Reducing lung strain after pneumonectomy impairs oxygen diffusing capacity but not ventilation-perfusion matching

2003 ◽  
Vol 95 (4) ◽  
pp. 1370-1378 ◽  
Author(s):  
Connie C. W. Hsia ◽  
Robert L. Johnson ◽  
Eugene Y. Wu ◽  
Aaron S. Estrera ◽  
Harrieth Wagner ◽  
...  

After pneumonectomy (Pnx), mechanical strain on the remaining lung is an important signal for adaptation. To examine how mechanical lung strain alters gas exchange adaptation after Pnx, we replaced the right lung of adult dogs with a custom-shaped inflatable silicone prosthesis. The prosthesis was kept 1) inflated (Inf) to reduce mechanical strain of the remaining lung and maintain the mediastinum in the midline, or 2) deflated (Def) to allow lung strain and mediastinal shift. Gas exchange was studied 4-7 mo later at rest and during treadmill exercise by the multiple inert gas elimination technique while animals breathed 21 and 14% O2in balanced order. In the Inf group compared with Def group during hypoxic exercise, arterial O2saturation was lower and alveolar-arterial O2tension difference higher, whereas O2diffusing capacity was lower at any given cardiac output. Dispersion of the perfusion distribution was similar between groups at rest and during exercise. Dispersion of the ventilation distribution was lower in the Inf group at rest, associated with a much higher respiratory rate, but rose to similar levels in both groups during hypoxic exercise. Mean pulmonary arterial pressure at a given cardiac output was higher in the Inf group, whereas peak cardiac output was similar between groups. Thus creating lung strain by post-Pnx mediastinal shift primarily enhances diffusive gas exchange with only minor effects on ventilation-perfusion matching, consistent with the generation of additional alveolar-capillary surfaces but not conducting airways and blood vessels.

2001 ◽  
Vol 90 (6) ◽  
pp. 2057-2062 ◽  
Author(s):  
Kyle K. Henderson ◽  
Richard L. Clancy ◽  
Norberto C. Gonzalez

The objective of these experiments was to determine whether living and training in moderate hypoxia (MHx) confers an advantage on maximal normoxic exercise capacity compared with living and training in normoxia. Rats were acclimatized to and trained in MHx [inspired Po 2(Pi O2 ) = 110 Torr] for 10 wk (HTH). Rats living in normoxia trained under normoxic conditions (NTN) at the same absolute work rate: 30 m/min on a 10° incline, 1 h/day, 5 days/wk. At the end of training, rats exercised maximally in normoxia. Training increased maximal O2 consumption (V˙o 2 max) in NTN and HTH above normoxic (NS) and hypoxic (HS) sedentary controls. However,V˙o 2 max and O2 transport variables were not significantly different between NTN and HTH:V˙o 2 max 86.6 ± 1.5 vs. 86.8 ± 1.1 ml · min−1 · kg−1; maximal cardiac output 456 ± 7 vs. 443 ± 12 ml · min−1 · kg−1; tissue blood O2 delivery (cardiac output × arterial O2 content) 95 ± 2 vs. 96 ± 2 ml · min−1 · kg−1; and O2 extraction ratio (arteriovenous O2 content difference/arterial O2 content) 0.91 ± 0.01 vs. 0.90 ± 0.01. Mean pulmonary arterial pressure (Ppa, mmHg) was significantly higher in HS vs. NS ( P < 0.05) at rest (24.5 ± 0.8 vs. 18.1 ± 0.8) and during maximal exercise (32.0 ± 0.9 vs. 23.8 ± 0.6). Training in MHx significantly attenuated the degree of pulmonary hypertension, with Ppa being significantly lower at rest (19.3 ± 0.8) and during maximal exercise (29.2 ± 0.5) in HTH vs. HS. These data indicate that, despite maintaining equal absolute training intensity levels, acclimatization to and training in MHx does not confer significant advantages over normoxic training. On the other hand, the pulmonary hypertension associated with acclimatization to hypoxia is reduced with hypoxic exercise training.


