Cardiovascular physiology

2011 ◽  
pp. 258-286
Author(s):  
Dr Mark Harrison
Keyword(s):  
Cardiac Output ◽  
Cardiac Cycle ◽  
Cardiovascular Physiology ◽  
Peripheral Vascular ◽  
Vascular Physiology

3.1 Systemic overview, 259 3.2 Cardiac cycle I, 262 3.3 Cardiac cycle II, 267 3.4 Cardiac cycle III, 269 3.5 Cardiac output, 272 3.6 Peripheral vascular physiology I, 276 3.7 Peripheral vascular physiology II, 278 3.8 Peripheral vascular physiology III, 282 See Table C.3.1...

Cardiovascular physiology

2017 ◽  
Author(s):  
Mark Harrison
Keyword(s):  
Emergency Medicine ◽  
Cardiac Output ◽  
Cardiovascular Physiology ◽  
Peripheral Vascular ◽  
Vascular Physiology

This chapter describes cardiovascular physiology as it applies to Emergency Medicine, and in particular the Primary FRCEM examination. The chapter gives a systemic overview and outlines the key details of cardiac cycles I, II, and III, cardiac output, and peripheral vascular physiology I, II, and III. This chapter is laid out exactly following the RCEM syllabus, to allow easy reference and consolidation of learning.

Normal function of the cardiovascular system

2018 ◽  
Author(s):  
Manish Kalla ◽  
Neil Herring
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cardiovascular System ◽  
Cardiac Cycle ◽  
Normal Function ◽  
Cardiac Physiology ◽  
Local Blood Flow ◽  
System P ◽  
Vascular Physiology ◽  
Flow Capillary

This chapter discusses normal function of the cardiovascular system, including cardiac physiology (the cardiac cycle, ECG, blood flow and heart sounds, control of cardiac output), vascular physiology (control of local blood flow, capillary transfer), integrated cardiovascular control,

HAEMODYNAMIC CHANGES AND ADRENAL FUNCTION IN MAN DURING INDUCED HYPOGLYCAEMIA

1963 ◽  
Vol 44 (3) ◽  
pp. 430-442 ◽  
Author(s):  
B. Arner ◽  
P. Hedner ◽  
T. Karlefors ◽  
H. Westling
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Mean Arterial Blood Pressure ◽  
Peripheral Vascular ◽  
Adrenocortical Activity ◽  
Arterial Blood ◽  
Haemodynamic Changes ◽  
The Mean ◽  
Temporary Rise ◽  
Catechol Amines

ABSTRACT Observations were made on healthy volunteers during insulin induced hypoglycaemia (10 cases) and infusion of adrenaline (3 cases) or cortisol (1 case). In all cases a rise in the cardiac output was registered during insulin hypoglycaemia. The mean arterial blood pressure was relatively unchanged and the calculated peripheral vascular resistance decreased in all cases. A temporary rise in plasma corticosteroids was observed. After infusion of adrenaline similar circulatory changes were observed but no rise in plasma corticosteroids was found. Infusion of cortisol caused an increased plasma corticosteroid level but no circulatory changes. It is concluded that liberation of catechol amines and increased adrenocortical activity following hypoglycaemia are not necessarily interdependent.

Euvolemic cirrhotic dogs in sodium balance maintain normal systemic hemodynamics

1988 ◽  
Vol 66 (1) ◽  
pp. 80-83 ◽  
Author(s):  
M. Levy ◽  
Elizabeth Maher ◽  
Marvin J. Wexler
Keyword(s):  
Cardiac Output ◽  
Liver Function ◽  
Vascular Resistance ◽  
Volume Expansion ◽  
Systemic Hemodynamics ◽  
Peripheral Vascular Resistance ◽  
Sodium Balance ◽  
Biliary Cirrhosis ◽  
Sodium Retention ◽  
Peripheral Vascular

Dogs with chronic biliary cirrhosis and portal hypertension commonly develop plasma volume expansion, urinary sodium retention, ascites, and perturbed systemic hemodynamics, i. e., a rise in cardiac output and a fall in peripheral vascular resistance. Our laboratory has previously demonstrated that creating a side-side portacaval anastomosis in such animals, and so venting hepatoportal pressure, will prevent sodium retention and ascites formation and will maintain the animals euvolemic. In the present study, in four cirrhotic dogs with such an anastomosis, observations made at 12 weeks postbiliary duct ligation, and in the presence of grossly disturbed liver function and morphology, failed to demonstrate any change from control conditions in arterial blood pressure, cardiac output, or peripheral vascular resistance. We conclude that venting hepatoportal pressure in cirrhotic dogs with markedly disturbed liver function prevents the advent of a hyperdynamic circulation, possibly by preventing volume expansion.

