When arrhythmias complicate heart failures

Transcription

1 When arrhythmias complicate heart failures Throughout the years, heart failure complicates usually with anomalies of the cardiac rhythm. These anomalies can have an atrial, a ventricular or an atrioventricular origin. A very high percentage of patients suffering heart failures, present various types of rhythm anomalies. Atrial arrhythmias are almost exclusively atrial fibrillations, and in a much minor scale, atrial flutter. About a third of heart failure patients are in atrial fibrillation. The appearance of this arrhythmia decreases the ventricular contractility with secondary decline in the exercise tolerance. If the atrial fibrillation has a very high ventricular rate, the ventricular diastolic time diminishes as well as the left ventricular filing, resulting in a decreased cardiac output (the amount of blood which the left ventricle pumps in a minute). This can only worsen the heart failure patient s condition which already presents a below average cardiac output (Figure 2).

2 Figure 1 Multiple mechanisms by which atrial fibrillation affects symptoms, cardiac output and the general outcome of the patients with heart failure. HF, heart failure; DF, diastolic filling; CO, cardiac output; PE, pump efficiency; ER, embolic risk; AF, atrial fibrillation; HR, heart rate.

3 More than this a fibrillating atrium loses contraction (or atrial kick from the American authors) and this results in a 20%-30% decrease in the efficiency of the heart as a pump. This results in a second factor which deteriorates the heart s pumping function. The most vulnerable hearts to atrial kick loss are the hypertrophic and/or the very dilated ones. This loss of cardiac efficiency only increases the patient s symptoms: the shortness of breath increases, just like the fatigue, the sleepiness, the mental confusion and the disordered breathing patterns during sleep can be accentuated. For the same exact reason, the retention of liquids increases, as the body weight and the lower legs edema appears. The most frequent cause of death in patients with heart failure and atrial fibrillation in the embolic stroke. In the atrial fibrillation, the loss of atrial contraction determines a sort of stagnation of the blood into the atria. This phenomenon, together with the often associated atrial enlargement, determine favourable conditions to the formations of blood clots (thrombus), inside the atrium itself. The risk associated with this event, is that a clot may detach from the inside of the atrium, and following the blood stream, exit the heart and obstruct an artery. This phenomenon is called thromboembolism (see Figure 2) and if this phenomenon involves a cerebral artery an embolic stroke is induced.

4 Figure 2 Anatomy of the heart, ascending aorta e carotid arteries. CE, cerebral embolism; LA, left atrium; LV, left ventricle; PE, peripheral embolism. Keeping in mind that the first arteries that are in the same direction as the blood that leaves the heart are the carotid arteries, we can understand why embolisms are mainly cerebral. The heart failure patient, even if with a normal cardiac rhythm, still presents an elevated embolic risk, and the appearance of atrial fibrillation, for the reasons mentioned above, can not but increase this risk. Due to all the above dangers, atrial fibrillation appearances worsen the outcomes of the patients in heart failure. The atrial fibrillation s incidence increases dramatically with the gravity of the heart failure (the NYHA class): the more the patient finds himself/herself in a higher NYHA class,

5 the more the arrhythmia s prevalence increases. The atrial fibrillation often represents a worsening cause for the heart failure, and this worsening, by itself, generates atrial fibrillation. A vicious cycle is created between heart failure and atrial fibrillation (Figure 3). Figure 3 Vicious cycle between atrial fibrillation and heart failure. HF, heart failure; AF, atrial fibrillation. On the other hand we can still provide two positive news. The first one would be that when possible, curing atrial fibrillation and restoring sinus rhythm, while improve the clinical picture of the failing heart. The second is that the restoration of the normal rhythm also improves the outcome of heart failure patients. For these and many more other reasons we always need to do all that is possible in order to defeat atrial fibrillation. Ventricular arrhythmias are represented by ventricular ectopic beats, accelerated idioventricular rhythm, non-sustained ventricular rhythm, sustained ventricular tachycardia and the feared ventricular fibrillation. These arrhythmias are identified during 24hr ECG recordings or during continuous monitoring (telemetry monitoring systems) for hospitalized patients (Figure 4). Figure 4 Telemetry monitoring of a patient who develops during the hospitalization a short run of non-sustained ventricular tachycardia. Arrhythmias can be asymptomatic or may present themselves with palpitations, light-headedness, dizziness, near-syncope, syncope or with even more severe symptoms (refer to When symptoms don t correspond to the disease but at times they do). The

6 prevalence of these ventricular rhythm disturbances in heart failure patients is high, but inferior to the atrial fibrillation one. In most cases, arrhythmias (both atrial and ventricular) occur due to the same underlying heart disease, but in other circumstances they can be only adverse effects of drugs we use to treat this syndrome. I am referring to positive inotropic drugs like catecholamines or phopshodiesterase inhibitors mainly used during acute heart failure therapy, or dgitalis and diuretic used in chronic therapies as well. Needs to be mentioned that diuretics do not present direct arrhythmogenic effects, but through electrolytic disturbances (hypokalemia and/or hypomagnesemia) which can incur. On the other hand, we also have drugs which can decrease arrhythmias incidence in cardiac failure: aside from the proper anti-arrhythmic drugs, we have the betablockers, the statins, ACE inhibitors and aldosterone antagonists. Every day, in our electrophysiology lab, for patients with cardiac failure and rhythm disturbances we apply particularly sophisticated techniques in order to eliminate the negative effect of arrhythmias on the failing heart s ventricular function, and to facilitate the ventricles to work more harmoniously with each other. Vladimir Guluta, MD