Maximum heart rate does not limit cardiac output at rest or during exercise in the American alligator (Alligator mississippiensis)

In most vertebrates, increases in cardiac output result from increases in heart rate (fH) with little or no change in stroke volume (Vs), and maximum cardiac output (Q̇) is typically attained at or close to maximum fH. We therefore tested the hypothesis that increasing maximum fH may increase maximum Q̇. To this end, we investigated the effects of elevating fH with right atrial pacing on Q̇ in the American alligator ( Alligator mississippiensis) at rest and while swimming. During normal swimming, Q̇ increased entirely by virtue of a tachycardia (29 ± 1 to 40 ± 3 beats/min), whereas Vs remained stable. In both resting and swimming alligators, increasing fH with right atrial pacing resulted in a parallel decline in Vs that resulted in an unchanged cardiac output. In swimming animals, this reciprocal relationship extended to supraphysiological fH (up to ~72 beats/min), which suggests that maximum fH does not limit maximum cardiac output and that fH changes are secondary to the peripheral factors (for example vascular capacitance) that determine venous return at rest and during exercise.

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Cardiovascular function and norepinephrine-thermogenesis in cold-acclimatized rats

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1963.204.5.888 ◽

1963 ◽

Vol 204 (5) ◽

pp. 888-894 ◽

Cited By ~ 30

Author(s):

Eugene Evonuk ◽

John P. Hannon

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Arterial Pressure ◽

Stroke Volume ◽

Room Temperature ◽

Metabolic Response ◽

Atrial Pressure ◽

Right Atrial ◽

Right Atrial Pressure ◽

Systemic Resistance

The cardiovascular and metabolic actions of norepinephrine (NE) and their inter-relationships were studied at normal room temperature in anesthetized, warm-acclimatized (W-A) (26 ± 1 C) and cold-acclimatized (C-A) (3 ± 1 C) rats. The cardiac output, heart rate, stroke volume, arterial pressure, right atrial pressure, and systemic resistance were measured prior to NE infusion; during NE infusion (2 µg/min) at the 25, 50, 75, and 100% levels of increased metabolism; and after infusion of NE had ceased. Norepinephrine caused a greater increase in the cardiac output, heart rate, stroke volume, and right atrial pressure in the C-A animals than it did in W-A animals. During the early metabolic response to NE (i.e., up to 25% increase in O2 consumption) there was a marked increase in the arterial pressure of both W-A and C-A rats, with the latter showing the greater maximum response. Beyond the 25% level of increased metabolism the arterial pressure and concomitantly the systemic resistance of the C-A animals declined sharply to the preinfusion levels where they remained throughout the course of infusion. In contrast to this, the arterial pressure and systemic resistance of the W-A animals remained high. It was concluded that norepinephrine-calorigenesis in the C-A rat is supported by a greater capacity to increase the cardiac output and an ability to preferentially reduce the systemic resistance to actively metabolizing areas (i.e., the viscera).

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Distribution of fetal cardiac output: importance of pacemaker location

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1976.231.1.204 ◽

1976 ◽

Vol 231 (1) ◽

pp. 204-208 ◽

Cited By ~ 5

Author(s):

PT Pitlick ◽

SE Kirkpatrick ◽

WF Friedman

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Left Atrial ◽

Left Ventricular ◽

Right Atrial ◽

Atrial Pacing ◽

Foramen Ovale ◽

Rate Versus ◽

Left Ventricular Output ◽

The Right

Important questions exist about the relative roles of changes in heart rate versus extent of myocardial shortening in regulating fetal cardiac output, because increases in heart rate created by left atrial pacing have been shown to increase right ventricular output and decrease left ventricular output. Since the pacemaker site could importantly influence foramen ovale flow and, hence, each ventricle's output, changes in individual ventricular outputs were examined when both the right and left atria were paced at a rate of 270 beats/min in five acute and in eight chronically instrumented fetal lamb studies. With pacing of either atrium, total cardiac output was unchanged compared to control values. However, the right ventricle contributed more to total cardiac output with left atrial pacing (73% acute, 65% chronic) than with right atrial pacing (51% acute, 57% chronic). Converse changes were observed in left atrial pacing (27% acute, 35% chronic) as compared to right atrial pacing (49% acute, 43% chronic). Thus the disparity that exists normally in the contributions of the right and left ventricles to total cardiac output is accentuated with left atrial pacing and minimized with right atrial pacing. Pressure measurements demonstrated changes in the atrial pressure relations that would be expected to alter flow across the foramen ovale depending on the chamber initially activated. Previous experimental differences can, therefore, be attributed to changes in the magnitude of shunting across the foramen ovale and depend on pacemaker location.

