Left ventricular failure in acute myocardial infarction

Lassers, B. W.; George, Michael E.D.; Anderton, J. L.; Higgins, Michael R.; Philp, T.

doi:10.1016/0002-9149(70)90589-8

Cited by 70 publications

(10 citation statements)

References 29 publications

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“…Although microvascular hypertension is a frequent cause of pulmonary edema in this setting, occasionally the two do not co-exist. Discrepancies between pulmonary wedge pressure on the one hand and lung water measurements (Biddle et al, 1974), clinical (Nixon and Durth, 1968;Timmis et al, 1981), and radiographic (Lassers et al, 1970;Kostuk et al, 1978) evidence of pulmonary edema on the other usually have been attributed to a phase lag between lowering of pressure and water clearance from the lung. Nonhydrostatic mediation has not generally been suspected.…”

Section: Discussionmentioning

confidence: 99%

“…Pulmonary edema which develops in the setting of an acute myocardial infarction (MI) is generally believed to result solely from high pulmonary microvascular pressure, since depressed myocardial contractility, decreased left ventricular compliance, and peripheral venoconstriction commonly raise the pressure of the lesser circulation during acute MI. However, radiographic and clinical signs of pulmonary edema during MI are noted occasionally despite the presence of normal pulmonary wedge pressure (Nixon and Durth, 1968;Lassers et al, 1970; Kostuk et al, 1978;Timmis et …”

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confidence: 99%

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Non-hydrostatic pulmonary edema after coronary artery ligation in dogs. Protective effect of indomethacin.

Richeson¹,

Paulshock²,

Yun³

1982

Circulation Research

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SUMMARY Pulmonary edema which develops during acute myocardial infarction is generally believed to result solely from pulmonary microvascular hypertension. However, patients with myocardial infarction and pulmonary edema occasionally are found to have normal pulmonary wedge pressure. We report data indicating that pulmonary edema develops after coronary artery ligation despite stable microvascular pressure. Four groups of open-chest dogs were studied: (1) nine dogs with left anterior descending coronary artery ligation, (2) seven dogs with sham coronary ligation, (3) seven dogs ligated after beginning an infusion of indomethacin (5 mg/kg per hr), and (4) five dogs ligated after an infusion of the drug's vehicle was begun. Extra vascular lung water and pulmonary blood volume were measured at hourly intervals during the 2 hours before and after coronary ligation or sham ligation. Gravimetric lung water was measured immediately thereafter. Changes of net pulmonary intravascular driving force (the difference of microvascular hydrostatic and oncotic pressure) after ligation or sham ligation were small and comparable in all groups. Pulmonary blood volume did not change in any group. Pulmonary extravascular water volume remained constant in the sham group but rose significantly in the ligated group. Gravimetric lung water also was significantly higher in the latter group. We interpret these results to indicate that factors other than microvascular pressure can mediate the formation of edema during acute myocardial infarction; increased pulmonary microvascular permeability may be responsible. Indomethacin infusion blocked the formation of edema after coronary ligation, even though net microvascular driving force was highest in this group. Infusion of the vehicle alone did not prevent edema. The mechanism by which indomethacin exerts this protective effect is unclear but is probably a result of its inhibition of cyclo-oxygenase or cyclic nucleotide phosphodiesterase. Circ Res 50: 301-309, 1982PULMONARY edema is commonly categorized as "cardiogenic" or "non-cardiogenic," with the implication that the former type is mediated by pulmonary microvascular hypertension, whereas altered endothelial permeability accounts for the development of the latter form (Robin et al., 1972;Staub, 1974aStaub, , 1978. Pulmonary edema which develops in the setting of an acute myocardial infarction (MI) is generally believed to result solely from high pulmonary microvascular pressure, since depressed myocardial contractility, decreased left ventricular compliance, and peripheral venoconstriction commonly raise the pressure of the lesser circulation during acute MI. However, radiographic and clinical signs of pulmonary edema during MI are noted occasionally despite the presence of normal pulmonary wedge pressure (Nixon and Durth, 1968;Lassers et al., 1970; Kostuk et al., 1978;Timmis et

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Non-hydrostatic pulmonary edema after coronary artery ligation in dogs. Protective effect of indomethacin.

Richeson¹,

Paulshock²,

Yun³

1982

Circulation Research

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“…Most doctors use chest radiography as a main guide to diuretic requirements. 2 We have drawn attention to a small subgroup in whom the appearances may mislead. When cardiac output is adequate excess diuretics cause relatively little harm; but for patients with low cardiac output a further reduction in left ventricular filling pressure will precipitate or worsen cardiogenic shock.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary oedema without critical increase in left atrial pressure in acute myocardial infarction.