Circulatory and renal control by prostaglandins and renin in low cardiac output in dogs

1989 ◽  
Vol 256 (4) ◽  
pp. H1079-H1086 ◽  
Author(s):  
G. A. Riegger ◽  
D. Elsner ◽  
E. P. Kromer
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Glomerular Filtration Rate ◽  
Renal Blood Flow ◽  
Plasma Levels ◽  
Filtration Rate ◽  
Sympathetic Nerve Activity ◽  
Peripheral Vascular ◽  
Nerve Activity ◽  
Low Cardiac Output

Changes of neurohumoral factors including vasodilatory prostaglandins (PGs) were investigated in an experimental model of moderate low-cardiac-output status induced by rapid right ventricular pacing (240 beats/min). After 7 days of pacing, we studied the response of renal, hormonal, and hemodynamic parameters to cyclooxygenase inhibition by indomethacin and the effects of the renin system by converting-enzyme blockade in addition to the inhibition of PG synthesis. Lowering cardiac output increased plasma levels of norepinephrine and atrial natriuretic peptide. Plasma renin concentration was suppressed, despite a fall in cardiac output and blood pressure and a stimulation of sympathetic nerve activity. Urinary excretion of PGE2 was increased (P less than 0.04); plasma levels of PGE2 and 6-keto-PGF1 alpha were unchanged as measured in blood from the renal vein, pulmonary artery, and aorta. During low cardiac output, we found a significant decrease of glomerular filtration rate, whereas renal blood flow and renal and peripheral vascular resistances were unchanged. Administration of indomethacin decreased plasma and urinary PGs significantly, markedly reduced renal blood flow, and increased renal vascular resistance without affecting peripheral vascular resistance. The additional blockade of the renin-angiotensin system by captopril showed mainly a vasodilator effect on peripheral arterial resistance vessels, resulting in an increase of cardiac output. Our results suggest that, in moderate low-cardiac-output status, renal blood flow is maintained by renal vasodilator PGs, which counterbalance vasoconstrictor mechanisms like the activated sympathetic nerve activity. We indirectly showed the importance of angiotensin II in preserving glomerular filtration rate, which declines when renin secretion is suppressed, as it may be the case in moderate heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic response of normal men to graded treadmill exercise

1964 ◽  
Vol 19 (3) ◽  
pp. 457-464 ◽  
Author(s):  
Burton S. Tabakin ◽  
John S. Hanson ◽  
Thornton W. Merriam ◽  
Edgar J. Caldwell
Keyword(s):  
Carbon Dioxide ◽  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Treadmill Exercise ◽  
Minute Volume ◽  
Peripheral Vascular ◽  
Carbon Dioxide Elimination ◽  
Oxygen Utilization

The physiologic variables defining the circulatory and respiratory state in normal man have been measured in recumbency, standing at rest and during progressively severe grades of exercise approaching near-maximal levels. Indicator-dilution technique was used for determination of cardiac output with simultaneous radio-electrocardiographic recordings of heart rate. Direct intra-arterial pressure measurements were utilized for calculation of peripheral vascular resistance. Minute volume of ventilation, oxygen utilization, and carbon dioxide elimination were obtained from analysis of expired air collected at the time of each cardiac output determination. A peak mean workload of 1,501 kg-m/min was realized during the treadmill exercise. Increases in cardiac output over the range of exercise employed correlated well with indices of workload such as heart rate, oxygen utilization, and minute volume of ventilation. There was no correlation of stroke volume with these indices. It is concluded from examination of individual stroke-volume responses that a progressive increase in stroke volume is not a necessary or constant phenomenon in adapting to increasing workload. cardiac output in treadmill exercise; dye-dilution cardiac output determinations; arterial pressure during upright exercise; stroke-volume response to graded treadmill exercise; exercise response of cardiac output and stroke volume; peripheral vascular resistance response to position and exercise; treadmill exercise—effects on cardiac output, stroke volume, and oxygen uptake; minute ventilation, cardiac output, and stroke volume during exercise; carbon dioxide elimination during treadmill exercise; heart rate and cardiac output during treadmill exercise; exercise; physiology Submitted on July 12, 1963

Cardiac output in Xenopus laevis tadpoles during development and in response to an adenosine agonist

1996 ◽  
Vol 270 (5) ◽  
pp. R997-R1004
Author(s):  
Y. Y. Tang ◽  
C. M. Rovainen
Keyword(s):  
Cardiac Output ◽  
Xenopus Laevis ◽  
Cardiac Cycle ◽  
Normal Development ◽  
Volume Overload ◽  
Adenosine Agonist ◽  
Video Frames ◽  
Blood Pressures ◽  
Aquarium Water ◽  
Accelerated Growth

We test the hypothesis that the heart and arteries enlarge with increased cardiac output (CO) during development and volume overload. Transparent albino tadpoles of Xenopus laevis at stages 43-50 were anesthetized in 0.3-0.5 mM benzocaine. Areas and radii [maximum and minimum radius (Rmax and Rmin, respectively)] of the ventricle were measured in digitized video frames during the cardiac cycle. Stroke volume (SV) and CO were calculated from Rmax and Rmin. Maximal velocities of 3.4-microns fluorescent beads were measured in the aortic arches. Arterial pressure was estimated by the Landis method. During normal development, the radii of the ventricle and aortic arch diameters increased with lengths of tadpoles, and SV (0.7 microliters/g) and CO (70 microliters.g-1.min-1) with wet weights. Volume overload was induced by a vasodilatory adenosine agonist 5'-N-ethylcarboxamidoadenosine (NECA) in the aquarium water. Acute (0.5-4 h) NECA significantly increased Rmax and heart rate. Chronic (> 1 wk) NECA significantly increased both Rmax and Rmin. SV and CO increased more than two times, blood pressures decreased, and specific vascular conductances increased more than five times. It is concluded that NECA increases CO in Xenopus tadpoles through a combination of increased filling and accelerated growth.

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