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Cardiac performance: independence of adrenergic inotropic and chronotropic effects

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1978.234.5.h525 ◽

1978 ◽

Vol 234 (5) ◽

pp. H525-H532

Author(s):

A. Ilebekk ◽

J. Lekven ◽

F. Kiil

Keyword(s):

Heart Rate ◽

Stroke Volume ◽

Ventricular Volume ◽

Left Ventricular ◽

Right Atrial ◽

Diastolic Filling ◽

Atrial Pacing ◽

Heart Rates ◽

Systolic Volume ◽

End Diastolic Volume

During right atrial pacing in open-chest anesthetized dogs, the relationships between reduction in stroke volume and rise in heart rate were identical in control experiments, during intravenous infusion of isoproterenol, and after blockade of adrenergic beta-receptors by propranolol. To examine the mechanism of this constant relationship, left ventricular volume was estimated by continuous recordings of myocardial chord length (MCL) between ultrasonic elements inserted into the anterior ventricular wall. Diastolic filling curves were curtailed by raising heart rate and end-diastolic MCL was reduced. At constant heart rate, end-diastolic MCL was not altered by isoproterenol infusion, except for a slight rise at heart rates exceeding 220 beats/min. End-systolic MCL, however, was reduced, accounting for larger stroke volume during isoproterenol than during propranolol infusion. The reduction in end-systolic MCL was constant at all heart rates examined. Hence, chronotropic changes influence end-diastolic volume and inotropic changes influence end-systolic volume; their effects on stroke volume regulation are, therefore, virtually independent.

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Effect of lactic acidosis on canine hemodynamics and left ventricular function

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1990.258.4.h1193 ◽

1990 ◽

Vol 258 (4) ◽

pp. H1193-H1199 ◽

Cited By ~ 4

Author(s):

K. Teplinsky ◽

M. O'Toole ◽

M. Olman ◽

K. R. Walley ◽

L. D. Wood

Keyword(s):

Cardiac Output ◽

Lactic Acidosis ◽

Stroke Volume ◽

Venous Return ◽

Diastolic Pressure ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

Ventricular Pressure ◽

Right Atrial ◽

Lactic Acidemia

Hypoperfusion states cause lactic acidosis, and the acidemia further reduces the inadequate cardiac output. Conceivably, the adverse effect of lactic acidemia on cardiac output is due to depressed contractility demonstrated in isolated myocardium. Alternatively, factors governing venous return cause a relative hypovolemic state and/or acidemic pulmonary vasoconstriction-induced right ventricular dysfunction. We reasoned that examination of left ventricular pressure-volume relationships at end systole and end diastole would determine which of these potential mechanisms accounted for reduced cardiac output during progressive lactic acidosis in anesthetized, mechanically ventilated dogs. Left ventricular (LV) volume was estimated from two pairs of epicardial ultrasonic crystals placed in the anterior-posterior and longitudinal planes, and LV pressure was obtained rom a catheter-tipped transducer. During progressive acidemia induced by a continuous intravenous infusion of 0.5 N lactic acid, cardiac output, stroke volume, and mean systemic arterial pressure fell significantly while mean pulmonary artery pressure and right atrial pressure increased significantly. These variables did not change with time in control (no-acid infusion) dogs. Lactic acidemia caused a 40% reduction in stroke volume, which could be attributed to depressed LV contractility, characterized by a decrease in maximum dP/dt as well as a fall in slope (Emax) with no change in volume intercept (Vo) of the left ventricular pressure-volume relationship at end systole. Neither the measured left ventricular end-diastolic pressure nor the estimated left ventricular end-diastolic volume (LVEDV) decreased with acidemia, suggesting that the reduced venous return did not result from relative hypovolemia. However, acidemic pulmonary hypertension may have interfered with the expected response to myocardial depression, which is an increase in LVEDV.

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Hubungan Volume Cairan dengan Cardiac Output dan Venous Return pada Pasien Kritis

JAI (Jurnal Anestesiologi Indonesia) ◽

10.14710/jai.v11i3.25251 ◽

2019 ◽

Vol 11 (3) ◽

pp. 164-177

Author(s):

