ANESTHESIOLOGY FAST REVIEW

ANESTHESIOLOGY_FAST_REVIEWKAPAK1-0-25

CARDIOVASCULAR PHISIOLOGY

Erbil Türksal

Ankara Atatürk Sanatoryum Training and Research Hospital, Department of Anesthesiology and Reanimation, Ankara, Türkiye

Türksal E. Cardiovascular Phisiology. In: Kazancı D, editor. Anesthesiology Fast Review. 1st ed. Ankara: Türkiye Klinikleri; 2025. p.9-22.

ABSTRACT

  • The cardiac muscle consists of atrial and ventricular contractile cells, specialized pacemaker cells, and conduction cells.
  • Each cardiac cycle begins with the spontaneous generation of an action potential in the sinoatrial (SA) node. Compared to ventricular muscle action potentials, this process occurs more slowly, without a distinct spike or plateau.
  • Although most anesthetic agents suppress SA node automaticity, this does not necessarily result in bradycardia. However, exaggerated responses may be observed, particularly in pathological conditions such as aging, heart failure, and arrhythmias.
  • Myocardial contractile force is directly dependent on the influx of Ca2+ from the extracellular space into the cell.
  • Digoxin, a cardiac glycoside, is used in the treatment of heart failure as it increases intracellular Ca2+ levels. Most local, volatile, and intravenous anesthetics suppress myocardial contractility. Anesthetic-induced cardiac depression is more pronounced in patients with hypocalcemia or those receiving calcium channel blockers and/or b-blockers.
  • The heart is innervated by sympathetic nerves originating from T1-2 to T5-6 and by the parasympathetic (vagus) nerve. The right sympathetic and parasympathetic nerves primarily influence the SA node, whereas the left sympathetic and parasympathetic nerves primarily affect the atrioventricular (AV) node.
  • Atrial emptying begins with the opening of the tricuspid and mitral valves, during which the majority (70-80%) of blood passively enters the ventricles.
  • The cardiac cycle is divided into four phases: isovolumetric contraction and ventricular ejection occur during systole, whereas isovolumetric relaxation and ventricular filling take place during diastole.
  • Ventricular performance is typically assessed based on the volume of blood pumped by the heart per minute, known as cardiac output, which is calculated as the product of stroke volume and heart rate.
  • Mean arterial pressure is directly proportional to systemic vascular resistance and cardiac output.
  • When baroreceptors detect a decrease in blood pressure, compensation occurs through tachycardia, increased contractility, and elevated systemic vascular resistance. All volatile and intravenous anesthetics inhibit the baroreflex response, thereby impairing this compensatory mechanism.

Keywords: Heart; Cardiovascular physiology; Heart conduction system; Myocardial contraction; Cardiac output; Blood pressure; Anesthetic agents

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