Cardiac abnormalities arrest

Patients with pre-existing cardiac abnormalities are particularly susceptible to effects such as hypertension, pulmonary edema, atrial and ventricular dysrhythmias, and cardiac arrest, which can occur when naloxone is given to reverse opioid effects. 

The main adverse effects of the opioid antagonists fall into two groups. The first are those caused by a reversal of opioid actions these include hypotension, pulmonary edema, atrial and ventricular dysrhythmias, and cardiac arrest. The risk of such effects is increased in patients with pre-existing cardiac abnormalities. The second group of effects results from direct actions of the opioid antagonists and their actions on the central nervous system, that is typical opioid effects, including dependence. 

Lethal Arrhythmias. Arrhythmias are a second significant source of cardiovascular problems. An arrhythmia is an abnormal or irregular heart rhythm. Bradyarrhythmias result in heart rates that are too slow tachyarrhythmias cause abnormally fast rates. A bradyarrhythmia can be debiUtating, causing a person to be short of breath, unable to climb stairs, black out, or even to go into cardiac arrest. Tachyarrhythmias can be un settling and painful at best, life-threatening at worst. 

Sinus bradycardia. An abnormally low sinoatrial impulse rate (<60/min) can be raised by parasympatholytics. The quaternary ipratropium is preferable to atropine, because it lacks CNS penetrability (p. 107). Sympathomimet-ics also exert a positive chronotropic action they have the disadvantage of increasing myocardial excitability (and automaticity) and, thus, promoting ectopic impulse generation (tendency to extrasystolic beats). In cardiac arrest epinephrine can be used to reinitiate heart beat... 

The accidental release of several tons of MIC in 1984 at Bhopal, India, resulted in a very heavy death toll (approximately 1850) and, in survivors, significant impairment of health. Immediate symptoms were difficulty in breathing, skin and eye irritation, vomiting, and unconsciousness. Only a few deaths were recorded in the first few hours, with the maximum number of fatalities occurring between 24 and 72 hours. The predominant cause of death was cardiac arrest following severe pulmonary edema. Lung function abnormalities have persisted years after exposure. Ophthalmic effects included lacrimation, lid edema, photophobia, and ulceration of the corneal epithelium. A follow-up study 3 years after exposure showed excess irritation, eyelid infection, cataract, and a decrease in visual acuity, but corneal erosion was resolved. ... 

Parenteral.Hyperkalemia Adverse reactions involve the possibility of potassium intoxication. Signs and symptoms include paresthesias of extremities flaccid paralysis muscle or respiratory paralysis areflexia weakness listlessness mental confusion weakness and heaviness of legs hypotension cardiac arrhythmias heart block ECG abnormalities such as disappearance of P waves, spreading and slurring of the QRS complex with development of a biphasic curve and cardiac arrest. 

Parenfera/- The most important treatment-emergent adverse effects were hypotension, asystole/cardiac arrest/electromechanical dissociation (EMD), cardiogenic shock, CFIF, bradycardia, liver function test abnormalities, VT, and AV block. The most common adverse effects leading to discontinuation of IV therapy were hypotension, asystole/cardiac arrest/EMD, VT, and cardiogenic shock. Adverse reactions occurring in at least 3% of patients include nausea. 

The primary cause of death in acute diazinon poisoning is a depression of the neurons in the brainstem (medulla), collectively known as the respiratory center, resulting in loss of respiratory drive or, in the case of managed treatment, cardiac failure due to electrical impulse or beat conduction abnormalities in cardiac muscles (fatal arrhythmias). Other effects, such as bronchoconstriction, excessive bronchial secretions, and paralysis of the respiratory muscles (intercostal muscles and diaphragm) may also contribute to respiratory insufficiency and death. Thus, death results from loss of respiratory drive and paralysis of the respiratory muscles, or cardiac failure, or both, with attendant asphyxia or cardiac arrest (Klaassen et al. 1986 Shankar 1967, 1978 Williams and Burson 1985). 

Another study used PET to measure perfusion and glucose metabolism after cardiac arrest (Scha afsma et al. 2003). It revealed a nearly 50% decrease of glucose consumption, but was unable to detect patterns of metabolic or perfusion changes that would predict clinical outcome or imaging abnormalities. See Chap. 16 for detailed information on this matter. 

