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Updated on November 11, 2011

Right sided exudative pleuritis

X-ray of patient with chronic bronchitis (COPD) and respiratory failure. The signs are characteristic to main disease.
X-ray of patient with chronic bronchitis (COPD) and respiratory failure. The signs are characteristic to main disease. | Source
X-ray of patient with cystic fibrosis and respiratory failure. The signs are characteristic to main disease.
X-ray of patient with cystic fibrosis and respiratory failure. The signs are characteristic to main disease. | Source

Pulmonary insufficiency or some degree of respiratory failure occurs when the exchange of respiratory gases between the circulating blood and the ambient atmo sphere is impaired. The terms are used synonymously though the term respiratory failure generally refers to more severe lung dysfunction. The gaseous composition of arterial blood with respect to 02 and C02 pressures is normally maintained within restricted limits; pulmonary insufficiency occurs when the Pao2 is < 60 mmHg and the Paco2 is > 50 mm Hg, but pulmonary insufficiency or respiratory failure may be manifested by a reduced Pao2, with a normal, low, or elevated Paco2.

There are 3 pathogenic categories of diseases of the respiratory apparatus: (1) those manifested mainly by airways obstruction; (2) those largely affecting the lung parenchyma but not the bronchi; and (3) those in which the lungs may be anatomically intact but the regulation of ventilation is defective because of abnor mal musculoskeletal structure and function of the chest wall or primary dysfunc tion of the CNS respiratory center. The etiology and mechanisms of disease leading to the physiologic disturbances in each of these categories may differ, but the pattern of physiologic disturbance of lung function is quite similar. Lists the most commonly recognized chronic lung disorders in these catego­ries. These and acute disorders (e.g., pulmonary edema, pneumonia, shock lung) which may lead to pulmonary insufficiency.



1. Airways Obstruction

Chronic bronchitis (picture 1)


Cystic fibrosis (mucoviscidosis) (picture 2)


2. Abnormal Pulmonary Interstitium (Pulmonary Alveolitis, Interstitial Fibrosis)



Progressive systemic sclerosis

Rheumatoid lung

Disseminated carcinoma

Idiopathic fibrosis (Hamman-Rich syndrome)

Drug sensitivity (hydralazine, busulfan, etc.)

Hodgkin's disease

Systemic lupus erythematosus



Leukemia (all cell types)

3. Alveolar Hypoventilation Without Primary Bronchopulmonary Disease

Functional: Sleep, chronic exposure to CO2, metabolic alkalosis Anatomic abnormal respiratory center (Ondine's curse), abnormal chest cage (kyphoscoliosis, fibrothorax) Disordered neuromuscular function: Myasthenia gravis, infectious potyneuritis, muscular dystrophy, poliomyelitis, polymyositis Obesity.Hypothyroidism.

Pathophysiologic Changes in Airways Obstruction

The diseases in this category induce an abnormally high resistance to airflow in the bronchial tree. The causes vary with the etiology but include secretions, bron chial mucosal edema, bronchial smooth muscle spasm, or structural weakness of bronchial wall supports. An abnormally high effort, and therefore energy expendi ture, is required for ventilation to produce the necessary pressure differences be tween the mouth and alveoli during expiration and inspiration. The high resistance to airflow can profoundly affect the gas exchanging function of the lung in the alveoli by disturbing the distribution of ventilation to various parts of the lung with respect to regional perfusion by mixed venous blood.

The ventilation/perfusion ratio must be close to 1 for Pao2; and Paco2 to remain normal (80 to 100 mm Hg for Pao2; 40 ± 4 mm Hg for Paco2). Paco2 is below normal if there is high alveolar ventilation for the level of perfusion; high regional perfusion with respect to ventilation reduces 02 tension and content of pulmonary capillary blood, a more dire occurrence. The mixing of blood from such over-perfused regions with blood from regions with a normal ventilation/perfusion ratio causes hypoxemia, which is determined quantitatively by the proportion and composition of blood mixing with the normally oxygenated blood. A true shunt of 50% of mixed venous blood (02; saturation 75%) mixing with a similar proportion of fully oxygenated blood results in an Sao2 of 87% or a Pao2 of 53 mm Hg. Hypercapnia or a high Paco2 will not occur as long as regions of the lung are over-ventilated with respect to the regional perfusion (a high ventilation/perfusion ratio) so that C02 is expelled from the blood in large volumes and the regional capillary Pco2 is below the normal 40 mm Hg. The net mixed Paco2 remains normal in the presence of persistent hypoxemia. Arterial hypercapnia develops when total ventilation or regional ventilation is depressed so that regional hyperventilation sufficient to maintain the Paco2 at normal can no longer occur. Hyper capnia may occur with exacerbations of bronchitis, pneumonia, or status asthmaticus, or suppression of total pulmonary ventilation due to pharmacologic depression of the respiratory center by such agents as codeine, morphine, barbitu rates, or other sedatives.

The characteristic changes in lung volumes and ventilatory tests in intrathoracic airways obstruction are (1) reduced VC, (2) increased RV and FRC so that TLC may be normal or increased, and (3) reduced MW, FEV1, and airflow rates on expiration at all phases of the forced expiratory volume.

Diffuse Interstitial Fibrosis and Alveolitis

The pattern of physiologic abnormality in these diseases is strikingly different from that in airways obstruction. VC is reduced, usually with reduced RV, so that TLC is also reduced. However, tests of airways obstruction (e.g., the FEV1 and the MW) are usually normal. The Paco2 is usually normal and often below nor mal because of hyperventilation, and is almost never elevated. The Pao2, however, is mildly to moderately reduced at rest and more markedly reduced during exercise. The hypoxemia is caused by ventilation/perfusion imbalance and diffusion limitation by the structurally abnormal alveolar capillary membrane or by reduc tion in the total lung area for diffusion. Lung diffusing capacity for CO2 or O2 is characteristically low at rest and during exercise.

Unlike the case in obstuctive lung diseases, the major mechanical abnormality is increased lung stiffness (reduced lung compliance) with normal airway resist ance. Ventilatory drive is also increased, frequently causing hyperventilation at rest and during exercise, with associated hypocapnia. The reduced lung compli ance and the increased ventilatory drive and hypoxemia contribute to dyspnea, the outstanding symptom in this group of diseases.

Alveolar Hypoventilation Without Primary Bronchopulmonary Disease

Alveolar hypoventilation of this type occurs when pulmonary structure is intact but the regulatory function of ventilation in relation to whole body metabolism is disturbed. The pathognomonic manifestation of this imbalance between ventila tory and metabolic function is an elevated Paco2 (normal = 40 ± 4 mm Hg) and a concomitantly reduced PaO2 (PaO2 falls as alveolar Pco2 rises). Ventilation/perfu sion imbalances are usual in addition to alveolar hypoventilation. The alveolar to arterial 02 tension difference is therefore increased, contributing further to arte rial hypoxemia. Sometimes (e.g., in central depression of the respiratory center), the elevated Paco2 also results from a total alveolar hypoventilation; other times (e.g., in obesity and severe kyphoscoliosis), elevated Paco2 may result from both ventilation/perfusion imbalance and reduced overall alveolar ventilation.

The pathologic basis of alveolar hypoventilation in the presence of normal lung structure (see TABLE )vanes from weakness or paralysis of the ventilatory muscles (as in myasthenia gravis and infectious polyneuritis) to acquired or con genital damage to the medullary respiratory center. In most cases except obesity, lung compliance and airway resistance are unimpaired and voluntary hyperventi lation usually markedly improves blood gas composition.

Consequences of Respiratory Failure

Depressed arterial and tissue O2 tensions affect the cellular metabolism of all organs and, if severe, can cause irreversible damage in minutes. In addition, even moderate (< 60 mm Hg) alveolar hypoxia over days or weeks can induce pulmo nary arteriolar vasoconstriction and increased pulmonary vascular resistance which leads to pulmonary hypertension, right ventricular hypertrophy (cor pulmonale), and eventually right ventricular failure.

Elevated arterial and tissue CO2 tensions, however, affect mainly the CNS and the acid-base balance. Paco2 elevations, usually > 70 mm Hg, are associated with marked cerebral vasodilation, increased CSF pressure, and changes in sensorium ranging from confusion to narcosis. Papilledema occurs at these levels of hypercapnia when they persist for many days; it is reversed on lowering of the Paco2.

Ventilatory responsiveness to CO2 as a stimulus to breathing is diminished by persistent hypercapnia, largely due to the increase in blood and tissue buffers resulting from the generation of bicarbonate by the kidney in response to the elevated Paco2. The increased buffering capacity which also occurs in the CNS diminishes the decrease in pH which occurs with increases in plasma and tissue C02 levels. The contribution of pH to the ventilatory stimulus of CO2 is therefore diminished. This can be seen in the relationship between pH, bicarbonate concen tration, and Paco2 in the Henderson-Hasselbalch equation. This effect on ventila tory responsiveness is reversed when the Paco2 returns to normal.

Sudden rises in Paco2 occur much faster than compensatory rises in extracellu lar buffer base; this causes marked acidosis (pH < 7.3), which additionally contributes to pulmonary arteriolar vasoconstriction, reduced myocardial contractility, hyperkalemia, hypotension, and cardiac irritability. This type of acidosis is rapidly reversed by increasing alveolar ventilation by mechanical hy­perventilation if necessary and rapidly lowering Paco2 to normal levels.


The nebulizer is designed for inhalation therapy and treatment of asthma, bronchitis, emphysema and upper respiratory tract disorders. A mouthpiece for adults and children or a mask for infants accompanies the machine
The nebulizer is designed for inhalation therapy and treatment of asthma, bronchitis, emphysema and upper respiratory tract disorders. A mouthpiece for adults and children or a mask for infants accompanies the machine
Continuous Positive Airway Pressure (CPAP) devices maintain open airways in patients who have been diagnosed with Obstructive Sleep Apnea (OSA). This device provides airflow at pressures prescribed by a patient's doctor during sleep. MedNow carries m
Continuous Positive Airway Pressure (CPAP) devices maintain open airways in patients who have been diagnosed with Obstructive Sleep Apnea (OSA). This device provides airflow at pressures prescribed by a patient's doctor during sleep. MedNow carries m

Pulse oxymetry

Objective measures of monitoring for hypoxaemia include pulse oximetry. This is a good bedside monitor if its limitations are recognised. It is a continuous and non-invasive monitor. Its principal limitation is that, in patients who are receiving supplemental oxygen, it will not reliably detect hypoventilation. Hypoventilation must, in the clinical environment, usually be confirmed by measurement of the PaCO2 by arterial blood gas analysis.

Infrequently, inadequate oxygenation with normal oxygen saturation may occur in cases with very gross anaemia or in situations where the cells are unable to utilise oxygen such as severe sepsis or cyanide poisoning. Mixed venous oxygen saturation measurements may be helpful in these situations but this is only practical in an intensive care setting with a pulmonary artery catheter in situ. Inaccurate readings may also be obtained in patients who have high carboxyhaemoglobin or methaemoglobin concentrations, high concentrations of endogenous or exogenous pigments such as bilirubin or methylene blue as well as with cold extremities and movement artifact.

In most circumstances, the trend in oxygen saturation is more important than the value per se as this can indicate whether the patient is responding to therapy or deteriorating.

Arterial blood gases

This is the ‘gold standard’ monitor of ventilation. Arterial blood gases are needed to obtain accurate data, in particular, evidence of hypoventilation (raised PaCO2) as a reason for hypoxaemia. Arterial blood gases may also give an indication of the metabolic effects of clinically important hypoxaemia. Formal blood gas analysis may also afford accurate estimates of carboxyhaemoglobin and methaemoglobin, the former being particularly important in patients rescued from fires. However, a blood gas is a painful, invasive and intermittent procedure that is time consuming in the setting of a busy ward.

A spectrum of treatments exist for the hypoxic patient. These range from supplemental oxgyen therapy and simple measures such as altering posture. Even sitting a patient up improves FRC, compared with the patient lying down. Physiotherapy can be useful, but most specifically in those patients with copious airways secretions. If the patient is still hypoxic after these ward-based treatments, measures such as continuous positive airway pressure, non-invasive ventilation or invasive ventilation may be required, usually in the setting of an intensive care unit.

Therapy of Respiratory Failure

The detection of respiratory failure from any cause and its therapy depend on analysis of arterial blood Po2, Pco2. and pH; faculties for such analyses are essential for effective therapy.

When the Paco2 is not elevated and only hypoxemia exists, the therapy of respi ratory failure may be different than when both blood gas abnormalities are pres ent. All available technics for reducing airways obstruction (i.e., bronchodilators, tracheal suction, moisturization, and chest physiotherapy) may be required in the treatment of respiratory failure. Ultimate recovery demands recognition of every factor leading to respiratory failure and use of therapeutic agents that can reverse these factors while the patient receives respiratory support by mechanical ventila tion and high O2 mixtures.

Oxygenation: The concentration of enriched O2 selected to overcome hypoxe mia should be the lowest concentration that will provide an acceptable Pao2. Inspired O2 concentrations exceeding 80% have significant toxic effects on the alveolar capillary endothehum and bronchi and should be avoided unless neces sary for the patient's survival. Concentrations of inspired O2 of < 60% are well tolerated for long periods without manifest toxicity. Most patients tolerate a Pao2 > 55 mm Hg quite well. However, Pao2 values in the range of 60 to 80 mm Hg are most desirable for adequate delivery of 02 to tissues and prevention of increases in pulmonary artery pressure from alveolar hypoxia. Pao2 values between 55 and 80 mm Hg are acceptable. For pulmonary insufficiency resulting from ventila­tion/perfusion imbalances as associated with obstructive lung disease or with combined diffusion limitation and ventilation/perfusion imbalance, inspired O2 concentrations of > 40% are usually not required. Most patients with these types of physiologic dysfunctions receive adequate oxygenation with 25 to 35% inspired O2. Such concentrations can be given readily by face masks designed to deliver specific concentrations at the mouth, or by nasal cannulas. With face masks, the flow of O2 required for a given percentage is predetermined by the mask design.

With nasal cannulas, the flow of 02 can only be estimated. Such estimates require knowledge of the total minute ventilation of the patient in room air and the duration of inspiration and expiration. If the time m both phases of ventila tion is equal, only half the flow of 100% 02 from the 02 reservoir can be assumed to be delivered to the patient. Thus, for a ventilatory rate of 10 L/min and a 4 L/min flow of 100% 02 through nasal cannulas, the 02 concentration delivered to the patient would be estimated at

(2 X 100%) + (8 X 21%) = 37% O2


If the minute ventilation rises and the 02 flow is unchanged, the inspired concen tration of O2 decreases. Because of the uncertainties in such estimates (including the admixture of 02 with room air, mouth breathing, varying respiratory rate), the actual Pao2 tension must be monitored regularly to determine the results of ther apy.

When higher concentrations of 02 must be delivered at the nose and mouth to achieve acceptable Pao2 levels (e.g., in severe pulmonary infection, shock lung, pulmonary edema), concentrations of O2 delivered by nasal cannulas are inadequate and tight-fitting face masks capable of delivering up to 100% inspired O2 may be necessary.

If adequate oxygenation by face mask requires continuous administration of O2 concentrations of more than 80%, tracheal intubation and mechanical ventilation can usually provide adequate oxygenation with a lower concentration of inspired O2, minimizing the risk of O2 toxicity. This provides larger tidal volumes and a more favorable ventilation/perfusion ratio than does spontaneous breathing.

No matter which technic of O2 delivery is used, the patient's comfort and bron chial clearance demand that the inspired gas be moisturized by passing it through a water trap.

Managing elevated PaCO2: In airways obstruction or when the ventilatory appa ratus or its CNS control fails, elevated blood and tissue Pco2, as well as hypoxemia, must be treated. The urgency and necessity of rapid lowering of an abnormally elevated arterial and tissue Poo2 may be questioned when respiratory acidosis is compensated. Elevated Paco2, whatever the primary cause, indicates low alveolar ventilation with respect to body metabolism. A Paco2 even to levels of 70 or 80 mm Hg is generally well tolerated as long as compensated by an increase in buffer base, which keeps arterial pH near normal; the primary consid eration must always be adequate oxygenation and the state of acidosis of the blood. If supplying enriched 02 during spontaneous ventilation leads to a continuously rising Paco2 and acidosis, then mechanical ventilatory assistance is required to control the Paco2.

Mechanical ventilation: In nonacutely ill patients with respiratory failure, an IPPB apparatus can be applied by a mouthpiece and nose clip or a face mask for intermittent therapy throughout the day. This technic is not effective if respiratory failure is acute and severe. If continuous mechanical ventilatory assistance is re quired, the patient should have tracheal intubation through either the mouth or nose. Intubation allows easier suctioning and a wide variety of technics of me chanical ventilation to be applied as required. After the trachea is intubated, the tube may be left in place for as long as 10 to 14 days if necessary before a tracheostomy must be performed or the patient returns to spontaneous ventila tion. Short-term tracheal intubation without tracheostomy may be adequate for treating acute episodes of respiratory failure due to pulmonary infection, severe left heart failure, pulmonary edema, inadvertent depression of ventilation by sedatives and analgesic agents, uncontrolled bronchospasm, pneumothorax, or combinations of the above.

Any mechanical ventilator, particularly if the driving pressure into the lung is high, may cause reduced venous return to the thorax, reduced cardiac output, and a consequent drop in systemic BP.This is particularly common when inspiratory positive pressures are high, hypovolemia is present, and vasomotor control is inadequate due to drugs, peripheral neuropathy, or muscle weakness.

There are 3 main types of mechanical ventilators for treating acute respiratory failure: (1) pressure-controlled, (2) volume-controlled, and (3) body-tank-type.

Intermittent positive pressure breathing (IPPB) apparatus: Ventilation is induced with a mechanical ventilator which delivers positive pressure during inspiration but allows the pressure in the airway to return to atmospheric pressure during the expiratory phase by spontaneous exhalation (see above). Various kinds of appara tus will introduce gas into the lungs by delivering the desired inspired mixture at a higher than atmospheric pressure through a face mask, mouthpiece, or intratracheal tube. All have similar features of control and performance. Ventilatory as sistance is provided only during inspiration; expiration is passive. A slight inspiratory effort by the patient (about 1 cm H20 negative pressure) opens a valve that initiates the flow of gas from the apparatus to the lungs. In most types of apparatus, a sensitivity control knob determines the ease with which inspiratory effort initiates inspiratory flow. Flow ceases when the pressure in the mouth or intratracheal tube reaches a positive pressure that has been preset by the pressure control on the apparatus. When inspiratory flow ceases, expiration occurs pas sively through an expiratory valve. The tidal volume delivered to the patient de­pends on the preset pressure at which the inspiratory flow ceases. In normal individuals, peak positive pressures of 15 cm H20 usually provide tidal volumes of 800 to 1000 ml. If bronchial obstruction, obesity, stiff lungs, or thoracic deformity is present, positive pressures > 20 cm H20 may be required to achieve normal tidal volumes. Newer devices can achieve inspiratory pressures of up to 60 cm H20. Such pressures may be required under circumstances of severely reduced lung compliance or increased airway resistance.

Moisture in the inspired gas or aerosol medications can be delivered by a nebu lizer connected to the inspired gas flow.

Inspired gas flow rates of about 40 to 60 L/min are usually adequate, even in tachypndc states in which higher than normal flows are required. Excessively high flow rates may accentuate uneven distribution of inspired gas, especially in bron chial obstruction, and may result in high positive pressures in the proximal bron chi before an adequate tidal volume can be introduced. The inspiratory phase may then be unnecessarily short and the tidal volume inadequate for effective gas exchange.

In pressure-controlled ventilators, breathing frequency may be determined by allowing the patient to initiate the inspiratory effort and determine his own rate, or, when necessary, an automatic frequency control predetermines a rate and will initiate breathing automatically. The frequency control on most apparatus also allows automatic initiation of a tidal volume in a patient breathing spontaneously if a period of apnea longer than a preset duration occurs.

Volume-controlled ventilators: A preset tidal volume is delivered to the patient regardless of the pressure required to deliver the inspiratory volume. Expiration is passive. Controls vary the inspired 02mixture, inspiration and expiration time, and ventilatory frequency. Humidification and nebulization are provided. These ventilators are particularly useful for maintaining adequate alveolar ventilation regardless of rapid changes in the airway resistance or pulmonary compliance while the patient is being ventilated. Volume-controlled ventilators are in general selected most commonly for ventilatory support in the setting of intensive care.

