Complications
Beta-blockers may cause bronchospasm. They should be avoided in patients with known asthma or history of lung disease with prominent history of wheezing.
Demand ischaemia can result from poor rate control.
Patients usually have paroxysmal to persistent atrial flutter with risk factors to thromboembolic events, such as left atrial dilation, congestive heart failure, hypertension, diabetes, hyperlipidaemia, and advanced age.
Controversy exists as regards treatment of established embolic acute stroke in the presence of acute atrial flutter. Anticoagulation in this setting may cause haemorrhagic stroke. Consultation with specialist (neurologist) is highly recommended. Novel approaches to interrupt thrombus propagation by intravascular devices are being studied.
Secondary to atrioventricular (AV) nodal blocking effects of beta-blockers and calcium-channel blockers.
Can occur due to profound effects on the AV node while in atrial flutter or to the effects on the sinus node when in sinus rhythm, particularly in patients with underlying sinus node dysfunction.
Can occur with anti-arrhythmic drugs (e.g., flecainide or amiodarone) as well.
May require changing drug, or adding permanent pacing.
Secondary to the vasodilatory effects of beta-blockers and calcium-channel blockers, as well as the atrioventricular (AV) nodal effects slowing the heart rate.
If this occurs, may resolve with lowering the dosage.
Other causes of hypotension should also be explored.
If the strategy was rate control only, consider AV nodal ablation for rate control; can also reconsider rhythm control in some patients.
Due to the negative inotropic effects of beta-blockers and calcium-channel blockers, as well as some anti-arrhythmic drugs.
These drugs should be used cautiously in patients with poor left ventricular function and not at all in patients with overt clinical heart failure until the heart failure is treated and compensated.
If heart rate control or rhythm control is the goal, amiodarone can be used to afford rate control or rhythm control with little depression of contractility.
Optimisation of heart failure regimen is also helpful.
May take many forms depending on the type and drug used. The most dangerous is ventricular arrhythmias such as ventricular tachycardia or torsades de pointes. Occurs with anti-arrhythmic drugs that prolong the QT or with drugs that prolong conduction in patients with underlying coronary disease.
Amiodarone contains iodine.
Elevated thyroid-stimulating hormone and hypothyroidism more common than hyperthyroidism unless the patient has a predilection to hyperthyroidism or a previous goiter.
Can replace thyroid hormone orally for hypothyroidism but usually need to discontinue the drug if hyperthyroid and treat the symptoms of hyperthyroidism.
Complications vary with the technique and experience, and some have decreased with modification of ablation strategies. However, ablation for atrial flutter is generally quite safe.[46][47]
May include pneumothorax (0.2%), atrioventricular (AV) fistulae, haematomas (<0.3%), congestive heart failure exacerbation (<0.1%), cerebrovascular events (0% to 4%), pericardial effusion usually uncomplicated (25%), pericardial tamponade (1%), organized atrial tachyarrhythmias (13%), AV block (<1%), need for a pacemaker (<0.2%), and pulmonary embolus (<1%). Procedure-related death is extremely rare (estimated at 0.03%).[46]
Most complications are handled acutely.
From poor rate control and loss of active atrial contraction, a cardiomyopathy can result and support the need for rhythm conversion.
Acute toxicity presents as acute respiratory distress syndrome within hours of giving amiodarone.
The long-term toxicity causes inflammation and/or fibrosis.
Symptoms of an unexplained cough or dyspnoea should trigger investigation with a chest x-ray and pulmonary function tests (PFTs) with a diffusion capacity.
PFTs should be considered as routine follow-up every 6 to 12 months while using the drug.
Will require discontinuation of the drug in most cases.
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