Heart Failure With Preserved Ejection Fraction: A Comprehensive Review and Update of Diagnosis, Pathophysiology, Treatment, and Perioperative Implications.

Almost three-quarters of all heart failure patients who are older than 65 have heart failure with preserved ejection fraction (HFpEF). The proportion and hospitalization rate of patients with HFpEF are increasing steadily relative to patients in whom heart failure occurs as result of reduced ejection fraction. The predominance of the HFpEF phenotype most likely is explained by the prevalence of medical conditions associated with an aging population. A multitude of age-related, medical, and lifestyle risk factors for HFpEF have been identified as potential causes for the sustained low-grade proinflammatory state that accelerates disease progression. Profound left ventricular (LV) systolic and diastolic stiffening, elevated LV filling pressures, reduced arterial compliance, left atrial hypertension, pulmonary venous congestion, and microvascular dysfunction characterize HFpEF, but pulmonary arterial hypertension, right ventricular dilation and dysfunction, and atrial fibrillation also frequently occur. These cardiovascular features make patients with HFpEF exquisitely sensitive to the development of hypotension in response to acute declines in LV preload or afterload that may occur during or after surgery. With the exception of symptom mitigation, lifestyle modifications, and rigorous control of comorbid conditions, few long-term treatment options exist for these unfortunate individuals. Patients with HFpEF present for surgery on a regular basis, and anesthesiologists need to be familiar with this heterogeneous and complex clinical syndrome to provide successful care. In this article, the authors review the diagnosis, pathophysiology, and treatment of HFpEF and also discuss its perioperative implications.

The Physiology of Oxygen Transport by the Cardiovascular System: Evolution of Knowledge.

The heart, vascular system, and red blood cells play fundamental roles in O2 transport. The fascinating research history that led to the current understanding of the physiology of O2 transport began in ancient Egypt in 3000 BC, when it was postulated that the heart was a pump serving a system of distributing vessels. Over 4 millennia elapsed before William Harvey (1578-1657) made the revolutionary discovery of blood circulation, but it was not until the 20th century that a lucid and integrative picture of O2 transport finally emerged. This review describes major research achievements contributing to this evolution of knowledge. These achievements include the discovery of the systemic and pulmonary circulations, hemoglobin within red blood cells and its ability to bind O2, and diffusion of O2 from the capillary as the final step in its delivery to tissue. The authors also describe the classic studies that provided the initial description of the basic regulatory mechanisms governing heart function (Frank-Starling law) and the flow of blood through blood vessels (Poiseuille's law). The importance of technical advances, such as the pulmonary artery catheter, the blood gas analyzer and oximeter, and the radioactive microsphere technique to measure the regional blood flow in facilitating O2 transport-related research, is recognized. The authors describe how religious and cultural constraints, as well as superstition-based medical traditions, at times impeded experimentation and the acquisition of knowledge related to O2 transport.

Right Ventricular Perfusion: Physiology and Clinical Implications.

Regulation of blood flow to the right ventricle differs significantly from that to the left ventricle. The right ventricle develops a lower systolic pressure than the left ventricle, resulting in reduced extravascular compressive forces and myocardial oxygen demand. Right ventricular perfusion has eight major characteristics that distinguish it from left ventricular perfusion: (1) appreciable perfusion throughout the entire cardiac cycle; (2) reduced myocardial oxygen uptake, blood flow, and oxygen extraction; (3) an oxygen extraction reserve that can be recruited to at least partially offset a reduction in coronary blood flow; (4) less effective pressure-flow autoregulation; (5) the ability to downregulate its metabolic demand during coronary hypoperfusion and thereby maintain contractile function and energy stores; (6) a transmurally uniform reduction in myocardial perfusion in the presence of a hemodynamically significant epicardial coronary stenosis; (7) extensive collateral connections from the left coronary circulation; and (8) possible retrograde perfusion from the right ventricular cavity through the Thebesian veins. These differences promote the maintenance of right ventricular oxygen supply-demand balance and provide relative resistance to ischemia-induced contractile dysfunction and infarction, but they may be compromised during acute or chronic increases in right ventricle afterload resulting from pulmonary arterial hypertension. Contractile function of the thin-walled right ventricle is exquisitely sensitive to afterload. Acute increases in pulmonary arterial pressure reduce right ventricular stroke volume and, if sufficiently large and prolonged, result in right ventricular failure. Right ventricular ischemia plays a prominent role in these effects. The risk of right ventricular ischemia is also heightened during chronic elevations in right ventricular afterload because microvascular growth fails to match myocyte hypertrophy and because microvascular dysfunction is present. The right coronary circulation is more sensitive than the left to α-adrenergic-mediated constriction, which may contribute to its greater propensity for coronary vasospasm. This characteristic of the right coronary circulation may increase its vulnerability to coronary vasoconstriction and impaired right ventricular perfusion during administration of α-adrenergic receptor agonists.

Isoflurane and the Coronary Steal Controversy of the 1980s: Origin, Resolution, and Legacy.

Isoflurane was introduced for general clinical use in North America in 1981. Shortly thereafter, in 1983, a study suggested that the anesthetic was a potent coronary vasodilator that could cause coronary steal and myocardial ischemia in patients with coronary artery disease. Myocardial ischemia results from small-vessel dilation which leads to increased blood flow to well-perfused myocardium and decreased blood flow to myocardium with borderline perfusion. This action of isoflurane raised concerns and threatened its use. By the early 1990s, these concerns were resolved by carefully performed clinical and experimental studies demonstrating no evidence of adverse cardiac changes during isoflurane administration as long as hemodynamic variables were tightly controlled. Indeed, the controversy sparked by the 1983 study led to a chain of experimental studies that ultimately demonstrated ironically that isoflurane has a preconditioning, cardioprotective effect. This chapter in anesthesia history underscores the importance of allowing the passage of time before assessing the clinical and scientific impact of a research finding.