Acute cardiac disease, effects

Ari pi prazole, olanzapine, quetiapine, risperidone, and ziprasidone are effective as monotherapy or as add-on therapy to lithium or valproate for acute mania. Prophylactic use of antipsychotics can be needed for some patients with recurrent mania or mixed states, but the risks versus benefits must be weighed in view of long-term side effects (e.g., obesity, type 2 diabetes, hyperlipidemia, hyperprolactinemia, cardiac disease, and tardive dyskinesia). 

Lithium should not be administered to patients with fluctuating or unstable renal function. Because hthium may affect functioning of the cardiac sinus node, patients with sinus node dysfunction (e.g., sick sinus syndrome) should not receive hthium. Although hthium also has acute and chronic effects on the thyroid, patients with hypothyroidism may receive hthium if the thyroid disease is adequately treated and monitored. Laboratory tests that should be performed before initiation of hthium are listed in Table 5-1. 

Most but not all forms of recurrent ventricular tachycardia occur in patients with extensive heart disease. Ventricular tachycardia occurring in a patient without heart disease is sometimes referred to as idiopathic ventricular tachycardia and may take several forms. " Fascicular tachycardia arises from a fascicle of the left bundle branch (usually posterior) and usually is not associated with severe underlying heart disease. Calcium channel blockers (but not adenosine) are effective in terminating an acute episode of fascicular ventricular tachycardia. Ventricular outflow tract tachycardia (usually originating from the right ventricular outflow tract and thus abbreviated RVOT) originates from near the pulmonic valve (or uncommonly the aortic) and also occurs in patients with normal LV without discernible cardiac disease. Unlike other forms of ventricular tachycardia, RVOT... 

Effects on the myocardium are not significant in normal individuals. In patients with coronary artery disease but no acute medical problems, 8-15 mg morphine administered intravenously produces a decrease in oxygen consumption, left ventricular end-diastolic pressure, and cardiac work effects on cardiac index usually are slight. In patients with acute myocardial infarction, the cardiovascular responses to morphine may be more variable than in normal subjects, and hypotension may be more pronounced. 

B. Euthyroid persons and children appear to have a high tolerance to the effects of an acute overdose. Patients with preexisting cardiac disease and those with chronic overmedication have a lower threshold of toxicity. Sudden deaths have been reported after chronic thyroid hormone abuse in healthy adults. 

Beriberi is caused by a deficiency of thiamin (also called thiamine, aneurin(e), and vitamin Bj). Classic overt thiamin deficiency causes cardiovascular, cerebral, and peripheral neurological impairment and lactic acidosis. The disease emerged in epidemic proportions at the end of the nineteenth century in Asian and Southeast Asian countries. Its appearance coincided with the introduction of the roller mills that enabled white rice to be produced at a price that poor people could afford. Unfortunately, milled rice is particularly poor in thiamin thus, for people for whom food was almost entirely rice, there was a high risk of deficiency and mortality from beriberi. Outbreaks of acute cardiac beriberi still occur, but usually among people who live under restricted conditions. The major concern today is subclinical deficiencies in patients with trauma or among the elderly. There is also a particular form of clinical beriberi that occurs in patients who abuse alcohol, known as the Wer-nicke-Korsakoff syndrome. Subclinical deficiency may be revealed by reduced blood and urinary thiamin levels, elevated blood pyruvate/lactate concentrations and a-ketoglutarate activity, and decreased erythrocyte transketolase (ETKL) activity. Currently, the in vitro stimulation of ETKL activity by thiamin diphosphate (TDP) is the most useful functional test of thiamin status where an acute deficiency state may have occurred. The stimulation is measured as the TDP effect. 

Cardiovascular Effects. Chronic cardiovascular disease has not been reported in workers occupationally exposed to low levels of trichloroethylene (El Ghawabi et al. 1973), although deaths following acute high-level inhalation exposures to trichloroethylene have been attributed to cardiac arrhythmias. Case studies have described cardiac arrhythmias that in some instances led to death after occupational exposure (Bell 1951 Kleinfeld and Tabershaw 1954 Smith 1966), poisoning (Dhuner et al. 1957 Gutch et al. 1965), or... 

Injection - Heart failure secondary to chronic lung disease cardiac arrhythmias brain tumor acute alcoholism delirium tremens idiosyncrasy to the drug increased intracranial or CSF pressure head injuries acute bronchial asthma upper airway obstruction. Because of its stimulating effect on the spinal cord, morphine should not be used in convulsive states (eg, status epilepticus, tetanus, strychnine poisoning) concomitantly with MAOIs or in those who have received such agents within 14 days. 

Cardiac effects Hypertension, in some cases severe, requiring acute treatment, has been reported in patients receiving bupropion alone and in combination with nicotine replacement therapy. Exercise care if bupropion is used in in patients with a recent history of Ml or unstable heart disease. 

In patients with longstanding hypothyroidism and those with ischemic heart disease, rapid correction of hypothyroidism may precipitate angina, cardiac arrhythmias, or other adverse effects. For these patients, replacement therapy should be started at low initial doses, followed by slow titration to full replacement as tolerated over several months. If hypothyroidism and some degree of adrenal insufficiency coexist, an appropriate adjustment of the corticosteroid replacement must be initiated prior to thyroid hormone replacement therapy. This prevents acute adrenocortical insufficiency that could otherwise arise from a thyroid hormone-induced increase in the metabolic clearance rate of adrenocortical hormones. 

Shock is a complex acute cardiovascular syndrome that results in a critical reduction in perfusion of vital tissues and a wide range of systemic effects. Shock is usually associated with hypotension, an altered mental state, oliguria, and metabolic acidosis. If untreated, shock usually progresses to a refractory deteriorating state and death. The three major mechanisms responsible for shock are hypovolemia, cardiac insufficiency, and altered vascular resistance. Volume replacement and treatment of the underlying disease are the mainstays of the treatment of shock. Although sympathomimetic drugs have been used in the treatment of virtually all forms of shock, their efficacy is unclear. 

The effects of coenzyme Q10 on coronary artery disease and chronic stable angina are modest but appear promising. A theoretical basis for such benefit could be metabolic protection of the ischemic myocardium. Double-blind, placebo-controlled trials have demonstrated that coenzyme Q10 supplementation improved a number of clinical measures in patients with a history of acute myocardial infarction (AMI). Improvements have been observed in lipoprotein a, high-density lipoprotein cholesterol, exercise tolerance, and time to development of ischemic changes on the electrocardiogram during stress tests. In addition, very small reductions in cardiac deaths and rate of reinfarction in patients with previous AMI have been reported (absolute risk reduction 1.5%). 

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