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NEW FINDINGS: What is the central question of this study? Does chronic mountain sickness (CMS) alter sympathetic neural control and arterial baroreflex regulation of blood pressure in Andean (Quechua) highlanders? What is the main finding and its importance? Compared to healthy Andean highlanders, basal sympathetic vasomotor outflow is lower, baroreflex control of muscle sympathetic nerve activity is similar, supine heart rate is lower and cardiovagal baroreflex gain is greater in mild CMS. Taken together, these findings reflect flexibility in integrative regulation of blood pressure that may be important when blood viscosity and blood volume are elevated in CMS. ABSTRACT: The high-altitude maladaptation syndrome chronic mountain sickness (CMS) is characterized by excessive erythrocytosis and frequently accompanied by accentuated arterial hypoxaemia. Whether altered autonomic cardiovascular regulation is apparent in CMS is unclear. Therefore, during the 2018 Global REACH expedition to Cerro de Pasco, Peru (4383 m), we assessed integrative control of blood pressure (BP) and determined basal sympathetic vasomotor outflow and arterial baroreflex function in eight Andean natives with CMS ([Hb] 22.6 ± 0.9 g·dL(-1) ) and seven healthy highlanders ([Hb] 19.3 ± 0.8 g·dL(-1) ). R-R interval (RRI, electrocardiogram), beat-by-beat BP (photoplethysmography) and muscle sympathetic nerve activity (MSNA; microneurography) were recorded at rest and during pharmacologically induced changes in BP (modified Oxford test). Although [Hb] and blood viscosity (7.8 ± 0.7 vs. 6.6 ± 0.7 cP; d = 1.7, P = 0.01) were elevated in CMS compared to healthy highlanders, cardiac output, total peripheral resistance and mean BP were similar between groups. The vascular sympathetic baroreflex MSNA set-point (i.e. MSNA burst incidence) and reflex gain (i.e. responsiveness) were also similar between groups (MSNA set-point, d = 0.75, P = 0.16; gain, d = 0.2, P = 0.69). In contrast, in CMS the cardiovagal baroreflex operated around a longer RRI (960 ± 159 vs. 817 ± 50 ms; d = 1.4, P = 0.04) with a greater reflex gain (17.2 ± 6.8 vs. 8.8 ± 2.6 ms·mmHg(-1) ; d = 1.8, P = 0.01) versus healthy highlanders. Basal sympathetic vasomotor activity was also lower compared to healthy highlanders (33 ± 11 vs. 45 ± 13 bursts·min(-1) ; d = 1.0, P = 0.08). In conclusion, our findings indicate adaptive differences in basal sympathetic vasomotor activity and heart rate compensate for the haemodynamic consequences of excessive erythrocyte volume and contribute to integrative blood pressure regulation in Andean highlanders with mild CMS.

We report a new pulmonary circulation model during cardiopulmonary bypass that is able to cause pulmonary congestion but without left heart failure. This kind of congestion is characterized by right and left heart output mismatching. The pathophysiological mechanism, clinical manifestations, diagnosis, differential diagnosis, and treatment of this pulmonary congestion are reviewed and discussed in the following article.

This paper aims to explore the diagnostic value of noninvasive cardiac function measurement for hypertension in pregnancy. One hundred and fifty-eight cases of gestational hypertension in our hospital were analyzed retrospectively while 30 healthy pregnant women were served as normal controls. The heart function parameters in the two groups were measured with noninvasive cardiac function analyzer, such as myocardial contractive force indexes (JP, VP), impedance indexes (RTM, RS), volume load indexes (GCV, LVDP) and left heart output index (LCI). In all 158 cases of gestational hypertension, the myocardial contractive force indexes, impedance indexes and left heart output index increased unusually. The difference between the two groups was statistically significant (P

In this review, we present the relation between power generation capabilities and pulmonary oxygen uptake during incremental cycling exercise in humans and the effect of exercise intensity on the oxygen cost of work. We also discuss the importance of oxygen delivery to the working muscles as a factor determining maximal oxygen uptake in humans. Subsequently, we outline the importance of coronary blood flow, myocardial oxygen uptake and myocardial metabolic stability for exercise tolerance. Finally, we describe mechanisms of endothelium-dependent regulation of coronary and skeletal muscle blood flow, dysregulation of which may impair exercise capacity and increase the cardiovascular risk of exercise.

We determined whether store-operated channels (SOC) are involved in neonatal pulmonary artery function under conditions of acute and chronic hypoxia, using newborn sheep gestated and born either at high altitude (HA, 3,600 m) or low altitude (LA, 520 m). Cardiopulmonary variables were recorded in vivo, with and without SOC blockade by 2-aminoethyldiphenylborinate (2-APB), during basal or acute hypoxic conditions. 2-APB did not have effects on basal mean pulmonary arterial pressure (mPAP), cardiac output, systemic arterial blood pressure, or systemic vascular resistance in both groups of neonates. During acute hypoxia 2-APB reduced mPAP and pulmonary vascular resistance in LA and HA, but this reduction was greater in HA. In addition, isolated pulmonary arteries mounted in a wire myograph were assessed for vascular reactivity. HA arteries showed a greater relaxation and sensitivity to SOC blockers than LA arteries. The pulmonary expression of two SOC-forming subunits, TRPC4 and STIM1, was upregulated in HA. Taken together, our results show that SOC contribute to hypoxic pulmonary vasoconstriction in newborn sheep and that SOC are upregulated by chronic hypoxia. Therefore, SOC may contribute to the development of neonatal pulmonary hypertension. We propose SOC channels could be potential targets to treat neonatal pulmonary hypertension.

