Wedge Pressure In Patients Research Articles

The Relationship Between Central Venous Pressure and Pulmonary Capillary Wedge Pressure in Patients with Aortic Stenosis

The Relationship Between Central Venous Pressure and Pulmonary Capillary Wedge Pressure in Patients with Aortic Stenosis

Relation between pulmonary venous flow and pulmonary wedge pressure: Influence of cardiac output

Multiple factors affect the systolic and diastolic components of pulmonary venous flow. It has been suggested that left ventricular function might influence the effects of filling pressures on indexes of pulmonary venous flow. The present study was designed to evaluate the effect of the pulmonary wedge pressures, left ventricular function, and cardiac output on the pulmonary vein flow pattern. Forty-five patients undergoing cardiac surgery were included in this study. Pulmonary venous flow and mitral flow variables were obtained by transesophageal echocardiography with hemodynamic variables obtained simultaneously. In the total group, there was no consistent relation between the pulmonary venous flow or the mitral flow parameters and the capillary wedge pressures. When patients were grouped according to normal (>2.2 L/min/m 2) or low (<2.2 L/min/m 2) cardiac index, a significant and positive relation was found between the systolic component of the pulmonary venous flow and the pulmonary wedge pressure in patients with normal cardiac index ( r = 0.69; p = 0.003). Conversely, in patients with low cardiac index there was also a significant although negative correlation between the systolic velocity integral and the pulmonary wedge pressure ( r = −0.58; p < 0.001). In conclusion, the systolic component of the pulmonary venous flow correlates closely and significantly with the capillary wedge pressures. The direction of this relation depends to a large extent on the total cardiac output and to a lesser extent on the left ventricular systolic function as assessed by the ejection fraction.

Doppler-derived mitral deceleration time of early filling as a strong predictor of pulmonary capillary wedge pressure in postinfarction patients with left ventricular systolic dysfunction

Objectives. The aim of this study was to investigate the correlations between Doppler-derlved transmitral flow velocity variables and pulmonary capillary wedge pressure in patients with severe left ventricular systolic dysfunction.Background. Abnormal relaxation and increased chamber stiffness have opposing effects on the left ventricular filling pattern. When both abnormalities are present at the same time, as often occurs in patients with systolic dysfunction, the ability of Doppler recording to assess diastolic function and predict left ventricular fillng pressure may be significantly compromised.Method. Pulmonary capillary wedge pressure and Doppler transmitral flow velocity profile were simultaneously recorded in 140 postinfarction patients with ejection fraction ≤35%.Results. Correlation between the ratio of mitral peak low velocity in early diastole to peak low velocity in late diastole (E/A ratio) and pulmonary capillary wedge pressure was weak (r = 0.65). Although the specificity of E/A ≥ 2 in predicting ≥29 mm Hg in pulmonary capillary wedge pressure was high (99%), its sensitivity was low (43%). Conversely, a very close negative correlation was found between mitral deceleration time of early filling and pulmonary capillary wedge pressure (r = −0.91). Sensitivity and specificity of ≤120 ms in deceleration time in predicting ≥20 mm Hg in pulmonary capillary wedge pressure were 100% and 99%, respectively.Conclusions. Doppler-derived mitral deceleration time of early filling provides a simple and accurate means of estimating pulmonary capillary wedge pressure that is particularly useful in patients with a normal or normalized mitral low velocity pattern.

Regional distribution of lung perfusion and ventilation in patients with chronic congestive heart failure and its relationship to cardiopulmonary hemodynamics

To study the relationship between the distribution of pulmonary blood flow, pulmonary ventilation, and pulmonary capillary wedge pressure, we studied six patients with chronic congestive heart fallure (CHF) (New York Heart Association classes II and III) at rest and during exercise. We used krypton 81 m ( 81mKr) and technetium 99m ( 99mTc) to assess lung ventilation and perfusion at rest and during exercise. Hemodynamic measurements were obtained with a balloon floatation thermodilution catheter. At rest, the upper lung zones of patients with CHF received significantly higher proportions of the blood flow compared with previously published data in normal volunteers. During exercise, however, the fractional perfusion to apices did not change, which suggests that apical flow redistribution is already maximized at rest. Measured pulmonary capillary wedge pressure failed to correlate with the upper zone or the ratio of upper-to-lower zone perfusion counts. Our findings suggest that upper zone flow redistribution may be associated with high, normal, or low capillary wedge pressure and therefore does not correlate with the pulmonary capillary wedge pressure in patients with chronic CHF.

