Chapter 12_ Answers to Study Questions


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Chapter 1

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1 1. The lungs always receive more blood flow than any other organ because 100% of the cardiac output always passes through the lungs.
1 2. False. Flow through any vascular bed depends on its resistance to flow and the arterial pressure. As long as this pressure is maintained constant (a critical point), alterations in flow through any individual bed will have no influence on flow through other beds in parallel with it.
1 3. A leaky aortic valve will cause a diastolic murmur. Normally, the aortic valve is closed during diastole when there is a large reverse pressure difference between the aorta and left ventricle.
1 4. False. Slowing conduction through the AV node will have no effect on heart rate but will increase the time interval between atrial and ventricular excitation. Heart rate is normally slowed by decreases in the rate of action potential initiation by pacemaker cells in the SA node.
1 5. The blood flow rate through the lungs (L) must equal the cardiac output (CO) because of the way the cardiovascular system is arranged. (L) is equal to the pressure drop across the lungs (PL) divided by the resistance to flow through the lungs (RL).

1 6.

1 7. Significant blood loss has a profound negative effect on cardiac pumping because there is not enough blood left to fill the heart properly. This results in decreased cardiac output because of Starling's law of the heart. The consequence of decreased cardiac pumping ability is a lessened pressure difference between arteries and veins. Because of the basic flow equation, less P causes less flow through the systemic organs. Interstitial homeostasis is compromised when there is abnormally low blood flow through capillaries. Improper interstitial conditions impair nerve function and cognitive ability in the brain and cause weakness in skeletal muscles.
1 8. Norepinephrine is the normal sympathetic neurotransmitter substance, so the same cardiovascular effects that normally accompany activation of sympathetic nerves should be predicted. These include increased heart rate, increased forcefulness of cardiac contraction, arteriolar constriction, and venous constriction.
1 9. Arteriolar and venous constriction would be expected because the sympathetic nerve effects on these vessels are normally mediated via alpha receptors
There would be no direct effects on the heart expected because the sympathetic effects on the heart are mediated by beta receptors.
1 10. Among other effects, -adrenergic receptor blockade tends to reduce heart rate and the forcefulness of ventricular contraction. Both these results tend to decrease cardiac output. -Receptor blockade does not directly influence arteriolar smooth muscle and thus does not directly change the resistance to flow through the systemic vasculature. According to the basic flow equation, less flow through a constant resistance implies a smaller pressure difference exists (P = x R). Because the venous pressure is normally 0 mmHg, and P is arterial minus venous pressure, this translates to a lowered arterial pressure.
1 11. Plasma sodium concentration will be 140 mEq/L because serum is just plasma minus a few clotting proteins. Interstitial sodium ion concentration will also be 140 mEq/L because sodium ions are in diffusional equilibrium across capillary walls. Intracellular sodium ion concentration cannot be predicted because sodium is actively pumped out of all cells.
1 12. Severe dehydration that often accompanies loss of body fluids results in a decrease in the fluid volume of all body components, including the plasma volume. In this situation, since blood cells are not lost, hematocrit will increase.

