- In contrast to action potentials in axons, the spike in cardiac action potentials is followed by a plateau phase that lasts 0.2-0.3 sec. Whereas the action potential for skeletal muscle and nerves is due to the abrupt opening of voltage-gated sodium channels in the cell membrane, in cardiac muscle it is initiated by voltage-gated sodium channels (the spike) and maintained by voltage-gated calcium channels (the plateau).
- Potent inhalational agents depress sinoatrial (SA) node automaticity. These agents seem to have only modest direct effects on the atrioventricular (AV) node, prolonging conduction time and increasing refractoriness. This combination of effects likely explains the frequent occurrence of junctional tachycardia when an anticholinergic agent is administered for sinus bradycardia during inhalation anesthesia; junctional pacemakers are accelerated more than those in the SA node.
- Studies suggest that volatile anesthetics depress cardiac contractility by decreasing the entry of Ca2+ into cells during depolarization (affecting T- and L-type calcium channels), altering the kinetics of its release and uptake into the sarcoplasmic reticulum, and decreasing the sensitivity of contractile proteins to calcium.
- Because the normal cardiac index (CI) has a wide range, it is a relatively insensitive measurement of ventricular performance. Abnormalities in CI therefore usually reflect gross ventricular impairment.
- In the absence of hypoxia or severe anemia, measurement of mixed venous oxygen tension (or saturation) is an excellent estimate of the adequacy of cardiac output.
- Patients with reduced ventricular compliance are most affected by loss of a normally timed atrial systole.
- Cardiac output in patients with marked right or left ventricular impairment is very sensitive to acute increases in afterload.
- The ventricular ejection fraction, the fraction of the end-diastolic ventricular volume ejected, is the most commonly used clinical measurement of systolic function.
- Left ventricular diastolic function can be assessed clinically by Doppler echocardiography in a transthoracic or transesophageal examination.
- Because the endocardium is subjected to the greatest intramural pressures during systole, it tends to be most vulnerable to ischemia during decreases in coronary perfusion pressure.
- The failing heart becomes increasingly dependent on circulating catecholamines. Abrupt withdrawal in sympathetic outflow or decreases in circulating catecholamine levels, such as can occur following induction of anesthesia, may lead to acute cardiac decompensation.
Anesthesiologists must have a thorough understanding of cardiovascular physiology both for its scientific significance in anesthesia and for its practical applications to patient management. Anesthetic successes and failures are often directly related to the skill of the practitioner in manipulating cardiovascular physiology. This chapter reviews the physiology of the heart and the systemic circulation and the pathophysiology of heart failure.
The circulatory system consists of the heart, blood vessels, and blood. Its function is to provide oxygen and nutrients to the tissues and to carry away the products of metabolism. The heart propels blood through two vascular systems arranged in series. In the normally low-pressure pulmonary circulation, venous blood flows past the alveolar-capillary membrane, takes up oxygen, and eliminates CO2. In the high pressure systemic circulation, ...