Operation Everest II: preservation of cardiac function at extreme altitude

1987 ◽  
Vol 63 (2) ◽  
pp. 531-539 ◽  
Author(s):  
J. T. Reeves ◽  
B. M. Groves ◽  
J. R. Sutton ◽  
P. D. Wagner ◽  
A. Cymerman ◽  
...  
Keyword(s):  
Heart Rate ◽  
Stroke Volume ◽  
Cardiac Function ◽  
Barometric Pressure ◽  
Right Atrial ◽  
O2 Uptake ◽  
Arterial Blood ◽  
Extreme Altitude ◽  
Chronic Hypoxemia ◽  
Ventricular Filling

Hypoxia at high altitude could depress cardiac function and decrease exercise capacity. If so, impaired cardiac function should occur with the extreme, chronic hypoxemia of the 40-day simulated climb of Mt. Everest (8,840 m, barometric pressure of 240 Torr, inspiratory O2 pressure of 43 Torr). In the five of eight subjects having resting and exercise measurements at the barometric pressures of 760 Torr (sea level), 347 Torr (6,100 m), 282 Torr (7,620 m), and 240 Torr, heart rate for a given O2 uptake was higher with more severe hypoxia. Slight (6 beats/min) slowing of the heart rate occurred only during exercise at the lowest barometric pressure when arterial blood O2 saturations were less than 50%. O2 breathing reversed hypoxemia but never increased heart rate, suggesting that hypoxic depression of rate, if present, was slight. For a given O2 uptake, cardiac output was maintained. The decrease in stroke volume appeared to reflect decreased ventricular filling (i.e., decreased right atrial and wedge pressures). O2 breathing did not increase stroke volume for a given filling pressure. We concluded that extreme, chronic hypoxemia caused little or no impairment of cardiac rate and pump functions.

Effect of sympathetic blockade on diurnal variation of hemodynamic patterns

1989 ◽  
Vol 256 (3) ◽  
pp. R778-R785 ◽  
Author(s):  
M. I. Talan ◽  
B. T. Engel
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Base Line ◽  
Sympathetic Blockade ◽  
Selective Blockade ◽  
Arterial Blood

Heart rate, stroke volume, and intra-arterial blood pressure were monitored continuously in each of four monkeys, 18 consecutive h/day for several weeks. The mean heart rate, stroke volume, cardiac output, systolic and diastolic blood pressure, and total peripheral resistance were calculated for each minute and reduced to hourly means. After base-line data were collected for approximately 20 days, observation was continued for equal periods of time under conditions of alpha-sympathetic blockade, beta-sympathetic blockade, and double sympathetic blockade. This was achieved by intra-arterial infusion of prazosin, atenolol, or a combination of both in concentration sufficient for at least 75% reduction of response to injection of agonists. The results confirmed previous findings of a diurnal pattern characterized by a fall in cardiac output and a rise in total peripheral resistance throughout the night. This pattern was not eliminated by selective blockade, of alpha- or beta-sympathetic receptors or by double sympathetic blockade; in fact, it was exacerbated by sympathetic blockade, indicating that the sympathetic nervous system attenuates these events. Because these findings indicate that blood volume redistribution is probably not the mechanism mediating the observed effects, we have hypothesized that a diurnal loss in plasma volume may mediate the fall in cardiac output and that the rise in total peripheral resistance reflects a homeostatic regulation of arterial pressure.

Analysis of heart rate-based control of arterial blood pressure

1996 ◽  
Vol 271 (2) ◽  
pp. H812-H822 ◽  
Author(s):  
W. C. Rose ◽  
J. S. Schwaber
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Vascular System ◽  
Reciprocal Relation ◽  
Arterial Baroreflex ◽  
Arterial Blood ◽  
Limited Effectiveness ◽  
Filling Time

Vagal control of the heart is the most rapidly responding limb of the arterial baroreflex. We created a mathematical model of the left heart and vascular system to evaluate the ability of heart rate to influence blood pressure. The results show that arterial pressure depends nonlinearly on rate and that changes in rate are of limited effectiveness, particularly when rate is increased above the basal level. A 10% change in heart rate from rest causes a change of only 2.4% in arterial pressure due to the reciprocal relation between heart rate and stroke volume; at higher rates, insufficient filling time causes stroke volume to fall. These findings agree well with published experimental data and challenge the idea that changes in heart rate alone can strongly and rapidly affect arterial pressure. Possible implications are that vagally mediated alterations in inotropic and dromotropic state, which are not included in this model, play important roles in the fast reflex control of blood pressure or that the vagal limb of the baroreflex is of rather limited effectiveness.

