Congenital heart disease: Congestive heart failure

Published on 07/02/2015 by admin

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Last modified 07/02/2015

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Congenital heart disease: Congestive heart failure

William C. Oliver, Jr., MD

Anesthetic management of a patient with congenital heart disease (CHD) and congestive heart failure (CHF) requires a thorough understanding of human anatomy and physiology. Anesthesia is more frequently employed in the setting of cardiac surgery; however, as life expectancy increases in this patient population, anesthesia is increasingly necessary for the performance of noncardiac procedures.

The fetal circulation is perfectly designed to adapt to the intrauterine environment; the anatomic and physiologic characteristics of the fetal circulation also allow the fetus to tolerate CHD. It is with the transition from fetal to postnatal circulation that characteristic physiologic changes usually appear that point to the presence of a cardiac anomaly. The degree of “fetal” circulation that persists after birth determines the impact of extrauterine life; consequently, the diagnosis of CHD may be made immediately after birth or may be delayed for days to months. Certain CHDs typically result in poor ventricular function and hemodynamics with progression to CHF. Unfortunately, the cause of CHF is not always readily apparent in neonates and infants. In addition to CHF, patients with CHD may have secondary effects, such as pulmonary hypertension.

CHD has been classified using numerous systems that represent the biases and interests of their authors, but none have been universally accepted. For this discussion, CHD will be classified according to the presence or absence of cyanosis. Cyanotic lesions are caused by shunting of blood from the pulmonary circulation to the systemic circulation, which results in poor pulmonary blood flow and progressive arterial desaturation. In contrast, lesions without cyanosis (acyanotic) are characterized by pulmonary overcirculation because of shunt from the systemic to pulmonary circulation that eventually causes CHF. Excessive blood to the lung reduces lung compliance and increases the work of breathing by two mechanisms: (1) increased left atrial pressure resulting in pulmonary venous congestion and pulmonary edema, which decreases the compliance of the lung itself, and (2) increased size of pulmonary vessels, causing greater obstruction to airflow in both large and small airways. A typical example of acyanotic CHD with CHF is the preterm infant with a ductus arteriosus that does not close postnatally (patent ductus arteriosus, or PDA). A large left-to-right (L-to-R) shunt causes systemic circulatory steal, pulmonary overcirculation, and diastolic hypotension. Pharmacologic or surgical closure of the PDA is required to resolve the CHF.

The orifice of the shunt in a PDA may be described as restrictive or nonrestrictive. If the orifice is restrictive, the primary determinant of shunt fraction is the radius of the orifice and pressure gradient. If the orifice is nonrestrictive, the shunt direction and magnitude depend on the relative resistances of the pulmonary and systemic vascular circulations, which can be manipulated as part of the care of individuals until closure of the PDA.

CHF can also occur from obstructive cardiac defects more quickly than from L-to-R shunts and may progress to circulatory collapse without immediate intervention. Obstructive defects are characterized as subvalvular, primary valvular, or supravalvular obstructions causing reduced left ventricular reserve, hypotension, and ventricular hypertrophy. Furthermore, myocardial ischemia is especially common in obstructive lesions of both ventricles, which show signs of failure. Patients with obstructive defects are at increased risk for developing arrhythmias, such as ventricular fibrillation, in part because of the tenuous myocardial O₂ supply-to-demand ratio. Isolated obstructive lesions can be seen in the right ventricle and are exacerbated by increased pulmonary vascular resistance (PVR), resulting in right-sided heart failure.

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