1982 ◽  
Vol 52 (6) ◽  
pp. 1575-1580 ◽  
Author(s):  
R. L. Capen ◽  
W. W. Wagner

We have previously shown that airway hypoxia causes pulmonary capillary recruitment and raises diffusing capacity for carbon monoxide. This study was designed to determine whether these events were caused by an increase in pulmonary vascular resistance, which redistributed blood flow toward the top of the lung, or by an increase in cardiac output. We measured capillary recruitment at the top of the dog lung by in vivo microscopy, gas exchange surface area of the whole lung by diffusing capacity for carbon monoxide, and blood flow distribution by radioactive microspheres. During airway hypoxia recruitment occurred, diffusing capacity increased, and blood flow was redistributed upward. When a vasodilator was infused while holding hypoxia constant, these effects were reversed; i. e., capillary “derecruitment” occurred, diffusing capacity decreased, and blood flow was redistributed back toward the bottom of the lung. The vasodilator was infused at a rate that left hypoxic cardiac output unchanged. These data show that widespread capillary recruitment during hypoxia is caused by increased vascular resistance and the resulting upward blood flow redistribution.


2007 ◽  
Vol 102 (4) ◽  
pp. 1448-1455 ◽  
Author(s):  
Connie C. W. Hsia ◽  
Robert L. Johnson ◽  
Paul McDonough ◽  
D. Merrill Dane ◽  
Myresa D. Hurst ◽  
...  

Mammals native to high altitude (HA) exhibit larger lung volumes than their lowland counterparts. To test the hypothesis that adaptation induced by HA residence during somatic maturation improves pulmonary gas exchange in adulthood, male foxhounds born at sea level (SL) were raised at HA (3,800 m) from 2.5 to 7.5 mo of age and then returned to SL prior to somatic maturity while their littermates were simultaneously raised at SL. Following return to SL, all animals were trained to run on a treadmill; gas exchange and hemodynamics were measured 2.5 years later at rest and during exercise while breathing 21% and 13% O2. The multiple inert gas elimination technique was employed to estimate ventilation-perfusion (V̇a/Q̇) distributions and lung diffusing capacity for O2 (DlO2). There were no significant intergroup differences during exercise breathing 21% O2. During exercise breathing 13% O2, peak O2 uptake and V̇a/Q̇ distributions were similar between groups but arterial pH, base excess, and O2 saturation were higher while peak lactate concentration was lower in animals raised at HA than at SL. At a given exercise intensity, alveolar-arterial O2 tension gradient (A-aDo2) attributable to diffusion limitation was lower while Dlo2 was 12–25% higher in HA-raised animals. Mean systemic arterial blood pressure was also lower in HA-raised animals; mean pulmonary arterial pressures were similar. We conclude that 5 mo of HA residence during maturation enhances long-term gas exchange efficiency and DlO2 without impacting V̇a/Q̇ inequality during hypoxic exercise at SL.


2001 ◽  
Vol 281 (5) ◽  
pp. L1279-L1287 ◽  
Author(s):  
C. C. W. Hsia ◽  
E. Y. Wu ◽  
E. Wagner ◽  
E. R. Weibel

To examine the effects of mechanical lung strain on regenerative growth of alveolar septal tissue after pneumonectomy (PNX), we replaced the right lungs of adult dogs with a custom-shaped inflatable silicone prosthesis. The prosthesis was either inflated (Inf) to maintain the mediastinum at the midline or deflated to allow mediastinal shift. The animals were euthanized ∼15 mo later, and the lungs were fixed at a constant distending pressure. With the Inf prostheses, lung expansion, alveolar septal tissue volumes, surface areas, and diffusing capacity of the tissue-plasma barrier were significantly lower than with the deflated prostheses; the expected post-PNX tissue responses were impaired by 30–60%. Capillary blood volume was significantly higher with Inf prostheses, consistent with microvascular congestion. Measurements in the Inf group remained consistently and significantly higher than those expected for a normal left lung, indicating persistence of partial compensation. In one dog, delayed deflation of the prosthesis 9–10 mo after PNX led to vigorous lung expansion and septal tissue growth, particularly of type II epithelial cells. We conclude that mechanical lung strain is a major signal for regenerative lung growth; however, other signals are also implicated, accounting for a significant fraction of the compensatory response to PNX.