Tank-type body ventilators: These can be used when ventilation is to be me chanically maintained for a prolonged period and when tracheostomy or tracheal intubation is not indicated. Such ventilators were commonly used prior to the availability of the mechanical ventilators discussed above. A new type of thoracic ventilator allows the patient to lie in a flexible plastic garment extending from the neck to the thighs with a rigid support overlying the thorax only, leaving the patient's arms free.

Positive end-expiratory pressure (PEEP): This term refers to ventilation in which a positive pressure is imposed in the airway at the end of expiration. Thus with PEEP, inspiration proceeds by imposing a positive pressure in the airway. After peak pressure and tidal volume are reached, expiration proceeds unobstructed. However, exhalation ceases at a preset expiration pressure that is set by an exha lation valve sensitive to pressure and placed in the exhalation part of the ventila tor or tracheal tube. If a Pao2 of 50 to 70 mm Hg cannot be achieved with 60% inspired 02 using positive pressure ventilatory assistance, a continuous PEEP of 3 to 15 cm H20 may be tried to induce further expansion of the lung, improve the ventilation/perfusion ratio, and reduce shunting. Since the procedure is not innocuous and complications are directly related to the magnitude of the endexpiratory pressure, the lowest level of PEEP that achieves an adequate Pao2 should be applied. The major complications of PEEP are decreased venous return, reduced cardiac output, and pneumothorax. Application of PEEP to a severely ill patient is best done by an individual experienced with this technic.

Continuous positive airway pressure (CPAP): In this technic, during spontane ous breathing, a positive pressure is applied during the entire respiratory cycle (during inspiration and expiration). In this regard, exhalation bears some rela tionship to pursed-Up breathing. The technic may be applied by a head canopy that controls the ambient airway pressure with or without intubation. When the patient has an intratracheal tube, CPAP can be applied by a specially modified T piece in which a reservoir bag is placed in the expiratory line and the expiratory pressure is controlled by varying the degree of occlusion of the tailpiece of the bag. The term continuous positive pressure breathing (CPPB) is synonymous with CPAP and the term continuous positive pressure ventilation (CPPV) has been used instead of CPPB when ventilation is controlled by a mechanical ventilator rather than spontaneously

Maintenance of clear airways: Clearing of secretions from upper and lower air ways is crucial to treating respiratory failure. Since alveolar gas is 100% humidi fied at body temperature, room air or inspired gas delivered from a tank tends to dry out mucous membranes and add to the difficulty of raising secretions. The inspired stream delivered through a positive pressure breathing apparatus must be fully moisturized to ensure reduced viscosity of secretions. This can sometimes be achieved by heated nebulization, which highly moisturizes the inspiratory stream.

Physical therapy technics such as chest percussion several times/day in severely ill patients loosen secretions, allowing their removal by tracheal suction or spon taneous cough.

Tracheal suction should be performed frequently through the mouth, nose, or tracheal tubes using sterile catheters and following other such precautions to minimize infection. In general, tracheal and lower airways suction without an intratracheal tube or tracheostomy by insertion of the suctioning catheter into the posterior pharynx is usually unsuccessful because of the difficulty of introducing the catheter past the vocal cords. Inadequate removal of secretions is an indica tion for tracheal intubation, which allows easy access to the upper and lower airways and minimizes the risk of aspiration of stomach contents.

Patient on Long Term Oxygen Therapy
Patient on Long Term Oxygen Therapy | Source
The internal auto-recharge power cartridge enables easy movement between AC power outlets without interruption of oxygen therapy and can keep the oxygen flowing for up to 5.1 hours. Long lengths of tangled oxygen tubing are no longer needed to move a
The internal auto-recharge power cartridge enables easy movement between AC power outlets without interruption of oxygen therapy and can keep the oxygen flowing for up to 5.1 hours. Long lengths of tangled oxygen tubing are no longer needed to move a | Source


Long Term Oxygen Therapy (picture 3) relates to the provision of oxygen therapy for continuous use at home for patients with chronic hypoxaemia (PaO2 at or below 7.3kPa (55mg). The oxygen flow rate must be sufficient to raise the waking oxygen tension above 8 KPa, (60mmHg).

Clincians usually prescribe LTOT where this is needed for at least 15 hours per day. For children this may cover 24 hours per day, but often apply to sleeping periods only.

Ambulatory oxygen may also be indicated in patients on LTOT to facilitate their mobility and quality of life.

Vitalair's dedicated oxygen concentrator service is there to help and support patients undergoing Long Term Oxygen Therapy. Having a ready supply of oxygen at home will help improve patients' quality of life, allowing them to enjoy the benefits of living at home.

Vitalair has invested in new concentrator technologies capable of delivering up to 5 litres per minute of therapeutic oxygen in the home. Each unit is known for its high performance, easy maintenance, and unmatched reliability.

Vitalair (picture 4) has also developed a longer-lasting high capacity cylinder, which can provide up to 20 hours of back-up oxygen supply. The size makes it easier to handle and to store, while the capacity means fewer changeovers are needed when administering oxygen. The permanently live contents gauge allows patients to see how much gas is left in the cylinder at all times.

Since patients only use back-up cylinders very occasionally, we cannot predict when a cylinder replacement is needed.


A Oxygen Concentrator
Now you can have the freedom to travel with ease or relax at home in comfort with a portable, reliable and quiet oxygen concentrator.

B Devilbiss Pulse Dose Oxygen Conserving Device
Pulse dose oxygen conserving technology is on the leading edge of oxygen therapy. Unlike other oxygen regulators that simply limit the flow of oxygen, the Devilbiss Pulse Dose delivers a consistent dose of oxygen at the very moment it is most beneficial.

C Portable Compressed Oxygen System
Using light weight aluminum cylinders, portable compressed oxygen systems can meet the needs of ambulatory patients or for short trips in the outdoors.

D Invacare HomeFill Oxygen System
The HomeFill oxygen system allows patients to fill there own high pressure cylinders from a concentrator. The HomeFill is a multi-stage pump that simply and safely compresses oxygen from a specially equipped concentrator into oxygen cylinders.


A Devilbiss 9000D CPAP
The quietest CPAP available. Convenient touch keypad control. Operating pressure range. 0, 10, 20, 30 or 45 minute pressure delay options. Push button altitude compensation. Monitors compliance while breathing. Includes travel bag for transporting.

B HC220 Fisher & Paykel
The HC220 humidified CPAP system offers an adjustable range of warm to heated humidification. Heated humidification with CPAP provides more effective treatment, so you too can have the lifestyle only a good night's sleep can bring.

C Remstar® Plus CPAP System
Full featured unit. All-new icon based display. Integrated humidification controls. Easy set-up. Unique new session meter records number of sessions that last more than 4 hours.

Picture 5

Liquid oxygen is another type of oxygen therapy alternative. It consists of a stationary unit that is filled with oxygen that is cooled to below zero then is given to the patient in a comfortable gas form. Liquid oxygen has portable units as well tha
Liquid oxygen is another type of oxygen therapy alternative. It consists of a stationary unit that is filled with oxygen that is cooled to below zero then is given to the patient in a comfortable gas form. Liquid oxygen has portable units as well tha
CPAP Moisture Therapy gel
CPAP Moisture Therapy gel | Source
This is a Non-Petroleum-Based Skin Care Emollient with Aloe Vera, Emu Oil, Vit. A & E to prevent the skin lesions in oxygen therapy.
This is a Non-Petroleum-Based Skin Care Emollient with Aloe Vera, Emu Oil, Vit. A & E to prevent the skin lesions in oxygen therapy. | Source
Hyperbaric oxygen therapy device
Hyperbaric oxygen therapy device | Source
Hyperbaric oxygen therapy device in action
Hyperbaric oxygen therapy device in action | Source

CPAP Moisture Therapy

Apply CPAP Moisture Therapy to facial area where mask meets the skin and inside the the nasal passage before beginning therapy (picture 6).

Repeat this process as often as needed to maintain soft skin and eliminate discomfort from dry/cracking skin.

Technology using CPAP therapy to assist those who have been diagnosed with sleep apnea problems may often result in skin irritation and discomfort in the nasal area. For this reason, CPAP Moisture Therapy may be useful to reduce this trauma.

CPAP Moisture Therapy is offered as a preventative to the skin irritation that may accompany this therapy for sleep apnea and may promote a greater compliance to treatment.


The problem with dry nose associated with oxygen delivery by means of plastic cannula has been well documented by care givers at every level for decades.

Nasal dryness as well as other skin dryness can occur apart from the use of oxygen or continuous positive airway pressure (CPAP) devices due to dry climates as well as changing seasons. It may be useful in addressing these issues (picture 7).

Oxygen users
Apply RoEzIt Dermal Care before beginning oxygen therapy and at intervals as needed during treatment to lubricate nasal passages, as well as over the ear where friction from tubing may cause discomfort.

Main forms of respiratory insufficiency (according to B. E. Votchal).

1. Central form – is the result of inhibition of respiratory center (narcosis, drugs, trauma, atherosclerosis, stroke etc.).

2. Neuro-muscular form – is the result of disturbance of conduction of signals from central nervous system to muscules (miastenia, poliemielitis etc.).

3. Thoraco-diafragmal form – is the result of reduction of chest movements (chest degormation, kifoscoliosis etc.).

4. Pulmonary form – is the result of pulmonary problems:

a) decrease of pulmonary tissue (pneumonia, tumor);

b) decrease of pulmonary tissue elasticity (fibrosis);

c) narrowing of bronchial system (asthma, stenosis).

Clinical and instrumental characteristics of main types of ventilation insufficiency: obstructive, restrictive and mixed.

1. Obstructive type is caused by:

a) spasm; b) mucous odema; c) hypersecretion; d) scar narrowing; e) endobronchial tumor; f) external pressuring of bronchus.

Diagnostic crireria: dyspnoe after physical execiesing, dry cough, dry rales. Increasing of expiration period, on spirography– decrease of FEV1.

2. Restrictive type is caused by:

a) fibrosis; b) pleural disorders; c) pleural exudation; d) pneumoconiosis; e) tumors of lungs; f) pulmonectomia.

Diagnostic crireria: on spirography– decrease of VC.

3. Mixed type: both causes are aviable.


We can better understand the concepts behind hyperbaric oxygen (HBO) therapy by first gaining an understanding of some basic terms:

Hyperbaric Oxygen Therapy
Hyperbaric oxygen therapy describes a person breathing 100 percent oxygen at a pressure greater than sea level for a prescribed amount of time—usually 60 to 90 minutes.

Atmospheric Pressure
The air we breathe is made up of 21 percent oxygen, 78 percent nitrogen and 1 percent carbon dioxide and all other gases. The air exerts pressure because air has weight and this weight is pulled toward the earth's center of gravity. This pressure is expressed as atmospheric pressure. Atmospheric pressure at sea level is 14.7 pounds per square inch (psi).

Hydrostatic Pressure
As we climb above sea level the atmospheric pressure decreases because the amount of air above us weighs less. When we dive below sea level the opposite occurs (the pressure increases) because water has weight that is greater than air. Thus, the deeper one descends under water the greater the pressure. This pressure is called hydrostatic pressure.

Atmospheres Absolute (ATA)
The combination (or the sum) of the atmospheric pressure and the hydrostatic pressure is called atmospheres absolute (ATA). In other words, the ATA or atmospheres absolute is the total weight of the water and air above us.

Terms Used to Measure Pressure
We use various terms to measure pressure. HBO therapy involves the use of pressure greater than that found at the earth's surface at sea level. This is called hyperbaric pressure. The terms or units used to express hyperbaric pressure include millimeters or inches of mercury (mmHg, inHg), pounds per square inch (psi), feet or meters of sea water (fsw, msw), and atmospheres absolute (ATA).

One atmosphere absolute, or 1-ATA, is the average atmospheric pressure exerted at sea level, or 14.7 psi. Two-atmosphere absolute, or 2-ATA, is twice the atmospheric pressure exerted at sea level. If a physician prescribes one hour of HBO treatment at 2-ATA, the patient breathes 100 percent oxygen for one hour while at two times the atmospheric pressure at sea level. The devices for HBO are presented on pictures 8-9.

While some of the mechanisms of action of HBO, as they apply to healing and reversal of symptoms,are yet to be discovered, it is known that HBO:

1) greatly increases oxygen concentration in all body tissues, even with reduced or blocked blood flow;

2) stimulates the growth of new blood vessels to locations with reduced circulation, improving blood flow to areas with arterial blockage;

3) causes a rebound arterial dilation after HBOT, resulting in an increased blood vessel diameter greater than when therapy began, improving blood flow to compromised organs;

4) stimulates an adaptive increase in superoxide dismutase (SOD), one of the body's principal, internally produced antioxidants and free radical scavengers; and,

5) aids the treatment of infection by enhancing white blood cell action and potentiating germ-killing antibiotics.

While not new, HBO has only lately begun to gain recognition for treatment of chronic degenerative health problems related to atherosclerosis, stroke, peripheral vascular disease, diabetic ulcers, wound healing, cerebral palsy, brain injury, multiple sclerosis, macular degeneration, and many other disorders Wherever blood flow and oxygen delivery to vital organs is reduced, function and healing can potentially be aided with HBO. When the brain is injured by stroke, CP, or trauma, HBO may wake up stunned parts of the brain to restore function.

Contributors and acknowledgements

Pulmonology facet of the department of internal medicine, Ternopil state medical University, Ternopil- Ukraine. Special thanks to Dr. Andrei Lepyavko Andreivich (MD)
Pulmonology facet of the department of internal medicine, Ternopil state medical University, Ternopil- Ukraine. Special thanks to Dr. Andrei Lepyavko Andreivich (MD) | Source
The greatest mukite
The greatest mukite | Source

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      Funom Theophilus Makama 7 years ago from Europe

      yeah, just as I have said earlier. Dr. Henry, thanks for your comments. Try following my clinical hubs and it will surprise you how I get comments from these medical establishments... How they know about my profile? Seriously I am yet to know about that, notwithstanding, I am enjoying and loving it. Thank you all.

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      Dr. Henry! 7 years ago

      All these comments? When? This is really intimidating just as you said earlier. But I think you are doing a great job

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      Detroit Medical Center, MI 7 years ago

      Patients with severe acute respiratory failure (ARF) should be referred for treatment using extracorporeal membrane `oxygenation (ECMO), rather than using conventional ventilator management, to improve their chances of survival without disability. ECMO would be cost-effective in the UK and other countries with similar health care costs. These are the conclusions of an Article published Online First and in a forthcoming edition of The Lancet, written by Dr Giles Peek, Department of Cardiothoracic Surgery and Extracorporeal Membrane Oxygenation, Glenfield Hospital, Leicester, UK, Professor Miranda Mugford, University of East Anglia, UK, and Professor Diana Elbourne of the London School of Hygiene and Tropical Medicine, UK, and colleagues. ECMO has already been a vital tool for battling swine flu and will be essential during the northern hemisphere winter when cases could rise dramatically again.

      Severe ARF causes high mortality in adults despite improvements in ventilation techniques and other treatments (eg, steroids, inhaled nitric oxide). Conventional management is by intermittent positive-pressure ventilation where oxygen-enriched air is blown into the lungs at high pressure, this in turn causes oxygen toxicity and pressure injury to the lung tissue on top of the underlying lung disease, delaying or preventing recovery. ECMO is an alternative which uses heart-lung bypass technology to provide gas exchange outside the body, allowing time for the lung treatment and recovery. Heparin is also given to prevent the blood clotting when it passes through the ECMO system. In this study, the authors compared treatment by a specialised ECMO team with care from specialist intensive care unit teams using conventional ventilation, and also assessed the cost-effectiveness of referral for ECMO care. In this UK-based randomised controlled trial, 180 adults were randomly assigned to receive continued conventional management (90) or ECMO (90). Eligible patients were aged 18-65 years and had severe but potentially reversible respiratory failure. The primary outcome was death or severe disability at 6 months after randomisation. Data about resource use and economic outcomes (quality-adjusted life-years [QALYs]) were collected.

      The researchers found that 68 of the 90 patients (75%) assigned to consideration of ECMO actually received it. Of those referred for consideration of ECMO, 63% survived to 6 months without disability compared to 47% of those who were assigned to conventional management. This is equivalent to 1 extra survivor without disability for every 6 patients treated. Consideration of ECMO treatment led to a gain of 0.03 QALYs at 6-month follow-up. Use of modelling, making assumptions about life expectancy, costs and quality of life after 6 months, predicted that the cost per QALY of ECMO referral as £19,252. The cost per case was twice that for conventional treatment, but the cost-effectiveness was still well within the range regarded as cost-effective by health technology assessment organisations such as the UK's National Institute for Health and Clinical Excellence (NICE).

      The authors say: "This study shows a significant improvement in survival without severe disability at 6 months in patients transferred to a specialist centre for consideration for ECMO treatment compared with continued conventional ventilation."

      They conclude: "The cost-effectiveness of ECMO would be improved if costs of both transport and provision of the technique could be reduced...We are confident that ECMO is a clinically effective treatment for acute respiratory distress syndrome, which also promises to be cost effective in comparison with other techniques competing for health resources."

      Dr Peek adds*: "Swine flu causes a viral pneumonia which can result in severe respiratory failure in young adults, we have already used ECMO during the first wave of the pandemic with good effect and we are expecting ECMO to prove an invaluable weapon in the fight against the winter resurgence of the infection, as has already been seen during the Australasian winter."

      In an accompanying Comment, Dr Joseph B Zwischenberger, University of Kentucky College of Medicine, Lexington, KY, USA, and James E Lynch, ECMO programme director, University of Texas Medical Branch, Galveston, TX, USA, conclude: "The CESAR group should be congratulated on completion of such a complex and large trial. The debate that will surround this study reflects the difficulty of this type of research in the critically ill patient. This study will likely provide ammunition for both those in favour and those against the use of ECMO in the adult population."


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      Marshfield Clinic 7 years ago

      What is "Chronic Obstructive Pulmonary Disease" or "COPD"?

      Chronic obstructive pulmonary disease or COPD is a very common disorder in the United States, and most of the world. Smoking cessation programmes in the United States have started to lessen the impact of chronic obstructive pulmonary disease, especially emphysema. However in other countries; in Europe, China, and Japan, smoking is rampant. Everybody's doing it, so chronic obstructive pulmonary disease continues to be a really serious problem, especially emphysema. Emphysema is most commonly caused by smoking. There are forms of emphysema that are inherited. There are some chemical disorders that can occur in the body, such as alpha-1 antitrypsin deficiency, that can cause a form of emphysema, but those are relatively rare. Smoking is, by and large, the main issue. We need to address the fact that the more you smoke, the higher your chances of developing these very, very debilitating disorders.

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      Contra Costa Regional Medical Center 7 years ago

      What is respiratory failure?

      Respiratory failure is a condition where the lungs have failed and they failed either in one of two areas. They've either failed in their ability to bring oxygen into the bloodsteam in adequate amounts or they failed in their inability to clear CO2. C2 is the fumes of metabolism and if they accumulate too high can cause death. The process of moving your carbon dioxide levels in your bloodstream from normal up a place where it causes death, the intermediate stages will cause unconsciousness, inability to even function or think clearly. Just like oxygen, if it gets too low in your bloodstream can cause serious malfunctioning of not only of your brain but your heart and when it gets so low that it can no longer support metabolism or cellular respiration then the organism will die.

      What are the most common causes of respiratory failure?

      Most common causes of respiratory failure include chronic obstructive pulmonary disease which is the fourth major cause of death in the United States now, emphysema, chronic bronchitis and of the four top ones is the only one that is increasing in frequency. The others are starting to lessen just a little bit like cancer, stroke, heart attack and the rest. But COPD, chronic obstructive pulmonary disease, is still on the increase. And it causes death by a combination of too high C2 too low oxygen. We also have other problems such as the adult respiratory distress syndrome which is the form of pulmonary edema that will kill a patient because they can't get enough oxygen into their bloodstream, however, the most common cause of death in that situation continues, the way a person continues on in ARDS is usually from infection not from hypoxemia which is the word for too low oxygen in the blood. The other main problem though with death from respiratory failure includes pneumonias, interstitial lung disease, all of these chronic illnesses that will afflict the lung can lead eventually to respiratory failure and then to death.

