Normal function of the cardiovascular system

Author(s):  
Manish Kalla ◽  
Neil Herring

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,

Author(s):  
Dr Mark Harrison

2.1 Control of blood pressure and heart rate, 445 2.2 Control of heart rate, 446 2.3 Cardiac output (CO), 447 2.4 Measurement of cardiac output (CO), 450 2.5 Blood flow peripherally, 451 2.6 The cardiac cycle, 454 2.7 ECG, 458 2.8 Pharmacological manipulation of the heart and peripheral circulation, ...


1983 ◽  
Vol 245 (5) ◽  
pp. G697-G702 ◽  
Author(s):  
P. T. Nowicki ◽  
B. S. Stonestreet ◽  
N. B. Hansen ◽  
A. C. Yao ◽  
W. Oh

Regional and total gastrointestinal (GI) blood flow, O2 delivery, and whole-gut O2 extraction and O2 consumption were measured before and 30, 60, and 120 min after feeding in nonanesthetized, awake 2-day-old piglets. Cardiac output and blood flow to kidneys, heart, brain, and liver were also determined. Blood flow was measured using the radiolabeled microsphere technique. In the preprandial condition, total GI blood flow was 106 +/- 9 ml X min-1 X 100 g-1, while O2 extraction was 17.2 +/- 0.9% and O2 consumption was 1.99 +/- 0.19 ml O2 X min-1 X 100 g-1. Thirty minutes after slow gavage feeding with 30 ml/kg artificial pig milk, O2 delivery to the GI tract and O2 extraction rose significantly (P less than 0.05) by 35 +/- 2 and 33 +/- 2%, respectively. The increase in O2 delivery was effected by a significant increase in GI blood flow, which was localized to the mucosal-submucosal layer of the small intestine. O2 uptake by the GI tract increased 72 +/- 4% 30 min after feeding. Cardiac output and blood flow to non-GI organs did not change significantly with feeding, whereas arterial hepatic blood flow decreased significantly 60 and 120 min after feeding. The piglet GI tract thus meets the oxidative demands of digestion and absorption by increasing local blood flow and tissue O2 extraction.


1980 ◽  
Vol 48 (2) ◽  
pp. 281-283 ◽  
Author(s):  
L. E. Boerboom ◽  
J. N. Boelkins

Although man is being exposed to hyperbaric environments more frequently, the effects of these environments and the inert gases used are not clearly defined. We therefore designed an experiment to examine both the effects of helium and elevated pressure on the cardiovascular system in conscious rabbits exposed to normoxic levels of a helium-oxygen (He-O2) gas mixture at 1 and 11 atmospheres absolute (ATA) for 2 h. Variables studied included heart rate, blood pressure, cardiac output, systemic vascular resistance, organ blood flow, and resistance to flow. The only change observed was a decrease in heart rate from a control of 284 +/- 7 (mean +/- SE) to 246 +/- 12 beats/min after 2 h of breathing He-O2 at 1 ATA. We therefore conclude that the cardiovascular system is not adversely affected by helium or elevated pressure as used in this experiment.


1992 ◽  
Vol 263 (4) ◽  
pp. E740-E747 ◽  
Author(s):  
R. J. Playford ◽  
M. A. Benito-Orfila ◽  
P. Nihoyannopoulos ◽  
K. A. Nandha ◽  
J. Cockcroft ◽  
...  

Peptide YY (PYY) reverses the increased intestinal secretion stimulated by vasoactive intestinal peptide (VIP) in humans. VIP also dilates blood vessels, so we investigated the effect of PYY on the cardiovascular system. Six volunteers received PYY, 0.4 and 1.2 pmol.kg-1 x min-1 i.v. for 2 h, reproducing plasma levels seen postprandially and during a diarrheal illness, respectively. Cardiac function was assessed by echocardiography. PYY infused at 0.4 pmol.kg-1 x min-1 had no effect on cardiovascular parameters. PYY infused at 1.2 pmol.kg-1 x min-1 caused a fall in both stroke volume from 128 +/- 8 to 110 +/- 8 ml/beat (mean +/- 95 confidence interval, P < 0.01) and cardiac output from 7.2 +/- 0.4 to 6.1 +/- 0.4 l/min (P < 0.01). Effects of infusion of PYY into the brachial artery at doses of 0-16 pmol/min were assessed using venous occlusion plethysmography in six subjects. PYY infusion caused a dose-dependent fall in forearm blood flow. Six subjects received VIP, 5 pmol.kg-1 x min-1 i.v., causing a rise in heart rate from 55 +/- 3 to 70 +/- 3 beats/min and increased cardiac output from 7.3 +/- 1.1 to 13.1 +/- 1.1 l/min. The addition of PYY, 0.4 pmol.kg-1 x min-1 i.v., did not affect the heart rate significantly but decreased the cardiac output to 10.4 +/- 1.1 l/min (P < 0.01). Infusions of PYY into the brachial artery at 5 pmol/min decreased local vasodilation induced by VIP infused at 2 pmol/min at the same site by 40% (P < 0.01), even though this dose of PYY had no significant effect on local blood flow when given alone.(ABSTRACT TRUNCATED AT 250 WORDS)


Author(s):  
Dr Mark Harrison

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...


