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(BQ) Part 2 book Cardiovascular physiology presents the following contents: The arterial system, the microcirculation and lymphatics, the peripheral circulation and its control, control of cardiac output - Coupling of heart and blood vessels, coronary circulation, special circulations, interplay of central and peripheral factors that control the circulation.
7 THE ARTERIAL SYSTEM O B J E C T I V E S 1. Explain how the pulsatile blood flow in the large arteries is converted into a steady flow in the capillaries 3. Explain the factors that determine the mean, systolic, and diastolic arterial pressures and the arterial pulse pressure 2. Discuss arterial compliance and its relation to stroke volume and pulse pressure 4. Describe the common procedure for measuring the arterial blood pressure in humans THE HYDRAULIC FILTER CONVERTS PULSATILE FLOW TO STEADY FLOW The principal functions of the systemic and pulmonary arterial systems are to distribute blood to the capillary beds throughout the body The arterioles, which are the terminal components of the arterial system, regulate the distribution of flow to the various capillary beds In the region between the heart and the arterioles, the aorta and pulmonary artery, and their major branches constitute a system of conduits of considerable volume and distensibility This system of elastic conduits and high-resistance terminals constitutes a hydraulic filter that is analogous to the resistancecapacitance filters of electrical circuits Hydraulic filtering converts the intermittent output of the heart to a steady flow through the capillaries This important function of the large elastic arteries has been likened to the Windkessels of antique fire engines The Windkessel in such a fire engine contains a large volume of trapped air The compressibility of the air trapped in the Windkessel converts the intermittent inflow of water to a steady outflow of water at the nozzle of the fire hose The analogous function of the large elastic arteries is illustrated in Figure 7-1 The heart is an intermittent pump The cardiac stroke volume is discharged into the arterial system during systole The duration of the discharge usually occupies about one third of the cardiac cycle In fact, as shown in Figure 4-13, most of the stroke volume is pumped during the rapid ejection phase This phase constitutes about half of systole Part of the energy of cardiac contraction is dissipated as forward capillary flow during systole The remaining energy in the distensible arteries is stored as potential energy (Figure 7-1A and B) During diastole, the elastic recoil of the arterial walls converts this potential energy into capillary blood flow If the arterial walls had been rigid, capillary flow would have ceased during diastole 135 136 CARDIOVASCULAR PHYSIOLOGY Compliant arteries Systole Arterial blood flows through the capillaries throughout systole Diastole Arterial blood continues to flow through the capillaries throughout diastole Capillaries Capillaries Left atrium Left atrium Aorta Aorta Left ventricle A Left ventricle When the arteries are normally compliant, a substantial fraction of the stroke volume is stored in the arteries during ventricular systole The arterial walls are stretched B During ventricular diastole the previously stretched arteries recoil The volume of blood that is displaced by the recoil furnishes continuous capillary flow diastole Rigid arteries Systole A volume of blood equal to the entire stroke volume must flow through the capillaries during systole Diastole Flow through the capillaries ceases during diastole Capillaries Capillaries Left atrium Left atrium Aorta Aorta Left ventricle C When the arteries are rigid, virtually none of the stroke volume can be stored in the arteries Left ventricle D Rigid arteries cannot recoil appreciably during diastole FIGURE 7-1 n A to D, When the arteries are normally compliant, blood flows through the capillaries throughout the cardiac cycle When the arteries are rigid, blood flows through the capillaries during systole, but flow ceases during diastole THE ARTERIAL SYSTEM Hydraulic filtering minimizes the cardiac workload More work is required to pump a given flow intermittently than steadily; the steadier the flow, the less is the excess work A simple example illustrates this point Consider first that a fluid flows at the steady rate of 100 mL per second (s) through a hydraulic system that has a resistance of mm Hg/mL/s This combination of flow and resistance would result in a constant pressure of 100 mm Hg, as shown in Figure 7-2A Neglecting any inertial effect, hydraulic work, W, may be defined as: t W = ∫ t12 PdV (1) that is, each small increment of volume, dV, pumped is multiplied by the pressure, P, that exists at that time The products are integrated over the time interval, t2 – t1, to yield the total work When flow is steady, W = PV (2) In the example in Figure 7-2A, the work done in pumping the fluid for s would be 10,000 mm Hg mL (or 1.33 × 107 dyne-cm) Next, consider an intermittent pump that generates a constant flow of fluid for 0.5 s, and then pumps nothing during the next 0.5 s Hence, flow is generated at the rate of 200 mL/s for 0.5 s, as shown in Figure 7-2B and C In panel B, the conduit is rigid, and the fluid is incompressible However, the system has the same resistance to flow as in panel A During the pumping phase of the cycle (systole), the flow of 200 mL/s through a resistance of 1 mm Hg/mL/s would produce a pressure of 200 mm Hg During the filling phase (diastole) of the pump, the pressure in this rigid system would be mm Hg The work done during systole would be 20,000 mm Hg mL This value is twice that required in the example shown in Figure 7-2A If the system were very distensible, hydraulic filtering would be very effective and the pressure would remain virtually constant throughout the entire cycle (Figure 7-2C) Of the 100 mL of fluid pumped during the 0.5 s of systole, only 50 mL would be emitted through the high-resistance outflow end of the system during systole The remaining 50 mL would be stored by the distensible conduit during systole, and it would flow out during diastole Hence the pressure would be 137 virtually constant at 100 mm Hg throughout the cycle The fluid pumped during systole would be ejected at only half the pressure that prevailed in Figure 7-2B Therefore, the work would be only half as great If filtering were nearly perfect, as in Figure 7-2C, the work would be identical to that for steady flow (Figure 7-2A) Naturally, the filtering accomplished by the systemic and pulmonic arterial systems is intermediate between the examples in Figures 7-2B and C The additional work imposed by the intermittent pumping, in excess of that for steady flow, is about 35% for the right ventricle and about 10% for the left ventricle These fractions change, however, with variations in heart rate, peripheral resistance, and arterial distensibility The greater cardiac energy requirement imposed by a rigid arterial system is illustrated in Figure 7-3 In a group of anesthetized dogs, the cardiac output pumped by the left ventricle was allowed to flow either through the natural route (the aorta) or through a stiff plastic tube to the peripheral arteries The total peripheral resistance (TPR) values were virtually identical, regardless of which pathway was selected The data (see Figure 7-3) from a representative animal show that, for any given stroke volume, the myocardial oxygen consumption ( MV˙ O2 ) was substantially greater when the blood was diverted through the plastic tubing than when it flowed through the aorta This increase in MV˙ O2 indicates that the left ventricle had to expend more energy to pump blood through a less compliant conduit than through a more compliant conduit ARTERIAL ELASTICITY COMPENSATES FOR THE INTERMITTENT FLOW DELIVERED BY THE HEART The elastic properties of the arterial wall are determined by the composition and mechanical properties of the vessel Two important constituents of the arterial wall are elastic fibers, composed of elastin and microfibrils, and collagen Elastin is elaborated by endothelial cells and is found in the tunica intima, whereas collagen is derived from myofibroblasts and located in the tunica adventitia A Continuous flow pump R=1 mm Hg mL/s P = 100 mm Hg Pumped flow: 100 mL/s W = P × V = 100 ì 100 = 10,000 mm Hg mL each s A, Outflow (mL/s) Pressure (mm Hg) CARDIOVASCULAR PHYSIOLOGY Outflow = 100 mL/s for s 200 100 200 100 Time (s) 2 The pump flow is steady, and pressure will remain constant regardless of the distensibility of the conduit Rigid tube B Intermittent pump R=1 mm Hg mL/s P = Downstroke: R × Q = × 200 = 200 mm Hg Upstroke: R × Q = × = mm Hg Pumped flow: Downstroke: 200 mL/s for 0.5 s Upstroke: mL/s for 0.5 s W = P × V = 200 × 100 = 20,000 mm Hg • mL each s 200 mL/s for 0.5 s Outflow = mL/s for 0.5 s Outflow (mL/s) Pressure (mm Hg) 138 200 100 200 100 Time (s) B, The flow (Q) produced by the pump is intermittent; it is steady for half the cycle and ceases for the remainder of the cycle Compliant tube C Intermittent pump R=1 mm Hg mL/s P = constant at 100 mm Hg Pumped flow: Downstroke: 200 mL/s for 0.5 s Upstroke: mL/s for 0.5 s W = P × V = 100 ì 100 = 10,000 mm Hg mL each s Outflow = 100 mL/s for s Outflow (mL/s) Pressure (mm Hg) The conduit is rigid and therefore, the flow produced by the pump during its downstroke must exit through the resistance during the same 0.5 s that elapses during the downstroke The pump must twice as much work as the pump in A 200 100 200 100 Time (s) C, The pump operates as in B, but the conduit is infinitely distensible This results in perfect filtering of the pressure; that is, the pressure is steady, and the outflow through the resistance is also steady The work equals that in A FIGURE 7-2 n A to C, The relationships between pressure and flow for three hydraulic systems In each the overall flow is 100 mL/s and the resistance is mm Hg/mL/s 139 0.1 24 20– 275 250 Plastic tubing 225 0.05 Native aorta 10 15 Stroke volume (mL) FIGURE 7-3 n The relationship between myocardial oxygen consumption (mL/100 g/beat) and stroke volume (mL) in an anesthetized dog whose cardiac output could be pumped by the left ventricle either through the aorta or through a stiff plastic tube to the peripheral arteries. (Modified