      What are the most common symptoms of respiratory failure?

      The most common symptoms of respiratory failure of course is breathlessness, the feeling that you're sufficating, that you're struggeling with each breathe. We have a term that says the work of breathing. With the term work of breathing what we mean by that is that the work that a person has to put into taking a breath is very minumal. For instance if you look at how much oxegyn you consume per minute, and then allocate each of the ten organ systems with a certain percentage of the consumption of that oxegyn. You'll find that the lung in order to do its job requires about 3 percent of the oxygen that is consumed by minute to work the pumps, and get the oxygen in, and distribute it to the rest of the body.The other organ systems like the brain, and the kidneys, and the heart consume a lot more oxygen than does the machinary in the body that brings in the oxygen. In resporitory failure, that work of breathing starts to decline dramatically. So you may see a patient in resporitory failure that the lung is requiring 25% of the oxygen just to take a breathe and move the air in and out. When that happens that means you're stealing oxygen away from the other systems that are much more used to higher levels of oxygen, and they start to shut down. So that oxygen becomes the sailable component with in this whole system much like a business. Where one part starts to shut down, requires more and more of the resources to run it and after a while it can kill the whole organism. So when the lung goes into resporitory failure, it starts demanding more of the oxygen than it would normally use. That then puts big stresses on other portions of the body such as the hearts ability to contract pump by pump goes down with the lack of oxygen. It needs a lot of oxygen to do its job. If it's not getting it because the lungs are demanding it then it starts to fail, as do the kidneys, as do the brain, and GI tract.

      How is respiratory failure treated?

      Respiratory failure is almost always treated by placing the patient in the intensive care unit, and then as we start to administer oxygen we check blood gases. That means that we take a little needle and place it into the artery, pull off arterial blood and then analyze it for its oxygen content, its CO2 content, and also its PH. Given that information, we can tell then, quite precisely, how much oxygen to add. Or, if the CO2 is climbing, we know that we are going to have to put a tube through the mouth, down into the lungs, blow up a little cuff at the end of the tube so it seals everything off, and then supply pressure to keep the lungs open, and then flush out the CO2. CO2's concentration in the lung is directly proportional to the volume of gas that you can get down in there to flush it out. So, as it starts to climb, you have to add more and more alveolar ventilation in order to flush that out. We find that we can do a lot to correct respiratory failure, which is determined, you have to remember, by two things: oxygenation and ventilation. Ventilation is the way we control CO2, and oxygenation is where, by virtue of the fact that we add more and more oxygen, we may add completely 100% oxygen to a patient that we are having a hard time oxygenating. Bearing in mind that we are starting off at approximately 21% oxygen on room air, we can go to 30%, 40%, 50%, and keep adding as much as we need to resolve that aspect of respiratory failure; whereas, with CO2, we can add more volume, more volume, more volume, and more volume to help flush out that CO2. There are limits, and at some point in time we can start getting into lung injury by too high an oxygen content; oxygen can burn the lung, too much volume and we can pop the lung. So, it has to be done very carefully and very knowledgably, and, at times, we run out of space and we do lose the patient because the respiratory failure overwhelms even our ability to do this. Nonetheless, there is a lot to do to resolve respiratory failure.


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      Alberta Health Services 7 years ago

      Drugs/Products Used in the Treatment of This Disease:

      Asmol CFC-free Inhaler (Salbutamol sulfate)

      Asmol uni-dose (Salbutamol sulfate)

      Atrovent Nebulising Solution (Ipratropium bromide)

      Chem mart Ipratropium (Ipratropium bromide)

      Chem mart Salbutamol (Salbutamol sulfate)

      GenRx Ipratropium (Ipratropium bromide)

      healthsense Ipratropium (Ipratropium bromide)

      healthsense Salbutamol (Salbutamol)

      Ipratropium (Terry White Chemists) (Ipratropium bromide)

      Salbutamol (Terry White Chemists) (Salbutamol sulfate)

      Ventolin Disks (Salbutamol sulfate)

      Ventolin Respirator Solution and Nebules (Salbutamol sulfate)

      Ventolin Rotacaps (Salbutamol sulfate)


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      Thomas Jefferson University Hospital 7 years ago

      How is Respiratory failure Diagnosed?

      The following basic investigations are useful to monitor patients with respiratory failure:

      Tidal volume and vital capacity - these measurements can be taken by simple 'spirometry'. They are especially useful to monitor progress in patients with respiratory inadequacy due to neuromuscluar problems, such as Guillain-Barre syndrome, in which the vital capacity decreases as the weakness increases.

      Blood gas analysis - blood gas measurements are required for diagnosis of respiratory failure by definition (see Disease Site). Alterations in oxygenation are also useful in monitoring respiratory failure. In addition, blood gas analysis enables disturbances in acid-base balance (acidosis or alkalosis) to be identified.

      Pulse oximetry - a light clip placed on the finger or earlobe gives a measure of blood oxygen saturation. This is not as reliable as arterial blood gas analysis, but is much easier and gives a continuous reading.

      Prognosis of Respiratory failure

      Respiratory failure is a severe condition that is generally terminal unless treated. Patients can be given supplemental oxygen, and mechanically ventilated if needed - although long-term ventilation has significant consequences. This may be because the patient's respiratory muscles become weak, or difficulties weaning the patient from the respirator - they may not be able to breathe for themselves (especially COPD patients).

      How is Respiratory failure Treated?

      The treatment of respiratory failure involves the following measures:

      supplemental oxygen - given initially via face mask

      control of secretions (physiotherapy)

      treatment of lung infection (antibiotics)

      control of airways obstruction (e.g. using bronchodilators, corticosteroids)

      limiting pulmonary oedema

      reducing load on respiratory muscles

      Finally, if the above measures are not effective, some form of respiratory support needs to be considered. There are many different devices and techniques used in providing respiratory support; they will not be discussed in detail. Broadly speaking, respiratory support techniques can be split into non-invasive and invasive techniques.

      Non-invasive techniques are used in conscious, cooperative patients, and are administered via face mask or nasal prongs.

      Invasive respiratory support is administered via an endotracheal tube or tracheostomy. The endotracheal tube is passed through the mouth, down the throat and through the larynx. A balloon is inflated at its tip to keep it lodged in the trachea, just under the larynx. Tracheostomy involves making an incision in the neck, and placing the tube directly into the trachea.

      Invasive respiratory support may cause significant complications, including: cardiac failure, lung infection, and barotrauma (e.g. Pneumothorax). Respiratory support also weakens the respiratory muscles, so spontaneous respiration has to be resumed gradually.

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      NHS Worcestershire Health Services 7 years ago

      What is Respiratory failure?

      Respiratory failure is a disease of the lungs.The respiratory system basically consists of a gas exchanging organ (the lungs) and a ventilatory pump (respiratory muscles and the thorax). Either or both of these can fail and cause respiratory failure. Respiratory failure occurs when gas echange at the lungs is sufficiently impaired to cause a drop in blood levels of oxgyen (hypoxaemia); this may occur with or without an increase in carbon dioxide levels. The definition of respiratory failure is PaO2 7kPa (55mmHg). Respiratory failure is divided into type I and type II.

      Type I respiratory failure involves low oxygen, and normal or low carbon dioxide levels.

      Type II respiratory failure involves low oxygen, with high carbon dioxide.

      Statistics on Respiratory failure?

      Respiratory failure is common, as it occurs in any severe lung disease - it can also occur as a part of multi-organ failure.

      Risk Factors for Respiratory failure

      Causes of Type I respiratory failure: disease that damage lung tissue, including pulmonary oedema, pneumonia, acute respiratory distress syndrome, and chronic pulmonary fibrosing alveoloitis.Causes of Type II respiratory failure: the most common cause is chronic obstructive pulmonary disease (COPD). Others include chest-wall deformities, respiratory muscle weakness (e.g. Guillain-Barre syndrome) and central depression of the respiratory centre (e.g. heroin overdose).

      Progression of Respiratory failure

      Type I respiratory failure occurs because of damage to lung tissue. This lung damage prevents adequate oxygenation of the blood (hypoxaemia); however, the remaining normal lung is still sufficient to excrete the carbon dioxide being produced by tissue metabolism. This is possible because less functioning lung tissue is required for carbon dioxide excretion than is needed for oxygenation of the blood.

      Type II respiratory failure is also known as 'ventilatory failure'. It occurs when alveolar ventilation is insufficient to excrete the carbon dioxide being produced. Inadequate ventilation is due to reduced ventilatory effort, or inability to overcome increased resistance to ventilation - it affects the lung as a whole, and thus carbon dioxide accumulates.Complications include: damage to vital organs due to hypoxaemia, CNS depression due to increased carbon dioxide levels, respiratory acidosis (carbon dioxide retention). This is ultimately fatal unless treated. Complications due to treatment may also occur.


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      Universitair Medisch Centrum St. Radboud 7 years ago

      Respiratory (RES-pi-rah-tor-e) failure is a condition in which not enough oxygen passes from your lungs into your blood. Your body's organs, such as your heart and brain, need oxygen-rich blood to work well.

      Respiratory failure also can occur if your lungs can't properly remove carbon dioxide (a waste gas) from your blood. Too much carbon dioxide in your blood can harm your body's organs.

      Both of these problems—a low oxygen level and a high carbon dioxide level in the blood—can occur at the same time.

      Diseases and conditions that affect your breathing can cause respiratory failure. Examples include COPD (chronic obstructive pulmonary disease) and spinal cord injuries. COPD prevents enough air from flowing in and out of the airways. Spinal cord injuries can damage the nerves that control breathing.


      To understand respiratory failure, it helps to understand how the lungs work. When you breathe, air passes through your nose and mouth into your windpipe. The air then travels to your lungs' air sacs. These sacs are called alveoli (al-VEE-uhl-eye).

      Small blood vessels called capillaries run through the walls of the air sacs. When air reaches the air sacs, the oxygen in the air passes through the air sac walls into the blood in the capillaries. At the same time, carbon dioxide moves from the capillaries into the air sacs. This process is called gas exchange.

      In respiratory failure, gas exchange is impaired.

      Respiratory failure can be acute (short term) or chronic (ongoing). Acute respiratory failure can develop quickly and may require emergency treatment. Chronic respiratory failure develops more slowly and lasts longer.

      Signs and symptoms of respiratory failure may include shortness of breath, rapid breathing, and air hunger (feeling like you can't breathe in enough air). In severe cases, signs and symptoms may include a bluish color on your skin, lips, and fingernails; confusion; and sleepiness.

      One of the main goals of treating respiratory failure is to get oxygen to your lungs and other organs and remove carbon dioxide from your body. Another goal is to treat the underlying cause of the condition.

      Acute respiratory failure usually is treated in an intensive care unit. Chronic respiratory failure can be treated at home or at a long-term care center.


      The outlook for respiratory failure depends on how severe its underlying cause is, how quickly treatment begins, and your overall health.

      People who have severe lung diseases may need long-term or ongoing breathing support, such as oxygen therapy or the help of a ventilator (VEN-til-a-tor). A ventilator is a machine that helps you breathe. It blows air—or air with increased amounts of oxygen—into your airways and then your lungs


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      West Penn Allegheny Health System 7 years ago

      Indications for ventilation in respiratory failure

      This is a difficult decision and should always take place in consultation with a senior doctor. If the patient is causing you or the referring medical or nursing staff significant worry, discuss with your seniors immediately.

      Click on indications for ventilation in the table on the left to obtain further essential information.

      The non-invasive methods of respiratory support described below are useful if the patient is likely to respond quickly (e.g. LVF, acute exacerbation of COPD). If the patient is in respiratory failure because of an illness that is likely to be prolonged (e.g. ARDS, pneumonia) then invasive ventilation is usually more appropriate.


      Continuous Positive Airway Pressure (CPAP) is an extremely useful technique for some forms of respiratory failure. CPAP systems can deliver high FiO2. CPAP works particularly well for cardiogenic pulmonary oedema and can allow time for medical therapy to work. It may also help in ARDS. The effect is more variable in other forms of respiratory failure.

      Non-Invasive Ventilation (NIV)

      Patients with hypercapnic, acidotic exacerbations of COPD should be offered Non Invasive Ventilation (NIV) on the medical wards at an early stage in the illness. This reduces mortality and the need for intubation. Most NIV equipment cannot deliver high FIO2.

      Think about NIV When called to see any patient with respiratory failure. Beware that if the patient is in distress then NIV is not appropriate. In this case the correct course of action would be to proceed to invasive ventilation as soon as possible. Always discuss with your senior cover.

      If the underlying disease is not likely to resolve quickly (e.g. pneumonia) and the patient becomes dependent on NIV, then invasive ventilation is likely to be the best option. This is because this group of patients do not tolerate even short periods without NIV. This will make it difficult to deliver other aspects of patient care e.g. feeding, drinking, mouth care..etc. This is different to COPD patients with acute exacerbations, as they can normally tolerate a few minutes off NIV to eat or drink.

      NIV can also be used as a bridge to invasive ventilation, but always discuss with your senior cover.

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      Mount Sinai Medical Center New York 7 years ago

      Acute Respiratory Distress Syndrome (ARDS) & Acute Lung Injury (/ALI)

      Acute Respiratory Distress Syndrome (ARDS) is under diagnosed. Often the diagnosis is never changed from the underlying condition (pneumonia, aspiration, pancreatitis etc). The diagnostic criteria are listed in the table opposite.

      It is the commonest cause of difficulty with ventilation in ICU. It is usually seen as part of a generalised inflammatory response with other organ dysfunction. If the lungs are the only failing organs, be suspicious of another cause of respiratory failure.

      Treatment is based on the treatment of the underlying disease. Supportive therapy with ventilation allows time to treat the cause. Ventilation can worsen the inflammatory process and cause further deterioration unless care is taken to avoid ventilator induced lung injury. There are no specific treatments. Diuresis is reasonable, but often difficult to achieve without worsening other organ perfusion.

      The underlying conditions that trigger ARDS can be either direct, if they affect the lungs (thoracic ARDS), or indirect (extrathoracic ARDS).

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      Landstinget Gavleborg 7 years ago

      Management of acute respiratory failure

      There are two components to the management of respiratory failure: emergency management (resuscitation), and definitive diagnosis and treatment of the underlying condition.

      Emergency management

      As always, this commences with an assessment of ABCDE. This approach is detailed elsewhere in this induction programme and most doctors will be very familiar with its principles. Make sure the airway is patent and protected, examine the patient and deal with life threatening emergencies. Gain i.v. access. Think about fluid therapy.

      How much oxygen?

      The simple answer to this is ‘enough’. If the SpO2 is normal, oxygen is not required.

      If the SpO2 is low, then high flow oxygen in the short term will do little harm. It should be titrated quickly downwards using SpO2 as a guide. Aim for SpO2 of 92%.

      In very few patients (those with clinically severe COPD who have compensated type II respiratory failure – a high bicarbonate with a high CO2) oxygen should be titrated upwards carefully with regular checks of the clinical status (mental state, ventilatory pattern) and blood gases (is CO2 rising?). These patients may hypoventilate when given too much oxygen. This may cause a respiatory arrest in severe circumstances, but more commonly will lead to profound hypoxaemia. This occurs when the FiO2 is reduced following a rise in CO2 (the hypoxia from the reduced FiO2 exacerbated by the high alveolar CO2).

      In these patients, aim for SpO2 of 88 –92%. Always assess the response of the patient to your intervention: e.g. has the SpO2 increased, has the CO2 increased?

      Definitive diagnosis and treatment

      Respiratory failure is NOT an adequate diagnosis. It is a description of a condition that results from many underlying disorders. It is impossible to properly direct further investigation and treatment without a diagnosis. Treatment of the underlying problem is beyond the scope of this review but thought should be given to diseases listed in the table on the left.

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      Vancouver Island Health Authority 7 years ago

      Ventilation – Perfusion (V/Q) mismatch

      V/Q mismatch is the presence of a degree of shunt and a degree of dead space in the same lung. It is a component of most causes of respiratory failure and is the commonest cause of hypoxaemia.

      Because of the complicated structure of the lungs, it is impossible to describe this condition in anatomical terms. A patient with this condition is likely to have areas in the lungs that are better perfused than ventilated and areas that are better ventilated than perfused. This occurs in normal lungs to some extent. The difference in V/Q mismatch is that the extent to which this occurs is significantly increased.

      Because of the flat upper portion of the Oxyhaemoglobin dissociation curve (fig 4), blood leaving the relatively healthy alveoli will have an oxygen saturation of about 97%. Blood leaving alveoli that do not have optimum V/Q ratios will have a much lower oxygen saturations . The admixture of all the blood leaving the alveoli results low oxygen saturations and hypoxaemia.

      In general, this cause of respiratory failure responds to oxygen therapy, although the response varies depending on the precise nature and size of the V/Q mismatch.

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      Universitatsklinikum Schleswig-Holstein 7 years ago


      Shunt occurs when venous blood mixes with arterial blood either by bypassing the lungs completely (extra-pulmonary shunt) or by passing through the lungs without adequate oxygenation (intra-pulmonary shunt).


      Extra pulmonary (cardiac) shunting is not commonly seen in adult practice. Even when a lesion causes communication between the right and left heart, initially the blood flow will be from left to right. This will cause a reduction in cardiac output and volume overload of the right heart but not shunt. Eventually, compensatory changes may take place, which cause blood to flow from the right to the left heart.


      Shunt occurs when blood is transported through the lungs without taking part in gas exchange. The commonest causes are alveolar filling (with pus, oedema, blood or tumour) and atelectasis, fig 3.

      Increasing FiO2 does not normally correct hypoxia caused by pure shunt. This is because the shunted blood in the diseased alveoli does not come in contact with alveolar gas. The deoxygenated blood leaving the diseased alveoli mixes with blood coming from healthy alveoli. In the relatively healthy alveoli, the oxygen saturation will be around 97-99% regardless of the increase in FiO2. The effect of increasing FiO2 on the blood leaving these alveoli will only be an increase in dissolved oxygen, which contributes little to oxygen delivery to tissues.

      Despite this, it is almost always worth trying to increase FiO2, either for the small increase in PO2, or to assess the effect on the other areas of lung where different processes might also be taking place.

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      Universitair Ziekenhuis Leuven 7 years ago

      Diffusion deficit

      This means that a pathological process is affecting the barrier which is normally present between alveolar gas and the capillary blood. In health, this barrier is very thin and is made of the alveolar epithelial cell, the interstitial space and the capillary endothelium, fig 2.

      The most common acute cause is interstitial pulmonary oedema. The most common chronic cause is pulmonary fibrosis.

      Diffusion deficit from fluid or fibrosis often contributes to respiratory failure in combination with other conditions, but rarely causes it on its own in ICU. When chronic fibrosis causes respiratory failure, patients do not benefit from ventilatory support. Acute fibrosis (e.g. non specific interstitial pneumonitis) presents in a very similar fashion to pneumonia and may respond to immunosuppression.

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      Georgia Hospital Association 7 years ago


      Two things cause alveolar hypoventilation:

      1. A reduction in minute ventilation.

      2. An increase in the proportion of dead space ventilation which can either be anatomical or physiological.

      The characteristic of hypoventilation is CO2 retention (Type 2 respiratory failure). PaCO2 is inversely related to alveolar ventilation, see fig 1. A rise in PaCO2 in the alveoli leads to an increase in oxygen requirements because the accumulated CO2 molecules displace O2 molecules(alveolar gas equation).

      Almost every cause of respiratory failure might eventually cause CO2 retention because of respiratory muscle fatigue. Some conditions normally present with Type 1 respiratory failure, but when severe present with marked CO2 retention (e.g. cardiogenic pulmonary oedema). This is because of a profound V/Q mismatch.

      Hypoxaemia caused by hypoventilation is easily corrected with low dose oxygen supplementation. If high dose oxygen is required, there is an additional or alternative cause of hypoxaemia.

