Mechanism of arterial hypoxemia following pulmonary thromboembolism in dogs

Levy, Steven E.; Simmons, Daniel H.

doi:10.1152/jappl.1975.39.1.41

Cited by 43 publications

(11 citation statements)

References 25 publications

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“…result of decreased transit time of blood through a reduced pulmonary capillary bed with resulting failure of alveolar-end capillary equilibration (18). Recently, VA/Q inequality and intrapulmonary shunt have been implicated as causes for the hypoxemia (19)(20)(21). A low cardiac output state with resulting reduction of mixed venous saturation has also been reported (22), but its impact on arterial hypoxemia has not been evaluated.…”

Section: Resultsmentioning

confidence: 99%

Mechanisms of gas exchange abnormality in patients with chronic obliterative pulmonary vascular disease.

Dantzker¹,

Bower²

1979

J. Clin. Invest.

129

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A B S T R A C T We have examined the mechanisiis of abnormal gas exchange in seven patients with chroniic obliteration of the pulmonary vascular bed secondary to recurrent pulmonary emboli or idiopathic pulmonary hypertension. All ofthe patients had a widened alveolararterial oxygen gradient and four were significantly hypoxemic with arterial partial pressures of oxygen <80 torr. Using the technique of multiple inert gas elimination, we found that ventilation-perfusion (VA/Q) relationships were only minimally abnormlal w\ith a imiean of 10% (range, 2-19%) of cardiac output perfusing abnormal units. These units consisted of shunt ancd units with VA/0 ratios <0.1. In addition, the dead space was found to be normal in each patient. There was no evidence for diffusion impairment, and the widenied alveolar-arterial oxygen gradient was completely explained by VA/Q inequality. Significanit hypoxemila occurred only when VA/Q inequality was combined with a low mixed venous oxygen content.

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Section: Resultsmentioning

confidence: 99%

Mechanisms of gas exchange abnormality in patients with chronic obliterative pulmonary vascular disease.

Dantzker¹,

Bower²

1979

J. Clin. Invest.

129

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“…Hypoxemia and impaired gas exchange indices calculated as a function of inspired oxygen concentration include PaO2/FiO2, a/APO2 and AaDO2. 5,13,14 In the present study, ROC curve analysis found that PaO2/FiO2 was inferior to both the a/APO2 and AaDO2 for comparing gas exchange under room air. If FiO2 was more than 0.21, the area under the ROC curve for PaO2/FiO2 was slightly smaller than that for a/APO2 (0.709 vs 0.714).…”

Section: Mechanisms Of Impaired Gas Exchange and Index Of Gas Exchangmentioning

confidence: 41%

“…9 Other proposed mechanisms have been reported and revealed minor roles. [10][11][12][13] Several parameters are derived from ABG analysis. Hypoxemia and impaired gas exchange indices calculated as a function of inspired oxygen concentration include PaO2/FiO2, a/APO2 and AaDO2.…”

Section: Mechanisms Of Impaired Gas Exchange and Index Of Gas Exchangmentioning

confidence: 99%

Prognostic Value of Arterial/Alveolar Oxygen Tension Ratio (a/APO2) in Acute Pulmonary Embolism

Hsu

Chu

Chang

et al. 2007

Circ J

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“…Air shift from the embolized lung areas has been demonstrated in animal models [15,16]. In humans this component is not demonstrated.…”

Section: Discussionmentioning

confidence: 99%

The assessment of gas exchange by automated analysis of O2 and CO2 alveolar to arterial differences

Paoletti

Fornai

et al. 1986

International Journal of Clinical Monitoring and Computing

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A computer program to measure breath by breath alveolar pressure (PA) and alveolar to arterial difference (AaD) for O2 and CO2, by a mass-spectrometer has been implemented. The program allows the determination of alveolar gas by different methods: 1. Bohr's equation (BE); 2. ideal alveolar air equation for O2 (IDO2); 3. end-tidal (ET); 4. by the Rahn's definition of 'mean alveolar gas', i.e., alveolar pressures are defined when instantaneous respiratory exchange ratio (IRQ) equals mean respiratory exchange ratio (MRQ). This automated technique has been used in 16 patients with chronic obstructive lung disease (COLD) and 15 patients with pulmonary embolism (APE). In both groups of patients it was always possible to find in each breath the point where IRQ = MRQ and therefore to measure AaD by RD. IDO2 was significantly lower than PAO2 by the other methods. Also ET values of O2 and CO2 were significantly different from RD and BE in both groups of patients, however the difference was consistently higher in COLD patients. The different shape of the expirograms (steeper expirograms in COLD) is responsible for this different result. RD and BE AaD characterize gas exchange more precisely than ET, because the contribution of high VA/Q units is also evaluated. This is particularly important in COLD patients. Consideration on dead space measurements are also reported both for COLD and APE patients. In conclusion this automated technique provides the assessment of gas exchange for the use in clinical respiratory physiology and for the monitoring of gas-exchange in critically ill patients.

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Mechanism of arterial hypoxemia following pulmonary thromboembolism in dogs

Cited by 43 publications

References 25 publications

Mechanisms of gas exchange abnormality in patients with chronic obliterative pulmonary vascular disease.

Mechanisms of gas exchange abnormality in patients with chronic obliterative pulmonary vascular disease.

Prognostic Value of Arterial/Alveolar Oxygen Tension Ratio (a/APO2) in Acute Pulmonary Embolism

The assessment of gas exchange by automated analysis of O2 and CO2 alveolar to arterial differences

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