Increased cardiac output, not pulmonary artery systolic pressure, increases blood flow through intrapulmonary arteriovenous anastomoses and impairs pulmonary gas exchange efficiency (717.2)

Background: One barrier to accurate interpretation of changes in hemodynamic pressures and cardiac output is lack of data about what constitutes a normal fluctuation. Few investigators have examined normal fluctuations in these parameters and none have done so in patients with left ventricular dysfunction. Aims: To describe normal fluctuations in pulmonary artery pressures and cardiac output in patients with left ventricular dysfunction. Methods: Hemodynamically stable advanced heart failure patients ( N=39; 55±6 years old; 62% male) with left ventricular dysfunction (mean ejection fraction 22±5%) were studied. Cardiac output and pulmonary artery pressures were measured every 15 min for 2 h. Results: Mean±standard deviation fluctuations were as follows: pulmonary artery systolic pressure=7±4 mmHg; pulmonary artery diastolic pressure=6±3 mmHg; pulmonary capillary wedge pressure=5±3 mmHg; cardiac output=0.7±0.3 l/min. The coefficient of variation for fluctuations in pulmonary artery systolic pressure was 6.7%, in pulmonary artery diastolic pressure was 9.3%, in pulmonary capillary wedge pressure was 9.2%, and in cardiac output was 7.2%. Conclusions: Values that vary <8% for pulmonary artery systolic pressure, <11% for pulmonary artery diastolic pressure, <12% for pulmonary capillary wedge pressure, and <9% for cardiac output from baseline represent normal fluctuations in these parameters in patients with left ventricular dysfunction.

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Unilateral lung edema: effects on pulmonary gas exchange, hemodynamics, and pulmonary perfusion distribution

Journal of Applied Physiology ◽

10.1152/jappl.2000.89.4.1513 ◽

2000 ◽

Vol 89 (4) ◽

pp. 1513-1521 ◽

Cited By ~ 8

Author(s):

Klaus Slama ◽

Mareike Gesch ◽

Johannes C. Böck ◽

Sylvia M. Pietschmann ◽

Walter Schaffartzik ◽

...

Keyword(s):

Blood Flow ◽

Gas Exchange ◽

Pulmonary Artery ◽

Venous Pressure ◽

Pulmonary Gas Exchange ◽

The Other ◽

Lung Edema ◽

Pulmonary Perfusion ◽

Central Venous ◽

Fluorescent Microspheres

Two types of unilateral lung edema in sheep were characterized regarding their effects on pulmonary gas exchange, hemodynamics, and distribution of pulmonary perfusion. One edema type was induced with aerosolized HCl (0.15 M, pH 1.0) and the other with NaCl (0.15 M, pH 7.4). Both aerosols were nebulized continuously for 4 h into left lungs. In HCl-treated animals, pulmonary gas exchange deteriorated [from a partial arterial O2 pressure-to-inspired O2 fraction ratio (PaO2 /Fi O2 ) of 254 at baseline to 187 after 4 h HCl]. In addition, pulmonary artery pressure and total pulmonary vascular resistance increased (from 16 to 19 mmHg and from 133 to 154 dyn · s · cm−5, respectively). In NaCl-treated animals, only the central venous pressure significantly increased (from 7 to 9 mmHg). Distribution of pulmonary perfusion (measured with fluorescent microspheres) changed differently in both groups. After HCl application, 6% more blood flow was directed to the treated lung, whereas, after NaCl, 5% more blood flow was directed to the untreated lung. HCl and NaCl treatment both induce an equivalent lung edema, but only HCl treatment is associated with gas exchange alteration and tissue damage. Redistribution of pulmonary perfusion maintains gas exchange during NaCl treatment and decreases it during HCl inhalation.

