Bradycardia and

The side effects and toxic reactions to verapamil iaclude upper GI upset, constipation, di22iaess, headaches, flushing and burning, edema, hypotension, bradycardia, and various conduction disturbances. Verapamil has negative iaotropic activity and may precipitate heart failure ia patients having ventricular dysfunction (1,2). 

Phenylephrine. Phenylephrine hydrochloride is an a -adrenoceptor agonist. Phenylephrine produces powerful vasoconstrictor and hypertensive responses. This results in baroreceptor activation of a reflex bradycardia and thus is useful in the treatment of supraventricular tachyarrhythmias. Unlike epinephrine [51-43-4] the actions of which are relatively transient, phenylephrine responses are more sustained (20 min after iv dosing and 50 min after subcutaneous dosing) (86). 

Better antihypertensive effect of P-adrenoceptor blockers is found in patients having high PRA and most are not efficacious in patients having low PRA or in elderly patients. P-Adrenoceptor blockers usually lower arterial blood pressure about 10 mm Hg (1.3 kPa). Side effects include lethargy, dyspnea, nausea, dizziness, headache, impotency, cold hands and feet, vivid dreams and nightmares, bronchospasm, bradycardia, and sleep disturbances. 

In high concentrations it blocks calcium channels and, thus, exerts prominent negative inotropic effects. Its adverse effects include proarrhythmic effects, worsening of heart failure and (due to (3-adrenoceptor blockade) bradycardia and bronchospasm. 

Cardiovascular—flushing of die face, peripheral circulatory collapse, tachycardia, bradycardia, and palpitations... 

Because narcoticanalgesicsdepressthe CNS(see Chap. 19), the nurse should not administer a barbiturate or miscellaneous sedativesand hypnoticsapproximately 2 hoursbefore or after administration of a narcoticanalgesic or other CNS depressant. If the time interval between administration of a narcotic analgesic and a sedative or hypnotic is less than 2 hours the patient may experien ce severe respiratory depres-son, bradycardia, and unresponsiveness. 

ADMINISTERING PROPRANOLOL. Cardiac monitoring is recommended when the drug is given IV because severe bradycardia and hypotension may be seen. The nurse obtains written instructions from the primary health care provider for propranolol administration. For example, tire primary health care provider may want the drug to be withheld for a systolic blood pressure less than 90 mm Hg or a pulse rate less than 50 bpm. 

Use only one medication initially for rate or rhythm control. Occasionally, two agents may need to be utilized. Combination therapy may cause hypotension, bradycardia, and might be arrhythmogenic. 

Electrocardiogram (ECG) May be normal or could show numerous abnormalities including acute ST-T-wave changes from myocardial ischemia, atrial fibrillation, bradycardia, and LV hypertrophy. 

Blockers are contraindicated in patients with severe bradycardia (heart rate less than 50 beats per minute) or AV conduction defects in the absence of a pacemaker. (3-Blockers should be used with particular caution in combination with other agents that depress AV conduction (e.g., digoxin, verapamil, and diltiazem) because of increased risk for bradycardia and heart block. Relative contraindications include asthma, bronchospastic disease, severe depression, and peripheral vascular disease. (3,-Selective blockers are preferred in patients with asthma or chronic obstructive pulmonary... 

The most serious side effects of P-blocker administration early in ACS are hypotension, bradycardia, and heart block. While initial, acute administration of P-blockers is not appropriate for patients who present with decompensated heart failure, initiation of P-blockers maybe attempted before hospital discharge in the majority of patients following treatment of acute heart failure. P-Blockers are continued indefinitely. 

Compare and contrast appropriate nonpharmacologic and pharmacologic treatment options for sinus bradycardia and AV nodal blockade. 

American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiac care, part 7.3. Management of symptomatic bradycardia and tachycardia. Circulation 2005 112 IV-67 to IV-177. 

Bradycardia and absence of wheezing may indicate impending respiratory failure. 

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. 

Using the ECG, the heart rate may be determined by calculating the time from the beginning of one P wave to the beginning of the next P wave, or from peak to peak of the QRS complexes. A normal resting heart rate in adults is approximately 70 beats/min. A heart rate of less than 60 beats/min is referred to as bradycardia and a heart rate of more than 100 beats/min is referred to as tachycardia. 

Opium and its derivatives have been employed for centuries for the treatment of pain. Morphine was first synthesized in 1805 and has proven to be one of the most effective analgesic agents available [1], Morphine and its analogs are particularly useful because they diminish pain sensation while maintaining consciousness. However, opiates induce severe side-effects including respiratory depression, nausea, bradycardia and constipation and long-term use of opiates can cause addiction [2]. 

Kitten, 3 months old, died in 6 h following hypersalivation, ataxia, depression, and seizures. No histopathology at necropsy brain AChE activity normal. Fenvalerate residues, in pg/kg, were 345,000 in skin, 230 in kidney, 150 in liver, 10 in brain. Adult (4-year-old) showed signs of toxicosis 4 h after topical application by 30 h, animal had lowered body temperature, bradycardia, and other signs of fenvalerate poisoning. At death, shortly thereafter, fenvalerate residues were 1000 pg/kg in skin and 20 pg/kg in liver... 

Treatment of sinus node dysfunction involves elimination of symptomatic bradycardia and possibly managing alternating tachycardias such as AF. Asymptomatic sinus bradyarrhythmias usually do not require therapeutic intervention. 

Blockers are contraindicated in patients with decompensated heart failure unless it is caused solely by tachycardia (high output). Other contraindications include sinus bradycardia, concomitant therapy with monoamine oxidase inhibitors or tricyclic antidepressants, and patients with spontaneous hypoglycemia. Side effects include nausea, vomiting, anxiety, insomnia, lightheadedness, bradycardia, and hematologic disturbances. 

Physical signs include coarse skin and hair, cold or dry skin, periorbital puffiness, bradycardia, and slowed or hoarse speech. Objective weakness (with proximal muscles being affected more than distal muscles) and slow relaxation of deep tendon reflexes are common. Reversible neurologic syndromes such as carpal tunnel syndrome, polyneuropathy, and cerebellar dysfunction may also occur. 

Side effects include drowsiness, fatigue, sleep disturbances, vivid dreams, memory disturbance, depression, G1 intolerance, sexual dysfunction, bradycardia, and hypotension. 

TAdrenergic blockers Fivefold increase in propranolol serum concentration bradycardia and hypotension... 

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