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      Seton Family of Hospitals 7 years ago

      Respiratory failure is, by definition, a failure of gas exchange. There are two types

      Type 1: hypoxaemia with a normal or low CO2

      Type 2: hypoxaemia with a high CO2

      The main symptom is shortness of breath. Signs of repiratory failure are listed in this table.

      There are several pathophysiological mechanisms underlying respiratory failure; they are:

      Alveolar hypoventilation

      Diffusion deficit


      Ventilation – perfusion mismatch


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      National Naval Medical Center 7 years ago

      Respiratory acidosis

      Respiratory acidosis is a condition that occurs when the lungs cannot remove all of the carbon dioxide the body produces. This disrupts the body's acid-base balance causing body fluids, especially the blood, to become too acidic.


      Causes of respiratory acidosis include:

      Diseases of the airways (such as asthma and chronic obstructive lung disease), which send air into and out of the lungs

      Diseases of the chest (such as scoliosis), which make the lungs less efficient at filling and emptying

      Diseases affecting the nerves and muscles that "signal" the lungs to inflate or deflate

      Drugs that suppress breathing (including powerful pain medicines, such as narcotics, and "downers," such as benzodiazepines), especially when combined with alcohol

      Severe obesity, which restricts how much the lungs can expand

      Chronic respiratory acidosis occurs over a long period of time. This leads to a stable situation, because the kidneys increase body chemicals, such as bicarbonate, that help restore the body's acid-base balance.

      Acute respiratory acidosis is a severe condition in which carbon dioxide builds up very quickly and before the kidneys can return the body to a state of balance.


      Symptoms may include:


      Easy fatigue


      Shortness of breath


      Exams and Tests

      Arterial blood gas (measures levels of oxygen and carbon dioxide in the blood; in respiratory acidosis, the level of carbon dioxide is too high)

      Chest x-ray

      Pulmonary function test


      Treatment is aimed at the underlying lung disease, and may include:

      Bronchodilator drugs to reverse some types of airway obstruction

      Noninvasive positive-pressure ventilation (sometimes called CPAP or BiPAP) or mechanical ventilation if needed

      Oxygen if the blood oxygen level is low

      Treatment to stop smoking

      Outlook (Prognosis)

      How well you do depends on the disease causing the respiratory acidosis.

      Possible Complications

      Poor organ function

      Respiratory failure


      When to Contact a Medical Professional

      Severe respiratory acidosis is a medical emergency. Seek immediate medical help if you have symptoms of this condition.

      Call your health care provider if you have symptoms of lung disease.


      Do not smoke. Smoking leads to the development of many severe lung diseases that can cause respiratory acidosis.

      Losing weight may help prevent respiratory acidosis due to obesity (obesity-hypoventilation syndrome).

      Be careful about taking sedating medicines, and never combine these medicines with alcohol.

      Alternative Names

      Ventilatory failure; Respiratory failure; Acidosis - respiratory


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      Vu Medical Center Amsterdam 7 years ago

      Lung (or respiratory) failure is a condition in which the level of oxygen in the blood becomes too low or the level of carbon dioxide in the blood becomes too high. Acute respiratory distress syndrome (ARDS) is a cause of sudden and severe lung failure.

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      Saarland University Hospital 7 years ago

      The signs of respiratory failure are signs of respiratory compensation, increased sympathetic tone, end-organ hypoxia, haemoglobin desaturation

      Signs of respiratory compensation


      tachypnoea is a very good indicator of a severely ill patient

      use of accessory muscles

      nasal flaring

      intercostal, suprasternal or supraclavicular recession

      Increased sympathetic tone




      End-organ hypoxia

      altered mental status

      bradycardia and hypotension (late signs)

      Haemoglobin desaturation


      Pulse oximetry

      estimates arterial saturation not PaO2 using absorption of two different wavelengths of infrared light

      the relationship between saturation and PaO2 is described by the oxyhaemoglobin dissociation curve

      a pulse oximetry saturation (SpO2) ~90% is a critical threshold. Below this level a small fall in PaO2 produces a sharp fall in SpO2

      sources of error

      poor peripheral perfusion. This will often lead to a discrepancy between the heart rate displayed by the pulse oximeter and the heart rate measured by other means (eg ECG). Look for any discrepancy when assessing the SpO2

      dark skin (oximeter over-reads slightly)

      false nails or nail varnish



      lipid infusion for TPN

      propofol infusion

      bright ambient light

      poorly adherent probe

      excessive motion

      carboxyhaemoglobin (SpO2 > SaO2)


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      Landspitalinn National University Hospital 7 years ago

      The most common cause for hypoxaemic respiratory failure in ICU patients is perfusion of non-ventilated alveoli (shunting).


      form of ventilation-perfusion mismatch in which alveoli which are not ventilated (eg due to collapse or pus or oedema fluid) but are still perfused. As a result blood traversing these alveoli is not oxygenated. The animation shows an alveolus with normal ventilation and perfusion and an alveolus in which shunting is occurring.

      this form of respiratory failure is relatively resistant to oxygen therapy. Increasing the inspired oxygen concentration has little effect because it can not reach alveoli where shunting is occurring and blood leaving normal alveoli is already 100% saturated

      commonest cause of hypoxaemic respiratory failure in critically ill patients

      hypoxic pulmonary vasoconstriction reduces the blood flow to non-ventilated alveoli and reduces the severity of the hypoxaemia

      causes of shunting:


      any cause of a right to left shunt eg Fallot's tetralogy, Eisenmenger's syndrome



      pulmonary oedema



      pulmonary haemorrhage

      pulmonary contusion

      Ventilation without perfusion

      this is the opposite extreme of ventilation-perfusion mismatch

      gas passes in and out of the alveoli but no gas exchange occurs because the alveoli are not perfused. and the ventilation is ineffective. In this respect these alveoli are behaving like other parts of the lung that are ventilated but do not take part in gas exchange (eg the major airways) and these alveoli therefore make up what is called physiological dead space

      unless the patient is able to compensate for it the reduction in effective ventilation results in an increase in PaCO2.

      causes include:

      low cardiac output

      high intra-alveolar pressure leading to compression or stretching of alveolar capillary (mechanically ventilated patients)

      Diffusion abnormality

      less common

      may be due to an abnormality of the alveolar membrane or a reduction in the number of alveoli resulting in a reduction in alveolar surface area

      causes include:

      Acute Respiratory Distress Syndrome

      fibrotic lung disease

      Alveolar hypoventilation

      as carbon dioxide passes into the alveolus and oxygen passes into the blood the pressure gradients between alveolar gas and blood are gradually reduced. Ventilation is required to restore the pressure gradients

      hypoventilation is marked by a rise in PaCO2 and a fall in PaO2

      Causes of hypoventilation


      brainstem injury due to trauma, haemorrhage, infarction, hypoxia, infection etc

      metabolic encephalopathy

      depressant drugs

      Spinal cord

      trauma, tumour, transverse myelitis

      Nerve root injury



      neuropathy eg Guillain Barre

      motor neuron disease

      Neuromuscular junction

      myasthenia gravis

      neuromuscular blockers

      Respiratory muscles


      disuse atrophy



      Respiratory system

      airway obstruction (upper or lower)

      decreased lung, pleural or chest wall compliance

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      Universitätsklinikum Leipzig Aör 7 years ago


      acute respiratory failure occurs when the pulmonary system is no longer able to meet the metabolic demands of the body

      hypoxaemic respiratory failure: arterial partial pressure of oxygen (PaO2) less than or equal to 6.7 kPa when breathing room air

      hypercapnic respiratory failure: arterial partial pressure of carbon dioxide (PaCO2) more than or equal to 6.7 kPa

      Basic respiratory physiology

      The major function of the lung is to get oxygen into the body and carbon dioxide out.

      Gas exchange requires a pressure gradient between alveolar air and blood, a short distance for diffusion of gases and intervening tissues which are permeable to oxygen and carbon dioxide

      Getting oxygen in

      the alveolar partial pressure of oxygen (PAO2) is dependent on the total alveolar pressure and the partial pressures of the other gases in the alveolus

      the sum of the partial pressures of all the gases is equal to the total alveolar pressure

      partial pressure of each gas in a mixture of gases is directly related to the proportions in which they are present

      therefore partial pressure of oxygen can be increased by:

      increasing alveolar pressure or

      increasing the proportion of oxygen in the mixture

      increasing the inspired oxygen concentration increases the proportion of oxygen in alveolar gas while reducing the proportion of nitrogen

      the alveolar partial pressure of water vapour remains largely constant and therefore does not contribute to changes in PAO2. The proportion of carbon dioxide in alveolar gas does, however, change and therefore factors which affect PACO2 also affect PAO2

      as carbon dioxide passes into the alveolus and oxygen passes into the blood the PACO2 rises and the PAO2 falls. Ventilation is required replenish the alveolar gas with fresh gas.

      thus the factors that result in changes in PAO2 are:


      alveolar pressure

      inspired oxygen concentration


      Getting carbon dioxide out

      CO2 elimination is largely dependent on alveolar ventilation (CO2 crosses the alveolar membrane very readily and so diffusion abnormalities and shunting (see below) have little effect on CO2 elimination).

      Alveolar ventilation = Respiratory rate x (tidal volume-dead space)

      Anatomical dead space is constant but physiological dead space depends on the relationship between ventilation and perfusion.

      Therefore changes in PACO2 are dependent on:

      respiratory rate

      tidal volume

      ventilation-perfusion matching


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      Klinikum Greifswald Klinik und Poliklinik für Hautkrankheiten Universität Greifswald 7 years ago

      The number of adults with tetralogy of Fallot now exceeds the number of children with the disorder due to childhood surgical successes. After surgical repair, however, most patients are left with pulmonary regurgitation that, over time, results in right ventricular volume overload, enlargement, and dysfunction. Usually well tolerated for 20 years or more, ongoing pulmonary insufficiency is at the core of late complications that include right ventricular failure, exercise intolerance, atrial and ventricular arrhythmias, and sudden death. Though late pulmonary valve replacement appears to attenuate this risk, prostheses have a finite life span. Thus, the timing of surgery must be carefully considered, weighing the up-front risks of surgery and possible repeat surgery against the risk of ongoing pulmonary regurgitation.


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      Kyoto University Hospital 7 years ago

      Over 90 % of the normal population has trivial to mild pulmonary regurgitation (PR) detected by color Doppler echocardiogram. This is what we call physiologic PR and is an incidental finding when the patient is undergoing a color Doppler echocardiogram for other reasons. This type of PR does not need any type of follow-up or intervention, as the pulmonary valve is normal.

      There are other cases where the pulmonary valve does not close completely, causing the blood to leak backward from the main pulmonary artery into the right ventricle.


      As mentioned above, a structurally normal pulmonary valve may have a little amount of PR, which is clinically irrelevant. It is found in most normal hearts.

      In some cases, the pulmonary regurgitation is caused by a malformed or thickened pulmonary valve. It may also be seen in patients with pulmonary stenosis who have undergone balloon valvuloplasty. A small subset of patients with complex heart defects may require a pulmonary conduit (tube), which may start leaking as it gets older. It may also be found in some cases of heart surgery for certain types of congenital heart defects. Finally, it may be seen in patients with pulmonary hypertension (high pressure in the lung vessels).

      In extremely rare cases, the pulmonary valve may be absent (absent pulmonary valve syndrome). There may be a combination of pulmonary stenosis with severe PR.

      Pulmonary regurgitation can be caused by infectious diseases such as endocarditis or by carcinoid heart disease, a very rare condition.


      Most patients with mild to moderate pulmonary valve regurgitation do not experience any symptoms. They may lead a normal life. Patients with a more severe degree of PR may experience some of these symptoms:

      ? Fatigue

      ? Shortness of breath, especially during exertion

      ? Chest pain

      ? Palpitations

      ? Enlarged liver

      ? Fainting with exercise

      ? Exercise intolerance

      Symptomatic patients undergo further testing and may require surgical intervention.


      An echocardiogram (ECHO) is a painless test that uses ultrasound waves to examine the heart. The echocardiogram is a very sensitive test, which will detect any trivial amount of leakage even in a structurally normal pulmonary valve. This is a very common finding in echocardiogram studies and most cardiologists do not mention it as it may cause unnecessary concern to the parents. There are other heart valves that may have a very small amount of leakage that may be physiologic too.

      The echocardiogram is very useful detecting the amount of pulmonary regurgitation in cases of “real” leakage. The test also helps to determine the size and function (contractility) of the right ventricle.

      Patients with severe pulmonary regurgitation may benefit from an MRI. This study will help determine the need and timing of surgery.


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      Intermountain Healthcare, ID 7 years ago

      Pulmonary valve insufficiency (or incompetence, or regurgitation) is a condition where the pulmonary valve is not strong enough to prevent backflow into the right ventricle. If it is secondary to pulmonary hypertension it is referred to as a "Graham Steell" murmur.

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      Karolinska Institute & University Hospital 7 years ago

      The backward or retrograde flow of blood through the pulmonary valve into the right ventricle during diastole; may be acute or chronic.


      Pulmonary hypertension (causing insufficiency secondary to dilatation of the valve ring)

      Infective endocarditis

      Rheumatic heart disease

      Congenital abnormalities (e. g., tetralogy of Fallot, ventricular septal defect, valvular pulmonic stenosis)

      Carcinoid heart disease

      Pulmonary valve repair

      Signs and Symptoms

      May be tolerated for years without problems



      Right heart failure

      Cardiac Auscultation

      Low-pitched murmur, usually best heard along the third or fourth intercostal spaces adjacent to the left sternal border; may be accentuated with inspiration

      When the pulmonary artery systolic pressure exceeds 70 mm Hg, dilatation of the pulmonary artery ring results in Graham-Steell's murmur, a high-pitched, blowing decrescendo murmur heard best along the left parasternal region

      Wide splitting of S2

      Right-sided S3 may be audible and Accentuated with inspiration

      Right-sided S4 may be audible and accentuated with inspiration


      Right ventricular hypertrophy

      Right bundle branch block

      Chest X-ray

      Enlarged pulmonary artery

      Enlarged right ventricle


      Pulmonary insufficiency is usually well tolerated

      Valvuloplasty/valve replacement


      Right ventricular enlargement

      Right ventricular volume overload pattern (see TR)

      Fine diastolic flutter of the tricuspid valve

      Premature opening of the pulmonic valve (defined as pulmonic valve opening on or before the QRS complex) due to severe acute pulmonary insufficiency


      Anatomic basis for the presence of pulmonary insufficiency (e.g. infective endocarditis, valvular pulmonic stenosis)

      Dilatation of the right ventricle

      Right ventricular volume overload pattern

      PW Doppler

      Up to 87% of normal patients appear to have pulmonary insufficiency Calculate the length and duration of the regurgitant jet to differentiate between true and physiologic insufficiency (< 1 cm in length and not holodiastolic in duration)

      Determine the severity of pulmonary insufficiency with mapping technique

      CW Doppler

      Compare the regurgitant Doppler spectral display with the pulmonic outflow Doppler spectral display

      Determine the pulmonary artery end-diastolic pressure

      Color Flow Doppler

      Determine the length and width of the pulmonary insufficiency

      Proximal acceleration (flow convergence) may indicate 3+ or 4+ pulmonary insufficiency

      Pulmonary Insufficiency Severity Scales

      PW and Color flow Doppler

      Physiologic : < 1 cm in length and not holodiastolic in duration

      Borderline : 1 to 2 cm in length and holodiastolic in duration

      Clinically significant : > 2 cm in length with a peak velocity > 1. 5 m/sec and holodiastolic in duration

      CW Doppler Spectral Strength of Regurgitant Jet

      Grade 1+ : Spectral tracing stains sufficiently for detection, but not enough for clear delineation

      Grade 2+ : Complete spectral tracing can just be seen

      Grade 3+ : Distinct darkening of spectral tracing is visible but density is less than antegrade flow

      Grade 4+ : Dark-stained spectral tracing


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      Children's Memorial Hospital of Chicago 7 years ago

      Incomplete closure of the pulmonary valve in the heart, allowing blood to return from the pulmonary artery into the right ventricle. 2. Respiratory insufficiency in which the lungs cannot take in enough oxygen or expell enough carbon dioxide to meet the needs of the body.


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      St. Vincent Hospitals and Health Services 7 years ago

      MYOSIN-LOSS (Acute Quadriplegic; Critical Illness) MYOPATHIES2

      General Syndrome

      Rapidly Evolving Myopathy with Myosin-Deficient Fibers

      Clinical features


      Progressive proximal > distal weakness over days to weeks

      Unexplained, persistent weakness after respiratory support or neuromuscular paralysis


      Age: Mean 6th decade

      Sex: Males & Females involved


      Diffuse: Proximal > Distal; Neck flexors


      Respiratory failure (80%)

      Severe cases: Face & occasional EOM

      Mild cases: Monophasic; May have Proximal arm weakness

      Often associated with some rhabdomyolysis

      Sensory: Normal, or Mild distal loss

      Tendon reflexes: Reduced


      Slow improvement in weakness (months) when steroids tapered

      High mortality (30% to 50%) from associated disorders

      Associated factors

      Corticosteroids (80%): Especially higher doses

      Transplant: Lung; Liver

      Systemic disease


      Myasthenia gravis

      Renal disease & Dialysis

      Severe "critical" illness

      Multi[ple organ failure

      Post-Paralysis Paralysis


      Paralytic treatment for Status asthmaticus or other disorders

      Treatment with NMJ blocking agents

      Non-depolarizing agents; e.g. Vecuronium; ?Corticosteroids

      Treatment > 1 week

      Inability to wean from respirator

      Persistent weakness


      Serum CK: Elevated or Normal

      High in 1st 2 weeks in status asthmaticus patients

      Normal in all after 2 weeks



      CMAP: Small

      Normal: Nerve conduction velocity; Distal Latencies; Sensory potentials


      Often normal, or mild non-specific changes

      Irritative changes

      Occur early in course: Some patients


      Positive sharp waves

      Myopathic changes

      Occur in some patients: Later in course

      Action potentials: Low amplitude, Short duration

      Repetitive nerve stimulation

      Occasional decrement early: 1st week after discontinuation of paralytic agent

      Normal late

      Muscle fibers may be electrically inexcitable

      Muscle Pathology

      Myosin loss in muscle fibers on ATPase stain (ATPase, pH 9.4 & 4.3)


      pH 9.4: Fibers with staining intensity less than type 1

      pH 4.3: Fibers with reduced staining intensity at pH 9.4 also show reduced staining at pH 4.3

      Some biopsies show loss diffuse loss within muscle fibers

      Others show focal regions of myosin loss within fibers

      Myosin loss present in scattered muscle fibers throughout musle biopsy: Not focal or diffuse regions


      Normal myosin/actin ratio in muscle: 1.31 to 1.57

      Critical illness myopathy myosin/actin ratio is low: 0.37

      Differential diagnosis

      Dermatomyositis in focal regions of muscle fiber damage

      HIV with nemaline rods

      Muscle fiber necrosis

      Atrophic muscle fibers

      Basophilic, atrophic type II muscle fibers (60%)

      All fibers atrophic (30%)

      Enlarged nuclei in atrophic muscle fibers

      Degeneration & Regeneration of muscle fibers: Occasional; Early

      Sarcolemma: Reduced NOS1 (nNOS) staining

      NOS1 staining also lost after denervation

      NOS1 activity, but not amount, increased with Caveolin-3 mutations

      Weakness: Pathophysiology

      Muscle membrane inexcitability

      Animal (rat) model

      Denervate hindlimb + High dose dexamethasone

      Loss of myosin with preservation of actin

      Increased glucocorticoid receptors in muscle membrane

      Muscle membrane changes


      Reduced Membrane impedance 2° to Increased Cl- conductance

      Reduced Na+ current amplitudes

      Reduced number of Na+ channels

      Reduced Na+ channel conductance or voltage-dependent gating

      Myosin loss

      ? via Calpain pathway

      ? Related to Increased general muscle catabolism

      Protein degradation pathways possibly involved4



      Also see: Critical illness polyneuropathy

      Cough & Neuromuscular Disorders

      HSN + Cough & GE reflux

      CMT 1B

      Autonomic disorders

      Holmes-Adie syndrome

      Acute pandysautonomia

      Vagal mononeuropathy

      Hoarse voice & Neuromuscular Disorders

      HSN + Cough & GE reflux

      HMSN 2C

      HMSN 4A

      HMN 7


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      UniverstätsSpitals Zürich 7 years ago

      Respiratory failure: Evaluation & Management


      Forced vital capacity (FVC): Reliable; May miss some respiratory problems

      Other testing

      FVC while supine

      Formal pulmonary function testis

      Nocturnal disorders of breathing


      Early: Non-invasive nocturnal ventilation, preferably NIPPV

      Assist cough when needed

      Avoid early tracheostomy

      Maintain ideal body weight.

