Shock in Pediatric

Shock is most simply conceptualised as failure of the circulation to provide adequate delivery of oxygen and essential nutrients to the tissues to ensure normal cell respiration. The process leading to this state may be single or multifactorial. In the management of sick and injured children, the emphasis lies in swift recognition of shock followed by rapid assessment of the nature of the circulatory failure. The latter is essential because avoidance of significant morbidity and mortality relies on the clinician’s ability to determine the origin(s) of the shock accurately and initiate appropriate and specific management.

At a cellular level inadequate oxygen delivery leads to lactic acid formation and the development of metabolic acidosis. Up to a point the body compensates for this by redistributing blood flow away from non-essential tissues (e.g. mesenteric circulation, skin) to the vital organs (e.g. brain and heart). This state of compensated shock is completed by increased extraction of oxygen from the blood by these essential organs to maintain oxygen delivery. Uncompensated shock develops when despite these mechanisms the pathological insult makes it impossible for the body’s vital organs to overcome the inadequacy of oxygen delivery. Untreated, uncompensated shock will inevitably lead to a spiralling deterioration. An inflammatory cascade ensues at the endothelium causing cellular tissue damage. If prolonged, this damage becomes irreversible and indeed restoration of adequate circulation at this stage may lead to reperfusion injury, itself exacerbating the damage. Multi-organ failure will follow, which in many cases will be unrecoverable. However, compensated and early, uncompensated shock are treatable and so this chapter focuses on the clinician’s recognition, assessment and initial management of shock in the Pediatric Emergency Department.

Heart Condition During Shock

Shock can be thought of in terms of three key elements that affect the heart’s ability to provide an adequate circulation, namely preload, contractility and afterload.

Preload

Preload refers to the degree of tension placed upon the cardiac muscle as it begins to contract. It is usually considered to be the end-diastolic pressure at the completion of ventricular filling. A sufficient degree of stretch to the myocardium is required to produce a level of contraction as governed by the Frank-Starling mechanism. This stretch is produced by venous return, itself inherently linked to actual circulating volume. A fall in circulating volume will reduce venous return, myocardial stretch, force of myocardial contraction and cardiac output.

Contractility

The force generated during ventricular contraction defines ventricular contractility. Contractility is maximised in a neutral homeostatic environment when myocardial oxygen delivery is adequate, acidosis absent, electrolytes in balance, etc. Improvement in contractility increases cardiac output through improved stroke volume.

Afterload

Afterload may be thought of as the resistance against the heart as it exerts its force during contraction. It is actually the pressure created in the artery leading from the ventricle during ventricular systole. Whilst it is true that too high an afterload would result in a reduction in the output by the ventricle, too low an afterload itself poses significant problems since adequate organ perfusion relies on a finely balanced relationship between preload, contractility and afterload.