Charles Reuse

Right ventricular dysfunction in septic shock: assessment by measurements of right ventricular ejection fraction using the thermodilution technique.

Right ventricular ejection fraction (RVEF) was measured by the thermodilution technique in a scries of 127 consecutive critically ill patients monitored with a modified pulmonary artery (PA) catheter equipped with a fast response thermistor. Thermodilution RVEF was significantly lower in septic shock (23.8 8.2%, 93 measurements) than in sepsis without shock (30.3 10.1%, 118 measurements) or in the absence of sepsis or cardiopulmonary impairment (32.5 7.1%, 62 measurements). Both myocardial depression and pulmonary hypertension could account for this impairment of RV function. RVEF decreased from 35.1 9.8 to 24.2 10.4% (P < 0.01) during development of septic shock and increased from 25.0 7.6 to 29.8 8.5%, (P < 0.05) during recovery (14 patients). Initial RVEF in septic shock was 27.8 8.6% in 11 patients who survived but only 20.9 6.7% (P < 0.02) in the 23 patients who eventually died. Thus, RV dysfunction is common during septic shock, is directly related to its severity, and can easily be recognized in patients monitored with a PA catheter.

Effects on right ventricular function of a change from dopamine to dobutamine in critically ill patients

In 15 critically ill patients requiring adrenergic support, right ventricular ejection fraction (RVEF) and right ventricular (RV) volumes were measured by the thermodilution technique receiving 5 micrograms/kg.min of dopamine and after replacement by the same dose of dobutamine. Shift from dopamine to dobutamine resulted in significant increases in stroke index from 28.1 +/- 3.6 to 31.0 +/- 3.8 ml/m2 (p less than .01) and significant decreases in pulmonary artery balloon-occluded pressure from 15.1 +/- 1.0 to 13.9 +/- 1.2 mm Hg (p less than .05) and right atrial pressure (RAP) from 14.0 +/- 1.3 to 12.2 +/- 1.1 mm Hg (p less than .05). RVEF increased slightly but significantly from 21.5 +/- 2.7% to 23.7 +/- 2.9% (p less than .01) so that RV end-diastolic volume (RVEDVI) was unchanged (140 +/- 12 vs. 141 +/- 12 ml, nonsignificant). RVEDVI/RAP ratio increased from 11.3 +/- 1.0 to 12.9 +/- 1.1 ml/mm Hg (p = .037). These results support the view that dobutamine has more favorable effects on RV function than dopamine in critically ill patients in the absence of profound hypotension and also indicates that higher filling pressures under dopamine administration can be related to changes in ventricular pressure/volume relationship.

Bretylium tosylate versus lidocaine in experimental cardiac arrest

Bretylium tosylate has been shown effective in the treatment of ventricular fibrillation and in the prevention of its recurrence. However, lidocaine is generally preferred because bretylium could have adverse hemodynamic effects related to its antiadrenergic action. To explore further the differences between these two antiarrhythmic agents, the authors compared the effects of bretylium, lidocaine, and saline on a standardized dog model of ventricular fibrillation followed by electromechanical dissociation (EMD). The protocol included three successive episodes of cardiac arrest in each animal. Three minutes before each episode of ventricular fibrillation, 5 mg/kg of bretylium tosylate (n = 11), 1 mg/kg of lidocaine (n = 9) or saline (n = 12) were administered blindly. There was no difference in the duration of cardiac arrest (bretylium, 8 min 18 sec; lidocaine, 7 min 54 sec; saline, 8 min 20 sec) or the total doses of epinephrine required to resuscitate the animals. Both bretylium and lidocaine appeared to preserve cardiac function 5 minutes after recovery, as stroke volume increased from 17.8 +/- 6.7 to 18.7 +/- 6.7 mL (NS) after bretylium and from 17.7 +/- 7.7 to 19.0 +/- 7.0 mL (NS) after lidocaine, but decreased from 19.0 +/- 5.3 to 14.6 +/- 6.0 mL (P less than .05) after saline. During the first 10 minutes of EMD, ventricular fibrillation or ventricular tachycardia recurred in 4 dogs treated with lidocaine, 3 dogs treated with saline, but no dog treated with bretylium (P less than .05 between bretylium and saline).(ABSTRACT TRUNCATED AT 250 WORDS)

Right ventricular function in septic shock

In critical states, right ventricular (RV) function is commonly altered by an increase in RV afterload or a depressed contractility. Severe sepsis can be associated with both. RV afterload can be increased by the pulmonary hypertension related to the release of various mediators and the development of microthrombi in the pulmonary circulation [1, 2]. Myocardial depression is also a relatively early event in the course of septic shock, even when cardiac output is normal or elevated [3, 4]. The release of circulating substances, various metabolic disorders, myocardial edema and decreased coronary perfusion have been incriminated [4]. Recent studies have well demonstrated that left ventricular ejection fraction could be depressed early during septic shock [3]. Right ventricular dysfunction might be more severe than left ventricular dysfunction, since the left ventricular afterload is typically reduced while RV afterload is usually increased (Fig. 1). Measurements of right ventricular ejection fraction (RVEF) have been recently available at the bedside by the thermodilution technique and could represent an additional parameter that can be routinely measured. RVEF values obtained by the thermodilution technique correlate well with those obtained by other techniques [58].

Thermodilution for measurement of cardiac output during artificial ventilation

polyuria (HP) characterized by a positive response to water deprivation. As we wrote in the discussion and conclusion of our paper, WE is first probably explained by a partial functional inhibition of the hypothalamo-neuro-hypophyseal axis and consequently by a partial deficit o f ADH release occurring after surgical manipulation of adenomas with suprasellar expansion. From this point of view, we agree with Martinez Chuecos et al., considering that all cases of HP we observed, could probably correspond to the same illness with different degrees of intensity. However, we found it difficult to accept that this pathophysiological mechanism is the one responsible for WE. Indeed, partial neurogenic diabetes insipidus is usually associated with increased serum osmolality and hypernatremia; ADH secretion is impaired at all levels of serum osmolality and urine concentration is possible only when the serum osmolality is greatly increased [1, 2]. In our patients who developed a WE pattern, hypotonlc polyuria was always of short duration (a few hours), and we never observed hypernatremia after water deprivation leading to urine concentration. On the other hand, when applying the logistic discriminant analysis, we found that prolactin secretion was a statistically significant predictive factor of WE, as compared with normal diuresis or diabetes insipidus. Therefore, the type of hormone secretion is demonstrated to play a role in producing WE, whatever the degree of expansion or the localization of the adenoma. Moreover, as mentioned in our paper, there are experimental arguments supporting a role for prolactin in the regulation of sodium and water balance. In conclusion, if a partial neurogenic diabetes insipidus is probably the first mechanism which has to be invoked to explain WE in our patients, we cannot exclude a possible influence of an endogenous fluid overload, on the basis o f biological and hormonal findings. These two mechanisms are not necessarily incompatible with regard to the pathogenesis of H E