Sinus arrest causes

MisraM, ThakurR,BhandariK. Sinus arrest caused by atenolol-verapamil combination. Clin Cardiol 9%1) 0, 365-7. 

Sick sinus syndrome Use only with extreme caution the drug may cause sinus bradycardia, sinus pause, or sinus arrest. The frequency probably increases with higher trough plasma levels. 

Adenosine 20-100 xg Have the same indications as sodium nitroprusside Can cause sinus arrest/AV block when high doses are used, especially in the RCA (an effect which is reversible within seconds)... 

Bradycardia often occurs with the combination of a potent short-acting opioid with suxamethonium during induction of anesthesia, and alfentanil has been reported to have caused sinus arrest in three patients (SEDA-17,79) (3). 

Patients with impaired function of the sinus node or impaired atrioventricular conduction can develop sinus bradycardia, sinus arrest, heart block, hypotension and shock, and even asystole, with verapamil (139) or diltiazem. These drugs should not be given to patients with aberrant conduction pathways associated with broad-complex tachydysrhythmias, and they can cause severe conduction disturbances in hypertrophic cardiomyopathy. 

In a 49-year-old otherwise healthy woman undergoing craniotomy for aneurysm clipping, inadvertent overdose with phenytoin (1500 mg) by rapid infusion caused intraoperative sinus arrest, which was managed successfully with standard resuscitative measures (5). 

Encainide, a class 1C antiarrhythmic agent, is available on a limited basis only to patients with life-threatening ventricular arrhythmias. Encainide slows conduction velocity, inhibits automaticity, and increases the ratio of the effective refractory period to action potential duration. It blocks the sodium channel of Purkinje fibers and the myocardium. Encainide is absorbed well, reaches peak plasma level in 30 to 90 minutes, becomes metabolized to 0-demethyl encainide (ODE) and 3-methoxy-O-demethyl encainide (MODE), which are active antiarrhythmic agents, and the metabolites are excreted by the kidneys. In renal impairment, the clearance of ODE and MODE is decreased, and hence the dosage should be reduced. Encainide may either worsen or create new arrhythmias, especially in electrolyte-imbalanced patients. Encainide is known to have caused sinus bradycardia, sinus pause, or sinus arrest (see also Eigure 84). 

Sotalol should be used cautiously in pregnant patients and patients with renal failure or diabetes mellitus. Sotalol should be used with extreme caution in patients with sick-sinus syndrome associated with symptomatic arrhythmias, because the drug can cause sinus bradycardia, sinus pauses, or sinus arrest. 

Overdose may cause sedation, confusion, coma, seizures, respiratory arrest, and cardiac toxicity (sinus arrest, atrioventricular [AV] block, asystole. 

With chronic use, amiodarone may cause ventricular arrhythmias (mono-morphic or polymorphic ventricular tachycardia see p 14) or bradyanhyth-mias (sinus arrest, AV block). Amiodarone may cause pneumonitis or pulmonary fibrosis, hepatitis, photosensitivity dermatitis, comeal deposits, hypothyroidism or hyperthyroidism, tremor, ataxia, and peripheral neuropathy. 

A. Cardiotoxic effects of the type la agents include sinus bradycardia sinus node arrest or asystole PR, QRS, or QT interval prolongation sinus tachycardia (caused by anticholinergic effects) polymorphous ventricular tachycardia (torsade de pointes) and depressed myocardial contractility, which, along with alpha-adrenergic or ganglionic blockade, may result in hypotension and occasionally pulmonary edema. 

However, in some cases combining two or more antihypertensives has led to severe, first-dose hypotension, see Alpha blockers + ACE inhibitors , p.84. Further, life-threatening bradycardia, asystole and sinus arrest can occur when antihypertensives that cause cardiodepression are given together (see beta blockers and diltiazem , (p.840)). 

Caused by the inability of the SAN to activate the atiia, leading to an absence of P waves on the ECG. These blocks can be classified as either complete or incomplete SA blocks. Incomplete blocks cause the occasional loss of beats. Complete SA block occurs when no impulses leave the SAN leading to Sinus Arrest , a complete lack of heart beats (no PQRS or T waves present). 

