Classification of shock
The diagnosis of shock is purely clinical. It is possible to classify shock into physiological categories but in reality there is usually overlap between these in individual patients. Classification may be useful in diagnosis since clinical signs may differ between types, as may treatment. Shock is most commonly classified by the anatomical site of the circulation failure.
1. Hypovolemic Shock
Hypovolemic shock results from a fall in actual circulating volume within the intravascular space. In children there are:
• Common causes
• dehydration, e.g. diarrhea and vomiting
• hemorrhage
• sepsis (due to fluid redistribution secondary to increased capillary permeability)
• Less common
•burns
• peritonitis
Compensatory mechanisms will be employed in response to a fall in circulating volume.
Cardiac output is maintained or augmented by tachycardia and peripheral vasoconstriction, the latter maintaining afterload. Renal perfusion is reduced as blood is diverted to the brain and heart, resulting in activation of the renin-angiotensin system and a subsequent increase in circulating volume by sodium and water reabsorption.
2. Cardiogenic shock
Cardiogenic shock refers to situations where myocardial contractility is compromised resulting in reduced cardiac output and tissue perfusion. It is less common than hypovolemia as the primary etiology in the shocked child but, since reduced perfusion will always eventually affect myocardial function, it is an inevitable consequence wherever shock is prolonged (see Figure 3.1). Causes are as follows:
• heart failure
• cardiac surgery
• intrinsic myocardial disease, e.g. acute viral myocarditis, cardiomyopathy
• drug toxicity
• electrolyte and acid-base disturbances
• dysrhythmias.
Reduction in cardiac output brings about compensatory manoeuvres as with hypovolemia.
3. Obstructive shock
Obstructive shock describes a scenario where despite adequate contractility the heart is unable to pump out an adequate volume of blood to be oxygenated and/or distributed to the tissues. Causes include:
• obstructive congenital cardiac lesion, e.g. aortic coarctation or critical aortic valve
stenosis
• tension pneumothorax
• cardiac tamponade.
4. Distributive shock
Distributive shock is usually a complication of severe infection. It is the principal pathophysiological process that defines septic shock. In the presence of overwhelming sepsis an unchecked, generalised inflamma-tory response develops. Inflammatory mediators such as TNFα, inter-leukin-1 and lipopolysaccharide endotoxin are produced causing local cell damage particularly to vascular endothelium. The vasoactive effects of these mediators on the endothelium produce variation in vascular tone. Whilst areas of vasoconstriction and vasodilatation may coexist side-by-side, the overall effect is that of peripheral vasodilatation and a fall in systemic vascular resistance (SVR). This means that blood is not distributed efficiently to the tissues despite a state of high cardiac output, which may exist in septic shock. Adults in septic shock secondary to Gram negative bacteremia classically present with this picture where good peripheral perfusion mediated by profound vasodilatation gives rise to the description of ‘warm shock’. In children, however, the more common presentation is that of cold peripheries, skin mottling and prolonged capillary refill time. Causes of distributive shock include:
• Septic
• meningococcemia
• Gram negative bacteremia
• streptococcal infection (group B streptococcus in neonates, pneumococcus in older children)
• Non-septic
• anaphylaxis
• neurogenic, e.g. following transection of the spinal cord
• drugs, e.g. vasodilators or anesthetics
5. Dissociative shock
Dissociative shock occurs when there is inadequate oxygen capacity. It occurs in:
• profound anemia
• methemoglobinemia
• carbon monoxide poisoning
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