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Biomedical subjects

P Mols

Publications and source records attributed to P Mols.

At least 19 recordsLinked to original sources
PubMed1999

Ventricular fibrillation secondary to ergotamine in a healthy young woman.

A 34-year-old woman collapsed secondary to ventricular fibrillation 3 hours following the ingestion of ergotamine tartrate for migraine. She underwent defibrillation and recovered rapidly without any subsequent consequences. The mechanism of action and the side effects of ergotamine and other antimigraine drugs are discussed. We hypothesize that a coronary spasm induced by ergotamine could be the aetiologic factor leading to ischaemic ventricular fibrillation.

Adult↗
PubMed1998

A comparison of repeated high doses and repeated standard doses of epinephrine for cardiac arrest outside the hospital. European Epinephrine Study Group.

BACKGROUND: Clinical trials have not shown a benefit of high doses of epinephrine in the management of cardiac arrest. We conducted a prospective, multicenter, randomized study comparing repeated high doses of epinephrine with repeated standard doses in cases of out-of-hospital cardiac arrest. METHODS: Adult patients who had cardiac arrest outside the hospital were enrolled if the cardiac rhythm continued to be ventricular fibrillation despite the administration of external electrical shocks, or if they had asystole or pulseless electrical activity at the time epinephrine was administered. We randomly assigned 3327 patients to receive up to 15 high doses (5 mg each) or standard doses (1 mg each) of epinephrine according to the current protocol for advanced cardiac life support. RESULTS: In the high-dose group, 40.4 percent of 1677 patients had a return of spontaneous circulation, as compared with 36.4 percent of 1650 patients in the standard-dose group (P=0.02); 26.5 percent of the patients in the high-dose group and 23.6 percent of those in the standard-dose group survived to be admitted to the hospital (P=0.05); 2.3 percent of the patients in the high-dose group and 2.8 percent in the standard-dose group survived to be discharged from the hospital (P=0.34). There was no significant difference in neurologic status according to treatment among those discharged. High-dose epinephrine improved the rate of successful resuscitation in patients with asystole, but not in those with ventricular fibrillation. CONCLUSIONS: In our study, long-term survival after cardiac arrest outside the hospital was no better with repeated high doses of epinephrine than with repeated standard doses.

Adrenergic Agonists↗
PubMed1994

Early defibrillation by EMTs: the Brussels experience.

Considering that in Brussels the first-aid ambulance team reaches the patient in cardiac arrest 10 min before the physician-manned ambulance, we instituted a feasibility study of early defibrillation by emergency medical technicians (EMTs). Three hundred EMTs received a 20-h automatic external defibrillation (AED) training course followed by a refresher course every 6 months. Of 316 cardiac arrests included in this study, asystole was encountered in 53% and ventricular fibrillation/ventricular tachycardia (VF/VT) in 33% of the cases on arrival of the EMTs. In the VF/VT group, defibrillation was performed by EMTs with a Laerdal Heartstart 7-9 min before the medical team arrived. The overall cardiac arrest survival rate improved from 7% in 1989 to 19% in 1992. However, the long-term survival rate (14/105) of ventricular fibrillation remained low because of excessive delays in emergency medical service (EMS) access and in early ACLS. In conclusion, this work shows that in Brussels: (1) early defibrillation of cardiac arrest victims in VF is feasible by EMTs when a training and a follow-up program are implemented; (2) the weakest link of the chain of survival is the early EMS access, and the early ACLS; and (3) AED program increases the interest and the efficacy of EMTs and medical teams in the management of cardiac arrests.

Aged↗
PubMed1994

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 Disease↗
PubMed1994

Semi-automatic external defibrillation.

Malignant arrhythmia, which is responsible for most of the out-of-hospital cardiac arrests, is ventricular fibrillation (VF). The best treatment of VF is a controlled electric shock on the chest administered in a short delay. The emergency medical technicians (EMTs) qualified to carry out this treatment in Belgium and in districts often succeed in arriving on the spot 8 minutes earlier than the people of the Service Mobile d'Urgence et de Réanimation (SMUR). The delegation of defibrillation to ambulance crew members however implies a specific teaching, training and a medical control. The Brussels experience shows that semi-automatic external defibrillation by EMT-Ds (SAED) is feasible when criteria for applying SAED in the pre-hospital phase are applicable.

Aged↗
PubMed1993

Acute effects of nifedipine on systolic and diastolic ventricular function in patients with chronic obstructive pulmonary disease.

