Changes in (a-A)CO2 difference and pulmonary artery pressure in anesthetized man.

Askrog, V

doi:10.1152/jappl.1966.21.4.1299

Cited by 56 publications

(16 citation statements)

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“…Changes in pulmonary blood flow due to myocardial infarction might result from pulmonary hypotension due to an acute reduction in cardiac output or from pulmonary hypertension due to pulmonary venous hypertension with left ventricular failure. Despite a wide range of pulmonary artery pressure and cardiac output in our data we were unable to demonstrate any simple correlation between VD/VT ratio and pulmonary haemodynamics such as that shown in other situations (West and Jones, 1965 ;Saunders, 1966;Askrog, 1966).…”

Section: Methodscontrasting

confidence: 82%

Disturbances of pulmonary function after acute myocardial infarction.

Pain¹,

Stannard²,

Sloman³

1967

BMJ

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have shown a high incidence of arterial hypoxaemia in patients studied after myocardial infarction. McNicol et al. suggested that pulmonary congestion with venoarterial shunting was the basic cause of this hypoxaemia and that treatment with diuretics would improve blood oxygenation presumably by removing transudated fluid from the lungs.This paper reports studies carried out in an attempt to further elucidate the mechanisms responsible for disturbed pulmonary function after myocardial infarction. Measurements of arterial blood gases, uniformity of ventilation, ventilation-perfusion relations, and pulmonary haemodynamics were made shortly after the onset of myocardial infarction. Materials and MethodsThe subjects, aged 39 to 77, were patients with a clinical diagnosis, subsequently confirmed by electrocardiograms and serum enzyme abnormalities, of acute transmural myocardial infarction. Studies were undertaken within four hours of admission to a coronary-care ward and within 12 hours of the onset of infarction. Throughout the procedures the patient was horizontal, with the head supported by one pillow. Papaveretum intravenously (10 mg.) was used to relieve pain if necessary.Blood Gases.-Arterial blood was sampled from a nylon catheter placed in one brachial artery. Care was taken to keep this catheter patent with heparin-saline solution, and the dead space of the catheter was always flushed with blood before taking the actual samples. These were taken with the subject breathing room air and after the administration of 100% oxygen for 10 minutes. Patients were allowed to breathe in their natural pattern. The blood was drawn into 10-ml. syringes with their dead space filled with heparin-saline, capped, and immediately placed in a flask containing ice This was regarded as sufficient to describe the washout as being linear or alinear, and multicompartment analysis of alinear curves was not performed.Haemodynamic Measurements.-In 17 subjects measurements of pulmonary artery or right ventricular pressure and cardiac output were made. Whenever possible these were performed within four hours of admission, but in six patients these measurements were separated by up to 24 hours from the gasexchange measurements.-Right heart pressures were measured with a fine polyethylene catheter (P.E. 60) 80 cm. long, which was passed percutaneously from a median cubital vein. With a Sanborn transducer (267A), preamplifier, and direct-writing recorder (296), the dynamic response is flat (± 5 %) to 4 c.p.s. Cardiogreen (5 mg.) was injected into the right atrium, and blood from the brachial artery was passed through a Waters densitometer (XP 302). Cardiac output was calculated from dye-curve analysis.All the above procedures were not performed in every subject. Of the 33 patients studied, 29 had blood-gas analysis-and

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Section: Methodscontrasting

confidence: 82%

Disturbances of pulmonary function after acute myocardial infarction.

Pain¹,

Stannard²,

Sloman³

1967

BMJ

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“…Although no data are available for patients undergoing AAA repair, it seems that the area under the threshold correlates to outcome during surgical aortic arch repair [10]. EtCO 2 is a trend monitor for continuously assessment of P a CO 2 and EtCO 2 is typically 0.5 kPa lower than P a CO 2 , but we acknowledge that this ratio differs with changes in pulmonary circulation, volume of dead space, and ventilatory strategy applied during anesthesia [35,36]. Diminished cerebrovascular CO 2 reactivity may result in a linear relationship between S c O 2 and MAP, however, the individual CO 2 reactivity was not assessed before surgical incision.…”

Section: Discussionmentioning

confidence: 99%

Near-infrared spectroscopy assessed cerebral oxygenation during open abdominal aortic aneurysm repair: relation to end-tidal CO2 tension

Sørensen

Nielsen

Secher

2015

J Clin Monit Comput

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During open abdominal aortic aneurism (AAA) repair cerebral blood flow is challenged. Clamping of the aorta may lead to unintended hyperventilation as metabolism is reduced by perfusion of a smaller part of the body and reperfusion of the aorta releases vasodilatory substances including CO2. We intend to adjust ventilation according end-tidal CO2 tension (EtCO2) and here evaluated to what extent that strategy maintains frontal lobe oxygenation (ScO2) as determined by near infrared spectroscopy. For 44 patients [5 women, aged 70 (48-83) years] ScO2, mean arterial pressure (MAP), EtCO2, and ventilation were obtained retrospectively from the anesthetic charts. By clamping the aorta, ScO2 and EtCO2 were kept stable by reducing ventilation (median, -0.8 l min(-1); interquartile range, -1.1 to -0.4; P < 0.001). During reperfusion of the aorta a reduction in MAP by 8 mmHg (-15 to -1; P < 0.001) did not prevent an increase in ScO2 by 2 % (-1 to 4; P < 0.001) as EtCO2 increased 0.5 kPa (0.1-1.0; P < 0.001) despite an increase in ventilation by 1.8 l min(-1) (0.9-2.7; P < 0.001). Changes in ScO2 related to those in EtCO2 (r = 0.41; P = 0.0001) and cerebral deoxygenation (-15 %) was noted in three patients while cerebral hyperoxygenation (+15 %) manifests in one patient. Thus changes in ScO2 were kept within acceptable limits (±15 %) in 91 % of the patients. For the majority of the patients undergoing AAA repair ScO2 was kept within reasonable limits by reducing ventilation by approximately 1 l min(-1) upon clamping of the aorta and increasing ventilation by approximately 2 l min(-1) when the lower body is reperfused.

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“…The improved CO 2 excretion is due to better perfusion of upper parts of the lung. 37 Askrog found an inverse linear correlation between pulmonary artery pressure and (a-ET)PCO2 .37 Thus, under conditions of constant lung ventilation, PETCO 2 monitoring can be used as a monitor of pulmonary blood flow. 2'45…”

Section: Cardiac Output and (A-et)pcomentioning

confidence: 98%