      Control oral secretions

      Aggressively treat URI’s.

      Give Influenza vaccine & Pneumovax.

      Avoid supplemental O2 unless addressing hypoventilation fails

      Outcomes in patients with chronic neuromuscular disease,

      Prolongs life

      Reduces symptoms

      Improves quality of life

      Prevents acute respiratory failure & delays tracheostomy

      End of life

      Prevent dyspnea and discomfort with O2

      Use of narcotics & benzodiazepines

      Terminal weaning: Not sudden withdrawal of support

      Respiratory failure: Exacerbating factors

      Reduced central drive

      Primary: Myotonic dystrophy

      Drugs: Sedatives hypnotics

      Supplemental oxygen

      Physical impediments

      Obesity: Increased work of chest wall movement


      Supine position: Inhibition of diaphragmatic movement

      Kyphoscoliosis: Reduced chest wall compliance

      Primary lung disease: Obstructive disease

      FEV1/FVC ratio reduced

      Increased airway resistance slows expiration

      Restrictive ventilatory defects are characterized by proportional decreases in FVC and FEV1, leaving the FEV1/FVC normal or even slightly elevated. Any lesion affecting the lung, chest wall, or respiratory muscles that reduces the ability to take in a normal amount of air but does not affect the conducting airways is classified as a restrictive lung disease.

      Obstructive defects are characterized by their involvement of the airways and the resultant reduction in expiratory flow. Spirometric studies of obstructive lung disease generally show a reduced FEV1, FEV1/FVC and flow rates with a relatively normal FVC. In severe obstructive lung disease, the FVC may also be reduced.

      Home ventilation: Types

      Pressure-limited: BiPAP


      Patient initiates breath

      Machine senses negative pressure

      Air delivered until set pressure is reached

      End inspiration pressure drops to set (positive) level

      Typical settings

      IPAP: 12 to 20 cm H2O

      EPAP: 3 to 4 cm H2O


      1st step: When hypoventilation in only nocturnal

      Can deliver breaths without patient triggering: For sleep apnea

      Simple to operate




      Can't deliver large volumes: No cough assist

      Most unit have no battery



      Patient initiates breath

      Machine senses negative pressure

      Air delivered until set volume is reached

      No compenstaion for air leakage: Set for large volumes (10 to 15 cc/kg)


      Battery back-up

      Back-up alarms

      Better for full time respiratory support

      Adjustable flow rates

      Can increase voice volume & cough



      Units may be heavy: But can be place on power wheelchai


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      Lifebridge Health 7 years ago

      The respiratory therapist has a number of methods available to help patientsovercome respiratory failure. They include:

      Suctioning the lungs through a small plastic tube passed through the nose, in order to remove secretions from the airways that the patient cannot cough up.

      Postural drainage, in which the patient is propped up at an angle or tilted to help secretions drain out of the lungs. The therapist may clap the patient on the chest orback to loosen the secretions, or a vibrator may be used for the same purpose.

      Breathing exercises after the patient recovers sufficiently to help strengthen the muscles that aid breathing.

      The prognosis (outlook) for patients with respiratory failure depends chieflyon its cause. When respiratory failure develops slowly, pressure may build up in the lung's blood vessels, a condition called pulmonary hypertension. This condition may damage blood vessels and cause the heart to fail. If it is not possible to provide enough oxygen to the body, complications involving either the brain or the heart may also prove fatal. If the kidneys fail or the diseased lungs become infected, the prognosis is poor. In some cases, the primary disease causing respiratory failure is irreversible. Then, the patient, family, and physician together must decide whether to prolong life by ventilator support. Occasionally, lung transplantation is an option; however, this itis a highly complex procedure and availability of healthy lungs is small. Ifthe underlying disease can be effectively treated, however, the outlook is usually good. Care is needed not to expose the patient to polluting substancesin the atmosphere as it could tip the balance against recovery.

      The best prevention of respiratory failure is early treatment of any lung disease or respiratory disease. Once serious respiratory failure is present, treatment in an intensive care unit with specialized personnel and equipment isdesirable.

      Read more: Respiratory failure, Information about Respiratory failure

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      Clalit Health Services 7 years ago

      Respiratory failure is nearly any condition that affects breathing and ultimately results in failure of the lungs to function properly. The main tasks ofthe lungs and chest are to get oxygen into the bloodstream from air that is inhaled (breathed in) and, at the same to time, to eliminate carbon dioxide (C02) from the bloodstream through air that is exhaled (breathed out). In respiratory failure, either the level of oxygen in the blood becomes dangerously low, and/or the level of C02 becomes dangerously high.

      Respiratory failure often is divided into two main types. One type is hypoxemic respiratory failure. This occurs when something interferes with normal gasexchange and too little oxygen gets into the blood (hypoxemia). All organs and tissues in the body suffer as a result. Respiratory distress syndrome, high altitudes (where there is less oxygen in the air), various forms of lung disease, severe anemia, and blood vessel disorders, can all prevent the lungs from extracting sufficient oxygen from the air.

      The other type of respiratory failure is ventilatory failure. This occurs when breathing is not strong enough to rid the body of C02, which then builds up in the blood. This can happen when the respiratory center in thebrainstem fails to drive breathing, when muscle disease keeps the chest wallfrom expanding when breathing in, or when chronic obstructive lung disease ispresent, making it difficult to exhale. Many respiratory conditions cause both too little oxygen (hypoxemia) and too much C02 (ventilatory failure).

      The major categories of respiratory failure, with specific examples of each,are:

      Obstruction of the airways. Examples are chronic bronchitis withheavy secretions; emphysema; cystic fibrosis; asthma (a condition in which itis very hard to get air in and out through narrowed breathing tubes).

      Weak breathing. This can be caused by drugs or alcohol, which depress therespiratory center; extreme obesity; or sleep apnea, where patients frequently stop breathing during sleep.

      Muscle weakness. This can be caused by muscular dystrophy; polio; a stroke that paralyzes the respiratory muscles;injury of the spinal cord; or Lou Gehrig's disease.

      Lung diseases.These include severe pneumonia; pulmonary edema (fluid in the lungs); heart disease; respiratory distress syndrome; pulmonary fibrosis and other scarringdiseases of the lung; radiation exposure; smoke inhalation; and widespread lung cancer.

      An abnormal chest wall. This condition can be caused by scoliosis or severe injury to the chest wall.

      Both low blood oxygen and high blood C02 can impair mental functions. Patients may become confused and disoriented and find it impossible to carry out their normal activities or do their work. Marked C02 excess can cause headaches and, in time, a semi-conscious state, or even coma. Lowblood oxygen causes the skin to take on a bluish tinge. It also can cause anabnormal heart rhythm (arrhythmia). Lung disease may cause abnormal chest sounds upon examination with a stethoscope such as wheezing in asthma, and "crackles" in obstructive lung disease. Patients often breathe rapidly, are restless, and have a rapid pulse. A patient with ventilatory failure is prone to gasp for breath, and may use the neck muscles to help expand the chest.

      The primary symptom of respiratory failure is shortness of breath. Other signs and symptoms are not specific but depend upon what is causing the failure.Good general health and some degree of "reserve" lung function will help a patient through an episode of respiratory failure. The key diagnostic method isto measure the amounts of oxygen, C02, and acid in the blood at regular intervals.

      In treating respiratory failure, most patients are first given oxygen, then the underlying cause of respiratory failure must be treated. For example, antibiotics are used to fight a lung infection, or, for an asthmatic patient, a drug to open up the airways is commonly prescribed. A patient whose breathingremains very poor will require a mechanical ventilator to aid breathing. A plastic tube is placed through the nose or mouth into the windpipe and attachedto a machine that forces air into the lungs. This can be a lifesaving treatment and should be continued until the patient's own lungs can take over the work of breathing. It is very important to use no more pressure than is necessary to provide sufficient oxygen, otherwise ventilation may cause further lung damage. Drugs are given to keep the patient calm, and the amount of fluid in the body is carefully adjusted so that the heart and lungs can function asnormally as possible. Steroids, which combat inflammation, may sometimes be helpful but they can cause complications, including weakening the breathing muscles.

      Read more: Respiratory failure, Information about Respiratory failure

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      Uf & Shands Jacksonville The University of Florida Health System 7 years ago

      The process of returning the patient to unassisted and spontaneous breathing is called weaning. Weaning is a complex process that requires the understanding and cooperation of the patient. It can cause great fatigue and depression in patients because of the slow- and long-term nature of the treatment procedures.

      Weaning a patient too rapidly or prematurely can be dangerous. Some patients, particularly those who had severe underlying cardiac disease and prolonged episodes of acute illnesses, may require weeks to months to wean. The doctor considers weaning only when the patient is awake, has good nutrition, and is able to cough and breathe deeply.

      Discontinuation of Ventilatory Support

      The difficult question of whether and when to discontinue life-sustaining mechanical ventilation to the patient who is not responding to any treatment is sometimes faced by the doctor and the family. The legal, ethical, and financial implications of continuing or withholding treatment to the patient in terminal respiratory failure are important issues addressed at family, professional, and government levels. Respecting the rights and wishes of the patient and helping the patient achieve a dignified and peaceful end while continuing to assure care and comfort is a responsibility shared by both the caregivers and the family. The family with a good understanding of respiratory failure in all its dimensions is best equipped to play its part in sharing this responsibility.

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      More About Some Common Lung Diseases Leading to Or Characterized by Respiratory Failure


      The hallmarks of asthma are obstruction to air flow and bronchoconstriction, tightening of the muscles in the walls of the bronchi, that is usually relieved by drugs called bronchodilators. Acute asthma attacks that persist, do not respond to bronchodilator therapy, and threaten life are referred to as status asthmaticus. Due to the heavy work of breathing, patients eventually tire and decrease their respiratory efforts. Patients in this condition are prone to develop respiratory failure. Respiratory failure is more common in women with asthma, in patients over 40 years of age, and in patients in whom treatment is delayed, or oral corticosteroid therapy is stopped suddenly.

      During an attack of asthma, airways obstruction from mucus secretions and thickened bronchial tissue can lead to severe hypoxemia, hypercapnia, and acidosis. Other potential complications are pneumonia and accumulation of air in pleural spaces. Patients with hypercapnia are at increased risk of death.

      In children with asthma, respiratory muscle fatigue and interrupted breathing (apnea) are indications of existing or developing respiratory failure.

      Chronic Obstructive Pulmonary Disease (COPD)

      COPD patients may develop acute respiratory failure when their chronic airway obstruction is complicated by infections, pulmonary emboli, heart failure, and drug- induced respiratory depression. Influenza often precipitates respiratory failure even without evidence of pneumonia in COPD patients. The hallmark of respiratory failure in COPD is increasing dyspnea and worsening blood gas abnormalities. Depending on the triggering event, various other clinical features may appear. The most dire sign is a decline in the patient's condition associated with PaO2 of less than 50 mm Hg and a PaCO2 greater than 50 mm Hg during air breathing. Uncontrolled administration of oxygen to patients with COPD and acute respiratory failure without therapy directed at reducing the work of breathing can result in further hypercapnia, acidosis, stupor, and coma.


      Patients with very severe pneumonia go into respiratory failure because of lung inflammation and accumulation of fluid that interferes with gas exchange. They breathe hard and become exhausted; their respiratory muscles are unable to keep up the pace. Blood carbon dioxide rises and oxygen in the blood falls further. Sedation, at the time of respiratory stress, may worsen the situation by depression of the brain activity which is needed to keep respiratory muscles working at high levels. This, in turn, decreases the amount of breathing and may promote the development of respiratory failure.

      Respiratory Distress Syndrome of the Newborn

      One type of respiratory failure in the newborn infant, especially those born prematurely, is commonly referred to as "respiratory distress syndrome." It is also called hyaline membrane disease because of the formation of an abnormal, hyaline (glassy and transparent under the microscope), protein-containing membrane in alveoli. RDS may also occur in full-term babies born to diabetic mothers.

      The causes of RDS are complex, but it is believed that the major problem is a poorly developed lung. Surfactant, a unique fat-containing protein necessary to reduce the surface tension in the alveoli of the lung to prevent their collapse, is deficient in RDS babies. The most effective treatment for RDS is the administration of surfactant. Surfactant replacement therapy for RDS, available since 1989, has brought about a 30 percent reduction in death rate for neonatal RDS in the United States (from 89.9 deaths per 100,000 live births in 1989 to 58.3 deaths per 100,000 in 1992). The National Heart, Lung, and Blood Institute (NHLBI) is supporting the development and testing of several different surfactant preparations useful in replacement therapy for RDS.

      Adult or Acute Respiratory Distress Syndrome

      Acute respiratory failure in adults as a clinical entity was first reported in 1967. Respiratory failure usually occurred following a catastrophic event in individuals with no previous lung disease and who did not respond to ordinary methods of respiratory support. Regardless of the event causing the lung injury, the patients exhibited common signs and symptoms, x-ray findings, and tissue changes. Because many of its features resembled the respiratory distress syndrome of the newborn, RDS, the adult disease was called "ARDS." As with RDS, there is increasing evidence that loss of surfactant function may also be associated with ARDS.

      Inhalation of gastric contents (aspiration), pulmonary infections, shock, trauma, burns, extrapulmonary sepsis, inhalation of toxic gases, drug overdose, and near-drowning are some of the different situations that can cause ARDS. An estimated 150,000 cases of ARDS occur yearly in the United States. The estimated mortality rate of ARDS is 50-70 percent.

      ARDS is often associated with multiple organ failure (heart, liver, kidneys, and lungs). Patient survival usually depends on the number of organs which fail, the degree and nature of damage, and the age and previous health status of the patient. The incidence of multiple organ failure is particularly high when sepsis or hypotension from loss of blood are the underlying causes of ARDS.

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      Keeping on Top of Your Condition

      Keeping in tune with your disease or condition not only makes treatment less intimidating but also increases its chance of success, and has been shown to lower a patients risk of complications. As well, as an informed patient, you are better able to discuss your condition and treatment options with your physician.


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      Uniklinik Köln - Klinikum der Universitat Zu Köln 7 years ago

      Patients with respiratory failure who have excessive lung secretions are sometimes helped by fiberoptic bronchoscopy, a technique for accessing the interior of the bronchi, the larger air passages of the lungs. The bronchoscope is a flexible tube with a light at the end that is passed through the nose or mouth into the trachea and bronchi. Fluid or tissue can be removed from the bronchi (aspiration), and cells for microscopic examination can be obtained by washing the interior of the larger breathing tubes (lavage). Bronchoscopy is useful for placing or removing endotracheal tubes, removing foreign bodies from the lung, and collecting tissue samples for diagnosis.

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      Intravenous Nutritional Support

      Nutritional supplementation is essential to maintain or restore strength when weakness and loss of muscle mass prevent patients from breathing adequately without ventilatory support. Appropriate nutrients (fats, carbohydrates, and predigested proteins) are fed intravenously for this purpose.


      Physiotherapy includes chest percussion (repeated sharp blows to the chest and back to loosen secretions), suction of airways, and regular changes of body position. It helps drain secretions, maintains alveolar inflation and prevents atelectasis, incomplete expansion of the lung.

      X-ray Monitoring

      X-ray images of the chest help the doctor monitor the progress of lung and heart disease in respiratory failure. The portable chest radiograph taken with an x-ray machine brought to the bedside is often used for this purpose in the intensive care unit.

      Lung Transplantation

      Lung transplantation currently offers the only hope for certain patients with end-stage pulmonary disease. The shortage of suitable donors and the high cost of the procedure continue to be major obstacles that limit its use.

      Complications of Treatment

      Oxygen toxicity, pulmonary embolism (closure of the pulmonary artery or one of its branches by a blood clot or a fat globule), cardiovascular problems, barotrauma (injury to the lung tissue from excessive ventilatory pressure), pneumothorax (air in the pleural space), and gastrointestinal bleeding are some of the complications of treatment. They result from fluid overload, mechanical ventilation, PEEP, and other procedures used in the management of respiratory failure.

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      Bjc Healthcare 7 years ago

      The patient with respiratory failure cannot be adequately treated in the general care areas of the hospital. Therefore, patients in severe respiratory failure are usually treated in the intensive care unit. Current therapy for all forms of respiratory failure attempts, first, to provide support for the heart, lungs, and other affected vital organs; and second, to identify and treat the underlying cause.

      Since the immediate threat to patients with respiratory failure is due to the inadequate level of oxygen delivered to the tissues, oxygenation is the basic therapy for acute respiratory failure due to lung disease. Oxygen-enriched air is usually given to the patient by nasal prongs, oxygen mask, or by placing an airtube into the trachea (windpipe). Since prolonged high oxygen levels can be toxic, the concentration of oxygen must be carefully controlled for both short- and long-term treatment. Assisted ventilation with mechanical devices may be the first priority for neuromuscular disease patients going into respiratory failure. Additional treatments employ ventilation which helps to keep the lungs inflated at low lung volumes (positive end-expiratory pressure, PEEP), and fluid and nutritional management.

      Endotracheal Intubation

      Endotracheal intubation involves insertion of a tube into the trachea. It permits delivery of precisely determined amounts of oxygen to the lungs and removal of secretions, and ensures adequate ventilation. Combined with mechanical ventilation, endotracheal intubation is the cornerstone of therapy for respiratory failure.

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      Mechanical Ventilation

      If the patient is tiring despite ongoing therapy, a mechanical ventilator, also called a respirator, is used. The ventilator assists or controls the patient's breathing.

      Positive End-Expiratory Pressure (PEEP)

      Positive end-expiratory pressure is used with mechanical ventilation to keep the air pressure in the trachea at a level that increases the volume of gas remaining in the lung after breathing out (expiration). This keeps the alveoli open, reduces the shunting of blood through the lungs, and improves gas exchange. Most ventilators have a PEEP adjustment.

      Extracorporeal Membrane Oxygenator (ECMO)

      The extracorporeal membrane oxygenator (ECMO) is essentially an artificial lung. It is an appropriately cased artificial membrane which is attached to the patient externally (extracorporeally), through a vein or artery. Although the best substitute for a diseased lung that cannot handle gas exchange adequately is a healthy human lung, such substitution is often not possible. Circulating the patient's blood through the ECMO offers another approach. Gas exchange using ECMO keeps the patient alive while the damaged lungs have a chance to heal.

      In 1974, the National Heart, Lung, and Blood Institute (NHLBI) organized a carefully designed clinical trial, to determine the effectiveness of ECMO for patients with acute respiratory distress syndrome. In this study, ECMO appeared to be no more useful than conventional therapy. On the other hand, ECMO seems to be an effective option in some infants with respiratory failure when treatment with mechanical ventilation fails. However ECMO is expensive, is associated with nonrespiratory complications, and is available only in a few specialized centers.

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      Management of Fluids and Electrolytes

      Pulmonary edema, the buildup of abnormal amounts of fluid in the lung tissues, often occurs in respiratory failure. Therefore fluids are carefully managed and monitored to maintain fluid balance and avoid fluid overload which may further worsen gas exchange.

      Pharmacologic Therapy

      Because respiratory failure may be the end result of several different diseases, no single drug therapy is effective in all situations.

      Antibiotics help when infections (sepsis) as well as pneumonia are involved in respiratory failure.

      Bronchodilators, for example, theophylline compounds, sympathomimetic agents (albuterol, metaproterenol, isoproterenol), anticholinergics (ipratropium bromide), and corticosteroids, reverse bronchoconstriction and reduce tissue inflammation.

      Other drugs, such as digitalis, improve cardiac output, and drugs which increase blood pressure in shock can improve blood flow to the tissues.

      No single drug therapy is effective in all situations.

