<i>Pulmonary Circulation at Sea Level and at High Altitudes</i>

Canepa, A; Chávez, Roberto; Hurtado, Alberto; Rotta, Andrés; Velasquez, T.

doi:10.1152/jappl.1956.9.3.328

Cited by 194 publications

(51 citation statements)

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“…Our study showed an increase in HR to similar levels in both hypoxic exposures which had not reached a plateau by the end of the 8 h exposure. This is consistent with data obtained by other workers over longer periods of time in humans (for example, Grover, Reeves, Maher, McCullough, Cruz, Denniston & Cymerman, 1976;Hoon, Balasubramanian, Mathew, Tiwari, Sharma & Chadha, 1977) and in sheep (Krasney et al 1984(Krasney et al , 1985, although HR may return to sea level values in well-acclimatized subjects up to an altitude of 4500 m (Rotta, Canepa, Hurtado, Velasquez & Chavez, 1956;Peniazola, Sime, Branchero, Gamboa, Cruz & Marticorena, 1963). Any slow components of the response persisting during the recovery period have not been studied in detail, although data from a study by Hoon et al (1977) suggest that HR might still be elevated several hours after the relief of hypoxia.…”

Section: Techniquessupporting

confidence: 92%

Effects of 8h of eucapnic and poikilocapnic hypoxia on middle cerebral artery velocity and heart rate in humans

Clar

Pedersen²,

Poulin³

et al. 1997

Experimental Physiology

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SUMMARYThis study examines the effects of prolonged hypoxia, with and without control of end-tidal CO2 partial pressure (PET,CO2), on the intensity-weighted mean velocity of blood flow in the middle cerebral artery (VIwM) and on heart rate (HR). Specifically, the time course of the responses, their reversibility with brief periods of hyperoxia and the recovery phase following prolonged hypoxia were all investigated. Twelve subjects were studied, of whom nine provided satisfactory data. A purpose-built chamber was used for the prolonged control of the end-tidal gases, and an end-tidal forcing system was used for generating the brief variations in end-tidal gases. Three 16 h protocols were employed: (1) 8 h eucapnic (average PET,CO, 39 mmHg) hypoxia (end-tidal 02 partial pressure, PETO, = 55 mmHg) followed by 8 h eucapnic euoxia (PETO2 = 100 mmHg); (2) 8 h poikilocapnic (average PET,Co2 4 mmHg below eucapnia) hypoxia (PET,02 = 55 mmHg) followed by 8 h poikilocapnic euoxia (PET,O0 = 100 mmHg); and (3) control (air inspired throughout). VIwM (using Doppler ultrasound) and HR were measured during brief exposures to hypoxic/euoxic and hyperoxic conditions with PET,CO, held 1-2 mmHg above eucapnia, at 0, 20, 240 and 480 min in the first 8 h, and at the same times in the second 8 h. There were no significant trends in VIWM under hypoxic conditions for either hypoxic protocol (ANOVA) and no significant differences between the three protocols for VIwM in hyperoxia (ANOVA). In contrast to VIWM, there was a significant increase in HR over time during both hypoxic exposures (P < 0.01, ANOVA). HR increased to a similar extent for the two types of hypoxia, and there was some suggestion that HR remained elevated after the relief of hypoxia. The results suggest that, with the level of hypoxia employed, progressive changes in HR occur, but that this level and duration of hypoxia has little sustained effect on VIWM.

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Section: Techniquessupporting

confidence: 92%

Effects of 8h of eucapnic and poikilocapnic hypoxia on middle cerebral artery velocity and heart rate in humans

Clar

Pedersen²,

Poulin³

et al. 1997

Experimental Physiology

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“…[17]. Table I lists the \,alucs obtaincd for intracardiac and great vcssel prcssurcs, which were generally similar to thosc in the literature [I, 4,5,16,18,19,[22][23][24]261.…”

Section: Lpft ~Lentriclementioning

confidence: 53%

Hemodynamic Findings in Normal Children

et al. 1967

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ExtractWe have studied cardiac function and dynamics in 29 apparently normal children under 20 years of age. Table I lists the values obtained for intracardiac and great vessel pressures. There was no correlation of these pressures with either age or increasing body size. Except for the possibility that our data is inadequate for patients under one week of age, these pressures as well as the ratio between pulmonary artery mean to systemic artery mean (fig. l ) , appear to be constant throughout the pediatric age range. Arterio-venous differences ranged from 28 to 78 ml of 0,/1 of blood. The mean was 44.3 ml/l with a S.D. of 15.0.Left ventricular cavity diameters are shown for 11 normal children from our series and 9 patients from the literature (fig.4). The two measurements recorded in the youngest subjects are elevated, probably as a result of our inability to distinguish that area of left ventricular 'wall' occupied by the thymus. The ratio of the left ventricular cavity diameter to wall thickness was 7.0 ( fig. 5).Calculated systemic, total pulmonary and pulmonary arteriolar resistances appeared to be inversely related to age, height, and weight. Therefore, it seemed that non-linear regression formulae employing the inverse of age, height and weight would be more suitable (table 111). Height alone gave the best correlation with all cardiac functions except output.Calculated resistances for both systemic and pulmonary circulations fall with increasing age at approximately the same rate (figs. 6-8). As systemic blood flow increases to accommodate the needs of increasing body size, the denominator of the DC resistance term increases and 'resistance' decreases.Since in the absence ofshunts, pulmonary blood flow must parallel the increase in systemic blood flow, pulmonary 'resistance' decreases pari passu. SpeculationHigh speed digital computers now make the development of regression equations increasingly simple. These equations will be increasingly employed by clinical investigators in place of 'surface area'.I t is also obvious that calculated 'resistances' tell us far less about the vascular bed than was formerly believed. Input impedance calculation will be employed in the future, particularly as better methods for measuring instantaneous flow become available.

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“…An inverse relationship between SpO 2 and PAP was reported as early as 1957 at 4540m 44 50 , and blood viscosity 29 . To provide insight into this latter point, we corrected both lowlander and Sherpa PASP values to a sea level HCT (45%).…”

Section: Discussionmentioning

confidence: 93%

Chemoreceptor Responsiveness at Sea Level Does Not Predict the Pulmonary Pressure Response to High Altitude

Hoiland

Foster

Donnelly

et al. 2015

Chest

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Abstract:The hypoxic ventilatory response (HVR) at sea level (SL) is moderately predictive of the change in pulmonary artery systolic pressure (PASP) to acute normobaric hypoxia. However, because of progressive changes in the chemoreflex control of breathing and acid-base balance at high altitude (HA), HVR at SL may not predict PASP at HA. We hypothesized that resting peripheral oxyhemoglobin saturation (SpO 2 ) at HA would correlate better than HVR at SL to PASP at HA. In 20 participants at SL, we measured normobaric, isocapnic HVR (L/min·-%SpO 2 -1 ) and resting PASP using echocardiography.Both resting SpO 2 and PASP measures were repeated on day 2 (n=10), days 4-8 (n=12), and 2-3 weeks (n=8) after arrival at 5050m. These data were also collected at 5050m on life-long HA residents (Sherpa; n=21

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Pulmonary Circulation at Sea Level and at High Altitudes

Cited by 194 publications

References 0 publications

Effects of 8h of eucapnic and poikilocapnic hypoxia on middle cerebral artery velocity and heart rate in humans

Effects of 8h of eucapnic and poikilocapnic hypoxia on middle cerebral artery velocity and heart rate in humans

Hemodynamic Findings in Normal Children

Chemoreceptor Responsiveness at Sea Level Does Not Predict the Pulmonary Pressure Response to High Altitude

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