Chapter 2

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2 1. a. The potassium equilibrium potential will become less negative because a lower electrical potential is required to balance the decreased tendency for net K+ diffusion out of the cell. [EeqK+ = ( 61.5 mV) log([K+]i/[K+]o).]
   b. Because the resting membrane is most permeable to K+, the resting membrane potential is always close to the K+ equilibrium potential. Lowering the absolute value of the K+ equilibrium potential will undoubtedly also lower the absolute resting membrane potential (ie, depolarize the cells).
   c. Two things happen when the resting membrane potential is decreased: (1) the potential is closer to the threshold potential which should increase excitability and (2) the fast sodium channels become inactivated, making the cell less excitable. Thus small increases in [K+]o may increase excitability whereas large increases in [K+]o decrease excitability.
2 2. Elevations in extracellular potassium depolarize cardiac muscle cell membranes as can be ascertained from the Nernst equation (see question 2 1). This depolarization will inactivate sodium and calcium channels, making the cells inexcitable and thus relaxing the heart. This significantly reduces oxygen demands and helps protect the heart tissue against hypoxic injury.
2 3. a. Sodium channel blockers delay the opening of the fast sodium channels in cardiac myocytes. This will slow the rate of depolarization during the action potential (phase 0) which will in turn slow conduction velocity. This results in a prolongation of the PR interval and a widening of the QRS complex.
   b. Calcium channel blockers slow the firing rate of SA nodal cells by blocking the calcium component of the diastolic depolarization. They will reduce the rate of rise of the AV nodal cell action potential (which is largely due to calcium entry into the cells) and slow the rate of conduction through the AV node. In addition, calcium channel blockers will decrease the amount of calcium made available to the contractile machinery during excitation-contraction coupling and thus will decrease the tension-producing capabilities of the cardiac muscle cell.
   c. Potassium channel blockers inhibit the delayed increase in potassium permeability that contributes importantly to the initiation and rate of repolarization of the cardiac myocyte. This prolongs the duration of the plateau phase of the action potential, prolongs the QT interval of the ECG, and prolongs the effective refractory period of the cell.
2 4. False. It is true that increases in sympathetic activity will increase heart rate (a positive chronotropic effect). However, the electrical refractory period of cardiac cells extends throughout the duration of the cell's contraction. This prevents individual twitches from ever occurring so closely together that they could summate into a tetanic state.
2 5. The correct answers are a and c. Increases in preload increase the amount of shortening by increasing the starting length of the muscle whereas increases in contractility increase the amount of shortening from a given starting length. Increases in afterload limit the amount of shortening because of an increase tension requirement. (See Figures 2 9 and 2 10.)

Chapter 3

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3 1. The ventricular systolic pressure is also 24 mmHg since the normal pulmonic valve provides negligible resistance to flow during ejection. The right ventricular diastolic pressure, however, is determined by systemic venous pressure and will be close to 0 mmHg.
3 2. False. Although there may be minor beat-to-beat inequalities, the average stroke volumes of the right and left ventricles must be equal or blood would accumulate in the pulmonic or systemic circulation.
3 3. All of them are correct answers: a by increasing preload, b by decreasing afterload, and c and d by augmenting contractility.
3 4.

3 5. One cannot tell from the information given because the two alterations would have opposite effects on cardiac output. A complete set of ventricular function curves, as well as quantitative information about the changes in filling pressure and sympathetic tone, would be necessary to answer the question. (See Figure 3 8.)
3 6. True. (See Figure 3 6.)

Chapter 4

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4 1. The correct answer is c.
4 2. The correct answer is b. According to the standard ECG polarity conventions, the P, R, and T waves will normally all be downward deflections on lead aVR.
4 3. According to the electrocardiographic conventions, the electrical axis is at 45 and falls within the normal range (in the patient's lower left quadrant). The smallest amplitude deflection will occur on the lead to which the electrical axis is most perpendicular. Lead III and lead aVL are both within 15 of being perpendicular to 45 and therefore will have equally small deflections.

Chapter 5

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5 1. a and b, because filling time is reduced; c, if ventricular rate is rapid; d, for obvious reasons; but not e, because ventricular pacemakers produce a lower heart rate, which is usually associated with a larger stroke volume.
5 2. (a) Aortic stenosis produces a significant pressure difference between the left ventricle and the aorta during systolic ejection.
   (b) Mitral stenosis produces a significant pressure difference between the left atrium and the left ventricle during diastole.
5 3. Tricuspid insufficiency. With proper positioning of the patient, pulsations in the neck veins can be observed. Regurgitant flow of blood through a leaky tricuspid valve during systole produces this large abnormal wave.
5 4. Irregular giant a-waves (called cannon waves) are observed in the jugular veins whenever the atrium contracts against a closed tricuspid valve (ie, during ventricular systole). Since in third-degree heart block the atria and ventricles are beating independently, this situation may occur at irregular intervals.

Chapter 6

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6 1. The Fick principle states that

6 2.

