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Biomedical subjects

B M Groves

Publications and source records attributed to B M Groves.

At least 73 records · Page 4Linked to original sources
PubMed1987

Operation Everest II: elevated high-altitude pulmonary resistance unresponsive to oxygen.

High altitude increases pulmonary arterial pressure (PAP), but no measurements have been made in humans above 4,500 m. Eight male athletic volunteers were decompressed in a hypobaric chamber for 40 days to a barometric pressure (PB) of 240 Torr, equivalent to the summit of Mt. Everest. Serial hemodynamic measurements were made at PB 760 (sea level), 347 (6,100 m), and 282/240 Torr (7,620/8,840 m). Resting PAP and pulmonary vascular resistance (PVR) increased from sea level to maximal values at PB 282 Torr from 15 +/- 0.9 to 34 +/- 3.0 mmHg and from 1.2 +/- 0.1 to 4.3 +/- 0.3 mmHg.l-1 X min, respectively. During near maximal exercise PAP increased from 33 +/- 1 mmHg at sea level to 54 +/- 2 mmHg at PB 282 Torr. Right atrial and wedge pressures were not increased with altitude. Acute 100% O2 breathing lowered cardiac output and PAP but not PVR. Systemic arterial pressure and resistance did not rise with altitude but did increase with O2 breathing, indicating systemic control differed from the lung circulation. We concluded that severe chronic hypoxia caused elevated pulmonary resistance not accompanied by right heart failure nor immediately reversed by O2 breathing.

Adult↗
PubMed1987

Operation Everest II: preservation of cardiac function at extreme altitude.

Hypoxia at high altitude could depress cardiac function and decrease exercise capacity. If so, impaired cardiac function should occur with the extreme, chronic hypoxemia of the 40-day simulated climb of Mt. Everest (8,840 m, barometric pressure of 240 Torr, inspiratory O2 pressure of 43 Torr). In the five of eight subjects having resting and exercise measurements at the barometric pressures of 760 Torr (sea level), 347 Torr (6,100 m), 282 Torr (7,620 m), and 240 Torr, heart rate for a given O2 uptake was higher with more severe hypoxia. Slight (6 beats/min) slowing of the heart rate occurred only during exercise at the lowest barometric pressure when arterial blood O2 saturations were less than 50%. O2 breathing reversed hypoxemia but never increased heart rate, suggesting that hypoxic depression of rate, if present, was slight. For a given O2 uptake, cardiac output was maintained. The decrease in stroke volume appeared to reflect decreased ventricular filling (i.e., decreased right atrial and wedge pressures). O2 breathing did not increase stroke volume for a given filling pressure. We concluded that extreme, chronic hypoxemia caused little or no impairment of cardiac rate and pump functions.

Adult↗
PubMed1987

Operation Everest II: pulmonary gas exchange during a simulated ascent of Mt. Everest.

Eight normal subjects were decompressed to barometric pressure (PB) = 240 Torr over 40 days. The ventilation-perfusion (VA/Q) distribution was estimated at rest and during exercise [up to 80-90% maximal O2 uptake (VO2 max)] by the multiple inert gas elimination technique at sea level and PB = 428, 347, 282, and 240 Torr. The dispersion of the blood flow distribution increased by 64% from rest to 281 W, at both sea level and at PB = 428 Torr (heaviest exercise 215 W). At PB = 347 Torr, the increase was 79% (rest to 159 W); at PB = 282 Torr, the increase was 112% (108 W); and at PB = 240 Torr, the increase was 9% (60 W). There was no significant correlation between the dispersion and cardiac output, ventilation, or pulmonary arterial wedge pressure, but there was a correlation between the dispersion and mean pulmonary arterial pressure (r = 0.49, P = 0.02). When abnormal, the VA/Q pattern generally had perfusion in lung units of zero or near zero VA/Q combined with units of normal VA/Q. Alveolar-end-capillary diffusion limitation of O2 uptake (VO2) was observed at VO2 greater than 3 l/min at sea level, greater than 1-2 l/min VO2 at PB = 428 and 347 Torr, and at higher altitudes, at VO2 less than or equal to 1 l/min. These results show variable but increasing VA/Q mismatch with long-term exposure to both altitude and exercise. The VA/Q pattern and relationship to pulmonary arterial pressure are both compatible with alveolar interstitial edema as the primary cause of inequality.

