Cardiogenic shock is caused by an abnormality in myocardialfunction and is expressed as depressed myocardial contractility and cardiac output with poor tissue perfusion. Compensatory mechanisms may contribute to the progression of shock bydepressing cardiac function further. Neurohormonal vasoconstrictor responses increase afterload and add to the work of thefailing ventricle. Tachycardia may impair coronary blood flow,which decreases myocardial oxygen delivery. Increased central blood volume caused by sodium and water retention andby incomplete emptying of the ventricles during systole resultsin elevated left ventricular volume and pressure, which impairsubendocardial blood flow. As compensatory mechanisms areovercome, the failing left ventricle produces increased ventricularend-diastolic volume and pressure, which leads to increased leftatrial pressure, resulting in pulmonary edema. This sequence alsocontributes to right ventricular failure because of increased pulmonary artery pressure and increased right ventricular afterload.
Primary cardiogenic shock may occur in children who have congenital heart disease. Cardiogenic shock also may occur in previously healthy children secondary to viral myocarditis, dysrhythmias, or toxic or metabolic abnormalities or after hypoxic-ischemic injury (see Chapters 142, 145, and 147, as well as Table 40-1).
Obstructive shock results from mechanical obstruction of ventricular outflow. Causes include congenital lesions such as coarctation of the aorta, interrupted aortic arch, and severe aortic valvular stenosis, along with acquired diseases (e.g., hypertrophic cardiomyopathy) (see Table 40-1). For neonates presenting in shock, obstructive lesions must be considered.
Dissociative shock refers to conditions in which tissue perfusion is normal, but cells are unable to use oxygen because the hemoglobin has an abnormal affinity for oxygen, preventing its release to the tissues (see Table 40-1).
All forms of shock produce evidence that tissue perfusion and oxygenation are insufficient (increased heart rate, abnormal blood pressure, alterations of peripheral pulses). The etiology of shock may alter the initial presentation of these signs and symptoms.
Hypovolemic shock is distinguished from other causes of shock by history and the absence of signs of heart failure or sepsis. In addition to the signs of sympathoadrenal activity (tachycardia, vasoconstriction), clinical manifestations include signs of dehydration (dry mucous membranes, decreased urine output) or blood loss (pallor). Recovery depends on the degree of hypovolemia, the patient’s preexisting status, and rapid diagnosis and treatment. The prognosis is good, with a low mortality in uncomplicated cases.
Patients with distributive shock usually have tachycardia and alterations of peripheral perfusion. In early stages, when cytokine release results in vasodilation, pulses may be bounding, and vital organ function may be maintained (an alert patient, with rapid capillary refill and some urine output in warm shock). As the disease progresses untreated, extremities become cool and mottled with a delayed capillary refill time. At this stage, the patient has hypotension and vasoconstriction. If the etiology of distributive shock is sepsis, the patient often has fever, lethargy, petechiae, or purpura, and he or she may have an identifiable source of infection.
Cardiogenic shock results when the myocardium is unable to supply the cardiac output required to support tissue perfusion and organ function. Because of this self-perpetuating cycle, heart failure progressing to death may be rapid. Patients with cardiogenic shock have tachycardia and tachypnea. The liver is usually enlarged, a gallop is often present, and jugular venous distention may be noted. Because renal blood flow is poor, sodium and water are retained, resulting in oliguria and peripheral edema.