• CI = HR × SV/BSA (normal values are 2.5 – 4.2 L/min/m²)

where MAP is mean arterial pressure, CVP is central venous pressure, CI is cardiac index, HR is heart rate, SV is stroke volume, and BSA is body surface area.

• Contractility is related to the rate of myocardial muscle shortening, which in turn depends on the intracellular calcium concentration during systole. Norepinephrine, sympathomimetic drugs, and secretion of epinephrine from the adrenal glands increase contractility via β₁-receptor activation.

• Myocardial contractility is depressed by anoxia, acidosis, depletion of catecholamine stores within the heart, and loss of functioning muscle mass as a result of ischemia or infarction. Most anesthetics and antiarrhythmic agents are negative inotropes (i.e., they decrease contractility).

Abnormal Cardiac Function

• Ventricular wall abnormalities: Hypokinesis (decreased contraction), akinesis (failure to contract), and dyskinesis (paradoxic bulging) during systole reflect increasing degrees of contraction abnormalities. Although contractility may be normal or even enhanced in some areas, abnormalities in other areas of the ventricle can impair emptying and reduce SV.

• Valvular dysfunction: Whereas stenosis of an AV valve reduces SV by decreasing ventricular preload, stenosis of a semilunar valve reduces SV by increasing ventricular afterload. Regurgitation can reduce SV by regurgitant volume with each contraction.

Regulation of Vascular Tone

• Most tissue beds regulate their own blood flow (autoregulation). These phenomena are likely caused by both an intrinsic response of vascular smooth muscle to stretch and the accumulation of vasodilatory metabolic byproducts. The latter may include K⁺, H⁺, CO₂, adenosine, and lactate.

• The vascular endothelium secretes or modifies substances that control blood pressure or flow such as vasodilators (e.g., nitric oxide, prostacyclin [PGI₂]), vasoconstrictors (endothelins, thromboxane A₂), anticoagulants (e.g., thrombomodulin, protein C), fibrinolytics (tissue plasminogen activator), and factors that inhibit platelet aggregation (nitric oxide and PGI₂).

• Autonomic control of the entire vasculature except the capillaries is primarily sympathetic via the thoracic and the first two lumbar segments. Sympathetic-induced vasoconstriction (via α₁-adrenergic receptors) can be potent in skeletal muscle, kidneys, the gut, and the skin; it is least active in the brain and heart. The most important vasodilatory fibers are those to skeletal muscle, mediating an increase in blood flow (via β₂-adrenergic receptors) in response to exercise. Vasodepressor (vasovagal) syncope, which can occur after intense emotional strain associated with high sympathetic tone, results from reflex activation of both vagal and sympathetic vasodilator fibers.

• Vascular tone and autonomic influences on the heart are controlled by vasomotor centers in the reticular formation of the medulla and lower pons. They are also responsible for the adrenal secretion of catecholamines as well as the enhancement of cardiac automaticity and contractility.

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