Changes in the levels of plasma atrial natriuretic peptide, hemodynamic measurements, and the levels of vasoactive hormones during the clinical course of congestive heart failure.

To investigate the mechanism for the release of human atrial natriuretic peptide (hANP) and the pathophysiological role of hANP in patients with congestive heart failure (CHF), plasma hANP levels in patients with dilated cardiomyopathy (DCM) or acute myocardial infarction (AMI) were determined serially, and the relationship between plasma ANP levels and hemodynamic measurements or various vasoactive hormones was analyzed during the clinical course of congestive heart failure. In 63 patients with either AMI or DCM, plasma hANP, plasma renin activity, aldosterone concentration, and catecholamines were measured over 4 weeks, during the course of CHF. Cardiac catheterization with a Swan-Ganz catheter was also performed. Plasma hANP in patients with DCM was elevated continuously during the clinical course. Plasma hANP levels in patients with AMI of Groups II and IV of Forrester's class decreased on days 7 and 14 and those in patients with AMI of Group I changed within normal limits. Plasma hANP levels were correlated positively with pulmonary artery pressure and pulmonary capillary wedge pressure in patients with AMI or DCM. Plasma renin activity, noradrenaline, and adrenaline levels were elevated in the acute phase of myocardial infarction and had a tendency to decrease upon improvement in clinical status. Plasma renin activity and noradrenaline level correlated positively with plasma hANP levels. These data indicate that plasma hANP levels are regulated by atrial distension and severity of cardiac impairment, and that plasma hANP and plasma renin activity or catecholamines correlated closely during the clinical course of CHF, indicating that these hormones may be involved in the volume and electrolytes status in CHF.

Cardiovascular time course after digoxin administration in left ventricular dysfunction after coronary artery bypass grafting

Intravenous digoxin, 1 mg, was administered over 8 hours to 10 cardiac patients with left ventricular (LV) dysfunction after coronary artery bypass grafting. The cardiovascular effects of digoxin were monitored over 20 hours by indwelling pulmonary artery and radial artery lines and were compared with those of a control group of 10 patients who had normal postoperative LV function. Digoxin administration produced an increased cardiac index and mean arterial blood pressure within 2 hours. Within 4 hours after digoxin administration pulmonary artery wedge pressure in patients receiving digoxin was significantly lower than in control patients. At 16 hours there was a significant increase in both the LV stroke work and LV stroke work index in patients receiving digoxin vs control patients. Two patients receiving digoxin and 3 control patients had changes in cardiac rhythm during the study. Thus, digoxin can be safely administered to postoperative patients with LV dysfunction and is an acceptable inotropic agent.

Response of normal and diseased epicardial coronary arteries to vasoactive drugs: quantitative arteriographic studies

Coronary vasodilators known to be effective in effort and vasospastic angina were studied in 93 patients undergoing catheterization for evaluation of chest pain. The ischemia-provoking stresses were isometric handgrip (25% of maximum for 4 to 5 minutes) or ergonovine maleate (0.2 mg intravenously). Hemodynamic changes and changes in angiographic diameter of epicardial coronary arteries were measured during these stresses, with and without drug administration. Drugs included intravenous diltiazem (0.25 mg/kg load + 0.003 mg/ kg/min), intravenous verapamil (0.14 mg/kg load + 0.0075 mg/kg/min) and intracoronary (0.012 mg/min X 4 minutes) and sublingual (0.4 mg) nitroglycerin. From these studies, the following statistically valid conclusions were reached. First, nitroglycerin is a potent dilator of epicardial coronary arteries, increasing normal luminal area an average of 28% and luminal area in significantly stenotic segments by 29%. Second, verapamil and diltiazem are nonsignificant epicardial coronary dilators (9% and 4% luminal area increase, respectively). Similarly, diltiazem does not dilate significant coronary stenoses. Third, sustained isometric handgrip increases systemic blood pressure and heart rate by reflex activation of the sympathetic nervous system. By this means, handgrip also constricts luminal area in normal and diseased coronary segments by 20% and 22%, respectively. One result of these changes is a handgrip-induced, ischemic 56% rise in pulmonary wedge pressure in patients with significant stenosis. Fourth, intracoronary nitroglycerin, in very small doses, does not block the systemic hemodynamic response to handgrip, but prevents handgrip-induced coronary constriction and the associated ischemic left ventricular dysfunction. Thus, in states of sympathetic activation, vasotonic constriction of significant lesions is a major mechanism of the ischemic response, and its prevention is a major mechanism of the nitroglycerin response. Last, verapamil and diltiazem infusions block the coronary constriction observed during handgrip in normal and diseased coronary segments. Verapamil almost completely abolishes the coronary constriction seen after ergonovine. Thus, unlike nitroglycerin, verapamil and diltiazem are not direct epicardial coronary dilators, but act by preventing the constriction of diseased coronary segments induced by α-adrenergic and serotonergic coronary receptor stimulation.