To evaluate how nifedipine influences systolic and diastolic ventricular function, the effects of 20 mg sublingual nifedipine were studied in 13 stable COPD patients. Nifedipine induced no change in mean pulmonary arterial pressure, decreased mean arterial pressure, pulmonary and systemic vascular resistance index, and increased heart rate and cardiac index. It also caused an increase in right and left ventricular ejection fractions. The end-diastolic volume index of both ventricles remained unchanged, whereas the end-systolic volume index tended to decrease without reaching a significant level, and the right ventricular contractility increased. After nifedipine administration, right and left ventricular compliance increased. This study suggests that short-term administration of nifedipine improves the systolic function by a decrease in ventricular afterload and an increase in ventricular contractility and increases the ventricular compliance by a reflex sympathetic stimulation and an afterload reduction.

Administration, Sublingual↗
PubMed1993

Dose dependency of aminophylline effects on hemodynamic and ventricular function in patients with chronic obstructive pulmonary disease.

The effects of aminophylline on pulmonary vascular tone, systemic hemodynamics, and ventricular ejection fractions reported in the literature show some discrepancies. We therefore studied in COPD patients the effects of aminophylline on hemodynamics, on ventricular ejection fractions, and on systolic and diastolic functions of each ventricle, and we measured simultaneously the blood level of the drug. The analysis of the data revealed a relationship between the blood level of aminophylline and the variations of right ventricular ejection fraction (RVEF) (r = 0.83, p = 0.005), left ventricular ejection fraction (LVEF) (r = 0.76, p = 0.017), pulmonary vascular resistance index (PVRI) (r = -0.58, p = 0.096), systemic vascular resistance index (SVRI) (r = -0.60, p = 0.08), and right ventricular peak systolic pressure/end-systolic volume index (RVPSP/ESVI) (r = -0.75, p = 0.02). Modifications of ejection fractions and vascular resistance indices were correlated for both ventricles (RVEF vs PVRI, r = -0.77, p = 0.01; LVEF vs SVRI, r = -0.76, p = 0.02). Finally, RVEF modifications was also correlated to RVPSP/ESVI variation (r = 0.78, p = 0.01). These results suggest that even within the therapeutic range (10 to 20 mg/L), the effects of aminophylline seemed to depend on its blood level. This dose dependency could explain the contradictory data reported in the literature concerning the effects of aminophylline on pulmonary and systemic hemodynamics and on ventricular function.

Aged↗
PubMed1992

Estimation of right ventricular ejection fraction by means of 99Tcm-macroaggregates.

A method is described for assessing right ventricular ejection fraction (RVEF) by means of 99Tcm-macroaggregates (MAA). The method consists of performing, in right anterior oblique (RAO) projection, a direct ECG-gated data acquisition over 120 s, as soon as the intravenous administration of the tracer is started. The activity returning to the left heart being negligible, background is limited to the lung activity overlapping the right ventricle. The distribution of lung activity in the gated frames is, however, exactly the same as that in the lung perfusion image, it can therefore be subtracted using static lung scintigraphy acquired directly after the gated study. Considering the count density distributions in the corrected end-diastolic (ED) and end-systolic (ES) frames and the first harmonic phase and amplitude images, ED and ES RV regions of interest (ROIs) are delineated for the calculation of RVEF. It has been shown that using 5 mCi 99Tcm-MAA, the ED count obtained is similar to that usually observed during a 20 mCi 99Tcm first-pass study. Intraobserver variation is acceptable and there is a good correlation between the RVEF calculated by this method and that obtained by means of a steady-state ECG-gated 81Krm technique. As the method presents similar advantages to those offered by 81Krm while using 99Tcm, it constitutes, in our opinion, a good approach for estimating RVEF in routine clinical practice.

Humans↗
PubMed1991

Volumetric response of right ventricle during progressive supine exercise in men.

Right ventricular (RV) adaptation to supine exercise has been studied in 10 young male volunteers by 81mKr electrocardiogram (ECG)-gated radionuclide ventriculography. During progressive supine exercise, the ejection fraction gradually increased from a mean value of 46% at rest up to 60% at a maximal exercise level. End-diastolic volume however remained unchanged at a low exercise level and even slightly decreased at a higher exercise level. Little or no change in end-diastolic volume and an increase in ejection fraction produced a significant decrease in end-systolic volume and a net increase in stroke volume. These results indicate that the Frank-Starling mechanism does not contribute to the increase in right ventricular stroke volume during progressive supine exercise, but the increase in right ventricular stroke volume rather seems related to an increased contractility, presumably mediated by an increased sympathetic activity.

Adult↗
PubMed1989

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)

Adult↗
PubMed1989

Enhancement of hypoxic pulmonary vasoconstriction by low dose almitrine bismesylate in normal humans.

