The Unpredictable Effect of Changing Cardiac Output on Hypoxemia after Acute Pulmonary Thromboembolism

2008 ◽  
Vol 2 ◽  
pp. CCRPM.S773
Author(s):  
John Y. C. Tsang ◽  
Wayne J. E. Lamm ◽  
Blazej Neradilek ◽  
Nayak L. Polissar ◽  
Michael P. Hlastala
Keyword(s):  
Cluster Analysis ◽  
Blood Flow ◽  
Cardiac Output ◽  
Gas Exchange ◽  
Clinical Setting ◽  
Pulmonary Thromboembolism ◽  
Regional Blood Flow ◽  
The Other ◽  
Fluorescent Microspheres ◽  
Acute Pulmonary Thromboembolism

Previous studies reported that the degree of hypoxemia following acute pulmonary thromboembolism (APTE) was highly variable and that its mechanism was mainly due to the creation of many high and low ventilation/perfusion (V/Q) units, as a result of the heterogeneous regional blood flow (Q) caused by embolic obstruction. We studied the effect of changing cardiac output (Qt) on gas exchange after APTE in 5 embolized piglets (23 ± 3 Kg), using Dobutamine intermittently at approximately 20 μg/kg/min for 120 minutes. The distribution of ventilation (V) and perfusion (Q) at various times was mapped using fluorescent microspheres in 941 ± 60 lung regions. After APTE, increase in Qt by Dobutamine improved venous oxygen tension (PvO2) but arterial PaO2 did not change consistently. On the other hand, cluster analysis showed that the V/Q ratio of most lung regions was lowered due to increases in Q at the same time. We concluded that the effect of changing cardiac output on gas exchange following APTE was affected by the simultaneous and varying balance between the changing V/Q mismatch and the concomitantly changing PvO2, which might explain the unpredictability of PaO2 in the clinical setting.

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

2000 ◽  
Vol 89 (4) ◽  
pp. 1513-1521 ◽  
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.

Endothelin receptor blockade does not improve hypoxemia following acute pulmonary thromboembolism

2007 ◽  
Vol 102 (2) ◽  
pp. 762-771 ◽  
Author(s):  
John Y. C. Tsang ◽  
Wayne J. E. Lamm ◽  
Blazej Neradilek ◽  
Nayak L. Polissar ◽  
Michael P. Hlastala
Keyword(s):  
Pulmonary Thromboembolism ◽  
Regional Blood Flow ◽  
Venous Catheter ◽  
Main Peak ◽  
Fluorescent Microspheres ◽  
Minimal Impact ◽  
Acute Pulmonary Thromboembolism ◽  
The Mean ◽  
Group 2 ◽  
Group 1

We studied the roles of endothelins in determining ventilation (V̇a) and perfusion (Q̇) mismatch in a porcine model of acute pulmonary thromboembolism (APTE), using a nonspecific endothelin antagonist, tezosentan. Nine anesthetized piglets (∼23 kg) received autologous clots (∼20 g) via a central venous catheter at time = 0 min. The distribution of V̇a and Q̇ at five different time points (−30, −5, 30, 60, 120 min) was mapped by fluorescent microspheres of 10 different colors. Five piglets ( group 1) received tezosentan (courtesy of Actelion) starting at time = 40 min for 2 h, and four piglets ( group 2) received only saline and served as control. Our results showed that, in all of the animals at 30 min following APTE but before tezosentan, the mean V̇a/Q̇ was increased, as was V̇a/Q̇ heterogeneity (log SD V̇a/Q̇), which represented a widening of its main peak. Afterwards, tezosentan attenuated the pulmonary hypertension in group 1 but also produced moderate systemic hypotension. However, it did not improve arterial Po2 or V̇a/Q̇ mismatch. We concluded that endothelin antagonism had minimal impact on gas exchange following APTE and confirmed our earlier observation that the main mechanism for hypoxemia in APTE was due to the mechanical redistribution of pulmonary regional blood flow away from the embolized vessels, resulting in the creation of many divergent low and high V̇a/Q̇ regions.

Spatial distribution of ventilation and perfusion in anesthetized dogs in lateral postures

2002 ◽  
Vol 92 (2) ◽  
pp. 745-762 ◽  
Author(s):  
Hung Chang ◽  
Stephen J. Lai-Fook ◽  
Karen B. Domino ◽  
Carmel Schimmel ◽  
Jack Hildebrandt ◽  
...  
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Regional Blood Flow ◽  
Linear Regression Analysis ◽  
Regional Distribution ◽  
Left Lung ◽  
Vertical Gradient ◽  
Fluorescent Microspheres ◽  
Lateral Decubitus ◽  
Ventilation And Perfusion

We aimed to assess the influence of lateral decubitus postures and positive end-expiratory pressure (PEEP) on the regional distribution of ventilation and perfusion. We measured regional ventilation (V˙a) and regional blood flow (Q˙) in six anesthetized, mechanically ventilated dogs in the left (LLD) and right lateral decubitus (RLD) postures with and without 10 cmH2O PEEP. Q˙ was measured by use of intravenously injected 15-μm fluorescent microspheres, and V˙a was measured by aerosolized 1-μm fluorescent microspheres. Fluorescence was analyzed in lung pieces ∼1.7 cm3 in volume. Multiple linear regression analysis was used to evaluate three-dimensional spatial gradients ofQ˙, V˙a, the ratio V˙a/Q˙, and regional Po 2 (PrO2 ) in both lungs. In the LLD posture, a gravity-dependent vertical gradient in Q˙ was observed in both lungs in conjunction with a reduced blood flow and PrO2 to the dependent left lung. Change from the LLD to the RLD or 10 cmH2O PEEP increased localV˙a/Q˙ and PrO2 in the left lung and minimized any role of hypoxia. The greatest reduction in individual lung volume occurred to the left lung in the LLD posture. We conclude that lung distortion caused by the weight of the heart and abdomen is greater in the LLD posture and influences both Q˙ andV˙a, and ultimately gas exchange. In this respect, the smaller left lung was the most susceptible to impaired gas exchange in the LLD posture.