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Increased cardiac output, not pulmonary artery systolic pressure, increases intrapulmonary shunt in healthy humans breathing room air and 40% O2

The Journal of Physiology ◽

10.1113/jphysiol.2014.274829 ◽

2014 ◽

Vol 592 (20) ◽

pp. 4537-4553 ◽

Cited By ~ 26

Author(s):

Jonathan E. Elliott ◽

Joseph W. Duke ◽

Jerold A. Hawn ◽

John R. Halliwill ◽

Andrew T. Lovering

Keyword(s):

Cardiac Output ◽

Pulmonary Artery ◽

Systolic Pressure ◽

Pulmonary Artery Systolic Pressure ◽

Intrapulmonary Shunt ◽

Healthy Humans ◽

Breathing Room

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Nitric oxide and cardiopulmonary hemodynamics in Tibetan highlanders

Journal of Applied Physiology ◽

10.1152/japplphysiol.00205.2005 ◽

2005 ◽

Vol 99 (5) ◽

pp. 1796-1801 ◽

Cited By ~ 76

Author(s):

Brian D. Hoit ◽

Nancy D. Dalton ◽

Serpil C. Erzurum ◽

Daniel Laskowski ◽

Kingman P. Strohl ◽

...

Keyword(s):

Nitric Oxide ◽

Blood Flow ◽

Pulmonary Artery ◽

High Altitude ◽

Sea Level ◽

Pulmonary Blood Flow ◽

Geometric Mean ◽

Systolic Pressure ◽

Pulmonary Artery Systolic Pressure ◽

Exhaled No

When O2 availability is reduced unavoidably, as it is at high altitude, a potential mechanism to improve O2 delivery to tissues is an increase in blood flow. Nitric oxide (NO) regulates blood vessel diameter and can influence blood flow. This field study of intrapopulation variation at high altitude tested the hypothesis that the level of exhaled NO (a summary measure of pulmonary synthesis, consumption, and transfer from cells in the airway) is directly proportional to pulmonary, and thus systemic, blood flow. Twenty Tibetan male and 37 female healthy, nonsmoking, native residents at 4,200 m (13,900 ft), with an average O2 saturation of hemoglobin of 85%, participated in the study. The geometric mean partial pressure of NO exhaled at a flow of 17 ml/s was 23.4 nmHg, significantly lower than that of a sea-level reference group. However, the rate of NO transfer out of the airway wall was seven times higher than at sea level, which implied the potential for vasodilation of the pulmonary blood vessels. Mean pulmonary blood flow (measured by cardiac index) was 2.7 ± 0.1 (SE) l/min, and mean pulmonary artery systolic pressure was 31.4 ± 0.9 (SE) mmHg. Higher exhaled NO was associated with higher pulmonary blood flow; yet there was no associated increase in pulmonary artery systolic pressure. The results suggest that NO in the lung may play a key beneficial role in allowing Tibetans at 4,200 m to compensate for ambient hypoxia with higher pulmonary blood flow and O2 delivery without the consequences of higher pulmonary arterial pressure.

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Sympathetic innervation of canine pulmonary artery and morphometric and functional analysis in dehydromonocrotaline-induced models after pulmonary artery denervation

Interactive CardioVascular and Thoracic Surgery ◽

10.1093/icvts/ivaa166 ◽

2020 ◽

Vol 31 (5) ◽

pp. 708-717

Author(s):

Xiaomin Jiang ◽

Juan Zhang ◽

Ling Zhou ◽

Jie Luo ◽

Jinsong Wang ◽

...

Keyword(s):