The result is positive, indicating net movement of fluid out of the capillaries.
6 3. All do: a and d by allowing interstitial protein buildup, b by raising PC, and c for obvious reasons.
6 4. (a) By the parallel resistance equation, the equivalent resistance (Rp) for the parallel pair is Rp = Re/2.
   Then by the series resistance equation

   (b) Since more resistance precedes the junction (Re) than follows it (Re/2), Pj will be closer to Po than to Pi.
   (c) The flow through the network (which equals the flow through the inlet vessel) is

   The pressure drop across the inlet vessel is equal to its resistance times the flow through it

6 5.

6 6. False. TPR is less than the resistance to flow through any of the organs. Each organ, in effect, provides an additional pathway through which blood may flow; thus the individual organ resistances must be greater than the total resistance and

6 7. False. Since

a decrease in renal resistance must increase 1/TPR and therefore decrease TPR. When the resistance of any single peripheral organ changes, TPR changes in the same direction.
6 8. True. Since arteriolar constriction tends to reduce the hydrostatic pressure in the capillaries, reabsorptive forces will exceed filtration forces and net reabsorption of interstitial fluid into the vascular bed will occur.
6 9. True. A = CO x TPR
6 10. False. Increases in cardiac output are often accompanied by decreases in total peripheral resistance. Depending on the relative magnitude of these changes, mean arterial pressure could rise, fall, or remain constant.
6 11. True. Pp  SV/CA. Acute changes in arterial compliance usually do not occur.
6 12. False. An increase in TPR (with CO constant) will produce approximately equal increases in PS and PD and increase A with little influence on pulse pressure.
6 13.

6 14. (a) Recall that SV Pp x CA. Pp increased by a factor of 1.15 (from 39 to 45 mmHg) during exercise. Since CA is a relatively fixed parameter in the short term, the increase in Pp must have been produced by an increase in stroke volume of about 15%.
   (b) Recall that CO = HR x SV. HR increased by a factor of 2 (from 70 to 140 beats per minute) during exercise, and since SV increased by a factor of about 1.15, cardiac output must have increased by about 130%. [2.0(1.15) = 2.3 times the original level.]
   (c) Recall that TPR = A/CO. PA increased by a factor of 1.13 (from 93 to 105 mmHg) during exercise while CO increased about 2.3 times. Thus, total peripheral resistance must have decreased by about 55% (1.13/2.3 = 0.45 of the original level).

Chapter 7

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7 1. The correct answers are a, b, and c.
7 2. False. Autoregulation of blood flow implies that vascular resistance is adjusted to maintain constant flow in spite of changes in arterial pressure.
7 3. All, because they all increase myocardial oxygen consumption. Myocardial blood flow is controlled primarily by local metabolic mechanisms.
7 4. False. Sympathectomy will cause some dilation of skeletal muscle arterioles but not a maximal dilation because skeletal muscle arterioles have a strong inherent basic tone.
7 5. Hyperventilation decreases the blood PCO2 level. This, in turn, causes cerebral arterioles to constrict (recall that cerebral vascular tone is highly sensitive to changes in PCO2). The increased cerebral vascular resistance causes a decrease in cerebral blood flow, which produces dizziness and disorientation.
7 6. It is likely that the increased metabolic demands evoked by the exercising skeletal muscle cannot be met by an appropriate increase in blood flow to the muscle. This patient may have some sort of arterial disease (atherosclerosis) that provides a high resistance to flow that cannot be overcome by local metabolic vasodilator mechanisms.
7 7. High left ventricular pressures must be developed to eject blood through the stenotic valve (Figure 5 4). This increases myocardial oxygen consumption, which tends to increase coronary flow. At the same time, however, high intraventricular pressure development enhances the systolic compression of coronary vessels and tends to decrease flow. The local metabolic mechanisms may be adequate to compensate for the increased compressional forces and meet the increased myocardial metabolic needs in a resting individual. However, they may not have enough "reserve" to meet additional needs such as those that accompany exercise. Coronary perfusion pressure may also be decreased if the systemic arterial pressure is lower than normal.

