Shock: Definition, Classification And Pathophysiology
What is Shock?
Shock is a clinical syndrome resulting from gross impairment of tissue perfusion and widespread cellular dysfunction caused by diminution in oxygen delivery.
1. Cardiogenic Shock: This is caused by rapid reduction in the cardiac output, let's note the following points:
- It is secondary to tachy- or bradyarrhythmias.
- It is secondary to obstructive or regurgitant lesions
- It is secondary to impairment of myocardial function.
- Obstructive lesions such as cardiac tamponade occurring in pericardial effusion, pulmonary hypertension and aortic dissection.
2. Hypovolemic shock: In this condition, the circulating blood volume is absolutely or relatively reduced. Let's note the following points
- Can be due to External or internal hemorrhage
- Fluid loss or sequestration-grastrointestinal, urinary or cutaneous
3. Toxic and metabolic shock
- Late stages of renal/hepatic/respiratory failure.
- Drug overdosages, e.g, hypotensives and diuretics, intoxications e.g, organo-phosphorus.
- Severe acidosis and alkalosis.
4. Endocrinologic causes
- Addison's disease
- Diabetic ketoacidosis, diabetes insipidus.
- Myxedema coma, thyrotoxic crisis, parathyroid dysfunction
5. Miscellaneous causes
- Septic shock caused by bacterial infection
- Anaphylactic shock caused by type I hypersensitivity reaction.
- Neurogenic shock caused by loss of vasomotor tone.
In shock, there is a disparity between the blood volume and the circulatory bed. This may be due to loss of blood volume, diminished cardiac output or loss of vascular tone affecting the circulatory bed. Shock is reversible in the early stages. Compensatory phenomena such as sympathetic overactivity leading to vasoconstriction and reflex tachycardia serve to maintain the blood pressure and systemic perfusion. These vascular responses are maximal in the vessels of the skin, kidneys, splanchnic areas, and skeletal muscles. These vasomotor phenomena serve to redirect the available blood to the vital organs like brain and heart. If shock persists or becomes severe, the compensatory mechanisms fail and progressive tissue damage occurs. Blood supply to the vital organs also suffers.
When the perfusion of tissues and delivery of oxygen are decreased, anaerobic metabolism supervenes. Hypoxia, hypercapnia and acidosis (both metabolic and lactic) ensue. Integrity of the capillary wall is lost leading to extravasation of protein-rich fluid into the extravasation space. Intense ischemia damages the intestinal mucosa resulting in the entry of bacteria and toxins into the circulation. This leads to further aggravation of hypotension and shock. Release of histamine and histamine-like substances enhance vasodilatation and capillary permeability. Disseminated intravascular coagulation results from the release of thromboplastic substances and this further damages the microcirculation of vital organs. This worsens the shock. Irrespective of the primary cause persistence of shock leads to myocardial dysfunction and further reduction in cardiac output.
© 2013 Funom Theophilus Makama