Circulation
-
The absorption and disposition of quinidine were measured in nine patients following single oral and intravenous dosing. A new specific chromatographic method was used to measure the drug in plasma and urine. After intravenous administration, the plasma half-life (t1/2beta) was 7.8+/-0.7 h, the volume of distribution (Vd) was 3.0+/-0.5 liters/kg, and the total body clearance was 4.8+/-0.8 ml/min/kg. ⋯ Mean quinidine concentrations were estimated in 42 patients on chronic therapy by averaging blood levels during a dosing interval. In patients without heart failure, these corresponded well to mean drug levels predicted from the pharmacokinetic parameters measured after a single intravenous dose, but in patients with heart failure, the values for mean quinidine concentrations were higher than predicted. This suggests that impaired elimination of the drug or a decreased volume of its distribution, or both, may develop in heart failure.
-
The circulatory effects of supraventricular tachycardia (SVT) were studied in eight patients who reported disabling symptoms during paroxysms of the arrhythmia. Supraventricular tachycardia was induced in each patient by rapid atrial pacing or with atrial premature stimuli. Hemodynamic parameters in sinus rhythm and following the initiation of SVT were recorded and compared. ⋯ Large waves appeared in the right atrium during SVT due to atrial contraction against closed tricuspid valves. Pulsus alternans were observed in each case during SVT. Despite the presence of chest pain during SVT, the coronary arteries were normally patent in four patients who underwent coronary arteriography.
-
Five patients with double outlet right ventricle, ventricular septal defect, pulmonary arterial hypertension and pulmonary vascular obstructive disease and three patients with complete d-transposition of the great arteries, ventricular septal defect, pulonary arterial hypertension and pulmonary vascular obstructive disease underwent an elective Mustard baffle operation. The ventricular septal defect was not closed. A large patent ductus arteriosus was divided in three patients. ⋯ In pre and postoperative hemodynamic studies in four patients, systemic arterial oxygen saturation and effective pulmonary blood flow increased from mean values of 70% to 90% and 1.7/min/m2 to 3.3 L/mon/m2, respectively. Absolute systemic and pulmonary flows, and pressures and resistances, were not significantly altered. Criteria for selection of patients with transposition of the great arteries of double outlet right ventricle who would benefit from a palliative Mustard procedure (Mustard atrial baffle without closure of the ventricular spetal defect) are: 1) severe symptoms; 2) pulmonary arteiral hypertension (75% systemic) with pulmonary vascular obstructive disease; and 3) pulmonary artieral oxygen saturation greater than systemic (ascending aorta) arterial oxygen saturation by approximately 10%.
-
Case Reports
Nitroglycerin-induced severe hypotension and bradycardia in patients with acute myocardial infarction.
Seven episodes of simultaneous severe systemic arterial hypotension and absolute or relative bradycardia were observed in five patients receiving either sublingual nitroglycerin (two patients) or intravenous nitroglycerin (three patients) within the first 24 hours of onset of symptoms of acute myocardial infarction. Left ventricular filling pressure, measured as pulmonary artery diastolic pressure, decreased simultaneously in all four patients in whom pulmonary artery pressures were monitored. ⋯ Possible mechanisms producing simultaneous bradycardia and hypotension during nitroglycerin administration are considered. The patient studies emphasize the importance of careful hemodynamic monitoring during administration of sublingual or intravenous nitroglycerin to patients with acute myocardial infarction.
-
Onset of QRS was compared between simultaneously recorded conventional ECG leads in 84 subjects with clinically normal hearts from a defined population sample. Mean onset of QRS was 6.4 msec earlier in lead V1 and 7.4 msec earlier in V2 than in lead II. ⋯ Interobserver differences equivalent to greater than 1 msec occurred in 3.9% of timeline measurements, but in in 38% of QRS onset measurements. The lower precision in measuring QRS onset may be attributed to baseline oscillations and to the relatively slow rate of voltage change at the onset of ventricular depolarization.