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      Universitätsklinikums Münster 7 years ago

      When the process of gas exchange is faulty, there is not enough oxygen in the blood (hypoxemia) to fuel the body's metabolic activity. In addition, sometimes there is also an accumulation of carbon dioxide, a waste product of metabolism, in the blood and tissues (hypercapnia). Hypercapnia makes blood more acidic; this condition is called acidemia. Eventually the body tissues become acidic. This condition, called acidosis, injures the body's cells and interferes with the functions of the heart and central nervous system. Ultimately, lack of oxygen in the blood causes death of the cells in the brain and other tissues. If not adequately treated, respiratory failure is fatal.

      Hypoxemic Respiratory Failure

      When a lung disease causes respiratory failure, gas exchange is reduced because of changes in ventilation (the exchange of air between the lungs and the atmosphere), perfusion (blood flow), or both. Activity of the respiratory muscles is normal. This type of respiratory failure which results from a mismatch between ventilation and perfusion is called hypoxemic respiratory failure. Some of the alveoli get less fresh air than they need for the amount of blood flow, with the net result of a fall in oxygen in the blood. These patients tend to have more difficulty with the transport of oxygen than with removing carbon dioxide. They often overbreathe (hyperventilate) to make up for the low oxygen, and this results in a low CO2 level in the blood (hypocapnia). Hypocapnia makes the blood more basic or alkaline which is also injurious to the cells.

      If not adequately treated, respiratory failure is fatal.

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      Hypercapnic Respiratory Failure

      Respiratory failure due to a disease of the muscles used for breathing ("pump or ventilatory apparatus failure") is called hypercapnic respiratory failure. The lungs of these patients are normal. This type of respiratory failure occurs in patients with neuromuscular diseases such as myasthenia gravis, stroke, cerebral palsy, poliomyelitis, amyotrophic lateral sclerosis, muscular dystrophy, postoperative situations limiting ability to take deep breaths, and in depressant drug overdoses. Each of these disorders involves a loss or decrease in neuromuscular function, inefficient breathing and limitation to the flow of air into the lungs. Blood oxygen falls and the carbon dioxide increases because fresh air is not brought into the alveoli in needed amounts. In general, mechanical devices that help move the chest wall help these patients.

      Conditions That May Progress To Respiratory Failure

      Almost all lung diseases including asthma, chronic obstructive pulmonary disease (COPD), AIDS-related pneumonia, other pneumonias and lung infections, and cystic fibrosis may eventually lead to respiratory failure particularly if the diseases are inadequately treated. These patients find it very hard to breathe and the result is low oxygen and high carbon dioxide blood levels.

      People whose normal lungs have been injured, such as from exposure to noxious gases, steam, or heat during a fire, can subsequently go into respiratory failure. Adult respiratory distress syndrome (ARDS), also referred to as acute respiratory distress syndrome, is a form of acute respiratory failure caused by extensive lung injury following a variety of catastrophic events such as shock, severe infection, and burns. ARDS can occur in individuals with or without previous lung disease.

      Hyaline membrane disease or respiratory distress syndrome of the newborn (RDS), the most common respiratory illness affecting premature babies, is another kind of respiratory failure. In this condition, the baby's lungs do not have enough surfactant, a substance that makes it possible for air to pass into the alveoli by lowering surface tension and preventing their collapse.

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      Symptoms Of Respiratory Failure

      The clinical features of respiratory failure vary widely in individual patients because so many different conditions can lead to this disorder. There are no physical signs unique to respiratory failure. At extremely low arterial oxygen (PaO2) levels, patients have rapid heart rates, rapid breathing rates, and they are confused, sweaty, and cyanotic (blue). Chronically low arterial oxygen makes patients irritable, and elevated carbon dioxide produces headaches and sleepiness. Difficult, rapid, or labored breathing (dyspnea) is a consistent symptom in the awake patient.

      The functions of the heart and blood vessels are often severely impaired in patients with respiratory failure. In some cases, chronic hypoxemia produces narrowing of the blood vessels in the lung which, along with the lung damage or the associated treatments, may weaken the heart and the circulatory system. Some of the signs of inadequate circulation are constriction of blood vessels in the skin, cold extremities, and low urine output.

      Diagnosis Of Respiratory Failure

      It is impossible to estimate the extent of hypoxemia and hypercapnia by observing a patient's signs and symptoms, and mild hypoxemia and hypercapnia may go entirely unnoticed. Blood oxygen must fall markedly before changes in breathing and heart rate occur.

      The clinical features of respiratory failure vary widely in individual patients.

      The way to diagnose respiratory failure, therefore, is to measure oxygen (PaO2) and carbon dioxide (PaCO2) in the arterial blood. However the levels that indicate respiratory failure are somewhat arbitrary. Depending on age, a PaO2 less than 60 mm Hg or PaCO2 greater than 45 mm Hg generally mean that the patient is in respiratory failure.

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      Scott and White Memorial Hospital 7 years ago

      Almost everyone who has a critically ill friend or relative may expect to hear the term, respiratory failure. Although failure to breathe normally was recognized even in ancient times as an ominous sign, the term, "respiratory failure," did not appear in the medical literature until the 1960s. Doctors now understand that respiratory failure is a serious disorder caused by a variety of different medical problems that may or may not start in the lung. Healthy people as well as patients with either pulmonary (lung) or nonpulmonary diseases can develop respiratory failure.

      The recognition of respiratory failure as a life-threatening problem led to the development of the concept of the intensive care unit (ICU) in modern hospitals. ICU personnel and equipment support vital functions to give patients their best chance for recovery. Today's sophisticated ICU facilities with their novel mechanical life support devices evolved as doctors and scientists learned more and more about the causes of respiratory failure and how to treat it.

      This fact book is a brief overview of the unique changes in lung function that are typical of respiratory failure and the widely different medical conditions that can cause those changes. It also discusses the methods that are used to restore normal respiration and prolong life, and the related dilemma of deciding if and when to withdraw or withhold life support from a hopelessly sick patient.

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      Who Can Get Respiratory Failure

      Many different medical conditions can lead to respiratory failure. Listed below are a few examples of people who may develop respiratory failure.

      A patient with a long history of asthma, emphysema, or chronic obstructive lung disease

      A patient who is undergoing major surgery in the abdomen, heart, or lung

      A person who has taken an overdose of sleeping pills or certain depressant drugs

      A premature baby who weighs less than 3 pounds

      A baby with bronchopulmonary dysplasia

      A patient suffering from AIDS

      A person who has received multiple physical injuries

      A person who has suffered extensive burns

      A person who has bled extensively from a gunshot wound

      A person who has almost drowned

      A patient with severe heart failure

      A patient with severe infections

      A person who is extremely obese

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      Breathing and Respiratory Failure

      The term, "respiratory failure," is used when the lungs are unable to perform their basic task - gas exchange. This process involves transfer of oxygen from inhaled air into the blood and of carbon dioxide from the blood into the lungs, with the result that the arterial blood, blood circulating through the body from the heart, has enough oxygen to nourish the tissues.

      Gas exchange occurs in tiny air sacs in the lung, called alveoli. When a person breathes in (inspiration), air is brought into the alveoli by the action of the respiratory muscles - the diaphragm, the muscles between the ribs, and the accessory muscles (those between the neck and the chest wall). These are collectively called "the ventilatory apparatus." The activity of the respiratory muscles is controlled by respiratory centers in the brain. The brain's respiratory centers in turn are controlled by chemoreceptors, special cells that are sensitive to the amounts of carbon dioxide or oxygen in the blood. The chemoreceptors that are sensitive to oxygen concentration are located in the large arteries in the neck in the carotid bodies. When they sense a fall in the level of oxygen in the blood, they send messages that stimulate the respiratory center in the brain so that there will be an increase in the rate or depth of breathing.

      Whenever any part of the ventilatory apparatus and/or the respiratory centers fails to work properly, the result can be respiratory failure. Both adults and babies can develop respiratory failure. In infants, however, respiratory failure occurs mostly in premature babies whose lungs have not yet fully developed.

      Transfer of oxygen of inhaled air into the blood and of waste carbon dioxide of blood into the lungs occurs in the alveolus.


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      Dana Farber Cancer Institute Boston 7 years ago

      Respiratory failure occurs when the respiratory system fails in oxygenation and/or carbon dioxide elimination. Respiratory failure may be:1

      Hypoxaemic respiratory failure (type I respiratory failure): PaO2 is less than 60 mmHg (8kPa) with a normal or low PaCO2. This is caused by ventilation-perfusion mismatch with either/both:

      Under-ventilated alveoli (e.g. pulmonary oedema, pneumonia or acute asthma).

      Venous blood bypasses ventilated alveoli (e.g. right to left cardiac shunts).

      Hyperventilation increases CO2 removal but does not increase oxygenation as blood leaving unaffected alveoli is almost fully saturated.

      Hypercapnic respiratory failure (type II respiratory failure): PaCO2 is more than 50 mmHg (6.5kPa) and indicates inadequate alveolar ventilation. Any ventilation-perfusion mismatch will affect PaO2 and therefore hypoxaemia is also common.

      Respiratory failure may be acute or chronic. The clinical markers of long-standing hypoxaemia include polycythaemia and cor pulmonale.


      Common causes of type I respiratory failure

      Chronic obstructive pulmonary disease


      Pulmonary oedema

      Pulmonary fibrosis



      Pulmonary embolism

      Pulmonary arterial hypertension

      Cyanotic congenital heart disease


      Adult respiratory distress syndrome



      Common causes of type II respiratory failure

      Chronic obstructive pulmonary disease

      Severe asthma

      Drug overdose, poisoning

      Myasthenia gravis



      Muscle disorders

      Head and neck injuries


      Pulmonary oedema

      Adult respiratory distress syndrome



      The cause of respiratory failure is often clear from the history and physical examination.


      The history may indicate the underlying cause, e.g. paroxysmal nocturnal dyspnoea, and orthopnoea in pulmonary oedema.

      Both confusion and reduced consciousness may occur.


      Localised pulmonary findings are determined by the underlying cause.

      Neurological features may include restlessness, anxiety, confusion, seizures, or coma.

      Tachycardia and cardiac arrhythmias may result from hypoxaemia and acidosis.


      Polycythaemia is a complication of long-standing hypoxaemia.

      Cor pulmonale: pulmonary hypertension is frequently present and may induce right ventricular failure, leading to hepatomegaly and peripheral oedema.


      Arterial blood gas analysis: confirmation of the diagnosis.

      Chest x-ray

      Full blood count: anaemia can contribute to tissue hypoxia; polycythaemia may indicate chronic hypoxaemic respiratory failure.

      Renal and hepatic function: may provide clues to the aetiology or identify complications associated with respiratory failure. Abnormalities in electrolytes such as potassium, magnesium, and phosphate may aggravate respiratory failure and other organ function.

      Serum creatine kinase and troponin I: to help exclude recent myocardial infarction. An elevated creatine kinase may also indicate myositis.

      Thyroid function tests

      Echocardiography: if a cardiac cause of acute respiratory failure is suspected.

      Pulmonary function tests are useful in the evaluation of chronic respiratory failure.

      ECG: to evaluate a cardiovascular cause and may also detect dysrhythmias resulting from severe hypoxaemia or acidosis.

      Right heart catheterisation: should be considered if uncertainty about cardiac function, adequacy of volume replacement, and systemic oxygen delivery.

      Pulmonary capillary wedge pressure may be helpful in distinguishing cardiogenic from non-cardiogenic oedema.


      A patient with acute respiratory failure generally needs prompt admission to hospital. Most patients with chronic respiratory failure can be treated at home with oxygen as well as therapy for their underlying disease.

      Immediate resuscitation may be required.

      Correction of hypoxaemia: ensure adequate oxygen delivery to tissues, generally achieved with a PaO2 of 60 mmHg or an arterial oxygen saturation (SaO2) of greater than 90%.

      Beware the prolonged use of high concentration oxygen in chronic sufferers who have become reliant on their hypoxic drive to maintain an adequate ventilation rate. Elevating the PaO2 too much may reduce the respiratory rate so that the PaCO2 may rise to dangerously high levels.

      Hypercapnia and respiratory acidosis: correct the underlying cause and/or provide assisted ventilation.

      Mechanical ventilation is used to increase PaO2 and to lower PaCO2. Mechanical ventilation also rests the respiratory muscles and is an appropriate therapy for respiratory muscle fatigue. Weaning patients with chronic respiratory failure off of mechanical ventilation may be very difficult.

      Appropriate management of the underlying disease.


      Pulmonary: e.g. pulmonary embolism, pulmonary fibrosis, and complications secondary to the use of mechanical ventilation.

      Cardiovascular: e.g. cor pulmonale, hypotension, reduced cardiac output, arrhythmias, pericarditis, and acute myocardial infarction.

      Gastrointestinal: e.g. haemorrhage, gastric distention, ileus, diarrhoea, and pneumoperitoneum. Stress ulceration is common in patients with acute respiratory failure.


      Hospital acquired infection: e.g. pneumonia, urinary tract infections, and catheter-related sepsis, are frequent complications of acute respiratory failure.

      Renal: acute renal failure and abnormalities of electrolytes and acid-base homeostasis are common in critically ill patients with respiratory failure.

      Nutritional: including malnutrition and complications related to administration of enteral or parenteral nutrition. Complications associated with naso-gastric tubes, e.g. abdominal distention and diarrhoea.


      The mortality rate associated with respiratory failure varies according to the underlying aetiology.

      The mortality rate for adult respiratory distress syndrome is approximately 40%.

      In patients with COPD and acute respiratory failure, the overall mortality rate is approximately 10%.


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      Shriners Hospitals for Children 7 years ago

      Respiratory failure (lung failure) is a condition in which the level of oxygen in the blood becomes dangerously low or the level of carbon dioxide becomes dangerously high.

      Conditions that block the airways, damage lung tissue, weaken the muscles that control breathing, or decrease the drive to breathe may cause lung failure.

      People may be very short of breath, have a bluish coloration to the skin, and be confused or sleepy.

      Doctors use blood tests to detect low levels of oxygen or high levels of carbon dioxide in the blood.

      Oxygen is given.

      Sometimes people need the help of a machine to breathe until the underlying problem can be treated.

      Respiratory failure is a medical emergency that can result from long-standing, progressively worsening lung disease or from severe lung disease that develops suddenly, such as the acute respiratory distress syndrome (see Respiratory Failure and Acute Respiratory Distress Syndrome: Acute Respiratory Distress Syndrome (ARDS)), in otherwise healthy people.


      Almost any condition that affects breathing or the lungs can lead to respiratory failure. Certain disorders, such as hypothyroidism or sleep apnea, can decrease the unconscious reflex that drives people to breathe. An overdose of opioids or alcohol also can decrease the drive to breathe by causing profound sedation. Obstruction of the airways, injury to the lung tissues, damage to the bones and tissues around the lungs, and weakness of the muscles that normally inflate the lungs are also common causes. Respiratory failure can occur if blood flow through the lungs becomes abnormal, as happens in pulmonary embolism (see Pulmonary Embolism (PE): Pulmonary Embolism). This disorder does not stop air from moving in and out of the lungs, but without blood flow to a portion of the lungs, oxygen is not properly extracted from the air.

      Did You Know?

      Age-related reductions in lung function place older people at higher risk of severe symptoms after developing pneumonia.


      Low oxygen levels in the blood can cause shortness of breath and result in a bluish coloration to the skin (cyanosis). Low oxygen levels, high carbon dioxide levels, and increasing acidity of the blood cause confusion and sleepiness. If the drive to breathe is normal, the body tries to rid itself of carbon dioxide by deep, rapid breathing. If the lungs cannot function normally, however, this breathing pattern may not help. Eventually, the brain and heart malfunction, resulting in drowsiness (sometimes to the point of becoming unconscious) and abnormal heart rhythms (arrhythmias), both of which can lead to death.

      Some symptoms of respiratory failure vary with the cause. A child with an obstructed airway due to the inhalation (aspiration) of a foreign object (such as a coin or a toy) may suddenly gasp and struggle for breath (see First Aid: Choking). People with acute respiratory distress syndrome may become severely short of breath over a period of hours. Someone who is intoxicated or weak may quietly slip into a coma.


      A doctor may suspect respiratory failure because of the symptoms and physical examination findings. A blood test done on a sample taken from an artery confirms the diagnosis when it shows a dangerously low level of oxygen or a dangerously high level of carbon dioxide. Chest x-rays and other tests are done to determine the cause of respiratory failure.

      What Causes Respiratory Failure?

      Underlying Problem


      Airway obstruction

      Chronic obstructive pulmonary disease, asthma, bronchiectasis, cystic fibrosis, bronchiolitis, inhaled foreign bodies

      Poor breathing (decrease in the drive to breathe)

      Obesity, sleep apnea, hypothyroidism, drug or alcohol intoxication

      Muscle weakness

      Myasthenia gravis, muscular dystrophy, polio, Guillain-Barré syndrome, polymyositis, certain strokes, amyotrophic lateral sclerosis (ALS), spinal cord injury

      Abnormality of lung tissue

      Acute respiratory distress syndrome (ARDS), pneumonia, pulmonary edema (excess fluid in the lungs) from heart or kidney failure, drug reaction, pulmonary fibrosis, widespread tumors, radiation, sarcoidosis, burns

      Abnormality of chest wall

      Scoliosis, chest wound, extreme obesity, deformities resulting from chest surgery


      People with respiratory failure are treated in an intensive care unit. Oxygen is given initially, usually in a greater amount than is needed, but the amount of oxygen can be adjusted at a later time. Occasionally, in people in whom carbon dioxide levels have remained high for some time, excess oxygen can result in slowing of the movement of air (ventilation) in and out of the lungs and a dangerous further increase in the carbon dioxide level. In such people, the dosage of oxygen needs to be more carefully regulated.

      The underlying disorder causing the respiratory failure must also be treated. For example, antibiotics are used to fight bacterial infection, and bronchodilators are used in people with asthma to open the airways. Other drugs may be given, for example, to decrease inflammation or treat blood clots. Mechanical ventilation is necessary unless respiratory failure resolves rapidly.


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      OhioHealth 7 years ago



      Common pulmonary complications of acute respiratory failure include pulmonary embolism, barotrauma, pulmonary fibrosis, and complications secondary to the use of mechanical devices.

      Patients are also prone to develop nosocomial pneumonia.

      Regular assessment should be performed by periodic radiographic chest monitoring.

      Pulmonary fibrosis may follow acute lung injury associated with acute respiratory distress syndrome (ARDS).

      High oxygen concentrations and the use of large tidal volumes may worsen acute lung injury.


      Common cardiovascular complications in patients with acute respiratory failure include hypotension, reduced cardiac output, arrhythmia, pericarditis, and acute myocardial infarction.

      These complications may be related to the underlying disease process, mechanical ventilation, or the use of pulmonary artery catheters.


      The major gastrointestinal complications associated with acute respiratory failure are hemorrhage, gastric distention, ileus, diarrhea, and pneumoperitoneum.

      Stress ulceration is common in patients with acute respiratory failure; the incidence can be reduced by routine use of antisecretory agents or mucosal protectants.


      Nosocomial infections, such as pneumonia, urinary tract infections, and catheter-related sepsis, are frequent complications of acute respiratory failure.

      These usually occur with the use of mechanical devices.

      The incidence of nosocomial pneumonia is high and associated with significant mortality.


      Acute renal failure and abnormalities of electrolytes and acid-base homeostasis are common in critically ill patients with respiratory failure.

      The development of acute renal failure in a patient with acute respiratory failure carries a poor prognosis and high mortality. The most common mechanisms of renal failure in this setting are renal hypoperfusion and the use of nephrotoxic drugs (including radiographic contrast material).


      These include malnutrition and its effects on respiratory performance and complications related to administration of enteral or parenteral nutrition.

      Complications associated with nasogastric tubes, such as abdominal distention and diarrhea, also may occur.

      Complications of parenteral nutrition may be mechanical due to catheter insertion, infectious, or metabolic (eg, hypoglycemia, electrolyte imbalance).


      The mortality rate for acute respiratory distress syndrome (ARDS) is approximately 40%. Younger patients (

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      St. John Health System Warren, Michigan 7 years ago


      Patients generally are prescribed bed rest during early phases of respiratory failure management. However, ambulation as soon as possible helps ventilate atelectatic areas of the lung.