Cardiac Output ◽

Pulmonary Artery ◽

Sympathetic Nerve ◽

Nerve Conduction ◽

Nerve Conduction Velocity ◽

Sympathetic Innervation ◽

Systolic Pressure ◽

Pulmonary Artery Systolic Pressure ◽

Control Group ◽

Mean Pressure

Abstract OBJECTIVES We aimed to describe the anatomic distribution of periarterial pulmonary sympathetic nerves and to observe the long-term morphometric and functional changes after pulmonary artery denervation (PADN), a novel therapy for pulmonary arterial hypertension (PAH). METHODS A total of 45 beagles were divided into a sympathetic innervation group (n = 3, 33.3% were females), a PAH group (n = 35, 34.3% were females) and a control group (n = 7, 28.5% were females). The PAH group was randomly divided into no-PADN (n = 7), instant-PADN (n = 7), 1M-PADN (n = 7), 2M-PADN (n = 7) and 3M-PADN (n = 7) subgroups. The sympathetic innervation group was sacrificed to reveal the sympathetic innervation of pulmonary arteries. PAH was induced by injecting dehydromonocrotaline (DHMCT) through the right atrium. The pulmonary capillary wedge pressure, right ventricular systolic pressure, right ventricular mean pressure, pulmonary artery systolic pressure and pulmonary artery mean pressure of each group were continuously measured. The cardiac output was detected to calculate the pulmonary vascular resistance. PAH and control groups were subjected to immunofluorescence assay, sympathetic nerve conduction velocity measurement and transmission electron microscopy. RESULTS The no-PADN group had significantly higher PVSP, PVMP, pulmonary artery systolic pressure, pulmonary artery mean pressure and pulmonary vascular resistance but lower cardiac output than those of the control group (P < 0.05). Instant-PADN, 1M-PADN, 2M-PADN and 3M-PADN groups had significantly lower PVSP, PVMP, pulmonary artery systolic pressure, pulmonary artery mean pressure and pulmonary vascular resistance but higher cardiac output than those of the no-PADN group (P < 0.05). Most sympathetic nerves were located within 2.5 mm of the intimae of the bifurcation and proximal trunk, mainly in the left trunk. The diameter and cross-sectional area of myelinated fibres in the PAH group were significantly larger than those of the control group. Sympathetic nerve conduction velocity of the PAH group gradually decreased, and nerve fibres were almost demyelinated 3 months after PADN. CONCLUSIONS PADN effectively relieved dehydromonocrotaline-induced canine PAH and decreased sympathetic nerve conduction velocity.

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AltitudeOmics: effect of reduced barometric pressure on detection of intrapulmonary shunt, pulmonary gas exchange efficiency, and total pulmonary resistance

Journal of Applied Physiology ◽

10.1152/japplphysiol.00474.2017 ◽

2018 ◽

Vol 124 (5) ◽

pp. 1363-1376 ◽

Cited By ~ 5

Author(s):

Frank A. Petrassi ◽

James T. Davis ◽

Kara M. Beasley ◽

Oghenero Evero ◽

Jonathan E. Elliott ◽

...

Keyword(s):

Blood Flow ◽

Gas Exchange ◽

Sea Level ◽

Oxygen Tension ◽

Pulmonary Blood Flow ◽

Contrast Echocardiography ◽

Barometric Pressure ◽

Arteriovenous Anastomoses ◽

Pulmonary Resistance ◽

Flow Through

Blood flow through intrapulmonary arteriovenous anastomoses (QIPAVA) occurs in healthy humans at rest and during exercise when breathing hypoxic gas mixtures at sea level and may be a source of right-to-left shunt. However, at high altitudes, QIPAVA is reduced compared with sea level, as detected using transthoracic saline contrast echocardiography (TTSCE). It remains unknown whether the reduction in QIPAVA (i.e., lower bubble scores) at high altitude is due to a reduction in bubble stability resulting from the lower barometric pressure (PB) or represents an actual reduction in QIPAVA. To this end, QIPAVA, pulmonary artery systolic pressure (PASP), cardiac output (QT), and the alveolar-to-arterial oxygen difference (AaDO2) were assessed at rest and during exercise (70–190 W) in the field (5,260 m) and in the laboratory (1,668 m) during four conditions: normobaric normoxia (NN; [Formula: see text] = 121 mmHg, PB = 625 mmHg; n = 8), normobaric hypoxia (NH; [Formula: see text] = 76 mmHg, PB = 625 mmHg; n = 7), hypobaric normoxia (HN; [Formula: see text] = 121 mmHg, PB = 410 mmHg; n = 8), and hypobaric hypoxia (HH; [Formula: see text] = 75 mmHg, PB = 410 mmHg; n = 7). We hypothesized QIPAVA would be reduced during exercise in isooxic hypobaria compared with normobaria and that the AaDO2 would be reduced in isooxic hypobaria compared with normobaria. Bubble scores were greater in normobaric conditions, but the AaDO2 was similar in both isooxic hypobaria and normobaria. Total pulmonary resistance (PASP/QT) was elevated in HN and HH. Using mathematical modeling, we found no effect of hypobaria on bubble dissolution time within the pulmonary transit times under consideration (<5 s). Consequently, our data suggest an effect of hypobaria alone on pulmonary blood flow. NEW & NOTEWORTHY Blood flow through intrapulmonary arteriovenous anastomoses, detected by transthoracic saline contrast echocardiography, was reduced during exercise in acute hypobaria compared with normobaria, independent of oxygen tension, whereas pulmonary gas exchange efficiency was unaffected. Modeling the effect(s) of reduced air density on contrast bubble lifetime did not result in a significantly reduced contrast stability. Interestingly, total pulmonary resistance was increased by hypobaria, independent of oxygen tension, suggesting that pulmonary blood flow may be changed by hypobaria.