Interaction of hyperthermia and heart rate on stroke volume during prolonged exercise

2010 ◽  
Vol 109 (3) ◽  
pp. 745-751 ◽  
Author(s):  
Joel D. Trinity ◽  
Matthew D. Pahnke ◽  
Joshua F. Lee ◽  
Edward F. Coyle
Keyword(s):  
Heart Rate ◽  
Stroke Volume ◽  
Heat Dissipation ◽  
Low Dose ◽  
Prolonged Exercise ◽  
Treatment Time ◽  
Placebo Control ◽  
Experimental Conditions ◽  
Time Interaction ◽  
Ventricular Filling

People who become hyperthermic during exercise display large increases in heart rate (HR) and reductions in stroke volume (SV). It is not clear if the reduction in SV is due primarily to hyperthermia or if it is a secondary effect of an elevation in HR reducing ventricular filling. In the present study, the upward drift of HR during prolonged exercise was prevented by a very small dose of the β1-adrenoreceptor blocker (atenolol; βB), thus allowing SV to be compared at a given HR during normothermia and hyperthermia. Eleven men cycled for 60 min at 57% of peak O2 uptake after receiving placebo control (PL) or a low dose (0.2 mg/kg) of βB. Hyperthermia was induced by reducing heat dissipation during exercise. Four experimental conditions were studied: normothermia-PL, normothermia-βB, hyperthermia-PL, and hyperthermia-βB. Hyperthermia increased skin and core temperature by 4.3°C and 0.8°C ( P < 0.01), respectively. βB prevented HR elevation with hyperthermia: HR values were similar at minute 60 during normothermia-PL and hyperthermia-βB (155 ± 11 and 154 ± 13 beats/min, respectively, P = 0.82). However, SV was increased by 7% during the final 20 min of exercise during hyperthermia-βB compared with normothermia-PL (treatment × time interaction, P = 0.03). In conclusion, when matched for HR, mild hyperthermia increased SV during exercise. Furthermore, the reduction in SV throughout prolonged exercise under normothermic and mildly hyperthermic conditions appears to be due to the increase in HR.

Heart Rate/Stroke Volume Relationship During Upright Exercise in Long-Term Diabetics

1993 ◽  
Vol 18 (2) ◽  
pp. 148-162
Author(s):  
R. G. Haennel ◽  
K. K. Teo ◽  
A. Suthijumroon ◽  
M. P. J. Senaratne ◽  
M. Hetherington ◽  
...  
Keyword(s):  
Heart Rate ◽  
Stroke Volume ◽  
Cardiac Function ◽  
Autonomic Function ◽  
Valsalva Maneuver ◽  
Peak Exercise ◽  
Initial Increase ◽  
Key Words Diabetes Mellitus ◽  
Key Words Diabetes ◽  
Deep Breathing

The changes in stroke volume (SV) during upright exercise were studied in 20 insulin-dependent diabetics (IDDM) and 20 age- and sex-matched controls. None of the diabetics had any cardiovascular symptoms. In addition, tests of autonomic function were conducted in the diabetics, assessing changes in heart rate (HR) during deep breathing and the Valsalva maneuver. During exercise the SV in the controls gradually increased and then remained essentially unchanged until maximum HR was achieved. Seven of the diabetics failed to sustain an initial increase in SV (fall > 15%), eight showed a "delayed" increase in SV, and the remaining five demonstrated an increasing SV over the range from rest to peak exercise. Abnormal autonomic function results were found during deep breathing (four diabetics) and the Valsalva maneuver (four diabetics). Findings indicate that cardiac function could be abnormal in IDDM without evidence of autonomic dysfunction. This abnormality could be due to a specific cardiomyopathy. Key words: diabetes mellitus, cardiac function, upright exercise, autonomic neuropathy, cardiomyopathy

scholarly journals CARDIAC FUNCTION DURING MINI-INVASIVE REPAIR OF PECTUS EXCAVATUM WITH THE NUSS PROCEDURE

2021 ◽  
Vol 74 (8) ◽  
pp. 1809-1815
Author(s):  
Ulbolhan A. Fesenko ◽  
Ivan Myhal
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Cardiac Index ◽  
Stroke Volume ◽  
Cardiac Function ◽  
Epidural Anaesthesia ◽  
Pectus Excavatum ◽  
Stroke Volume Index ◽  
Volume Index ◽  
Nuss Procedure

