SECTION III THE CARDIONASOULAR SYSTEM 且eart Block An 80-year-old mam had problems with his AV conduction system and his cardiologist decided that an artificial paceraker was required.Imediately after the pacemaker had heem installed,the cardiologist tested the effects of different pacing frequencies to deternine the optimal settings for the patiemt.Some of the results were as follows:When the heart was paced at 60 beats/nin.the patient's stroke volume was 80 ml.his cardiac output was 4.8 1/nin,and his total peripheral resistance was 20 mm Hg/L/min.When the heart was paced at 100 beats/min,the stroke volune was 48 ml,his cardiac output was 4.8 L/nin,and his total peripheral resistance vas 20 m Hg/L/ain. 1.What was the patient's mean arterial pressure while he was being paced at heart rates of 60 and 100 beats/min? 2.What directional changes in the arterial systolic.diastolic,and pulse pressures would you expect when the paced heart rate was switched from 60 to 100 beats/min? ANSVER 1.The cardiac output (Ch)and total peripheral resistance (Rt)in this example were not affected by the pacing frequency.The mean arterial pressure (Pa)can be determined from the definition of total peripheral resistance (Rt):that is.Rt Pa Pv)/gh Thus,Pa Pv Rt.gh,which equals 20 x 4.8 96 mm Hg.regardless of the pacing frequency.Because Pv is usually only slightly greater than 0,Pa is essentially the product of peripheral resistance and cardiac output (in this case, about 96 mm Hg).Any change in cardiac output will evoke a proportionate change in
SECTION III THE CARDIOVASCULAR SYSTEM Heart Block An 80-year-old man had problems with his AV conduction system, and his cardiologist decided that an artificial pacemaker was required. Immediately after the pacemaker had been installed, the cardiologist tested the effects of different pacing frequencies to determine the optimal settings for the patient. Some of the results were as follows: When the heart was paced at 60 beats/min, the patient's stroke volume was 80 ml, his cardiac output was 4.8 L/min, and his total peripheral resistance was 20 mm Hg/L/min. When the heart was paced at 100 beats/min, the stroke volume was 48 ml, his cardiac output was 4.8 L/min, and his total peripheral resistance was 20 mm Hg/L/min. 1. What was the patient's mean arterial pressure while he was being paced at heart rates of 60 and 100 beats/min? 2. What directional changes in the arterial systolic, diastolic, and pulse pressures would you expect when the paced heart rate was switched from 60 to 100 beats/min? ANSWER 1. The cardiac output (Qh) and total peripheral resistance (Rt) in this example were not affected by the pacing frequency. The mean arterial pressure (Pa)can be determined from the definition of total peripheral resistance (Rt); that is, Rt = Pa – Pv)/Qh Thus, Pa – Pv = Rt · Qh, which equals 20 x 4.8 = 96 mm Hg, regardless of the pacing frequency. Because Pv is usually only slightly greater than 0, Pa is essentially the product of peripheral resistance and cardiac output (in this case, about 96 mm Hg). Any change in cardiac output will evoke a proportionate change in
Pa,regardless of whether that change in cardiac output was achieved by a change in stroke volume,in heart rate,or in both. 2.While the left ventricle is ejecting blood into a normally distensible aorta during systole,some blood is continually running out of the arteries,traversing the resistance vessels.and entering the veins.At any time during vemtricular ejection,the increment in arterial volune equals the disparity between the volume of blood already ejected by the ventricle into the arteries and the anount of peripheral runoff"from the arteries through the nicrocirculation and into the veins.During the imitial phase of ejectfon (the rapid ejection phase),the rate of ejection exceeds the rate of runoff.and arterial volune (and hence also arterial pressure)progressively increases.During the secondary phase of ejection (the reduced ejectfon phase),the rate of runoff exceeds the rate of ejection,and arterial volume (and hence also arterial pressure)progressively decreases. The volune of blood in the arteries just before ventricular ejection is the minimm arterial volume:it is this blood volume that determines the diastolic arterial pressure (Pd).During ventricular ejection,the naximum increase in arterial volume above this minimn volume may be called the maximun volume increnent (AVa).The maximm arterial volume,which prevails at the end of the rapid ejection phase of ventricular systole,accounts for the systolie arterial pressure (Ps)and the maximun volue increment (AVa)accounts for the pulse pressure (Ps -Pd).For a given arterial compliance (Ca),the relation between (Ps Pd)and AVa is (Ps -Pd)■△Va/Ca During pacing at a heart rate of 60 heats/min.the patient's stroke volune was 80 nl,whereas when the pacing rate was increased to 100 beats/ain,the stroke volume decreased to 48 ml.A ventricular ejection of 80 ml would be expected to induce a substantially larger arterial volune increment than would a ventricular ejection of only 48 ml.Hence.the stroke volune of 80 ml would be expected to elicit a substantially greater pulse pressure than would a stroke volume of 48 ml.Because
Pa, regardless of whether that change in cardiac output was achieved by a change in stroke volume, in heart rate, or in both. 2. While the left ventricle is ejecting blood into a normally distensible aorta during systole, some blood is continually running out of the arteries, traversing the resistance vessels, and entering the veins. At any time during ventricular ejection, the increment in arterial volume equals the disparity between the volume of blood already ejected by the ventricle into the arteries and the amount of "peripheral runoff” from the arteries through the microcirculation and into the veins. During the initial phase of ejection (the rapid ejection phase), the rate of ejection exceeds the rate of runoff, and arterial volume (and hence also arterial pressure) progressively increases. During the secondary phase of ejection (the reduced ejection phase), the rate of runoff exceeds the rate of ejection, and arterial volume (and hence also arterial pressure) progressively decreases. The volume of blood in the arteries just before ventricular ejection is the minimum arterial volume; it is this blood volume that determines the diastolic arterial pressure (Pd). During ventricular ejection, the maximum increase in arterial volume above this minimum volume may be called the maximum volume increment (∆Va). The maximum arterial volume, which prevails at the end of the rapid ejection phase of ventricular systole, accounts for the systolic arterial pressure (Ps) and the maximum volume increment (∆Va) accounts for the pulse pressure (Ps – Pd). For a given arterial compliance (Ca), the relation between (Ps – Pd) and ∆Va is (Ps – Pd) = ∆Va/Ca. During pacing at a heart rate of 60 beats/min, the patient's stroke volume was 80 ml, whereas when the pacing rate was increased to 100 beats/min, the stroke volume decreased to 48 ml. A ventricular ejection of 80 ml would be expected to induce a substantially larger arterial volume increment than would a ventricular ejection of only 48 ml. Hence, the stroke volume of 80 ml would be expected to elicit a substantially greater pulse pressure than would a stroke volume of 48 ml. Because
the mean arterial pressures were shown above to be equal at the two pacing rates, the arterial pressure characteristics during pacing at the slower rate would be characterized by a lower diastolic pressure and a higher systolic pressure than would prevail during pacing at the faster rate
the mean arterial pressures were shown above to be equal at the two pacing rates, the arterial pressure characteristics during pacing at the slower rate would be characterized by a lower diastolic pressure and a higher systolic pressure than would prevail during pacing at the faster rate