1990 ◽  
Vol 68 (1) ◽  
pp. 181-186
Author(s):  
G. G. Giesbrecht ◽  
M. Younes

The mechanism of ventilatory stimulation that accompanies increases in cardiac output is unknown. Previous studies addressing this issue have been inconclusive. However, only steady pulmonary blood flow was used. The effect of flow pulsatility merits consideration, because increasing cardiac output raises not only mean pulmonary arterial pressure but also pulse pressure; mechanoreceptors with an important dynamic component to their responses may cause a response to pulsatile, but not steady, flow. Studies were done on anesthetized cats (n = 4) and dogs (n = 4). The right pulmonary artery was cannulated within the pericardium, and systemic blood was pumped from the left atrium to the right pulmonary artery. The right pulmonary circulation was perfused at different levels of flow, which was either steady or pulsatile. Steady-state flow of up to 150 ml.kg-1.min-1 (270 ml.kg-1.min-1 when corrected for the proportion of lung tissue perfused) did not affect breathing pattern. When high pulmonary flow was made pulsatile (pulse pressure approximately 23 mmHg), breath duration decreased from 3.7 +/- 0.72 to 3.4 +/- 0.81 (SD) s (P less than 0.01), representing a change in frequency of only 9%. There was no change in peak inspiratory activity. It was concluded that pulmonary vascular mechanoreceptors are not likely to contribute significantly to the increase in ventilation in association with increases in cardiac output.


2004 ◽  
Vol 97 (4) ◽  
pp. 1567-1574 ◽  
Author(s):  
Priya Ravikumar ◽  
Cuneyt Yilmaz ◽  
D. Merrill Dane ◽  
Robert L. Johnson ◽  
Aaron S. Estrera ◽  
...  

After pneumonectomy (PNX), mechanical strain on the remaining lung is greatly increased. To assess whether remaining lobes expand uniformly after left or right PNX (removing 42 and 58% of lung mass, respectively), we performed high-resolution computed tomography (CT) scans at 45 ml/kg above end-expiratory lung volume on adult male foxhounds after left or right PNX, which were compared with adult Sham controls. Air and tissue volumes were separately measured in each lobe. After left PNX, air and tissue volumes in the right upper and cardiac lobes increased ∼2.2-fold above and below the heart, whereas volumes in right middle and lower lobes did not change significantly. After right PNX, air and tissue volumes in the left upper and middle lobes increased 2.3- to 2.7-fold across the midline anterior to the heart, whereas the left lower lobe expanded ∼1.9-fold posterior to the heart. Regional changes in volume density of tissue post-PNX estimated by CT scan parallel postmortem estimates by morphometric analyses. Data indicate heterogeneous regional distribution of mechanical lung strain, which could influence the differential cellular compensatory response following right and left PNX.


2013 ◽  
Vol 16 (6) ◽  
pp. 319 ◽  
Author(s):  
Kim Maguire ◽  
Calvin Leung ◽  
Visali Kodali ◽  
Brice Taylor ◽  
Jacques-Pierre Fontaine ◽  
...  

Tension hydrothorax is a rare complication of pneumonectomy for pleural mesothelioma and an exceptionally rare cause of heart failure. We describe a patient who had undergone extrapleural pneumonectomy, chemotherapy, and radiation for pleural mesothelioma and who developed heart failure symptoms within months of the completion of treatment. Investigation showed a massive left pleural effusion resulting in tension hydrothorax, mediastinal shift, and evidence of right heart failure with constrictive physiology and low cardiac output. Therapeutic thoracentesis resulted in increase in cardiac output and symptomatic improvement.


