PULMONARY INSUFFICIENCY, (RESPIRATORY FAILURE)
Right sided exudative pleuritis
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.
DISORDERS CAUSING CHRONIC 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
Idiopathic fibrosis (Hamman-Rich syndrome)
Drug sensitivity (hydralazine, busulfan, etc.)
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.
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.
SOME DEVICES THAT ARE USEFUL IN PATIENTS WITH CHRONIC RESPIRATORY FAILURE
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.
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).
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.
HYPERBARIC OXYGEN THERAPY
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.
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).
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
sources and references
- Allewelt M, Schuler P, Bolcskei PL. Ampicillin + sulbactam vs clindamycin +/- cephalosporin for the treatment of aspiration pneumonia and primary lung abscess. Clin Microbiol Infect. Feb 2004;10(2):163-70.
- Appelbaum PC, Spangler SK, Jacobs MR. Beta-lactamase production and susceptibilities to amoxicillin, amoxicillin-clavulanate, ticarcillin, ticarcillin-clavulanate, cefoxitin, imipenem, and metronidazole of 320 non-Bacteroides fragilis Bacteroides isolates and 129 fusobacteria from 28 U.S. Antimicrob Agents Chemother. Aug 1990;34(8):1546-50.
- Bandt PD, Blank N, Castellino RA. Needle diagnosis of pneumonitis. Value in high-risk patients. JAMA. Jun 19 1972;220(12):1578-80.
- Bartlett JG, Gorbach SL, Tally FP. Bacteriology and treatment of primary lung abscess. Am Rev Respir Dis. May 1974;109(5):510-8.
- Bartlett JG, Finegold SM. Anaerobic infections of the lung and pleural space. Am Rev Respir Dis. Jul 1974;110(1):56-77.
- Bartlett JG. HIV infection and surgeons. Curr Probl Surg. Apr 1992;29(4):197-280.
- Finegold SM, George WL, Mulligan ME. Anaerobic infections. Part II. Dis Mon. Nov 1985;31(11):1-97.
- Finegold SM, Rolfe RD. Susceptibility testing of anaerobic bacteria. Diagn Microbiol Infect Dis. Mar 1983;1(1):33-40.
- Herth F, Ernst A, Becker HD. Endoscopic drainage of lung abscesses: technique and outcome. Chest. Apr 2005;127(4):1378-81.
- Hirshberg B, Sklair-Levi M, Nir-Paz R. Factors predicting mortality of patients with lung abscess. Chest. Mar 1999;115(3):746-50.
- Howe C, Sampath A, Spotnitz M. The pseudomallei group: a review. J Infect Dis. Dec 1971;124(6):598-606.
- La Scola B, Michel G, Raoult D. Isolation of Legionella pneumophila by centrifugation of shell vial cell cultures from multiple liver and lung abscesses. J Clin Microbiol. Mar 1999;37(3):785-7.
- Mansharamani N, Balachandran D, Delaney D. Lung abscess in adults: clinical comparison of immunocompromised to non-immunocompromised patients. Respir Med. Mar 2002;96(3):178-85.
- Mansharamani NG, Koziel H. Chronic lung sepsis: lung abscess, bronchiectasis, and empyema. Curr Opin Pulm Med. May 2003;9(3):181-5.
- Narushima M, Suzuki H, Kasai T. Pulmonary nocardiosis in a patient treated with corticosteroid therapy. Respirology. Mar 2002;7(1):87-9.
- Perlino CA. Metronidazole vs clindamycin treatment of anaerobic pulmonary infection. Failure of metronidazole therapy. Arch Intern Med. Oct 1981;141(11):1424-7.
- Pohlson EC, McNamara JJ, Char C. Lung abscess: a changing pattern of the disease. Am J Surg. Jul 1985;150(1):97-101.
- Sanders CV, Hanna BJ, Lewis AC. Metronidazole in the treatment of anaerobic infections. Am Rev Respir Dis. Aug 1979;120(2):337-43.
- Light RW. Clinical practice. Pleural effusion. N Engl J Med. Jun 20 2002;346(25):1971-7.
- Light RW, ed. Pleural Diseases. 5th ed. Baltimore, Md: Lippincott Williams & Wilkins; 2007.
- Light RW, Jenkinson SG, Minh VD, George RB. Observations on pleural fluid pressures as fluid is withdrawn during thoracentesis. Am Rev Respir Dis. May 1980;121(5):799-804.
- Marchi E, Teixeira LR, Vargas FS. Management of malignancy-associated pleural effusion: current and future treatment strategies. Am J Respir Med. 2003;2(3):261-73.
- Romero Candeira S, Hernбndez Blasco L, Soler MJ, Muсoz A, Aranda I. Biochemical and cytologic characteristics of pleural effusions secondary to pulmonary embolism. Chest. Feb 2002;121(2):465-9.
- Sahn SA. Management of complicated parapneumonic effusions. Am Rev Respir Dis. Sep 1993;148(3):813-17.
- Sahn SA. State of the art. The pleura. Am Rev Respir Dis. Jul 1988;138(1):184-234.
- Sahn SA, Good JT Jr. Pleural fluid pH in malignant effusions. Diagnostic, prognostic, and therapeutic implications. Ann Intern Med. Mar 1988;108(3):345-9.
- Sallach SM, Sallach JA, Vasquez E, Schultz L, Kvale P. Volume of pleural fluid required for diagnosis of pleural malignancy. Chest. Dec 2002;122(6):1913-7.
- Seibert AF, Haynes J Jr, Middleton R, Bass JB Jr. Tuberculous pleural effusion. Twenty-year experience. Chest. Apr 1991;99(4):883-6.
- Shaw P, Agarwal R. Pleurodesis for malignant pleural effusions. Cochrane Database Syst Rev. 2004;CD002916.
- Stark P. The pleura. In: Taveras JM, Ferrucci JT, eds. Radiology: Diagnosis/Imaging/Intervention. Philadelphia, Pa: Lippincott-Raven; 2000:1-29.
- Walker-Renard PB, Vaughan LM, Sahn SA. Chemical pleurodesis for malignant pleural effusions. Ann Intern Med. Jan 1 1994;120(1):56-64.
- West SD, Davies RJ, Lee YC. Pleurodesis for malignant pleural effusions: current controversies and variations in practices. Curr Opin Pulm Med. Jul 2004;10(4):305-10.
More by this Author
Rheumatic fever is an inflammatory disease affecting the heart, joints, central nervous system and subcutaneous tissue. It derives its name from involvement of joints and the presence of fever in acute stage. The major...
The estimated incidence is 1 million cases per year, with most effusions caused by congestive heart failure, malignancy, infections, and pulmonary emboli. The estimated prevalence is 320 cases per 100,000 people in...
- 5Nonspecific infections of the bladder-Acute and Chronic cystitis and Acute urethral syndrome in Women
The urinary system showing the bladder The three major nonspecific infections of the bladder are: Acute cystitis, chronic cystitis and Acute urethral syndrome in women. But before we go into these three diseases in...