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Biomedical subjects

J R Malm

Publications and source records attributed to J R Malm.

At least 37 records · Page 2Linked to original sources

Muscular ventricular septal defects repaired with left ventriculotomy.

Between 1974 and 1979 nine patients, aged 10 months to 4 years, underwent left ventriculotomy for closure of single or multiple defects in the muscular ventricular septum. The vertical incision paralleled the anterior descending branch of the left coronary artery near the apex of the left ventricle and ranged from 2.5 to 3.5 cm in length. Four patients also had a right ventriculotomy with closure of a high perimembranous ventricular defect in two. Serial electrocardiograms indicated changes of myocardial ischemia or necrosis. Left bundle branch block did not develop in any patient. Three patients died in the early postoperative period. The six surviving patients are living and well 2 to 7 years later. There is apparent complete closure of the ventricular defects, which was documented by cardiac catheterization in four cases. Two patients had cardiomegaly and left ventricular dysfunction as assessed with echocardiographic and angiographic study, whereas four displayed good cardiac function. In three of the latter patients, cardioplegia or deep hypothermia techniques were utilized intraoperatively. The observations indicate that left ventriculotomy of limited size is an acceptable approach to the difficult problem of repair of muscular ventricular defects but may involve some risk of compromise of the coronary circulation.

Child, Preschool↗

The arrhythmogenic actions of histamine on human atrial fibers.

We used standard microelectrode techniques to study the effects of histamine on right atrial tissues from patients undergoing corrective cardiac surgery. In the 10(-6) to 10(-4) M range, histamine increased maximum diastolic potential, action potential amplitude, and automaticity. In some preparations, histamine also induced delayed afterdepolarizations and triggered activity. The potency of histamine in increasing automaticity was about 10 times less than that of epinephrine. Propranolol (2 x 10(-7)M), which abolished the chronotropic effect of epinephrine, did not alter the effect of histamine. Conversely, the effect of histamine but not that of epinephrine was antagonized by cimetidine (3 x 10(-6) to 1 x 10(-5) M). This suggests that H2 receptors mediate the chronotropic effects of histamine on the human heart. The slow channel blocker verapamil (2 x 10(-8) to 2 x 10(-6) M) counteracted the effects of histamine on automaticity, delayed afterdepolarizations, and triggered activity, suggesting that in human atrium histamine may act by increasing slow inward (presumably Ca2+) current. If one considers these arrhythmogenic effects of histamine and the fact that human cardiac tissue contains large amounts of histamine, our experiments lend further support to the concept that histamine release can induce arrhythmias.

Action Potentials↗

Tetralogy of Fallot.

Based on our experience and the data presented here the following general approach may be used in the management of patients with tetralogy of Fallot: 1. Symptomatic infants under 6 months of age should be considered for an initial palliative shunt, preferably a Blalock-Taussig shunt or a Gore-tex modification of that procedure. 2. Symptomatic patients older than 6 months of age should be considered candidates for total correction, unless there are anatomic contraindications (anomalous left anterior descending artery, severe hypoplasia of the main pulmonary artery, multiple branch stenoses, multiple ventricular septal defects, or pulmonary atresia), or the predicted PRV/LV is greater than 0.7. 3. Total correction with closure of shunt should be undertaken in all patients prior to 5 years of age.

Adolescent↗

Acute hemodynamic alterations after mitral valve replacement with the glutaraldehyde-treated porcine heterograft prosthesis.