from Kelly RP, Tunin R, Kass DA: Effect of reduced aortic compliance on cardiac efficiency and contractile function of in situ canine left ventricle Circ Res 71:490, 1992.) The elastic properties of the arterial wall may be appreciated by considering first the static pressurevolume relationship for the aorta To derive the curves shown in Figure 7-4, aortas were obtained at autopsy from individuals in different age groups All branches of each aorta were ligated and successive volumes of liquid were injected into this closed elastic system After each increment of volume, the internal pressure was measured In Figure 7-4, the curve that relates pressure to volume in the youngest age group (curve a) is sigmoidal Although the curve is nearly linear, the slope decreases at the upper and lower ends At any point on the curve, the slope (dV/dP) represents the aortic compliance Thus, in young individuals the aortic compliance is least at very high at low pressures and greatest at intermediate pressures This sequence of compliance changes resembles the familiar compliance changes encountered in inflating a balloon The greatest difficulty in introducing air into the balloon is experienced at the beginning of inflation and again at near-maximal volume, just before the balloon ruptures At intermediate volumes, the balloon is relatively easy to inflate; that is, it is more compliant Increase in volume (%) O2 consumption (mL O2/100 g/beat) THE ARTERIAL SYSTEM a 29–3 175 b 36–42 150 c 47–5 125 d 200 100 e 75 71–78 50 25 0 25 50 75 100 125 150 175 200 225 Pressure (mm Hg) FIGURE 7-4 n Pressure-volume relationships for aortas obtained at autopsy from humans in different age groups (ages in years denoted by the numbers at the right end of each of the curves). (Redrawn from Hallock P, Benson IC: Studies on the elastic properties of human isolated aorta J Clin Invest 16:595, 1937.) Figure 7-4 reveals that the pressure-volume curves derived from subjects in different age groups are displaced downwards, and the slopes diminish as a function of advancing age Thus, for any pressure above about 80 mm Hg, the aortic compliance decreases with age This manifestation of greater rigidity (arteriosclerosis) is caused by progressive changes in the collagen and elastin contents of the arterial walls The previously described effects of the subject’s age on the elastic characteristics of the arterial system were derived from aortas removed at autopsy (see Figure 7-4) Such age-related changes have been confirmed in living subjects by ultrasound imaging techniques These studies disclosed that the increase in the diameter of the aorta produced by each cardiac contraction is much less in elderly persons than in young persons (Figure 7-5) The effects of aging on the elastic modulus of the aorta in healthy subjects are 140 CARDIOVASCULAR PHYSIOLOGY 22 yr Consequently, the increase in elastic modulus with aging (see Figure 7-6) and the decrease in compliance with aging (see Figure 7-4) both reflect the stiffening (arteriosclerosis) of the arterial walls as individuals age 63 yr ∆D mm 1s FIGURE 7-5 n The pulsatile changes in diameter (ΔD), measured ultrasonically, in a 22-year-old man and a 63-year-old man. (Modified from Imura T, Yamamoto K, Kanamori K, et al: Non-invasive ultrasonic measurement of the elastic properties of the human abdominal aorta Cardiovasc Res 20:208, 1986.) Ep (x 10 N/m2) 0 10 20 30 40 50 60 70 80 90 Age (yr) FIGURE 7-6 n The effects of age on the elastic modulus (Ep) of the abdominal aorta in a group of 61 human subjects. (Modified from Imura T, Yamamoto K, Kanamori K, et al: Non-invasive ultrasonic measurement of the elastic properties of the human abdominal aorta Cardiovasc Res 20:208, 1986.) shown in Figure 7-6 The elastic modulus, Ep , is defined as: Ep = Δ P /(Δ D / D) (3) where ΔP is the aortic pulse pressure, (Figure 7-7), D is the mean aortic diameter during the cardiac cycle, and ΔD is the maximal change in aortic diameter during the cardiac cycle The fractional change in diameter (ΔD/D) of the aorta during the cardiac cycle reflects its change in volume (ΔV) as the left ventricle ejects its stroke volume into the aorta each systole Thus Ep is inversely related to compliance, which is the ratio of ΔV to ΔP THE ARTERIAL BLOOD PRESSURE IS DETERMINED BY PHYSICAL AND PHYSIOLOGICAL FACTORS The determinants of the pressure within the arterial system of intact subjects cannot be evaluated precisely Nevertheless, arterial blood pressure is routinely measured in patients, and it provides a useful clue to cardiovascular status We therefore take a simplified approach to explain the principal determinants of arterial blood pressure To accomplish this, the determinants of the mean arterial pressure, defined in the next section, are analyzed first Systolic and diastolic arterial pressures are then considered as the upper and lower limits of the periodic oscillations about this mean pressure The determinants of the arterial blood pressure may be subdivided arbitrarily into “physical” and “physiological” factors (Figure 7-8) The arterial system is assumed to be a static, elastic system The only two “physical” factors are considered to be the blood volume within the arterial system and the elastic characteristics (compliance) of the system The following “physiological” factors will be considered: namely, (1) the cardiac output, which equals heart rate × stroke volume, and (2) the peripheral resistance Such physiological factors operate through one or both of the physical factors Mean Arterial Pressure The mean arterial pressure is the pressure in the large arteries, averaged over time The mean pressure may be obtained from an arterial pressure tracing, by measuring the area under the pressure curve This area is divided by the time interval involved, as shown in Figure 7-7 The mean arterial pressure, Pa , can usually be determined satisfactorily from the measured values of the systolic (Ps) and diastolic (Pd) pressures, by means of the following empirical formula: Pa ≅ Pd + (Ps − Pd ) (4) Pressure (mm Hg) THE ARTERIAL SYSTEM Systolic pressure 120 Pulse pressure Mean pressure Diastolic pressure 80 − Pa = 40 141 t2 t1 Pa dt t2 – t1 FIGURE 7-7 n Arterial systolic, diastolic, pulse, and mean pressures The mean arterial pressure ( Pa ) represents the area under the arterial pressure curve (colored area) divided by the cardiac cycle duration (t2 – t1) t2 t1 Time Physiological factors Cardiac output (Heart rate × Stroke volume) Peripheral resistance Physical factors Arterial blood volume Arterial compliance Arterial blood pressure FIGURE 7-8 n Arterial blood pressure is determined directly by two major physical factors, the arterial blood volume and the arterial compliance These physical factors are affected in turn by certain physiological factors, primarily the heart rate, stroke volume, cardiac output (heart rate × stroke volume), and peripheral resistance The mean arterial pressure depends mainly on the mean blood volume in the arterial system and on the arterial compliance (see Figure 7-8) The arterial volume, Va, in turn depends (1) on the rate of inflow, Qh, from the heart into the arteries (cardiac output), and (2) on the rate of outflow, Qr, from the arteries through the resistance vessels This constitutes the peripheral runoff Expressed mathematically, dVa / dt = Qh − Qr (5) This equation is an expression of the law of conservation of mass The equation states that the change in arterial blood volume per unit time (dVa/ dt) represents the difference between the rate (Qh) at which blood is pumped into the arterial system by the heart, and the rate (Qr) at which the blood leaves the arterial system through the resistance vessels If the arterial inflow exceeds the outflow, the arterial volume increases, the arterial walls are stretched, and the arterial pressure rises The converse happens when the arterial outflow exceeds the inflow When the inflow equals the outflow, the arterial pressure remains constant 142 CARDIOVASCULAR PHYSIOLOGY Cardiac Output The change in pressure in response to an alteration of cardiac output can be appreciated better by considering some simple examples Under control conditions, let cardiac output be L/min and let mean arterial pressure ( Pa ) be 100 mm Hg (Figure 7-9A) From the definition of total peripheral resistance, R = (Pa − Pra ) / Qr (6) where Pra is right atrial pressure If Pra (mean right atrial pressure) is negligible compared with Pa , R ≅ Pa / Qr (7) Therefore in the example, R is 100/5, or 20 mm Hg/L/min Now let cardiac output, Qh, suddenly increase to 10 L/min (Figure 7-9B) Pa will remain unchanged Because the outflow, Qr, from the arteries depends on Pa and R, Qr will also remain unchanged Therefore Qh, now 10 L/min, will exceed Qr, still only L/min This will increase the mean arterial blood volume (Va ) From equation 5, when Qh > Qr, dVa /dt > 0; that is, volume is increasing Because Pa depends on the mean arterial blood volume, Va and on the arterial compliance, Ca, an increase in Va will raise the Pa By definition, Ca = dVa / dPa (8) dVa = Ca dPa (9) dVa / dt = Ca dPa / dt (10) dPa / dt = (Qh − Qr ) / Ca (11) Therefore, and From equation 5, Hence Pa will rise when Qh > Qr, it will fall when Qh < Qr, and it will remain constant when Qh = Qr In this example, Qh suddenly increased to 10 L/ min, and Pa continued to rise as long as Qh exceeded Qr Equation shows that Qr will not attain a value of 10 L/min until Pa reaches a level of 200 mm Hg Thereafter, R will remain constant at 20 mm Hg/L/min Hence, as Pa approaches 200, Qr will approach the value of Qh, and Pa will rise very slowly When Qh begins to rise, however, Qh exceeds Qr, and therefore Pa will rise sharply The pressure-time tracing in Figure 7-10 indicates that, regardless of the value of Ca, the slope gradually diminishes as pressure rises, and thus the final value is approached asymptomatically Furthermore, the height to which Pa will rise does not depend on the elastic characteristics of the arterial walls Pa must rise to a level such that the peripheral runoff will equal the cardiac output; that is, Qr = Qh Equation shows that Qr depends only on the pressure gradient and the resistance to flow Hence Ca determines only the rate at which the new equilibrium value of Pa will be approached, as illustrated in Figure 7-10 When Ca is small (as in rigid