Studies in clinical shock and hypotension: VI. Relationship between left and right ventricular function.

Left ventricular end diastolic (LVEDP) and mean right atrial (RAP) pressures were recorded simultaneously in 30 patients with shock (14 acute myocardial infarction, 10 acute pulmonary embolism or severe bronchopulmonary disease, and 6 sepsis). Myocardial infarction was characterized by a predominant increase in LVEDP, pulmonary disease by a predominant increase in RAP, and sepsis by a normal relationship between LVEDP and RAP. In all three groups a significant positive correlation was noted between RAP and LVEDP, with the regression line in cor pulmonale deviated significantly toward the RAP axis and the regression line in myocardial infarction exhibiting a zero RAP intercept at an elevated LVEDP.Low cardiac outputs with elevated LVEDP in myocardial infarction indicated severe left ventricular failure. Low outputs with elevated RAP in cor pulmonale were consistent with right ventricular overload. Although cardiac outputs often were normal in sepsis, low outputs with elevated cardiac filling pressures in some patients were consistent with a hemodynamic or humoral-induced generalized depression of cardiac performance.Vasoconstrictor and inotropic drugs often produced a functional disparity between the two ventricles, with the gradient between LVEDP and RAP increasing, apparently because of an increase in left ventricular work or an inadequacy of left ventricular oxygen delivery. Acute plasma volume expansion with dextran in patients with pulmonary vascular disease resulted in a somewhat more rapid rise in RAP than in LVEDP. In septic and myocardial infarction shock, however, LVEDP and RAP usually rose proportionally, with the absolute rise of LVEDP surpassing that of RAP. Although the absolute level of the central venous pressure thus may not be a reliable indicator of left ventricular function in shock, changes in venous pressure during acute plasma volume expansion should serve as a fairly safe guide to changes in LVEDP.

Persistence of normal BP after withdrawal of drug treatment in mild hypertension.

Antihypertensive therapy was discontinued in 24 patients with mild hypertension whose BPs had been well controlled with diuretics alone. Eleven patients (46%) maintained normal diastolic BPs (less than or equal to 90 mm Hg) for six months after stopping treatment and five patients (21%) for 12 months. All patients who remained normotensive for six to 12 months had mean diastolic BPs of 82 mm Hg or less during treatment. There was no significant correlation between maintenance of normotension and any of the following: pretreatment BP, presence of target-organ damage, duration of known hypertension, family history of hypertension, heart rate, body weight, weight gain after stopping diuretic therapy, 24-hour urinary sodium and potassium excretion, serum electrolyte values or renin profile. This study demonstrates that hypertension may be favorably modified, sometimes for many months, by effective antihypertensive treatment.

Treatment of severe hypertension with intravenous labetalol.

The effectiveness of repeated intravenous injections of labetalol in reducing blood pressure (BP) was evaluated in patients with severe hypertension. The subjects were 10 patients who were 29 to 61 yr old and who had diastolic blood pressure (DBP) of 125 mm Hg or higher. Repeated injections titrated from 20 to 80 mg were given at 15-min intervals until there was a reduction in DBP of 30 mm Hg or until 300 mg had been administered. The average reduction of BP ranged from 201 +/- 5/132 +/- 1 to 157 +/- 6/108 +/- 4 mm Hg (mean +/- SEM). Four patients responded with a reduction in DBP of 30 mm Hg or more with total doses of 60 to 220 mg. Of the remaining six who received the full dose, in four there was a 20 to 29 mm Hg reduction in DBP, in one there was a 10 mm Hg fall, and in one there was no reduction. There was a positive correlation between age and response to intravenous labetalol. No severe side effects were encountered. Intravenous labetalol is useful and well tolerated in patients with severe hypertension.

Diuretic-induced hypokalemia in uncomplicated systemic hypertension: effect of plasma potassium correction on cardiac arrhythmias.

Sixteen patients with diuretic-induced hypokalemia underwent 24-hour ambulatory electrocardiographic monitoring during and after correction of hypokalemia. Plasma potassium averaged 2.83 +/- 0.08 mEq/liter before and 3.73 +/- 0.06 mEq/liter after correction with potassium chloride, triamterene or both. Premature atrial contractions decreased in 6 patients, increased in 6 and remained unchanged in 4. There was no improvement in ventricular ectopic activity after plasma potassium correction. Ventricular ectopic activity improved in 5 patients, worsened in 10 and remained unchanged in 1. Ventricular tachycardia was not observed in either phase. Plasma magnesium remained normal throughout. The investigators conclude that in patients with uncomplicated hypertension, correction of diuretic-induced hypokalemia does not significantly reduce the occurrence of spontaneous atrial or ventricular ectopic activity.

Initial and long-term effects of prazosin on sympathetic vasopressor responses in essential hypertension.

In 10 untreated hypertensive patients who received an initial dose of 3 to 5 mg prazosin, supine blood pressure (BP) decreased significantly, from an average of 171 +/- 24/96 +/- 10 to 157 +/- 22/90 +/- 10 mm Hg (p less than 0.025). The Valsalva overshoot, response to cold pressor test and digital vasoconstrictor response to a deep breath were not inhibited. However, during 55 degrees passive headup tilt there was a significant decrease in BP. Seven patients received prazosin for a period of 3 months. After long-term therapy BP returned to baseline levels and a dose of prazosin similar to that given initially produced an average decrease in BP from 174 +/- 20/101 +/- 8 to 167 +/- 23/99 +/- 7 mm Hg. Upright tilting no longer resulted in a decrease in BP. The Valsalva overshoot, cold pressor test and digital vasoconstrictor responses remained unchanged. Orthostatic hypotension after the first dose of prazosin without blockade of the other sympathetic reflex responses suggests that the drug has a greater blocking effect on capacitance vessels than on resistance vessels. Prazosin showed a loss of antihypertensive effectiveness during long-term treatment.

Systemic vasoconstrictor and renal vasodilator effects of PLV-2 (octapressin) in man.

The systemic and renal hemodynamic effects of PLV-2 (octapressin) were studied in patients with hypotension or decompensated cirrhosis of the liver. Low doses (0.004 to 0.02 units/min) increased renal blood flow (indicator-dilution technique), reduced renal vascular resistance, and produced a slight increase in arterial pressure and systemic vascular resistance. Higher doses (0.1 to 0.5 units/min) produced a sharp increase in arterial pressure and systemic resistance while renal resistance increased moderately and renal blood flow usually was maintained above control levels. Renal fraction was increased at all dose levels. The increased renal blood flow was accompanied by more rapid intrarenal dye transit time and slight increase in renal extraction ratio of paraaminohippurate suggesting a rise in cortical blood flow. It is concluded that PLV-2 in small doses produces renal vasodilation and in larger doses preferential extra-renal vasoconstriction resulting in redistribution of blood flow to the kidney.

Furosemide compared with hydrochlorothiazide. Long-term treatment of hypertension.

In a double-blind crossover study, the effectiveness of furosemide, 40 mg twice daily, was compared with hydrochlorothiazide, 50 mg twice daily, in hypertensive patients. Both hydrochlorothiazide and furosemide significantly reduced blood pressure (BP) during three months of therapy. However, the fall in BP was consistently greater with hydrochlorothiazide than with furosemide, although the difference was significant only with respect to systolic BP. The somewhat greater antihypertensive effectiveness of hydrochlorothiazide may be related to its longer action permitting a more continuous diuretic effect and, hence, maintenance of reduced extracellular fluid volume throughout the 24-hour period.