Enalapril: a review of human pharmacology.

Enalapril, an orally-active, long-acting, nonsulphydryl angiotensin-converting enzyme (ACE) inhibitor, is extensively hydrolysed in vivo to enalaprilat, its bioactive form. Bioactivation probably occurs in the liver. Metabolism beyond activation to enalaprilat is not observed in man. Administration with food does not affect the bioavailability of enalapril; excretion of enalapril and enalaprilat is primarily renal. Peak serum enalaprilat concentrations are reached 4 hours post-dose, and the profile is polyphasic with a prolonged terminal half-life (greater than 30 hours) due to the binding of enalaprilat to ACE. Steady-state is achieved by the fourth daily dose, with no evidence of accumulation. The effective accumulation half-life following multiple dosing is 11 hours. Higher serum concentrations and delayed urinary excretion occur in patients with severe renal insufficiency. Enalapril reduces blood pressure in hypertensive patients by decreasing systemic vascular resistance. The blood pressure reduction is not accompanied by an increase in heart rate. Furthermore, cardiac output is slightly increased and cardiovascular reflexes are not impaired. Once- and twice-daily dosage regimens reduce blood pressure to a similar extent. Enalapril increases renal blood flow and decreases renal vascular resistance. Enalapril also augments the glomerular filtration rate in patients with a glomerular filtration rate less than 80 ml/min. Enalapril reduces left ventricular mass, and does not affect cardiac function or myocardial perfusion during exercise. There is no rebound hypertension after enalapril therapy is stopped. Enalapril does not produce hypokalaemia, hyperglycaemia, hyperuricaemia or hypercholesterolaemia. When combined with hydrochlorothiazide, enalapril attenuates the undesirable diuretic-induced metabolic changes. Therapeutic doses of enalapril do not affect serum prolactin and plasma cortisol in healthy volunteers or T3, rT3, T4 and TSH in hypertensive patients. Enalapril has natriuretic and uricosuric properties. The antihypertensive effect of enalapril is potentiated by hydrochlorothiazide, timolol and methyldopa, but unaffected by indomethacin and sulindac. No interactions occur between enalapril and frusemide, hydrochlorothiazide, digoxin and warfarin. The bioavailability of enalapril is slightly reduced when propranolol is coadministered, but this does not appear to be of any clinical significance. Enalapril increases cardiac output and stroke volume and decreases pulmonary capillary wedge pressure in patients with congestive heart failure refractory to conventional treatment with digitalis and diuretics.(ABSTRACT TRUNCATED AT 400 WORDS)

Prospective study comparing different echocardiographic measurements of pulmonary capillary wedge pressure in patients with organic heart disease other than mitral stenosis

In 25 patients with cardiac disease, but free of left ventricular inflow obstruction, the electrocardiogram and M-mode echocardiogram of the aortic root, left atrium and both the mitral and the aortic valves were obtained simultaneously with the pulmonary artery wedge pressure (PAWP) during right heart catheterization. The echocardiographic measurements of the left atrial size, PR-AC interval, left atrial emptying index and the ratio between the electrocardiographic Q wave to mitral valve closure (Q-MVC) and between aortic valve closure to the mitral E point (AVC-E) were correlated to the pulmonary artery wedge pressure by means of linear regression analysis. A formula in which PAWP = 36.6 (Q-MVC/AVC-E)-- 2 was prospectively used to study the measured pressure in the current group of patients. The pulmonary artery wedge pressure derived from these latter measurements correlated well with the invasive measurement of this pressure (r = 0.91). The pulmonary artery wedge pressure calculated by echocardiography differed from the pulmonary artery wedge pressure measured by catheterization by 3 mm Hg or less in 19 of the 25 patients, by 4 mm Hg or less in 22 patients and by 6 mm Hg or less in 24 patients. Although the correlation between the (Q-MVC/AVC-E) ratio and measured pulmonary artery wedge pressure was highly significant (r = 0.91, probability [p] less than 0.001, n = 25), the left atrial emptying index, PR-AC and left atrial size revealed poor correlation coefficients (r = 0.45, r = 0.45 and r = 0.56 [p less than 0.05]), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Estimation of pulmonary artery wedge pressure from chest radiograph in patients with chronic congestive cardiomyopathy and ischaemic cardiomyopathy.

