Handbook of Clinical Anesthesia

Chapter 10

cardiovascular Anatomy and Physiology

  1. Introduction

(Kampine JP, Stowe DF, Pagel PS: Heart and peripheral circulation. In Clinical Anesthesia. Edited by Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC. Philadelphia: Lippincott Williams and Wilkins, 2009, pp 207–232).

  1. Functional Anatomy of the Heart
  2. Synchronous contraction of the left ventricular (LV) muscles shortens the long axis of the heart, decreases the circumference of the LV, and lifts the apex toward the anterior chest wall. This action produces the familiar palpable point of maximum impulse, which is normally located in the fifth or sixth intercostal space in the mid-clavicular line.
  3. The pulmonary circulation is a low-pressure, low-resistance system into which the right ventricle (RV) transfers blood.
  4. During contraction, LV pressure increases from end-diastolic values of 10 to 12 mm Hg to a peak pressure of 120 to 140 mm Hg during systole. The peak pressures generated by the LV reflect the requirement to circulate blood through the high resistance systemic circulation.
  5. Efficient pumping action of the heart requires two pairs of unidirectional valves. One pair is located at the outlets of the RV and LV (pulmonic and aortic valves, respectively). The atrioventricular (AV) valves separating the atria from the ventricles are the tricuspid and mitral valve on the right and left sides of the heart, respectively.
  6. The RV and LV are the major cardiac pumping chambers, but the atria play a critically important supporting roles. The atria function as reservoirs, conduits,

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and contractile chambers and facilitate the transition between continuous, low-pressure venous to phasic, high-pressure arterial blood flow. When atrial contraction is absent or ineffective (e.g., in atrial failure, atrial fibrillation or flutter), the heart may be capable of compensating for the loss of the atrial contractile function and continue to function effectively under resting conditions.

  1. The Cardiac Cycle
  2. LV systole is commonly divided into the isovolumic contraction, rapid ejection, and slower ejection phases. Closure of both the tricuspid and mitral valves occurs when RV and LV pressures exceed corresponding atrial pressure and cause the source of the first heart sound (Fig. 10-1).
  3. The normal LV end-diastolic volume is about 120 mL. The average ejected stroke volume is 80 mL, and the normal ejection fraction (EF) is approximately 67%. A decrease in EF below 40% is typically observed when the myocardium is affected by ischemia, infarction, or cardiomyopathic disease processes.
  4. Disease processes known to reduce LV compliance (myocardial ischemia, pressure-overload hypertrophy) attenuate early filling and increase the importance of atrial systole to overall LV filling.
  5. Diastolic dysfunction may independently cause heart failure, even in the presence of relatively normal contractile function. This “heart failure with normal systolic function” has been increasingly recognized as a major underlying cause of congestive heart failure.
  6. Determinants of Cardiac Output
  7. Cardiac output is the product of heart rate and stroke volume and may be normalized to the body surface area (cardiac index).
  8. Cardiac output is a function of preload, afterload, myocardial contractility (inotropic state), and heart rate.
  9. Systemic vascular resistance (the ratio of driving pressure to cardiac output) is the most commonly used nonparametric expression of peripheral resistance and is primarily affected by autonomic nervous system activity.

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Figure 10-1. Mechanical and electrical events of the cardiac cycle showing also the ventricular volume curve and the heart sounds. Note the isovolumic contraction (ICP) and the relaxation period (IRP) during which there is no change in ventricular volume because all valves are closed. The ventricle decreases in volume as it ejects its contents into the aorta. During the first third of systolic ejection (the rapid ejection period), the curve of emptying is steep. ECG = electrocardiogram.

