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PubMed1997

[Acute and chronic heart failure].

Cardiac failure is a syndrome which comprises ventricular dysfunction (confirmed by echocardiography) and compensating mechanisms (immediate activation of the sympathetic nerve and functioning of Starling's mechanism, within hours or days activation of RAAS within days or weeks hypertrophy of the heart). Cardiac failure develops rapidly either in a previously healthy subject (first extensive IM, diffuse myocarditis, acute aortic or mitral regurgitation) or in a damaged heart (IHD, KMP, defect) as a result of sudden excessive burdening (ischaemia, arrythmia, infection, surgery etc.) or spontaneously (end-stage). It is manifested above all by "backward" failure (pulmonary oedema). The pulmonary pressure must be rapidly reduced: i.v. nitrovasodilators act immediately, i.v. furosemide acts within 10-15 min. (in can, however, reduce the circulating volume which has not increased during the first failure). Also O2, anodynes. In the subacute stage (without any precise time limits) which may develop in serious cases from acute failure, or develop as a result of deterioration of chronic failure, in addition to congestion, symptoms caused by "forward" failure are in the foreground. These are symptoms caused by a reduced minute output and hyperfusion of tissue. It is indicated to administer substances which improve work tolerance, i.e. positive inotropics (digitalis, beta-agonist or phosphodiesterase inhibitors). If the blood pressure drops, a combination of dopamine and dobutamine should be administered; if the respiratory volume drops, artificial pulmonary ventilation, in case of persisting oedema continuous arteriovenous haemofiltration, in severe failure intraaorrtic balloon contrapulsation etc. In an irreversible state urgent or elective orthoptic transplantation of the heart should be considered. In chronic heart failure an important component of comprehensive treatment is in addition to treatment of congestion and hypoperfusion, prevention of "cardiovascular remodelling" by means of angiotensin convertase inhibitors etc. Which improve the quality of life and survival. Arrhythmias are an independent prognostic factor.

Acute Disease↗
PubMed1997

Shy Drager syndrome.

Shy Drager Syndrome (SDS) is a movement disorder which is often referred to as a parkinson plus syndrome or Multiple System Atrophy (MSA). For patients afflicted with this condition, rigidity and bradykinesia are the primary extrapyramidal symptoms which are present. The "plus" refers to autonomic nervous system dysfunction which leads to much of the disability seen in this disorder. Syncope, urinary incontinence, impotence, constipation, fecal incontinence, cardiac arrythmias as well as other symptoms occur as a result of widespread pathological changes in multiple areas of the central and autonomic nervous system. The goal of this paper is to provide an overview of the pathophysiology, signs and symptoms of and treatment for SDS. Nursing Care of the patient and family coping with Shy Drager Syndrome and the challenges it presents to the Movement Disorder Nurse are discussed. A coordinate, multidisciplinary team approach is suggested.

Adult↗
PubMed1997

[Subtotal pericardectomy with the use of extracorporeal circulation].

The results of surgical treatment of 91 patients with constrictive pericarditis are analysed. There were 2 groups of patients: In 71 patients (1st group) the "closed" pericardectomy was used, 20 patients (2d group) were operated with the use of extracorporeal circulation. Both groups were comparable in terms of their preoperative status. The rate of hospital mortality was 7.6% (7 patients). In the 1st group the rate of mortality was 8.4%, while in the 2d group no patients died. The trauma of myocardium and coronary arteries, as well as acute arrythmias were the main factors of mortality. To achieve a positive result the ventricles should be completely released of the constricting capsule. The use of extracorporeal circulation provides favorable conditions for such a release and decreases the rate of mortality.

Adolescent↗
PubMed1998

Tachycardia: an important determinant of coronary risk in hypertension.

