Heart sudden failure

Syncope is the abrupt and transient loss of consciousness due to a temporary reduction in cerebral blood flow. It is associated with an absence of postural tone and followed by a rapid and usually complete recovery. Syncope may be both benign or the only warning before an episode causing sudden death (1). Recurrent episodes of syncope may result from a variety of disorders, all of which cause a temporary reductiou iu cerebral blood flow sufficient to disturb the normal functions of the brain. Neurocardiogenic (vasovagal) syncope is the most common of a group of reflex (neurally mediated) syncopes, characterized by a sudden failure of the autonomic nervous system (ANS) to maintain blood pressure, and occasionally heart rate, at a level sufficient to maintain cerebral perfusion and consciousness (2-4). Syncope accounts for 3.5% of all emergency room visits and 1-6% of all hospital admissions annually in the USA (5). 

In broilers of modern fast growing, meat production genotypes, most deaths are due to sudden heart failure and parasite infections (see also Chapter 12). Also such genotypes suffer from leg disorders (perosis, tibial dyschondroplasia, etc.) and muscle diseases to such an extent that they have difficulty in walking normally. They are thought to suffer severe pain and consequently spend much longer lying down. This in turn may lead to serious breast blisters. 

The long-term goals after MI are to (1) control modifiable coronary heart disease (CHD) risk factors (2) prevent development of systolic heart failure (3) prevent recurrent MI and stroke and (4) prevent death, including sudden cardiac death. 

VF is electrical anarchy of the ventricle resulting in no cardiac output and cardiovascular collapse. Sudden cardiac death occurs most commonly in patients with ischemic heart disease and primary myocardial disease associated with LV dysfunction. VF associated with acute MI may be classified as either (1) primary (an uncomplicated MI not associated with heart failure [HF]) or (2) secondary or complicated (an MI complicated by HF). 

Adverse events include ulceration of nasal mucosa and nasal septal collapse, tachycardia, heart failure, hyperthermia, shock, seizures, psychosis (similar to paranoid schizophrenia), and sudden death. 

Adrenalin is rapidly destroyed by the enzyme amino-oxadize and is therefore ineffective orally. It may be injected, snorted or possibly dissolved under the tongue. It is of considerable value to restore heart beat after sudden heart failure. This is due to its powerful stimulating effect. 

At present, we suspect that toxin-LR causes heart failure in mice, perhaps due to suddenly increased resistance to pulmonary blood flow. Heart failure in mammals is known to cause engorgement of the liver with blood. Pulmonary vascular occlusion may also cause secondary hypoxemia and shock. However, biochemical pathways that are initiated by toxin-LR and that lead to the onset of discernable signs of illness after 30 min are unidentified. The 30 min asymptomatic period following toxin injection may be associated with a toxin-initiated cascade of biochemical events which lead to overt signs of illness. 

SCD-HeFT = Sudden Cardiac Death in Heart Failure Trial. 

The results of MADIT II were met with some skepticism, but later confirmed by the recent Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) [24]. This study evaluated the benefit of ICD therapy versus amiodarone or placebo as primary prevention in over 2,500 patients with stable NYHA class II or III heart failure and EF < 35%, without the requirement for NSVT or EPS. Patients with both ischemic and nonischemic etiologies for cardiomyopathy were included. Over a follow-up of 4 years, there was no benefit of amiodarone over placebo for overall mortality, but ICD therapy resulted in a significant 23% reduction in overall mortality [p = 0.007] (Fig. 3.5). The benefit of ICD therapy was comparable for ischemic and nonischemic cardiomyopathy. 

Solomon SD, Zelenkofske S, McMurray JJ, et al. Sudden death in patients with myocardial infarction and left ventricular dysfunction, heart failure, or both. NEnglJMed. Jun 23 2005 352(25) 2581-2588. 

The symptom of syncope in a patient with ischemic heart disease and heart failure should initially prompt concern about ventricular dysrhythmias. Based on the results of recent clinical trials of sudden death prevention in heart failure [27, 28], most patients with low ejection fraction and advanced ischemic heart disease will likely be treated with an... 

Baldasseroni S, Opasich C, Gorini M, et al. Left bundle-branch block is associated with increased 1-year sudden and total mortality rate in 5517 outpatients with congestive heart failure a report from the Italian network on congestive heart failure. Am. Heart J. 2002 143 398-405. 

There is an increased risk of death in older patients with dementia. Although the causes of death were varied, most of the deaths appeared to be either cardiovascular (e.g., heart failure, sudden death) or infectious (e.g., pneumonia) in nature. This drug is not approved for treatment of patients with dementia-related psychosis. 

Propranolol 13- Adrenoceptor blockade Direct membrane effects (sodium channel block) and prolongation of action potential duration slows SA node automaticity and AV nodal conduction velocity Atrial arrhythmias and prevention of recurrent infarction and sudden death Oral, parenteral duration 4-6 h Toxicity Asthma, AV blockade, acute heart failure Interactions With other cardiac depressants and hypotensive drugs... 

Mitochondrial P oxidation of fatty acids is the principal source of energy for the heart. Consequently, inherited defects of fatty acid oxidation or of carnitine-assisted transport often appear as serious heart disease (inherited cardiomyopathy). These may involve heart failure, pulmonary edema, or sudden infant death. 

Marks, A. R. (2001). Ryanodine Receptors/Calcium Release Channels in Heart Failure and Sudden Cardiac Death. . / Mol Cell Cardiol 33(4) 615-24. 

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