      The pharmacotherapy of cardiogenic pulmonary edema and acute exacerbations of COPD is discussed here. The goals of therapy in cardiogenic pulmonary edema are to achieve a pulmonary capillary wedge pressure of 15-18 mm Hg and a cardiac index greater than 2.2 L/min/m2, while maintaining adequate blood pressure and organ perfusion. These goals may need to be modified for some patients. Diuretics, nitrates, analgesics, and inotropics are used in the treatment of acute pulmonary edema.


      First-line therapy generally includes a loop diuretic such as furosemide, which inhibits sodium chloride reabsorption in the ascending loop of Henle.

      Furosemide (Lasix)

      Administer loop diuretics IV because this allows for both superior potency and a higher peak concentration despite increased incidence of adverse effects, particularly ototoxicity.






      10-20 mg IV for patients symptomatic with CHF not already using diuretics

      40-80 mg IV for patients already using diuretics

      80-120 mg IV for patients whose symptoms are refractory to initial dose after 1 h of administration or who have significant renal insufficiency

      Higher doses and more rapid redosing may be appropriate for patients in severe distress


      Not established

      Metolazone (Mykrox, Zaroxolyn)

      Has been used as adjunctive therapy in patients initially refractory to furosemide. Has been demonstrated to be synergistic with loop diuretics in treating refractory patients and causes a greater loss of potassium. Potent loop diuretic that sometimes is used in combination with Lasix for more aggressive diuresis. Also used in patients with a degree of renal dysfunction for initiating diuresis.






      5-10 mg PO before redosing with furosemide


      Not established


      These agents reduce myocardial oxygen demand by lowering preload and afterload. In severely hypertensive patients, nitroprusside causes more arterial dilatation than nitroglycerin. Nevertheless, due to the possibility of thiocyanate toxicity and the coronary steal phenomenon associated with nitroprusside, IV nitroglycerin may be the initial therapy of choice for afterload reduction.

      Nitroglycerin (Nitro-Bid, Nitrol)

      SL nitroglycerin and Nitrospray are particularly useful in the patient who presents with acute pulmonary edema with a systolic blood pressure of at least 100 mm Hg. Similar to SL, onset of Nitrospray is 1-3 min, with a half-life of 5 min. Administration of Nitrospray may be easier, and it can be stored for as long as 4 y. One study demonstrated significant and rapid hemodynamic improvement in 20 patients with pulmonary edema who were given Nitrospray. Topical nitrate therapy is reasonable in a patient presenting with class I-II CHF. However, in patients with more severe signs of heart failure or pulmonary edema, IV nitroglycerin is preferred because it is easier to monitor hemodynamics and absorption, particularly in patients with diaphoresis. Oral nitrates, due to delayed absorption, play little role in the management of acute pulmonary edema.






      Nitrospray: 1 puff (0.4 mg) equivalent to a single 1/150 SL; may repeat q3-5min as hemodynamics permit, not to exceed 1.2 mg

      Ointment: Apply 1-2 inches of nitropaste to chest wall

      Injection: Start at 20 mcg/min IV and titrate to effect in 5- to 10-mcg increments q3-5min


      Not established

      Nitroprusside sodium (Nitropress)

      Produces vasodilation of venous and arterial circulation. At higher dosages, may exacerbate myocardial ischemia by increasing heart rate. Easily titratable.






      10-15 mcg/min IV; titrate to effective dose range of 30-50 mcg/min and a systolic blood pressure of at least 90 mm Hg


      Not established


      Morphine IV is an excellent adjunct in the management of acute pulmonary edema. In addition to being both an anxiolytic and an analgesic, its most important effect is venodilation, which reduces preload. Also causes arterial dilatation, which reduces systemic vascular resistance and may increase cardiac output.

      Morphine sulfate (Duramorph, Astramorph, MS Contin)

      DOC for narcotic analgesia due to reliable and predictable effects, safety profile, and ease of reversibility with naloxone. Morphine sulfate administered IV may be dosed in a number of ways and commonly is titrated until desired effect is obtained.






      2-5 mg and repeated q10-15min IV unless respiratory rate is

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      Hamad Medical Corporation 7 years ago

      Weaning from mechanical ventilation

      Weaning or liberation from mechanical ventilation is initiated when the underlying process that necessitated ventilatory support has improved. In some patients, such as those recovering from uncomplicated major surgery or a toxic ingestion, withdrawal of ventilator support may be done without weaning. In patients who required more prolonged respiratory therapy, the process of liberating the patient from ventilatory support may take much longer.

      A patient who has stable underlying respiratory status, adequate oxygenation (eg, PaO2/FiO2 >200 on PEEP

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      L’Institut Curie 7 years ago

      Obstructive airway diseases

      In patients with COPD or asthma, institution of mechanical ventilation may worsen dynamic hyperinflation (auto-PEEP or intrinsic PEEP [PEEPi]). The dangers of auto-PEEP include a reduction in cardiac output and hypotension (because of decreased venous return) and barotrauma.

      The goals of mechanical ventilation in obstructive airway diseases are to unload the respiratory muscles, achieve adequate oxygenation, and minimize the development of dynamic hyperinflation and its associated adverse consequences.

      Following the initiation of mechanical ventilation, patients with status asthmaticus frequently develop severe dynamic hyperinflation, which is often associated with adverse hemodynamic effects. The development of dynamic hyperinflation can be minimized by delivering the lowest possible minute ventilation in the least possible time. Therefore, the initial ventilatory strategy should involve the delivery of relatively low tidal volumes (eg, 8-10 mL/kg) and lower respiratory rates (eg, 8-12 breaths per min) with a high inspiratory flow rate.

      In the absence of hypoxia, hypercapnia generally is well tolerated in most patients. Even marked levels of hypercapnia are preferable to attempts to normalize the PCO2, which could lead to dangerous levels of hyperinflation.

      Patients often require large amounts of sedation and occasionally paralysis until the bronchoconstriction and airway inflammation have improved.

      If a decision is made to measure trapped-gas volume (VEI), as recommended by some investigators, an attempt should be made to keep it below 20 mL/kg. The routine measurement of VEI is not recommended because measurement of plateau pressure and auto-PEEP provide similar information and are much easier to perform.

      Patients with COPD have expiratory flow limitation and are prone to the development of dynamic hyperinflation. Here again, the goal of mechanical ventilation is to unload the respiratory muscles while minimizing the degree of hyperinflation. The use of extrinsic PEEP may be considered in spontaneously breathing patients in order to reduce the work of breathing and to facilitate triggering of the ventilator. Care must be exercised to avoid causing further hyperinflation, and the set level of PEEP should always be less than the level of auto-PEEP.

      Facilitating patient-ventilator synchrony

      During mechanical ventilation, many patients sometimes experience asynchrony between their own spontaneous respiratory efforts and the pattern of ventilation imposed by the ventilator. This can occur with both controlled and patient-initiated modes of ventilation.

      In order to achieve synchrony, the ventilator must not only sense and respond quickly to the onset of the patient's inspiratory efforts, it also must terminate the inspiratory phase when the patient's "respiratory clock" switches to expiration. Asynchronous interactions, commonly referred to as "fighting the ventilator," may occur when ventilator breaths and patient efforts are out of phase. This may lead to excessive work of breathing, increased respiratory muscle oxygen consumption, and decreased patient comfort.

      Patient-ventilator asynchrony should be minimized, and a variety of ways is available to achieve this. Modern ventilators are equipped with significantly better valve characteristics compared to older-generation ventilators. Flow-triggering (with a continuous flow rate) appears to be more sensitive and more responsive to patient's spontaneous inspiratory efforts.

      Patient-ventilator asynchrony often occurs in the presence of auto-PEEP. Auto-PEEP creates an inspiratory threshold load and thereby decreases the effective trigger sensitivity. This may be partially offset by the application of external PEEP.

      Sometimes, additional sedation may be necessary to achieve adequate patient-ventilator synchrony.

      Noninvasive ventilatory support

      The application of ventilatory support through a nasal or full face mask in lieu of ETT is being used increasingly for patients with acute or chronic respiratory failure.

      Noninvasive ventilation should be considered in patients with mild-to-moderate acute respiratory failure. The patient should have an intact airway, airway-protective reflexes, and be alert enough to follow commands.

      In clinical trials, noninvasive positive-pressure ventilation (NPPV) has proven beneficial in acute exacerbations of COPD and asthma, decompensated CHF with mild-to-moderate pulmonary edema, and pulmonary edema from hypervolemia. Reports conflict regarding its efficacy in acute hypoxemia due to other causes (eg, pneumonia). A variety of methods and systems are available for delivering noninvasive ventilatory support.

      The benefits of NPPV depend on the underlying cause of respiratory failure. In acute exacerbations of obstructive lung disease, NPPV decreases PaCO2 by unloading the respiratory muscles and supplementing alveolar ventilation. The results of several clinical trials support the use of NPPV in this setting.

      In a large randomized trial comparing NPPV with a standard ICU approach, the use of NPPV was shown to reduce complications, duration of ICU stay, and mortality.8 In patients in whom NPPV failed, mortality rates were similar to the intubated group (25% vs 30%).

      Plant and colleagues recently published the largest prospective randomized study comparing NPPV with standard treatment in patients with COPD exacerbation. NPPV was administered on the ward; the nurses were trained for 8 hours in the preceding 3 months. Treatment failed in significantly more patients in the control group (27% vs 15%), and in-hospital mortality rates were significantly reduced by NPPV (20% to 10%).

      In addition, 3 Italian cohort studies with historical or matched control groups have suggested that long-term outcome of patients treated with NPPV is better than that of patients treated with medical therapy and/or endotracheal intubation.

      In acute hypoxemic respiratory failure, NPPV also helps maintain an adequate PaO2 until the patient improves.

      In cardiogenic pulmonary edema, NPPV improves oxygenation, reduces work of breathing, and may increase cardiac output.

      When applied continuously to patients with chronic ventilatory failure, NPPV provides sufficient oxygenation and/or carbon dioxide elimination to sustain life by reversing or preventing atelectasis and/or resting the respiratory muscles.

      Patients with obesity-hypoventilation syndrome benefit from NPPV by reversal of the alveolar hypoventilation and upper airway obstruction.

      Most studies have used NPPV as an intermittent rather than continuous mode of support. Most trials have used inspiratory pressures of 12-20 cm water; expiratory pressures of 0-6 cm water; and excluded patients with hemodynamic instability, uncontrolled arrhythmia, or a high risk of aspiration

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      Continuum Health Partners 7 years ago

      Hypoxemia is the major immediate threat to organ function. Therefore, the first objective in the management of respiratory failure is to reverse and/or prevent tissue hypoxia. Hypercapnia unaccompanied by hypoxemia generally is well tolerated and probably is not a threat to organ function unless accompanied by severe acidosis. Many experts believe that hypercapnia should be tolerated until the arterial blood pH falls below 7.2. Appropriate management of the underlying disease obviously is an important component in the management of respiratory failure.

      A patient with acute respiratory failure generally should be admitted to a respiratory care or intensive care unit. Most patients with chronic respiratory failure can be treated at home with oxygen supplementation and/or ventilatory assist devices along with therapy for their underlying disease.

      Extracorporeal membrane oxygenation (ECMO) may be more effective than conventional management for patients with severe but potentially reversible respiratory failure. Peek et al found that survival without severe disability was significantly higher in patients who were transferred to a single specialized center for consideration of ECMO. In a randomized, controlled trial in 180 patients with a Murray lung injury score of 3.0 or higher, or uncompensated hypercapnia with a pH less than 7.20 despite optimal conventional treatment, 36.7% of patients in the ECMO arm had died or were severely disabled 6 months after randomization compared with 52.9% of patients in the conventional treatment arm. Although average total costs were more than twice as high for ECMO than for conventional care, lifetime quality-adjusted life-years (QALYs) gained were 10.75 for the ECMO group compared with 7.31 for the conventional group.5

      Airway management

      Assurance of an adequate airway is vital in a patient with acute respiratory distress.

      The most common indication for endotracheal intubation (ETT) is respiratory failure.

      ETT serves as an interface between the patient and the ventilator.

      Another indication for ETT is airway protection in patients with altered mental status.

      Correction of hypoxemia

      After securing an airway, attention must turn to correcting the underlying hypoxemia, the most life-threatening facet of acute respiratory failure.

      The goal is to assure adequate oxygen delivery to tissues, generally achieved with a PaO2 of 60 mm Hg or an arterial oxygen saturation (SaO2) of greater than 90%.

      Supplemental oxygen is administered via nasal prongs or face mask; however, in patients with severe hypoxemia, intubation and mechanical ventilation are often required.

      Coexistent hypercapnia and respiratory acidosis may need to be addressed. This is done by correcting the underlying cause or providing ventilatory assistance.

      Mechanical ventilation is used for 2 essential reasons: (1) to increase PaO2 and (2) to lower PaCO2. Mechanical ventilation also rests the respiratory muscles and is an appropriate therapy for respiratory muscle fatigue.

      Ventilator management

      The use of mechanical ventilation during the polio epidemics of the 1950s was the impetus that led to the development of the discipline of critical care medicine.

      Prior to the mid 1950s, negative-pressure ventilation with the use of iron lungs was the predominant method of ventilatory support.

      Currently, virtually all mechanical ventilatory support for acute respiratory failure is provided by positive-pressure ventilation. Nevertheless, negative-pressure ventilation still is used occasionally in patients with chronic respiratory failure.

      Over the years, mechanical ventilators have evolved from simple pressure-cycled machines to sophisticated microprocessor-controlled systems. A brief review of mechanical ventilation is presented as follows.

      Overview of mechanical ventilation

      Positive-pressure versus negative-pressure ventilation: In order for air to enter the lungs, a pressure gradient must exist between the airway and alveoli. This can be accomplished either by raising pressure at the airway (positive-pressure ventilation) or by lowering pressure at the level of the alveolus (negative-pressure ventilation). The iron lung or tank ventilator is the most common type of negative-pressure ventilator used in the past. These ventilators work by creating subatmospheric pressure around the chest, thereby lowering pleural and alveolar pressure, and thus facilitating flow of air into the patient's lungs. These ventilators are bulky, poorly tolerated, and are not suitable for use in modern critical care units. Positive-pressure ventilation can be achieved by an endotracheal or tracheostomy tube or noninvasively through a nasal mask or face mask.

      Controlled versus patient-initiated (ie, assisted): Ventilatory assistance can be controlled (AC) or patient-initiated. In controlled modes of ventilation, the ventilator delivers assistance independent of the patient's own spontaneous inspiratory efforts. In contrast, during patient-initiated modes of ventilation, the ventilator delivers assistance in response to the patient's own inspiratory efforts. The patient's inspiratory efforts can be sensed either by pressure or flow-triggering mechanisms (see Triggering mechanism, below).

      Pressure-targeted versus volume-targeted: During positive-pressure ventilation, either pressure or volume may be set as the independent variable. In volume-targeted (or volume preset) ventilation, tidal volume is the independent variable set by the physician and/or respiratory therapist, and airway pressure is the dependent variable. In volume-targeted ventilation, airway pressure is a function of the set tidal volume and inspiratory flow rate, the patient's respiratory mechanics (compliance and resistance), and the patient's respiratory muscle activity. In pressure-targeted (or pressure preset) ventilation, airway pressure is the independent variable and tidal volume is the dependent variable. The tidal volume during pressure-targeted ventilation is a complex function of inspiratory time, the patient's respiratory mechanics, and the patient's own respiratory muscle activity.

      Interface between patient and ventilator (mask vs endotracheal intubation)

      Mechanical ventilation requires an interface between the patient and the ventilator. In the past, this invariably occurred through an endotracheal or tracheostomy tube, but in recent years, an increasing trend has occurred towards noninvasive ventilation, which can be accomplished by the use of either a full face mask (covering both the nose and mouth) or a nasal mask (see Noninvasive ventilatory support, below).6

      Care of an endotracheal tube includes correct placement of the tube, maintenance of proper cuff pressure, and suctioning to maintain a patent airway.

      Following intubation, the position of the tube in the airway (rather than esophagus) should be confirmed by auscultation of the chest and, ideally, by a carbon dioxide detector. As a general rule, the endotracheal tube should be inserted to an average depth of 23 cm in men and 21 cm in women (measured at the incisor). Confirming proper placement of the endotracheal tube with a chest radiograph is recommended.

      The tube should be secured to prevent accidental extubation or migration into the mainstem bronchus, and the endotracheal tube cuff pressure should be monitored periodically. The pressure in the cuff generally should not exceed 25 mm Hg.

      Endotracheal suctioning can be accomplished by either open-circuit or closed-circuit suction catheters. Routine suctioning is not recommended because suctioning may be associated with a variety of complications, including desaturation, arrhythmias, bronchospasm, severe coughing, and introduction of secretions into the lower respiratory tract.

      Specific modes of ventilatory support

      Pressure support ventilation (PSV): PSV can be categorized as patient-initiated, pressure-targeted ventilation. With PSV, ventilatory assistance occurs only in response to the patient's spontaneous inspiratory efforts. With each inspiratory effort, the ventilator raises airway pressure by a preset amount. When the inspiratory flow rate decays to a minimal level or to a percentage of initi

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      Douglas Hospital Douglas Mental Health University Institute 7 years ago

      Laboratory Studies

      Respiratory failure may be associated with a variety of clinical manifestations. However, these are nonspecific, and very significant respiratory failure may be present without dramatic signs or symptoms. This emphasizes the importance of measuring arterial blood gases in all patients who are seriously ill or in whom respiratory failure is suspected.

      A complete blood count may indicate anemia, which can contribute to tissue hypoxia, whereas polycythemia may indicate chronic hypoxemic respiratory failure.

      A chemistry panel may be helpful in the evaluation and management of a patient in respiratory failure. Abnormalities in renal and hepatic function may either provide clues to the etiology of respiratory failure or alert the clinician to complications associated with respiratory failure. Abnormalities in electrolytes such as potassium, magnesium, and phosphate may aggravate respiratory failure and other organ function.

      Measuring serum creatine kinase with fractionation and troponin I helps exclude recent myocardial infarction in a patient with respiratory failure. An elevated creatine kinase with a normal troponin I may indicate myositis, which occasionally can cause respiratory failure.

      In chronic hypercapnic respiratory failure, serum thyroid-stimulating hormone should be measured to evaluate the possibility of hypothyroidism, a potentially reversible cause of respiratory failure.

      Imaging Studies

      Chest radiograph

      Chest radiography is essential because it frequently reveals the cause of respiratory failure. However, distinguishing between cardiogenic and noncardiogenic pulmonary edema often is difficult.

      Increased heart size, vascular redistribution, peribronchial cuffing, pleural effusions, septal lines, and perihilar bat-wing distribution of infiltrates suggest hydrostatic edema; the lack of these findings suggests acute respiratory distress syndrome (ARDS).


      Echocardiography need not be performed routinely in all patients with respiratory failure. However, it is a useful test when a cardiac cause of acute respiratory failure is suspected.

      The findings of left ventricular dilatation, regional or global wall motion abnormalities, or severe mitral regurgitation support the diagnosis of cardiogenic pulmonary edema.

      A normal heart size and normal systolic and diastolic function in a patient with pulmonary edema would suggest acute respiratory distress syndrome (ARDS).

      Echocardiography provides an estimate of right ventricular function and pulmonary artery pressure in patients with chronic hypercapnic respiratory failure.

      Other Tests

      Patients with acute respiratory failure generally are unable to perform pulmonary function tests (PFTs). However, PFTs are useful in the evaluation of chronic respiratory failure.

      Normal values of forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) suggest a disturbance in respiratory control.

      A decrease in FEV1 -to-FVC ratio indicates airflow obstruction, whereas a reduction in both the FEV1 and FVC and maintenance of the FEV1 -to-FVC ratio suggest restrictive lung disease.

      Respiratory failure is uncommon in obstructive diseases when the FEV1 is greater than 1 L and in restrictive diseases when the FVC is more than 1 L.

      An ECG should be performed to evaluate the possibility of a cardiovascular cause of respiratory failure; it also may detect dysrhythmias resulting from severe hypoxemia and/or acidosis.


      Right heart catheterization

      This remains a controversial issue in the management of critically ill patients.

