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Review
. 2009 Sep;27(3):497-517.
doi: 10.1016/j.anclin.2009.07.008.

Diastolic dysfunction, cardiovascular aging, and the anesthesiologist

Affiliations
Review

Diastolic dysfunction, cardiovascular aging, and the anesthesiologist

David Sanders et al. Anesthesiol Clin. 2009 Sep.

Abstract

As the number of persons aged 65 years and older continues to increase, the anesthesiologist will more frequently encounter this demographic. Cardiovascular changes that occur in this patient population present difficult anesthetic challenges and place these patients at high risk of perioperative morbidity and mortality. The anesthesiologist should be knowledgeable about these age-related cardiovascular changes, the pathophysiology underlying them, and the appropriate perioperative management. Whether presenting for cardiac or general surgery, the anesthesiologist must identify patients with altered physiology as a result of aging or diastolic dysfunction and be prepared to modify the care plan accordingly. With a directed preoperative assessment that focuses on certain aspects of the cardiovascular system, and the assistance of powerful echocardiographic tools such as tissue Doppler, this can be achieved.

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Figures

Figure 1
Figure 1
Age-related arterial stiffness and pressure waveform shapes. (Reprinted with permission from Dudley M, Groban L. Current Reviews in Clinical Anesthesia 2009;29:263-75.)
Figure 2
Figure 2
Schematic of blood pressure as a result of ejection of blood (e.g., stroke volume) into a series of tubes whose diameters vary with pulsating pressure. In the young adult, the aorta cushions the cardiac pulsation by converting pressure energy into elastic energy through distension. Once the heart ceases ejection and the pressure falls, the walls of the aorta recoil and the elastic energy is reconverted into pressure energy. This reduces the magnitude of pressure change and allows for a steady flow beyond the arterioles. This accounts for the diastolic component of BP. With aging and hypertension, the aorta and other major conduit vessels become rigid leading to a loss of “cushioning” of the ejected energy. Accordingly, this loss of stored energy manifests in extremes in pressure--increased pulse pressure and very low diastolic pressure. (Adapted from Baird RN, Abbott WM. Lancet 1976;2:948-41.)
Figure 3
Figure 3
Cardiac cycle with phases of diastole.
Figure 4
Figure 4
Doppler criteria for classification of diastolic function. (Reprinted with permission from Chest 2005;128:3652–3663.) (Figure 4)
Figure 5
Figure 5
Top: Schematic of the midesophageal four-chamber view with pulsed wave Doppler (PWD) imaging sample volume at the level of the tips of the open mitral valve leaflets. Bottom: Transmitral blood flow velocity profile obtained with PWD imaging at the midesophageal four-chamber view. (Reprinted with permission from Chest 2005;128:3652–3663.) (Figure 2A and B)
Figure 6
Figure 6
Top: Schematic of the midesophageal four-chamber view with pulsed Doppler imaging sample volume located at the lateral mitral annular wall for tissue Doppler imaging (TDI) assessment of diastolic function. Bottom: Lateral mitral annular tissue Doppler waveforms for the assessment of left ventricular diastolic function. (Reprinted with permission from Chest 2005;128:3652–3663.) (Figures 7A and B)
Figure 7
Figure 7
Transmitral Doppler imaging, pulmonary view Doppler imaging, and tissue Doppler imaging (TDI) profiles corresponding to normal, delayed relaxation, pseudonormal, and restrictive filling patterns. (Reprinted with permission from Chest 2005;128:3652–3663.) (Figure 5)

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