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  2. The inotropic state is the intrinsic force of myocardial contraction independent of changes in preload, afterload, or heart rate.
  3. The primary determinant of myocardial oxygen consumption is heart rate because the more frequently the heart performs pressure-volume work, the more oxygen must be consumed. At high heart rates, particularly in patients with heart disease, there may not be adequate diastolic filling time to maintain cardiac output and coronary artery perfusion (which is highly dependent on the duration of diastole). Such events may cause acute myocardial ischemia or infarction.
  4. Measures of Cardiac Function
  5. Clinical indicators of contractile performance include cardiac output, EF, fractional shortening or area change of the LV short axis, and LV systolic wall thickening.
  6. These indices of contractility are dependent on heart rate, preload, and afterload but nevertheless may be measured with reasonable reliability using echocardiographic techniques and remain useful indices of contractile performance.
  7. Cellular and Molecular Biology of Cardiac Muscle Function
  8. Ultrastructure of the Cardiac Myocyte.The heart contracts and relaxes nearly 3 billion times during an average lifetime (heart rate, 70 bpm; life expectancy, 75 years). A review of cardiac myocyte ultrastructure provides important insights into how the heart accomplishes this astonishing performance.
  9. Proteins of the Contractile Apparatus. Myosin, actin, tropomyosin, and the three-protein troponin complex make up the six major components of the contractile apparatus.
  10. Calcium–Myofilament Interaction. Binding of calcium to troponin C precipitates a series of conformational changes in the troponin–tropomyosin complex that lead to the exposure of the myosin-binding site on the actin molecule.
  11. Myosin–Actin Contraction Biochemistry. The biochemistry of cardiac muscle contraction is most often described using a simplified four-component model (Fig. 10-2).

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Figure 10-2. Schematic illustration of the actin filaments and its individual monomers and active myosin binding sites (m; left panel). The myosin head is dissociated from actin by binding with adenosine triphosphate (ATP). Subsequent ATP hydrolysis and release of inorganic phosphate (Pi) “cocks” the head group into a tension-generating configuration. Attachment of the myosin head to actin allows the head to apply tension to the myosin rod and the actin filament. The right panel illustrates calcium binding to troponin C, which causes troponin I to decrease its affinity for actin. As a result in a conformational shift in tropomyosin position (see text), seven sites on actin monomers are revealed. ADP = adenosine diphosphate.

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Figure 10-3. Major waves (P, QRS, and T) of the electrocardiogram are indicated as well as the timing of the activation of some of the key conductive structures. AV = atrioventricular; SA = sinoatrial.

III. Electrical Properties of The Heart

  1. The clinical electrocardiogram(ECG) consists of a regular series of deflections from the isoelectric line. The first deflection of the ECG is the P-wave. (Figs. 10-3 and 10-4). (Einthoven, who developed the system, began his depiction of the ECG in the middle of the alphabet.) The QT interval is the duration between the onset of ventricular depolarization (indicated by the QRS complex) and

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completion of repolarization (as signified by the end of the T-wave). The QT interval varies inversely with heart rate and may precipitate malignant ventricular arrhythmias when shortened or prolonged by administration of vasoactive drugs (volatile anesthetics) or in the presence of intrinsic cardiac pathology (prolonged QT syndrome).

 

Figure 10-4. Top: Electrocardiogram (ECG) recorded from the body surface. Bottom: Intracardiac ECG.

  1. Role of Ion Channels. The action potentials of individual groups of excitable cardiac myocytes are quite different (Figs. 10-5 and 10-6).
  2. The sinoatrial (SA) and AV nodes and accessory pacemaker cells have unstable, spontaneously depolarizing properties. The magnitude and slope of spontaneous depolarization (also known as automaticity) of SA node cells are important in the regulation of heart rate and are dependent on sympathetic and vagal (parasympathetic) neural innervation and activity.
  3. The SA node pacemaker may be displaced by a latent pacemaker elsewhere in the heart during myocardial ischemia because of primary suppression of the SA node or because of spontaneous discharge of a latent pacemaker at a higher intrinsic rate.
  4. Neural Innervation of the Heart and Blood Vessels
  5. Baroreflex Regulation of Blood Pressure
  6. The heart is innervated by the parasympathetic and sympathetic nervous systems.
  7. Aside from their effects on heart rate, excitability, and conduction, the parasympathetic fibers do not substantially influence contractility.
  8. Activation of cardiac sympathetic fibers produces positive chronotropic, dromotropic, inotropic, and lusitropic effects (increases in heart rate, conduction velocity, myocardial contractility, and the rate of myofibrillar relaxation).
  9. The afferent innervation of the heart consists of mechanoreceptors with primarily vagal afferent pathways and receptors with spinal afferent pathways.
  10. Activation of the ventricular receptors by nociception or stretch, such as may occur in response to a sudden increase in ventricular volume, causes a vagal depressor response with a decrease in heart rate and mean arterial pressure (MAP; Bezold-Jarisch reflex).

