Cardiac ventricular arrhythmias

Occurs when the volume of extracellular fluid is significantly diminished. Examples include hemorrhage, fluid loss caused by burns, diarrhea, vomiting, or excess diuresis Occurs when the heart is unable to deliver an adequate cardiac output to maintain perfusion to the vital organs. Examples include as the result of an acute myocardial infarction, ventricular arrhythmias, congestive heart failure (CHF), or severe cardiomyopathy. 

These dm are primarily used in the treatment of hypertension (see the Summary Drug Table Adrenergic Blocking Drugs also see Chap. 39) and certain cardiac arrhythmias (abnormal rhythm of the heart), such as ventricular arrhythmias or supraventricular tachycardia They are used to prevent reinfarction in patients with a recent myocardial infarction (1—4 weeks after MI). Some of these dm have additional uses, such as the use of propranolol for migraine headaches and nadolol for angina pectoris. 

Mr. Summers has a ventricular arrhythmia and is placed on a cardiac monitor. The primary health care provider prescribes IV lidocaine. Discuss preadministration assessments you would perform on Mr. Summers. Analyze which adverse reactions would be most important to monitor for during the ongoing assessment. Determine what reactions should be reported immediately. 

Cardiovascular Effects. In one case study, a woman who had accidentally consumed about 20 mL of trichloroethylene was reported to have suffered a myocardial infarction within 2 hours of ingestion (Morreale 1976). In two other case studies, men who ingested 350 and 500 mL of trichloroethylene had ventricular arrhythmias that persisted for up to 3 days (Dhuner et al. 1957). The arrhythmias were described as ventricular tachycardia with extrasystoles from different ventricular foci. Cardiac arrhythmia was also reported in a women who drank an unknown amount of trichloroethylene (Perbellini et al. 1991). 

Increased oxygen demand secondary to increased heart rates and blood pressure has been hypothesized to lead to myocardial infarction (especially in patients with fixed coronary disease) and/or ventricular arrhythmias. In patients with no history of cardiac disease, cocaine is thought to induce acute isehemie complications via vasospasm of the coronaries (Ascher et al. 1988). In addition, Virmani et al. (1988) have reported a 20 percent incidence of myocarditis thought to be secondary to accumulated microvascular injuries. 

Tachycardia and increased contractility (due to SNS activation) Increase cardiac output Increased MV02 Shortened diastolic filling time P,-Receptor down-regulation, decreased receptor sensitivity Precipitation of ventricular arrhythmias Increased risk of myocardial cell death... 

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. 

Inhalation of certain hydrocarbons, including some anesthetics, can make the mammalian heart abnormally sensitive to epinephrine, resulting in ventricular arrhythmias, which in some cases can lead to sudden death (Reinhardt et al. 1971). The mechanism of action of cardiac sensitization is not completely understood but appears to involve a disturbance in the normal conduction of the electrical impulse through the heart, probably by producing a local disturbance in the electrical potential across cell membranes. The hydrocarbons themselves do not produce arrhythmia the arrhythmia is the result of the potentiation of endogenous epinephrine (adrenalin) by the hydrocarbon. 

The decreased work capacity of the in-farcted myocardium leads to a reduction in stroke volume (SV) and hence cardiac output (CO). The fall in blood pressure (RR) triggers reflex activation of the sympathetic system. The resultant stimulation of cardiac 3-adreno-ceptors elicits an increase in both heart rate and force of systolic contraction, which, in conjunction with an a-adren-oceptor-mediated increase in peripheral resistance, leads to a compensatory rise in blood pressure. In ATP-depleted cells in the infarct border zone, resting membrane potential declines with a concomitant increase in excitability that may be further exacerbated by activation of p-adrenoceptors. Together, both processes promote the risk of fatal ventricular arrhythmias. As a consequence of local ischemia, extracellular concentrations of H+ and K+ rise in the affected region, leading to excitation of nociceptive nerve fibers. The resultant sensation of pain, typically experienced by the patient as annihilating, reinforces sympathetic activation. 

Inhalation of concentrations in the range of 5000-20,OOOppm have been used to produce light anesthesia. Recovery from unconsciousness is usually uneventful, but ventricular arrhythmias and death from cardiac arrest have occurred rarely. Exposure of volunteers to 500-1000 ppm has resulted in some symptoms of CNS disturbance such as dizziness, lightheadedness, lethargy, and impairment in visual-motor response tests. In general, no significant signs of toxicity or impaired performance have been noted in subjects acutely exposed to 300 ppm or less. 

Amiodarone (16) has been the center of much interest because of its activity as a cardiac depressant useful in treating ventricular arrhythmia and many analogues have been prepared [4. I he originally patented procedure concludes simply by etherification of benzofuran-containing iodonated phenol 15 with 2-halodiethylaminoethane to give amiodarone (16) [5]. The synthesis t)f 15 is not detailed in the reference but the synthesis of benzbromarone contains closely analo-goii.s steps [6]. 

Strophanthin is used in severe cardiovascular insufficiency, in particular after myocardial infarction, for chronic cardiac insufficiency, cardiac decompensation, supraventricular tachycardia, and ventricular arrhythmia. Synonyms of this drug are combetin, strofopan, and others. 

Tocainide is used for suppressing symptoms of ventricular arrhythmia and tachycardia, and for premature cardiac contractions. A synonym of this drug is tonocard. 

Mortality In the National Heart, Lung, and Blood Institute s Cardiac Arrhythmia Suppression Trial (CAST), a long-term, multicentered, randomized, double-blind study in patients with asymptomatic nonlife-threatening ventricular arrhythmias who had an Ml more than 6 days but less than 2 years previously, an excessive mortality or nonfatal cardiac arrest rate was seen in patients treated with encainide or flecainide (7.7%) compared with that seen in patients assigned to matched placebo-treated groups (3%). The averaged duration of treatment with encainide or flecainide in this study was 10 months. 

IV Acute management of ventricular arrhythmias occurring during cardiac manipulation, such as cardiac surgery or in relation to acute myocardial infarction (Ml). 

Bepridll History of serious ventricular arrhythmias uncompensated cardiac insufficiency congenital QT interval prolongation use with other drugs that prolong QT interval. 

Proarrhythmia Like other antiarrhythmic agents, sotalol can provoke new or worsened ventricular arrhythmias in some patients, including sustained ventricular tachycardia or ventricular fibrillation, with potentially fatal consequences. Because of its effect on cardiac repolarization, is the most common form of proarrhythmia associated with sotalol, occurring in approximately 4% of high-risk patients. 

Concomitant use of calcium channel blockers (atenolol) Bradycardia and heart block can occur and the left ventricular end diastolic pressure can rise when beta-blockers are administered with verapamil or diltiazem. Patients with preexisting conduction abnormalities or left ventricular dysfunction are particularly susceptible. Recent acute Ml (sotalol) Sotalol can be used safely and effectively in the long-term treatment of life-threatening ventricular arrhythmias following an Ml. However, experience in the use of sotalol to treat cardiac arrhythmias in the early phase of recovery from acute Ml is limited and at least at high initial doses is not reassuring. 

Sildenafil - Serious cardiovascular, cerebrovascular, and vascular events, including Ml, sudden cardiac death, ventricular arrhythmia, cerebrovascular hemorrhage, transient ischemic attack, hypertension subarachnoid and intracerebral hemorrhages, and pulmonary hemorrhage have been reported postmarketing in temporal association with sildenafil. 

---