A pilot study aimed to introduce intraoperative monitoring of liver surgery using transoesophageal echocardiography (TEE) is described. A set of TEE measurements was established as a protocol, consisting of left atrial (LA) dimension at the aortic valve plane; mitral velocity flow integral, calculation of stroke volume and cardiac output (CO); mitral annular plane systolic excursion; finally, right atrial area. A total of 165 measurements (on 21 patients) were performed, 31 occurring during hypotension. The conclusions reached were during acute blood loss LA dimension changed earlier than CVP, and, in one patient, a dynamic left ventricular (LV) obstruction was observed; in 3 patients a transient LV systolic dysfunction was documented. The comparison between 39 CO paired measurements obtained by TEE and PiCCO2 revealed a statistically significant correlation (P<0.001,r=0.83). In this pilot study TEE successfully answered the questions raised by the anesthesiologists. Larger cohort studies are needed to address this issue.

Purpose. Despite the increasing popularity of marathon running, there are no data on the responses of stroke volume (SV) and cardiac output (CO) to exercise in this context. We sought to establish whether marathon performance is associated with the ability to sustain high fractional use of maximal SV and CO (i.e, cardiac endurance) and/or CO, per meter (i.e., cardiac cost).Methods. We measured the SV, heart rate (HR), CO, and running speed of 14 recreational runners in an incremental, maximal laboratory test and then during a real marathon race (mean performance: 3 hr 30 min±45 min).Results. Our data revealed that HR, SV and CO were all in a high but submaximal steady state during the marathon (87.0±1.6%, 77.2±2.6%, and 68.7±2.8% of maximal values, respectively). Marathon performance was inversely correlated with an upward drift in the CO/speed ratio (mL ofCO×m−1) (r=−0.65,P<0.01) and positively correlated with the runner’s ability to complete the race at a high percentage of the speed at maximal SV (r=0.83,P<0.0002).Conclusion. Our results showed that marathon performance is inversely correlated with cardiac cost and positively correlated with cardiac endurance. The CO response could be a benchmark for race performance in recreational marathon runners.

In three clinical centres, we compared a new method for measuring cardiac output with conventional thermodilution. The new method computes beat-to-beat cardiac output from radial artery pressure by simulating a three-element model of aortic input impedance, and includes non-linear aortic mechanical properties and a self-adapting systemic vascular resistance. We compared cardiac output by continuous model simulation (MF) with thermodilution cardiac output (TD) in 54 patients (18 female, 36 male) undergoing coronary artery bypass surgery. We made three or four conventional thermodilution estimates spread equally over the ventilatory cycle. In 490 series of measurements, thermodilution cardiac output ranged from 2.1 to 9.3, mean 5.0 litre min(-1). MF differed +0.32 (1.0) litre min(-1) on average with limits of agreement of -1.68 and +2.32 litre min(-1). Differences decreased when the first series of measurements in a patient was used to calibrate the model. In 436 remaining series, the mean difference became -0.13 (0.47) litre min(-1) with limits of agreement of -1.05 and +0.79 litre min(-1). When consecutive measurements were made, the change was greater than 0.5 litre min(-1), on 204 occasions. The direction of change was the same with both methods in 199. The difference between the methods remained near zero during surgery suggesting that a single calibration per patient was adequate. Aortic model simulation with radial artery pressure as input reliably monitors changes in cardiac output in cardiac surgery patients. Before calibration, the model cannot replace thermodilution, but after calibration the model method can quantitatively replace further thermodilution estimates.

It is generally accepted that the left ventricle (LV) hypertrophies (LVH) to normalize systolic wall stress (ςs) in chronic pressure overload. However, LV filling pressure (Pv) may be elevated as well, supporting the alternative hypothesis of end-diastolic wall stress (ςd) normalization in LVH. We used an LV time-varying elastance model coupled to an arterial four-element lumped-parameter model to study ventricular-arterial interaction in hypertension-induced LVH. We assessed model parameters for normotensive controls and applied arterial changes as observed in hypertensive patients with LVH (resistance +40%, compliance −25%) and assumed 1) no cardiac adaptation, 2) normalization of ςs by LVH, and 3) normalization of ςs by LVH and increase in Pv, such that ςd is normalized as well. In patients, systolic and diastolic blood pressures increase by ∼40%, cardiac output (CO) is constant, and wall thickness increases by 30–55%. In scenarios 1 and 2, blood pressure increased by only 10% while CO dropped by 20%. In scenario 2, LV wall thickness increased by only 10%. The predictions of scenario 3 were in qualitative and quantitative agreement with in vivo human data. LVH thus contributes to the elevated blood pressure in hypertension, and cardiac adaptations include an increase in Pv, normalization of ςs, and preservation of CO in the presence of an impaired diastolic function.

