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Heart failure is increasingly being recognized as a growing health problem worldwide. It is estimated that the lifetime risk of developing heart failure is approximately 20% for patients older than 40 years.1 Clinical anesthesiologists can therefore expect to see cases involving patients suffering from heart failure with increasing frequency. Symptomatic heart failure is associated with high risk of morbidity and mortality as a result of perioperative ischemia/infarction, dysrhythmias, worsening heart failure, postoperative cognitive dysfunction, and stroke.2,3 Asymptomatic left ventricular dysfunction, which is considered a precursor of symptomatic heart failure and is assumed to have similar prevalence as symptomatic heart failure, is also associated with high perioperative mortality.4 Since most anesthetics interfere with cardiovascular performance, either by direct myocardial depression or by depression of sympathetic activity, on which these patients rely, an appropriate anesthetic technique must be selected to minimize hemodynamic changes and maintain a near-normal physiologic status. This chapter discusses the aspects of dose reduction, titration of drugs, and the pharmacodynamic effects of each class of anesthetic drugs. As an example, the chapter provides a practical guide to the selection and use of general anesthetic agents in patients with poor cardiac function undergoing colectomy and discusses the pharmacologic management of acute cardiac deterioration.




Heart failure is a complex clinical syndrome, but the basic problem is the heart's inability to pump blood at a rate commensurate with the requirements of the metabolizing tissues or ability to do so only at elevated filling pressures. It can be broadly subdivided into 2 distinct forms. The first form, termed diastolic dysfunction, and is due to inadequate ventricular relaxation preventing adequate end-diastolic filling.5,6 The second, termed systolic dysfunction, is due to inadequate force generation to eject blood normally. Therefore, it is important to be aware of the influence of anesthetics on both systolic and diastolic dysfunction.


In the failing ventricle, various adaptive mechanisms are initiated to help maintain arterial pressure and cardiac output (CO). The body activates several neurohumoral pathways to increase circulating blood volume. The sympathetic nervous system increases heart rate and contractility, causes arteriolar vasoconstriction in nonessential vascular beds, and stimulates secretion of renin from the juxtaglomerular apparatus of the kidney. Stimulation of the renin–angiotensin system results in further arteriolar vasoconstriction, sodium and water retention, and release of aldosterone. The increased aldosterone, in turn, also leads to sodium and water retention. Additionally, baroreceptor and osmotic stimuli lead to vasopressin release from the hypothalamus, causing reabsorption of water in the renal collecting duct. Although these neurohumoral pathways initially are beneficial, eventually they become deleterious and aggravate ischemia, potentiate dysrhythmias, cause endothelial dysfunction, promote cardiac remodeling, and are directly toxic to myocytes (Figure 22–1).

Figure 22–1

Pathophysiology of cardiac failure and its effects on pharmacokinetics.

(Modified with permission from Benowitz NL, Meister W. Pharmacokinetics ...

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