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Biomedical subjects

N O Fowler

Publications and source records attributed to N O Fowler.

At least 55 records · Page 3Linked to original sources
PubMed1979

Indications for surgical replacement of the mitral valve. With particular reference to common and uncommon causes of mitral regurgitation.

Mitral valve replacement is considered when there is severe mitral stenosis, severe mitral insufficiency or a combination of the two. Ordinarily, surgical replacement is considered only for patients who are in functional classes III or IV and do not respond to medical management. Patients with symptomatic mitral stenosis should be treated with mitral commissurotomy whenever possible. Patients selected for commissurotomy should have a pliable valve, no other major valve dysfunction, sinus rhythm, no systemic embolism and good left ventricular function. Early operation is not ordinarily required. Mitral insufficiency may require mitral valve replacement in six rather common settings: rheumatic disease, rupture of mitral chordae tendineae, postinfarction rupture of a papillary muscle, intractable infective endocarditis, floppy mitral valve and malfunction of a prosthetic valve. Rupture of mitral chordae tendineae can usually be recognized from the history, physical examination, echocardiogram and angiocardiogram. Severe left ventricular papillary muscle dysfunction is usually due to cardiac infarction, and occurs within the first 9 days of infarction. When only a papillary muscle tip is ruptured the patient may survive long enough for a mitral valve replacement. In infective endocarditis, operation is more often needed because of congestive heart failure than because of refractory infection. Evidence of mitral stenosis or insufficiency in a patient with a previously implanted prosthetic valve usually indicates an urgent need for study and early operation. Uncommon causes of mitral incompetence that may require valve replacement are endocardial fibroelastosis, Marfan's syndrome, calcified mitral anulus, osteogenesis imperfecta, methysergide-induced heart disease and carcinoid heart disease.

Adult↗
PubMed1978

Hemodynamic effects of nitroprusside and hydralazine in experimental cardiac tamponade.

Cardiac tamponade is associated with decreased cardiac output and increased systemic vascular resistance. Thus, vasodilator drugs might lower systemic resistance and increase cardiac output. Three groups of dogs were studied during tamponade. Group I received nitroprusside only; group II received blood transfusion and then nitroprusside; group III received hydralazine. In group I, nitroprusside lowered right artrial pressure and systemic resistance; cardiac output was unchanged. In group II, transfusion raised right atrial pressure but not cardiac output. Then nitroprusside raised cardiac output significantly. Hydralazine decreased right atrial pressure less than nitroprusside but decreased vascular resistance and raised cardiac output. Both nitroprusside and hydralazine decreased systemic vascular resistance during tamponade, but only hydralazine raised cardiac output probably because of its lesser effect upon the capacitance vessels. Nitroprusside maintained cardiac output during tamponade despite lowered right atrial pressure but increased cardiac output only after transfusion.

Animals↗
PubMed1977

Echocardiographic study of cardiac tamponade.

We studied 14 patients with cardiac tamponade and pulsus paradoxus; 11 were studied after relief of tamponade by pericardiocentesis. Right ventricle diastolic diameter increased during inspiration in each of 12 patients; left ventricle diastolic diameter decreased during inspiration in each of 13. Mitral valve DE amplitude decreased with inspiration in 13 of 14 patients. Mitral valve E-F slope could be measured in eight patients, and was rounded and not measurable in six. Six of the eight showed inspiratory decrease in mitral E-F slope. Similar changes were observed in two other patients with pulsus paradoxus who had chronic obstructive airway disease. Twenty patients with large pericardial effusions and no tamponade did not show these changes. These results suggest inspiratory augmentation of right ventricular filling and inspiratory diminution of left ventricular filling, not only in cardiac tamponade, but in obstructive airway disease associated with pulsus paradoxus.

Aortic Valve↗
PubMed1976

Electrocardiographic changes and cardiac arrhythmias in patients receiving psychotropic drugs.