Heart rate and blood pressure are highly correlated and in large population studies, individuals with high blood pressure tend to have high heart rates. Fast heart rate precedes the development of high blood pressure and serves as an early indicator of coronary heart disease. Not only does the heart rate predict coronary mortality, but also the non-cardiovascular mortality and is, therefore, an overall predictor of longevity. In the Tecumseh Blood Pressure study, we have seen that 37% of all patients with borderline hypertension have the 'hyperkinetic hypertension state', which consists of elevated cardiac output, high heart rate, high sympathetic tone, and decreased parasympathetic tone. In this population, evidence of high heart rate exists in these individuals as children, and persists through early adulthood. This suggests that tachycardia is a reliable marker of high sympathetic tone. High sympathetic tone might be the mechanism whereby heart rate is associated with high insulin, insulin resistance, dyslipidemia, high hematocrit and excess weight. These mechanisms are discussed in details in this review. Tachycardia is a strong risk factor for sudden death and arrythmia. Heart rate, as one of the prime determinants of cardiac work, may contribute to greater cardiac strain. Animal studies have shown that a higher heart rate may be associated with a greater development of atherosclerotic plaque in coronary vasculature. Therefore, heart rate elevation is not merely a sign of underlying pathology, but it may also cause further damage that leads to increased mortality. In the treatment of hypertension, reducing heart rate by pharmacologic and non-pharmacologic measures may have a greater effect on coronary mortality than blood pressure reduction alone.

Autonomic Nervous System↗
PubMed1996

[Mitral valve replacement under beating heart in 137 cases].

To avoid damage of myocardial ischemia, myocardial hypoxia and reperfusion injury, we designed mitral valve replacement in beating heart under extracorporeal circulation with low dose temperature of 31 degrees C to 35 degrees C in 137 cases of rheumatic heart disease, congenital heart disease mitral stenosis and mitral insufficiency, or concurrent aortic insufficiency. The patients were rept in unblocking aorta, unfilling cardiac arrest perfusion, idle pulse and dradycardia of 40-50 times/min, nose temperature of 32 +/- 1 degrees C. Patients with concurrent aortic insufficiency should first undergo replacement of aorta under cold cardiac arrest and then replacement mitral valve under beating heart to reduce the time of cold heart ischemia. Plastic surgery for tricuspid valve was done under beating heart. Good postoperative prognosis was nated: an average arterial pressure of 9.5-10.5 kPa (70 to 80 mmHg), dose of dopamine was obviously reduced. No low cardiac output syndrome, acute renal failure and severe arrythmia were observed in 137 cases, except 4 deaths due to infection and blood coagulation (2.9%). A left cardiac chamber no-level air removal device and aorta perfusioner leading flow device were designed for exsufflation of left pneumatocardia.

Adolescent↗
PubMed1998

[Long QT syndrome: from clinical discovery to molecular etiopathogenesis].

Before the era of Molecular Biology the etiopathogenic mechanism of the long QT Syndrome (LQTS) was hypothetized to be an inhomogeneity in the innervation of the myocardium by the sympathetic system resulting in abnormal myocardial repolarisation, prolongation of the QT interval and various rhythm disorders. The progress of Molecular Biology has led to abandon this hypothesis; it is now agreed that the etiopathology of the various forms of the LQTS and of the arrythmias which are associated with it lies in the presence of mutations localized on genes coding either for cardio-specific ionic channels or for proteins which modulate the activity of these ionic channels. Thus, the alterations, direct or indirect, of these cardio-specific ionic channels lead to a delayed repolarization of myocardial cells which manifest itself on the electrocardiogram by a prolongation of the QT interval. This delayed repolarization of myocardial cells would induce a reactivation of myocardial ionic channels of the L-Ca++ type which leads to the development of secondary late depolarization which represent the underlying cellular mechanisms for "torsade de pointes". This hypothesis is experimentally reinforced by the observation both in animals and in men of a prolongation of the QT interval as well as aspecific tachyarrythmias after pharmacologic blockade of myocardial potassium channels. Therefore the long QT syndromes probably find their origin in genetic abnormalities of the electro-ionic system of the heart whereas the mechanical function and the autonomic innervation appear to be entirely normal.

Animals↗
PubMed1998

[Sotalol--atrial fibrillation, reduced renal function and sudden death].

Sotalol is a betablocker with additional antiarrythmic properties. Its pharmacokinetic properties may lead to increased serum levels of the drug in patients with reduced kidney function. We report on a case in which kidney failure in a patient using sotalol for paroxysmal atrial fibrillation gave rise to torsade de pointes ventricular tachycardia and, eventually, sudden death. Gradual prolongation of the QT interval suggested an overdose of sotalol. Sotalol has been commonly used in cases of angina pectoris and hypertension. The recently published SWORD study has, however, changed the indications for its use, and sotalol should now only be used in cases of severe supraventricular and ventricular arrythmias.

Acute Kidney Injury↗