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The American Dental Association and several dental specialty organizations have published guidelines that detail requirements for monitoring patients during various levels of sedation and, in some cases, general anesthesia. In general, all of these are consistent with those guidelines suggested by the American Society of Anesthesiologists Task Force for Sedation and Analgesia by Non-Anesthesiologists. It is well-accepted that the principal negative impact of sedation and anesthesia pertains to the compromise of respiratory function, but attentive monitoring of cardiovascular function is also important. While monitoring per se is a technical issue, an appreciation of its purpose and the interpretation of the information provided require an understanding of basic cardiovascular anatomy and physiology. The focus of this continuing education article is to address essential physiological aspects of cardiovascular function and to understand the appropriate use of monitors, including the interpretation of the information they provide.Abstract
The cardiac cycle (ventricular volumes). At the end of diastole, the left ventricle illustrated here contains approximately 130 mL of blood, which is described appropriately as end-diastolic volume (EDV). Notice that approximately 50 mL of blood remains in the ventricle at the end of systole. This volume is called end-systolic volume (ESV). The volume ejected during systole is the stroke volume and, in this example, equals approximately 80 mL. (EDV – ESV = SV).
Arterial (aortic) blood pressure. Examine the aortic pressure curve and the ventricular pressure curve. As ventricular systole commences, ventricular pressure increases from 0 to 80 mm Hg, and this opens the aortic valve. The force of blood ejected into the aorta increases its pressure to 120 mm Hg. This is systolic pressure and is produced by ventricular ejection. Notice that during ventricular diastole (relaxation), ventricular pressure approaches zero. However, aortic pressure does not drop below 80 mm Hg. This is diastolic pressure and is essentially a function of arterial resistance. These pressures are transmitted throughout the arterial tree and are recorded indirectly using the familiar sphygmomanometer.
Frank-Starling law of the heart. As the heart is stretched by greater venous return or end-diastolic volume (EDV), it ejects a greater stroke volume. Notice the tracing labeled “A.” When EDV (preload) increases, the stroke volume also increases. However, there is a point at which a limit is reached and stroke volume begins to decline. Notice the difference in the tracing labeled “B,” which represents a heart that is in failure. With each increase in preload, stroke volume does not increase as much, and the decline in stroke volume commences with a lower amount of preload.
Determinants of arterial pressure. Mean arterial pressure (MAP) is the time-weighted average of systolic blood pressure (SBP) and diastolic blood pressure (DBP). The principal determinant of SBP is stroke volume, which is increased by venous return (preload) and contractility. DBP is determined primarily by arterial resistance, which also provides afterload against which the ventricles must work to eject stroke volume (dotted arrow). + indicates positive influence; −, negative influence.
Exemplary automated noninvasive blood pressure unit.
Specialized neural conductive tissues and their approximate firing rates.
Einthoven's triangle and standard limb leads.
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ISSN: 0003-3006