Lung Water in Patients with Acute Myocardial Infarction

Biddle, Theodore L.; Khanna, P. K.; Yu, Paul N.; Hodges, Morrison; Shah, Pravin M.

doi:10.1161/01.cir.49.1.115

Cited by 31 publications

(9 citation statements)

References 29 publications

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“…The intensity of lung liquid accumulation is determined by left ventricular function [28], and its sequence of accumulation was well described by STAUB et al [29]. In the present study, histopathological analysis showed significant alveolar and bronchial liquid accumulation only in the presence of infarction in animals not being administered propranolol (group I).…”

Section: Discussionsupporting

confidence: 84%

Pulmonary morphofunctional effects of acute myocardial infarction

Faffe¹,

Chagas²,

Medeiros³

et al. 1999

Eur Respir J

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Acute myocardial infarction (AMI) may yield several respiratory changes. Nevertheless, no comprehensive pulmonary morphological/physiological correlation has been performed under this condition. The aims of the present investigation were: 1) to determine the respiratory parameters in an experimental model of coronary artery occlusion, 2) to relate these results to findings from lung histopathology, and 3) to evaluate the effects of propranolol used prior to AMI.Twenty-eight rats were anaesthetized and mechanically ventilated. In the control group (C), a suture line was passed around the left anterior descending coronary artery (LADCA). The infarct group (I) was similarly prepared but the LADCA was ligated and infarct resulted. In the control/propranolol (CP) and infarct/propranolol (IP) groups, propranolol was intravenously injected 5 min before surgery as performed in groups C and I, respectively. Lung static (EL,st) and dynamic (EL,dyn) elastances, airway resistance (RL,int), and viscoelastic/inhomogeneous pressure (DP2L) were determined before and 30, 60 and 120 min after surgery.In group I, EL,st, EL,dyn, RL,int and DP2L increased progressively throughout the experiment, and were higher than those found in groups C, CP and IP. All respiratory parameters but EL,st remained unaltered in group IP. Lung histopathological examination demonstrated alveolar, interstitial and intrabronchial oedema in group I. Group IP showed only interstitial oedema.Acute myocardial infarction yields lung resistive, elastic and viscoelastic changes. The last two results from alveolar and interstitial oedema, respectively. The previous use of propranolol diminishes respiratory changes.

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Section: Discussionsupporting

confidence: 84%

Pulmonary morphofunctional effects of acute myocardial infarction

Faffe¹,

Chagas²,

Medeiros³

et al. 1999

Eur Respir J

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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%

“…al., 1981), and increased lung water (PEV) has been measured in about 15% of patients with MI and normal pulmonary wedge pressure (Biddle et al, 1974).…”

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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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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“…The patients during acute coronary syndrome are vulnerable to develop backpressure changes on pulmonary bed presenting as the pulmonary oedema (1–3), and the associated ventilation perfusion mismatch (4,5). Short‐term better outcome of active smokers ‘smokers paradox’ during ACS has been reported (8,9).…”

Section: What’s Knownmentioning

confidence: 99%