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Figure 10-5. Cardiac action potentials throughout the conductance system from the sinoatrial (SA) node through the ventricular muscle during one cardiac cycle. Note the automatic pacemaker activity (slow, spontaneous depolarization) of the SA and atrioventricular (AV) nodal cells and the lack of spontaneous activity of atrial, Purkinje, and ventricular muscle cells. ECG = electrocardiogram; LV = left ventricle.

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Figure 10-6. Changes in four ionic currents responsible for action potential (AP) depolarization and repolarization in a sinoatrial (SA) nodal pacemaker cell. Two are increasing inward currents (ii and iCa), and two are decreasing outward currents (delayed rectifier [iK] and inward rectifier [iK1]).

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  1. Other Cardiovascular Reflexes.Other reflexogenic areas within the cardiovascular system regulate hemodynamics through arterial chemoreceptors and the central nervous system (CNS) response to ischemia.
  2. In addition to the baroreceptor responses, severe hypotension also causes arterial vaso- and venoconstriction in response to brainstem hypoxia. This CNS ischemic response may be activated when MAP is reduced below 50 mm Hg.
  3. Somatic pain increases heart rate and MAP by activation of sympathetic efferent nerves. In contrast, visceral pain or distention of a hollow viscus (small intestine, bladder) may produce reflex vagal bradycardia and hypotension.
  4. The oculocardiac reflex is activated by pressure on the ocular globe and causes pronounced bradycardia and hypotension by activation of vagal nerve fibers innervating the SA node.
  5. The Valsalva maneuver consists of forced expiration against a closed glottis. This maneuver reduces venous return to the right heart, decreases cardiac output and MAP, and increases heart rate.
  6. The Coronary Circulation
  7. Anatomy of the Coronary Arterial and Venous Systems.The heart is the only organ that furnishes its own blood supply (Fig. 10-7).
  8. Coronary Microcirculation.As in other capillary beds, the coronary capillaries are the sites for exchange of O2 and CO2 and for the movement of larger molecules across the endothelial cell lining, where it is devoid of vascular smooth muscle.
  9. Mechanics of Coronary Blood Flow
  10. Blood supply to the LV is directly dependent on the difference between the aortic pressure and LV end-diastolic pressure (coronary perfusion pressure) and inversely related to the vascular resistance to flow, which varies to the fourth power of the radius of the vessel (Poiseuille's law). Two other determinants of coronary flow are vessel length and viscosity of the blood, but these factors are generally constant.
  11. Resting coronary blood flow in adults is approximately 250 mL/min (1 mL/g), representing approximately 5% of the cardiac output.

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Figure 10-7. The anterior view (left) shows the right coronary and left anterior descending arteries. The posterior view (right) shows the left circumflex and posterior descending arteries. Note that the right coronary or left circumflex artery may form the latter artery. The anterior cardiac veins from the right ventricle and the coronary sinus, which primarily drain the left ventricle, empty into the right atrium.

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  2. Aortic pressure is slightly less than LV pressure during systole. As a result, blood flow in the LV subendocardium occurs only during diastole (Fig. 10-8). Coronary blood flow is also compromised when aortic diastolic pressure is reduced (severe aortic insufficiency).
  3. In contrast to left coronary blood flow, right coronary artery flow is continuous throughout the cardiac cycle because the lower pressure in the RV compared with the LV causes substantially less extravascular compression (Fig. 10-8).
 

Figure 10-8. Schematic representation of blood flow in the left and right coronary arteries during phases of the cardiac cycle. Note that most left coronary flow occurs during diastole, and right coronary flow (and coronary sinus flow) occurs mostly during late systole and early diastole.

