Cardiogenic shock (CS) is a life-threatening state where the heart fails as a pump, resulting in a low cardiac output that cannot meet the body’s metabolic demands. This primary failure of myocardial function leads to inadequate tissue perfusion and oxygen delivery, rapidly progressing to organ dysfunction. Within the Pediatric Advanced Life Support (PALS) framework, understanding the cause of CS is paramount, as the type of heart failure dictates the immediate treatment. This condition differs significantly from other forms of shock, such as hypovolemic or distributive, because the core problem is the pump itself, not primarily the fluid volume or vessel tone.
Defining Pediatric Cardiogenic Shock
Pediatric cardiogenic shock is characterized by significantly impaired myocardial contractility, leading to a depressed stroke volume and a low cardiac output. The cardiovascular system tries to compensate for this reduced output by increasing the heart rate (tachycardia) and constricting blood vessels (vasoconstriction), which increases systemic vascular resistance (SVR). While these are initial attempts to maintain blood pressure, the increased SVR forces the weakened heart to pump against a higher resistance, ultimately worsening the problem by increasing the heart’s oxygen demand.
Children are uniquely vulnerable to this cycle because their cardiac output is highly dependent on their heart rate, as their ventricles are less compliant and cannot increase stroke volume as effectively as an adult heart. The physiologic response often becomes detrimental, as the persistently high heart rate further reduces the time for ventricular filling, which compounds the low stroke volume. A distinguishing feature is pulmonary edema, indicated by increased work of breathing and crackles, resulting from blood backing up into the pulmonary circulation. This differentiates it from hypovolemic shock, where the patient is typically fluid-depleted.
Congenital and Structural Cardiac Defects
Structural heart defects are a frequent cause of cardiogenic shock, particularly in neonates and young infants, often presenting after the transitional period from fetal circulation. These defects cause shock by creating either an obstruction to blood flow or a severe volume overload that overwhelms the heart muscle. The most acute presentations are often seen with duct-dependent systemic circulation lesions, where the survival of the newborn relies on the patent ductus arteriosus (PDA) remaining open to supply the body.
Conditions like Hypoplastic Left Heart Syndrome (HLHS), critical coarctation of the aorta, or critical aortic stenosis all obstruct the outflow of blood from the left side of the heart. When the PDA naturally begins to close, the systemic circulation is suddenly cut off or severely restricted, leading to profound shock and collapse. Immediate intervention to reopen or maintain the ductus is necessary to re-establish blood flow to the body.
Other structural defects, such as large ventricular septal defects (VSDs) or atrioventricular canal defects (AVCDs), can lead to cardiogenic shock over a longer period. These lesions cause a large volume of blood to shunt from the high-pressure left side of the heart to the low-pressure right side and back to the lungs. This excessive pulmonary blood flow causes chronic volume overload, leading to severe heart failure and eventually cardiogenic shock, typically presenting weeks or months after birth.
Acquired Myocardial Disease
A second major category involves diseases that directly damage previously healthy heart muscle after birth, causing acquired myocardial dysfunction. These are more common causes of cardiogenic shock in older infants and children than congenital defects. The primary mechanism is a widespread reduction in the contractility of the heart muscle fibers, meaning the muscle simply cannot squeeze hard enough to circulate blood effectively.
Myocarditis is a common acquired cause, typically resulting from a viral infection that triggers an inflammatory response in the heart muscle. This inflammation causes the heart muscle to swell and become severely weakened, leading to acute pump failure. Cardiomyopathies, which are diseases of the heart muscle structure or function, are also significant culprits, with dilated cardiomyopathy being a frequent form where the left ventricle is enlarged and weak.
Severe systemic illness, such as overwhelming sepsis, can also induce a form of acquired myocardial disease known as septic cardiomyopathy. Toxins produced by bacteria or the body’s own inflammatory response during sepsis can directly depress the heart muscle’s function, leading to a state of combined distributive and cardiogenic shock. This direct injury to the myocardium is a severe complication, accounting for many cardiogenic shock cases in children admitted for acute decompensated heart failure.
Rate and Rhythm Disturbances
Rate and rhythm disturbances, or arrhythmias, can compromise cardiac output dramatically, even in a structurally normal heart, leading to cardiogenic shock. The mechanical timing of the heart is compromised, overriding the heart’s ability to fill and eject blood efficiently. The most common pathological rhythm disturbance in children is supraventricular tachycardia (SVT), which involves an excessively fast heart rate originating above the ventricles.
When the heart rate exceeds a certain threshold, often above 220 beats per minute in infants, the ventricles do not have enough time to fill completely with blood between beats. This inadequate filling time severely limits the stroke volume, causing a rapid decline in overall cardiac output and precipitating shock. Conversely, profound bradycardia, or an abnormally slow heart rate, can also cause shock because the child’s heart cannot compensate for the low rate by increasing the stroke volume significantly. The resulting mechanical failure, whether too fast or too slow, necessitates prompt rhythm correction to restore normal hemodynamics.