Effects of increasing left ventricular filling pressure in patients with acute myocardial infarction

Russell, Richard O.; Rackley, Charles E.; Pombo, Jaoquin; Hunt, David; Potanin, Constantine; Dodge, Harold T.

doi:10.1172/jci106371

Cited by 147 publications

(9 citation statements)

References 27 publications

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“…Although increased preload has been shown to increase ventricular performance in ischemic heart failure in man (28) or in the experimental animal (29), the present experiments suggest that this increase is achieved at the expense of an increase in the ischemic area, particularly in the deep regions of the heart. It has recently been observed (30) that acutely increased left ventricular preload with low molecular weight dextran reduces the anginal threshold in patients with ischemic heart disease.…”

Section: Control Preloadcontrasting

confidence: 55%

Mechanism for Flow Distribution in Normal and Ischemic Myocardium during Increased Ventricular Preload in the Dog

Kjekshus

1973

Circulation Research

123

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The effects of increased ventricular preload on the distribution of regional blood flow in normal and ischemic myocardium were determined in deep and superficial regions of the left ventricle by using labeled microspheres. The ratio of flow in deep regions to flow in superficial regions in nonischemic tissue was 1.06 ± 0.06 and increased to 1.14 ± 0.06 when left ventricular end-diastolie pressure was raised from 4.8 ± 1 mm Hg to 18 ± 2 mm Hg by intravenous infusion of blood. In ischemic areas the ratio of flow in deep regions to flow in superficial regions fell simultaneously from 0.71 ±0.12 to 0.45 ±0.07 ( P < 0.001). Control of coronary flow during increased preload was studied in a separate preparation in which coronary flow was decreased in steps by reducing coronary perfusion pressure during periods of constant cardiac performance. The increased preload was associated with loss of autoregulation of coronary flow. It is suggested that, in myocardium with unrestricted coronary supply, regional distribution of flow is independent of gradients in tissue pressure during the described changes in preload due to an autoregulatory mechanism. However, when autoregulation of coronary flow is abolished by coronary artery occlusion, the coronary bed is fully dilated, and distribution of flow is directly dependent on gradients in myocardial tissue pressure. Increased ventricular preload consequently augments the underperfusion of the subendocardial regions of an ischemic area.

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Section: Control Preloadcontrasting

confidence: 55%

Mechanism for Flow Distribution in Normal and Ischemic Myocardium during Increased Ventricular Preload in the Dog

Kjekshus

1973

Circulation Research

123

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“…When it is not possible to obtain pulmonary capillary wedge pressure, pulmonary arterial diastolic pressure may be used as an equivalent. Such substitution has been shown to be valid for patients without chronic pulmonary vascular disease (RUSSELL et al 1970). However, pulmonary arterial diastolic pressure, and even left atrial pressure, reflect only the mean left ventricular filling pressure.…”

Section: Calculated Parametersmentioning

confidence: 99%

Hemodynamic Response to Different Anesthetics during Open‐Heart Surgery

Maunuksela

1977

Acta Anaesthesiol Scand

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“…After myocardial infarction, there is a relative increase in this zone of hypo perfusion at the lung base, an increase in the zone 4 phenomenon. This is most likely due to an element of left ventricular failure and elevated pulmonary venous pressure, which are present at the time of infarction (18)(19)(20) but return to normal in the subsequent 2 to 3 days, as was demonstrated in 6 of the patients in whom pulmonary artery and wedge pressures and cardiac output measurements were done. This transient failure results in extravasation of fluid into the lung interstitium and increased interstitial pressure, a finding in conformity with experimental evidence that with increased pulmonary venous pressure, edema first appears in the interstitium of the dependent zone of the lung (21) and most prominently in the perivascular space (22).…”

Section: Discussionmentioning

confidence: 93%

Arterial Hypoxemia and Distribution of Pulmonary Perfusion after Uncomplicated Myocardial Infarction^1–³

Fj¹,

Kazemi²

1972

Am Rev Respir Dis

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__________________________________________________ ___To assess the consequences of myocardial infarction on the lung, pulmonary gas exchange and distribution of pulmonary perfusion and ventilation were studied after uncomplicated myocardial infarction in 35 patients in whom no clinical or radiographic evidence of congestive failure was apparent. Studies were performed in some of the patients during the first and third weeks after infarction and in 7 patients 2 to 6 months later.During the first week, the mean arterial oxygen tension was decreased to 72 mm Hg and the mean alveolar-arterial oxygen tension gradient increased to 47 mm Hg; both values improved in the convalescent phase. The mean arterial oxygen tension was 447 mm Hg and the mean alveolararterial oxygen tension gradient was 203 mm Hg while breathing 100 per cent oxygen during the first week after infarction; both values returned to normal in the 2-to 6-month follow-up studies. Distribution of pulmonary perfusion was abnormal in the first week. There was diminution of the normally occurring vertical gradient of perfusion in the lung, with relative hypoperfusion of lung base, increased perfusion of lung base, and increased perfusion of the apex. This abnormality returned toward normal in the follow-up period.No other hemodynamic abnormalities were demonstrated. The underlying mechanism of both hypoxemia and perfusion maldistribution appeared to be fluid accumulation in the lung interstitium secondary to transient left ventricular failure at the time of acute myocardial infarction.

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Effects of increasing left ventricular filling pressure in patients with acute myocardial infarction

Cited by 147 publications

References 27 publications

Mechanism for Flow Distribution in Normal and Ischemic Myocardium during Increased Ventricular Preload in the Dog

Mechanism for Flow Distribution in Normal and Ischemic Myocardium during Increased Ventricular Preload in the Dog

Hemodynamic Response to Different Anesthetics during Open‐Heart Surgery

Arterial Hypoxemia and Distribution of Pulmonary Perfusion after Uncomplicated Myocardial Infarction^1–³

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Effects of increasing left ventricular filling pressure in patients with acute myocardial infarction

Cited by 147 publications

References 27 publications

Mechanism for Flow Distribution in Normal and Ischemic Myocardium during Increased Ventricular Preload in the Dog

Mechanism for Flow Distribution in Normal and Ischemic Myocardium during Increased Ventricular Preload in the Dog

Hemodynamic Response to Different Anesthetics during Open‐Heart Surgery

Arterial Hypoxemia and Distribution of Pulmonary Perfusion after Uncomplicated Myocardial Infarction1–3

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Arterial Hypoxemia and Distribution of Pulmonary Perfusion after Uncomplicated Myocardial Infarction^1–³