vessels), a relatively slight increment in Va would increase Pa greatly This increment in Pa is caused by a transient excess of Qh over Qr Hence Pa attains its new equilibrium level quickly Conversely, when Ca is large, considerable volumes can be accommodated with relatively small pressure changes Therefore the new equilibrium value of Pa is reached at a slower rate Peripheral Resistance Similar reasoning may now be applied to explain the changes in Pa that accompany alterations in peripheral resistance Let the control conditions be identical to those of the preceding example, that is, Qh = 5, Pa = 100, and R = 20 (see Figure 7-9A) Then, let R suddenly be increased to 40 (see Figure 7-9D) Pa would not change appreciably When Pa = 100 and R = 40, Qr would equal Pa /R, which would then equal 2.5 L/min Thus, the peripheral runoff would be only 2.5 L/min, even though cardiac output equals L/min If Qh remains constant at L/min, Qh would exceed Qr and Va would increase; and therefore Pa would rise Pa will continue to rise until it reaches 200 mm Hg (see Figure 7-9, E) At this pressure level, Qr = 200/40 = L/min, which equals Qh Pa will remain at this new, elevated level, as long as Qh and R not change It is evident, therefore, that the level of the mean arterial pressure depends on cardiac output and peripheral resistance This dependency applies regardless of whether the change in cardiac output is accomplished by an alteration of heart rate or of stroke volume Any change in heart rate that is balanced by a concomitant, oppositely directed change in stroke volume, will not alter Qh Hence Pa will not be affected THE ARTERIAL SYSTEM 2.5 L/min L/min 10 L/min A 143 Control conditions Pa = 100 mm Hg Qr = L/min 20 mm Hg R= L/min Qh = L/min Qr = Pa 100 = =5 R 20 A, Under control conditions Qh = L/min, Pa = 100 mm Hg, and R = 20 mm Hg/L/min Qr must equal Q h , and therefore the mean blood volume (Va) in the arteries will remain constant from heartbeat to heartbeat B Instantaneous increase in cardiac output D Instantaneous increase in peripheral resistance Pa = 100 Pa = 100 Qr = L/min Qh = 10 L/min R= Qr = 20 mm Hg L/min Pa 100 = =5 R 20 Qr = B, If Q h suddenly increases to 10 L/min, Q h will initially exceed Qr, and therefore Pa will begin to rise rapidly C Qr = 2.5 L/min 40 mm Hg R= L/min Qh = L/min Steady-state increase in cardiac output Pa 100 = = 2.5 R 40 D, If R abruptly increases to 40 mm Hg/L/min, Qr suddenly decreases and therefore Q h exceeds Qr Thus Pa will rise progressively E Steady-state increase in peripheral resistance Pa = 200 Pa = 200 Qr = 10 L/min Qh = 10 L/min 20 mm Hg R= L/min Qr = Pa 200 = = 10 R 20 C, The disparity between Q h and Qr progressively increases arterial blood volume The volume continues to increase until Pa reaches a level of 200 mm Hg Qr = L/min Qh = L/min R= Qr = 40 mm Hg L/min Pa 200 = =5 R 40 E, The excess of Qh over Qr accumulates blood in the arteries Blood continues to accumulate until Pa rises to a level of 200 mm Hg FIGURE 7-9 n The relationship of mean arterial blood pressure ( Pa ) to cardiac output (Qh), peripheral runoff (Qr), and peripheral resistance (R) under control conditions (A), in response to an increase in cardiac output (B and C), and in response to an increase in peripheral resistance (D and E) CARDIOVASCULAR PHYSIOLOGY V4 Small Ca 200 Large Ca 100 Increase cardiac output Volume Arterial pressure (mm Hg) 144 B2 VB B V3 B1 V2 VA V1 A A2 A1 Time FIGURE 7-10 n When cardiac output is suddenly increased, the arterial compliance (Ca) determines the rate at which the mean arterial pressure will attain its new, elevated value but will not determine the magnitude of the new pressure Pulse Pressure Let us assume (see Figure 7-8) that the arterial pressure, Pa, at any moment depends on the two physical factors, namely (1) the arterial blood volume, Va, and (2) the arterial compliance, Ca Hence, the arterial pulse pressure (that is, the difference between systolic and diastolic pressures) is principally a function of the stroke volume and the arterial compliance Stroke Volume The effect of a change in stroke volume on pulse pressure may be analyzed when Ca remains virtually constant Ca is constant over any linear region of the pressure-volume curve (see Figure 7-11) Volume is plotted along the vertical axis, and pressure is plotted along the horizontal axis; the slope, dV/dP, equals the compliance, Ca In an individual with such a linear Pa:Va curve, the arterial pressure would oscillate about a mean value ( Pa in Figure 7-11) This value depends entirely on cardiac output and peripheral resistance, as explained above The mean pressure reflects a specific mean arterial blood volume, Va The coordinates, Pa and Va , define point A on the graph During diastole, peripheral runoff from the arterial system occurs in the absence of the ventricular ejection of blood Furthermore, Pa and Va diminish to the minimal values, P1 and V1, just before the next ventricular ejection P1 defines the diastolic pressure P1 PA P2 P3 PB P4 Pressure FIGURE 7-11 n Effect of a change in stroke volume on pulse pressure in a system in which arterial compliance is constant over the range of pressures and volumes involved A larger volume increment (V4 – V3 as compared with V2 – V1) results in a greater mean pressure (PB as compared with (PA ) and a greater pulse pressure (P4 – P3 as compared with P2 – P1) During the rapid ejection phase of systole, the volume of blood introduced into the arterial system exceeds the volume that exits through the arterioles Arterial pressure and volume therefore rise from point A1 toward point A2 in Figure 7-11 The maximal arterial volume, V2, is reached at the end of the rapid ejection phase (see Figure 4-13); this volume corresponds to the peak pressure, P2, which is the systolic pressure The pulse pressure is the difference between the systolic and diastolic pressures (P2 – P1 in Figure 7-11), and it corresponds to some arterial volume increment, V2 – V1 This increment equals the volume of blood discharged by the left ventricle during the rapid ejection phase, minus the volume that has run off to the periphery during this same phase of the cardiac cycle When a healthy heart beats at a normal frequency, the volume increment during the rapid ejection phase is a large fraction (about 80%) of the stroke volume It is this increment that raises the arterial volume rapidly from V1 to V2 Consequently, the arterial pressure will rise from the diastolic to the systolic level (P1 to P2 in Figure 7-11) During the remainder of the cardiac cycle, peripheral runoff will exceed cardiac ejection During 278 CARDIOVASCULAR PHYSIOLOGY c the arterial chemoreceptors reflexly induced the parasympathetic nerves to the skin to release neuropeptide Y d the arterial baroreceptors reflexly induced the sympathetic nerves to the skin to release nitric oxide e the arterial baroreceptors reflexly induced the sympathetic nerves to the skin to release norepinephrine The patient’s arterial blood pressure, 85/65 mm Hg, indicates that: a the patient’s left ventricle was pumping an abnormally low cardiac output and low stroke volume b the patient’s left ventricle was pumping more blood than her right ventricle c the patient’s left ventricle was pumping an abnormally low cardiac output but a normal stroke volume d the patient’s left ventricle was pumping a normal cardiac output and an abnormally low stroke volume e the patient’s left ventricle was pumping less blood than her right ventricle If the patient’s bleeding had stopped before she arrived at the hospital, which of the following changes would be expected in the patient’s blood hour after she had arrived at the hospital? a The individual red blood cells would be larger than normal b The hematocrit ratio would be reduced c The lymphocyte count would be abnormally high d The plasma albumin concentration would be increased e The plasma globulin concentration would be increased APPENDIX C A S E S T U D Y A N S W E R S CASE 1-1 b is correct The circulation time will be shortened because some blood passes through the shunt (short circuit) CASE 2-1 c is correct When the extracellular K+ concentration increases, the Nernst equation indicates that the transmembrane potential will become less negative d is correct When the extracellular K+ concentration increases and depolarizes the membrane, the rate of rise of the action potential is diminished because some Na+ channels are inactivated by the persistent depolarization d is correct The Purkinje fibers are automatic fibers, and they generate action potentials at a low frequency whenever they are not depolarized by action potentials that originate in higher- frequency pacemaker sites a is correct When ventricular pacing at 75 beats per minute was discontinued, spontaneous pacemaker activity in the ventricles was suppressed for several seconds because the preceding period of artificial pacing had hyperpolarized the ventricular pacemaker cells (Purkinje fibers) CASE 3-1 c is correct because the PR interval, which indicates the time for conduction from atria through the AV node and ventricular conducting system to the ventricle, is normal 2 e is correct because the QT interval measures the duration of the average ventricular action potential a is correct because heart rate can be taken from either the R-R or the P-P interval when conduction is normal d is correct because there is greater activation of repolarizing K channels when heart rate increases CASE 4-1 d is correct The murmur is characteristic of mitral stenosis c is correct The pulse is totally irregular b is correct A “loop” diuretic like furosemide would relieve the excessive preload and allow the cardiac output to improve and the edema and ascites to subside b is correct The elevated left atrial pressure would be transmitted back to the wedged catheter (wedge pressure) c is correct 300 mL O2/min /[(18 − 8) mL O2/100 mL blood] = 3000 mL/min = L/min CASE 5-1 d is correct A decrease in arterial pressure would reflexly increase sympathetic activity and thereby increase the neuronal release of norepinephrine d is correct The ACh released from vagal fibers acts on muscarinic receptors on SA node automatic cells, and these receptors interact very quickly with specific K+ channels because no second messenger intervenes 279 280 CARDIOVASCULAR PHYSIOLOGY a is correct The cardiac responses