Role of cardiac output in mediating arterial blood pressure oscillations

1996 ◽  
Vol 271 (3) ◽  
pp. R641-R646 ◽  
Author(s):  
D. S. O'Leary ◽  
D. J. Woodbury
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Low Frequency ◽  
Left Ventricular ◽  
Right Atrial ◽  
Total Power ◽  
Av Block ◽  
Arterial Blood ◽  
Low Frequency Oscillations

The objective of this study was to determine the role of cardiac output in mediating spontaneous fluctuations in mean arterial pressure (MAP) conscious dogs. Dogs were chronically instrumented to monitor MAP and cardiac output. Atrioventricular (AV) block was induced, and left ventricular and right atrial electrodes were implanted. After recovery, MAP was observed for 5 min under two conditions: 1) normal variation in heart rate and cardiac output via triggering the ventricular stimulator with each atrial depolarization (effectively reversing the AV block, AV-linked stimulation) and 2) computer control of ventricular rate to maintain cardiac output constant on a by-beat basis at the same level as observed during normal variations in heart rate and cardiac output. When cardiac output was held constant, large-amplitude, low-frequency oscillations in MAP were readily apparent. Spectral analysis by fast Fourier transform revealed that during constant cardiac output the power observed at low frequencies in the MAP spectrum represented 95.0 +/- 2.7% of the total power compared with 75.5 +/- 4.6% during normal variations in heart rate and cardiac output (P < 0.05). In addition, when cardiac output was held constant, the power observed at higher frequencies markedly decreased from 24.5 +/- 4.6% of total power during AV-linked stimulation to only 5.0 +/- 2.7% of total power during constant cardiac output (P < 0.05). We conclude that low-frequency oscillations in MAP are due to changes in peripheral resistance, whereas a significant amount of high-frequency changes in MAP stems from spontaneous changes in cardiac output.

scholarly journals Respiratory-related heart rate variability in progressive experimental heart failure

2005 ◽  
Vol 289 (4) ◽  
pp. H1729-H1735 ◽  
Author(s):  
Sophie Motte ◽  
Myrielle Mathieu ◽  
Serge Brimioulle ◽  
Anne Pensis ◽  
Lynn Ray ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Spectral Analysis ◽  
Left Ventricular ◽  
Right Atrial ◽  
Left Ventricular Ejection ◽  
Total Power ◽  
Progressive Heart Failure ◽  
Atrial Natriuretic

Heart failure is associated with autonomic imbalance, and this can be evaluated by a spectral analysis of heart rate variability. However, the time course of low-frequency (LF) and high-frequency (HF) heart rate variability changes, and their functional correlates during progression of the disease are not exactly known. Progressive heart failure was induced in 16 beagle dogs over a 7-wk period by rapid ventricular pacing. Spectral analysis of heart rate variability and respiration, echocardiography, hemodynamic measurements, plasma atrial natriuretic factor, and norepinephrine was obtained at baseline and every week, 30 min after pacing interruption. Progressive heart failure increased heart rate (from 91 ± 4 to 136 ± 5 beats/min; P < 0.001) and decreased absolute and normalized (percentage of total power) HF variability from week 1 and 2, respectively ( P < 0.01). Absolute LF variability did not change during the study until it disappeared in two dogs at week 7 ( P < 0.05). Normalized LF variability increased in moderate heart failure ( P < 0.01), leading to an increased LF-to-HF ratio ( P < 0.05), but decreased in severe heart failure ( P < 0.044; week 7 vs. week 5). Stepwise regression analysis revealed that among heart rate variables, absolute HF variability was closely associated with wedge pressure, right atrial and pulmonary arterial pressure, left ventricular ejection fraction and volume, ratio of maximal velocity of early (E) and atrial (A) mitral flow waves, left atrial diameter, plasma norepinephrine, and atrial natriuretic peptide (0.45 < r < 0.65, all P < 0.001). In tachycardia-induced heart failure, absolute HF heart rate variability is a more reliable indicator of cardiac dysfunction and neurohumoral activation than LF heart rate variability.

scholarly journals The Influence ofNrf2on Cardiac Responses to Environmental Stressors

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Reuben Howden ◽  
Eva Gougian ◽  
Marcus Lawrence ◽  
Samantha Cividanes ◽  
Wesley Gladwell ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
High Frequency ◽  
Low Frequency ◽  
Therapeutic Strategies ◽  
Environmental Stressors ◽  
Total Power ◽  
Airborne Pollutants ◽  
Cardiac Responses

