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Chapter: Clinical Anesthesiology: Anesthetic Management: Cardiovascular Physiology & Anesthesia

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Effects of Anesthetic Agents on Heart

Effects of Anesthetic Agents on Heart
Most volatile anesthetic agents are coronary vasodilators.

EFFECTS OF ANESTHETIC AGENTS

Most volatile anesthetic agents are coronary vasodi-lators. Their effect on coronary blood flow is vari-able because of their direct vasodilating properties, reduction of myocardial metabolic requirements (and secondary decrease due to autoregulation), and effects on arterial blood pressure. The mecha-nism is not clear, and these effects are unlikely to have any clinical importance. Halothane and iso-flurane seem to have the greatest effect; the former primarily affects large coronary vessels, whereas the latter affects mostly smaller vessels. Vasodilation due to desflurane seems to be primarily autonomi-cally mediated, whereas sevoflurane seems to lack coronary vasodilating properties. Dose-dependent abolition of autoregulation may be greatest with isoflurane.

Volatile agents exert beneficial effects in experi-mental myocardial ischemia and infarction. They reduce myocardial oxygen requirements and protect against reperfusion injury; these effects are mediated by activation of ATP-sensitive K + (KATP) channels. Some evidence also suggests that volatile anesthetics enhance recovery of the “stunned” myocardium (hypocontractile, but recoverable, myocardium after ischemia). Moreover, although volatile anesthetics decrease myocardial contractility, they can be poten-tially beneficial in patients with heart failure because most of them decrease preload and afterload.

The Pathophysiology of Heart Failure

Systolic heart failure occurs when the heart is unable to pump a sufficient amount of blood to meet the body’s metabolic requirements. Clinical manifesta-tions usually reflect the effects of the low cardiac output on tissues (eg, fatigue, dyspnea, oxygen debt, acidosis), the damming-up of blood behind the failing ventricle (dependent edema or pulmo-nary venous congestion), or both. The left ventricle is most commonly the primary cause, often with secondary involvement of the right ventricle. Iso-lated right ventricular failure can occur in the set-ting of advanced disease of the lung parenchyma or pulmonary vasculature. Left ventricular failure is most commonly the result of myocardial dysfunc-tion, usually from coronary artery disease, but may also be the result of viral disease, toxins, untreated hypertension, valvular dysfunction, arrhythmias, or pericardial disease.

Diastolic dysfunction can be present in the absence of signs or symptoms of heart failure. Symp-toms arising from diastolic dysfunction are the result of atrial hypertension (Figure 20–13). Failure of the heart to relax during diastole leads to elevated left ventricular end-diastolic pressure, which is trans-mitted to the left atrium and pulmonary vasculature. Common causes of diastolic dysfunction include hypertension, coronary artery disease, hypertrophic cardiomyopathy, valvular heart disease, and peri-cardial disease. Although diastolic dysfunction can occasionally cause symptoms of heart failure, even in the presence of normal systolic function (normal left ventricular ejection fraction), it nearly always occurs in association with systolic dysfunction in patients with heart failure.

Diastolic dysfunction is diagnosed echocar-diographically. Placing the pulse wave Doppler sample gate at the tips of the mitral valve during


left ventricular filling will produce the characteris-tic diastolic flow pattern (Figure 20–9). In patients with normal diastolic function, the ratio between the peak velocities of the early (E) and the atrial (A) waves is from 0.8 to 2. In the early stages of diastolic dysfunction, the primary abnormality is impaired relaxation. When left ventricular relaxation is delayed, the initial pressure gradient between the left atrium and the left ventricle is reduced, result-ing in a decline in early filling, and, consequently, a reduced peak E wave velocity. The A wave veloc-ity is increased relative to the E wave, and the E/A ratio is reduced. As diastolic dysfunction advances, the left atrial pressure increases, restoring the gradi-ent between the left atrium and left ventricle with an apparent restoration of the normal E/A ratio. This pattern is characterized as “pseudonormal-ized.” Using the E/A ratio alone cannot distinguish between a normal and pseudonormalized pattern of diastolic inflow. As diastolic dysfunction worsens further, a restrictive pattern is obtained. In this sce-nario, the left ventricle is so stiff that pressure builds in the left atrium, resulting in a dramatic peak of early filling and a prominent, tall, narrow E wave. Because the ventricle is so poorly compliant, the atrial contraction contributes little to filling, result-ing in a diminished A wave and an E/A ratio greater than 2:1.Doppler patterns of pulmonary venous flow have been used to distinguish between a pseudonormalized and normal E/A ratio. Currently, most echocardiographers use tissue Doppler to examine the movement of the lateral annulus of the mitral valve during ventricular filling (Figure 20–9). Tissue Doppler allows the echocardiographer to determine both the velocity and the direction of the movement of the heart. During systole, the heart contracts toward the apex, away from a TEE transducer in the esophagus. This motion produces the s’ wave of systole. During early and late diastolic filling, the heart moves toward the transducer pro-ducing the e’ and a’ waves. Like the inflow patterns achieved with pulse wave Doppler, characteristic patterns of diastolic dysfunction are reflected in the tissue Doppler trace. An e’ wave less than 8 cm/sec is consistent with diastolic dysfunction. Of note, the tissue Doppler trace does not produce a pseudonor-malized pattern permitting the echocardiographer to readily distinguish between normal and abnor-mal diastolic function.


Cardiac output may be reduced at rest with heart failure, but the key point is that the heart is incapable of appropriately increasing cardiac output and oxygen delivery in response to demand. Inad-equate oxygen delivery to tissues is reflected by a low mixed venous oxygen tension and an increase in the arteriovenous oxygen content difference. In com-pensated heart failure, the arteriovenous difference may be normal at rest, but it rapidly widens during stress or exercise.

Heart failure is less commonly associated with an elevated cardiac output. This form of heart fail-ure is most often seen with sepsis, thyrotoxicosis, and other hypermetabolic states, which are typically associated with a low SVR.

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