Eight patients had cardiac manifestations that were life-threatening in five while taking psychotropic drugs, either phenothiazines or tricyclic antidepressants. Although most patients were receiving several drugs, Mellaril (thioridazine) appeared to be responsible for five cases of ventricular tachycardia, one of which was fatal in a 35 year old woman. Supraventricular tachycardia developed in one patient receiving Thorazine (chlorpromazine). Aventyl (nortriptyline) and Elavil (amitriptyline) each produced left bundle branch block in a 73 year old woman. Electrocardiographic T and U wave abnormalities were present in most patients. The ventricular arrhythmias responded to intravenous administration of lidocaine and to direct current electric shock; ventricular pacing was required in some instances and intravenous administration of propranolol combined with ventricular pacing in one. The tachyarrhythmias generally subsided within 48 hours after administration of the drugs was stopped. Five of the eight patients were 50 years of age or younger; only one clearly had antecedent heart disease. Major cardiac arrhythmias are a potential hazard in patients without heart disease who are receiving customary therapeutic doses of psychotropic drugs. A prospective clinical trial is suggested to quantify the risk of cardiac complications to patients receiving phenothiazines or tricyclic antidepressant drugs.

Adrenergic Agonists↗
PubMed1976

Pericarditis caused by Histoplasma capsulatum.

Sixteen patients with pericarditis caused by Histoplasma capsulatum were studied. Fourteen were less than 30 years old, and no patient had an underlying illness or was receiving immunosuppressive therapy. All patients experienced a flu-like prodromal illness lasting from 2 weeks to 4 months. Pneumonitis or hilar adenopathy, or both, was found in 12; pleural effusion, uncommon in primary pulmonary histoplasmosis, was found in seven patients. Pericardial fluid, pleural fluid and bone marrow cultures yielded no growth. All patients demonstrated a fourfold or greater change in complement-fixing antibody titers. No patient had disseminated disease, and only one required treatment with ampholericin B. The illness ran a protracted course, and in six patients symptomatic pericarditis recurred. Ultimately all recovered. Ten patients were restudied 6 months to 12 years after recover. Only one patient had pericardial calcification, and none had constrictive pericarditis. This form of granulomatous pericarditis, unlike that caused by Mycobacterium tuberculosis, appears to carry a good prognosis.

Adolescent↗
PubMed1975

Blood viscosity and cardiac output in acute experimental anemia.

The significance of blood viscosity alterations during anemia was evaluated in dogs under morphine-chloralose anesthesia. In group I, anemia (mean hematocrit 18.1 +/- 1.3 vol %) was produced by exchange transfusion with clinical dextran (avg mol wt 70,000). In group II, anemia was produced (mean hematocrit 19.9 +/- 0.88 vol %) with 500,000 molecular weight dextran, thus preventing the decrease in blood viscosity in group I. The cardiac output increase in group I (93.4%) with low-viscosity anemia was significantly greater than in group II (43.3%) with unchanged blood viscosity. Group III animals were transfused with a clinical dextran-red cell mixture, and group IV animals received a 500,000 mol wt dextran-red cell mixture. In group III, blood viscosity and cardiac output did not change. In group IV, blood viscosity rose and cardiac output fell significantly. The results suggest that a change in blood viscosity exerts a significant effect upon cardiac output, especially during acute dextran-exchange anemia.

Anemia↗
PubMed1975

Influence of acute hypertension on aortic valve competence.

The effect of acutely induced hypertension on aortic valve competence was studied in anesthetized dogs. Aortic pressure was increased by infusion of methoxamine or mechanically; aortic valve competence was evaluated by aortogrphy and by indicator dye. The aortic valve was normally competent; aortic insufficiency appeared with increase of mean pressure by as little as 20-50 mmHg; 6 of 9 animals showed aortic incompetence when mean aortic pressure was elevated 45-70 mmHg, but the valve remained competent in 2 of 9 animals with mean pressure increments of 60-90 mmHg. The aortic root was appreciably less distensible than was the proximal descending aorta; this factor may limit the degree of aortic insufficiency in response to acute hypertension in the dog.

Animals↗