The effect of almitrine bismesylate on hypoxic pulmonary vasoconstriction (HPV) remains controversial. We therefore investigated in a double-blind, placebo-controlled, randomized design the effects of low dose of almitrine bismesylate (4 micrograms/kg/min given intravenously) on blood gases, pulmonary hemodynamics, and ventilation-perfusion (VA/Q) distributions in normal subjects breathing a hypoxic mixture (FIO2, 0.125), room air (FIO2, 0.21), and oxygen (FIO2, 1.0) in a random sequence. In the placebo group (7 subjects), no change was recorded. In the almitrine group (10 subjects), arterial PO2 improved during hypoxia (from 42 +/- 2 to 47 +/- 1 mm Hg, p less than 0.05, mean +/- SEM) and normoxia (from 99 +/- 3 to 104 +/- 2, p less than 0.05). Pulmonary arterial mean pressure and pulmonary vascular resistance index increased with almitrine during hypoxia, respectively, from 20 +/- 1 to 23 +/- 1 mm Hg (p less than 0.01) and from 207 +/- 22 to 283 +/- 35 dyne.s.cm-5.m2 (p less than 0.01), and during normoxia, respectively, from 12 +/- 1 to 14 +/- 1 mm Hg (p less than 0.05) and from 90 +/- 11 to 137 +/- 13 dyne.s.cm-5.m2 (p less than 0.05). The VA/Q distribution improved during hypoxia, with a shift of the blood flow distribution to better oxygenated lung units with higher VA/Q ratios. We conclude that in normal humans low dose of almitrine improves gas exchange by an enhancement of HPV.

Adult↗
PubMed1989

Prediction of pulmonary arterial pressure in chronic obstructive pulmonary disease by radionuclide ventriculography.

Pulmonary arterial hypertension represents an important parameter for the assessment of the severity of chronic bronchitis. The measurement of the pulmonary arterial pressure, however, requires invasive techniques of limited routine use because of costs and associated risks. The aim of this study is to evaluate whether the 81mKr right ventricular ejection fraction and parameters derived from equilibrium 99mTc red blood cells' right ventricular curve allow a better estimation of PAP than the 99mTc RVEF. In 41 patients with severe chronic bronchitis, the linear correlation between PAP and 99mTc RVEF was -0.61 (p less than 0.001). None of the parameters derived from the right ventricular curve was better correlated to PAP than the 99mTc RVEF. In 16 other chronic bronchitis patients, the 81mKr RVEF correlated moderately to PAP. In conclusion, the alternative isotopic methods proposed in this work do not provide a reliable estimation of pulmonary arterial pressure in patients with chronic bronchitis.

Blood Pressure↗
PubMed1988

How does salbutamol improve the ventricular performance in patients with chronic obstructive pulmonary disease?

To evaluate the influence of beta 2 mimetics on ventricular contractility and pump function, radionuclide ventriculography and right heart catheterization were simultaneously performed in 10 patients with severe chronic obstructive pulmonary disease. After a 60 min constant infusion of 17 micrograms/min salbutamol, cardiac index increased by 60%, heart rate by 39%, and stroke volume index by 14%. Mean pulmonary artery pressure remained unchanged and mean arterial pressure decreased slightly but not significantly. Right ventricular (RV) function improved as attested to by an increase of RV ejection fraction (+8%), a decrease of RV end-diastolic pressure (-5 mm Hg), and RV end-systolic volume index (-18%). Simultaneously, the pulmonary vascular resistance index decreased by 33% and RV contractility, appreciated by RV dP/dtmax, RV (dP/dtmax)/P, and RV end-systolic pressure/volume ratio, increased by 44, 77, and 27%, respectively. Left ventricular (LV) function also improved. The LV ejection fraction increased by 18% and LV end-systolic volume decreased by 34%. Concomitantly, the systemic vascular resistance index decreased by 40% and the LV end-systolic pressure/volume ratio increased by 50%. Our results suggest that the infusion of salbutamol improves ventricular performance by a decrease of ventricular afterload and by a positive inotropic effect.

Aged↗
PubMed1987

Hypoxic pulmonary vasoconstriction and pulmonary gas exchange in normal man.