In order to define the relation between chest x-ray findings and the level of pulmonary artery wedge pressure in patients with chronic congestive cardiomyopathy, 82 patients had chest radiographs before undergoing 92 haemodynamic studies. The studies were divided into three groups according to the level of pulmonary artery wedge pressure (PAWP) (group 1: less than 15 mmHg, group 2: 15 to 24 mmHg, group 3: greater than or equal to 25 mmHg. Venous distribution, interstitial oedema, pleural effusions, left atrial enlargement, and right ventricular enlargement each occurred in less than 10 per cent of group 1 studies. Radiological abnormalities generally distinguished group 1 from group 2, but none except cardiothoracic ratio distinguished group 2 from group 3. Cardiothoracic ratio correlated best with pulmonary artery wedge pressure (r = 0.70). Alveolar oedema was uncommon when PAWP greater than or equal to 25 mmHg, occurring in 32 per cent of group 3 studies. Stepwise multiple linear regression analysis showed that cardiothoracic ratio, alveolar oedema, interstitial oedema, and left atrial size each contributed independently to the prediction of PAWP. The regression analysis improved the accuracy of the estimation of PAWP from the findings noted on standard chest radiographs.

Relationship of wedge pressure to end-diastolic volume in patients undergoing myocardial revascularization

Myocardial performance is thought to follow changes in pulmonary capillary wedge pressure in patients undergoing myocardial revascularization. This theory is based on the assumption that changes in pulmonary capillary wedge pressure accurately reflect end-diastolic volume and, thus, fiber length of the left ventricle. To examine the validity of this assumption, we evaluated the relationship between pulmonary capillary wedge pressure and end-diastolic volume in 10 patients undergoing myocardial revascularization. A coaxial cardiac scintillation probe was used to obtain serial radiocardiograms on which ejection fraction is graphically displayed and a thermal dilution catheter was used to measure stroke volume. End-diastolic volume was derived by dividing stroke volume by ejection fraction. Following base-line measurement of pulmonary capillary wedge pressure and end-diastolic volume, the circulation of each patient was volume loaded from the pump oxygenator. Multiple measurements made at different volume loading conditions before and after bypass showed no correlation between end-diastolic volume and pulmonary capillary wedge pressure in the over-all patient population. When the end-diastolic volume was small (105 ml or less), the mean pulmonary capillary wedge pressure was 9 ± 0.8 torr. When the end-diastolic volume increased by 50%, the pulmonary capillary wedge pressure was statistically unchanged, 10.3 ± 1 torr. A substantial increase in end-diastolic volume may occur with minimal change in pulmonary capillary wedge pressure. These data suggest that overdistention of the ventricle may be undetected when one relies on wedge pressure to assess myocardial performance. It may be detrimental, therefore, to seek an arbitrarily elevated pulmonary capillary wedge pressure at the termination of cardiopulmonary bypass (CPB).

Isosorbide dinitrate in acute and chronic heart failure.

The hemodynamic effects of sublingual isosorbide dinitrate (ISD) were studied in 12 patients with congestive heart failure (CHF) of many causes. The duration of CHF in the chronic group varied from 3 to 62 months (mean, 29.5). Hemodynamic parameters were obtained serially before and 10, 20, 30, 45, 60, and 120 min after a 5 to 15 mg dose of ISD sublingually. The hemodynamic effects were pronounced at 45 min and returned to control levels in 120 min. Heart rate did not change. Hemodynamic parameters that changed after ISD were mean arterial pressure (-7%, p less than 0.05), mean pulmonary artery pressure (-17%, p less than 0.05), and mean pulmonary capillary wedge pressure (-29%, p less than 0.005). Mean cardiac index (+3%, p = NS) and mean stroke work index rose (+9.4%, P X NS); mean total systemic resistance fell (-10%, p = NS). Thus the duration of hemodynamic effects of ISD is less than 2 hr and sublingual ISD induces beneficial reduction of pulmonary capillary wedge pressure in patients with acute and chronic CHF without increasing cardiac index and stroke work index.

