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Biomedical subjects

G M Domenighetti

Publications and source records attributed to G M Domenighetti.

4 recordsLinked to original sources
PubMed1994

[Treatment of acute pulmonary hypertension caused by hypoxia--cosmetic or clinical benefits?].

Acute or chronic exacerbated hypoxic pulmonary hypertension (PH) is a frequent event in patients with severe respiratory failure, such as those presenting with acute exacerbation of chronic obstructive pulmonary disease (COPD) or with adult respiratory distress syndrome (ARDS). The increased pulmonary vascular tone may reduce right ventricular performance. This, in turn, may trigger a drop in cardiac output and in oxygen delivery; furthermore, in patients with ARDS, increased hypoxic vasoconstriction may enhance extravascular water accumulation. However, the increased pulmonary vascular tone acts as a natural defence mechanism on the level of the air-blood barrier and may reduce the intrapulmonary VA/Q mismatch. Systemic vasodilators may induce favourable hemodynamic effects in patients with a hypoxic PH and a reduced right ventricular performance. On the other hand, they may worsen gas exchange through a flow-diversion phenomenon (from normal lung units to units with a very low VA/Q relationship) or through inhibition of hypoxic vasoconstriction if PvO2 increases. Recently, nitric oxide (NO) has been recognized as an important endothelial factor with potent vasorelaxing properties; preliminary studies in patients with ARDS and in those with severe primary pulmonary hypertension have corroborated the power of this molecule in improving gas exchange and pulmonary hemodynamics without deleterious effects on the systemic circulation. However, further randomized controlled studies with NO are urgently needed in order to investigate the risk-benefit ratio and the prognostic significance of this promising new treatment. Until this occurs, patients with a hypoxic acute or chronic exacerbated PH should not be treated according to fixed criteria but on a reasonable case by case basis.

Acute Disease↗
PubMed1992

Short- and long-term hemodynamic effects of oral nifedipine in patients with pulmonary hypertension secondary to COPD and lung fibrosis. Deleterious effects in patients with restrictive disease.

STUDY OBJECTIVE: The present study was undertaken to evaluate at rest the short- and long-term effects of oral nifedipine (N) in patients with pulmonary hypertension (PH). DESIGN AND SETTING: A prospective study with ten consecutive cases during two years in a setting of a district acute hospital. PATIENTS OR PARTICIPANTS: Seven patients with advanced COPD and three with severe lung fibrosis (LF) during a period of stable condition. Three patients with COPD were eligible for the long-term investigation. INTERVENTIONS: Right heart catheterization with a 7F Swan-Ganz triple-lumen thermodilution catheter and radial cannulation with a 3F arterial catheter. MEASUREMENTS AND RESULTS: Measurement of CO, MAP, RAP, PAP, PWP, HR, and ABG and calculation of CI, TSR, PAR, and DO2 before and after 20 mg of N sublingually at rest. For the group as a whole, N induced a reduction in MAP and TSR, with a significant increase in CI and DO2. There were no significant changes in PAP, PAR (magnitude of the reduction: -10 percent), HR, and PaO2. The individual analysis of the driving pressures (PAP-PWP) in function of the cardiac output demonstrated that a real vasodilating effect in the pulmonary circulation occurred in only three COPD patients (magnitude of the PAR reduction: -43 percent), while in the three patients with LF, N induced a deleterious increase in PAP and PAR. After long-term treatment (10 mg of N daily every 4 h; average 12 months) in the former, despite a persistent beneficial hemodynamic effect (magnitude of the PAR reduction: -36 percent), there was the usually expected clinical worsening. CONCLUSIONS: N in small doses may be able in some patients with severe COPD to induce a beneficial short- and long-term hemodynamic effect on the pulmonary circulation when PH is present. On the other hand, N should not be used in patients with PH and advanced LF.

Aged↗
PubMed1984

Hyperadrenergic syndrome in severe tetanus: extreme rise in catecholamines responsive to labetalol.

The hyperadrenergic syndrome that occurs in tetanus is characterised by hypertension, tachycardia, and increased systemic arteriolar resistance. A 74 year old man with tetanus was found to have very high catecholamine concentrations--as high as those in phaeochromocytoma--and the fluctuations in blood pressure and heart rate were measured to see whether they paralleled changes in the catecholamine values. A labetalol infusion of 0.25-1 mg/min gradually stabilised the cardiovascular disturbances and the patient recovered.

Adrenergic Fibers↗