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Biomedical subjects

A Saadjian

Publications and source records attributed to A Saadjian.

15 recordsLinked to original sources

Vascular and cardiac reactivity in pulmonary hypertension due to chronic obstructive lung disease: assessment with various oxygen concentrations.

The aim of the present work was to evaluate vasoreactivity in patients with pulmonary hypertension related to chronic obstructive lung disease. This was done by comparing haemodynamic data recorded while patients were breathing room air, and hypoxic and hyperoxic mixtures. We estimated the role of vasoconstriction in determining the level of pulmonary hypertension. This study included 26 patients with moderate pulmonary hypertension mean pulmonary arterial pressure (MPAP) = 27.3 +/- 1.2 mmHg) secondary to chronic obstructive lung disease (COLD), forced expiratory volume in one second (FEV1) = 0.95 +/- 0.13 l; arterial oxygen tension (PaO2) = 8.7 +/- 0.25 kPa). After insertion of a thermodilution catheter in the pulmonary artery and a cannula in the femoral artery, mixtures containing 15, 21, 30 and 100% oxygen were randomly administered for 20 min each. As fractional inspiratory oxygen (FIO2) increased, MPAP decreased relatively less than cardiac index. Cardiac output was at its highest during room air breathing and the hypoxic mixture did not lead to a further increase. Unlike normal subjects, in whom adjustment of cardiac output is achieved by heart rate alone, haemodynamic regulation in these patients also involved stroke volume. Variations in MPAP and cardiac index were strongly correlated with arterial oxygen saturation (SaO2). The greatest variations were noted in the patients with the highest pulmonary hypertension. Under normoxic and hyperoxic condition the relationship between pulmonary artery driving pressure and cardiac index was linear and its slope steeper in patients having the highest pulmonary hypertension at steady-state.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged

Effects of nicardipine on pulmonary and systemic vascular reactivity to oxygen in patients with pulmonary hypertension secondary to chronic obstructive lung disease.

We compared the acute effects of nicardipine and a placebo on the response of pulmonary and systemic circulation to different inspiratory fractional concentrations of O2 (FiO2) in 10 patients with pulmonary hypertension secondary to chronic obstructive lung disease. After catheterization of the pulmonary and femoral arteries, gas mixtures containing 15, 21, and 30% O2 were randomly administered for 20 min each during infusion of saline and then nicardipine (0.06 mg/kg/min). Plasma nicardipine level was maintained at 30 ng/ml. During nicardipine infusion, cardiac index (CI) was significantly higher (+20%, p less than 0.05) than during placebo infusion, with no change in mean pulmonary artery pressure (MPAP). Pulmonary resistances also decreased significantly (-20%) during nicardipine. No change in arterial or mixed venous O2 contents was noted. Mean arterial pressure (MAP) and systemic resistances decreased significantly with nicardipine. Inhaling a hyperoxic mixture was followed by a significant decrease in arterial pressure during placebo infusion; this was not observed during nicardipine. In contrast with systemic circulation, the response of the pulmonary circulation to different FiO2 levels was unaffected by nicardipine.

Blood Gas Analysis

Heat and mass transfer of a thermal indicator in pulsatile flow through the cardio-pulmonary system. I. Modeling.

The construction of a physico-mathematical model which describes the mechanism of indicator dispersion in the circulation and which fits the thermal dilution curves (TDC) is presented. Because of its more evident physical meaning, formulation of the problem in terms of heat and mass transfer is preferred to stochastic theory. Hypotheses necessary to simplify the general system of governing equations are clearly defined and discussed. This deductive method leads to a one-dimensional convective heat transfer model in which pulsatility and form of injection appear naturally. Simulations of TDC in constant and pulsatile flow cases are performed on a digital mini-computer which demonstrates the model's ability to represent different experimental or clinical observations. This will facilitate hemodynamic parameter identification from TD techniques and will increase the accuracy of this identification.

Aorta

Heat and mass transfer of a thermal indicator in pulsatile flow through the cardio-pulmonary system. II. Identification of cardiac output.

Hamilton's celebrated formula for cardiac output measurement is simple but its validity is dependent on several methodologic requirements which are not generally fulfilled, particularly in thermal dilution. A quite different method, based on a physico-mathematical model of the indicator dispersion in the circulation, is proposed. It allows direct derivation of cardiac output once the model's parameters have been identified. Combined deconvolution and least squares procedures are used with truncated data for this identification. Numerical tests and application to clinical observations are presented. Both limitations and possibilities of further developments in estimation of pulsatile flow conditions from TD technique are discussed.

Blood Circulation

[Use of sodium nitroprusside in cardiology].