Acclimatization↗
PubMed1987

Primary pulmonary hypertension. A national prospective study.

A national registry was begun in 1981 to collect data from 32 centers on patients diagnosed by uniform criteria as having primary pulmonary hypertension. Entered into the registry were 187 patients with a mean age (+/- SD) of 36 +/- 15 years (range, 1 to 81), and a female-to-male ratio of 1.7:1 overall. The mean interval from onset of symptoms to diagnosis was 2 years. The most frequent presenting symptoms included dyspnea (60%), fatigue (19%), and syncope (or near syncope) (13%). Raynaud phenomenon was present in 10% (95% of whom were female) and a positive antinuclear antibody test, in 29% (69% female). Pulmonary function studies showed mild restriction (forced vital capacity [FVC], 82% of predicted) with a reduced diffusing capacity for carbon monoxide (DLCO), and hypoxemia with hypocapnia. The mean (+/- SD) right atrial pressure was 9.7 +/- 6 mm Hg; mean pulmonary artery pressure, 60 +/- 18 mm Hg; cardiac index, 2.3 +/- 0.9 L/min X m2; and pulmonary vascular resistance index, 26 +/- 14 mm Hg/L/min X m2 for the group. Although no deaths or sustained morbid events occurred during the diagnostic evaluation of the patients, the typically long interval from initial symptoms to diagnosis emphasizes the need to develop strategies to make the diagnosis earlier.

Adolescent↗
PubMed1986

Role of glomerular filtration rate in the impaired sodium and water excretion of patients with the nephrotic syndrome.

Hemodynamic and hormonal factors were monitored in nine patients with nephrotic syndrome who were evaluated relative to their capacity to excrete a 20-mL/kg water load (normal greater than 80%). In five "nonexcretor" patients (37% of water load excreted in five hours), as compared to four normal excretors (105% of water load excreted in five hours; P less than .01 v nonexcretors), neither BP (131/88 v 119/79 mm Hg), pulse (74 v 77 beats/min), cardiac index (3.7 v 3.1 L/min/m2), pulmonary wedge pressure (9.3 v 7.3 mm Hg), systemic vascular resistance (1537 v 1254 dynes-sec-cm-5), nor plasma volume (41.3 v 40.1 mL/kg) were different. Similarly, plasma renin activity (2.6 v 3.7 ng/mL/h), plasma aldosterone (12 v 10.9 ng/dL), and plasma norepinephrine (403 v 312 pg/mL) were not different between nonexcretor v excretor patients with nephrotic syndrome. Plasma vasopressin concentrations were also similar both before (3.1 +/- 0.8 v 2.4 +/- 1.2 pg/mL) and during the water load (0.9 +/- 0.3 v 1.0 +/- 0.4 pg/mL). Inulin clearances, however, were lower in the nonexcretor v the excretor nephrotic patients (37 v 78 mL/min/1.73 m2; P less than .02) and correlated with water excretion (r = .68; P less than .05). Head-out water immersion increased sodium (40 to 110 microEq/min; P less than .01) and water excretion (37% to 82%; P less than .025) in the nonexcretors; the improvement correlated with the increase in inulin clearance during immersion (r = .70; P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Antinuclear antibodies in primary pulmonary hypertension.