      Invasive monitoring probably is not routinely needed in patients with acute hypoxemic respiratory failure, but when significant uncertainty about cardiac function, adequacy of volume resuscitation, and systemic oxygen delivery remain, right heart catheterization should be considered.

      Measurement of pulmonary capillary wedge pressure may be helpful in distinguishing cardiogenic from noncardiogenic edema.

      The pulmonary capillary wedge pressure should be interpreted in the context of serum oncotic pressure and cardiac function.


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      Hadassah Medical Organization 7 years ago

      These diseases can be grouped according to the primary abnormality and the individual components of the respiratory system, as follows:

      Central nervous system disorders

      A variety of pharmacological, structural, and metabolic disorders of the CNS are characterized by depression of the neural drive to breathe.

      This may lead to acute or chronic hypoventilation and hypercapnia.

      Examples include tumors or vascular abnormalities involving the brain stem, an overdose of a narcotic or sedative, and metabolic disorders such as myxedema or chronic metabolic alkalosis.

      Disorders of the peripheral nervous system, respiratory muscles, and chest wall

      These disorders lead to an inability to maintain a level of minute ventilation appropriate for the rate of carbon dioxide production.

      Concomitant hypoxemia and hypercapnia occur.

      Examples include Guillain-Barré syndrome, muscular dystrophy, myasthenia gravis, severe kyphoscoliosis, and morbid obesity.

      Abnormalities of the airways

      Severe airway obstruction is a common cause of acute and chronic hypercapnia.

      Examples of upper airway disorders are acute epiglottitis and tumors involving the trachea; lower airway disorders include COPD, asthma, and cystic fibrosis.

      Abnormalities of the alveoli

      The diseases are characterized by diffuse alveolar filling, frequently resulting in hypoxemic respiratory failure, although hypercapnia may complicate the clinical picture.

      Common examples are cardiogenic and noncardiogenic pulmonary edema, aspiration pneumonia, or extensive pulmonary hemorrhage. These disorders are associated with intrapulmonary shunt and an increased work of breathing.

      Common causes of type I (hypoxemic) respiratory failure

      Chronic bronchitis and emphysema (COPD)


      Pulmonary edema

      Pulmonary fibrosis



      Pulmonary embolism

      Pulmonary arterial hypertension


      Granulomatous lung diseases

      Cyanotic congenital heart disease


      Adult respiratory distress syndrome

      Fat embolism syndrome



      Common causes of type II (hypercapnic) respiratory failure

      Chronic bronchitis and emphysema (COPD)

      Severe asthma

      Drug overdose


      Myasthenia gravis



      Primary muscle disorders


      Cervical cordotomy

      Head and cervical cord injury

      Primary alveolar hypoventilation

      Obesity hypoventilation syndrome

      Pulmonary edema

      Adult respiratory distress syndrome



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      Rigshospitalet 7 years ago

      The diagnosis of acute or chronic respiratory failure begins with clinical suspicion of its presence. Confirmation of the diagnosis is based on arterial blood gas analysis. Evaluation of an underlying cause must be initiated early, frequently in the presence of concurrent treatment for acute respiratory failure.

      The cause of respiratory failure is often evident after a careful history and physical examination.

      Cardiogenic pulmonary edema usually develops in the context of a history of left ventricular dysfunction or valvular heart disease.

      A history of previous cardiac disease, recent symptoms of chest pain, paroxysmal nocturnal dyspnea, and orthopnea suggest cardiogenic pulmonary edema.

      Noncardiogenic edema (eg, acute respiratory distress syndrome [ARDS]) occurs in typical clinical contexts such as sepsis, trauma, aspiration, pneumonia, pancreatitis, drug toxicity, and multiple transfusions.


      The signs and symptoms of acute respiratory failure reflect the underlying disease process and the associated hypoxemia or hypercapnia. Localized pulmonary findings reflecting the acute cause of hypoxemia, such as pneumonia, pulmonary edema, asthma, or COPD, may be readily apparent. In patients with acute respiratory distress syndrome (ARDS), the manifestations may be remote from the thorax, such as abdominal pain or long-bone fracture. Neurological manifestations include restlessness, anxiety, confusion, seizures, or coma.

      Asterixis may be observed with severe hypercapnia. Tachycardia and a variety of arrhythmias may result from hypoxemia and acidosis.

      Once respiratory failure is suspected on clinical grounds, arterial blood gas analysis should be performed to confirm the diagnosis and to assist in the distinction between acute and chronic forms. This helps assess the severity of respiratory failure and also helps guide management.

      Cyanosis, a bluish color of skin and mucous membranes, indicates hypoxemia. Visible cyanosis typically is present when the concentration of deoxygenated hemoglobin in the capillaries or tissues is at least 5 g/dL.

      Dyspnea, an uncomfortable sensation of breathing, often accompanies respiratory failure. Excessive respiratory effort, vagal receptors, and chemical stimuli (hypoxemia and/or hypercapnia) all may contribute to the sensation of dyspnea.

      Both confusion and somnolence may occur in respiratory failure. Myoclonus and seizures may occur with severe hypoxemia. Polycythemia is a complication of long-standing hypoxemia.

      Pulmonary hypertension frequently is present in chronic respiratory failure. Alveolar hypoxemia potentiated by hypercapnia causes pulmonary arteriolar constriction. If chronic, this is accompanied by hypertrophy and hyperplasia of the affected smooth muscles and narrowing of the pulmonary arterial bed. The increased pulmonary vascular resistance increases afterload of the right ventricle, which may induce right ventricular failure. This, in turn, causes enlargement of the liver and peripheral edema. The entire sequence is known as cor pulmonale.

      Criteria for the diagnosis of acute respiratory distress syndrome

      Clinical presentation - Tachypnea and dyspnea; crackles upon auscultation

      Clinical setting - Direct insult (aspiration) or systemic process causing lung injury (sepsis)

      Radiologic appearance - Three-quadrant or 4-quadrant alveolar flooding

      Lung mechanics - Diminished compliance (

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      University of Chicago Hospitals 7 years ago


      United States

      Respiratory failure is a syndrome rather than a single disease process, and the overall frequency of respiratory failure is not well known. The estimates for individual diseases mentioned here can be found in the appropriate eMedicine article.


      The mortality rate associated with respiratory failure varies according to the etiology. For acute respiratory distress syndrome, the mortality rate is approximately 45% in most studies; this percentage has not changed over the years.1,2 Acute exacerbation of COPD carries a mortality rate of approximately 30%. The mortality rates for other causative disease processes have not been well described.


      The relation between acute respiratory failure and race is still debated. A recent work by Khan et al suggested that no differences in mortality exist in patients of Asian and Native Indian descent with acute critical illness after adjusting for differences in case mix.3 Moss and Mannino, in a 2002 manuscript, showed worse outcome for African-Americans suffering from acute respiratory distress syndrome (ARDS) as compared with whites when adjusted for case mix.4

      As more prospective association studies are performed, we will have a better knowledge of the impact of race on the outcome of respiratory failure.

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      California Pacific Medical Center 7 years ago

      Respiratory failure can arise from an abnormality in any of the components of the respiratory system, including the airways, alveoli, CNS, peripheral nervous system, respiratory muscles, and chest wall. Patients who have hypoperfusion secondary to cardiogenic, hypovolemic, or septic shock often present with respiratory failure.

      Hypoxemic respiratory failure

      The pathophysiologic mechanisms that account for the hypoxemia observed in a wide variety of diseases are ventilation-perfusion (V/Q) mismatch and shunt. These 2 mechanisms lead to widening of the alveolar-arterial oxygen difference, which normally is less than 15 mm Hg. With V/Q mismatch, the areas of low ventilation relative to perfusion (low V/Q units) contribute to hypoxemia. An intrapulmonary or intracardiac shunt causes mixed venous (deoxygenated) blood to bypass ventilated alveoli and results in venous admixture. The distinction between V/Q mismatch and shunt can be made by assessing the response to oxygen supplementation or calculating the shunt fraction following inhalation of 100% oxygen. In most patients with hypoxemic respiratory failure, these 2 mechanisms coexist.

      Hypercapnic respiratory failure

      At a constant rate of carbon dioxide production, PaCO2 is determined by the level of alveolar ventilation (Va), in which VCO2 is ventilation of carbon dioxide and K is a constant value (0.863).

      (Va = K x VCO2)/PaCO2

      A decrease in alveolar ventilation can result from a reduction in overall (minute) ventilation or an increase in the proportion of dead space ventilation. A reduction in minute ventilation is observed primarily in the setting of neuromuscular disorders and CNS depression. In pure hypercapnic respiratory failure, the hypoxemia is easily corrected with oxygen therapy.

      Ventilatory capacity versus demand

      Ventilatory capacity is the maximal spontaneous ventilation that can be maintained without development of respiratory muscle fatigue. Ventilatory demand is the spontaneous minute ventilation that results in a stable PaCO2. Normally, ventilatory capacity greatly exceeds ventilatory demand. Respiratory failure may result from either a reduction in ventilatory capacity or an increase in ventilatory demand (or both). Ventilatory capacity can be decreased by a disease process involving any of the functional components of the respiratory system and its controller. Ventilatory demand is augmented by an increase in minute ventilation and/or an increase in the work of breathing.

      Pathophysiologic Mechanisms in Acute Respiratory Failure

      The act of respiration engages 3 processes: (1) transfer of oxygen across the alveolus, (2) transport of oxygen to the tissues, and (3) removal of carbon dioxide from blood into the alveolus and then into the environment. Respiratory failure may occur from malfunctioning of any of these processes. In order to understand the pathophysiologic basis of acute respiratory failure, an understanding of pulmonary gas exchange is essential.

      Physiology of gas exchange

      Respiration primarily occurs at the alveolar capillary units of the lungs, where exchange of oxygen and carbon dioxide between alveolar gas and blood takes place. Following diffusion into the blood, the oxygen molecules reversibly bind to the hemoglobin. Each molecule of hemoglobin contains 4 sites for combination with molecular oxygen, 1 g of hemoglobin combines with a maximum of 1.36 mL of oxygen. The quantity of oxygen combined with hemoglobin depends on the level of blood PaO2. This relationship, expressed as the oxygen hemoglobin dissociation curve, is not linear but has a sigmoid-shaped curve with a steep slope between a PaO2 of 10 and 50 mm Hg and a flat portion above a PaO2 of 70 mm Hg. The carbon dioxide is transported in 3 main forms: (1) in simple solution, (2) as bicarbonate, and (3) combined with protein of hemoglobin as a carbamino compound.

      During ideal gas exchange, blood flow and ventilation would perfectly match each other, resulting in no alveolar-arterial PO2 difference. However, even in normal lungs, not all alveoli are ventilated and perfused perfectly. For a given perfusion, some alveoli are underventilated while others are overventilated. Similarly, for known alveolar ventilation, some units are underperfused while others are overperfused. The optimally ventilated alveoli that are not perfused well are called high V/Q units (acting like dead space), and alveoli that are optimally perfused but not adequately ventilated are called low V/Q units (acting like a shunt).

      Alveolar ventilation

      At steady state, the rate of carbon dioxide production by the tissues is constant and equals the rate of carbon dioxide elimination by the lung. This relationship is expressed as PaCO2 = VCO2 x 0.862/Va. This relationship signifies whether the alveolar ventilation is adequate for metabolic needs of the body.

      The efficiency of lungs at carrying out of respiration can be further evaluated by measuring alveolar-to-arterial PaO2 difference. This difference is calculated by the following equation:

      PA O2 = FIO2 x (PB – PH2 O) – PA CO2/R

      For the above equation, PA O2 = alveolar PO2, FIO2 = fractional concentration of oxygen in inspired gas, PB = barometric pressure, PH2 O = water vapor pressure at 37°C, PA CO2 = alveolar PCO2, assumed to be equal to arterial PCO2, and R = respiratory exchange ratio. R depends on oxygen consumption and carbon dioxide production. At rest, VCO2/VO2 is approximately 0.8.

      Even normal lungs have some degree of V/Q mismatching and a small quantity of right-to-left shunt, alveolar PO2 is slightly higher than arterial PO2. However, an increase in alveolar-to-arterial PO2 above 15-20 mm Hg indicates pulmonary disease as the cause of hypoxemia.

      Pathophysiologic causes of acute respiratory failure

      Hypoventilation, V/Q mismatch, and shunt are the most common pathophysiologic causes of acute respiratory failure. These are described in the following paragraphs.


      Hyperventilation is an uncommon cause of respiratory failure and usually occurs from depression of the CNS from drugs or neuromuscular diseases affecting respiratory muscles. Hypoventilation is characterized by hypercapnia and hypoxemia. The relationship between PaCO2 and alveolar ventilation is hyperbolic. As ventilation decreases below 4-6 L/min, PaCO2 rises precipitously. Hypoventilation can be differentiated from other causes of hypoxemia by the presence of a normal alveolar-arterial PO2 gradient.

      V/Q mismatch

      V/Q mismatch is the most common cause of hypoxemia. V/Q units may vary from low to high ratios in the presence of a disease process. The low V/Q units contribute to hypoxemia and hypercapnia in contrast to high V/Q units, which waste ventilation but do not affect gas exchange unless quite severe. The low V/Q ratio may occur either from a decrease in ventilation secondary to airway or interstitial lung disease or from overperfusion in the presence of normal ventilation. The overperfusion may occur in case of pulmonary embolism, where the blood is diverted to normally ventilated units from regions of lungs that have blood flow obstruction secondary to embolism. Administration of 100% oxygen eliminates all of the low V/Q units, thus leading to correction of hypoxemia. Hypoxemia increases minute ventilation by chemoreceptor stimulation, but the PaCO2 level generally is not affected.


      Shunt is defined as the persistence of hypoxemia despite 100% oxygen inhalation. The deoxygenated blood (mixed venous blood) bypasses the ventilated alveoli and mixes with oxygenated blood that has flowed through the ventilated alveoli, consequently leading to a reduction in arterial blood content. The shunt is calculated by the following equation:

      QS/QT = (CCO2 – CaO2)/CCO2 – CvO2)

      QS/QT is the shunt fraction, CCO2 (capillary oxygen content) is calculated from ideal alveolar PO2, CaO2 (arterial oxygen content) is derived from PaO2 using the oxygen dissociation curve, and CVO2 (mixed venous oxygen content) can be assumed or measured by drawing mixed venous blood from pulmonary arterial catheter.

      Anatomical shunt exists in normal lungs because of the bronchial and thebesian circulations, a

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      Vancouver Coastal Health 7 years ago

      Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. In practice, respiratory failure is defined as a PaO2 value of less than 60 mm Hg while breathing air or a PaCO2 of more than 50 mm Hg. Furthermore, respiratory failure may be acute or chronic. Although acute respiratory failure is characterized by life-threatening derangements in arterial blood gases and acid-base status, the manifestations of chronic respiratory failure are less dramatic and may not be as readily apparent.

      Bilateral airspace infiltrates on chest radiograph film secondary to acute respiratory distress syndrome that resulted in respiratory failure.

      Classification of respiratory failure

      Respiratory failure may be classified as hypoxemic or hypercapnic and may be either acute or chronic.

      Hypoxemic respiratory failure (type I) is characterized by a PaO2 of less than 60 mm Hg with a normal or low PaCO2. This is the most common form of respiratory failure, and it can be associated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units. Some examples of type I respiratory failure are cardiogenic or noncardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage.

      Hypercapnic respiratory failure (type II) is characterized by a PaCO2 of more than 50 mm Hg. Hypoxemia is common in patients with hypercapnic respiratory failure who are breathing room air. The pH depends on the level of bicarbonate, which, in turn, is dependent on the duration of hypercapnia. Common etiologies include drug overdose, neuromuscular disease, chest wall abnormalities, and severe airway disorders (eg, asthma, chronic obstructive pulmonary disease [COPD]).

      Distinctions between acute and chronic respiratory failure

      Acute hypercapnic respiratory failure develops over minutes to hours; therefore, pH is less than 7.3. Chronic respiratory failure develops over several days or longer, allowing time for renal compensation and an increase in bicarbonate concentration. Therefore, the pH usually is only slightly decreased.

      The distinction between acute and chronic hypoxemic respiratory failure cannot readily be made on the basis of arterial blood gases. The clinical markers of chronic hypoxemia, such as polycythemia or cor pulmonale, suggest a long-standing disorder.


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      Asan Medical Center Seoul 7 years ago

      Pulmonary dysfunction



      Chronic Obstructive Pulmonary Disease



      Pulmonary contusion[1]


      Acute Respiratory Distress Syndrome (ARDS) is a specific and life-threatening type of respiratory failure.

      Cystic Fibrosis

      Cardiac dysfunction

      Pulmonary edema

      Cerebrovascular Accident


      Congestive heart failure

      Valve pathology


      Fatigue due to prolonged tachypnoea in metabolic acidosis

      Intoxication with drugs (e.g., morphine, benzodiazepines) that suppress respiration.

      Neurological Disease

      Toxic Epidermal Necrolysis


      Mechanical Ventilator

      Emergency treatment follows the principles of cardiopulmonary resuscitation. Treatment of the underlying cause is required. Endotracheal intubation and mechanical ventilation may be required. Respiratory stimulants such as doxapram may be used, and if the respiratory failure resulted from an overdose of sedative drugs such as opioids or benzodiazepines, then the appropriate antidote such as naloxone or flumazenil will be given.


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      National Jewish Medical and Research Center 7 years ago

      Type 1 respiratory failure is defined as hypoxemia without hypercapnia, and indeed the PaCO2 may be normal or low. It is typically caused by a ventilation/perfusion (V/Q) mismatch; the volume of air flowing in and out of the lungs is not matched with the flow of blood to the lungs. The basic defect in type 1 respiratory failure is failure of oxygenation characterized by:

      This type of respiratory failure is caused by conditions that affect oxygenation such as:

      Parenchymal disease (V/Q mismatch)

      Diseases of vasculature and shunts: right-to-left shunt, pulmonary embolism

      interstitial lung diseases: ARDS, pneumonia, emphysema.

      [edit]Type 2

      The basic defect in type 2 respiratory failure is characterized by:

      Type 2 respiratory failure is caused by increased airway resistance; both oxygen and carbon dioxide are affected. Defined as the build up of carbon dioxide levels (PaCO2) that has been generated by the body. The underlying causes include:

      Reduced breathing effort (in the fatigued patient)

      A decrease in the area of the lung available for gas exchange (such as in emphysema).


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      Academisch Medisch Centrum & Emma Kinderziekenhuis AMC Universiteit van Amsterdam * 7 years ago

      The term respiratory failure, in medicine, is used to describe inadequate gas exchange by the respiratory system, with the result that arterial oxygen and/or carbon dioxide levels cannot be maintained within their normal ranges. A drop in blood oxygenation is known as hypoxemia; a rise in arterial carbon dioxide levels is called hypercapnia. The normal reference values are: oxygen PaO2 greater than 60 mmHg (8.0 kPa), and carbon dioxide PaCO2 less than 45 mmHg (6.0 kPa). Classification into type I or type II relates to the absence or presence of hypercapnia respectively.


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      Funom Theophilus Makama 7 years ago from Europe

      Don't worry.... They will surely come... Just give them some time and then you'll see lots and lots (or rather read) of contributions.... TO be frank with you, my hubs and their posts make research easier... Anyone who wants to do any research on any medical case or clinical case, just have to come to my hubs where such contributions are made.... No need going to several sites again... I am so happy and blessed to be getting such comments from medical establishments round the world.

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      al_masculine 7 years ago

      ha ha ha ha ha ha! I totally agree with you Dchosen_01. I miss those hospitals and medical establishments..... We are all waiting...

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      Dchosen_01 7 years ago

      hmmm! Thanks for writing this, cos it took me three days to finish this in particula. But I enjoyed it anyway. I have a project to write on about this, so I guess its the right thing to do... Where are all those your affiliate hospitals and medical establishments? 12 days is sure too long for them not to have written their intimidating comments and contributions.... I am eagerly waiting...

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      Funom Theophilus Makama 7 years ago from Europe

      Counting towards 10 hubs now. One more to go. Knowledge of these diseases is very essential. Do not wait until you have them before knowing about them. Its not necessary to read all- about simply know the basics. Enjoy this hub and I wish to have feedbacks, recommendations, questions and as well-criticism. Cheers!