to vagal stimulation develop and decay rapidly, but the responses to sympathetic stimulation develop and decay very slowly Hence respiratory dysrhythmia is mediated almost entirely by the vagus nerves, and this dysrhythmia would be abolished by a potent muscarinic antagonist a is correct Heart rate increases during inspiration in this dysrhythmia, and this increase is mediated mainly by a reduction in vagal activity e is correct Acetylcholinesterase is abundant in atrial tissues, and especially in the SA and AV nodes CASE 8-1 d is correct 1[(44 − 8) − 0.7(23 − 3)] = 22 c is correct Portal-caval shunt (portal vein to inferior vena cava) could reduce the high venous pressure in the mesentery by allowing mesenteric blood to bypass the high vascular resistance in the liver This would aid in eliminating the ascites b is correct Albumin is small enough (low molecular weight) to exert the main osmotic force of plasma and large enough to remain within the vascular compartment CASE 8-2 CASE 6-1 b is correct (Pa − Pv)/Q—that is, [(100 − 80) + (80 − 10)]/300—equals 0.30 mm Hg/mL/min d is correct The left ([100 − 10]/500) and right ([100 − 10]/300) vascular resistances were 0.18 and 0.30 mm Hg/mL/min, respectively, and the reciprocals of those resistances were 5.56 and 3.33 mL/min/mm Hg, respectively Hence the reciprocal of the sum (8.89 mL/min/mm Hg) of these reciprocals equals 0.11 mm Hg/mL/min a is correct The pressure difference across the plaque (100 − 80 mm Hg), divided by the flow past the plaque (300 mL/min), equals 0.066 mm Hg/mL/min 1 e is correct The albumin concentration in the patient’s blood is low because of the loss of albumin from the burned tissues This results in a decreased plasma oncotic pressure, and that plus the loss of fluid from the damaged microvessels leads to a decreased blood volume and an increased red blood cell concentration Therefore a plasma transfusion, which supplies albumin plus saline without red blood cells, is the most effective treatment d is correct The small diameter (or radius) of the capillaries is responsible for the low wall tension, according to the law of Laplace, whereby T (wall tension) = P (pressure) × r (radius of capillary) The low wall tension protects against capillary rupture CASE 7-1 a is correct The mean arterial pressure in the systemic and pulmonary vascular beds depends on the outputs of the left and right ventricles and the systemic vascular resistances Over any substantial time interval, the outputs of the two ventricles are equal, but the systemic vascular resistance far exceeds the pulmonary vascular resistance c is correct When the arterial pressure rises, the arteries become less compliant (as does a balloon), and also the arterial compliance decreases with age CASE 9-1 b is correct The arterioles are maximally dilated secondary to the inadequate blood flow that causes the local release of vasodilator metabolites d is correct The ankle-brachial index is taken from the ratio of systolic pressure in the dorsalis pedis artery to that in the brachial artery (112 mm Hg/140 mm Hg = 0.80) a is correct Use of tobacco is believed to be a contributing factor to the cause and exacerbation of thromboangiitis obliterans APPENDIX 281 CASE 10-1 CASE 12-1 c is correct The blood loss would decrease the central venous pressure, and this reduction in cardiac preload would reduce the cardiac output a is correct A drug that improves cardiac contractility would increase cardiac output, a change that would tend to increase the arterial blood volume Hence, if total blood volume remains constant, the venous blood volume would decrease Consequently, the central venous pressure would decline e is correct Gravity acts to pool blood in the compliant, dependent veins, and hence the pressure in the foot veins increases The redistribution of the venous blood volume causes the central venous volume and pressure to diminish The consequent reduction in preload decreases the cardiac output b is correct When the heart rate is abnormally high (250 beats/min), cardiac filling is inadequate, and therefore stroke volume and cardiac output are decreased 1 a is correct The hepatic fibrosis increases the hepatic vascular resistance, and therefore the pressure in the vessels downstream to the liver is elevated Consequently, the balance of Starling forces in the splanchnic capillaries favors the movement of fluid out of the capillaries and into the abdominal cavity CASE 11-1 d is correct Two factors operate in bradycardia At the slower rate, more time is spent in diastole, thereby decreasing coronary resistance (less extravascular compression) However, at the slower rate the heart uses less oxygen and fewer vasodilator metabolites are present, permitting greater expression of basal tone (coronary constriction) The end result is the algebraic sum of these two opposing factors a is correct The coronary vessels are maximally dilated as a result of the accumulation of vasodilator metabolites consequent to an inadequate oxygen supply to the myocardial cells If any vasoconstriction occurred, it would be transient b is correct Endothelin is a powerful vasoconstrictor e is correct With exercise, a denervated heart increases stroke volume more than heart rate to meet the required cardiac output Any increase in heart rate must come from release of epinephrine and norepinephrine from the adrenal medulla CASE 12-2 b is correct The murmur, the high right ventricular systolic pressure with a normal right atrial pressure, the elevated Po2 of the right ventricular blood, and the absence of cyanosis indicated a left-to-right shunt through an interventricular septal defect CASE 12-3 d is correct The ankle-brachial index (ABI) is the ratio of systolic blood pressure in the dorsal pedal artery to that in the brachial artery The ratio (70 mm Hg/140 mm Hg) yields an ABI of 0.5 CASE 13-1 d is correct The patient’s heart became unable to pump enough blood per unit time owing to a decrease in stroke volume and hence in cardiac output a is correct The patient’s body temperature reached an alarmingly high level because of inadequate heat loss via the skin (vasoconstriction secondary to decrease in blood pressure) in the presence of the great heat production in the active muscles CASE 13-2 e is correct The hypotension would act via the arterial baroreceptors to activate the sympathetic nerves to the skin The consequent release of norepinephrine would constrict the cutaneous arterioles, and the skin temperature would drop 282 CARDIOVASCULAR PHYSIOLOGY a is correct The abnormally low mean arterial pressure (about 72 mm Hg) would signify an abnormally small cardiac output The low mean arterial pressure could not have been caused by arterial vasodilation because the baroreceptor reflex response to a low mean arterial pressure would be vasoconstriction, not dilation The low pulse pressure (20 mm Hg) would signify an abnormally small stroke volume 3 b is correct The decrease in capillary hydrostatic pressure draws interstitial fluid into the plasma compartment and thereby dilutes the red cell component of whole blood INDEX A A band, 56f–57f A receptors, 189 a wave, 72 ABI See Ankle-brachial index Accessory atrioventricular pathways, 42b Accumulated vasodilator metabolites, 268–269 Acetylcholine atrioventricular node N region fibers hyperpolarized by, 39 hyperpolarization induced by, 35, 35f muscarinic receptor interactions with, 112 vagal ending release of, 112 Acetylcholinesterase, 280 Acetylstrophanthidin, 43 Acid hydrolases, 275 Acidosis, 115 in hemorrhage, 274 ACTH See Adrenocorticotropic hormone Actin, 55–58 Actin filaments, 172 Action potential amplitude of, 26 contraction and, 12, 57f, 172 cycle length effects on, 28–29 definition of, 11–12 diltiazem effects on, 22f, 23 duration of, 28–29, 28f fast response changes to slow response, 13b conduction of, 25–27 description of, 12, 12f effective refractory period for, 27 excitability affected by, 27–28 voltage-dependent sodium channels and, 15–24 gate concept for, 19 ionic currents, 20f overshoot of, 15–17 phases of, 11–25, 12f plateau phase calcium conductance during, 21–23, 21f, 63–64, 108 definition of, 11–12 early afterdepolarization at end of, 43 genesis of, 20 potassium conductance during, 22–23 propagation of, 25 from Purkinje fibers, 40–41 rate of change of, 26 repolarization definition of, 11–12 Action potential (Continued) early, 20 final, 23 slow response in atrioventricular node N region, 37–38 conduction of, 27 description of, 12, 12f fast responses changed to, 13b ionic basis of, 24–25 relative refractory period during, 27 tetrodotoxin effects on, 13b, 13f, 16 transmembrane See Transmembrane potential types of, 12–13 upstroke of, 11–12, 15–19 Activation of calcium channels, 34, 111 of fast sodium channels, 16 Activation gate, 16 Active hyperemia, 182 Acute coronary artery occlusion, 233b Acute heart failure, 211b Addisonian crisis, 114b Addison’s disease, 114b Adenosine, 245 description of, 182 A1 receptor, 230 A2a receptor, 230, 231f Adenosine triphosphate (ATP), metabolism of, 81–83 sensitive KATP channels, 229, 265 Adenylyl cyclase, 21–22, 112 Adrenal medulla, 185 α-Adrenergic effect, 185 β-Adrenergic drugs, 228 β-Adrenergic effect, 185 β-Adrenergic receptors antagonists, 92 catecholamines and, 21–22, 110–111 β-Adrenoceptor-blocking agent, 228 α1-Adrenoceptors, 254 α-Adrenoceptors, 228 β1-Adrenoceptors, 254 β-Adrenoceptors, 228 Adrenocortical hormones, 113–114 Adrenocorticotropic hormone (ACTH), 275 Adrenomedullary hormones, 113 Afferent arterioles, 250–251 Afterdepolarizations delayed, 43–44 early, 43 triggered activity caused by, 42–44 Afterload cardiac function curve and, 198 definition of, 22b, 103–104 description of, 69 left ventricular, 212 Afterload reducing drugs, 22b A-H interval, 48 Albumin, 163–164, 280 Aldosterone, 189, 273 Alveolus, 245, 246f Ambient temperature, skin blood flow and, 239–240 Amplitude, 26 Anemia blood viscosity in, 130b high altitude and, 7b megaloblastic, 8f microcytic, hypochromic, 5–6, 8f sickle cell, 5–6, 8f, 132b spherocytic, 132b Angina pectoris, 189b, 234b Angioplasty, 233b Angiotensin I, 189, 253, 273 converting enzyme, 253 Angiotensin II, 189, 253, 273 Angiotensin-converting enzyme, 189 Angiotensinogen, 253 Ankle-brachial index (ABI), 148b, 280–281 Anomalous viscosity, 129 ANP See Atrial natriuretic peptide Antegrade impulse, 41–42 Anterior