Chapter 8

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8 1. None of the choices is correct. (The very small change in vascular volume that accompanies a decrease in arteriolar tone is not sufficient to have a significant effect on mean circulatory filling pressure.)
8 2. Central venous pressure always settles at the value that makes cardiac output and venous return equal. Therefore anything that shifts the cardiac function curve or the venous return curve affects venous pressure (see list of influences on PCV in Appendix C).
8 3. False. The Frank-Starling law says that, if other influences on the heart are constant, cardiac output decreases when central venous pressure decreases (eg, AB in Figure 8 7). In the intact cardiovascular system, where many things may happen simultaneously, cardiac output and central venous pressure may change in opposite directions (eg, BC in Figure 8 7).
8 4. None. Venous return must always equal cardiac output in the steady-state situation.
8 5. Because cardiac preload is central venous pressure, the physician will try to lower central venous pressure. This requires a left shift of the venous return curve. The two ways that can be done are decreasing circulating volume or decreasing venous tone. The former is often accomplished with diuretic drugs, and the latter can be achieved with certain vasodilator drugs.

Chapter 9

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9 1. a and b will increase; the rest will decrease.
9 2. Carotid sinus massage causes baroreceptors to fire, which in turn decreases sympathetic activity and increases parasympathetic activity from the medullary cardiovascular centers. Both act to slow the pacemaker activity and allow a more normal rhythm to be established.
9 3. a, b, and d increase mean arterial pressure; c and e decrease mean arterial pressure.
9 4. (1) The influence of sympathetic nerve activity on arteriolar tone will be blocked. Arteriolar tone will fall and thus so will TPR. An 1-blockade represents a pressure-lowering disturbance on the effector portion of the cardiovascular system.
   (2) The effector portion function curve will shift downward as shown in Figure 9 6B. (In this instance the effector function curve may also become less steep, because increases in TPR no longer aid in the production of increased A when sympathetic activity increases.)
   (3) A new steady state will be established within the arterial baroreceptor reflex pathway at lower than normal arterial pressure and higher than normal sympathetic nerve activity, as shown in Figure 9 6B.
   (4) Heart rate and cardiac output will increase because of the increased sympathetic activity. The cardiac function curve will shift upward, but the venous return curve will not because -receptor blockade blocks the effect of increased sympathetic activity on the veins. Consequently, central venous pressure will be lower than normal (see Figure 8 6).
9 5. a and d are disturbances to the effector portion of the arterial baroreceptor control system which reduce the arterial pressure produced for any given level of sympathetic activity. Thus, as indicated in Figure 9 6B, the net results of these disturbances and subsequent adjustments to them will be a new steady state at a lower than normal mean arterial pressure and a higher than normal sympathetic activity.
    b and c elicit set-point-increasing inputs to the neural portion of the arterial baroreceptor control system that result in a greater than normal sympathetic output for any given level of input from the arterial baroreceptors. Thus, as indicated in Figure 9 7A, in the presence of these disturbances the system will operate at higher than normal mean arterial pressure and sympathetic activity.
9 6. a and c. These disturbances would tend to directly lower blood pressure, which would then lead to a reflex increase in heart rate. Disturbances b and d have no direct effect on the heart or vessels. Rather they act on the medullary cardiovascular centers to raise the set point and cause an increase in sympathetic activity. Consequently, one would expect b and d to cause increases in both heart rate and mean arterial pressure.

