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Haemodynamic Effect of Deslanoside at Rest and During Exercise in Patients with Chronic Bronchitis

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Haemodynamic Effect of Deslanoside at Rest and During Exercise in Patients with Chronic Bronchitis Br Heart J: first published as 10.1136/hrt.35.1.2 on 1 January 1973. Downloaded from British HeartJournal, I973, 35) 2-8. Haemodynamic effect of deslanoside at rest and during exercise in patients with chronic bronchitis V. Jezek and F. Schrijen From Uniti I4 de l'I.N.S.E.R.M., Nancy, France The effect of intravenously administered deslanoside (Cedilanid) was studied in 24 patients with chronic bronchitis at rest and during exercise. No changes in ventilation, blood gases, and oxygen consumption were observed. In the patients without right heartfailure, deslanoside induced a slight reduction in cardiac output, right ventricular end-diastolic andpulmonary arterial wedge pressures, and increase ofsystemic andpulmonary vascular resistances. The effect of deslanoside was different in the patients with right heartfailure: an increase of cardiac output, stroke volume, right and left ventricular stroke work and stroke power, and a more pro- nounced decrease of RV end-diastolic and pulmonary arterial wedge pressures were observed, with no changes in vascular resistances. We failed to find a significant improvement in cardiac performance after deslanoside during exercise. The effect of deslanoside does not seem to be related to arterial hypoxaemia or hypercapnic acidosis at rest. The effect of digitalis glucosides has been studied less than 94%) was present in 75 per cent, arterial by different authors (Ferrer and Harvey, I959; hypercapnia (P8co2 over 43 mmHg) in 7I per cent, and Gray, Williams, and Gray, I952; Mounsey et al., pulmonary arterial hypertension at rest (PPA over 20 and Malmberg, mmHg) in 79 per cent of the cases. No patient received I952; Berglund, Widimsky, I963). digitalis glycosides at least 4 weeks before the study Particular attention has been drawn to the changes and no patient was in the period of acute respiratory http://heart.bmj.com/ in pulmonary arterial and right ventricular pressures, insufficiency. No patient had evidence ofvalvular disease, but pulmonary arterial wedge or left heart pressures atherosclerosis, or previous myocardial infarction. have been measured only occasionally. Therefore, When the diastolic systemic pressure was above go we have little information about the changes of pul- mmHg, the patient was omitted from the study. monary vascular resistance in acute digitalization. The patients were divided into the following groups: We know only one paper (Berglund et al., I963) Group i includes 9 patients without any history of car- which deals with the effect of digitalis in exercising diac failure, Group 2 includes 6 patients with a positive patients. history of cardiac failure from 4 weeks to 2 years before the study, and Group 3 includes 9 patients with signs of on September 27, 2021 by guest. Protected copyright. We tried to study the effect of acute digitalization right heart failure (leg oedema, liver congestion) at the in a group of patients with chronic bronchitis suffici- time of catheterization. No patients had clinical or ently large for statistical analysis. laboratory signs of tricuspid insufficiency. Catheterizations were performed in the postprandial Patients and examination procedure state, without premedication, by Cournand catheters No. 7 and 8 introduced via the antecubital vein. Zero The study was made in 24 patients with chronic bron- pressure level was placed I0 cm above the catheterization chitis, the diagnosis being made on the basis of a positive table. Ventilation, oxygen consumption, and carbon history of chronic productive cough. All the patients dioxide output were registered in the Metabograph.1 were of a physical and mental state to understand the The analyses of blood gases were made in the Radio- nature and full circumstances of the investigation, and meter2 equipment using Astrup's technique; blood oxy- all of them assented to take part in the study, though gen capacity was measured in the Van Slyke apparatus. they realized that it was not expected to be of direct Arterial blood was withdrawn from a Cournand needle advantage to themselves. Complete obstructive syn- inserted in the brachial artery. drome according to spirography was present in 67 per After introduction of the catheter in the wedge posi- cent of the cases and normal spirographic values were tion and insertion of the needle in the brachial artery, observed in 4 cases only. Arterial hypoxaemia (SaO2 1 Metabo, Lausanne, Switzerland. Received io April 1972. 