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Bradycardia

Treatment of Manic—Depressive Illness. Siace the 1960s, lithium carbonate [10377-37-4] and other lithium salts have represented the standard treatment of mild-to-moderate manic-depressive disorders (175). It is effective ia about 60—80% of all acute manic episodes within one to three weeks of adrninistration. Lithium ions can reduce the frequency of manic or depressive episodes ia bipolar patients providing a mood-stabilising effect. Patients ate maintained on low, stabilising doses of lithium salts indefinitely as a prophylaxis. However, the therapeutic iadex is low, thus requiring monitoring of semm concentration. Adverse effects iaclude tremor, diarrhea, problems with eyes (adaptation to darkness), hypothyroidism, and cardiac problems (bradycardia—tachycardia syndrome). [Pg.233]

Doridosine. Doridosine, AJ -methyhsoguanosine, (35) was isolated from the dorid nudibranchs of Anisodoris nobilis and the sponge, Tedania (106,107). The injection of (35) into the saphenous vein of anesthetized rats produces hypotension and bradycardia almost immediately. The observed changes in the electrocardiograms are minor and indicate Httie interference with conduction of the impulse within the heart (see Cardiovascularagents). [Pg.122]

After these reports there were many attempts to administer hemoglobin solutions to humans. Many of these patients did well, but others demonstrated hypertension, bradycardia, oliguria, and even anaphylaxis. These untoward effects were not correlated with specific biochemical properties of the solutions themselves. [Pg.161]

Arrhythmias Originating in the Sinus Node Sinus bradycardia Sick sinus syndrome Sinus tachycardia Disorders of Impulseformation ... [Pg.112]

Because of its brief half-life and minimal hpid solubihty, the side effects of esmolol are transient and include hypotension, cold extremities, dyspnea (from bronchospasms), bradycardia, nausea, vomiting, and headaches (41). [Pg.119]

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). [Pg.120]

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). [Pg.120]

Sotalol is rapidly and almost completely (>90%) absorbed. Bioavahabhity of absorbed dmg is 89—100%. Peak plasma levels are achieved in 2—4 h. Sotalol is 50% bound to plasma proteins. Plasma half-life of the compound is about 5.2 h. No metabolites of sotalol have been identified indicating littie metabolism. The dmg is excreted mainly by the kidneys (80—90%) and about 10% is eliminated in the feces. The plasma half-life is prolonged in patients having renal failure. Kinetics of the compound are not affected by changes in liver function (1,2). Sotalol has ah the adverse effects of -adrenoceptor blockers including myocardial depression, bradycardia, transient hypotension, and proarrhythmic effects (1,2). [Pg.121]

Patients having high plasma renin activity (PRA) (>8 ng/(mLh)) respond best to an ACE inhibitor or a -adrenoceptor blocker those having low PRA (<1 ng/(mLh)) usually elderly and black, respond best to a calcium channel blocker or a diuretic (184). -Adrenoceptor blockers should not be used in patients who have diabetes, asthma, bradycardia, or peripheral vascular diseases. The thiazide-type diuretics (qv) should be used with caution in patients having diabetes. Likewise, -adrenoceptor blockers should not be combined with verapamil or diltiazem because these dmgs slow the atrioventricular nodal conduction in the heart. Calcium channel blockers are preferred in patients having coronary insufficiency diseases because of the cardioprotective effects of these dmgs. [Pg.132]

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. [Pg.141]

Bradycardia Bradycardia is a slow heart rate (60 beats per minute or slower) that does not meet the body s metabolic demands. Symptoms of bradycardia include dizziness, extreme fatigue, shortness of breath, or fainting spells. This can be compared to tachycardia, which is an extremely rapid heart rate, usually signified by a pulse of over 100 beats per minute. Adults usually have a resting heart rate of 70-80 beats per minute, although well-trained athletes can have resting rates in the 50 s or 60 s. Newborn babies have a normal heart rate of 120-160 beats per minute. A slowed heart rate can lead to a variety of other problems. First aid treatment may include administration of oxygen. [Pg.522]

Bradycardia/AV- bio ck/renal vaso cons trict Hypotension/coronary vasodilation/platelet aggreg Mediator release... [Pg.171]

