Haemodynamic Effects of Intravenous Frusemide in Patients with Myocardial Infarction and Left Ventricular Failure

1974 ◽  
Vol 46 (2) ◽  
pp. 253-264 ◽  
Author(s):  
Anne E. Tattersfield ◽  
M. W. McNicol ◽  
R. W. Sillett
Keyword(s):  
Myocardial Infarction ◽  
Pulmonary Artery ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Pulmonary Artery Pressure ◽  
Left Ventricular ◽  
Left Ventricular Failure ◽  
Stroke Index ◽  
Ventricular Failure ◽  
Artery Pressure

1. Intravenous frusemide has been given to thirty-five patients with myocardial infarction and clinical signs of left ventricular failure. The haemodynamic changes following frusemide were then observed over the subsequent 6 h. 2. Frusemide produced a large diuresis, which was maximal during the first 2 h but fluid depletion was maintained at 24 h. The greatest diuresis occurred in patients with the highest stroke index. 3. All patients showed a fall in pulmonary artery pressure after frusemide. In patients with evidence of poor left ventricular function (low stroke index, high pulmonary artery pressure) this was associated with little change in stroke index. In patients with less severe impairment of left ventricular function there was an initial fall in stroke index at 1 and 2 h. 4. Six hours after frusemide there was a reduction in both pulmonary artery pressure and systemic arterial pressure; the latter correlated with the volume of the diuresis.

Relationship between Haemodynamic and Respiratory Function in Patients with Myocardial Infarction and Left Ventricular Failure

1972 ◽  
Vol 42 (6) ◽  
pp. 751-768 ◽  
Author(s):  
Anne E. Tattersfield ◽  
M. W. McNicol ◽  
R. W. Sillett
Keyword(s):  
Myocardial Infarction ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Clinical Signs ◽  
Left Ventricular ◽  
Left Ventricular Failure ◽  
Stroke Index ◽  
Ventricular Failure ◽  
Artery Pressure ◽  
Arterial Blood

1. Forty-five patients with myocardial infarction and clinical signs of left ventricular failure have been studied with measurements of pulmonary and brachial artery pressure, cardiac output, arterial blood gas pressures and expired air collections. 2. Pulmonary artery pressure was elevated and stroke index was reduced in the majority of patients (89% and 85% respectively). There was a close inverse correlation between these two measurements, both of which appear to be direct consequences of impaired left ventricular function. 3. Arterial hypoxaemia was common and only transiently relieved by hyperventilation. Dead space/tidal volume ratio and venous admixture were both increased, compatible with considerable ventilation/perfusion mismatching in the lung. Both measurements correlated directly with pulmonary artery pressure.

Right and Left Ventricular Function and Pulmonary Artery Pressure in Patients With Bronchiectasis

CHEST Journal ◽  
2008 ◽  
Vol 133 (2) ◽  
pp. 468-473 ◽  
Author(s):  
Abdulaziz H. Alzeer ◽  
Abdulellah F. Al-Mobeirek ◽  
Hadil A.K. Al-Otair ◽  
Usama A.F. Elzamzamy ◽  
Ismail A. Joherjy ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Pulmonary Artery Pressure ◽  
Left Ventricular ◽  
Artery Pressure

Decreased left ventricular function, myocarditis, and coronary arteriolar medial thickening following monocrotaline administration in adult rats

2007 ◽  
Vol 103 (1) ◽  
pp. 287-295 ◽  
Author(s):  
F. Akhavein ◽  
E. Jean St.-Michel ◽  
E. Seifert ◽  
C. V. Rohlicek
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Cardiac Function ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Pulmonary Artery Pressure ◽  
Left Ventricular ◽  
Control Group ◽  
Artery Pressure ◽  
Medial Thickening

Decreased right as well as left ventricular function can be associated with pulmonary hypertension (PH). Numerous investigations have examined cardiac function following induction of pulmonary hypertension with monocrotaline (MCT) assuming that MCT has no direct cardiac effect. We tested this assumption by examining left ventricular function and histology of isolated and perfused hearts from MCT-treated rats. Experiments were performed on 50 male Sprague-Dawley rats [348 ± 6 g (SD)]. Thirty-seven rats received MCT (50 mg/kg sc; MCT group) while the remainder did not (Control group). Three weeks later, pulmonary artery pressure was assessed echocardiographically in 20 MCT and 8 Control rats. The hearts were then excised and perfused in the constant pressure Langendorff mode to determine peak left ventricular pressure (LVP), the peak instantaneous rate of pressure increase (+dP/d tmax) and decrease (−dP/d tmax), as well as the rate pressure product (RPP). Histological sections were subsequently examined. Pulmonary artery pressure was higher in the MCT-treated group compared with the Control group [12.9 ± 6 vs. 51 ± 35.3 mmHg ( P < 0.01)]. Left ventricular systolic function and diastolic relaxation were decreased in the MCT group compared with the Control group (+dP/d tmax4,178 ± 388 vs. 2,801 ± 503 mmHg/s, LVP 115 ± 11 vs. 83 ± 14 mmHg, RPP 33,688 ± 1,910 vs. 23,541 ± 3,858 beats·min−1·mmHg−1, −dP/d tmax−3,036 ± 247 vs. −2,091 ± 389 mmHg/s; P < 0.0001). The impairment of cardiac function was associated with myocarditis and coronary arteriolar medial thickening. Similarly depressed ventricular function and inflammatory infiltration was seen in 12 rats 7 days after MCT administration. Our findings appear unrelated to the degree of PH and indicate a direct cardiotoxic effect of MCT.

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