Chapter 10

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10 1. Because capillaries have such a small radius, the tension in the capillary wall is rather modest despite very high internal pressures according to the law of Laplace (T = P x r).
10 2. Fainting occurs because of decreased cerebral blood flow when mean arterial pressure falls below about 60 mmHg. On a hot day, temperature reflexes override pressure reflexes to produce the increased skin blood flow required for thermal regulation. Thus TPR is lower when standing on a hot day than on a cool one. Consequently, mean arterial pressure falls below 60 mmHg with less lowering of cardiac output on a warm day than on a cool one.
10 3. The cardiovascular response to lying down is just the opposite of that shown in Figure 10 3. Therefore, patients tend to lose rather than retain fluid during extended bed rest and end up with lower than normal blood volumes. Thus they are less able to cope with an upright posture during the period required for blood volume to reach the value it had when periods of standing were part of the patient's normal routine.
10 4. The pressure produced by the water on the lower part of the body enhances reabsorption of fluid into the capillaries, compresses peripheral veins, reduces the peripheral venous volume, and increases the volume of blood in the central venous pool. This stimulates the cardiopulmonary mechanoreceptors and evokes a diuresis by way of the various neural and hormonal pathways discussed in Chapter 9.
10 5. R = A/. Skeletal muscle resistance must have decreased considerably during exercise because skeletal muscle flow increased 10-fold (1000%) whereas mean arterial pressure increased much less ( 11%).
10 6. TPR = A/CO. Total peripheral resistance must have decreased during exercise because cardiac output increased 3-fold (300%), which is relatively much larger than the 11% increase in mean arterial pressure.
10 7. (1) The heart rate during exercise is well above the intrinsic rate ( 100 beats per minute). This indicates activation of the cardiac sympathetic nerves because withdrawal of cardiac parasympathetic activity cannot increase heart rate above the intrinsic rate (Chapter 2).
   (2) Increased arterial pulse pressure and ejection fraction at constant central venous pressure indicates increased stroke volume and cardiac contractility and thus increased activity of cardiac sympathetic nerves (Chapter 3).
   (3) Decreased renal and splanchnic blood flows in spite of increased mean arterial pressure indicate sympathetic vasoconstriction (Chapter 4).
10 8. (a) SV = CO/HR
   SV = 6000/70 = 86 mL/beat at rest.
   SV = 18,000/160 = 113 mL/beat during exercise.
   [You may recall that, in the absence of other information, changes in SV can be estimated from changes in arterial pulse pressure, (Pp). The information in Figure 10 4 indicates that Pp increased 1.75 times (from 40 mmHg to 70 mmHg) as a result of exercise whereas SV actually increased only 1.32 times (from 86 mL to 113 mL), as calculated earlier. This discrepancy emphasizes that while SV is a major determinant of Pp, changes in other factors, such as the compliance of arteries (CA), can influence Pp as well (see Appendix C). Part of the increase in Pp that accompanies exercise is due to a decrease in effective arterial compliance. The latter is due to (1) an increase in mean arterial pressure with exercise, and (2) the nonlinear nature of the arterial volume-pressure relationship (see Figure 6 8).]
   (b) Ejection fraction = SV/EDV, or EDV = SV/ejection fraction
   EDV = 86/0.60 = 143 mL/at rest
   EDV = 113/0.80 = 141 mL during exercise
   [Recall that central venous pressure, PCV, is the cardiac filling pressure or preload and is therefore the primary determinant of EDV. The EDV changed little with exercise because exercise caused little or no change in PCV.]
   (c) SV = EDV ESV, or ESV = EDV SV
   ESV = 143 86 = 57 mL at rest
   ESV = 141 113 = 28 mL during exercise
   [Recall that the primary determinants of ESV are cardiac afterload (mean arterial pressure) and myocardial contractility (see Appendix C). Cardiac afterload increases during exercise and thus goes in the wrong direction to account for a decrease in ESV. Therefore, an increased myocardial contractility, secondary to increased cardiac sympathetic nerve activity, must be primarily responsible for the decrease in ESV that accompanies exercise.]
   (d)
   Key features:
   1. End-diastolic volume during both rest and exercise is about 140 mL.
   2. Ventricular ejection (decreasing ventricular volume) begins when intraventricular pressure reaches the diastolic aortic pressure and the aortic valve opens. Figure 10 4 indicates an arterial diastolic pressure of 80 mmHg both at rest and during exercise. Thus, ventricular ejection will begin at an intraventricular pressure of 80 mmHg in both situations.
   3 and 4. Peak intraventricular pressure normally equals peak (systolic) arterial pressure. Hence, the systolic arterial pressure values in Figure 10 4 indicate peak intraventricular pressures of 120 mmHg and 150 mmHg during rest and exercise, respectively.
   5 and 6. As calculated in c earlier, end-systolic volume is 57 mL at rest and decreases to 28 mL during exercise.
10 9. The external negative pressure served to expand the thorax and "pull" air into the lungs through the patient's airways in much the same way that the thoracic muscle and diaphragm expand the thorax in normal breathing. This method of ventilating the lungs did not have the adverse cardiovascular consequences that positive pressure ventilation has.
10 10. Blood flow through muscle is reduced or stopped by compressive forces on skeletal muscle vessels during an isometric muscle contraction. Thus, during an isometric maneuver, total peripheral resistance (TPR) may be higher than normal rather than much lower than normal as it is during phasic exercises such as running. In the absence of decreased TPR but the presence of strong set-point-raising influences (central command) from the cortex on the medullary cardiovascular centers, mean arterial pressure may be regulated to very high values (see point 2 in Figure 9 7A).