interatrial myocardial band, 36 Antidiuretic hormone, 98, 273 Antigen blood group based on, 7–8 definition of, Aorta aging effects on, 139–140 cardiac cycle changes, 140 characteristics of, 3f static pressure-volume relationship for, 139, 139f wall tension of, 156t Aortic arch, 185–186, 186f, 189 Aortic bodies, 189 Aortic compliance, 139 Aortic insufficiency, 75b Aortic pulse pressure, 139–140, 141f Aortic regurgitation, 145b Aortic stenosis, 75b, 121, 226b Page numbers followed by f indicate figures; t, tables; b, boxes 283 284 INDEX Aortic valve, 61f Apex of heart, 60–62 Apnea, 219–220 Apparent viscosity, 129 Aquaporins, 159 Arachidonic acid, 157f, 275 Arcuate arteries, 250 Arterial baroreceptors, 185–188 Arterial blood pressure, hemorrhage and, 270 Arterial compliance (Ca), 145–146, 200 Arterial diastolic pressure, 146–147 Arterial hypotension, 185 Arterial pulse pressure, 144 Arteries See also specific artery anatomy of, arcuate, 250 celiac, 254 characteristics of, 3f elastic, 135, 136f elasticity of, 137–140 frictional resistance in, functions of, 171 hepatic, 256 inferior mesenteric, 254 renal, 250 superior mesenteric, 254 Arteriogenesis, 233 Arteriolar resistance, 163 Arteriolar vasoconstriction, 270–271 Arterioles afferent, 250–251 anatomy of, 153–156 characteristics of, 3f constriction of, 180f cross-sectional image of, 173f functions of, 135, 171 histology of, 155f, 173f metarterioles, 153–154 nitric oxide effects on, 182 nitroprusside effects on, 179 prostaglandins’ effect on, 182 terminal, 3f, 154 Arterioluminal vessel, 223–224 Arteriosclerosis, 140 Arteriosinusoidal vessel, 223–224 Arteriovenous (AV) anastomoses, 237, 238f Artificial respiration, cardiac output and, 220–221 Ascending aorta, 147 ATP See Adenosine triphosphate Atria anatomy of, 60–62 left See Left atrium right See Right atrium Atrial conduction, 36 Atrial fibrillation, 50, 50f Atrial flutter, 51b Atrial natriuretic peptide (ANP), 98–99 Atrial pacemaker complex, 31 Atrial receptors heart rate regulation by, 98–99 urine volume affected by, 98 Atrial systole, 73 Atrioventricular block bradycardia and, 215b complete, 38–39, 38f, 39b Atrioventricular block (Continued) first-degree, 38, 38f, 39b second-degree, 38, 38f, 39b site of, 48, 48f third-degree, 38–39, 38f, 39b Atrioventricular (AV) node anatomy of, 36f, 37 in atrial fibrillation, 51b automaticity in, 35 cholinesterase in, 92–93 conduction in, 37–39 description in, 12 N region of, 37–38 NH region of, 37–38 AN region of, 37–38 regions of, 37 retrograde conduction through, 38 transmembrane potential from, 39f Atrioventricular pathways, accessory, 42b Atrioventricular valves, 61f, 62 Atropine, 92 Augmentation index, 148 Auricular appendage, 61f Ausculatory method, 149–150 Automaticity in atrioventricular node, 35 ionic basis of, 34–35 properties of, 31 Purkinje fibers, 32, 35 Autonomic nervous system, heart rate regulation by, 91–102 Autoregulation of coronary blood flow, 225 of intestinal circulation, 254 of renal hemodynamics, 252–253 of systemic blood flow, 166, 179–180 Auxiliary pump, 219–220 Auxiliary pumping mechanism, 220b AV node See Atrioventricular node B B lymphocytes, B receptors, 189 Bachmann’s bundle, 36 Bainbridge reflex, 98–99 Balloon angioplasty, 233b Baroreceptor reflex, 269 heart rate regulation by, 97–98 in hemorrhage, 270–272 myocardial performance affected by, 112–113 Baroreceptors arterial, 185–188 cardiopulmonary, 188–189 carotid sinus, 186 definition of, 185–186 sinoaortic, 273 Basal metabolism, 2b Basal tone, 182–183 Basophils, 6f Birth, circulatory system at, 259–260 Blanching, 239 Blood apparent viscosity of, 130 components of, 5–8 erythrocytes See Erythrocytes Blood (Continued) functions of, homeostatic functions of, leukocytes, 6–7 lymphocytes, mobilization of, from capacitance vessels, 185 rheologic properties of, 129–131 viscosity of, 129, 130f Blood clotting aberrations, in hemorrhage, 275 Blood flow arterial, autoregulation of, 179, 225 in capillaries, 3, 4f, 154 cerebral, 243–245 coronary See Coronary blood flow endothelial regulation of, 180–181 equation for, 119 hepatic, 256–257 intestinal, 256 local regulation of, 181–183 nutritional, 154–155 peak velocity of, 121, 121f peripheral See Peripheral blood flow physiological shunting of, 154–155 pressure gradient effects on, 120–121 pulmonary, 247–249 pulsatile arterial, renal, 252 resistance to, 125–127 right ventricle and, 211–214 to skin ambient temperature and, 239–240 body temperature and, 239–240 skin color and, 240 sympathetic nervous system and, 237–239 tissue metabolic activity effects on, 181–183 tissue perfusion alteration effects on, 179 velocity of, 91–102 Blood groups, 7–8 Blood pressure arterial, 140–147 hemorrhage and, 270 baroreceptors’ effect on arterial, 185–188 cardiopulmonary, 188–189 curves, 147–148 determinants of cardiac output See Cardiac output mean arterial pressure, 140–141 overview of, 140 peripheral resistance, 142 pulse pressure, 144 measurement of, 148–150 sphygmomanometer measurement of, 148–150, 149f vascular reflexes’ effect on, 185–189 Blood reservoirs, 206 Blood transfusion, cardiac output affected by, 99f Blood vessels See also specific vessel anatomy of, 1–2, 2f function of, 171 INDEX Blood vessels (Continued) in parallel, 126–127 parasympathetic nervous system, innervation of, 185 resistance, 171 schematic diagram of, 4f in series, 126–127 shear stress on, 128–129 Blood volume decreases in, 189 description of, 5–8, 140 distribution of, 3, 5t vascular function curve affected by, 205–206, 209–210 Blood-brain barrier, 244–245 Blushing, 239 Body temperature, skin blood flow and, 239–240, 281 Bowman capsule, 250–251 Brachial artery, 149–150 Bradycardia, 281 cerebral ischemia and, 272 complete atrioventricular block and, 215b description of, 47–48, 47f sick sinus syndrome and, 215b Bradykinin, 239 Bronchial vasculature, 246–247 Bundle branches anatomy of, 39, 40f block of, 40b left, 39–40, 40f right, 39–40, 40f Bundle of His description of, 17–18 electrogram of, 26f, 48 C c wave, 72 Ca See Arterial compliance Calcium calcium-induced release of, 64–65 delayed afterdepolarizations and, 44 excitation-contraction coupling mediated by, 63–65 intercellular concentration of, 63 from interstitial fluid, 63–64 myoplasmic concentration of, 14t, 172–174 systolic, 63–65 trigger, 63–64 Calcium channel(s) activation of, 34, 111 characteristics of, 21 L-type, 21 stretch effects on, 179 T-type, 21 voltage-gated, 176 Calcium channel antagonists dihydropyridine receptor, 63–64 transmembrane potential affected by, 34f Calmodulin, 172–174 cAMP See Cyclic adenosine monophosphate Capacitance vessels basal tone in, 184b blood mobilization from, 185 constriction of, 184 Capacitance vessels (Continued) description of, 153 sympathetic nerves’ regulation of, 184–185 Capillaries blood flow in, 3, 4f, 154 characteristics of, 3f density of, 154 diameter of, 156, 280 distribution of, 154 endothelial wall, 161f fenestrations in, 158f, 159 flow-limited transfer across, 161–162 hydrostatic pressure in, 163 illustration of, 160f–161f law of Laplace, 155 in myocardium, 58–60 permeability of, 158–159, 158f pinocytotic transfer across, 167 recruitment of, 166 wall tension of, 156t Capillary filtration, 163–165 coefficient, 165 Capillary pressure, 164–165 Capillary recruitment, 166, 265 Carbohydrate metabolism, 84–86 Carbon dioxide central chemoreceptors affected by, 189–190 myocardial performance affected by, 115 Carbon dioxide tension, description of, 189 Cardiac cells effective refractory period, 17–18 excitability of, 27–29 intracellular and extracellular ion concentrations in, 14t potassium concentration in, 13 sodium entry into, 17 sodium equilibrium potential for, 14 Cardiac cycle afterload during, 77–78 aorta changes during, 140 length of, 28–29 norepinephrine release during, 95 preload during, 77–78 pressure-volume graph of, 77 ventricular diastole, 73 ventricular systole, 72 Cardiac excitability, 27–29 Cardiac failure, in hemorrhage, 274 Cardiac fibers conduction in, 25–27 skeletal muscle fibers vs., 58 Cardiac function curve (CFC), 196–197 afterload and, 198 contractility and, 197–198 myocardial compliance and, 198–199 physiological function and, 199–200 Cardiac glycogen levels, 258 Cardiac glycosides, 65 Cardiac muscle characteristics of, 55–58 metabolism of ATP, 81–86 oxygen requirements, 58 skeletal muscle vs., 56f–57f, 58, 59f syncytium, 58 285 Cardiac O2 consumption, 86–88 Cardiac output (CO) artificial respiration and, 220–221 bleeding effects on, 99f blood transfusion effects on, 99f calculation of, 91 central venous pressure and, relationship between, 196–200, 281 description of, 140, 142 elements of, 141 factors controlling, 195–196, 196f Fick principle for measuring, 79–80 Frank-Starling mechanism, 106 gravity and, 216–218, 281 heart rate and, 214–216 indicator dilution technique for measuring, 80–81 mean arterial pressure and, 141f renal circulation and, 250–254 respiratory activity and, 219–220 venous pressure depends on, 205 venous return and, 207 Cardiac valves atrioventricular, 61f, 62 semilunar, 61f, 62 Cardiac work, 86–88 Cardiopulmonary baroreceptors, 188–189 Cardiovascular system, functions of, Cardioversion, 215b Carotid sinus anatomy of, 186f baroreceptors in, 185–186 denervation of, 188 Catecholamines, 272 adrenal medulla secretion of, 185 β-Adrenergic receptors and, 21–22, 110–111 calcium entry into cells affected by, 64–65 cardiac muscle contractility affected by, 21–22 contraction affected by, 65 vascular tone control by, 178 Celiac artery, 254 Cell membranes ionic conductance of, 19 permeability of, 13 Central chemoreceptors, 189–190 Central command, 264 Central nervous system, depression of, in hemorrhage, 274–275 Central terminal, 47 Central venous pressure cardiac output and, relationship between, 196–200, 281 right ventricle and, 211–214 Cerebral circulation, 243–245 Cerebral cortex, 191 Cerebral ischemia, 191b in hemorrhage, 272 CFC See Cardiac function curve cGMP See Cyclic guanosine monophosphate Chemoreceptor(s) central, 189–190 peripheral, 189 stimulation of, 189 286 INDEX Chemoreceptor reflex description of, 101–102 in hemorrhage, 272 Chemotactic substances, Cholecystokinin, 256 Cholinesterase, 92–93 Chord conductance equation, 15 Chordae tendineae, 62 Chronic heart failure, 106b, 211b Circulation, 2f cerebral, 243–245 cutaneous, 237–240 fetal, 257–260 hepatic, 256–257 