The aim of the study was to analyze cardiac function during Nuss procedure under the combination of general anesthesia with different variants of the regional block. Materials and methods: The observative prospective study included 60 adolescents (boys/girls=47/13) undergone Nuss procedure for pectus excavatum correction under the combination of general anaesthesia and regional blocks. The patients were randomized into three groups (n=20 in each) according to the perioperative regional analgesia technique: standart epidural anaesthesia (SEA), high epidural anaesthesia (HEA) and bilateral paravertebral anaesthesia (PVA). The following parameters of cardiac function were analyzed: heart rate, estimated cardiac output (esCCO), cardiac index (esCCI), stroke volume (esSV) and stroke volume index (esSVI) using non-invasive monitoring. Results: Induction of anesthesia and regional blocks led to a significant decrease in esCCO (-9.4%) and esCCI (-9.8%), while esSV and esSVI remained almost unchanged in all groups (H=4.9; p=0.09). At this stage, the decrease in cardiac output was mainly due to decreased heart rate. At the stage of sternal elevation we found an increase in esSV, which was more pronounced in the groups of epidural blocks (+23.1% in HEA and +18.5% in SEA). After awakening from anesthesia and tracheal extubation esSV was by 11% higher than before surgery without ingergroup difference. Conclusions: The Nuss procedure for pectus excavatum correction lead to improved cardiac function. increase in stroke volume and its index were more informative than cardiac output and cardiac index which are dependent on heart rate that is under the influence of anaesthesia technique.

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.

Altered hormonal regulation and blood flow distribution with cardiovascular deconditioning after short-duration head down bed rest

2007 ◽  
Vol 103 (6) ◽  
pp. 2018-2025 ◽  
Author(s):  
D. Fischer ◽  
P. Arbeille ◽  
J. K. Shoemaker ◽  
D. D. O'Leary ◽  
R. L. Hughson
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Stroke Volume ◽  
Vascular Resistance ◽  
Hormonal Regulation ◽  
Venous Pressure ◽  
Plasma Concentrations ◽  
Bed Rest ◽  
Arterial Blood

This study tested the hypothesis that cardiovascular and hormonal responses to lower body negative pressure (LBNP) would be altered by 4-h head down bed rest (HDBR) in 11 healthy young men. In post-HDBR testing, three subjects failed to finish the protocol due to presyncopal symptoms, heart rate was increased during LBNP compared with pre-HDBR, mean arterial blood pressure was elevated at 0, −10, and −20 mmHg and reduced at −40 mmHg, central venous pressure (CVP) and cardiac stroke volume were reduced at all levels of LBNP. Plasma concentrations of renin, angiotensin II, and aldosterone were significantly lower after HDBR. Renin and angiotensin II increased in response to LBNP only post-HDBR. There was no effect of HDBR or LBNP on norepinephrine while epinephrine tended to increase at −40 mmHg post-HDBR ( P = 0.07). Total blood volume was not significantly reduced. Splanchnic blood flow taken from ultrasound measurement of the portal vein was higher at each level of LBNP post-compared with pre-HDBR. The gain of the cardiopulmonary baroreflex relating changes in total peripheral resistance to CVP was increased after HDBR, but splanchnic vascular resistance was actually reduced. These results are consistent with our hypothesis and suggest that cardiovascular instability following only 4-h HDBR might be related to altered hormonal and/or neural control of regional vascular resistance. Impaired ability to distribute blood away from the splanchnic region was associated with reduced stroke volume, elevated heart rate, and the inability to protect mean arterial pressure.