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  1. Regulation of Coronary Blood Flow.The two major determinants of coronary blood flow (perfusion pressure and vascular resistance) vary substantially during the cardiac cycle. However, metabolic factors are the major physiologic determinants of coronary vascular tone and hence myocardial perfusion.
  2. Oxygen Delivery and Demand
  3. The heart normally extracts between 75% and 80% of arterial O2content, by far the greatest O2 extraction of all organs.
  4. The majority of O2demand is derived from the increase in LV pressure during isovolumic contraction.
  5. An increase in myocardial contractility enhances O2consumption, but heart rate is the primary determinant of O2 consumption.
  6. Cardiac O2extraction is near maximal under resting conditions and cannot be substantially increased during exercise. Thus, the primary mechanism by which myocardium meets its O2 demand is through enhanced O2 delivery, which is proportional to coronary blood flow at a constant hemoglobin concentration.
  7. Myocardial Ischemia and Infarction
  8. A large, acute coronary artery occlusion produces acute myocardial ischemia and often contributes to the development of a malignant ventricular arrhythmia because blood flow through coronary collaterals fails to provide sufficient perfusion to the ischemic zone (sudden death).
  9. If the coronary artery occlusion develops more slowly (atherosclerotic plaques), collateral formation in the watershed region may reduce the degree of myocardial damage associated with acute coronary occlusion. Atherosclerotic plaques are composed of cholesterol and other lipids that become deposited beneath the intima and fibrous tissue, which also frequently becomes calcified.
  10. Myocardial infarction may also occur without evidence of major coronary thromboses, emboli, or stenosis. This form of infarction is caused by excessive metabolic demands resulting from severe LV hypertrophy (critical aortic stenosis) or vasoactive drug ingestion (amphetamines, cocaine) or may also result from coronary artery vasospasm.
  11. Despite past arguments to the contrary, the vast majority of experimental and clinical evidence

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collected to date indicates that volatile anesthetics do not cause coronary artery steal unless profound hypotension (<50 mm Hg) is present. Volatile anesthetics are not potent vasodilators, unlike drugs such as adenosine and sodium nitroprusside that are known to produce coronary artery steal.

  1. The Pulmonary Circulation
  2. Comparison with the Systemic Circulation.The pulmonary circulation receives the blood pumped by the RV. Total pulmonary blood flow is equivalent to cardiac output. There are major differences in hemodynamics between the systemic and pulmonary circulations (Fig. 10-9).
  3. Regional Differences in Perfusion and V/Q Matching(Fig 10-10).
  4. Hypoxic Pulmonary Vasoconstriction. Pulmonary arteriolar vasoconstriction triggered by hypoxia shunts blood flow away from poorly to well-ventilated regions of the lung, thereby improving arterial O2saturation.
  5. Physiologic Modulation of the Pulmonary Circulation. The blood volume stored in the pulmonary circulation is substantial (≥900 mL), and when combined with the blood volume contained within the heart and proximal great vessels, this pulmonary blood volume provides a crucial, rapidly available source of reserve intravascular volume during acute, massive hemorrhage.
 

Figure 10-9. Comparison of pressure gradients (in mm Hg) along the high-pressure systemic and low-pressure pulmonary circulation.

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Figure 10-10. Relative ventilation and perfusion (V/Q) distribution in different areas of the lungs (upright position). The left side shows the percentage distribution of the total lung volume, and the right side shows the alveolar ventilation, pulmonary blood flow, and V/Q ratio of each horizontal slice of lung volume. Note that the upper zone is relative overventilated and the lower zone is relatively overperfused.

VII. The Cerebral Circulation

  1. Anatomy and Cerebral Autoregulation
  2. Blood flow to the brain is provided through the internal carotid and vertebral arteries. The vertebral arteries join to form the basilar artery, which (along with branches of the internal carotid arteries) forms the circle of Willis.
  3. The brain is approximately 2% of total body weight, yet this organ receives approximately 15% of cardiac output. This remarkably large cerebral blood flow (45 to 55 mL/100 g/min) reflects the high metabolic rate of the brain. Cerebral blood flow and metabolic rate are closely linked and are approximately four times greater in gray compared with white matter.
  4. Regulation of Cerebral Blood Flow: Hypercarbia, Hypoxia, and Arterial Pressure
  5. Cerebral blood flow remains relatively constant when MAP varies between 50 and 150 mm Hg in healthy subjects (Fig. 10-11).
  6. Autoregulation of cerebral blood flow may be shifted to the right in patients with chronic, poorly controlled essential hypertension.
  7. Cerebral autoregulation is inhibited by hypercarbia and higher end-tidal concentrations of volatile anesthetics.
  8. Arterial carbon dioxide partial pressure (PaCO2) is a major regulator of cerebral blood flow within the

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physiologic range of arterial CO2 tensions. Cerebral blood flow linearly increases 1 to 2 mL/100 g/min for each 1–mm Hg increase in PaCO2 (Fig 10-11).