intestinal, 254–256 pulmonary, 245–250 description of, 1–2 renal, 265 anatomy of, 250–251 cardiac output and, 250–254 hemodynamics of, 252–254 skeletal muscle, 240–243 regulation of, 240–243 splanchnic, 254–257, 265 systemic, 1–2, 245–250 Circulatory system, at birth, 259–260 CO See Cardiac output Compensatory pause, after premature ventricular depolarization, 49 Complete atrioventricular block, 38–39, 38f, 39b bradycardia and, 215b Compliance aortic, 139 arterial, 145–146 Conditioning, 269 Conductance, hydraulic, 127 Conduction and local circuit currents, 25 atrial, 36 atrioventricular node, 37–39 in right bundle branch, 39–40 ventricular, 39–41 Conduction system, 36, 36f Conduction velocity, 26 Congenital cardiac defects, 214b Congestive heart failure, 218b, 256b–257b arterial pulse pressure in, 145b description of, 75b Connexins, 25 Connexons, 58 Conservation of mass, 141 Contractility cardiac function curve and, 197–198 definition of, 78 drugs that affect, 78 heart rate affected by changes in, 107–110 hypoxia effects on, 115 myocardial, 209 norepinephrine effects on, 113, 114f sympathetic nervous system effects on, 110–112 thyroid hormones’ effect on, 114–115 ventricular function curve and, 106–107 Contraction action potential and, 172 atrial, 73 calcium and, 63 catecholamines’ effect on, 65 force of, 63–69 frequency of, 107 isovolumic, 70 skeletal muscle, 182 strength of, 109 velocity of, 69 Coronary artery disease, 27b Coronary artery occlusion, 226b acute, 233b Coronary atherosclerosis, 230b Coronary blood flow cardiac function and, 230–231 coronary collateral vessel development and, 233–234 metabolic factors, 228–230 neural factors of, 225–228 neurohumoral factors of, 225–228 physical factors of, 225–227 Coronary bypass surgery, 233b Coronary collateral vessel, development of, coronary blood flow and, 233–234 Coronary steal, 234b Coronary vessels, 223–224, 224f Corticomedullary junction, 250 Countercurrent exchange, 163, 254 Counterpulsation, 226b Coupled extrasystoles, 48 Coupling interval, 109, 113–114 Creatinine phospholipase (CPIC) equation, 81 Crista dividens, 258 Current calcium diastolic depolarization affected by, 34 inward, 107–108 inward hyperpolarization-induced, 34 transient, 44 potassium, 34 Cushing phenomenon, 245b Cutaneous circulation, 237–240 Cv See Venous compliance Cyclic adenosine monophosphate (cAMP) dependent protein kinase (PKA), 96f description of, 21–22, 95 prostacyclin effects on, 156 Cyclic guanosine monophosphate (cGMP), 34 cGMP-dependent protein kinase, 157 D DADs See Delayed afterdepolarizations Delayed afterdepolarizations (DADs), 43–44 Delayed rectifier potassium channels, 23 Denervation hypersensitivity, 238–239 Dependent variable, 200, 208 Depolarizations description of, 11–12 diastolic, 34 premature atrial, 41, 48, 49f premature ventricular, 48, 49f Depressor area, 183 Depressor effect, 185–186 Diacylglycerol, 178 Diastasis, 73 Diastole calcium removal during, 65 definition of, ventricular, 73 Diastolic depolarization, 34 Diastolic pressure arterial, 146–147 ausculatory method for measuring, 149–150 schematic diagram of, 141f Diffusion of lipid-insoluble molecules, 159–162 water and soluble transfer across endothelium by, 159, 161 Diffusion-limited transport, 162, 162f Digitalis, electrogenic pump affected by, 15 Dihydropyridine receptor, 63–64 Diltiazem, 22f, 23 2,3-Diphosphoglycerate, 7f Dipyridamole, 232 Dissecting aneurysm, 129b Dorsal motor nucleus of vagus, 92 Ductus arteriosus, 258 Ductus venosus, 257–258 Dysrhythmias atrioventricular block See Atrioventricular block definition of, 47 fibrillation, 49–51 premature depolarizations, 48–49 respiratory, 99–100 sinoatrial node rhythm alterations, 47–48 tachycardia See Tachycardia E EADs See Early afterdepolarizations Early afterdepolarizations (EADs), 43 Ectopic foci, 32b Ectopic pacemakers, 32b Edema, 168 pulmonary, 213b–214b EDRF See Endothelium-derived relaxing factor Effective refractory period, 17–18, 27 Einthoven triangle, 45, 46f Ejection rapid, 71 reduced, 71 Ejection fraction, 78, 112 Elastic modulus, 140 Electric shock, for fibrillation, 51 Electrocardiogram configuration of, 37f limb leads for, 45–47 P wave, 37, 45 PR interval, 45 premature atrial depolarization, 48, 49f QRS complex, 37, 45 scalar, 44–47 of supraventricular tachycardia, 50f T wave, 45 of ventricular tachycardia, 50f INDEX Electrocardiography, 44–47 benefits of, 44 scalar, 44–47 Electrogenic pump, 15 Electromechanical coupling, 179 Elephantiasis, 167b Emphysema, 247b End-diastolic pressure, 106 End-diastolic ventricular volume, 106 Endogenous vasoconstrictors, in hemorrhage, 272–273 β-Endorphin, 275 Endothelin, 157, 281 Endothelium blood flow regulation by, 180–181 lipid-soluble molecules across, 162–163 permeability of, 158–159 solute transfer across, 159, 161 water transfer across, 159, 161 Endothelium-derived relaxing factor (EDRF), 157, 157f Energy substrate metabolism, during myocardial ischemia, 231–233 Enkephalins, 275 Eosinophils, 6f Epinephrine, 185–189, 272 Equilibrium point, 208 Equilibrium potentials potassium, 14 sodium, 14 Erythroblast, 8f Erythroblastosis fetalis, 5–6, 8b, 8f Erythrocytes aggregation of, 131 deformability of, 131 description of, 5–6 diameter of, 131 fibrinogen concentration effects on, 131 lifespan of, morphology of, 6f production of, Erythropoiesis, Erythropoietin, Esophageal varices, 256b–257b Essential hypertension, 72b, 130b Excitation-contraction coupling calcium mediation of, 63–69 description of, 21 in vascular smooth muscle, 176 Exercise, 264–269, 281 arterial pressure increase during, 267–268 cardiac output increase in, 266–267 conditioning, 269 mild to moderate, 264–268 performance limits, 269 peripheral resistance declines during, 264–266 physical training, 269 postexercise recovery, 268–269 severe, 268 venous return enhanced in, 267 Extracoronary resistance, 225–226 Extrasystole, 43–44 Extravascular compression, 225–226 F F waves, 50 Fahraeus-Lindqvist phenomenon, 131 Fast response action potential changes to slow response, 13b conduction of, 25–27 description of, 12, 12f effective refractory period for, 27 excitability affected by, 27–28 voltage-dependent sodium channels and, 15–24 Fast sodium channels description of, 16 m gates in, 16 Fatty acid metabolism, 83–86 Febrile infectious diseases, 34b Fenestrations, 158f, 159 Fetal circulation, 257–260 Fetal oxyhemoglobin dissociation curve, 258 Fibrillation, 49–51 atrial, 50, 50f definition of, 49–50 description of, 41 electric shock treatment of, 51 mechanism of, 51 ventricular, 50–51, 50f, 220b Fibrinogen, 131 Fick principle, 79f for oxygen consumption, 80 Fick’s law of diffusion, 159 Filariasis, 167b Filling pressure, of heart, 196 Filtration, 165 Filtration coefficient, 165–167 First heart sound, 74, 74f First-degree atrioventricular block, 38, 38f, 39b Flow equation for, 119 laminar, 122, 123f, 127–128 Poiseuille’s law, 122, 125 pressure and, 122–125 resistance to, 125–127 steady, 122 streamlined, 127–128 turbulent, 128 velocity and, 119, 120f volume, 119 Foot protein, 63–64 Foramen ovale, 258 Force, 66–68 Fourth heart sound, 75 Frank-Starling mechanism cardiac output and, 106 history of, 103–104 in intact preparations, 106–107 premature beats and, 109 representation of, 106–107 Free radicals, Frictional resistance, Functional cardiac murmurs, 128b Functional hyperemia, 256 G Gallop rhythms, 75b Gamma globulins, 287 Gap junctions description of, 25, 58 histology of, 57f in intercalated disks, 57f, 58, 59f Gastrin, 256 GFR See Glomerular filtration rate Gibbs-Donnan effect, 164 Globin definition of, diseases caused by changes in, 5–6 Glomerular filtration rate (GFR), 252–253 Glomeruli, 250–251 Glucagon, 115 Glucose fatty acid cycle, 85 Glucose uptake, regulation of, 84 Glycocalyx, 63–64, 161 Glycolysis, regulation of, 84 G-protein-coupled receptor (GPCR), 96 Graves disease, 2b Gravity, cardiac output and, 216–218, 281 Guanylyl cyclase, 157, 157f H h gate, 16–18 H2 fields of Forel, 97 Heart anatomy of, 1–2 apex of, 60–62 conduction system of, 36, 36f filling pressure of, 196 function of, description of, 171 hypodynamic, 78, 78f mean electrical axis of, 46–47 pericardium of, 63 preload of, 196 sodium requirements of, 63 vasculature and, 207–211 Heart failure, 211b acute, 211b chronic, 106b, 211b congestive, 218b, 256b–257b arterial pulse pressure in, 145b atrial natriuretic peptide levels, 99b description of, 75b left, 247b right, 213, 214b Heart rate bleeding effects on, 99f blood transfusion effects on, 99f cardiac adaptation to alterations in, 105–106 cardiac output and, 214–216 chemoreceptor reflex effects on, 101–102 conditions that affect, 34b contractile force affected by changes in, 107–110 definition of, 91 hypothalamus influences on, 97 intrinsic, 92 lung stretch receptors’ effect on, 100 mean arterial pressure and, 97f normal, 91 peripheral chemoreceptor stimulation effects on, 101–102, 102f regulation of 288 INDEX Heart rate (Continued) autonomic nervous system, 112–113 Bainbridge reflex, 98–99 baroreceptor reflex, 97–98 overview of, 91 parasympathetic pathways, 92–93 sympathetic pathways, 93–97 ventricular receptor reflexes’ role in, 102 during sleep, 91 Heart sounds, 74–75, 74f Hematocrit ratio, 102f, 107, 130f Heme, Hemoglobin description of, iron moiety of, oxygen affinity for, oxygen bound, skin color and, 240 Hemoglobin S, 5–6 Hemorrhage, 269–276 arterial blood pressure and, 270 arterial pressure in, 166b arterial pulse pressure in, 145b compensatory mechanisms, 270–273 baroreceptor reflexes, 270–272 cerebral ischemia, 272 chemoreceptor reflexes, 272 endogenous vasoconstrictors, 272–273 renal conservation of salt and water, 273 tissue fluid reabsorption, 272 decompensatory mechanisms, 273–275 acidosis, 274 blood clotting aberrations, 275 cardiac failure, 274 central nervous system depression, 274–275 reticuloendothelial system depression, 275 positive and negative feedback mechanisms interact, 275–276 Hemorrhagic shock, 270 description of, 185 Heparin, 275 Hepatic acinus, 256 Hepatic arterial system, 256 Hepatic artery, 256 Hepatic circulation, 256–257 anatomy of, 256 blood flow regulation, 256–257 hemodynamics, 256 Hepatic cirrhosis, 256b–257b Homeostasis, Hormones adrenocortical, 113–114 adrenomedullary, 113 myocardial performance affected by, 113–116 thyroid, 114–115 Humoral immunity, H-V interval, 48 Hydraulic conductance, 127 Hydraulic filtering, 