Andrea Rimondini

Hemofiltration as short-term treatment for refractory congestive heart failure

Hemofiltration has been suggested as a new therapeutic tool in refractory heart failure. In this study, 11 patients with primary or ischemic heart disease in New York Heart Association class IV, in whom there was no response to medical treatment, were subjected to hemofiltration. The pathophysiologic adjustments promoted by subtraction of plasma water were investigated, and guidelines for an appropriate use of this procedure in heart failure are provided. Fluid was removed from plasma at a rate of 500 ml/hour until either normalization of the right atrial pressure (which was increased in all cases) was achieved or the hematocrit exceeded 50 percent. According to these criteria, the duration of treatment ranged from four to six hours and the total amount of fluid removed was 2,000 to 3,000 ml. In each case, hemofiltration promoted relief of dyspnea and of clinical and radiographic evidence of lung congestion and pleural effusion, and substantially reduced the dependent edema and abdominal girth. These effects were paralleled by progressive decrease of the right (-70 percent) and left (-45 percent) ventricular filling pressures and of the pulmonary arterial pressure and arteriolar resistance, without significant variations in heart rate, aortic pressure, cardiac index, and systemic vascular resistance. Changes in the right atrial and wedge pulmonary pressures are interpreted as reflecting a combined effect of a decrease in pressure on the outside of the heart due to fluid reabsorption (from lung interstitial spaces and pericardial, pleural and abdominal cavities) and of intravascular volume subtraction. The arterial partial pressure of oxygen was raised, the partial pressure of carbon dioxide and pH were unchanged, and urinary output was substantially enhanced by the procedure. The study indicates that: hemofiltration may be a short-term treatment for refractory cardiac insufficiency with overhydration; a filtration rate of 500 ml/hour is effective and safe; and the central venous pressure may be a reliable guide to volume subtraction.

Changes in circulating norepinephrine with hemofiltration in advanced congestive heart failure

In congestive heart failure (CHF), hemofiltration is associated with an obvious decrease in circulating norepinephrine. This method was used for investigating the mechanisms whereby plasma norepinephrine is increased in chronic CHF. In 23 cases of advanced CHF, hemofiltration (2,983 +/- 1,228 ml) lowered plasma norepinephrine by 515 +/- 444 pg/ml. This effect was prompt, persisted or became greater in the next 24 hours. It was not associated with significant changes in cardiac output, aortic pressure or systemic vascular resistance. It did not appear to depend on variations in parameters related to the sympathetic activity, such as plasma renin, right atrial, wedge pulmonary artery and renal perfusion pressures, and was independent of duration and amount of hemofiltration. These observations did not support the concept that the norepinephrine decrease was the main consequence of a neural sympathetic inhibition. Hemofiltration increased diuresis by 606 +/- 415 ml; changes were prompt and correlated inversely (r = -0.7; p less than 0.01) with those in plasma norepinephrine. The same unknown mechanism of the increased urinary output might potentiate the norepinephrine removal from the blood by the kidney, or hemofiltration and the augmented diuresis might result in a regression of congestion of lungs and kidneys, leading to an improved extraction of norepinephrine. In CHF, a relation may exist between fluid retention and norepinephrine and in advanced stages, circulating norepinephrine, although strikingly increased, is devoid of important cardiovascular effects. At these stages, plasma norepinephrine is probably unreliable as an index of the sympathetic neural activity.

Isolated ultrafiltration in cardiogenic pulmonary edema

Twenty patients (ten with mitral and/or aortic valve disease and ten with ischemic heart disease, all in the New York Heart Association class IV, aged between 18 and 74 yr, with cardiogenic pulmonary edema unresponsive to drug treatment) were treated with polysulphone membrane ultrafiltration (UF) in a veno-venous circuit. All patients had dyspnea, pulmonary rales, hypoxemia, tachycardia, hypotension, overhydration, radiologic evidence of engorged pulmonary vasculature, and Kerley-B lines.Systemic and pulmonary arterial pressures, cardiac output (by thermodilution), and intrapulmonary shunt fraction (Qsp/Qt) were determined and chest x-ray was obtained at the beginning and the end of UF. Average duration of the treatment was 150 ± 28 min; UF volume averaged 3000 ± 170 ml. UF reduced the Qsp/Qt by 58% from control condition, and did not significantly affect hemodynamic variables. Chest x-rays documented clearing of alveolar edema and venous congestion. These changes were associated with unequivocal clinical improvement and no mechanical ventilation was necessary to improve gas exchange. Short-term fluid subtraction did not result in undesired circulatory alterations. Because the ultrafiltrate composition is similar to plasmatic fluid, no modification in the plasma osmolarity was detected.In conclusion, UF may be considered an effective tool for the treatment of acute pulmonary edema refractory to drug therapy, as an alternative to mechanical ventilation, and as a remedy for excessive extravascular lung water.