Complete SA block otherwise known as sinus arrest has no such mathematical relationship. The pauses can last several seconds, and may cause patients to collapse (Fig. 7.15). The pause is normally terminated by an escape beat. As discussed earlier these escape beats originate further down the conduction system and are known as junctional or ventricular escape beats, depending upon their origin. These beats act as a safety net preventing Asystole. Treatment may require the use of drugs such as atropine or the insertion of an artificial pacemaker. 

Otherwise know as Brady-tachy syndrome features alternating periods of tachycardia and bradycardia on the same ECG (Fig. 7.16). Atrial fibrillation or flutter may also be seen on the ECG causing the tachycardia. The bradycardia is caused by sinus pauses or periods of sinus arrest. 

Depression or cardiac excitability and contractility may cause AV block, ventricular arrhythmias, or cardiac arrest. Symptoms of local anesthetic CNS toxicity, such as dizziness, tongue numbness, visual impairment or disturbances, and muscular twitching appear to occur before cardiotoxiceffects. Cardiotoxic effects include angina, QT prolongation, PR prolongation, atrial fibrillation, sinus bradycardia, hypotension, palpitations, and cardiovascular collapse. 

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. 

An overdose of acebutolol (6.4 mg) in a 48-year-old man caused cardiac arrest with ventricular tachycardia (5). An intravenous bolus of sodium bicarbonate 50 mmol produced sinus rhjThm. 

Encainide has been reported to cause sinus node arrest in association with prolonged sinus node recovery time (19). It also raises the pacing threshold in patients with chronic implanted pacemakers (20), although this has not been reported to increase the failure rate of pacemakers. 

Lidocaine can cause dysrhythmias and hypotension. The dysrhythmias that have been reported include sinus bradycardia, supraventricular tachycardia (11), and rarely torsade de pointes (12). There have also been rare reports of cardiac arrest (2) and worsening heart failure (13). Lidocaine can also cause an increased risk of asystole after repeated attempts at defibrillation (14). Lidocaine may increase mortality after acute myocardial infarction, and it should be used only in patients with specific so-called warning dysrhythmias (that is frequent or multifocal ventricular extra beats, or salvos) (15). 

Overdosage with mexiletine causes dizziness, drowsiness, nausea, hypotension, sinus bradycardia, paresthesia, seizures, intermittent left-bundle branch block, and temporary asystole. With massive overdoses, coma and respiratory arrest may occur (see also Eigure 84). 

TheophyUine decreases peripheral resistance, increases cardiac output, and causes a central vagal effect. Palpitations, sinus bradycardia, extrasystoles, hypotension, ventricular tachycardia, premature ventricular contractions (PVCs), and cardiac arrest have been reported. Although cardiovascular effects are generaUy mUd and transient, serious reactions, such as ventricular arrhythmias, can develop without warning. Patients should be carefuUy monitored. 

Lupanine has been substituted on the 2 (keto)-position, forming benzyl-lupanol and further altered to phenyldehydrosparteine by removal of a molecule of water from the 2 and 3 carbon atoms forming a double bond. With either of these derivatives, a tenfold increase in potency of effects on the isolated frog heart is obtained. Lower concentrations cause ventricular standstill (arrest), sinus bradycardia, and an increase in electrical current (threshold) producing fibrillation (78). 

A. Ataxia, nystagmus, ophthalmoplegia, movement disorders (dyskinesia, dystonia), mydriasis, and sinus tachycardia are common with mild to moderate overdose. With more serious intoxication, myoclonus, seizures (including status epilepticus), hyperthermia, coma, and respiratory arrest may occur. Atrioventricular (AV) block and bradycardia have been reported, particularly in the elderly. Based on Its structure similarity to tricyclic antidepressants, carbamazepine may cause QRS and QT interval prolongation and myocardial depression however, in case reports of overdose, QRS widening rarely exceeds 100-120 msec and Is usually transient. 

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