[Sexuality and cardiopathies]. / Sexualité et cardiopathies.

Every year, nearly 2.5 million Canadians are struck down by a heart attack. For many, the road to recovery is paved with great anxiety. This can take a number of forms, affecting career plans, physical activities, marital harmony and, worst of all, the couple's sex life. The author attempts to show how counselling by a qualified sexologist can make the difference by restoring the patient's sexuality. The article is part of a study conducted among more than 25 nurses at the Montreal Institute of Cardiology. A mini-review of the literature is presented, as well as the methodology used. The study revealed a clear need for more and better information on sexual relations following a heart attack.

A simple and disposable sweat collector.

Apart from in cystic fibrosis, where sweat analysis provides valuable diagnostic information, sweat yields remain an overlooked biological fluid. Technical problems (dilution, condensation, contamination, evaporation, etc.) linked to currently available collection procedures are of concern and thwart their use. To overcome some of these technical difficulties, an original sweat-collection technique is described. A collection capsule is created inside a flexible, adhesive and disposable anchoring membrane pasted onto the skin. A fluid-tight window is positioned in the upper part of the pocket and gives access to its content. Through the collection window, complete emptying of the sweat collector can be achieved repeatedly by suction using a vacutainer tube inserted in a tube holder equipped with a long dull needle. With prior addition of a suitable marker, fractional samplings can also be performed using a precision micropipette. This collecting method allows for kinetic studies on sweat rate and sweat content. The limited bias-inducing manipulations linked to the described technique, coupled with the ease of performing kinetic studies on sweat volume and content, make this original tool a reliable and accurate sweat-collection technique.

Effects of hypoxemia with and without acidemia on the isometric contraction time and the electromechanical delay of the fetal myocardium: an experimental study on the ovine fetus.

This study assessed the response of the preejection period during hypoxemia with and without acidemia. In five pregnant ewes, hypoxemia was created during 1 hour followed by fetal infusion of lactic acid during 2 hours. A micromanometer catheter positioned above the fetal aortic valve, an endocavitary phonocardiogram, and a fetal electrocardiogram allowed measurements of the two components of the preejection period--the isometric contraction time and the electromechanical delay. At the onset of hypoxemia, because of changes in isometric contraction time, the preejection period began to shorten. When acidemia was induced, the preejection period modified slowly in the opposite direction and lengthened, initially because of a prolongation of electromechanical delay and later because of an increase in the already shortened isometric contraction time. This process developed slowly and at the end of 2 hours of acidemia, preejection period were back to preexperimental values. It can be concluded that systolic time intervals can be normal and misleading when acidosis complicates hypoxemia.

Insulin and the resting potential of hypoxic substrate-deprived myocardium.

Insulin stimulates ionic transport by the sodium pump and induces hyperpolarization in skeletal and cardiac muscle among other cells. The insulin-induced hyperpolarization in most cases can be inhibited by exposure to cardiac glycosides or metabolic inhibition. However, extracellular accumulation of K ions leaking from hypoxic cells in superfused preparations may distort the effects of insulin on the resting potential. We used standard microelectrode techniques and perfused rabbit hearts submitted to hypoxia and substrate deprivation to reinvestigate the effects of insulin (6.4 nM) on the membrane potential. The membrane depolarized by about 6 mV and the action potential was reduced to a sharp spike without overshoot. Insulin restored the resting potential to control values but did not change the action potential configuration substantially. The insulin-induced repolarization was not due to reuptake of potassium as revealed by spectrophotometric determinations of myocardial K content. In addition, the diffusion component of the resting potential measured after inhibition of the sodium pump with 10(-4) M ouabain was not modified by insulin. Our results suggest that an increase in the contribution of electrogenic Na extrusion to the resting potential underlies the repolarizing effect of insulin of hypoxic substrate-deprived myocardium.

Cardiovascular status during ketamine anesthesia in the fetal lamb.

To determine the effects of maternal ketamine anesthesia on fetal hemodynamic and cardiac function, a study was carried out on 8 chronically catheterized fetal lambs. Ketamine was administered intravenously to the mother every 15 min during 1 h. The fetal PO2 and pH remained within physiological limits whereas the PCO2 decreased from 44.35 +/- 1.36 to 37.32 +/- 4.75 Torr (p less than 0.05). The following changes of the fetal heart systolic time intervals were observed: a progressive lengthening of the preejection period (PEP) (from 52 +/- 10 to 63 +/- 11 ms, p less than 0.01), a shortening of the ejection time (ET) and a significant increase of the PEP/ET ratio (from 0.32 +/- 0.04 to 0.47 +/- 0.01, p less than 0.01). The two components of PEP, electromechanical delay and the isovolumetric contraction time were both prolonged. A progressive rise of fetal systolic and diastolic pressures was also noted (p less than 0.01). Fetal heart rate increased (145 +/- 33 to 190 +/- 28 beats/min, p less than 0.01) and cardiac beat-to-beat variability decreased (from 0.028 to 0.009, p less than 0.01) during the ketamine anesthesia. This study demonstrates that maternal anesthesia with ketamine can alter indices of fetal myocardial function and other cardiac parameters used in fetal and neonatal monitoring, without affecting tissular oxygenation.