The association of positive antinuclear antibodies with the clinical and hemodynamic features of 43 patients with primary pulmonary hypertension and 16 patients with secondary pulmonary hypertension was investigated. Each patient had determinations of antinuclear antibodies using a KB cell substrate immunofluorescent test. Of the patients with primary pulmonary hypertension, 40% had positive antinuclear antibodies at titers of 1:80 dilutions or greater. There were no differences between patients with primary pulmonary hypertension and positive antinuclear antibodies compared with those with negative antinuclear antibodies in relation to clinical or hemodynamic status. A 6% incidence rate of antinuclear antibodies was found in patients with secondary pulmonary hypertension, similar to that in the normal population. The clinical, hemodynamic, serologic and histologic similarity between patients with primary pulmonary hypertension and those with unexplained pulmonary hypertension associated with collagen vascular disorders suggests that primary pulmonary hypertension in some patients may represent a collagen vascular disease confined to the lungs. The frequency of positive antinuclear antibody tests would place primary pulmonary hypertension between rheumatoid arthritis and scleroderma in the spectrum of collagen vascular diseases. Further studies are necessary, however, before one might expect that immunosuppressive therapy would be beneficial to these patients.

Adult↗
PubMed1986

The case for treatment of selected patients with primary pulmonary hypertension.

The treatment of primary pulmonary hypertension with pulmonary vasodilator agents is controversial. Some patients have benefited, while others have not. To shed light on the mater we reviewed published reports of 117 patients having acute vasodilator challenge and found that 53 reduced their pulmonary vascular resistance by 30% or more. Calcium antagonists (n = 46), hydralazine (n = 23), and diazoxide (n = 18) gave approximately equivalent acute reductions in resistance (30%, 35%, 32%, respectively), but captopril (n = 17) gave a poor response (-7%). The reports indicated that chronic treatment (3 months or longer) benefited only 4 of 64 patients (6%) having acute reduction in resistances of less than 30%. However, when resistance was lowered acutely by more than 30%, 33 of 53 patients (62%) improved with treatment. In 5 patients having multiple catheterization, improvement was sustained for the duration of follow-up (10 to 48 months). Except for captopril, the agents employed gave similar reductions in resistance, and perhaps the choice should be determined by avoidance of side-effects. Long-term benefit is never certain, but selecting patients with brisk acute vasodilator responses may predict the benefit from chronic vasodilator treatment.

Adult↗
PubMed1985

A comparison of the acute hemodynamic effects of prostacyclin and hydralazine in primary pulmonary hypertension.

In patients with primary pulmonary hypertension the administration of a vasodilating drug is often used to test pulmonary vasoreactivity. Hydralazine has been employed as a test drug, but because of its long duration of action there is a risk of sustained systemic arterial hypotension in patients with a fixed pulmonary vascular resistance. In this study we compared the acute hemodynamic effects of intravenous prostacyclin, a potent, short-acting vasodilator, with the effects of oral or intravenous hydralazine. Both prostacyclin and hydralazine increased cardiac output and decreased systemic pressure without changing pulmonary arterial pressure in seven patients with primary pulmonary hypertension. The average decrease in total pulmonary resistance with prostacyclin (-46% +/- 5%) was more than that with hydralazine (-32% +/- 6%). The respective decreases in total systemic resistance were -50% +/- 4% vs -43% +/- 6%. The percent changes in individual responses to the two agents were correlated (p less than 0.05) for pulmonary arterial pressure, systemic arterial pressure, total pulmonary resistance, and total systemic resistance. We concluded that the pulmonary hemodynamic effects of prostacyclin resembled those of hydralazine. Prostacyclin may predict the acute pulmonary hemodynamic effects of hydralazine in primary pulmonary hypertension and because of its prompt, brief action may provide greater patient safety.

Blood Pressure↗
PubMed1985

Rupture of left sinus of Valsalva aneurysm into the pulmonary artery.

Congenital sinus of Valsalva aneurysm is an uncommon lesion that frequently presents after rupture in adult life. This report describes a patient with a left sinus of Valsalva aneurysm that ruptured into the main pulmonary artery, a previously unreported anatomic variant. Anatomic and clinical features of previously reported cases of ruptured sinus of Valsalva aneurysm are reviewed.

Adult↗
PubMed1985

Interrelationship between cardiac output and vascular resistance as determinants of effective arterial blood volume in cirrhotic patients.