Nrf2protects the lung from adverse responses to oxidants, including 100% oxygen (hyperoxia) and airborne pollutants like particulate matter (PM) exposure, but the role ofNrf2on heart rate (HR) and heart rate variability (HRV) responses is not known. We hypothesized that genetic disruption ofNrf2would exacerbate murine HR and HRV responses to severe hyperoxia or moderate PM exposures.Nrf2-/-andNrf2+/+mice were instrumented for continuous ECG recording to calculate HR and HRV (low frequency (LF), high frequency (HF), and total power (TP)). Mice were then either exposed to hyperoxia for up to 72 hrs or aspirated with ultrafine PM (UF-PM). Compared to respective controls, UF-PM induced significantly greater effects on HR (P<0.001) and HF HRV (P<0.001) inNrf2-/-mice compared toNrf2+/+mice.Nrf2-/-mice tolerated hyperoxia significantly less thanNrf2+/+mice (~22 hrs;P<0.001). Reductions in HR, LF, HF, and TP HRV were also significantly greater inNrf2-/-compared toNrf2+/+mice (P<0.01). Results demonstrate thatNrf2deletion increases susceptibility to change in HR and HRV responses to environmental stressors and suggest potential therapeutic strategies to prevent cardiovascular alterations.

Effects of isoproterenol on the cardiovascular system of fetal sheep exposed to long-term high-altitude hypoxemia

1995 ◽  
Vol 78 (5) ◽  
pp. 1793-1799 ◽  
Author(s):  
M. Kamitomo ◽  
T. Ohtsuka ◽  
R. D. Gilbert
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Right Ventricular ◽  
High Altitude ◽  
Arterial Blood Pressure ◽  
Left Ventricular ◽  
Arterial Blood ◽  
Isoproterenol Infusion

We exposed fetuses to high-altitude (3,820 m) hypoxemia from 30 to 130 days gestation, when we measured fetal heart rate, right and left ventricular outputs with electromagnetic flow probes, and arterial blood pressure during an isoproterenol dose-response infusion. We also measured the distribution of cardiac output with radiolabeled microspheres during the maximal isoproterenol dose. Baseline fetal arterial blood pressure was higher in long-term hypoxemic fetuses (50.1 +/- 1.3 vs. 43.4 +/- 1.0 mmHg) but fell during the isoproterenol infusion to 41.3 +/- 1.4 and 37.5 +/- 1.4 mmHg, respectively, at the highest dose. Heart rate was the same in both groups and did not differ during isoproterenol infusion. Baseline fetal cardiac output was lower in the hypoxemic group (339 +/- 18 vs. 436 +/- 19 ml.min-1.kg-1) due mainly to a reduction in right ventricular output. During the isoproterenol infusion, right ventricular output increased to the same extent in both hypoxemic and normoxic fetuses (approximately 35%); however, left ventricular output increased only approximately 15% in the hypoxemic group compared with approximately 40% in the normoxic group. The percent change in individual organ blood flows during isoproterenol infusion in the hypoxemic groups was not significantly different from the normoxic group. All of the mechanisms that might be responsible for the differential response of the fetal left and right ventricles to long-term hypoxia are not understood and need further exploration.

Role of sinoaortic reflexes in hemodynamic patterns of natural defense behaviors in the cat

1981 ◽  
Vol 240 (3) ◽  
pp. H421-H429 ◽  
Author(s):  
G. Baccelli ◽  
R. Albertini ◽  
A. Del Bo ◽  
G. Mancia ◽  
A. Zanchetti
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Carotid Sinus ◽  
Emotional Behavior ◽  
Natural Defense ◽  
Arterial Blood ◽  
Hemodynamic Pattern ◽  
Before And After

To evaluate whether sinoaortic afferents contribute to the hemodynamic pattern of fighting, cardiovascular changes associated with fighting were studied in cats before and after sinoaortic denervation. Sinoaortic denervation exaggerates the decrease in heart rate, cardiac output, and arterial pressure during immobile confrontation (hissing, staring but no movement). During nonsupportive fighting (fighting with forelimbs while lying on one side) and supportive fighting ( fighting while standing on four feet) sinoaortic denervation reduces the increase in heart rate and cardiac output, minimizes the mesenteric vasoconstriction, induces a fall in arterial blood pressure, but does not affect iliac vasoconstriction or vasodilatation. The hemodynamic pattern of fighting is similarly changed by temporary inactivation of carotid sinus baroreflexes by common carotid occlusion as by chronic section of sinoaortic nerves. It is concluded that sinoaortic reflexes play an important role in the cardiovascular patterns accompanying natural fighting. They favor cardiac action and allow a marked visceral vasoconstriction to occur, thus minimizing or preventing a fall in blood pressure during emotional behavior.