Fowler¹,

Burwood²,

Gishen³

et al. 1981

BMJ

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pacemaker was working satisfactorily and there had been complete resolution of the pneumopericardiurn.Three months later the patient presented with pleuritic chest pain and was admitted to hospital after a syncopal episode. She was found to be feverish and to have radiological evidence of both pericardial and pleural effusions. In addition the epicardial pacemaker was intermittently failing to capture. Postcardiotomy syndrome was diagnosed and, though aspirin resulted in rapid improvement of symptoms and of the pericardial and pleural effusions, the pacemaker continued to show intermittent failure to capture. In view of the syncopal episode a new permanent endocardial pacing system was inserted electively through a right cephalic vein cut-down, using a wedged electrode. Thereafter she made an uncomplicated recovery and was discharged home. DiscussionIn most cases effective permanent cardiac pacing may be established with a low incidence of complications.'4 The common causes of early failure of endocardial pacing are poor positioning of the electrode initially and subsequent displacement.' Less common but well recognised are perforation of the myocardium, fracture of the lead, infection, and failure of the generator. Temporary endocardial pacing in our patient resulted in a pneumopericardium. Presumably the electrode had penetrated not only the right ventricle but also the pericardium into the adjacent lung.Pericarditis after epicardial pacing is a well-recognised complication.5 In our patient the early postoperative pericarditis was followed by recurrent attacks: these were thought to be due to the postcardiotomy syndrome as no infective, autoimmune, or other cause could be identified. The epicardial electrodes themselves, however, may result in focal inflammation and cause a relapsing pericarditis. Pulmonary oedema without critical increase in left atrial pressure in acute myocardial infarctionTwelve patients with acute myocardial infarction and radiological evidence of pulmonary oedema were observed in whom the left atrial pressure, measured indirectly as pulmonary artery end-diastolic pressure, was not critically increased (range 5-12 mm Hg with reference to sternal angle). Eight of the patients had been treated with frusemide, but only six had responded; hence in at least half of the series diuresis could not account for the anomalous finding. Six patients with low cardiac output were given infusions to expand plasma volume. Appreciable increments in mean values for cardiac index (1-6 to 2-0 1/min/ m2), stroke index (18 to 23 ml/beat/m2), mean arterial pressure (65 to 86 mm Hg), and pulmonary artery end-diastolic pressure (8 to 15 mm Hg) were recorded. This group, and the remaining six patients with higher cardiac output, survived to leave hospital.Delay in radiographic clearing after a fall of left atrial pressure was a possible explanation for the relaRoyal

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“…Hemodynamic studies have shown that heart failure is common in acute myocardial infarction (Lassers et al, 1970;Rackley and Russell, 1972;Ram0 el al., 1970;Wolk et al, 1972). Although furosemide has been found to be an effective and safe diuretic agent, there is still some difference of opinion as to whether it should be used routinely after myocardial infarction (Mond et al, 1974;Stock, 1970).…”

Section: Introductionmentioning

confidence: 99%

Evaluation of diuretic therapy by impedance cardiography in acute myocardial infarction

Gabriel

Ekelund

Orö

1980

Clinical Cardiology

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Summary:Changes in transthoracic electrical impedance (TEI) were recorded in 20 patients with acute myocardial infarction before, during, and 60 min after intravenous administration of furosemide (Impuganm). The major change was an increase in TEI (ZO) (6.2%, p0.05). Heart rate and blood pressure remained unchanged. It was possible to differentiate between two types of TEI changes after furosemide. In 10 patients there was an early and rapid increase in ZO (type A), while the rest of the patients showed a decreased or unchanged ZO followed by a slow increase (type-B). The line describing the mean ZO change in type A was significantly higher than that of type B and fell outside f 2 SEM of the line describing the mean ZO change found in five normal subjects (type C). The ZO change in type B was similar to that in type C. It is assumed that Z , change in type A may represent patients with an increased amount of extravascular fluid (heart failure), while the change in type B represents patients without heart failure. This assumption is based on the difference in dependency of TEI on extravascular volume versus intravascular volume changes. It is suggested that the impedance method may be used as a simple noninvasive method to assess the effect of diuretic therapy and may have the value of detecting extravascular thoracic fluids in acute myocardial infarction.

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Left ventricular failure in acute myocardial infarction

Cited by 70 publications

References 29 publications

Non-hydrostatic pulmonary edema after coronary artery ligation in dogs. Protective effect of indomethacin.

Non-hydrostatic pulmonary edema after coronary artery ligation in dogs. Protective effect of indomethacin.

Pulmonary oedema without critical increase in left atrial pressure in acute myocardial infarction.

Evaluation of diuretic therapy by impedance cardiography in acute myocardial infarction

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