Sudden death

There is a close correlation between myocardial infarctions and tachyarrhythmias, illustrated by the presence of complex ventricular arrhythmias among heart attack victims which are estimated to affect one-third of the survivors each year. Frequendy, the immediate cause of sudden death is ventricular fibrillation, an extreme arrhythmia that is difficult to detect or treat. In the majority of cases, victims have no prior indication of coronary heart disease. 

Cardiac arrhythmias are an important cause of morbidity and mortality approximately 400,000 people per year die from myocardial infarctions (MI) in the United States alone. Individuals with MI exhibit some form of dysrhythmia within 48 h. Post-mortem examinations of MI victims indicate that many die in spite of the fact that the mass of ventricular muscle deprived of its blood supply is often quite small. These data suggest that the cause of death is ventricular fibrillation and that the immediate availability of a safe and efficacious antiarrhythmic agent could have prolonged a number of Hves. The goals of antiarrhythmic therapy are to reduce the incidence of sudden death and to alleviate the symptoms of arrhythmias, such as palpitations and syncope. Several excellent reviews of the mechanisms of arrhythmias and the pharmacology of antiarrhythmic agents have been pubflshed (1,2). 

There have been a number of long-term trials with various P-adrenoceptor blockers in patients surviving acute MI (37—39) that demonstrated a reduction in mortaUty, sudden death, and nonfatal re-infarctions. The term cardioprotective has been used to describe this effect for the dmgs studied. The... 

Diuretics, such as those of the thiazide type, have been the cornerstone of first-line antihypertensive treatments for decades. However, popularity and use have eroded as a result of increases in sudden death in patients on diuretic therapy, and unfavorable effects on blood Hpids profile, ie, increasing cholesterol and triglyceride. These effects have been impHcated as possible causes for the lack of decrease in the mortaUty rate resulting from acute MI in patients treated with a diuretic (187,240,241). However, diuretics do protect against stroke and CHF. 

In the past, chloroform was used extensively as a surgical anesthetic, but this use was abandoned because exposure to narcotic concentrations often resulted in sudden death from effects on the heart and circulation or from severe injury to the Hver. In addition, chloroform for this and other consumer uses was harmed by FDA in 1976 with the discovery that it is carcinogenic in mice (38). When splashed into the eye, chloroform causes local pain and irritation, but serious injury is not expected. Skin contact for single, brief exposures ordinarily causes Htde or no local irritation. 

Hypokalemia. Hypokalemia associated with thia2ide diuretic therapy has been knpHcated in the increased incidence of cardiac arrhythmias and sudden death (82). Several large clinical trials have been conducted in which the effects of antihypertensive dmg therapy on the incidence of cardiovascular complications were studied. The antihypertensive regimen included diuretic therapy as the first dmg in a stepped care (SC) approach to lowering the blood pressure of hypertensive patients. 

It is prophetic that Firket (1), in speaking about public anxiety about potential catastrophes, said, "This apprehension was quite justified, when we think that proportionately, the public services of London, for example, might be faced with the responsibility of 3200 sudden deaths if such phenomenon occurred there" (p. 1192). In 1952, such a catastrophe occurred (see Section III,C). 

Concentrated potassium solutions are for IV mixtures only and should never be used undiluted. Direct IV injection of potassium could result in sudden death. When potassium is given IV, it is always diluted in 500 to 1000 mL of an IV solution. The maximum recommended concentration of potassium is 80 mEq in 1000 mL of IV solution (although in acute emergency situations a higher concentration of potassium maybe required). 

In a previous section we mentioned the significance of myosin filament structure. In nematodes two forms of myosin-II, myosin A and B, are required for proper filament stmcture (Epstein, 1988). The two forms of myosin are expressed at the proper time to allow for correct filament assembly. An accessory protein called paramyosin is also required for correct filament assembly. In vertebrate cardiac muscle, there are also two isoforms of myosin-II a-myosin and p-myosin. The proper ratio of these two proteins is of utmost importance for proper muscle activity. The incorrect synthesis of a- and P-myosins results in a severe cardiac disorder known as hypertrophic cardiomyopathy. Genetic transmission of the disease occurs in about 55% of families. The inherited condition is called familial hypertrophic cardiomyopathy (FHC), and this condition is a leading cause of sudden death in young athletes. 

Signs and symptoms of sympathetic nervous system activity are invariably found in MH. Levels of catecholamines are markedly increased in MH. Whether activation of the sympathetic nervous system is a primary or a secondary response in the syndrome has not been fully elucidated. Gronert reported that stress-induced sympathetic hyperactivity can initiate a malignant hyperthermic episode in susceptible swine without a triggering agent. Stress-induced MH in humans has been inferred because susceptible families have been shown to have an increased incidence of sudden death. Gronert s reasons that activation of the sympathetic... 