Blood gases, hemodynamics and ventilation were measured in 7 healthy volunteers at baseline while breathing room air (FIO2 0.21), during hypoxia (FIO2 0.125, 15 min) and after nifedipine 20 mg sublingually at FIO2 0.21 (45 min) and at FIO2 0.125 (15 min). Distributions of ventilation-perfusion ratios (VA/Q) were determined, using the multiple inert gas elimination technique, at baseline, during hypoxia, and again during hypoxia after nifedipine intake. Hypoxia was associated with an average increase in pulmonary vascular resistances by 104%, which was partially inhibited by nifedipine. The inert gas data showed a mild deterioration in the distribution of VA/Q ratios during hypoxia. However, when blood flow and ventilation were constrained to the baseline normoxic values in the distributions recovered during hypoxia ('normalization procedure') a slight improvement in VA/Q matching could be evidenced, which was blunted during hypoxia after nifedipine. This was interpreted as the functional effect of hypoxic pulmonary vasoconstriction (HPV). Using the 'normalized' distributions, we computed the relationship between the decrease in compartmental blood flow that occurred during hypoxia and the corresponding alveolar PO2, and calculated the gain due to HPV feedback using equations of the control theory. The contribution of HPV to the stability of compartmental VA/Q was greatest for alveolar PO2 values around 60 mm Hg, but at best the feedback had only a moderate efficiency.

Adult↗
PubMed1987

Measurement of right ventricular volumes from ECG-gated steady-state krypton-81m angiocardiography.

The physical characteristics of krypton-81m makes it particularly suited for the study of right ventricular function, but its ultrashort half-life (13.3 s) precludes in vitro measurements of blood pool specific activity needed for count based determination of ventricular volumes. A combined geometric count based method was developed to measure absolute right ventricular volumes during steady state krypton-81m angiocardiography: background corrected ventricular count rates were converted to volumes using a count to volume calibration factor calculated in an 'internal reference ROI' located in the right ventricular outflow tract. Stroke volumes calculated with this method were shown to be comparable to thermodilution determined stroke volumes and the ability of the method to monitor changes in right ventricular volumes was demonstrated during intervention studies.

Angiocardiography↗
PubMed1987

Pulmonary vascular tone improves pulmonary gas exchange in the adult respiratory distress syndrome.

Hemodynamics, blood gases, lung mechanics, and the distributions of ventilation-perfusion ratios (VA/Q) were studied before and after iv diltiazem, 0.5 mg/kg over 30 min, in 6 patients with pulmonary hypertension secondary to the adult respiratory distress syndrome (ARDS) ventilated with 7 to 20 cm H2O positive end-expiratory pressure (PEEP). Diltiazem decreased systemic and pulmonary arterial pressures without changes in cardiac output and in filling pressures of the heart, and with a slowing of heart rate. Pulmonary vascular resistances decreased from 401 +/- 59 to 329 +/- 58 dyne.s.cm-5.m2 (mean +/- SEM), p less than 0.01. Arterial Po2 decreased from 87 +/- 10 to 80 +/- 11 mm Hg (p less than 0.02) without changes in arterial PCO2, mixed venous PO2, and O2 consumption. Lung compliance and airway resistances did not change. Diltiazem increased true shunt from 23 +/- 5 to 30 +/- 7% of total blood flow (p less than 0.02) without other modification in the pattern of VA/Q distribution as measured by the multiple inert gas elimination technique. These results suggest that pulmonary vascular tone contributes to the maintenance of VA/Q matching in patients with ARDS.

Adult↗
PubMed1986

Treatment of hyponatremic cirrhosis with ascites resistant to diuretics by urea.

We have studied the efficacy of urea in the treatment of hyponatremia and hydrosaline retention in cirrhotic patients with ascites resistant to diuretics. In 5 patients with hyponatremia and ascites resistant to a major diuretic treatment (200-400 mg spironolactone combined with 40-160 mg furosemide/day for 4 of them), urea intake (30-90 g/day) induced the following changes: the daily weight changed from a gain of 0.01 +/- 0.06 kg/day to a loss of 1.03 +/- 0.12 kg/day (p less than 0.001) (mean +/- SEM), serum sodium concentration rose from 128 +/- 1.3 to 133 +/- 1.4 mmol/l (p less than 0.01), sodium output increased from 24 +/- 4 to 82.5 +/- 11 mmol/day, diuresis increased from 1.05 +/- 0.10 to 2.24 +/- 0.24 liters/day (p less than 0.01). Despite an important weight loss, the creatinine clearance did not change significantly (53.6 +/- 4.5 ml/min before and 70.0 +/- 8.2 ml/min during urea). In patients responding to classical diuretics, urea as a monotherapy was less effective. From the 6 patients with resistant ascites, only 1 developed prerenal uremia after urea treatment. In order to enhance urea efficacy, it is important to take it together with a long-loop diuretic. Intermittent urea intake seemed to be useful in cirrhotic patients with hyponatremia associated with ascites resistant to diuretics and with low or normal blood urea concentrations.

Adult↗