Chapter answers
Chapter 2
1 A. The conduction velocity of the AV node results in a PR interval that is always between 120–200 ms in a normal heart.
3 C. Since the T wave denotes the period during which ventricular repolarization takes place, the end of this wave corresponds to repolarization of the longest duration action potentials, which are those in the endocardial cells.
4 B. The duration of the QRS complex denotes the time taken for depolarization of the entire ventricular myocardium.
5 F. The AV valves open when ventricular muscle relaxation is complete and close at the beginning of ventricular contraction.
6 B. The normal velocity of impulse propagation through the ventricular syncytium causes depolarization of the whole muscle mass within 50–80 ms. If the time taken for ventricular depolarization is greater than 80 ms, then the velocity of action potential propagation is abnormally slow OR the normal conduction pathway is blocked at some point.
Chapter 3
2 D. Release of catecholamines increases contractility of all myocardial cells, but it is only atrial contraction that can contribute to ventricular filling. Other factors that aid filling are decreased intrathoracic pressure during inspiration and muscle pumping causing compression of limb veins. Increased heart rate may increase end-systolic volume, but does not affect ventricular filling.
3 C. Ventricular filling is limited by the increased stiffness of both myocardium and pericardium at high filling volumes and by the fact that the calcium channels that determine ventricular action potential plateau duration have a finite minimum cycle time, so that above a certain heart rate the diastolic filling time is shortened. With exercise modalities that elevate diastolic blood pressure, this rise in afterload also limits ventricular emptying. Sympathetic activation and catecholamine secretion continue to rise proportionately to exercise intensity up to maximum work capacity.
Chapter 4
1 E. Sympathetic activation increases stroke volume both by increasing cardiac filling (due primarily to mobilizing blood from venous reservoirs) and by increasing cardiac emptying (due to increased myocardial contractility). The effect on peak blood pressure of this larger stroke volume is enhanced by faster ejection by more rapid myocardial depolarization and by reduced aortic distension because of vascular muscle contraction.
2 A. Remember that the formula for calculation of mean blood pressure at rest is DBP + ⅓ PP or (SBP + 2DBP). Only at the high heart rates that occur during heavy exercise, DBP + 2/5 PP, may be slightly more accurate.
3 A. Conversion of laminar to turbulent flow is enhanced by increased velocity of flow and increased vessel diameter. This situation occurs where blood whose flow velocity has been increased by vessel compression under the cuff enters the wider, non-compressed segment immediately downstream. With cuff inflation to pressures between systolic and diastolic pressures, flow is necessarily intermittent. However, with the high flow velocities associated with high cardiac outputs, Korotkow sounds may still be heard when the cuff is inflated to pressures significantly below DBP and flow is continuous.
4 C. Decreased peripheral resistance will reduce DBP. If stroke volume and heart rate remain constant, then the pulse pressure will remain constant. Pulse pressure is inversely proportional to heart rate if all other factors remain unchanged, and is greater in peripheral arteries than in aorta because aortic compliance damps the pressure oscillations.
5 D. Peripheral resistance = mean BP/CO = 96/16 PRU. Remember that the PRU unit varies in magnitude depending on the way in which cardiac output is expressed. Here, the PRU incorporates cardiac output as expressed in l/min. If cardiac output was expressed in ml/min, then peripheral resistance would be 96/16 000 or 0.006 PRU.
Chapter 5
1 D. When sympathetic tone is high, a greater intravascular pressure is needed to balance the tendency of the vessel wall to contract inwards. Wall tension is proportional to transmural pressure and to the ratio of luminal diameter:wall thickness, so it rises with BP and is higher in large vessels with high intravascular pressures. The elastic properties of the aortic wall make it stretch in response to increased BP; the presence of collagen limits this expansion and the risk of rupture.
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