Left Ventricular Function in Massive Pulmonary Embolism

Alpert, Joseph S.; Francis, Gary S.; Vieweg, W. Victor R.; Thompson, Stanley; Stanton, Kathleen; Hagan, Arthur D.

doi:10.1378/chest.71.1.108

Cited by 26 publications

(6 citation statements)

References 10 publications

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“…18 An abnormal E to F slope of the anterior mitral valve leaflet persisting for four months after pulmonary embolectomy has been reported in a patient with pulmonary embolism. 13 This finding would be consistent with reduced ventricular filling but may also represent altered left ventricular compliance, possibly due to altered left ventricular geometry. 19 As further evidence of altered left ventricular filling and function secondary to a reduced right ventricular output, stroke volume index and systolic time intervals have been shown to be abnormal in both acute and chronic cases of pulmonary embolism.…”

Section: Discussionsupporting

confidence: 59%

“…6,12 This encroaches on the left ventricular cavity, altering left ventricular compliance and raising left ventricular end-diastolic pressure (LVEDP). 13 It is postulated that septal bulging might partly account for both the altered left ventricular compliance and function. 14 There is evidence in support of this theory from animal studies where acute constriction of the pulmonary artery, or an increase in right ventricular end-diastolic pressure in the presence of constant left ventricular filling leads to an increase in left ventricular end-diastolic pressure.…”

Section: Discussionmentioning

confidence: 99%

“…19 As further evidence of altered left ventricular filling and function secondary to a reduced right ventricular output, stroke volume index and systolic time intervals have been shown to be abnormal in both acute and chronic cases of pulmonary embolism. 10,13,[20][21][22] The assessment of left ventricular function during excess right ventricular systolic loading, which occurs with pulmonary embolism, is therefore complicated by the altered loading of the left ventricle. For this reason, conventional measures of left ventricular function such as ejection fraction and left ventricular end-diastolic pressure may be misleadingly normal when left ventricular muscle function, assessed by studies of contractile element velocity, is actually markedly abnormal.…”

Section: Discussionmentioning

confidence: 99%

“…While pulmonary oedema may occur in patients with anatomically normal hearts, the fact that it is much more common in patients with disorders of the coronary circulation or aortic valves 5 is highly suggestive that altered left ventricular function plays an important role in the aetiology of the pulmonary oedema associated with pulmonary embolism. However, there are reports of cases where left ventricular end-diastolic pressure (or pulmonary artery wedge pressure) have been found to be low 2,13 in the presence of pulmonary oedema and where a patient without any evidence of left ventricular failure had pulmonary oedema for many years after pulmonary embolism. 4 Furthermore, one study of 14 patients suffering massive pulmonary embolism showed evidence only of right ventricular pressure overload and left ventricular underfilling, with no evidence of impaired left ventricular function to account for a low cardiac index.…”

Section: Discussionmentioning

confidence: 99%

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Pulmonary embolism as a cause of pulmonary oedema

Montgomery

Marshall

Woolf

et al. 1995

Clinical Intensive Care

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Acute pulmonary oedema is a well-described complication of pulmonary embolism. However, the relationship between these two conditions is not widely appreciated by physicians and the diagnosis of an underlying pulmonary embolism in patients with pulmonary oedema may well be missed. We describe two cases in which pulmonary oedema complicated pulmonary embolism, and discuss the possible factors involved in the development of oedema. These include altered left ventricular (LV) function, increased lung microvascular permeability, overperfusion and reperfusion injury. We also emphasise the importance of considering the possibility of an underlying pulmonary embolism in patients with pulmonary oedema so that appropriate thrombolytic therapy can be given early. Case histories Case oneA 78-year-old male ex-smoker with no previous history of cardiorespiratory symptoms presented with a 10-day history of dyspnoea. This had begun six days after a transurethral resection of a bladder tumour when he was awoken by fleeting sharp chest pain, and breathlessness which persisted until admission. On examination he was in sinus rhythm (80 bpm), with an audible third heart sound, a blood pressure of 145/80 mmHg, a jugular venous waveform visible 3 cm above the sternal angle and bilateral pitting oedema up to the lower thigh. Electrocardiography (ECG) showed occasional runs of 10 beats of atrial fibrillation (160 bpm). Arterial blood gases breathing room air were: pH 7.49, PaO 2 10.7 kPa, PaCO 2 4.3 kPa. Plain posteroanterior chest radiography (CXR) showed upper lobe blood diversion and interstitial shadowing. Routine haematology and biochemistry were normal.Left ventricular failure and paroxysmal atrial fibrillation were diagnosed by the admitting junior doctor, and treated with intravenous heparin, diuretics, and amiodarone. Twentyfour hours later the PaO 2 fell to 4.8 kPa (on room air), and the

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Section: Discussionsupporting

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Pulmonary embolism as a cause of pulmonary oedema

Montgomery

Marshall

Woolf

et al. 1995

Clinical Intensive Care

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“…LV systolic dysfunction commonly results from decreased RV output [ 16 ]. Acute PE increases pulmonary vascular resistance secondary to direct physical obstruction of the vascular bed, hypoxemia, and vasoconstriction within the pulmonary arterial system [ 17 ] (Figure 5 ). The acute rise in afterload causes RV dilation, flattening the interventricular septum and altering LV diastolic compliance and interventricular interdependence via the so-called “reverse Bernheim effect” [ 18 - 20 ].…”

Section: Discussionmentioning

confidence: 99%

Acute Saddle Embolus With Thrombus in Transit: A Case Report and Review of the Literature

Doodnauth¹,

Choi²,

Dunkley³

et al. 2022

Cureus

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Pulmonary embolism is a life-threatening medical emergency associated with right ventricular failure. Rarely, it impacts the left ventricle to the point of compromising the left ventricular (LV) ejection fraction. We present a case of a 73-year-old African American male with a medical history pertinent for intravascular large B-cell lymphoma who developed an acute saddle embolus with a “clot-in-transit” and profound LV systolic dysfunction. Our report illustrates how an acute saddle embolus may be associated with LV systolic dysfunction via the “reverse Bernheim effect.” Additionally, the report highlights the significance of a “clot-in-transit” and LV systolic dysfunction, as they both directly correlate with increased risk of mortality.

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