Chest
Clinical Significance of Pulmonary Function TestsAlterations in Gas Exchange Following Pulmonary Thromboembolism
Section snippets
INTRAPULMONARY SHUNT
Right-to-left intrapulmonary shunts subsequent to pulmonary embolism have been demonstrated both in man and in experimental animals. Wilson et al1 studied 21 patients with angiographically-demonstrated pulmonary emboli while breathing room air and 100 percent oxygen. They found that intrapulmonary shunting accounted for most of the hypoxemia observed in their patients, and this shunting gradually diminished during the first month following embolization. The magnitude of the shunting did not
VENTILATION-PERFUSION INEQUALITY
The development of ventilation-perfusion inequality has also been demonstrated to provide a major contribution to the deranged gas exchange seen following pulmonary embolization. Kafer,9 for instance, studied 21 patients who were felt to have pulmonary thromboembolism on the basis of perfusion lung scan abnormalities. He measured their PaO2 while breathing room air and while breathing 100 percent oxygen and estimated the contribution of inequality and shunt to each patient's
DECREASED MIXED VENOUS OXYGEN CONTENT
A final element in the pathogenesis of alterations in arterial blood gas tension seen following pulmonary thromboembolism is a decrease in the oxygen content of mixed venous blood. Figure 4 shows that in the presence of inequality, arterial O2 content falls as the mixed venous oxygen tension falls. In patients with pulmonary thromboembolism, the mixed venous Po2 may fall due to decreases in cardiac output or inability of cardiac output to keep pace with increased tissue oxygen
ARTERIAL BLOOD GAS ABNORMALITIES IN MAN
Arterial hypoxemia is found in most patients who have experienced pulmonary thromboembolization. Figure 6 demonstrates the distribution of arterial partial pressure of oxygen (PaO2) during room air breathing in 54 previously reported patients without underlying lung disease.1, 19,20 All patients had their emboli demonstrated by pulmonary angiography and were studied within three weeks of the first symptoms suggesting pulmonary thromboembolism. Although many factors are likely to have
DEAD SPACE AND EXPIRED Co2 ALTERATIONS IN MAN
The Bohr dead space (VD/VT) as determined from measurement of the partial pressure of CO2 in arterial and mixed expired gas represents the sum of the anatomic dead space and the alveolar dead space. Anatomic dead space is constituted primarily by the large conducting airways and is relatively fixed in size. The alveolar dead space is determined by ventilation to lung units with ratios greater than the mean for that individual. In normal individuals, these units occur predominantly
SUMMARY
There is a broad spectrum of gas exchange abnormalities that result from pulmonary thromboembolism. The severity and mechanism of these abnormalities are likely to depend upon the size and location of emboli, the presence or absence of preexisting cardiopulmonary disease, and the time elapsed since embolization. Arterial blood gas alterations and changes in expired gas composition reflected in the Bohr dead space and arterial to end-tidal CO2 gradient are neither sufficiently sensitive nor
REFERENCES (27)
Respiratory function in pulmonary thromboembolic disease
Am J Med
(1969)- et al.
Gas exchange abnormalities produced by venous gas emboli
Resp Physiol
(1979) - et al.
The hemodynamic response to pulmonary embolism in patients without prior cardiopulmonary disease
Am J Cardiol
(1971) - et al.
Pulmonary embolism in the patient with chronic obstructive pulmonary disease
Chest
(1981) - et al.
Early diagnosis of chronic pulmonary vascular obstruction
Am J Med
(1968) - et al.
Hypoxemia in pulmonary embolism, a clinical study
J Clin Invest
(1971) Pulmonary hemodynamics and arterial oxygen saturation in pulmonary embolism
J Appl Physiol
(1965)- et al.
Effects of chronic pulmonary artery ligation on pulmonary mechanics and surfactant
J Appl Physiol
(1966) - et al.
Effects of pulmonary embolism on the pulmonary circulation with special reference to arteriovenous shunts in the lung
Circ Res
(1956) - et al.
Effect of pulmonary microembolism on arteriovenous shunt flow
J Thorac Cardiovasc Surg
(1978)
Lung vascular permeability following progressive pulmonary embolization
J Appl Physiol: Respir Environ Physiol
Lung fluid exchange after uneven pulmonary artery obstruction in sheep
Circ Res
Fluid leaks from extra-alveolar vessels in living dog lungs
J Appl Physiol: Respir Environ Exer Physiol
Cited by (45)
Pulmonary embolism and pregnancy
2021, Praticien en Anesthesie ReanimationDetection of Residual Pulmonary Vascular Obstruction by Ventilation-Perfusion Lung Scan Late After a First Pulmonary Embolism
2017, American Journal of CardiologyCitation Excerpt :First, we excluded patients with cardiopulmonary diseases and above all, we observed a strong relation between both persistent perfusion defects at 3 months (i.e., 3M-RPVO ≥15) and poor changes in perfusion defects (i.e., RC-RPVO ≤ −37.5%) and the occurrence of HF or worsening dyspnea at 5 years. In this context, it has previously been described that persistent thrombi cause partial or complete obliteration of pulmonary arteries, which may result in increased V-Q mismatch and dead space ventilation.16–18 RV dysfunction could also explain the temporal relation observed in our study between PE and the occurrence/worsening of HF.
Persistent dyspnea complaints at long-term follow-up after an episode of acute pulmonary embolism: Results of a questionnaire
2008, European Journal of Internal MedicineCitation Excerpt :Indeed, dead space ventilation as determined by V/Q-scans has been shown to correlate with lung perfusion defects in subjects with acute PE [18]. Also, the development of ventilation-perfusion inequality has been demonstrated to provide a major contribution to the deranged gas exchange seen following pulmonary embolization [19]. In addition, survivors of PE present signs of ventilation to perfusion mismatch at exertion 3.1 years on average after the thromboembolic event [20].
Pulmonary Embolism
2008, Pediatric Respiratory MedicineMajor pulmonary embolism: Review of a pathophysiologic approach to the golden hour of hemodynamically significant pulmonary embolism
2002, ChestCitation Excerpt :Among patients who had Pao2 values (≥ 80 mm Hg) and Paco2 values (≥ 35 mm Hg) that were not low and a normal P(A-a)O2, 38% of patients without CPD and 14% of patients with CPD had angiographically proven PE in PIOPED.128 Given the reported relationship between PE severity and Pao2 or P(A-a)O2,85130132 the preceding values most likely reflect the presence of minor PEs. McIntyre and Sasahara85 reported a linear relationship between PE severity (as assessed by the degree of angiographic obstruction, mPAP, and cardiac index) and Pao2 levels in patients without CPD, but no correlation was found in patients with CPD.
Understanding and Engineering the Pulmonary Vasculature
2023, Advances in Experimental Medicine and Biology