Facilitating influence of disopyramide on atrial flutter termination by overdrive pacing

Long-lasting (mean 30 days) type I atrial flutter was treated with overdrive pacing in 30 patients (mean age 69 years) with organic heart disease. To evaluate the effect of pretreatment with disopyramide, the study population was divided in 3 groups of 10 patients each: group A, no disopyramide therapy; group B, intravenous disopyramide (maximum dose 250 mg in 1 hour); and group C, oral disopyramide (400 mg daily for 4 days). There were no differences in baseline cycle length of atrial flutter among the 3 groups before drugs were given. The stimulation protocol included overdrive atrial pacing up to the shortest paced cycle of 150 ms performed at a maximum of 3 atrial sites. Reversion to sinus rhythm occurred in 2 patients in group A, 7 in group B (p less than 0.01) and 5 in group C. Pacing was performed from a mean number of 2.1 sites/patient in group A, 1.2 in group B and 2.0 in group C. Atrial fibrillation occurred in 7, 3 and 4 patients, respectively. Acceleration to a faster form of atrial flutter occurred in 3, 3 and 4 patients, respectively, and reversion to sinus rhythm occurred in all patients who had intravenous disopyramide and in 1 who took the drug orally. The administration of disopyramide before overdrive pacing improved the rate of conversion to sinus rhythm and allowed an easier stimulation protocol with a lower incidence of pacing-induced atrial fibrillation. Disopyramide is beneficial when overdrive atrial pacing is performed for the treatment of long-standing atrial flutter in patients with organic heart disease.

Type II atrial flutter interruption with transesophageal pacing: use of propafenone and possible change of the substrate.

Type II atrial flutter (AFII) is an arrhythmia which usually cannot be interrupted by atrial pacing: the underlying mechanism is considered to be a leading circle without an excitable gap. We investigated whether the administration of propafenone, an antiarrhythmic drug, which primarily decreases conduction velocity, has a beneficial effect on AFII interruption using transesophageal pacing. Twelve patients with an AFII were randomized into 2 groups in which pacing was performed without treatment (group A) or two hours after the administration of 600 mg of oral propafenone (group B). Sinus rhythm was attained in 0 of 6 patients in group A and in 4 of 6 patients in group B (P < 0.05). The baseline mean cycle length was the same in both groups (175 ± 7 (A) vs 168 ± 8 ms (B); it lengthened significantly after the administration of propafenone (219 ± 33 vs 168 ± 8 ms; P < 0.05). Propafenone did not significantly lengthen the cycle in the two patients in whom interruption of the arrhythmia was impossible. Our data show that propafenone has a facilitating effect on atrial pacing only when it significantly prolongs the cycle length of the arrhythmia, possible expression of a conversion of AFII into type I, with an anatomical substrate and an excitable gap allowing arrhythmia capture and interruption. In the two patients in whom sinus rhythm was not restored, the absence of a direct dependence of the cycle length on the change in conduction velocity induced by propafenone may be explained by the persistence of a functionally determined circuit, resistant to atrial pacing.

Increased cardiac electrical instability concomitant with pacing induced repolarisation abnormalities.

The relation between the occurrence of repolarisation abnormalities after right ventricular pacing and spontaneous arrhythmias was investigated in 16 patients in whom the sick sinus syndrome was suspected. All patients had normal QRS complexes and T waves in the electrocardiogram before pacing and required atrial stimulation and His bundle recording for diagnostic purposes. Patients were randomised into a study group or a control group. In the eight patients in the study group right ventricular pacing was performed for 12 hours, and was followed by inversion of the T wave in surface leads II, III, aVF, and V2-V5 and lengthening of the QTc interval. The frequency and complexity of ventricular arrhythmias increased after pacing in six patients who had ventricular extrasystoles in the baseline Holter recording. As the configuration of the T wave became normal the frequency of ventricular extrasystoles returned to baseline values. In the control group of eight patients ventricular pacing was not performed after the electrophysiological study and no changes were seen in T wave configuration and in the frequency of spontaneous arrhythmias. These results suggest that the post-pacing repolarisation abnormalities reflect abnormal electrical properties of the ventricle and that in some cases they lead to increased electrical instability.