Schwartz HJ, Squillace DL, Sher TH, Teigland JD, Yunginger JW Studies in stinging insect hypersensitivity postmortem demonstration of antivenom IgE antibody in possible sting-related sudden death. Am J Clin Pathol 1986 85 607-610. 

False. Sniffing solvents is highly dangerous. There is a danger of sudden death caused by overstimulation of the heart or asphyxiation caused by swelling of the throat tissues or inhalation of vomit. Users also expose themselves to a high level of accident risk whilst intoxicated. 

While VTE may initially cause few or no symptoms, the first overt manifestation of the disease may be sudden death.2 Death from PE can occur within minutes, before effective treatment can be given. In addition to the symptoms produced by the acute event, the long-term sequelae of VTE such as the post-thrombotic syndrome (PTS a complication of VTE occurring due to damage to the vein caused by a blood... 

Domperidone minimally crosses the BBB it acts in the CTZ which lies outside of the BBB. As such, domperidone is less likely to cause the centrally-mediated adverse effects seen with metoclopramide and has an estimated overall incidence of 5% to 10%.1,30 However, domperidone has been associated with prolonged QT intervals, cardiac arrhythmias, and sudden death.31 It should not be used for patients with underlying long QT interval or for those on other medications that prolong the QT interval. Both metoclopramide and domperidone can cause hyperprolactinemia, galactorrhea, and gynecomastia. 

Because the severity of symptoms and the absolute serum concentration are poorly correlated in some patients, institution of therapy should be dictated by the clinical scenario. All patients with hypercalcemia should be treated with aggressive rehydration normal saline at 200 to 300 mL/hour is a routine initial fluid prescription. For patients with mild hypocalcemia, hydration alone may provide adequate therapy. The moderate and severe forms of hypercalcemia are more likely to have significant manifestations and require prompt initiation of additional therapy. These patients may present with anorexia, confusion, and/or cardiac manifestations (bradycardia and arrhythmias with ECG changes). Total calcium concentrations greater than 13 mg/dL (3.25 mmol/L) are particularly worrisome, as these levels can unexpectedly precipitate acute renal failure, ventricular arrhythmias, and sudden death. 

Antidepressant medications appear to be useful for certain children and adolescents, particularly those who have severe or psychotic depression, fail psychotherapeutic measures, or experience chronic or recurrent depression. SSRIs generally are considered the initial antidepressants of choice, although comorbid conditions may favor alternative agents. Clinicians should be aware of the possibility of behavioral activation with the SSRIs, including such symptoms as impulsivity, silliness, daring conduct, and agitation.44 Desipramine should be used with caution in this population because of several reports of sudden death, and a baseline and follow-up electrocardiogram (ECG) may be warranted when this medication is used to treat pediatric patients.9... 

The tricyclic antidepressants (TCAs), such as imipramine, can alleviate symptoms of ADHD. Like bupropion, TCAs likely will improve symptoms associated with comorbid anxiety and depression. The mechanism of action of TCAs is in blocking norepinephrine transporters, thus increasing norepinephrine concentrations in the synapse the increase in norepinephrine is believed to alleviate the symptoms of ADHD. TCAs have been demonstrated to be an effective non-stimulant option for ADHD but less effective than stimulants. However, their use in ADHD has declined owing to case reports of sudden death and anticholinergic side effects6,13 (Table 39-3). Further, TCAs may lower seizure threshold and increase the risk of car-diotoxicity, (e.g., arrythmias). Patients starting on TCAs should have a baseline and routine electrocardiograms. 

Space and time scales can be combined to draw the distinctions between the risks due to these two types of release. Acute risks are usually associated with immediate effects of a release occurring within hours of the accident and confined to within a few kilometers or less of its location. Examples of this class of events are spills, fires, explosions and their effects such as property damage, traumatic injury, or sudden death. 

Staley J., Wetli C., Ruttenber A., DeamW., Mash D. Altered dopaminergic synaptic markers in cocaine psychosis and sudden death. Natl. Inst. Drug Abuse Res. Monogr. 153 491, 1995. 

In the epidemiological tracking of agitated delirium victims in Metropolitan Dade County, men with preterminal delirium comprised approximately 10% of the annual number of cocaine overdose deaths. The demographic trends show that the proportion of these cases remains consistent throughout the epidemic of cocaine abuse and tends to track the annual frequency of cocaine-related sudden deaths. This observation suggests that a certain percentage of cocaine addicts may be at risk for cocaine delirium with chronic abuse. 

Wetli, C.V. and Fishbain, D.A. Cocaine-induced psychosis and sudden death in recreational cocaine users. J. Forensic. Sci. 30 873, 1985. 

---