Low-frequency oscillations in arterial pressure and heart rate: a simple computer model

1989 ◽  
Vol 256 (6) ◽  
pp. H1573-H1579 ◽  
Author(s):  
J. B. Madwed ◽  
P. Albrecht ◽  
R. G. Mark ◽  
R. J. Cohen
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Computer Model ◽  
Low Frequency ◽  
Beta Adrenergic ◽  
Simple Computer ◽  
Effector Mechanism ◽  
Arterial Blood ◽  
Low Frequency Oscillations ◽  
Effector Mechanisms

We have previously reported that low-frequency oscillations in arterial blood pressure (ABP) and heart rate (HR) occur when conscious dogs experience severe blood loss. These low-frequency oscillations are generated by enhancement of the sympathetic nervous system and inhibition of the parasympathetic nervous system. We have developed a simple computer model to elucidate those properties critical to the generation of these oscillations. Our model incorporates several important features: 1) arterial baroreceptor feedback loops, which relate ABP to targeted HR and total peripheral resistance (TPR) values; 2) two effector outputs, HR and TPR, which are controlled by the outputs of vagal, beta-adrenergic, and alpha-adrenergic effector mechanisms; 3) a fixed beat-to-beat stroke volume; and 4) a wind-kessel model, which represents the peripheral circulation. Each effector mechanism is modeled as a low-pass filter in series with a delay. The vagal effector mechanism slows the HR after a 100-ms delay and reaches maximal HR at that time. The beta-adrenergic effector mechanism speeds HR after a 2.5-s delay and then increases to maximal HR 7.5 s later. The alpha-adrenergic effector mechanism begins vasoconstriction after a 5-s delay and then reaches maximal contraction 15 s later. Computer simulations of inhibition of the vagal effector mechanism and activation of the adrenergic effector mechanisms elicit low-frequency oscillations in ABP and HR. These oscillations are similar to those observed experimentally in the dog during hemorrhage. We conclude that the slow temporal response of the alpha-adrenergic effector mechanism controlling TPR is the critical element in predicting the observed low-frequency oscillations in ABP and HR.

Very-low-frequency oscillations in heart rate and blood pressure in periodic breathing: role of the cardiovascular limb of the hypoxic chemoreflex

2000 ◽  
Vol 99 (2) ◽  
pp. 125 ◽  
Author(s):  
Darrel P. FRANCIS ◽  
L. Ceri DAVIES ◽  
Keith WILLSON ◽  
Piotr PONIKOWSKI ◽  
Andrew J.S. COATS ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Low Frequency ◽  
Periodic Breathing ◽  
Very Low Frequency ◽  
Low Frequency Oscillations

scholarly journals Cardiovascular assessment in horses sedated with xylazine or amitraz

2008 ◽  
Vol 60 (2) ◽  
pp. 329-334 ◽  
Author(s):  
R.L. Linardi ◽  
J.C. Canola ◽  
C.A.A. Valadão
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular Effects ◽  
Left Ventricular ◽  
Av Block ◽  
Drug Injection ◽  
Arterial Blood ◽  
Cardiovascular Side Effects ◽  
Cardiovascular Assessment ◽  
Second Degree

Cardiovascular effects due to intravenous (IV) xylazine (1.0mg/kg) or amitraz (0.1 or 0.4mg/kg) were evaluated in horses. Left ventricular function indexes, heart rate (HR), and cardiac output (CO) were measured by echocardiography. Second degree atrioventricular (AV) block was detected by electrocardiography. Invasive arterial blood pressure (AP) was also evaluated. All parameters were measured immediately before and during 60 minutes after drug injection. HR, CO, and second degree AV block were different between xylazine and amitraz-0.4mg/kg groups. Xylazine induced initial hypertension 10 minutes after injection, and hypotension was observed 30 minutes after amitraz-0.4mg/kg administration. Except for the second degree AV block which occurred only at five minutes, there was no change in the echocardiographic measurements after administration of amitraz-0.1mg/kg. Thus, amitraz-0.4mg/kg and xylazine (1.0mg/kg) induced similar cardiovascular side effects, but long-lasting action of amitraz-0.4mg/kg in the cardiovascular system was observed.

