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Biomedical subjects

F A Finnerty

Publications and source records attributed to F A Finnerty.

At least 19 recordsLinked to original sources

Step 2 regimens in hypertension. An assessment.

A single-blind clinical trial compared step 2 combination therapy consisting of 50 or 100 mg of hydroflumethiazide plus either 0.125 to 0.250 mg of reserpine, 500 to 2,000 mg of methyldopa, or 80 to 320 mg of propranolol hydrochloride, in 59 patients whose elevated blood pressure (BP) failed to respond adequately to the thiazide alone. After nine weeks of treatment, diastolic BP was reduced below 90 mm Hg in all 20 patients treated with the reserpine-hydroflumethiazide combination, in 13 of the 19 patients treated with methyldopa and hydroflumethiazide, and in 16 of the 20 patients treated with propranolol and hydroflumethiazide. Changes in laboratory values were not substantial; adverse reactions occurred only in the methyldopa group. Although the three treatment regimens were similar with respect to safety and efficacy, the reserpine-hydroflumethiazide combination offers the advantages of more convenient dosage at lower cost.

Adult

Hypertension in the elderly: special considerations in treatment.

The goal of antihypertensive therapy in the elderly should be to reduce systolic blood pressure to 140 mm Hg and diastolic pressure to 100 mm Hg without disturbing cerebral or coronary blood flow or depressing cerebral function. This goal can usually be accomplished by using half doses of thiazide diuretics alone or in combination with half doses of hydralazine. Drugs which produce postural hypotension or depress cardiac output and cerebral function should not be used.

Aged

Diuretics as initial treatment for essential hypertension.

1 In the United States, the thiazide diuretics are considered the cornerstone of all antihypertensive regimens for four reasons: by themselves, they are capable of controlling the blood pressure in 60-70% of the hypertensive population; they prevent the sodium retention produced by all other antihypertensive agents; they can be given once a day; and they are inexpensive. 2 Despite these advantages, the thiazide do cause hypokalaemia hyperuricaemia and hyperglycaemia. The incidence of hypokalaemia (K less than 3.0 mEq/l) is only 2-4%; the incidence of hyperuricaemia (uric acid greater than 10 mg per cent is 3-4%; and the incidence of hyperglycaemia is 1-2%. 3 The possibility that a beta-blocking agent combined with a thiazide diuretic might produce better BP control, prevent thiazide-induced abnormalities and exert a coronary prevention action with once daily administration would suggest that such a combination should be the ideal initial therapy for most patients with hypertension.

Adrenergic beta-Antagonists

Management of hypertensive encephalopathy.

The hypertensive encephalopathy is a syndrome consisting of a sudden elevation of arterial pressure usually preceded by severe headache and followed by convulsions, coma or a variety of transitory cerebral phenomena. The syndrome may complicate acute glomerulonephritis, toxemia of pregnancy and essential or malignant hypertension. Two syndromes must be differentiated from true hypertensive encephalopathy: 1. acute anxiety state with labile hypertension and 2. acute pulmonary edema due to hypertensive heart disease. At least in patients with acute anxiety states, the use of antihypertensive agents is usually not indicated. Since encephalopathy is always accompanied by increased vascular resistance and since clinical experience has demonstrated clearing of the sensorium, cessation of convulsions and release of vasoconstriction following reduction of blood pressure, the primary aim of therapy should be prompt lowering of arterial pressure. The two agents of choice are diazoxide and sodium nitroprusside. Stroke is differentiated from encephalopathy by the persistence of lateralizing signs. The aggressiveness of antihypertensive therapy in this situation depends on the severity of the hypertensive process. Rapid reduction of blood pressure is indicated in patients found to have accelerated hypertension while a more gradual lowering of pressure appears warranted for patients with chronic arterial hypertension and evidence of generalized arteriosclerosis.

Brain Diseases

Sodium intake and furosemide administration in hypertensive patients with renal insufficiency.

The effects of various levels of sodium intake and loop diuretic (furosemide) administration upon arterial pressure and renal function were studied in 11 patients with impaired renal function and essential hypertension. The patients were hospitalized in a metabolic ward and continued taking their usual antihypertensive medications. After a stabilization period, all patients followed the following regiments for 5 to 7 days: period I, 20 mEq sodium diet without diuretic administration; period II, 80 mEq sodium diet and furosemide, 80 mg daily; and period III, 200 mEq sodium diet and furosemide, 240 mg daily. Supine diastolic pressure was lower (P is less than 0.05) during period II than during period I and both supine and standing systolic and diastolic pressures were significantly lower in period III than in period I (P is less than 0.01). No significant differences in the renal clearance of inulin were noted between any of the study periods. In patients with essential hypertension and impaired renal function, consumption of a moderate or liberal sodium diet combined with administration of a loop diuretic agent (furosemide) appears to result in better control of arterial pressure without significant changes in renal function than does strict sodium restriction without diuretic administration.

Adult

Vasodilator administration in the presence of beta-adrenergic blockade.

To explore the possibility that the presence of propranolol-induced beta-adrenergic blockade might have an adverse effect upon homeostatic circulatory reflexes activated by the administration of a potent vasodilator agent, arterial blood pressure and pulse rate response to rapid intravenous diazoxide injection was monitored before and after pretreatment with propranolol in ten hypertensive patients. It appeared that beta-adrenergic blockade had no clinically significant effect on the magnitude of hypotension or the degree of heart rate acceleration induced by the administration of the potent vasodilator diazoxide. This reflex vasodilator-induced cardio-acceleration after propranolol adminstration could be the result of incomplete blockade of endogenously released neurotransmitter, inhibition of the parasympathetic nervous system, or a direct pharmacologic action of diazoxide. Diazoxide administration to hypertensive patients in the presence of beta-adrenergic blockade was not associated with any clinically significant hemodynamic consequences.

Administration, Oral