 

Figure 10-11. Cerebral blood flow (CBF) is autoregulated (relatively unchanged) as mean systemic blood pressure increases between 50 to 150 mm Hg. However, CBF is nearly linearly increased with an increase in arterial carbon dioxide partial pressure (PaCO2) and increased if arterial oxygen partial pressure (PaO2) decreases below 50 mm Hg.

  1. Alterations in cerebral blood flow produced by changes in PaCO2are not sustained because bicarbonate is eventually transported out of the brain extracellular fluid, thereby returning pH to a normal value.
  2. In contrast to the effects of respiratory acidosis on cerebral blood flow, the actions of metabolic acidosis are more gradual because the blood–brain barrier is relatively impermeable to H+.
  3. Hypoxia-induced increases in cerebral blood flow occur at PaO2values below 60 mm Hg (Fig. 10-11).
  4. Neural control of the cerebral circulation plays a relatively minor role in regulation of cerebral blood flow despite the extensive sympathetic nervous system innervation of cerebral blood vessels.
  5. Effects of Increased Intracranial Pressure
  6. Along with the brain, the cerebral circulation is entirely constrained within the rigid cranial cavity. This unique anatomic arrangement implies that increases in cerebral blood flow must be matched by comparable increases in venous flow from the skull because the volume of blood and extracellular fluid within the brain is relatively constant.

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  1. An intracranial mass (tumor, hematoma) is inevitably accompanied by an increase in intracranial pressure (ICP). If ICP continues to increase, a compensatory increase in arterial pressure occurs (Cushing's reflex) that acts as a protective mechanism to maintain cerebral perfusion.

VIII. Renal Circulation

  1. Anatomy of the Renal Circulation: Determinants of Glomerular Blood Flow.The kidney has approximately 1 million glomeruli that filter plasma from circulating blood into Bowman's capsule surrounding each glomerulus capillary tuft. The entire glomerular capillary tuft is enveloped by Bowman's capsule, which collects the glomerular filtrate and transports it to the renal tubules, where urine is concentrated.
  2. Renal Hemodynamics
  3. The MAP in the glomerular capillaries is normally between 50 and 60 mm Hg, which favores the outward filtration of plasma water along the entire length of the capillary loop. Renal blood flow is approximately 20% of cardiac output and is heavily balanced toward perfusion of the renal cortex.
  4. Renal blood flow is very important for the delivery of the large volumes of blood to the glomeruli required for ultrafiltration.
  5. Renal blood flow remains relatively constant between MAP of 75 and 170 mm Hg but becomes pressure dependent beyond this range of autoregulation.
  6. Alterations in afferent arteriole resistance autoregulate glomerular filtration rate by constricting the diameter of afferent arterioles in response to increases in driving pressure.
  7. The Splanchnic and Hepatic Circulation
  8. Regulation of Gastrointestinal Blood Flow
  9. The intestinal circulation is weakly autoregulated compared with the cerebral, coronary, and renal vascular beds. Intestinal autoregulation appears to be primarily metabolic in origin.
  10. Pronounced sympathetic stimulation during acute hypovolemia produces gastrointestinal arterial

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constriction and venoconstriction, thereby shifting blood from a large vascular capacitance bed into the central circulation.

  1. Regulation of Hepatic Blood Flow
  2. The liver receives approximately 25% of total cardiac output, 75% of which is derived from the portal vein that contains venous blood from the gastrointestinal tract, spleen, and pancreas. The remaining 25% of hepatic blood flow is provided by the hepatic artery, which supplies the majority of O2to the liver.
  3. Blood flow in the portal venous and hepatic arterial systems tends to vary reciprocally, but these respective hepatic blood supplies do not fully interact. Thus, a reduction of blood flow in the portal vein may not be fully compensated by an increase in hepatic arterial flow.
  4. The hepatic arterial system (but not the portal venous system) is autoregulated.
  5. The liver contains about 15% of the total blood volume of the body and is an important volume reservoir that may be rapidly mobilized in response to sympathetic nervous system activation during acute hypovolemia.

Editors: Barash, Paul G.; Cullen, Bruce F.; Stoelting, Robert K.; Cahalan, Michael K.; Stock, M. Christine

Title: Handbook of Clinical Anesthesia, 6th Edition

Copyright ©2009 Lippincott Williams & Wilkins

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