Circulatory Emergencies: Shock

Abstract

Shock is an abnormal physiologic state of inadequate tissue perfusion that is a common end point for various diseases.Physiologic subtypes of shock include hypovolemic, cardiogenic, distributive, and obstructive shock. Multiple subtypes of shock can be present with a single disease.With the exception of cardiogenic shock, the most common mistake in management is not administering enough fl uids in a timely fashion.Use of goal-directed therapy for fl uid-refractory septic shock improves outcome.with only minimal changes in vital signs. 4,5 The term compensated shock is used for patients with shock physiology, but preservation of normal blood pressure. Decompensated shock is used when the patient has hypotension, and is usually a late sign of shock. If untreated, decompensated shock will become irreversible, leading to eventual death.Physiologic subtypes of shock include hypovolemic, cardiogenic, distributive, and obstructive shock. Hypovolemic shock is due to a defi ciency in intravascular volume either through insuffi cient intake or excessive loss of fl uid. Cardiogenic shock is due to failure of the heart to provide suffi cient cardiac output. Distributive shock is defi ned as a change in vascular capacitance resulting in peripheral vasodilation and abnormal redistribution of blood fl ow. Obstructive shock is due to an obstruction of outfl ow from the heart. The differential diagnosis for each type of shock is extensive (Table 8-1).While it is useful to distinguish between the physiologic subtypes of shock, recognition and treatment of the specifi c disorders that lead to shock is equally important. In addition, some diseases have multisystem involvement with several different subtypes of shock. For example, children with septic shock may be hypovolemic from fl uid loss and inadequate intake, and may have sepsis-induced myocardial depression that directly limits contractility and cardiac output. Recognition and ApproachKnowledge of physiologic compensatory responses can help clinicians identify shock subtypes and initiate appropriate management. Cardiac output is regulated by both the heart rate and the stroke volume of each contraction. Preload, cardiac contractility, and afterload determine stroke volume. Preload refl ects both the absolute intravascular volume and changes in venous capacitance. Afterload is related to systemic vascular resistance. The primary physiologic response to compensate for shock is via the sympathetic nervous system. Baroreceptors in the carotid sinus and chemoreceptors in the aorta and carotid bodies sense hypovolemia and hypoxemia, respectively, and activate the sympathetic adrenergic response. The release of catecholamines activates α 1 receptors in peripheral vascular smooth muscle, causing peripheral vasoconstriction. 6 Presynaptic α 2 receptors in the heart and vasculature are activated by norepinephrine released from sympathetic nerves and mediate negative feedback inhibition of further norepinephrine release.