Right atrial pressure and ANP release during prolonged exercise in a hot environment

1994 ◽  
Vol 76 (5) ◽  
pp. 1882-1887 ◽  
Author(s):  
H. Nose ◽  
A. Takamata ◽  
G. W. Mack ◽  
T. Kawabata ◽  
Y. Oda ◽  
...  
Keyword(s):  
Heart Rate ◽  
Prolonged Exercise ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Plasma Norepinephrine ◽  
Temperature Plasma ◽  
Blood Temperature ◽  
Hot Environment ◽  
Arterial Blood

To investigate the relationship between right atrial pressure (RAP) and atrial natriuretic peptide (ANP) release during prolonged exercise in a hot environment (30 degrees C, 20% relative humidity), we studied with a Swan-Ganz catheter five male volunteers exercising on a cycle ergometer at 60% of peak aerobic power for 50 min. The ANP level increased from 14 +/- 3 (SE) to 69 +/- 10 pg/ml (P < 0.001) during the first 10 min of exercise as RAP rose from 4.3 +/- 0.8 to 6.9 +/- 1.1 mmHg (P < 0.001). The 10-min ANP level was significantly correlated with RAP (r = 0.88, P < 0.05) but not with heart rate, pulmonary arterial blood temperature, plasma norepinephrine, or plasma epinephrine. The 10-min RAP value was inversely correlated with blood volume (r = -0.98, P < 0.01) and also with stroke volume (r = -0.96, P < 0.01). In the next 20 min of exercise, ANP continued to increase to 101 +/- 12 pg/ml (P < 0.02 vs. 10 min) and remained at this level until 50 min of exercise, whereas RAP decreased and reached a level not significantly different from baseline at 50 min (5.7 +/- 1.0 mmHg; P < 0.01 vs. 10 min). This dissociation of ANP and RAP may have been related to the significant increases from the 10-min values of heart rate, blood temperature, norepinephrine (all P < 0.01), and epinephrine (P < 0.02) during the same period. These results suggest that ANP release is primarily controlled by atrial distension at the onset of exercise but that other stimulators may be involved thereafter.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular function and norepinephrine-thermogenesis in cold-acclimatized rats

1963 ◽  
Vol 204 (5) ◽  
pp. 888-894 ◽  
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).

Maximum cardiac performance of rainbow trout (Oncorhynchus mykiss) at temperatures approaching their upper lethal limit

1996 ◽  
Vol 199 (3) ◽  
pp. 663-672 ◽  
Author(s):  
A Farrell ◽  
A Gamperl ◽  
J Hicks ◽  
H Shiels ◽  
K Jain
Keyword(s):  
Heart Rate ◽  
Rainbow Trout ◽  
Stroke Volume ◽  
Cardiac Function ◽  
Cardiac Performance ◽  
Preferred Temperature ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Lethal Limit ◽  
Q10 Values

Numerous studies have examined the effect of temperature on in vivo and in situ cardiovascular function in trout. However, little information exists on cardiac function at temperatures near the trout's upper lethal limit. This study measured routine and maximum in situ cardiac performance in rainbow trout (Oncorhynchus mykiss) following acclimation to 15, 18 and 22 &deg;C, under conditions of tonic (30 nmol l-1), intermediate (60 nmol l-1) and maximal (200 nmol l-1) adrenergic stimulation. Heart rate increased significantly with both temperature and adrenaline concentration. The Q10 values for heart rate ranged from 1.28 at 30 nmol l-1 adrenaline to 1.36 at 200 nmol l-1 adrenaline. In contrast to heart rate, maximum stroke volume declined by approximately 20 % (from 1.0 to 0.8 ml kg-1) as temperature increased from 15 to 22 &deg;C. This decrease was not alleviated by maximally stimulating the heart with 200 nmol l-1 adrenaline. Because of the equal and opposite effects of increasing temperature on heart rate and stroke volume, maximum cardiac output did not increase between 15 and 22 &deg;C. Maximum power output decreased (by approximately 10-15 %) at all adrenaline concentrations as temperature increased. This reduction reflected a poorer pressure-generating ability at temperatures above 15 &deg;C. These results, in combination with earlier work, suggest (1) that peak cardiac performance occurs around the trout's preferred temperature and well below its upper lethal limit; (2) that the diminished cardiac function concomitant with acclimation to high temperatures was associated with inotropic failure; (3) that Q10 values for cardiac rate functions, other than heart rate per se, have a limited predictive value at temperatures above the trout's preferred temperature; and (4) that heart rate is a poor indicator of cardiac function at temperatures above 15 &deg;C.

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