Listiana Dewi Sartika ◽

Erwin Pradian ◽

Nurita Dian ◽

Reza W Sudjud ◽

Ricky Aditya

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Stroke Volume ◽

Venous Return ◽

Filling Pressure ◽

Mean Systemic Filling Pressure ◽

Systemic Filling ◽

Systemic Filling Pressure

Pemberian cairan merupakan salah satu intervensi medis yang sering dilakukan pada pasien kritis di intensif care unit (ICU). Perkembangan ilmu mengenai cairan tubuh dulu lebih menitikberatkan pada fisiologi jantung kiri. Cardiac output, pada mulanya lebih dikenal sebagai fungsi jantung kiri dimana cardiac output ditentukan oleh jumlah darah yang dipompa dari ventrikel kiri dalam semenit (stroke volume) dan heart rate. Namun demikian, ternyata pemahaman fisiologi kardiovaskular tidak sesederhana itu. Menurut Starling, jantung hanya akan memompa darah yang masuk ke dalam jantung kanan. Dengan demikian, jumlah darah yang masuk ke jantung kanan harus sama dengan jumlah darah yang dipompa oleh jantung kiri, dimana keduanya adalah cardiac output. Ini kemudian diteliti lagi oleh Guyton. Guyton mencoba memandang cardiac output sebagai darah yang masuk ke jantung kanan (venous return). Terdapat banyak faktor yang menentukan kembalinya cairan ke jantung kanan. Faktor perbedaan tekanan antara mean systemic filling pressure (MSFP) dengan tekanan atrium kanan, serta faktor resistensi vena merupakan faktor penentu dalam fungsi venous return. Guyton juga mencari hubungan antara fungsi jantung dengan fungsi venous return. Pemahaman cardiac output secara utuh baik sebagai fungsi jantung dan sebagai venous return ini dapat menjelaskan banyak hal yang berhubungan dengan disfungsi kardiovaskular maupun gangguan ekstra kardiak pada pasien kritis dengan kondisi syok. Oleh karena itu, sangat penting bagi klinisi untuk memahami hubungan antara cairan tubuh dengan cardiac output dan venous return.

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Mechanisms of increase in cardiac output during acute weightlessness in humans

Journal of Applied Physiology ◽

10.1152/japplphysiol.01188.2010 ◽

2011 ◽

Vol 111 (2) ◽

pp. 407-411 ◽

Cited By ~ 20

Author(s):

Lonnie G. Petersen ◽

Morten Damgaard ◽

Johan C. G. Petersen ◽

Peter Norsk

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Stroke Volume ◽

Venous Return ◽

Water Immersion ◽

Parabolic Flight ◽

Cuff Inflation ◽

Lower Heart Rate ◽

Vascular Beds

Based on previous water immersion results, we tested the hypothesis that the acute 0-G-induced increase in cardiac output (CO) is primarily caused by redistribution of blood from the vasculature above the legs to the cardiopulmonary circulation. In seated subjects ( n = 8), 20 s of 0 G induced by parabolic flight increased CO by 1.7 ± 0.4 l/min ( P < 0.001). This increase was diminished to 0.8 ± 0.4 l/min ( P = 0.028), when venous return from the legs was prevented by bilateral venous thigh-cuff inflation (CI) of 60 mmHg. Because the increase in stroke volume during 0 G was unaffected by CI, the lesser increase in CO during 0 G + CI was entirely caused by a lower heart rate (HR). Thus blood from vascular beds above the legs in seated subjects can alone account for some 50% of the increase in CO during acute 0 G. The remaining increase in CO is caused by a higher HR, of which the origin of blood is unresolved. In supine subjects, CO increased from 7.1 ± 0.7 to 7.9 ± 0.8 l/min ( P = 0.037) when entering 0 G, which was solely caused by an increase in HR, because stroke volume was unaffected. In conclusion, blood originating from vascular beds above the legs can alone account for one-half of the increase in CO during acute 0 G in seated humans. A Bainbridge-like reflex could be the mechanism for the HR-induced increase in CO during 0 G in particular in supine subjects.

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Atriopeptin II lowers cardiac output in conscious sheep

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1985.249.6.r776 ◽

1985 ◽

Vol 249 (6) ◽

pp. R776-R780 ◽

Cited By ~ 4

Author(s):