135–137 Hydraulic resistance definition of, 125 in parallel, 126–127 in series, 126–127 Hydraulic resistance equation, 125 Hydrogen peroxide, Hydrostatic forces capillary filtration regulated by, 163 disturbances in, 166–167 osmotic forces and, balance between, 163–165 Hydrostatic pressure, 163–165, 218, 282 Hypercapnia, 189 Hyperpolarization, acetylcholine-induced, 35, 35f Hypertension, 218b characteristics of, 147b chronic, 147b description, 129b Hyperthyroidism, 115b Hypervolemia, 205 Hypotension, 226b, 267 orthostatic, 218b postural, 188b Hypothalamus, 190 Hypothyroidism, 115b Hypovolemia, 205 Hypovolemic shock, 248b Hypoxia high altitude and, 7b hypercapnia and, 189 I Idioventricular pacemakers, 32 Immunity, Impulse initiation, 47 Impulse propagation, 47 Inactivation, of fast sodium channels, 16, 18–19 Inactivation gate, 16 Incisura, 147 Independent variable, 200, 208 Indicator dilution technique, for cardiac output measurements, 80–81, 80f Inferior mesenteric artery, 254 Inflow pressure, 123 Inositol 1,4,5-trisphosphate IP3, 175, 177f smooth muscle receptor, 175, 175f Insulin, 115 Insulin levels, effects of, 86 Integrins, 158 Interlobar branches, 250 Interlobular branches, 250–251 Intermittent claudication, 243b Interstitial fluid (ISF) accumulation of, 167b description of, 164–165 Interventricular septum, 61f Intestinal blood flow, 256 Intestinal circulation, 254–256 anatomy of, 254 autoregulation, 254 neural regulation, 254 Intravascular pressure, 179 Intrinsic heart rate, 92 Inwardly rectified potassium current, 23 Inwardly rectifying potassium channels, 13–14 Ion channels, 13 Ischemia, description of, 13b, 230b Isoelectric line, 45 Isometric contraction, 70 Isoproterenol, 21–22, 94 Isovolumetric contraction, 70 Isovolumetric relaxation, 73 J Junctional processes, 63–64 Juxtamedullary glomeruli, 251 K Kidneys, blood flow in See Renal circulation Korotkoff sounds, 149–150 L Lactate oxidation, regulation of, 84–85 Laminar flow, 122, 123f, 127–128 Laplace equation, 155 Laplace relationship, 106 Lateral pressure, 120 Law of conservation of mass, 141 Law of Laplace, 155–156 Left anterior hemiblock, 40b Left atrium, 36f Left auricular appendage, 61f Left bundle branch, 39–40, 40f Left heart failure, 247b Left posterior hemiblock, 40b Left vagus nerve, 92 Left ventricle, 212, 225–226 anatomy of, 36f, 62 description of, 1–2 endocardial surface of, 41 pressure in, 226 ventricular systole effects on, 72 Left ventricular afterload, 212 Left ventricular failure, 213b–214b Left ventricular preload, 213 Less pressure work, 265 Leukocytes, 6–7 Leukotrienes, 275 Limb leads, for electrocardiogram, 45–47 Linear velocity, 119 Lipid-insoluble molecules, 159–162 Lipid-soluble molecules, 162–163 Local anesthetics, 16 Long QT syndrome, 24b Loop diuretic, 279 L-type calcium channels, 21 Lymphatic system, 167–168 Lymphocytes, 5, 6f Lysosomes, M m gate, 16 Macula densa, 253 Maximal dP/dt, 78 Mayer waves, 183–184 Mean arterial pressure, 140–141, 280 definition of, 140 representation of, 97f, 141f Mean circulatory pressure, 202 Mean electrical axis, 46–47 Mechanical restitution curve, 109 INDEX Medulla cardiovascular activity affected by, 183–184 depressor area of, 183 parahypoglossal area of, 97 pressor region of, 183 Megakaryocytes, Megaloblastic anemia, 8f Membrane resting potential, 12f, 13 Membranous septum, 61f Metabolic vasodilators, 264 Metamyelocytes, 6f Metarterioles, 153–154 Microcirculation endothelium’s role in regulation of, 156–157 schematic diagram of, 154f Microcytic, hypochromic anemia, 5–6, 8f Middle cervical ganglia, 93 Mitral insufficiency, 75b Mitral stenosis, 75b murmur and, 279 Mitral valve, 61f, 62 Monocytes, 5, 6f Monokines, 275 Müller maneuver, 219 Murmur, 281 mitral stenosis and, 279 Murmurs, 128b Muscarinic receptors, 228 acetylcholine interactions with, 112 antagonist of, 92 Muscular activity, venous valves and, 218–219 Myocardial cells, 55–60, 110–111 Myocardial compliance, cardiac function curve and, 198–199 Myocardial contractility, 209 Myocardial fibers, Frank-Starling mechanism See Frank-Starling mechanism Myocardial hibernation, 233b Myocardial infarction, 205b Myocardial ischemia, 230b energy substrate metabolism during, 231–233 Myocardial oxygen consumption, 137, 139f Myocardial performance acidosis effects on, 115 blood gases that affect, 115 carbon dioxide effects on, 115 hormones that regulate adrenocortical, 113–114 adrenomedullary, 113 insulin, 115 thyroid, 114–115 intrinsic mechanisms that regulate, 102–110 nervous system control of baroreceptor reflex, 112–113 parasympathetic, 112 sympathetic, 110–112 oxygen effects on, 115–116 Myocardial stunning, 232, 233b Myocardium capillaries in, 58–60 vagus nerve effects on, 112 Myoendothelial junctions, 172 Myofibrils, 56f–57f Myofilaments, 104–105 Myogenic mechanism, 179, 253 Myosin, 55–58 N Na+,K+-ATPase description of, 15, 27b overdrive suppression and, 35–36 Natural pacemaker, 31 Negative feedback mechanism, 270 Negative inotropic agents, 22b Nernst equation, 15–16, 279 Neuropeptide Y, 94f, 95 Neurovascular coupling, 244–245 Neutral proteases, 275 Neutrophils, 6f Newtonian fluids description of, 122, 124 viscosity of, 129 Nitric oxide (NO) arterioles affected by, 182 description of, 157 vasodilation caused by, 181 Nitric oxide synthase, 182 Nitroprusside, 179 NO See Nitric oxide Nonnewtonian fluids, 124 Norepinephrine, 272 cardiac cycle-related release of, 95 contractility affected by, 21–22, 113, 114f description of, 183–184 sympathetic nerve release of, 110–111, 279 Normovolemia, 205 Nucleus ambiguus, 92 Nucleus of the tractus solitarius, 185–186 Nutritional flow, 154–155 O Oncotic pressure, 164–165 Opioids, 275 Opsonic protein, 275 Orthostatic hypotension, 188b, 218b Osmotic forces capillary filtration regulated by, 163 disturbances in, 166–167 hydrostatic forces and, balance between, 163–165 Osmotic pressure, 163 Outflow pressure, 123 Overdrive suppression, 35–36 Overshoot, 15–17 Oxygen cardiac muscle requirements of, 71f hemoglobin binding to, myocardial performance affected by, 115 Oxygen bound hemoglobin, skin color and, 240 Oxygen consumption determination of, 80 Fick principle for, 80 myocardial, 137, 139f Oxygen free radicals, 275 Oxyhemoglobin, Oxyhemoglobin dissociation curve, 7f, 266 P 289 P wave, 37, 45 Pacemaker ectopic, 32b natural, 31 spontaneous activity of, 279 Pacemaker cells automaticity of, 35 discharge frequency of, 33, 33f overdrive suppression, 35–36 Pacemaker fibers, 33 Pacemaker potential, 33 Pacemaker shift, 33 Palpatory method, 149 Papillary muscles, 61f Parasympathetic nervous system blood vessels innervated by, 185 heart rate regulation by, 92–93 myocardial performance affected by, 112 Parasystole, 48 Paroxysmal supraventricular tachycardia, 49, 50f Paroxysmal tachycardia, 31–32 Paroxysmal ventricular tachycardia, 49, 105f Peak velocity, 121, 121f Pericardium definition of, 63 pressure-volume relationship and, 106 Peripheral blood flow description of, 171 endothelial regulation of, 180–181 extrinsic factors involved in description of, 183–191 intrinsic factors and, 191–192 intrinsic factors involved in description of, 179–183 extrinsic factors and, 191–192 myogenic mechanism effects on, 179–180 Peripheral chemoreceptors description of, 189 heart rate affected by, 101–102, 102f Peripheral resistance, 200 aortic baroreceptors’ effect on, 186 carotid sinus effects on, 186–187 description of, 142 total, 4, 146–147 vascular function curve affected by, 206–207, 210–211 Peripheral runoff, 141, 143f, 202 Peritubular capillaries, 251 Permeability of cell membranes, 13 Phagocytosis, Pharmacomechanical coupling, 176 Phasic pressure, 4f Phonocardiogram, 74, 74f Phosphodiesterase, 96f Phospholamban, 65, 110–111 Phospholipase C, 178 Physical training, 269 Physiological shunting, 154–155 Pinocytosis, 158–159, 167 Pitot tubes, 120 Plasma cells, Plasma proteins description of, 164 lymphatic system return of, 168 290 INDEX Plasma substrate, effects of, 86 Plasma transfusion, 280 Plateau phase calcium conductance during, 21–23, 21f, 63–64, 108 definition of, 11–12 early afterdepolarizations at end of, 43 genesis of, 20 potassium conductance during, 22–23 Platelets morphology of, 6f prostacyclin effects on, 156 Pluripotential stem, Poiseuille equation, 216 Poiseuille’s law, 122, 125, 165 Polycythemia, 7b, 130b Portacaval shunt, 256b–257b Portal vein, 256 Portal venous system, 256 Portal-caval shunt, 280 Positive feedback mechanisms, 273 Positive inotropic effect, 77–78 Postcapillary resistance, 256 Postexercise recovery, 268–269 Postextrasystolic potentiation, 109 Postganglionic gray branches, 183 Postganglionic nerves, 95 Postganglionic neurons, 93 Postganglionic sympathetic fibers, 183 Postrepolarization refractoriness, 28 Postsinusoidal, 256 Postural hypotension, 188b Potassium conductance of, during plateau phase, 22–23 extracellular concentration of, 63 Potassium channels, 279 acetylcholine-regulated, 95 delayed rectifier, 23 description of, 13–14 inwardly rectifying, 13–14 Potassium equilibrium potentials, 14 P-P interval, 47–48, 279 PR interval, 45, 279 Precapillary resistance, 165, 256 Precordial leads, 47 Preganglionic neurons, 93 Preganglionic white fibers, 183 Preload description of, 66–69 of heart, 196 left ventricular, 213 Premature atrial depolarizations, 41, 48, 49f Premature beats Frank-Starling mechanism and, 109 weakness of, 109 Premature depolarizations, 31–32 Premature ventricular depolarization, 48, 49f Premature ventricular systole, 109 Presinusoidal, 256 Pressor effect, 185–186 Pressor region, 183 Pressure equation for, 122 flow and, 122–125, 138f inflow, 123 outflow, 123 Pressure drop, 2, 4f Pressure gradient, 120–121 Pressure-volume loop, 77 Pressure-volume relationships, 75–79 active, 77 diastolic, 75–77 end-systolic, 77 passive, 75–77 Principle of “conservation of mass,”, 202 Propranolol, 92, 94 Prostacyclin, 156 Prostaglandins, 182, 275 Pulmonary artery wedge pressure, 247b Pulmonary blood flow, 247–249 Pulmonary circulation, 245–250 description of, 1–2 pressures in, 247 regulation of, 249–250 Pulmonary edema, 213b–214b Pulmonary embolism, 247b Pulmonary hemodynamics, 247–249 Pulmonary reflexes, 191 Pulmonary veins, 61f, 247 Pulmonic valve, 61f Pulsatile arterial blood flow, Pulse, 149–150, 279 Pulse pressure aortic, 139–140, 141f arterial, 144 arterial compliance effects on, 145 blood pressure and, 144 schematic