Pulmonary gas exchange during induction of pulmonary edema in anesthetized dogs

Said, Sami I.; Longacher, Joseph W.; Davis, R. Kim; Banerjee, Chandra M.; Davis, William M.; Wooddell, W. Jeff

doi:10.1152/jappl.1964.19.3.403

Cited by 35 publications

(8 citation statements)

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“…[63] It may occur due to perfusion of unventilated areas due to surfactant deficiency, pulmonary edema, and pulmonary arteriovenous anastomosis or patent foramen ovale. [6465] Preexisting pulmonary arterial-venous anastomosis may open up by the elevated pulmonary artery pressure. [66] PE may lead to the development of right ventricular failure and elevated right atrial pressure and when the right atrial pressure exceeds left atrial pressure, shunting occurs through the foramen ovale which remains patent in approximately 15% of patients.…”

Section: Bronchoconstriction and Dead Space Ventilationmentioning

confidence: 99%

“…Recanalization of thrombi occurs earlier than the clearance red blood cells and debris from the infracted alveolar area and improved perfusion to this underventilated area may cause shunt formation. [4965] Although PE reduces the elimination of CO 2 , hypercapnia is rare except in large emboli. Hyperventilation of normally functioning alveoli eliminates CO 2 .…”

Section: Bronchoconstriction and Dead Space Ventilationmentioning

confidence: 99%

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Mechanisms of hypoxemia

2017

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Oxygen is an essential element for life and without oxygen humans can survive for few minutes only. There should be a balance between oxygen demand and delivery in order to maintain homeostasis within the body. The two main organ systems responsible for oxygen delivery in the body and maintaining homeostasis are respiratory and cardiovascular system. Abnormal function of any of these two would lead to the development of hypoxemia and its detrimental consequences. There are various mechanisms of hypoxemia but ventilation/perfusion mismatch is the most common underlying mechanism of hypoxemia. The present review will focus on definition, various causes, mechanisms, and approach of hypoxemia in human.

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Section: Bronchoconstriction and Dead Space Ventilationmentioning

confidence: 99%

Section: Bronchoconstriction and Dead Space Ventilationmentioning

confidence: 99%

Mechanisms of hypoxemia

2017

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“…Said et al (1964), inducing acute pulmonary edema in anesthetized dogs by intravenous infusion of dextran in saline found that P a02 remained near normal until just before the edema became grossly apparent, when it fell precipitously; left atrial pressure mounted to a peak and then declined. In two patients with frank left ventricular failure and pulmonary edema after acute myocardial infarction, Mac Kenzie et al (1964) observed only a moderate depression of Pa02 and a response to high oxygen administration largely similar to that in unshocked patients or normal subjects, suggesting that the abnormality resulting in a low Pa02 is not related to the raised pressures behind the left heart and the resultant pulmonary changes.…”

Section: Discussionmentioning

confidence: 98%

Arterial pO<sub>2</sub>, pCO<sub>2</sub>, pH and Standard Bicarbonate in Patients with an Acute Myocardial Infarction

Ljungstrøm¹,

Johansson²,

Sievers³

1967

Cardiology

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“…Both atelectasis (45) and temporary airway closure due to pneumoconstriction (46) or pulmonary edema (47) can cause right-to-left shunting that can be temporarily reversed by deep breathing. Indeed pulmonary edema has been suggested as one source of hypoxemia in animals following starch embolism (3,48).…”

Section: Discussionmentioning

confidence: 99%

Hypoxemia in pulmonary embolism, a clinical study

Wilson¹,

Pierce²,

Johnson³

et al. 1971

J. Clin. Invest.

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A B S T R A C T The cause of hypoxemia was studied in 21 patients with no previous heart or lung disease shortly after an episode of acute pulmonary embolism. The diagnosis was based on pulmonary angiography demonstrating distinct vascular filling defects or "cutoffs." It was found that virtually all of the hypoxemia in patients with previously normal heart and lungs could be accounted for on the basis of shunt-like effect. The magnitude of the shunting did not correlate with the percent of the pulmonary vascular bed occluded nor with the mean pulmonary artery pressure. The shunts tended to gradually recede over about a month after embolism. Patients without pulmonary infarction were able to inspire 80-111% of their predicted inspiratory capacities, and this maneuver temporarily diminished the observed shunt. Patients with pulmonary infarcts were able to inhale only to 60-69% of predicted inspiratory capacity, and this did not reverse shunting. These data suggest that the cause of right-to-left shunting in patients with pulmonary emboli is predominantly atelectasis.When the elevation of mean pulmonary artery pressure was compared to cardiac index per unit of unoccluded lung, it fell within the range of pulmonary hypertension predicted from published data obtained in patients with exercise in all except one case. This observation suggests that pulmonary vasoconstriction following embolism is not important in humans, although these data are applicable only during the time interval in which our patients were studied and in patients receiving heparin.

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Pulmonary gas exchange during induction of pulmonary edema in anesthetized dogs

Cited by 35 publications

References 0 publications

Mechanisms of hypoxemia

Mechanisms of hypoxemia

Arterial pO<sub>2</sub>, pCO<sub>2</sub>, pH and Standard Bicarbonate in Patients with an Acute Myocardial Infarction

Hypoxemia in pulmonary embolism, a clinical study

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