Relationship between colloid osmotic pressure and pulmonary artery wedge pressure in patients with acute cardiorespiratory failure : Weil MH, Henning RJ, Morissette M. Michaels S: Am J Med 64: 643–650, 1978

Relationship between colloid osmotic pressure and pulmonary artery wedge pressure in patients with acute cardiorespiratory failure : Weil MH, Henning RJ, Morissette M. Michaels S: Am J Med 64: 643–650, 1978

Relationship between colloid osmotic pressure and pulmonary artery wedge pressure in patients with acute cardiorespiratory failure

Close relationships between progressive respiratory failure, roentgenographic signs of pulmonary opacification and decreases in the difference between colioid osmotic pressure of plasma and the pulmonary artery wedge pressure (colloid-hydrosatic pressure gradient) were demonstrated in 49 critically ill patients with multisystem failure, and especially in patients in shock. The potential Importance of this relationship is underscored by the observation that fatal progression of pulmonary edema was related to a critical reduction in the colloid-hydrostatic pressure gradient to levels of less than 0 mm Hg. More often, reduction in colloid osmotic pressure rather than Increases in left ventricular filling pressure (pulmonary artery wedge pressure) accounted for the decline in colloid-hydrostatic pressure gradient. Routine measurement of colloid osmotic pressure, preferably in conjunction with pulmonary artery wedge pressure, is likely to improve understanding of the mechanisms of acute pulmonary edema.

Combined Oral Hydralazine-Nitrate Therapy in Left Ventricular Failure: Hemodynamic Equivalency to Sodium Nitroprusside

Administration of sodium nitroprusside increases the cardiac output and decreases the pulmonary wedge pressure in patients with left ventricular failure. Drugs suitable for long-term oral administration have not been as effective as intravenous therapy with sodium nitroprusside. We compared the hemodynamic effects of combined oral therapy with hydralazine and isosorbide dinitrate (100 mg of hydralazine plus 10 to 50 mg of chewable isosorbide dinitrate) to the effects of intravenous therapy with sodium nitroprusside in 15 patients with congestive heart failure (class 3 to 4) due to cardiomyopathy. Therapy with sodium nitroprusside reduced the mean arterial pressure by 11.3 mm Hg and the pulmonary wedge pressure by 10.4 mm Hg while increasing the cardiac index by 0.72 L/min/sq m. The combined oral therapy also reduced the mean arterial pressure by 12.0 mm Hg and the pulmonary wedge pressure by 12.0 mm Hg while increasing the cardiac index by 0.81 L/min/sq m in the same patients. All changes were significant (P

Pulmonary edema related to changes in colloid osmotic and pulmonary artery wedge pressure in patients after acute myocardial infarction.

Pulmonary artery wedge and plasma colloid osmotic pressures and their relationship to pulmonary edema were investigated in 26 patients with acute myocardial infarction of whom 14 developed pulmonary edema. In the absence of pulmonary edema, both the pulmonary artery wedge pressure and plasma colloid osmotic pressure were in normal range; after onset pulmonary edema, a moderate increase in pulmonary wedge pressure and reduction in plasma colloid osmotic pressure were observed. When the gradient between the plasma colloid osmotic pressure and the pulmonary artery wedge pressure was calculated, highly significant differences were demonstrated (P less than 0.002). In the absence of pulmonary edema, this gradient averaged 9.7 (plus or minus 1.7 SEM) torr; following appearance of pulmonary edema, it was reduced to 1.2 (plus or minus 1.3) torr. During therapy with digoxin and furosemide, reversal of pulmonary edema was closely related to a concomitant change in the colloid osmotic-hydrostatic pressure gradient. These observations indicate that both increases in pulmonary capillary pressure and decreases in colloid osmotic pressure may follow the onset of pulmonary edema. Such decline in colloid osmotic pressure and especially the reduction in colloid osmotic-hydrostatic capillary pressure gradient may favor transudation of fluid into the lungs.

Distribution of blood flow in the lungs in acute pulmonary edema in dogs.

