f Post graduate mcqs and discussion : SHOCK

Saturday, April 7


 The term, shock, denotes a clinical state of poor perfusion to the extent that the body demands are not suitably met from a great increase in metabolic demands (oxygen consumption) and/or decrease in metabolic supply (oxygen delivery).


Two major types are recognized:

a. intravascular hypovolemia
b . intravascular normo- or hypervolemia.

a. Intravascular hypovolemia is caused by loss of volume in the form of loss of blood (severe hemorrhage), protein-rich fluid (nephrotic syndrome, burns), or protein-poor fluid (acute gastroenteritis), or decrease in vascular resistance (anaphylactic shock, drugs, denervation injuries and early “warm” septic shock).

b.  Intravascular normo- or hypervolemia is caused by cardiac dysfunction (coronary artery disease, myocarditis, cardiomyopathy, hypoxemia, metabolic insult), inflow obstruction (pericardial temponade, intracardiac tumors), outflow obstruction (malignant hypertension, congenital heart disease in the form of severe aortic stenosis or coarctation, or hypoplastic left heart syndrome), and arrhythmias (supraventricular tachycardia).

Clinical Manifestations 

These are by and large similar in the two types and include tachycardia, normal or low blood pressure, cool peripheral extremities due to profound vasoconstriction and hypoperfusion with the increasing severity of volume loss, there is tendency for the cooling to extent to the proximal parts. In shock due to loss of resistance, patients extremities are unduly warm due to vasodilatation. In addition, postural hypotension may be remarkable. An important example of this type of shock is septic shock associated with septicemia. As the vascular epithelium in this shock loses its integrity, it starts leaking fluid into the perivascular space, patient may develop adult respiratory distress syndrome (ARDS). With further progression, myocardial function decreases with reduced cardiac output together with secondary severe vasoconstriction. This is the stage of cold shock.


It is based on a good history, physical examination and laboratory support. As the laboratory results are likely to take time, resuscitation of the patient with cardiorespiratory collapse and rest of the initial treatment must never
be delayed, especially his oxygenation, ventilation and access to the vascular system through IV line or intraosseous line. Among laboratory tests of special importance are or packed cell volume (PCV), serum calcium, glucose, potassium, urea-nitrogen, creatinine, LFT, coagulation screen, blood culture, etc. Capillary refill time is a useful parameter of peripheral perfusion. Swan-Ganz catheterization of pulmonary artery is of value to demonstrate a reduced cardiac output/ index central venous pressure (CVP) and left atrial pressure (LAP), and very high systemic vascular resistance (SVR). Cardiac evaluation in nonvolemic shock should further include an ECG, a chest X-ray and echocardiography.


Treatment of hypovolemic shock due to loss of intravascular of volume is replacement of volume which is initially carried out by using isotonic solutions such as normal saline or lactated Ringer’s solution. Whole blood, fresh frozen plasma or 5% albumin is administered in specific etiologic situations. Treatment of hypovolemic shock due to decrease in vascular resistance is volume resuscitation and administration of a vasoconstrictor. Treatment of septic shock depends on it stage. In the initial “warm” stage, volume resuscitation and vaso-constrictors are needed. In the subsequent “cold” stage, therapy should include positive inotropes and afterload reduction. Broad-spectrum antibiotics are strongly recommended. Steroids are indicated only when Waterhouse-Friderichsen syndrome is suspected. Treatment of normovolemic/hypovolemic shock due to myocardial failure is volume resuscitation, antiarrhythmic, inotropic and afterload-reducing agents, and correction of hypoxemia and metabolic abnormalities.