2 Radiometer, Copenhagen, Denmark. Br Heart J: first published as 10.1136/hrt.35.1.2 on 1 January 1973. Downloaded from Haemodynamic effect of deslanoside 3 the patient breathed in a mask connected to the Metabo- of ventricular work, ventricular power, and tension-time graph. Pulmonary wedge, pulmonary arterial, right index were obtained by planimetry from the brachial ventricular, and brachial artery pressures were recorded artery and pulmonary artery pressure curves. Vascular and the blood for analysis was withdrawn after I0 min- resistances, ventricular work, stroke work, stroke power, utes steady state. This procedure was repeated after and stroke tension-time index (Samoff et al., I958), and pedalling (io minutes on the average) on the bicycle mean systolic ejection rate were calculated by the usual ergometer in the supine position. The work load was formulae. Pulmonary artery wedge pressure was used 40 W for I8 patients and 20 W for 3. Three patients instead of left ventricular end-diastolic pressure for the were not able to exercise. calculation of left ventricular work. Immediately after exercise, a dose of o-6 mg deslano- Statistical analysis was made by simple or paired t-test side diluted in I0 ml isotonic saline was introduced via and by calculation of correlation coefficients. The differ- the catheter. The same examination procedure and ences in mean pulmonary arterial pressure and pulmon- measurements were repeated after a rest of 30-40 ary vascular resistance between two exercise periods minutes. (before and after deslanoside) were not evaluated statis- Cardiac output was calculated according to the Fick tically because they are diminished by repeated exercise method. The pre-ejection period and systolic ejection itself (Widimsky, Berglund, and Malmberg, I963). time index were derived from the brachial artery pressure curve according to Weissler, Harris, and Schoenfeld Results (I968). In 6 patients from another study, it was shown that the systolic ejection time calculated from the brachial Differences between groups at rest artery and the ascending aorta pressure curves are The results are summarized in Table i. Groups i identical. The mean systolic pressures for the calculation and 2 differ only in the values of end-diastolic and TABLE i Haemodynamic changes after deslanoside in patients recovering from cardiac failure (Group 2) Value Rest Exercise Control Deslanoside Control Deslanoside VE (1. min -m 2) 4-4±+04 4-7±°03 I3-4±4-2 I3-7±5-I VAlVE (%) 56±7 56±3 58± 9 6I±9 Va2 (ml min m- ) I59±I9 I54+I2 459± I33 47I ± I35 P,O2 (mmHg) 66±9 6I+7 7I+I3 63 ±I4 http://heart.bmj.com/ Sa02(%) 88±7 86±6 87+9 85+I2 PcoC2 (mmHg) 46±3 42±I 48±5 46±5 [H+]a (n mol L-1) 40±4 38±4 45±3 43±3 Cardiac output (1. min m ) 4*3 ±I*2 3-9±I-0 7-I ±i8 6-9±I'7 Heart rate (min- 1) 77±I7 82 +19 I03 ±22 I06 +25 Stroke volume (ml m- 2) 54±7 47 ±6* 7I +20 65 ±9 RV end-diastolic pressure (mmHg) II5±+2-8 I0-0 +3--888±3-3 I72 ±5-6 Mean pulmonary arterial pressure (mmHg) 29 ±4 28 ±6 53 ±10 49± I2 Mean pulmonary arterial wedge pressure (mmHg) I3-6 ± 2-6 9-6 + 2.2* I9-5 ± 57 i8'3 ± 38 Mean brachial artery pressure (mmHg) I0o8 + 1 II I2I +8 I04+ I24±9 on September 27, 2021 by guest. Protected copyright. Systemic vascular resistance (dynes sec cm - 5m 12) 944±435 2055 ±570 1236 ± 257 I240 ± I97 Pulmonary vascular resistance (dynes sec Cm- 5m- 2) 237±54 300 ± 59* 280 ± I09 260+97 Exercise index II86 +I095 1220 +66I LV work (kg m min -m'2) 7 4 ±+'9 6-2+I-2 14'0 ±3-0 I'33 3±3 LV stroke work (g m m- 2) 94+22 75 +12 I39 ±37 125 ±20 LV stroke power (g m sec IM - 2) 327±67 268 ±47 519 ±I97 46I ±II3 Mean systolic ejection rate (ml sec) I84±24 I65±26 259 ±98 232+55 Pre-ejection period of cardiac contraction (msec) I44 + 22 I25 ±i8* III ± 15 98 +10 Systolic ejection time index (msec) 4I4 ±23 4I6 ±25 444±47 450±44 Stroke tension time index for LV (mmHg sec) 37 + 6 36 +±5 42 ± 4 41 +4 RV work (kg m min'-m 2) I-5±o-6 I-4±o-6 4-7 'I 3 4-3 ± I4 RV stroke work (gm m-2) I9±5 I7±5 45 ±8 40±6 RV stroke power (g m sec-m- 2) 59±I8 56±I8 I49±29 I28 +26 Stroke tension time index for RV (mmHg sec) 1I-5 ±2-1 Io-8 ±2-0 I9-6±4-8 I9-0 ±4-8 All values are given as a mean ± I standard deviation. Values during exercise were obtained in 5 patients of Group 2 and in 7 patients of Group 3. Statistical significance of the differences between control period and the measurements after deslanoside: * P < 005; t P < O-OI; * P<o-ooi. Symbols used in the Tables: VE = global ventilation; VA = alveolar ventilation; Vo2= oxygen consumption. PaO2 = arterial oxygen tension; S0o2= arterial oxygen saturation; PacO2= arterial carbon dioxide tension; [H+]a= arterial hydrogen ions. Exercise index = difference between cardiac output at rest and during exercise divided by the difference of oxygen consumption.
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