Cardiovascular effects of positive-pressure ventilation in normal subjects

1979 ◽  
Vol 47 (2) ◽  
pp. 453-461 ◽  
Author(s):  
S. S. Cassidy ◽  
W. L. Eschenbacher ◽  
C. H. Robertson ◽  
J. V. Nixon ◽  
G. Blomqvist ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Right Ventricular ◽  
Positive Pressure Ventilation ◽  
Normal Subjects ◽  
Left Ventricular ◽  
Right Atrial ◽  
Positive Pressure ◽  
Right Ventricular Filling ◽  
Ventricular Filling

In normal subjects during 15-min positive-pressure ventilation with 10 cmH2O end-expiratory pressure (PEEP), cardiac output fell 19% due to a fall in stroke volume. Transmural mean right atrial pressure rose 3.1 cmH2O and right ventricular end-diastolic diameter increased 15%. Simultaneously, left ventricular end-diastolic diameter decreased 21%, ejection time increased 11%, and velocity of circumferential fiber shortening fell 30%. Thus, right ventricular filling increased and left ventricular filling decreased. The function of the right ventricle was impaired and the function of the left ventricle may have been impaired. Cardiac output gradually increased due to a 7% increase in heart rate as PEEP was continued for 1 h and transmural mean right atrial pressure also increased further by 2.4 cmH2O. Compensation for the reduced stroke volume occurred as filling pressures and heart rate rose, but ventricular function remained impaired for the entire duration of PEEP. On resuming spontaneous breathing, cardiac output and ventricular function returned to base-line levels. We conclude that the reduced cardiac output during PEEP is not due to a direct mechanical reduction in right ventricular filling.

Distribution of fetal cardiac output: importance of pacemaker location

1976 ◽  
Vol 231 (1) ◽  
pp. 204-208 ◽  
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.

Effect of methylene blue on cardiac output response to exercise in dogs

1986 ◽  
Vol 61 (6) ◽  
pp. 2012-2017 ◽  
Author(s):  
N. Imai ◽  
J. I. Paley ◽  
H. S. Barold ◽  
C. S. Liang
Keyword(s):  
Heart Rate ◽  
Methylene Blue ◽  
Cardiac Output ◽  
Treadmill Exercise ◽  
Left Ventricular ◽  
O2 Consumption ◽  
Arterial Blood ◽  
Arterial Blood Lactate ◽  
Total Body ◽  
Pyruvate Ratio

To determine whether the increase in cardiac output during mild to moderate exercise is related to an increase in the tissue redox potential, we compared the responses of cardiac output, total body oxygen consumption, and arterial blood lactate-to-pyruvate ratio (a measure of NADH/NAD) to treadmill exercise between dogs treated with normal saline and those treated with a hydrogen acceptor, new methylene blue. Normal saline was infused into the left atrium in the first group of dogs at a rate of 0.38 ml/min throughout the treadmill exercise (2.5 mph and 5.0 mph on a 6% incline, each for 20 min). In the second group, methylene blue was administered as a loading dose (4 mg/kg) before exercise, followed by a continuous infusion (0.15 mg X kg-1 X min-1) throughout exercise. A similar infusion of methylene blue was given to a third group of dogs without exercise; it reduced the arterial lactate-to-pyruvate ratio from 6.70 +/- 0.35 to 4.12 +/- 0.27 but had no or little effects on cardiac output, heart rate, arterial pressure, and left ventricular dP/dt and (dP/dt)/P. Treadmill exercise doubled cardiac output and increased total body O2 consumption three- to fourfold in the first two groups but increased arterial blood lactate-to-pyruvate ratio only in group 1 (6.0 +/- 0.54 to 9.97 +/- 0.91). The relationship between cardiac output and total body O2 consumption was unaffected by the simultaneous administration of methylene blue during exercise. Groups 1 and 2 also did not differ in their heart rate, left ventricular dP/dt and (dP/dt)/P, and plasma catecholamine responses to exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Sign in / Sign up

Export Citation Format

Share Document