Perioperative hemodynamic changes following mitral valve replacement using the porcine heterograft prosthesis were measured in 21 patients with acquired mitral valve disease. Preoperatively, a state of compensatory cardiac failure was suggested by the following: an increased heart rate (HR) (96 beats per minute); low cardiac and stroke volume (SVI) indices (2.3 +/- 0.10 L/min/m2 and 25 +/- 2 ml/beat/m2); and increased systemic vascular resistance (SVR) (1,626 +/- 116 DYNE SEC CM-5). Bothe the mean pulmonary artery PAP) and pulmonary capillary wedge pressures (PCWP) were elevated as well (32 +/- 3 and 22 +/- 2 torr). Immediate hemodynamic improvement followed valve replacement. HR, SVR, PAP, and PCWP all decreased significantly. Twenty-four hours after valve replacement, PAP (23 +/- 1 torr) and PCWP (13 +/- 1 torr) demonstrated marked declines, SVR was reduced by one-third (1,173 +/- 87 dyne sec cm-5), HR had decreased by 10 beats per minute, and SVI had increased to 30 +/- 2 ml/beat/m2. The prompt circulatory improvement of patients soon after mitral valve replacement using the porcine heterograft compares favorably with studies in which other valve types were employed and in which postoperative cardiovascular depression was encountered frequently.

Adult↗

Methods for recording electrograms of the sinoatrial node during cardiac surgery in man.

Recent reports have shown that it is possible to record extracellular electrograms from the rabbit and dog sinoatrial (SA) node. We applied similar techniques to record SA nodal activity in 23 patients who underwent cardiac surgery for various forms of heart disease. Both a bipolar technique, using pairs of electrodes at various interelectrode distances, and a unipolar technique, using an exploring and an indifferent electrode, were used. To record SA nodal electrograms, polarity was reversed from the conventional electrocardiographic recording; high amplification (100 microV/cm) and low-pass filters (0.15-20 Hz) were used. SA nodal electrograms were recorded from eight of 12 patients using the bipolar method and from nine of 11 patients using the unipolar method. There were no significant differences in the success rate or quality of the recording between the two methods. However, the unipolar method allowed a more accurate localization of the SA node. Human SA nodal electrograms resembled those of the dog and rabbit and showed two distinct slopes: a diastolic slope and an upstroke slope preceding the P wave of the ECG, SA conduction times were 32.4 +/- 2.8 msec (mean +/- SEM) at sinus (PP) cycle lengths of 587.6 +/- 35.6 msec for the bipolar method, and 38.2 +/- 3.2 msec at sinus (PP) cycle lengths of 712.2 +/- 50.7 msec for the unipolar method. These methods for recording of extracellular SA nodal electrograms in man may prove useful in 1) localization of the SA node during open heart surgery and 2) assessment of SA nodal function in health and disease.

Adolescent↗

Pharmacologic antagonism of beta adrenergic blockade in dogs. II. Hemodynamic effects of simultaneous intravenous infusion of isoproterenol and dopamine during chronic propranolol administration.

Chronic beta adrenergic blockade was induced in eight dogs with 240 to 360 mg of oral propranolol dailty for 2 to 6 weeks. Beta blockade was confirmed by a minimal heart rate response to isoproterenol, 0.06 micrograms/kg/min, in a pentobarbital-anesthetized, open-chest preparation. Subsequent to confirmation of beta blockade, hemodynamic effects of isoproterenol and dopamine were examined individually and in combination. A desirable balance of arterial pressure and cardiac output was achieved by combining isoproterenol, 0.2 to 2.0 micrograms/kg/min, with dopamine, 5 to 20 micrograms/kg/min. This combination increased mean arterial pressure (109 +/- 9 versus 81 +/- 7), cardiac output (4.3 +/- .5 versus 2.8 +/- .3 L/min) and heart rate 156 +/- 4 versus 120 +/- 7) (p less than 0.05). The hemodynamic effects of combined isoproterenol-dopamine were superior to the effects of either drug alone and suggest a method for effective circulatory support of man during chronic beta adrenergic blockade.

Animals↗

Pharmacologic antagonism of beta-adrenergic blockade in dogs. I. Hemodynamic effects of isoproterenol, dopamine, and epinephrine in acute propranolol administration.

