Pierre Mols

Effect of vasopressin and somatostatin on hemodynamics and blood gases in patients with liver cirrhosis.

The effects of somatostatin and vasopressin on blood gases, pulmonary and systemic hemodynamics, and portal pressure assessed by the gradient between occluded and free hepatic vein pressures, were investigated in 18 patients with liver cirrhosis. In the first 10 patients, an iv bolus of 250 microgram somatostatin, followed by an infusion of 125 microgram somatostatin over 30 min, caused a sudden rise in pulmonary and systemic vascular pressures lasting 2 to 5 min and accompanied by bradycardia. There was a slight and transient increase in venous admixture (Qsp/Qt) and alveolar-arterial oxygen tension gradients (P(A-a)O2), and a transient reduction in O2 delivery (O2 del) (-11% of the baseline values) and portal pressures (-14%). In the next 8 patients, vasopressin, 0.4 U/min infused over 30 min, caused a more persistent pulmonary and systemic hypertension and bradycardia, a slight increase in P(A.a)O2 and Qsp/Qt, a reduction in O2 del (-27%) and a decrease in portal pressures (-32%). These effects were marked during the entire vasopressin infusion period. Both somatostatin and vasopressin had vasoconstrictive properties and exerted negative effects on hemodynamics and blood gases. Vasopressin appeared to be a more potent drug than somatostatin.

Systemic and regional hemodynamic effects of isosorbide dinitrate in patients with liver cirrhosis and portal hypertension

In a group of 17 cirrhotic patients with portal hypertension, we have investigated the effects of 5 mg sublingual administration of isosorbide dinitrate (IDN) on central hemodynamics, on regional (hepatic and renal) hemodynamics and on blood gases. Fifteen min after drug administration, we observed a decrease in the right atrial mean pressure from 4 +/- 1 to 3 +/- 1 mmHg (mean +/- S.E.M., P less than 0.02) and of pulmonary arterial wedge pressure from 7 +/- 1 to 4 +/- 1 mmHg (P less than 0.001) with decreases of the cardiac index from 4.2 +/- 0.2 to 3.7 +/- 0.2 l/min/m2 (P less than 0.001) and the mean arterial pressure from 89 +/- 4 to 72 +/- 3 mmHg (P less than 0.001) and an increase in heart rate from 86 +/- 4 to 94 +/- 5 beats/min (P less than 0.001). Arterial PO2 decreased from 73 +/- 2 to 66 +/- 2 mmHg (P less than 0.001). As a consequence of both cardiac index and arterial PO2 reductions, O2 transport to the tissues was reduced from 602 +/- 32 to 518 +/- 26 ml/min.m2 (P less than 0.001). The hepatic venous pressure gradient decreased from 17 +/- 1 to 14 +/- 1 mmHg (P less than 0.001) and hepatic vein PO2 did not change. The hepatic blood flow (HBF) determined in 7 patients remained unchanged. Renal blood flow (RBF) determined in 5 patients decreased from 0.76 +/- 0.11 to 0.68 +/- 0.11 l/min (P less than 0.001). In conclusion, isosorbide dinitrate reduces portal hypertension in patients with liver cirrhosis without compromising hepatic perfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Electroencephalographic mapping and 99mTc HMPAO single-photon emission computed tomography in carbon monoxide poisoning

STUDY OBJECTIVE To investigate whether topographic analysis of EEG mapping and technetium-99m (99mTc) hexamethylpropylenamine oxide (HMPAO) brain single-photon emission computed tomography (SPECT) can detect cerebral anomalies in the acute phase of carbon monoxide poisoning. DESIGN Twelve patients aged 18 to 55 years with severe carbon monoxide poisoning and no history of neurologic disorder were evaluated. Either nasal (5 patients) or hyperbaric (7 patients) oxygen therapy was administered. Criteria for hyperbaric oxygen therapy were blood CO of more than 20%, loss of consciousness, pregnancy, or signs of cardiac injury. After oxygen treatment, all patients had a blood CO value of 0% and no patient had persistent acute signs of toxicity. Patients then were investigated by confentional EEG, EEG mapping, and 99mTc HMPAO brain SPECT. These procedures were performed on the day of admission. PARTICIPANTS After nasal (5 patients) or hyperbaric (7 patients) oxygen therapy was administered, 12 adults with severe carbon monoxide poisoning were evaluated. All studies were performed on the day of admission. MEASUREMENTS Conventional EEG, EEG mapping, and 99mTc HMPAO brain SPECT. RESULTS While classic EEG was normal in 9 of 12 patients and showed diffuse anomalies in 3, EEG mapping and 99mTc HMPAO brain SPECT demonstrated unilateral or bilateral regional anomalies in 8 of 12 patients. Anomalies were localized in temporo-parieto-occipital areas, the watershed areas of the major cerebral arteries, or in temporal cortex. CONCLUSION These preliminary results suggest that EEG mapping and 99mTc HMPAO brain SPECT can be complementary tools to diagnose early regional cerebral anomalies in carbon monoxide-poisoned patients.

Acute hemodynamic effects of controlled oxygen therapy in decompensated chronic obstructive pulmonary disease.

The acute effects of controlled O2 therapy on hemodynamics and blood gases were investigated in 22 patients with decompensated chronic obstructive pulmonary disease (COPD). An inspired O2 fraction (FIO2) of 0.24 and 0.28 given to the first 12 patients markedly improved arterial and mixed-venous blood oxygenation with no (FIO2 0.24) or slight (FIO2 0.28) aggravation of hypercapnia, but did not change O2 delivery to the tissues. Higher FIO2 values of 0.35 and 0.40 in the next ten patients improved blood oxygenation even more, together with an increase in O2 delivery to the tissues and a significant aggravation of hypercapnia. All four FIO2 values reduced cardiac output without changing pulmonary vascular resistance. These results suggest that in patients with decompensated COPD, low-flow O2 improves oxygenation by diffusion rather than convection. On the other hand, controlled O2 therapy does not appear to be an immediately effective pulmonary vasodilating treatment in these patients.

Hypouricemia in cirrhosis reflects hemodynamic alterations

In a population of 27 consecutive patients with liver cirrhosis, systemic hemodynamics were investigated and correlated to uric acid concentrations, fractional uric acid excretion, and creatinine clearances. Mean serum uric acid concentration was lower than in normal controls, and this was related to abnormally high uric acid clearances. Uric acid concentrations correlated positively to total peripheral resistances and negatively to cardiac output. Fractional uric acid excretions correlated negatively to total peripheral resistances and positively to cardiac output. There was no correlation between creatinine clearances and any variable of systemic hemodynamics. Serum uric acid concentration and fractional uric acid excretion are dependent of the hemodynamic state in cirrhosis.