The effect of head-out water immersion (HWI) in decompensated cirrhotic patients to correct sodium and water excretion has been found to be incomplete and variable. The explanation may be that the efficacy of HWI in correcting a decreased effective arterial blood volume (EABV) in decompensated cirrhotic patients is limited by an accompanying decrease in systemic vascular resistance (SVR) and thus a relative increase in arterial vascular holding capacity. The present studies were undertaken to examine this possibility by maintaining SVR (dynes X sec X cm-5) nearly constant during HWI with an exogenous infusion of norepinephrine (HWI + NE). In six decompensated cirrhotic patients, neither HWI nor NE infusion alone significantly increased sodium excretion (UNaV, 13 vs. 19 and 13 microEq/min, respectively), but each maneuver increased the excretion of a 20 ml/kg water load (28 to 60 and 61%, respectively, both P less than 0.05). The combination of HWI + NE, however, significantly increased UNaV to 70 microEq/min (P less than 0.05) and percentage of water excretion to 95 (P less than 0.001), values significantly greater than those achieved with either maneuver alone. These differences were not explained by any changes in inulin clearance. With HWI alone, cardiac index (CI) increased (4.2 to 5.3 liter/min/m2, P less than 0.01), but SVR decreased (872 to 613 dynes X sec X cm-5, P less than 0.001) and mean arterial pressure (MAP) remained constant (83 vs. 78 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Regional myocardial blood flow in man during dipyridamole coronary vasodilation.

Regional myocardial blood flow before and after intravenous dipyridamole (0.56 mg/kg) was measured during cardiac catheterization in 11 patients using the 133Xe washout technique. Significant increases in heart rate (75 +/- 4 vs 87 +/- 6, p less than 0.004) and decreases in systolic blood pressure (144 +/- 8 vs 131 +/- 7, p less than 0.02) were observed with dipyridamole infusion. However, double product and cardiac output did not differ before or after drug infusion. Regional myocardial blood flow increased from 67 +/- 3 (SEM) to 117 +/- 3 ml/100 mg/min in myocardial segments supplied by nonobstructed coronary arteries. In stenotic coronary arteries, flow increased from 57 +/- 5 to 79 +/- 9 ml/100 mg/min with dipyridamole. We conclude that dipyridamole infusion results in flow differences which discriminate stenotic from nonstenotic coronary arteries.

Blood Pressure↗
PubMed1983

Mechanisms of improvement of water and sodium excretion by immersion in decompensated cirrhotic patients.

Eight patients with alcoholic liver disease, ascites, and edema were found to have impaired water (36 +/- 6% in 5 hr) and sodium (3.9 +/- 1.1 mEq/5 hr) excretion during a 20 ml/kg water load. These patients were submitted to a 5-hr head-out water immersion (HWI) with hemodynamic monitoring (Swan-Ganz). HWI increased cardiac index (3.3 to 4.2 liters/min/m2), right atrial pressure (RAP, 3.9 to 9.0 mm Hg), and wedge capillary pulmonary pressure (9.8 to 15.4 mm Hg) (all P less than 0.01). HWI decreased plasma renin activity (6.4 to 4.5 ng/ml/hr, P less than 0.001), aldosterone (73 to 43 ng/dl, P less than 0.001), arginine vasopressin (AVP, 1.03 +/- 0.15 to 0.76 +/- 0.08 pg/ml, P less than 0.005), norepinephrine (NE, 584 to 435 pg/ml, P less than 0.001) and increased the percentage of water load excreted (36 to 63%, P less than 0.005) and urinary sodium excretion (3.9 to 9.7 mEq/5 hr, P less than 0.05). The percentage of water load excreted was inversely correlated to AVP levels (r = 0.52, P less than 0.05) and directly correlated to RAP (r = 0.74, P less than 0.05). A significant positive correlation was also found between the increase in fractional excretion of sodium (delta FENa) and the increase in RAP (r = 0.77, P less than 0.001). FENa also correlated inversely with NE levels (r = 0.56, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Thermodilution method overestimates low cardiac output in humans.