Myocardial function and hemoglobin oxygen affinity during hyperglycemia in the fetal lamb.

To determine the effects of maternal hyperglycemia on fetal hemodynamic and cardiac function, a study was carried out on nine chronically catheterized fetal sheep. In six fetuses, glucose was infused intravenously with an initial dose of 5 mg/kg per min. Data were compared with controls. This dose was gradually increased to 16 mg/kg per min by the fifth day. The initial blood glucose was 14.7 +/- 3.0 mg/dl and increased to 54.6 +/- 16.4 mg/dl by the last day of the infusion period (P less than 0.001). The PO2 decreased from a baseline of 20.25 +/- 3.40 to 15.88 +/- 5.24 mmHg (P less than 0.01). Similarly significant decreases were also observed for the blood O2 content and O2 hemoglobin saturation: 8.5 +/- 1.7 to 6.4 +/- 2.2 ml/dl and 62.3 +/- 13.6 to 46.1 +/- 17.6%, respectively, during hyperglycemia (P less than 0.01). The duration of the preejection period (PEP) before the start of the experiment was 45 +/- 4 ms; a final value of 57 +/- 10 ms was obtained (P less than 0.01). However, the electromechanical delay and ejection time (ET) showed no significant variation. The ratio of the PEP/ET increased from 0.31 +/- 0.04 to 0.38 +/- 0.07 (P less than 0.01) during hyperglycemia. The reticulocytes increased from 1.4 +/- 1.8 to 3.1 +/- 2.9% (P less than 0.05) and the 2,3-diphosphoglycerate decreased from 4.4 +/- 1.1 to 2.8 +/- 1.2 mumol/g hemoglobin (P less than 0.005). This study demonstrated that fetal hyperglycemia depresses myocardial function in the fetal lamb. The changes in cardiac function could not be explained by the small drop in O2 saturation.

Effects of maternal alcohol intoxication on fetal circulation and myocardial function: an experimental study in the ovine fetus.

To determine whether acute alcohol ingestion during pregnancy could affect fetal myocardial function, studies were carried in six chronically catheterized fetal sheep during maternal alcohol infusion. Absolute ethyl alcohol (0.8 ml/kg) was administered to the mother over 10 minutes via the jugular vein. These infusions were repeated every 30 minutes during 3 hours, and peak maternal and fetal blood concentrations close to 200 mg/dl alcohol were reached. Fetal PCO2 decreased from a baseline of 43.15 +/- 3.75 to 36.13 +/- 2.6 torr 1 hour after the start of alcohol infusion (P less than 0.05). Similarly, pH rose from 7.37 +/- 0.027 to 7.44 +/- 0.015 (P less than 0.05). Both values returned to baseline level at the end of alcohol infusion. PO2 remained within physiologic limits. The systolic time intervals of the fetal heart showed a rapid and prolonged modification. The pre-ejection period from 58 +/- 8 to 66 +/- 4 msec (P less than 0.05) during the infusion; this change was related to an increase in the isometric contraction period. The ratio of the pre-ejection period over the ejection time was also significantly increased (P less than 0.01), and remained elevated until the end of the experiment (12 hours). A rise in fetal systolic and diastolic pressures was observed at about 2 hours after the start of the alcohol infusion, and lasted 4 hours. This study suggests that an episode of maternal alcohol intoxication causes rapid depression of fetal myocardial contractility that is maintained several hours after cessation of alcohol ingestion.

Physiologic modulations of the systolic time intervals in the fetal lamb.

To examine the modulation of fetal systolic time intervals of the ovine fetus in relation to fetal maturation, heart rate, respiratory activity, and circadian rhythm, studies were carried out on 13 fetal-maternal sheep preparations. The data obtained showed that there was a significant correlation between the ejection time (ET) and the RR intervals of the electrocardiogram. The pre-ejection period (PEP) and PEP/ET increased in relation to the fetal maturation (38 ms and 0.25 at 120 days to 52 ms and 0.33 at 145 days of gestation, respectively). When the circadian rhythmicity was analyzed, a relative tachycardia was in evidence during the 21- to 03-h period but systolic time intervals remained unchanged. Except for some tachycardia and cardiac rhythm variability, respiratory activity also had no influence on the systolic time intervals.