Effects of arteriovenous fistulas on cardiac oxygen supply and demand.BackgroundArteriovenous (AV) fistulas used for hemodialysis access may affect cardiac load by increasing the preload while decreasing the afterload. In dogs, AV fistulas have also been shown to affect coronary perfusion negatively. We investigated the net effect of AV fistulas on cardiac oxygen supply and demand.MethodsAortic pressure waves were reconstructed from finger pressure recordings obtained on the nonfistula arm using a wave-form filter. Changes in systolic, mean, and diastolic aortic pressure were calculated, together with changes in heart rate (HR), stroke volume (SV), cardiac output (CO), and systemic vascular resistance (SVR) during a 60-second compression of AV fistulas in 10 patients. Changes in cardiac supply and demand were estimated by calculating the area under the aortic pressure curve during diastole [diastolic pressure time index (DPTI)] and systole [systolic pressure time index (SPTI)], respectively.ResultsDuring fistula compression, systolic, mean and diastolic pressure increased by 4.2 ± 4.3, 2.6 ± 3.0, and 2.8 ± 2.9mm Hg (mean ± sd, all P < 0.05). The HR decreased by 3.8 ± 2.5 beats per minute (P < 0.01), and SV decreased 3.7 ± 6.1% (NS). CO decreased 9.4 ± 8.6%, and SVR increased 14.3 ± 11.7% (both P < 0.05). The SPTI increased by 1.5 ± 1.5mm Hg · sec (P < 0.01), and the DPTI increased by 7.6 ± 8.1mm Hg · sec (14.8% increase, P < 0.05) during compression. The ratio of supply and demand (DPTI/SPTI) improved by 13.5 ± 13.0% (P < 0.01) when the fistula was compressed.ConclusionAV fistulas have a small effect on left ventricular oxygen demand, but decrease cardiac oxygen supply considerably.

1. The effects of bed rest on the cardiovascular and muscular parameters which affect maximal O2 consumption (VO2,max) were studied. The fractional limitation of VO2,max imposed by these parameters after bed rest was analysed. 2. The VO2,max, by standard procedure, and the maximal cardiac output (Qmax), by the pulse contour method, were measured during graded cyclo-ergometric exercise on seven subjects before and after a 42-day head-down tilt bed rest. Blood haemoglobin concentration ([Hb]) and arterialized blood gas analysis were determined at the highest work load. 3. Muscle fibre types, oxidative enzyme activities, and capillary and mitochondrial densities were measured on biopsy samples from the vastus lateralis muscle before and at the end of bed rest. The measure of muscle cross-sectional area (CSA) by NMR imaging at the level of biopsy site allowed computation of muscle oxidative capacity and capillary length. 4. The VO2,max was reduced after bed rest (-16.6%). The concomitant decreases in Qmax (-30.8%), essentially due to a change in stroke volume, and in [Hb] led to a huge decrease in O2 delivery (-39.7%). 5. Fibre type distribution was unaffected by bed rest. The decrease in fibre area corresponded to the significant reduction in muscle CSA (-17%). The volume density of mitochondria was reduced after bed rest (-16.6%), as were the oxidative enzyme activities (-11%). The total mitochondrial volume was reduced by 28.5%. Capillary density was unchanged. Total capillary length was 22.2% lower after bed rest, due to muscle atrophy. 6. The interaction between these muscular and cardiovascular changes led to a smaller reduction in VO2,max than in cardiovascular O2 transport. Yet the latter appears to play the greatest role in limiting VO2,max after bed rest (> 70% of overall limitation), the remaining fraction being shared between peripheral O2 diffusion and utilization.

The dp/dt values and peripheral resistance were calculated by the Wigers method [3]: P = D/MO.1322, where P is the peripheral resistance (in dynes'sec'cm-S), D is the average arterial pressure (in mm Hg), and MV is the heart output (in ml/sec); RCV-D/CF, where RCV is coronary vessel resistance, D is the average arterial pressure (in mm Hg), and CF is the coronary flow (in ml/min); RFV = D/FF, where RFV is the resistance of the femoral vessels, D is the average arterial pressure (in mm Hg), and FF is the femoral flow rate (in ml/min).

That the heart output increases during pregnancy has been demonstrated in both animals and the human being.1In a normal pregnancy the cardiac output begins to increase at about the fourth month, from which time on there is a steady rise until term is reached. This increase in cardiac output during normal gestation, expressed in terms of volume of blood passing through the heart in unit time, is approximately 50 per cent. Following delivery the minute volume slowly returns to normal, reaching its nonpregnant level within four weeks. Unfortunately, as yet, we are ignorant of the cardiac output or work during the period of labor, although there is reason to believe that it is further augmented during parturition. It is evident that such a marked increase in the minute volume of the heart during gestation must be of the utmost importance in patients suffering from some cardiac disturbance. This