Author(s):  
Sethuraman Sankaran ◽  
Jeffrey A. Feinstein ◽  
Alison L. Marsden

Numerical simulations of blood flow in the human cardiovascular system are usually performed using custom Finite element methods and specialized boundary conditions. These simulations are performed to (a) understand the physics of blood flow in the human cardiovascular system and (b) a priori testing of proposed treatments/interventions whether surgical or endovascular. To perform these simulations, we require prior knowledge of parameters such as cardiovascular geometry, boundary conditions (inflow/outflow/pressure), etc. In the past, researchers have assumed exact values for these parameters. However, in reality, each of these parameters is uncertain. For example, inflow conditions into the model are dictated by the heart rate and cardiac output of the patient. Even during rest, there are variations in cardiac output and hence the corresponding blood inflow velocities need to be modeled as a random variable. Additionally, the cardiovascular geometry is built based on MRI-images. These are subject to uncertainties due to noise in the data and variability between users during model construction. We develop a computational toolbox that can account for uncertainties in such parameters in hemodynamic simulations. The uncertainties examined in this work include i) variation and accuracy of image-based model geometry ii) variability in inflow condition of the patient and iii) variability in the implementation of the final surgical design. The last source of uncertainty stems from the fact that optimally designed surgical parameters may not be exactly implemented in the operating room. We show numerical examples of (a) blood flow in stenotic vessels (b) effect of uncertainty in carotid sinus size on blood flow and (iii) develop a stochastic optimization technique to compute optimal parameters of an idealized Y-graft model for the Fontan surgery accounting for sources of uncertainties listed above.


Author(s):  
Mark Harrison

This chapter describes the pathophysiology of the cardiovascular system as it applies to Emergency Medicine, and in particular the Primary FRCEM examination. The chapter outlines the key details of the control of blood pressure and heart rate, cardiac output, blood flow, cardiac cycle, ECG, pharmacological manipulation of the heart, shock, oxygen delivery and consumption, body fluid homeostasis, crystalloid solutions, colloidal solutions, and exudates and transudates. This chapter is laid out exactly following the RCEM syllabus, to allow easy reference and consolidation of learning.


1963 ◽  
Vol 204 (2) ◽  
pp. 279-283 ◽  
Author(s):  
Margaret Beznak

Growth hormone, thyroxin, or growth hormone and thyroxin were given for a period of 4 weeks to rats hypophysectomized 2–3 months previously. The effect of these treatments on blood pressure, weight and rate of the heart, cardiac output, and work was measured under basal conditions and during acute loading (infusion of polyvinylpyrrolidone into the right side of the heart) as well as during chronic loading (constriction of the aorta). The changes in cardiovascular parameters in the basal state due to hypophysectomy could all be reversed by thyroxin treatment. Thyroxin alone was inadequate in restoring the response of the hearts to either acute or chronic loading. Growth hormone in combination with thyroxin could restore or even exaggerate the normal response to both chronic and acute loading as well as maintain the basal parameters. Growth hormone itself had comparatively little effect; it caused some increase in the weight of the heart and stroke volume. It is concluded that both thyroxin and growth hormone are necessary for the normal function of the cardiovascular system.


1964 ◽  
Vol 207 (3) ◽  
pp. 661-668 ◽  
Author(s):  
Edward S. Kirk ◽  
Carl R. Honig

Myocardial tissue pressure increases from epicardium to endocardium, and in the deeper layers exceeds ventricular blood pressure during one-third of the cardiac cycle (21). The effect of this tissue pressure gradient on local blood flow was studied using the depot clearance technique. Blood flow was found to be at least 25% lower in the deep regions as compared with superficial ones. With total coronary inflow held constant, vagal arrest of the heart removed the tissue pressure gradient, and simultaneously redistributed flow from superficial to deeper layers. We conclude that the gradient in tissue pressure, and hence in the extravascular component of coronary resistance, is at least in part, the cause of the nonhomogeneous blood flow across the wall. By use of the oxygen cathode, a gradient of oxygen tensions was observed which paralleled the blood flow gradient; mean oxygen tension in the subepicardium averaged twice that in the subendocardium. The gradient in oxygen tension appears to be of sufficient magnitude to determine a transmural gradient in aerobic metabolism.


1977 ◽  
Vol 232 (5) ◽  
pp. H534-H536
Author(s):  
D. G. Wantzelius ◽  
K. L. Goetz

We describe an inexpensive circuit designed to correct base-line drift of electromagnetic flowmeters automatically when cardiac output is being measured. The circuit measures the flowmeter output voltage during a portion of each diastole when blood flow in the aorta is assumed to be zero. Any deviation of the flowmeter output voltage from zero during this time represents either base-line offset or drift. The output voltage obtained during zero flow conditions is stored throughout the next cardiac cycle and subtracted continuously from the flowmeter output during each beat, thus giving a beat-by-beat correction of any base-line drift.


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