scholarly journals Regional CO2 tension quantitatively mediates homeostatic redistribution of ventilation following acute pulmonary thromboembolism in pigs

2009 ◽  
Vol 107 (3) ◽  
pp. 755-762 ◽  
Author(s):  
John Y. C. Tsang ◽  
Wayne J. E. Lamm ◽  
Erik R. Swenson
Keyword(s):  
Gas Exchange ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Airway Resistance ◽  
Pulmonary Thromboembolism ◽  
Regional Ventilation ◽  
Fluorescent Microspheres ◽  
Artery Pressure ◽  
Mean Pulmonary Artery Pressure ◽  
Acute Pulmonary Thromboembolism

Previous studies reported that regional CO2 tension might affect regional ventilation (V̇) following acute pulmonary thromboembolism (APTE). We investigated the pathophysiology and magnitude of these changes. Eight anesthetized and ventilated piglets received autologous clots at time = 0 min until mean pulmonary artery pressure was 2.5 times baseline. The distribution of V̇ and perfusion (Q̇) at four different times (−5, 30, 60, 120 min) was mapped by fluorescent microspheres. Regional V̇ and Q̇ were examined postmortem by sectioning the air-dried lung into 900–1,000 samples of ∼2 cm3 each. After the redistribution of regional Q̇ by APTE, but in the scenario assuming that no V̇ shift had yet occurred, CO2 tension in different lung regions at 30 min post-APTE (PXCO2) was estimated from the V̇/Q̇ data and divided into four distinct clusters: i.e., PXCO2 < 10 Torr; 10 < PXCO2 < 25 Torr; 25 < PXCO2 < 50 Torr; PXCO2 > 50 Torr. Our data showed that the clusters in higher V̇/Q̇ regions (with a PXCO2 < 25 Torr) received ∼35% less V̇ when measured within 30 min of APTE, whereas, in contrast, the lower V̇/Q̇ regions showed no statistically significant increases in their V̇. However, after 30 min, there was minimal further redistribution of V̇. We conclude that there are significant compensatory V̇ shifts out of regions of low CO2 tension soon following APTE, and that these variations in regional CO2 tension, which initiate CO2-dependent changes in airway resistance and lung parenchymal compliance, can lead to improved gas exchange.

Relationship among cardiac output, shunt, and inspired O2 concentration

1991 ◽  
Vol 71 (6) ◽  
pp. 2191-2197 ◽  
Author(s):  
P. D. Wagner ◽  
W. Schaffartzik ◽  
R. Prediletto ◽  
D. R. Knight
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Gas Exchange ◽  
Arteriovenous Fistulas ◽  
Dependent Behavior ◽  
O2 Concentration ◽  
Mongrel Dog ◽  
Receptor Blockers ◽  
Leukotriene Receptor ◽  
Opening And Closing

In comparing gas exchange responses of the methacholine- (MCh) challenged mongrel dog with leukotriene receptor blockers and placebo at different inspiratory O2 fractions (FIO2), we previously noted systematically different values of cardiac output as a function of drug administration and/or FIO2. This confounds identification of the effects of FIO2 and/or drugs on gas exchange, because shunt is well known to vary directly with cardiac output when other factors are equal. Accordingly, in six dogs we examined the dependence of combined shunt and low ventilation-perfusion (VA/Q) blood flow (“shunt”) on cardiac output in the MCh-challenged mongrel dog. Two dogs breathed 100% O2, another two breathed room air, and the final pair breathed 12% O2 while cardiac output was altered several times by sequentially opening and closing arteriovenous fistulas every 10 min for approximately 90 min after a standard MCh challenge. On 100% O2, shunt increased by 11.0% of the cardiac output per 1-l/min increase in cardiac output. On room air, the value was 7.4%. With 12% O2 breathing shunt rose by only 2.2% per 1-l/min rise in blood flow. This FIO2 -dependent behavior of the shunt-cardiac output relationship was highly reproducible, both within and between animals. It suggests that the increase in shunt with cardiac output depends more on vascular tone of noninjured areas than on tone of the low VA/Q regions (which are hypoxic at all FIO2 values).

Pushmi-Pullyu and the Right Atrium

2011 ◽  
pp. 55-62
Author(s):  
James R. Munis
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Right Ventricle ◽  
Flow Rate ◽  
Blood Flow Rate ◽  
The Other ◽  
Right Atrial ◽  
The One ◽  
The Right ◽  
Point Of Intersection

What does right atrial pressure (PRA) do to cardiac output (CO)? On the one hand, we've been taught that PRA represents preload for the right ventricle. That is, the higher the PRA, the greater the right ventricular output (and, therefore, CO). This is simply an application of Starling's law to the right side of the heart. On the other hand, we've been taught that PRA represents the downstream impedance to venous return (VR) from the periphery. That is, the higher the PRA, the lower the VR, and therefore, the lower the CO. The point of intersection between the 2 curves defines a unique blood flow rate, which is both CO and VR at the same time.

Cardiac output and regional blood flow in hypoxic woodchucks

1971 ◽  
Vol 220 (6) ◽  
pp. 1565-1568 ◽  
Author(s):  
RF Burlington ◽  
JA Vogel ◽  
TM Burton ◽  
IA Salkovitz
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Regional Blood Flow
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