All of the medical management provided to children with heart disease is directed toward increasing cardiac output in low-output states by alteration of the heart rate, preload, afterload, or inherent contractility. As mentioned previously, some of these parameters may be rather fixed due to the inherent limitations of the neonatal ventricular noncompliance.3
Heart rate is the most malleable of the cardiac physiologic parameters. Symptomatic bradycardias of all types are treated with oxygenation, atropine and, in severe cases, with epinephrine and/or isoproterenol followed by transthoracic pacemaker and transvenous pacemaker usage. Symptomatic tachycardia must be differentiated into sinus, supraventricular, or ventricular before specific therapy can be initiated.
Preload disorders are common in children and are most frequently due to shock states with resultant hypovolemia that causes the decreased preload. The hypovolemia may be due to increased loss of total body water, such as occurs in excessive diarrhea or vomiting, or it may be a relative loss of volume due to maldistribution. In the latter circumstance, distributive forms of shock such as in sepsis, neurogenic spinal shock, or anaphylaxis produce relative hypovolemia secondary to increased vasodilation and decreased venous return to the heart. In congestive heart failure, preload is markedly increased when the left atrial pressure becomes elevated. The resulting Starling forces produce pulmonary edema and its resultant hypoxemia. The hypoxemia reduces contractility, further increasing the left atrial pressure and accentuating the increased preload state. Treatment of such a state requires diuretics and vasodilation to reduce preload.
Adequate oxygen delivery is necessary for the myocardium during the diastolic filling phase. The oxygen supply depends on the P o2 of the blood, the hemoglobin concentration, and the coronary perfusion pressure. Hypoxemia results from deoxygenated venous blood entering the systemic circulation by vascular shunts that may be present at any location. Hypoxemia caused by most vascular shunts responds poorly to increasing ambient inspired oxygen. In contrast, most respiratory causes of hypoxemia respond to increasing oxygen.
Anemia profoundly decreases the amount of oxygen available to the tissues by decreasing the amount of oxygen bound to hemoglobin per unit of cardiac output. Transfusions of 10 mL packed red cells per kilogram will raise the hemoglobin approximately 1.5 g/dL and provide improved oxygen-carrying capacity to the tissues. In special circumstances, other competing agents, such as methemoglobinemia and carboxyhemoglobinemia, with increased affinity for oxygen must be excluded.
Myocardial perfusion can only occur during the relaxation phase provided during diastole. The perfusion is markedly impaired under conditions of low cardiac output. Because the coronary perfusion pressure is the difference between the diastolic pressure minus the coronary sinus venous pressure, it follows that any situation that lowers diastolic pressure to 30 to 40 mmHg can lead to poor coronary perfusion, myocardial ischemia, and subsequent ECG changes reflecting injury. Treatment of low diastolic pressure includes infusion with a-adrenergic agents such as phenylephrine, norepinephrine, and epinephrine to raise the diastolic pressure and coronary artery perfusion.
Other factors are also important to augment contractility, but are not as amenable to therapy by emergency physicians. Acidosis adversely affects myocardial contractility and may be persistent after hypovolemia has been corrected. Sodium bicarbonate may rapidly improve contractility in such situations. If acidosis is due to respiratory failure, airway control with endotracheal intubation and mechanical ventilation is useful to correct the hypercapnia and decrease the metabolic demand generated by trying to overcome respiratory failure. Temperature control is also important because elevations can cause an increase in oxygen consumption by 400 percent, causing a marginal cardiovascular system to fail. Ideally, a neutral thermal environment should be maintained to avoid such stress. Hypoglycemia frequently occurs during stressful events, and neonates are less able to respond because of decreased glycogen stores and minimal fat necessary for gluconeogenesis. Low serum glucose of less than 40 mg/dL should be corrected with an infusion of either 25% or 10% dextrose solution. Electrolyte disturbances can interfere with both inotropic and chronotropic responses to decreased cardiac output. Appropriate monitoring of concentrations of potassium, calcium, magnesium, sodium, chloride, phosphate, and bicarbonate is prudent. Finally, attempts must be made to minimize stress in ill neonates. Alleviation of external stressors such as tubing manipulation or skin care should be minimized to increase oxygen availability by decreasing agitation. All attempts to provide for parental care and the minimization of blood drawing are crucial to this goal.
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