Normal rhythmic activity is the result of the activity of the sinus node generating action potentials that are conducted via the atria to the atrioventricular node, which delays further conduction to the His-Tawara-Purkinje system. From the Purkinje fibres, action potentials propagate to the ventricular myocardium. Arrhythmia means a disturbance of the normal rhythm either resulting in a faster rhythm (tachycardia, still rhythmic) or faster arrhythmia (tachyarrhythmia) or slowed rhythm (bradycardia, bradyarrhythmia). [Pg.96]

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. [Pg.100]

Supraventricular bradycardia is treated by implantation of a pacemaker device or has been treated pharmacologically with atropine. Supraventricular paroxysmal tachycardia is treated with aj marine or praj marine. Supraventricular tachyarrhythmias or AV reentrant arrhythmia typically can be terminated using adenosine. [Pg.101]

Cardiac glycosides have a small ratio of toxic to therapeutic concentration. Possible adverse effects are nausea, vomiting, abdominal pain, diarrhoea, fatigue, headache, drowsiness, colour vision disturbances, sinus bradycardia, premature ventricular complexes, AV-block, bigeminy, atrial tachycardia with AV-Block, ventricular fibrillation. There are several mechanisms relevant for their toxic action (Table 2). [Pg.328]

Decreased activity of the thyroid gland results in hypothyroidism and, in severe cases, myxoedema. It is often of immunological origin and the manifestations are low metabolic rate, slow speech, lethargy, bradycardia, increased sensitivity to cold, and mental impairment. Myxoedema includes a characteristic thickening of the skin. Therapy of thyroid tumours is another cause of hypothyroidism. Thyroid deficiency... [Pg.610]

Cardiovascular—flushing of die face, peripheral circulatory collapse, tachycardia, bradycardia, and palpitations... [Pg.171]

Drowsiness, sedation, sleepiness, lethargy, constipation, diarrhea, bradycardia, tachycardia, rash... [Pg.189]

Drowsiness is the most common reaction seen with the use of skeletal muscle relaxants. Additional adverse reactions are given in die Summary Drug Table Drugp Used to Treat Musculoskeletal Disorders. Some of the adverse reactions tiiat may be seen with the administration of diazepam include drowsiness, sedation, sleepiness, letiiargy, constipation or diarrhea, bradycardia or tachycardia, and rash. [Pg.191]


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AV block, bradycardia

Alpha-adrenergic agents bradycardia caused

Arrhythmias bradycardia

Atenolol bradycardia

Atropine for bradycardia

Beta-adrenoceptor antagonists bradycardia

Bradycardia adult

Bradycardia algorithm

Bradycardia and

Bradycardia antagonists

Bradycardia atropine

Bradycardia beta-adrenoceptor

Bradycardia betaxolol

Bradycardia block

Bradycardia caffeine, effect

Bradycardia caused

Bradycardia cyanide exposure

Bradycardia definition

Bradycardia donepezil

Bradycardia due to opioids

Bradycardia epinephrine

Bradycardia evolution

Bradycardia glycosides causing

Bradycardia hypotension

Bradycardia isoprenaline

Bradycardia mexiletine

Bradycardia nerve agent exposure

Bradycardia pediatric

Bradycardia phenylephrine

Bradycardia physostigmine

Bradycardia physostigmine effects

Bradycardia treatment

Bradycardia vasopressin

Bradycardia verapamil

Bradycardia, pacing

Bradycardia, supraventricular

Bradycardia-tachycardia syndrome

Bradycardia/atrioventricular block caused

Carbamazepine bradycardia caused

Cholinergic agents bradycardia caused

Clonidine bradycardia caused

Esmolol bradycardia

Fentanyl bradycardia

Hydromorphone bradycardia

Ketamine bradycardia

Lidocaine profound bradycardia

Mild bradycardia

Nervous system toxicity bradycardia

Paclitaxel bradycardia

Reflex bradycardia

Remifentanil bradycardia

Sinus bradycardia

Sinus bradycardia and

Sinus bradycardia causes

Sinus bradycardia treatment

Transient bradycardia

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