diagram of, 141f stroke volume and, 141f Pump, 200 auxiliary, 219–220 Purkinje fibers action potentials from, 40–41, 44f anatomy of, 39–40, 40f automaticity properties of, 32, 35, 279 definition of, 39–40 description of, 12 Pyruvate oxidative, regulation of, 84–85 Q QRS complex, 37, 45 QT interval, 45, 279 long QT syndrome, 24b R Radial pulse, 149 Rapid ejection, 71 Rapid filling phase, 71f, 73 Rate of change of potential, 26 Rate-pressure product, 87 Raynaud’s disease, 240b Reactive hyperemia, 182f, 183, 239 Reentry bidirectional block, 41 conditions necessary for, 41 definition of, 41 unidirectional block, 41–42, 42f Reflection coefficient, 161–163 Refractory period effective, 17–18, 27 relative, 27 Relative hematocrit, 131 Relative refractory period, 27 Renal artery, 250 Renal circulation, 265 anatomy of, 250–251 cardiac output and, 250–254 Renal conservation, of salt and water, 273 Renal hemodynamics, 252 blood flow, 252 circulation, 252–254 autoregulation, 252–253 neural regulation, 253–254 segmental resistance, 252 Renin, 189, 273 Renin-angiotensin system, 253 Repolarization definition of, 11–12 early, 20 final, 23 Residual volume, 72 Resistance arteriolar, 163 blood flow, 125 definition of, 125 to flow, 125–127 hydraulic, 125 peripheral aortic baroreceptors’ effect on, 188 carotid sinus effect on, 188 description of, 142 total, 146–147 precapillary, 165 total peripheral, 146–147 Resistance vessels, 171 constriction, 184 description of, 153, 171 epinephrine effects on, 185 hemorrhage shock effects on, 185 sympathetic nerves’ regulation f, 184–185 Respiratory activity, cardiac output and, 219–220 Respiratory cardiac dysrhythmia, 99–100 Resting cell membrane, 13 Resting membrane potential, level of, 26 Resultant cardiac vector, 45 Reticulocytes, 8f Reticuloendothelial system, depression of, in hemorrhage, 275 Retrograde impulse, 41–42 Reynolds’s number, 128 Rh-negative, 7–8 Rh-positive, 7–8 Rhythmicity, 31 Right atrial pressure, description of, 104 Right atrium, 36f Right auricular appendage, 61f Right bundle branch, 39–40, 40f Right heart failure, 213, 214b Right vagus nerve, 92 Right ventricle anatomy of, 36f, 62 blood flow in, 1–2 blood flow regulation and, 211–214 central venous pressure and, 211–214 endocardial surface of, 41 INDEX Right ventricular ejection, 71–72 Ryanodine receptors, 63–64, 175f S SA See Sinoatrial node Sarcolemma, 56f Sarcomeres, definition of, 55–58 Sarcoplasmic reticulum adenosine triphosphate hydrolysis by, 114 anatomy of, 56f, 59f, 60 systolic calcium uptake by, 78 Scalar electrocardiography, 44–47 Scalar quantities, 44–45 Second heart sound, 74, 74f Second-degree atrioventricular block, 38, 38f, 39b Semilunar valves anatomy of, 61f, 62 ejection phase, 74 Severe exercise, 268 Shear rate, 124–125 Shear stress on blood vessel wall, 128–129 definition of, 124–125 Shear thinning, 131 Shock electric, for fibrillation, 51 hemorrhagic, 270 Shunting, physiological, 154–155 Sick sinus syndrome, 36b bradycardia and, 215b Sickle cell anemia, 5–6, 8f, 132b Sinoaortic baroreceptors, 273 Sinoatrial (SA) node, 32–34 anatomy of, 32, 32f cardiac ganglion cells in, 92 cells of, 32 cholinesterase in, 92–93 description of, 11–12 rhythm alterations, 47–48 slow response in, 27 tonic influence of, 91–92 transmembrane potential from, 32, 34f Sinus bradycardia, 47–48, 47f Sinus rhythm, 47f Sinus tachycardia, 47f Sinuses of Valsalva, 62 Skeletal muscle circulation, 240–243 regulation of, 240–243 fast, 58 Skin blood flow to ambient temperature and, 239–240 body temperature and, 239–240, 281 skin color and, 240 sympathetic nervous system and, 237–239 color of O2 bound hemoglobin, 240 skin blood flow and, 240 description of, 191 temperature of, 281 Slow diastolic depolarization, 35 Slow response, excitability affected by, 28 Slow response action potential in atrioventricular node N region, 37–38 conduction of, 27 description of, 12, 12f fast responses changed to, 13b ionic basis of, 24–25 relative refractory period during, 28 Smooth muscle skeletal muscle vs., 172–174 vascular cells of, 172 contractile state of, 181–182 cross-sectional image of, 173f description of, 172 Smooth muscle pump, 175f Sodium cardiac glycosides’ effect on, 65 heart requirements for, 63 transmembrane movement of, 16 Sodium-calcium exchange (NCX) cardiac muscle, 64f vascular smooth muscle, 175f, 176 Sodium channels, 279 current flow through, 20f fast, 16, 25–27 gating of, 16, 18f structure of, 17f Sodium equilibrium potentials, 14 Solutes endothelial transfer of, 159, 161 movement of, 161 Spherocytic anemia, 132b Sphygmomanometer, 148–150, 149f Splanchnic circulation, 254–257, 265 Split sound, 75 Staircase phenomenon, 107 Starling hypothesis, 165 Static pressure, 120, 202 Static pressure-volume relationship, 139 Steady flow, 122 Stem cells, erythrocytes from, Stokes-Adams attacks, 39b Streamlined flow, 127–128 Stretch receptors, 273 Stroke volume arterial compliance and, 145–146 changes in, 144f definition of, 104 pulse pressure and, 144–145 Superior mesenteric artery, 254 Supraventricular tachycardia, 215b description of, 42b paroxysmal, 49, 50f Sympathetic nerves, section of, 184–185 Sympathetic nervous system heart rate regulation, 93–97 myocardial performance affected by, 110–112 skin blood flow and, 237–239 vasoconstrictor fibers of, 184 Systemic circulation, 1–2, 245–250 Systole atrial, 73 calcium, 63–65 definition of, ventricular 291 Systole (Continued) description of, 69–73 premature, 109 Systolic pressure ausculatory method for measuring, 149–150 description of, 141f, 144 T T lymphocytes, T wave, 45 Tachycardia diastasis during, 73 ectopic, 49 paroxysmal, 31–32, 49 sinus, 47f supraventricular, 215b description, 42b paroxysmal, 49, 50f ventricular, 215b paroxysmal, 49, 50f Temperature ambient, skin blood flow and, 239–240 body, skin blood flow and, 239–240 of skin, 281 Terminal arterioles, 3f, 154 Tetrodotoxin action potential affected by, 13b, 13f, 16 sinoatrial node and, 32–33 Thalassemia, 5–6 Thebesian vessel, 223–224 Thermodilution, 81 Third heart sound, 75 Third-degree atrioventricular block, 38–39, 38f, 39b Thoracic duct, 168 Threshold, 15–16 Threshold potential, 16–17 Thrombi, 128b, 275 Thromboangitis obliterans, tobacco and, 280 Thromboxanes, 275 Thyroid hormones, 114–115 Tissue fluid, reabsorption of, in hemorrhage, 272 Tissue pressure, 163 Titin, 68–69 Tobacco, thromboangitis obliterans and, 280 Tone, definition of, 171 Total peripheral resistance, 146–147 Total pressure, 120 Transient inward current, 44 Transient outward current, 20 Transmembrane potential from atrioventricular node, 39f potassium effects on, 14 from sinoatrial node, 32, 34f sodium effects on, 14 vagal stimulus effect on, 35f Transmural pressure, 154, 249 Transverse tubules, 56f–57f, 58–60, 59f–60f Traube-Hering waves, 183–184 Treppe phenomenon, 107 Tricuspid valve, 61f, 62 292 INDEX Trigger calcium, 63–64 Triggered activity, 65–69 T-type calcium channel, 21 Tubuloglomerular feedback, 253 Turbulent flow, 128 U U tube, 216 Universal donors, 7–8 Universal recipients, 7–8 Upstroke of action potential, 11–12, 15–19 V v wave, 72 Vagus nerve, myocardial performance affected by, 112, 280 Valsalva maneuver, 220 Varicose veins, 219b, 242b Vasa recta, 251 Vascular endothelial growth factors (VEGFs), 167, 234 Vascular function curve (VFC), 196 blood volume and, 205–206, 209–210 central venous pressure and cardiac output, 200–207 mechanical analysis of, 203–205 peripheral resistance and, 206–207, 210–211 Vascular reflexes, blood pressure affected by, 185–189 Vascular resistance, epinephrine effects on, 185 Vascular smooth muscle cells of, 172 contractile state of, 181–182 cross-sectional image of, 173f description of, 172 Vascular system, bronchial, 246–247 Vasoconstriction, epinephrine-induced, 185 Vasoconstrictor tone, 191 Vasodilation interstitial fluid osmolarity as cause of, 182 mediators of, 182 Vasodilation (Continued) metabolites produced by, 181, 280 vascular resistance controlled by, 182–183 Vasomotion, 154 Vasopressin, 98, 273 Vasovagal syncope, 102b VEGFs See Vascular endothelial growth factors (VEGFs) Veins See also specific vein characteristics of, 3f Velocity flow and, 119, 120f linear, 119 peak, 121, 121f Venae cavae characteristics of, 3f cross-sectional area of, Venoconstriction, 270 Venomotor tone, 206 Venous compliance (Cv), 200 Venous pooling, 217 Venous pressure, cardiac output and, 205 Venous return, cardiac output and, 207 Venous valves, muscular activity and, 218–219 Ventricles anatomy of, 60–62 left See Left ventricle right See Right ventricle volume changes in, 104–105 Ventricular conduction, 39–41 Ventricular diastole, 73 Ventricular ejection, 62 Ventricular fibrillation, 50–51, 50f, 220b Ventricular filling, rapid phase, 71f, 73 Ventricular function curves, 106–107 Ventricular hypertrophy, 47b Ventricular receptors, 102b Ventricular systole description, 70–73 premature, 109 Ventricular tachycardia, 215b paroxysmal, 49, 105f Venules, 3f Vessels See also Blood vessels arterioluminal, 223–224 arteriosinusoidal, 223–224 coronary, 223–224, 224f coronary collateral, 233–234 thebesian, 223–224 VFC See Vascular function curve Viscosity anomalous, 129 apparent, 129 of blood, 129, 130f definition of, 124 dimensions of, 125 for newtonian fluid, 129 of plasma, 129–130 Viscous drag, 129 Voltage clamping, 14 Voltage-dependent phenomenon, 16–17 Voltage-dependent sodium channels description of, 16 fast response action potential affected by, 15–24 schematic diagram of, 17f Voltage-gated calcium channels, 21f, 176 Volume flow, 119 Vulnerable period, 51 W Wall thickness, 155 Waterfall effect, 248–249 Wedge pressure, 279 Windkessel, 135 Wolff-Parkinson-White syndrome, 42b Z Z line anatomy of, 55–58, 56f electrical stimulation, 63–64 Zero cardiac output, 205 ... Increase in volume (%) O2 consumption (mL O2/100 g/beat) THE ARTERIAL SYSTEM a 29 –3 175 b 36– 42 150 c 47–5 125 d 20 0 100 e 75 71–78 50 25 0 25 50 75 100 125 150 175 20 0 22 5 Pressure (mm Hg) FIGURE... Downstroke: R × Q = × 20 0 = 20 0 mm Hg Upstroke: R × Q = × = mm Hg Pumped flow: Downstroke: 20 0 mL/s for 0.5 s Upstroke: mL/s for 0.5 s W = P × V = 20 0 × 100 = 20 ,000 mm Hg • mL each s 20 0 mL/s for 0.5... peripheral resistance (D and E) CARDIOVASCULAR PHYSIOLOGY V4 Small Ca 20 0 Large Ca 100 Increase cardiac output Volume Arterial pressure (mm Hg) 144 B2 VB B V3 B1 V2 VA V1 A A2 A1 Time FIGURE 7-10 n When