Tricyclic antidepressants commonly produce abnormalities in cardiovascular function in children and adults, and there are reports of cardiac arrest and death in children. Cardiovascular function should be carefully monitored in children taking these drugs (Dulcan, 1994). 

Cardiac ischaemia may trigger abnormal electrical activity, causing fibrillation. Defibrillators deliver a large DC shock across the heart (cardioversion), to arrest abnormal activity and allow re-establishment of sinus rhythm. 

Buflomedil is generally considered to be innocuous at therapeutic dosages. Acute toxicity is due to accidental or intentional overdosage. Overdosage causes generalized seizures and cardiac conduction abnormalities, eventually leading to cardiac arrest (SEDA-21, 215). 

Ranitidine is generally well tolerated in therapeutic doses. Ranitidine has less central nervous system (CNS) penetration, endocrine effects, and cardiovascular effects than cimetidine. Reported CNS effects associated with ranitidine include hallucinations, depression, delirium, headaches, dystonia, and choreoathetosis. Cardiac arrest during infusion, bradycardia, and progressive AV block with syncope have been reported in association with ranitidine. Abnormal liver enzymes, interstitial nephritis, parotitis, leukopenia, granulocytopenia, thrombocytopenia, pancytopenia, eosinophilia, vasculitis, dermatitis, toxic epidermal necrolysis, sexual impotence, gynecomastia, and polymyositis have also been reported in association with ranitidine therapy. 

Abnormally high extracellular (hyperkalemia) concentrations produce symptoms of mental confusion, weakness, tinghng, flaccid paralysis of the extremities, and weakness of the respiratory muscles. Cardiac effects of hyperkalemia include bradycardia and conduction defects evident on the electrocardiogram by prolonged PR and QRS intervals and peaked T waves. Prolonged severe hyperkalemia >7.0 mmol/L can lead to peripheral vascular collapse and cardiac arrest. There is individual variability in the concentrations of at which symptoms become apparent, but symptoms are almost always present at concentrations >6.5 mmol/L. Concentrations >10.0 mmol/L are in most cases fatal. 

FIGURE 17-16. Example of an approach to the management of survivors of cardiac arrest (resuscitated VT/VF). Reversible causes of cardiac arrest (e.g., electrolyte abnormalities, acute phase of Ml) should be treated with specific therapy. AADs = antiarrhythmic drugs BBs = /i-blockers EPS = invasive electrophysio-logic studies ICD = implantable cardioverter-defibrillator VT/VF = ventricular tachycardia/ventricular fibrillation Ml = myocardial infarction. 

Hg accumulates in the heart, and exposures to organic and inorganic forms of this metal have been associated with blood-pressure alterations and abnormal cardiac function. Numerous reports of human poisonings have described marked hypertension and abnormal heart rate among victims. Autopsies of two boys who died of cardiac arrest after they were fed ethylmercury-contaminated pork over a period of several weeks revealed myocarditis. Two recent epidemiological studies have found associations between dietary exposure to very low levels of MeHg... 

In one of the cases reviewed by Sheikh and colleagues, a patient developed a generalized urticarial rash, nausea, and abdominal pain after ingestion of chaparral, but had been taking chaparral for 1 yr, had a history of allergies, and was also taking naproxen and ketorolac. Miscellaneous adverse effects associated with chaparral use include sudden unilateral loss of vision, tachycardia, electrolyte abnormalities with cardiac arrest, and syncopal episodes (Sheikh et al., 1997). 

Early trials of SAECG showed that an abnormal test was associated with an increased risk of VT, SCD, and total mortality (59). SAECG had a low PPV in these trials, but a high NPV of between 81 and 89%. However, few of these patients were treated with contemporary therapy, making their relevance in current risk stratification paradigms less clear. A more recent trial of 1925 patients with ischemic cardiomyopathy and NSVT found that a filtered QRS duration >114 msec independently predicted the primary end point of arrhythmic death or cardiac arrest (58). However, the five-year rate of the primary end point was 28% versus 17% in patients with an abnormal test versus a normal test (P = 0.0001), revealing the limited PPV and NPV of SAECG to risk stratify these patients. The predictive value of the test was enhanced when it was combined with a low LVEF. 

---