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Exercise- and hypoxia-induced blood flow through intrapulmonary arteriovenous anastomoses is reduced in older adults

Journal of Applied Physiology ◽

10.1152/japplphysiol.01125.2013 ◽

2014 ◽

Vol 116 (10) ◽

pp. 1324-1333 ◽

Cited By ~ 23

Author(s):

H. Cameron Norris ◽

Tyler S. Mangum ◽

Joseph W. Duke ◽

Taylor B. Straley ◽

Jerold A. Hawn ◽

...

Keyword(s):

Blood Flow ◽

Contrast Echocardiography ◽

Age Groups ◽

Systolic Pressure ◽

Arteriovenous Anastomoses ◽

Older Individuals ◽

Age Related ◽

Flow Through ◽

Pulmonary Arterial ◽

Exercise Induced

Mean pulmonary arterial pressure (Ppa) during exercise is significantly higher in individuals aged ≥50 yr compared with their younger counterparts, but the reasons for this are unknown. Blood flow through intrapulmonary arteriovenous anastomoses (IPAVA) can be detected during exercise or while breathing hypoxic gas mixtures using saline contrast echocardiography in almost all healthy young individuals. It has been previously hypothesized that a lower degree of exercise-induced blood flow through IPAVA is associated with high Ppa during exercise. This association may suggest that individuals who are known to have high Ppa during exercise, such as those ≥50 yr of age, may have lower blood flow through IPAVA, but the presence and degree of exercise-induced blood flow through IPAVA has not been specifically studied in older populations. Using transthoracic saline contrast echocardiography, we investigated the potential effects of age on exercise-induced blood flow through IPAVA in a cross-section of subjects aged 19–72 yr. To verify our findings, we assessed the effects of age on hypoxia-induced blood flow through IPAVA. Age groups were ≤41 yr (younger, n = 16) and ≥50 yr (older, n = 14). Qualitatively measured exercise- and hypoxia-induced blood flow through IPAVA was significantly lower in older individuals compared with younger controls. Older individuals also had significantly higher pulmonary arterial systolic pressure and total pulmonary resistance (TPR) during exercise. Low blood flow through IPAVA was independently associated with high TPR. The reasons for the age-related decrease in blood flow through IPAVA are unknown.

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Determinants of maximal oxygen uptake in severe acute hypoxia

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00155.2002 ◽

2003 ◽

Vol 284 (2) ◽

pp. R291-R303 ◽

Cited By ~ 136

Author(s):

J. A. L. Calbet ◽

R. Boushel ◽

G. Rådegran ◽

H. Søndergaard ◽

P. D. Wagner ◽

...