We compared 57 cardiac output measurements by the thermodilution and Fick methods in 26 patients and found that thermodilution values were higher in all 16 cases in which Fick outputs were less than 3.5 l/min. In 10 cases where Fick values were less than or equal to 2.5 l/min, thermodilution and Fick measurements differed by an average of 35%. When combined with the results of previous studies comparing the thermodilution, dye dilution, and Fick techniques, these findings suggest that the thermodilution method overestimates true cardiac output in the low output range. This overestimation probably is due to heat loss under conditions of low flow. Because the thermodilution method is used widely in patients with low output states, these findings have potentially important clinical implications.

Adolescent↗
PubMed1982

Functional significance of coronary collateral vessels in patients with coronary artery disease.

Regional myocardial perfusion was measured in 12 normal subjects and in 34 patients with coronary artery disease (CAD) at rest and during infusion of isoproterenol. Increments in regional flows normalized for change in heart rate-systolic product were 91 +/- 28% (S.D.) in normals, 71 +/- 44% in normal regions in diseased hearts, 58 +/- 33% in regions supplied by 50% to 70% stenosed arteries, 35 +/- 32% in regions supplied by arteries stenosed by more than 70%, and 16 +/- 27% in regions supplied by collateral vessels only. In 3 of 14 regions perfused entirely via collateral pathways, regional perfusion decreased with isoproterenol. Therefore the extent to which coronary flow reserve estimated with isoproterenol was compromised varied directly with the severity of anatomic coronary artery lesions and, in some regions entirely perfused by collateral vessels, an increase in heart rate-systolic pressure product was accompanied by a decrease in perfusion below resting levels. It is concluded that collateral vessels effectively maintain flow rates at normal levels at rest but tend to be inefficient at delivering blood when myocardial oxygen demand is increased.

Blood Pressure↗
PubMed1982

Multiclinic controlled trial of diltiazem for Prinzmetal's angina.

To assess the efficacy of a new calcium entry blocker, diltiazem (Cardizem), for prophylaxis of Prinzmetal's angina, 48 patients were studied in randomized, multiple crossover multiclinic study (2 weeks single-blind, 8 weeks double-blind). Diltiazem dosage in one crossover phase was 120 mg per day; in the other, 240 mg per day. Therapeutic response was measured by patients' diary records of angina frequency and nitroglycerin tablet consumption. Treatment with 120 mg of diltiazem per day reduced angina by 41 percent from the entry placebo period and 20 percent from the paired placebo period (p less than 0.005). Treatment with 240 mg of diltiazem per day reduced angina frequency by 68 percent from the entry placebo period and 43 percent from the paired placebo period (p less than 0.01). There were similar reductions in nitroglycerin consumption. Adverse experiences that may have been related to the medication were noted in only 5 percent of patients. There were no alterations in blood pressure or heart rate. The PR interval increased 3 percent at the 240 mg dosage level. We conclude that diltiazem is an effective and safe agent for control of symptoms of Prinzmetal's angina.

Adult↗
PubMed1982

Prostacyclin-induced acute pulmonary vasodilation in primary pulmonary hypertension.

To evaluate the effects of prostacyclin (prostaglandin I2) on pulmonary vascular tone in primary pulmonary hypertension (PPH), we performed right-heart catheterization on seven patients with PPH and made hemodynamic measurements before and after infusing incremental doses of prostacyclin. In maximal doses of 2-12 mg/kg/min (mean 5.7 +/0 3.1 ng/kg/min), prostacyclin reduced mean pulmonary arterial pressure from 62 +/- 15 to 55 +/- 16 mm Hg (p less than 0.05) and total pulmonary resistance from 17.1 +/- 8.7 to 9.7 +/- 5.9 units (p less than 0.005), and increased cardiac output from 4.22 +/- 1.64 to 6.57 +/- 2.04 l/min (p less than 0.01). Heart rate increased from 83 +/- 13 to 94 +/- 11 beats/min (p = 0.1) and mean systemic arterial pressure decreased from 90 +/- 12 to 77 +/- 4 mm Hg (p = 0.055). Three patients who received a continuous infusion of prostacyclin for 24-48 hours had sustained reductions in total pulmonary resistance during the infusion period. These data demonstrate that prostacyclin can increase cardiac output and reduce pulmonary arterial pressure and resistance in PPH.

Adolescent↗