2020 ◽  
Vol 13 (9) ◽  
pp. e235281
Author(s):  
Sanjan Asanaru Kunju ◽  
Prithvishree Ravindra ◽  
Ramya Kumar Madabushi Vijay ◽  
Priya Pattath Sankaran

A 20-year-old woman presented with abdominal pain and shortness of breath. She was in obstructive shock with absent breath sounds on the left haemithorax. Chest X-ray showed a large radiolucent shadow with absent lung markings and mediastinal shift to the right side with concerns for tension pneumothorax. Though tube thoracostomy was done on the left side of the chest, column movement was absent. To confirm the diagnosis CT with contrast was done that revealed a huge left side diaphragmatic defect with abdominal contents in the thorax and mediastinal structures are shifted to left. She underwent emergency laparotomy and postoperative period was uneventful.


2019 ◽  
Vol 34 (6) ◽  
pp. 1199-1207
Author(s):  
Thorir Svavar Sigmundsson ◽  
Tomas Öhman ◽  
Magnus Hallbäck ◽  
Eider Redondo ◽  
Fernando Suarez Sipmann ◽  
...  

AbstractRespiratory failure may cause hemodynamic instability with strain on the right ventricle. The capnodynamic method continuously calculates cardiac output (CO) based on effective pulmonary blood flow (COEPBF) and could provide CO monitoring complementary to mechanical ventilation during surgery and intensive care. The aim of the current study was to evaluate the ability of a revised capnodynamic method, based on short expiratory holds (COEPBFexp), to estimate CO during acute respiratory failure (LI) with high shunt fractions before and after compliance-based lung recruitment. Ten pigs were submitted to lung lavage and subsequent ventilator-induced lung injury. COEPBFexp, without any shunt correction, was compared to a reference method for CO, an ultrasonic flow probe placed around the pulmonary artery trunk (COTS) at (1) baseline in healthy lungs with PEEP 5 cmH2O (HLP5), (2) LI with PEEP 5 cmH2O (LIP5) and (3) LI after lung recruitment and PEEP adjustment (LIPadj). CO changes were enforced during LIP5 and LIPadj to estimate trending. LI resulted in changes in shunt fraction from 0.1 (0.03) to 0.36 (0.1) and restored to 0.09 (0.04) after recruitment manoeuvre. Bias (levels of agreement) and percentage error between COEPBFexp and COTS changed from 0.5 (− 0.5 to 1.5) L/min and 30% at HLP5 to − 0.6 (− 2.3 to 1.1) L/min and 39% during LIP5 and finally 1.1 (− 0.3 to 2.5) L/min and 38% at LIPadj. Concordance during CO changes improved from 87 to 100% after lung recruitment and PEEP adjustment. COEPBFexp could possibly be used for continuous CO monitoring and trending in hemodynamically unstable patients with increased shunt and after recruitment manoeuvre.


1975 ◽  
Vol 39 (1) ◽  
pp. 47-53 ◽  
Author(s):  
J. A. Loeppky ◽  
U. C. Luft

To clarify the role of O2 stores in the fluctuations in VO2 observed with changing posture, O2 intake (Veo2) and pulmonary capillary O2 transfer (Vpco2) were calculated breath by breath with a box-balloon sprometer and mass spectrometer. Changes in O2 stores of the lungs (O2L) and blood (O2b) were computed assuming metabolic rate (Vco2) constant (O2L = Veo2 - Vpco2; O2b = Vpco2 - Vco2). Measurements were made before, during, and after passive tilt to 60 degrees and on return to recumbency after 10 min erect. From supine to upright O2L increased rapidly and O2b dropped slowly, creating a net deficit in Veo2 of 130 ml in 10 min. Return to supine caused rapid loss in O2L and gain in O2b with a net Veo2 excess of 117 ml. Shifts in O2b were 2.5 times greater but opposite to shifts in O2L. Changes in O2b result from shifts in blood volume and flow more than from changes in cardiac output. Refilling of O2b, matching loss while upright, caused transient hypoxia with significant hyperpnea.


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