B. A. Breuhaus ◽

H. H. Saneii ◽

M. A. Brandt ◽

J. E. Chimoskey

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Smooth Muscle ◽

Arterial Pressure ◽

Stroke Volume ◽

Total Peripheral Resistance ◽

Peripheral Resistance ◽

Atrial Pressure ◽

Right Atrial ◽

Right Atrial Pressure

Atrial natriuretic peptides cause natriuresis, kaliuresis, diuresis, and hypotension. They relax vascular smooth muscle in vitro, and they dilate renal vessels in vivo. Hence, we tested the hypothesis that they produce hypotension by lowering total peripheral resistance. The studies were performed in conscious chronically instrumented sheep standing quietly in their cages. Atriopeptin II (AP II) was infused into the right atrium for 30 min at 0.1 nmol X kg-1 X min-1. Atriopeptin II lowers arterial pressure (9%, P less than 0.05) by lowering cardiac output (18%, P less than 0.05), stroke volume (28%, P less than 0.05), and right atrial pressure (2.3 mmHg, P less than 0.05). Heart rate and total peripheral resistance increase (16 and 13%, respectively, P less than 0.05). Partial ganglionic blockade with trimethaphan camsylate during AP II infusion prevents the increases in heart rate and total peripheral resistance. The changes in right atrial pressure, stroke volume, and cardiac output persist, and arterial pressure falls further (27%, P less than 0.05). These hemodynamic data are consistent with direct AP II-induced relaxation of venous smooth muscle with reduction of venous return, right atrial pressure, stroke volume, cardiac output, and arterial pressure, followed by reflex activation of the sympathetic nervous system to increase heart rate and total peripheral resistance. Because partial ganglionic blockade alone and AP II alone cause similar reductions in right atrial pressure (2.1 and 2.3 mmHg, respectively) but AP II causes a greater fall in stroke volume (28 vs. 13%), it is possible that AP II also causes coronary vasoconstriction.

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Cardiac output in muscular exercise at 5,800 m (19,000 ft)

Journal of Applied Physiology ◽

10.1152/jappl.1964.19.3.441 ◽

1964 ◽

Vol 19 (3) ◽

pp. 441-447 ◽

Cited By ~ 72

Author(s):

L. G. C. E. Pugh

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Sea Level ◽

Indirect Evidence ◽

Mean Value ◽

Muscular Exercise ◽

Maximum Output ◽

Work Intensity ◽

Maximum Heart Rate ◽

Sea Level Pressure

Cardiac output during muscular exercise was estimated by the acetylene technique on four members of the Himalayan Scientific and Mountaineering expedition 1960–1961 at sea level and 5,800 m (19,000 ft). The output for a given work intensity at 5,800 m (19,000 ft) was comparable with the output at the same work intensity at sea level, but the maximum output was reduced, the mean value being 16 liters/min, compared with 23 liters/min at sea level. Heart rates during light and moderate exercise were higher than the rates observed at the same work intensity at sea level. The maximum heart rate during exercise was limited to 130–150 beats/min compared with 180–196 beats/min at sea level. The stroke volume at altitude was lower than at sea level at each work rate. On breathing oxygen at sea-level pressure, heart rate for a given work intensity was reduced; but the maximum heart rate increased. Indirect evidence suggested that maximum cardiac output increased but probably not to the sea-level values because of the increased hemoglobin and lower heart rate. altitude acclimatization; cardiac function, work and altitude; hypoxia and cardiac output Submitted on July 29, 1963

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Physiological factors associated with the lower maximal oxygen consumption of master runners

Journal of Applied Physiology ◽

10.1152/jappl.1989.66.2.949 ◽

1989 ◽

Vol 66 (2) ◽

pp. 949-954 ◽

Cited By ~ 38

Author(s):

A. M. Rivera ◽

A. E. Pels ◽

S. P. Sady ◽

M. A. Sady ◽

E. M. Cullinane ◽

...

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Stroke Volume ◽

Maximal Oxygen Consumption ◽

Maximal Heart Rate ◽

Distance Runners ◽

Physiological Factors ◽

Factors Associated ◽

Older Athletes ◽

Maximal Cardiac Output

We examined the hemodynamic factors associated with the lower maximal O2 consumption (VO2max) in older formerly elite distance runners. Heart rate and VO2 were measured during submaximal and maximal treadmill exercise in 11 master [66 +/- 8 (SD) yr] and 11 young (32 +/- 5 yr) male runners. Cardiac output was determined using acetylene rebreathing at 30, 50, 70, and 85% VO2max. Maximal cardiac output was estimated using submaximal stroke volume and maximal heart rate. VO2max was 36% lower in master runners (45.0 +/- 6.9 vs. 70.4 +/- 8.0 ml.kg-1.min-1, P less than or equal to 0.05), because of both a lower maximal cardiac output (18.2 +/- 3.5 vs. 25.4 +/- 1.7 l.min-1) and arteriovenous O2 difference (16.6 +/- 1.6 vs. 18.7 +/- 1.4 ml O2.100 ml blood-1, P less than or equal to 0.05). Reduced maximal heart rate (154.4 +/- 17.4 vs. 185 +/- 5.8 beats.min-1) and stroke volume (117.1 +/- 16.1 vs. 137.2 +/- 8.7 ml.beat-1) contributed to the lower cardiac output in the older athletes (P less than or equal 0.05). These data indicate that VO2max is lower in master runners because of a diminished capacity to deliver and extract O2 during exercise.

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