Cardiogenic Shock

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Cardiogenic shock occurs when the heart fails as a pump to provide adequate circulation to meet the metabolic needs of the body. Although less common than other forms of shock, cardiogenic shock does occur in the pediatric population.The pathophysiology of cardiogenic shock is similar to that of other shock states. Adequate oxygen delivery at the tissue level is the primary concern and depends on cardiac output. Cardiac output is influenced by stroke volume and heart rate, represented by the following formula:Stroke volume is dependent on preload, contractility, and afterload. Preload is the end-diastolic stretch provided by filling of the ventricles, contractility is the force generated during ventricular systole, and afterload is the pressure needed to eject blood out of the ventricles. Factors within this formula can be manipulated to increase cardiac output and alleviate shock.Cardiogenic shock in the pediatric population may be related to congenital or acquired heart disease or due to noncardiac causes. Examples of congenital heart disease include left-to-right shunts such as large ventricular septal defects. These types of defects can cause reduced stroke volume due to decreased preload in the left ventricle. In obstructive lesions such as coarctation of the aorta, the heart may be unable to generate sufficient force to overcome the obstruction and provide adequate cardiac output. Acquired causes such as infectious cardiomyopathies can impede contractility, while arrhythmias may affect stroke volume through heart rate irregularities. Examples of noncardiac causes of reduced cardiac output include pneumothorax, large pulmonary embolus, or electrolyte abnormalities such as hyperkalemia or hypocalcemia.The clinical features of cardiogenic shock are direct manifestations of oxygen deprivation to vital organs. At first, symptoms may appear vague. Infants may present with poor feeding or appear less active and can quickly progress to lethargy. Older children may appear fatigued and complain of difficulty with breathing or chest pain. As shock progresses, they may experience syncope or an altered mental status. Physical examination may reveal tachycardia, tachypnea, pallor, cool or mottled extremities, or weak distal pulses. Signs of heart failure such as gallop rhythm, jugular venous distension, crackles (rales), and hepatomegaly may develop as back pressure of blood into the pulmonary and venous circulations worsens. If there is further deterioration to uncompensated shock, multisystem organ failure may ensue, leading to coma and death.When cardiogenic shock is suspected, diagnostic tests, including electrocardiography, chest radiography, and echocardiography, are helpful. Electrocardiography may reveal rhythm abnormalities or findings consistent with cardiomyopathy. Chest radiographs may show such signs of heart failure as pulmonary congestion or cardiomegaly or reveal a noncardiac cause of cardiogenic shock. The most informative tool for diagnosis of cardiogenic shock and its cause is two-dimensional echocardiography with Doppler. Echocardiography provides detailed information about structural abnormalities, which is particularly important when managing neonates who have potential congenital heart disease. Echocardiography also provides information about systolic and diastolic function, wall motion, contractility, valve function, and ejection fraction, which helps to guide management. Laboratory assessment of glucose, electrolytes, calcium, blood gas, cardiac enzymes, and viral titers may be helpful, depending on the clinical scenario.The goal of acute management of cardiogenic shock is to improve oxygen delivery to all organs. The body naturally attempts this by increasing the heart rate. The clinician’s role is to judiciously modulate preload, afterload, and contractility to achieve the same goal. Where possible, reducing the body’s oxygen demand can help ensure adequate distribution of this vitally important but limited resource. Securing a stable airway to provide oxygen and establishing access to deliver fluid and medications are essential. Calcium should be replaced if values are low because this mineral ensures effective ventricular contractions. Boluses of 5 to 10 mL/kg of isotonic fluids may help increase preload to yield larger stoke volumes. Neonates with ductal-dependent lesions in cardiogenic shock should be treated with prostaglandin E1 to maintain a patent ductus arteriosus. Sedation can be a useful adjunct to reduce oxygen demand of skeletal muscle in fussy or agitated infants and toddlers. Neonates and infants are also at higher risk of hypothermia; maintaining normothermia with a heating resuscitation bed can reduce their metabolic demand for heat generation.Finally, inotropic agents should be considered early to prevent volume overload. Vasopressors such as dopamine, dobutamine, and epinephrine help increase contractility to produce larger stroke volumes. Agents such as milrinone, nitroprusside, and inhaled nitric oxide help increase stroke volumes by reducing afterload. Phenylephrine and norepinephrine should be avoided because of their potent vasoconstrictive effects, which can worsen afterload. In cases of cardiogenic shock refractory to medications, extracorporeal membrane oxygenation or ventricular assist devices can be used.COMMENTS: One of the challenges in caring for pediatric patients who present in shock is differentiating those with hypovolemic or septic shock, which are more common in pediatrics, from those with cardiogenic shock. This is important because fluid boluses should be used more judiciously in cardiogenic shock. Patients with cardiogenic shock may present with hypovolemia, euvolemia, or hypervolemia. Diagnosis of cardiogenic shock can be assisted by a careful physical examination that reveals signs of congestive heart failure, third heart sound, hepatomegaly, or jugular venous distention. Because cardiac output is more strongly influenced by heart rate than stroke volume in young children, those who have less myocardial muscle mass may present with more subtle symptoms. Rapid identification of cardiogenic shock is essential to avoid overly aggressive fluid resuscitation and fluid overload but more rapid initiation of inotropic medication interventions.

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