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Gas Exchange ◽

Oxygen Uptake ◽

Maximal Oxygen Uptake ◽

Acute Hypoxia ◽

Cycle Ergometer ◽

Pulmonary Gas Exchange ◽

Leg Blood Flow ◽

Ergometer Exercise

To unravel the mechanisms by which maximal oxygen uptake (V˙o 2 max) is reduced with severe acute hypoxia in humans, nine Danish lowlanders performed incremental cycle ergometer exercise to exhaustion, while breathing room air (normoxia) or 10.5% O2 in N2(hypoxia, ∼5,300 m above sea level). With hypoxia, exercise PaO2 dropped to 31–34 mmHg and arterial O2 content (CaO2 ) was reduced by 35% ( P < 0.001). Forty-one percent of the reduction in CaO2 was explained by the lower inspired O2 pressure (Pi O2 ) in hypoxia, whereas the rest was due to the impairment of the pulmonary gas exchange, as reflected by the higher alveolar-arterial O2 difference in hypoxia ( P < 0.05). Hypoxia caused a 47% decrease inV˙o 2 max (a greater fall than accountable by reduced CaO2 ). Peak cardiac output decreased by 17% ( P < 0.01), due to equal reductions in both peak heart rate and stroke volume ( P < 0.05). Peak leg blood flow was also lower (by 22%, P < 0.01). Consequently, systemic and leg O2 delivery were reduced by 43 and 47%, respectively, with hypoxia ( P < 0.001) correlating closely with V˙o 2 max( r = 0.98, P < 0.001). Therefore, three main mechanisms account for the reduction ofV˙o 2 max in severe acute hypoxia: 1) reduction of Pi O2 , 2) impairment of pulmonary gas exchange, and 3) reduction of maximal cardiac output and peak leg blood flow, each explaining about one-third of the loss inV˙o 2 max.

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Mechanisms of improvement in pulmonary gas exchange during isovolemic hemodilution

Journal of Applied Physiology ◽

10.1152/jappl.1999.87.1.132 ◽

1999 ◽

Vol 87 (1) ◽

pp. 132-141 ◽

Cited By ~ 39

Author(s):

Steven Deem ◽

Richard G. Hedges ◽

Steven McKinney ◽

Nayak L. Polissar ◽

Michael K. Alberts ◽

...

Keyword(s):

Blood Flow ◽

Fractal Dimension ◽

Gas Exchange ◽

Spatial Correlation ◽

Pulmonary Blood Flow ◽

Minute Ventilation ◽

Flow Distribution ◽

Pulmonary Gas Exchange ◽

Normal Lung ◽

Blood Flow Distribution

Severe anemia is associated with remarkable stability of pulmonary gas exchange (S. Deem, M. K. Alberts, M. J. Bishop, A. Bidani, and E. R. Swenson. J. Appl. Physiol. 83: 240–246, 1997), although the factors that contribute to this stability have not been studied in detail. In the present study, 10 Flemish Giant rabbits were anesthetized, paralyzed, and mechanically ventilated at a fixed minute ventilation. Serial hemodilution was performed in five rabbits by simultaneous withdrawal of blood and infusion of an equal volume of 6% hetastarch; five rabbits were followed over a comparable time. Ventilation-perfusion (V˙a/Q˙) relationships were studied by using the multiple inert-gas-elimination technique, and pulmonary blood flow distribution was assessed by using fluorescent microspheres. Expired nitric oxide (NO) was measured by chemiluminescence. Hemodilution resulted in a linear fall in hematocrit over time, from 30 ± 1.6 to 11 ± 1%. Anemia was associated with an increase in arterial [Formula: see text] in comparison with controls ( P < 0.01 between groups). The improvement in O2 exchange was associated with reducedV˙a/Q˙heterogeneity, a reduction in the fractal dimension of pulmonary blood flow ( P = 0.04), and a relative increase in the spatial correlation of pulmonary blood flow ( P = 0.04). Expired NO increased with anemia, whereas it remained stable in control animals ( P < 0.0001 between groups). Anemia results in improved gas exchange in the normal lung as a result of an improvement in overallV˙a/Q˙matching. In turn, this may be a result of favorable changes in pulmonary blood flow distribution, as assessed by the fractal dimension and spatial correlation of blood flow and as a result of increased NO availability.

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