Sodium nitroprusside (SNP) is rarely used in cardiology. It is reserved traditionally for severe episodes of arterial hypertension. Certain states of refractory heart failure represent new indications for use, which implies a double haemodynamic monitoring system: continuous control of systemic blood pressure by intra-arterial catheterization; control of pulmonary pressure and repeated measurements of cardiac output. Prolonged treatment requires continuous biological monitoring of toxicity and careful control of kidney function. As a moderator of blood pressure, SNP is remarkably effective. The hypotensive effect is immediate, readily reversible and generally tachyphylaxis is not observed. The effect of SNP on cardiac work is one of double load reduction: mainly a reduction in afterload or pressure and systemic resistance and a reduction in preload or pressure of ventricular filling. In this respect, SNP can be used effectively for severe cases of heart failure intractable to traditional cardio-stimulatory and diuretic treatments and stemming from diverse causes: acute stage of myocardial infarction, ventricular dilatation, mitral papillary syndrome, heart failure, either subacute or chronic, of various causes. As a rule, the immediate results are positive. Taking the patient off the drug can be difficult and may cause a return to the previous haemodynamic situation.

Adult

[Hemodynamic profile of acute myocardial infarction as a function of electrocardiographic localization].

The haemodynamic profiles of 147 cases of myocardial infarction investigated within 30 hours of the clinical onset were studies in relation to the topography of the necrosis on the ECG: there were 36 inferior (I), 29 postero-inferior (PI), 22 antero-septal (AS), 38 antero-lateral (AL), 15 deep septal (DS), and 7 strictly posterior or lateral (PL). Simultaneous recordings of the diastolic pulmonary arterial pressures and the left ventricular diastolic pressures (pre-and post-a) have shown different degrees of correlation with the topographical site. The correlation found in AS, AL and I necrosis are clearer with respect to the pre-a. The PI necroses show no correlation. Graphs of left ventricular function as well as an analysis of the various other parameters show that the DS, the AL, and to a lesser extent the PI are associated with the grossest depression of left ventricular function. A study of the amplitude of the "a" wave also shows that the effect of infacts of the free wall of the left ventricule on the compliance is greater. A study of right ventricular function as well as the correlations between the pulmonary and right atrial pressures confirms the presence of right ventricular disfunction in DS and PI necroses. Impaired left ventricular function, impaired right ventricular function, and disorders of compliance seem to be the determining factors in changing the haemodynamics in the various ECG sites of infarction.

Acute Disease

Cardiac output measurement by thermodilution: methodologic problems.

In clinical practice, thermodilution technique for cardiac output measurement is generally applied to the right heart (injection of a saline cold bolus in the right atrium, temperature measurement downstream in the pulmonary artery). This technique is well adapted to repetitive measurements using a single catheter. However, its validity is dependent on several methodologic requirements: quantitation of the indicator, control of the catheter's dead-space effect, conservation and mixing of the cold bolus, accurate measurement of small thermal gradients. Calculations from the thermal dilution curve must be adapted to possible baseline shifts. All these different methodologic aspects are studied. Several solutions (heat exchanger, automatic injection, calculation method) are proposed. Comparison between an automatic thermodilution device and dye dilution has been performed successfully.

Cardiac Catheterization

[Approach to the prognosis of myocardial infarct from the initial hemodynamic examination].

Hemodynamic investigations (right and left heart catheterization, cardiac output measurement) were performed in 132 patients with acute myocardial infarction. Retrospective study of the first 100 patients allowed determination of prognostic indices. A new statistical method is proposed which was used prospectively in the 32 following patients and resulted in an error of prediction of about 3 per cent. The establishment of prognosis from hemodynamic data is a necessary condition prior to new therapeutic approaches of cardiac failure in acute myocardial infarction.

Adult

Mechanical aspect of the heart sound emission.

The present paper deals with a physical study of the relation between the phonocardiogram and left ventricular pressure (LVP) fluctuations. Fourier analysis comparison of the two signals-simultaneously recorded either on pathologic human hearts or during experiments on dogs-does not point out an obvious relation between the phonocardiogram and a linear combination of the first pressure derivatives.-A mechanical model of the heart enabling the description of the sound emission mechanism provides a qualitative relation between the phonocardiogram and LVP fluctuations: the acceleration of the thoracic area is equal to the product of LVP by a time function depending on the mechanical properties of the muscle. - A theoretical thoracic acceleration obtained by transformation of the experimental LVP is compared with the experimental phonocardiogram through linear filtering analysis. The theoretical signal is in good agreement with the experimental one.

Fourier Analysis