Chapter 11

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11 1. Intense sympathetic activation drastically reduces skin blood flow, promotes transcapillary reabsorption of fluids, increases heart rate and contractility (but may not restore stroke volume because of low central venous pressure), and reduces skeletal muscle blood flow. Cerebral blood flow falls if the compensatory mechanisms do not prevent mean arterial pressure from falling below 60 mmHg.
11 2. (a) Not helpful since gravity tends to promote peripheral venous blood pooling and cause a further fall in arterial pressure.
   (b) Not helpful if carried to an extreme. Cutaneous vasodilation produced by warming adds to the cardiovascular stresses.
   (c) Helpful if the victim is conscious and can drink since fluid will be rapidly absorbed from the gut to increase circulating blood volume.
   (d) Might be helpful as an initial emergency measure to prevent brain damage due to severely reduced blood pressure, but prolonged treatment will promote the decompensatory mechanisms associated with decreased organ blood flow.
11 3. (a) In hypovolemic shock from diarrhea, the hematocrit will probably increase because, even though the compensatory processes will evoke a substantial "auto transfusion" by shifting fluid from the intracellular and interstitial space into the vascular space, this amount of fluid is limited to a liter or less. Therefore, a substantial loss of fluid (without red blood cells) will raise the hematocrit significantly.
   (b) In cardiogenic shock, the hematocrit may decrease because compensatory actions evoked to maintain blood pressure may promote a fluid shift into the vascular space. However, since central venous pressure (and perhaps peripheral venous pressures) may also be elevated, capillary hydrostatic pressures (and thus fluid shifts) are difficult to predict.
   (c) In septic shock, peripheral vasodilation and peripheral venous pooling may actually promote filtration of fluid out of the vasculature in some beds (which would lead to an increased hematocrit) but the low arterial and central venous pressures may counteract this shift so changes in hematocrits are difficult to predict in this situation.
   (d) Chronic bleeding disorders are usually associated with low hematocrit and anemia because red blood cell production may not keep pace with red cell losses whereas the volume regulating mechanisms may be able to maintain a normal blood volume.
11 4. True. The law of Laplace states that when the radius (r) of a cylinder (or in this case the irregularly shaped ventricular chamber) increases, the wall tension (T) for a given internal pressure (P) must also increase: T = P x r
11 5. Excessive fluid retention can induce decompensatory mechanisms that further compromise an already weakened heart (eg, inadequate oxygenation of the blood as it passes through edematous lungs, marked cardiac dilation and increased myocardial metabolic needs, liver dysfunction due to congestion). Diuretic therapy reduces fluid volume and the high venous pressures that are the cause of these problems.
11 6. If blood volume and central venous pressure are reduced too far with diuretic therapy, cardiac output may fall to unacceptably low levels through the Frank-Starling law of the heart.
11 7. Because of the high resistance of the stenosis and the pressure drop across it, glomerular capillary pressure and therefore glomerular filtration rate are lower than normal when arterial pressure is normal. Thus, a renal artery stenosis reduces the urinary output rate caused by a given level of arterial pressure. The renal function curve is shifted to the right, and hypertension follows.

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Cardiovascular Physiology
Cardiovascular Physiology: Mosby Physiology Monograph Series, 9e (Mosbys Physiology Monograph)
ISBN: 0323034462
EAN: 2147483647
Year: 2006
Pages: 20

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