ArticleDistribution of blood flow in the lungs in acute pulmonary edema in dogs.A L Muir, D L Hall, P Despas, and J C HoggA L Muir, D L Hall, P Despas, and J C HoggPublished Online:01 Dec 1972https://doi.org/10.1152/jappl.1972.33.6.763MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByLung transplant after prolonged ex vivo lung perfusion: predictors of allograft function in swine31 July 2018 | Transplant International, Vol. 31, No. 12Pulmonary HemodynamicsPhosphoinositide 3-kinase, Src, and Akt modulate acute ventilation-induced vascular permeability increases in mouse lungsTakashige Miyahara, Kazutoshi Hamanaka, David S. Weber, Douglas A. Drake, Mircea Anghelescu, and James C. Parker1 July 2007 | American Journal of Physiology-Lung Cellular and Molecular Physiology, Vol. 293, No. 1The spatial distribution of pulmonary lesions in severe ARDS An autopsy study of 35 casesPathology - Research and Practice, Vol. 194, No. 7Experimental Hydrostatic Pulmonary Edema in Rabbit Lungs: MorphologyAmerican Review of Respiratory Disease, Vol. 147, No. 4A quantitative correlation of extravascular lung water accumulation with vascular permeability and hydrostatic pressure measurements: a positron emission tomography studyJournal of Critical Care, Vol. 5, No. 3The effects of norepinephrine on gas exchange and regional blood flows after massive bead embolizationJournal of Critical Care, Vol. 5, No. 3Respiratory and non-respiratory lung function indices during the development and resolution ofO,S,S-trimethyl phosphorodithioate-induced lung damage in the rat. A chemical model of adult respiratory distress syndromeJournal of Applied Toxicology, Vol. 7, No. 6Effect of edema on segmental vascular resistance in isolated lamb lungs determined by micropuncture.Circulation Research, Vol. 61, No. 2Pulmonary interstitial resistanceAnnals of Biomedical Engineering, Vol. 15, No. 2Gas Exchange in Acute Lung InjuryCritical Care Clinics, Vol. 2, No. 3Pulmonary Interstitial Spaces and Lymphatics1 January 2011Pulmonary EdemaVeterinary Clinics of North America: Small Animal Practice, Vol. 15, No. 5Sepsis and Pulmonary EdemaClinics in Chest Medicine, Vol. 6, No. 3Adult respiratory distress syndrome--I. Aetiology and mechanisms.Postgraduate Medical Journal, Vol. 60, No. 706The Influence of Cardiovascular Function on Gas ExchangeClinics in Chest Medicine, Vol. 4, No. 2Mechanisms and consequences of pulmonary edema: Cardiac lung, shock lung, and principles of ventilatory therapy in adult respiratory distress syndromeAmerican Heart Journal, Vol. 103, No. 1GAS EXCHANGE IN THE ADULT RESPIRATORY DISTRESS SYNDROMEClinics in Chest Medicine, Vol. 3, No. 1Regional edema formation in isolated perfused dog lungs.Circulation Research, Vol. 48, No. 1Pulmonary OedemaBritish Journal of Diseases of the Chest, Vol. 74Ozone exposure, adaptation, and changes in lung elasticityEnvironmental Research, Vol. 19, No. 2Der Einfluß von Blut und parenteral zugeführter Flüssigkeit auf die Lungenstrombahn und Methoden zur quantitativen Erfassung statischer und dynamischer Flüssigkeitsvolumina in der LungeRelationship between colloid osmotic pressure and pulmonary artery wedge pressure in patients with acute cardiorespiratory failureThe American Journal of Medicine, Vol. 64, No. 4Ventilatory management in acute pulmonary edemaThe American Journal of Medicine, Vol. 54, No. 5Lung water balance More from this issue > Volume 33Issue 6December 1972Pages 763-9 https://doi.org/10.1152/jappl.1972.33.6.763PubMed4643854History Published online 1 December 1972 Published in print 1 December 1972 Metrics

Left ventricular failure in acute myocardial infarction

In 30 patients with acute myocardial infarction complicated by either advanced atrioventricular or bundle branch block, pulmonary arterial wedge pressures were studied in relation to clinical and radiographic features of left ventricular failure, changes in central venous and pulmonary arterial pressures, and arterial hypoxemia. An increase in mean pulmonary arterial wedge pressure was poorly correlated with the presence of dyspnea, audible third or fourth heart sounds, or persistent basal rales; however, it was significantly related to radiographic evidence of pulmonary venous dilatation or edema, a systolic blood pressure of less than 100 mm Hg, gallop rhythm associated with tachycardia, and heart rate in patients with sinus rhythm and normal atrioventricular conduction. Increased mean right atrial pressure indicated increased mean pulmonary arterial wedge pressure in patients with isolated anterior infarction, but in several patients with isolated inferior infarction the level of right atrial pressure was disproportionately high. The pulmonary arterial diastolic pressure closely reflected the mean pulmonary arterial wedge pressure in the absence of obstructive airways disease or pulmonary embolism. The level of the arterial oxygen tension fell as the mean pulmonary arterial wedge pressure rose, but it was considerably reduced in some patients with only moderately increased pressures. However, the latter usually had radiographic evidence of pulmonary venous dilatation or edema, suggesting that the pressure had been elevated previously to higher levels.