Hemodynamic effects of isoproterenol, dopamine, and epinephrine were studied before and after acute beta-adrenergic blockade in 16 open-chest, anesthetized mongrel dogs. Beta blockade was induced with 1 mg. per kilogram of intravenous propranolol. Cardiac output measurements were obtained by thermal dilution, and pressure recordings were obtained in the right ventricle, pulmonary artery, left atrium, left ventricle, and aorta. Derived parameters included stroke volume, pulmonary and systemic vascular resistances, and peak left ventricular dP/dt. In the presence of propranolol, epinephrine became a lethal drug in large doses and did not increase cardiac output in standard doses. Dopamine, in 25 to 50 mcg. per kilogram per minute doses, increased arterial pressure and systemic resistance; cardiac output was diminished compared with dopamine, 10 mcg. per kilogram per minute, prior to propranolol, as a result of increased resistance and decreased LV contractility. Isoproterenol, 0.6 to 0.9 mcg. per kilogram per minute, 15 to 20 times standard dosages, had moderately positive inotropic effects and increased cardiac output. Left ventricular systolic pressure with isoproterenol after propranolol was reduced when compared with effects of smaller doses prior to propranolol. These observations suggest that none of the catecholamines studied would be optimal for circulatory support in heart failure in the presence of propranolol. The present results define a pharmacologic basis for design of appropriate drug combinations for circulatory support in beta-blocked animals.

Adrenergic beta-Antagonists↗

Intraoperative mapping in patients with univentricular hearts.

The location of the specialized cardiac conduction system in patients with univentricular hearts may be extremely variable. Electrophysiologic studies during open heart surgery identified the intraventricular conducting tissue to be consistently located in four sites. In patients with univentricular hearts without an outlet chamber, conducting tissue may be located either at 1. along the posterior wall or 2. along the anterior free wall of the ventricle. In patients with univentricular hearts and an outlet chamber, conducting tissue is uusally located anterior and superior to the bulboventricular foramen and then extends towards the atrium either 1. in between the bulboventricular foramen and the pulmonary valve or 2. along the right margin of the pulmonary artery over the anterior free wall of the ventricle towards the junction of the inter-atrial septum and the right atrial appendage. These electrophysiologic studies are consistent with previously described locations of conducting tissue in similar hearts by histologic methods. The different locations of the intraventricular conducting tissues in patients with univentricular hearts demonstrates the valve and the need for electrophysiologic mapping of the specialized cardiac conduction system during surgical repair of univentricular hearts.

Electrocardiography↗

Comparison of intraoperative nitroprusside unloading in mitral and aortic regurgitation.

To compare the hemodynamic effect of vasodilator therapy on different regurgitant lesions, we infused sodium nitroprusside intraooperatively in 12 patients with mitral regurgitation and 15 with aortic regurgitation. During the critical period preceding establishment of cardiopulmonary bypass, both groups had developed intense vasoconstriction and cardiac decompensation. All demonstrated improved cardiac function with vasodilator therapy; however, the degree of improvement with nitroprusside differed in the two groups. Stroke volume increased 10 ml. per beat per meter squared in those patients with aortic regurgitation and only 6 ml. per beat per meter squared in those with mitral regurgitation (p less than 0.05). The percent increase in stoke volume induced by nitroprusside was inversely correlated to the preoperative left ventricular ejection fraction (r = 0.44, p less than 0.02). Patients with aortic regurgitation had lower preoperative left ventricular ejection fractions than those with mitral regurgitation (0.53 versus 0.63, p less than 0.02). Therefore, we conclude that patients with aortic regurgitation derived greater intraoperative hemodynamic benefit from unloading with nitroprusside, because they came to surgery with greater impairment of left ventricular contractility. Although nitroprusside improved cardiac function in both groups, only the patients with aortic regurgitation achieved normal pulmonary artery pressure (17 torr) and pulmonary vascular resistance (2.1 units) as a result of unloading. Those with mitral regurgitation continued to have pulmonary hypertension (28 torr) and increased pulmonary vascular resistance (3.9 units) despite vasodilator therapy. Thus the data suggest that patients with mitral regurgitation derived less hemodynamic benefit from intraoperative nitroprusside therapy because they were also limited by right ventricular dysfunction and a less responsive pulmonary vasculature.

Adult↗