Sinus node dysfunction: decreased automaticity due to age, drugs, etc.
AV block: either in the AV node or His–Purkinje system due to age, ischemia, drugs, infections.
Tachyarrhythmias:
Increased automaticity: such as paroxysmal atrial tachycardia (AT) or multifocal atrial tachycardia (MAT).
Triggered activity: such as torsade des pointes or digoxin toxicity.
Re‐entry: most common cause of clinically significant tachycardias, e.g. atrioventricular nodal re‐entrant tachycardia (AVNRT), atrioventricular re‐entrant tachycardia (AVRT), atrial flutter (AFl), ventricular tachycardia (VT).
Predictive/risk factors
Age >70 years old.
Male gender.
APACHE score >25.
Underlying disease (cardiac/pulmonary/thyroid).
Metabolic derangement.
Volume fluctuations.
Electrolyte disturbances.
Vasopressors.
Prevention
Diagnosis
Although clinical history and laboratory tests are helpful, diagnosis is mainly based on ECG findings. Some common arrhythmias are defined below.
Sinus node dysfunction: characterized by sinus bradycardia, sinus arrest, or pauses.
Second degree AV block, Mobitz I (Wenckebach): there is a progressive lengthening of the PR interval until a P wave is not conducted. There is only one non‐conducted P wave. It is a result of delay within the AV node and is usually benign.
Second degree AV block, Mobitz II: characterized by episodic and unpredictable failure of the His–Purkinje pathway to conduct the impulse from the atria to the ventricles. There is no change in the PR interval prior to or after the non‐conducted P wave. Usually symptomatic and indicative of underlying disease of the His–Purkinje system, with high rates of progression to complete AV block.
Complete AV block: this presents with AV dissociation – variable PR intervals – and an escape rhythm that is either junctional or ventricular and with a slower rate than atrial rhythm (Figure 15.1). This is produced due to a complete failure of the AV node to conduct any impulses from the atria to the ventricles.
Atrial fibrillation (AF): there are no distinct P waves (atrial activity can be usually seen, however it is not regular and occurs at rates >300 bpm). The RR intervals follow no repetitive pattern (‘ventricular response irregularly irregular’).
Supraventricular tachycardia (SVT): regular narrow complex rhythms at rates of 140–220 bpm. P (antegrade or retrograde) wave can be often seen, particularly in inferior leads and V1 (Figure 15.2).
Monomorphic ventricular tachycardia (VT): regular wide QRS tachycardia with QRS morphology inconsistent with aberrancy (Figure 15.3). Other features that can be seen include AV dissociation, capture beats (normal conduction system has momentarily conducted one sinus beat, in the midst of AV dissociation, to produce a QRS complex of normal duration), fusion beats (combination beats that result when sinus and ventricular complexes simultaneously activate the ventricular myocardium creating a hybrid complex), and positive or negative concordance throughout the precordial leads.
Polymorphic VT: regular wide QRS tachycardia with frequent variations of the QRS axis, morphology, or both (Figure 15.4). Torsade des pointes (‘twisting around points’) is a subtype in which these variations take the form of a progressive, sinusoidal, cyclic alteration of the QRS axis. The peaks of the QRS complexes appear to ‘twist’ around the isoelectric line.
MAT: P waves can be seen (at least three different morphologies) AFl: underlying sawtooth waves
Narrow QRS tachycardias
AVNRT/AVRT AT/MAT Common AFl Atrial fibrillation (AF)
AVNRT/AVRT: breaks with adenosine AT/AFl: slow down with adenosine, but do not break. Sawtooth waves in AFl AF: irregular, no P waves
Wide QRS tachycardias
VT SVT with aberrance AF + WPW
VT: underlying heart disease. Dissociation P‐QRS, captures/fusions. Precordial concordance SVT: breaks with adenosine. Baseline bundle branch block. Similar morphology/axis ECG baseline and tachycardia AF + WPW: irregular ventricular response, variation of QRS widening
Typical presentation
The onset of all tachyarrhythmias is abrupt except sinus tachycardia, which is gradual. Symptoms can be palpitations, shortness of breath, dizziness, or chest pain – although underlying conditions may be driving these.
Bradyarrhythmias: symptoms range from asymptomatic to dizziness or pre‐syncopal or syncopal spells. There is shortness of breath from low cardiac output or worsening heart failure.
Clinical diagnosis
History
Diagnosis of arrhythmia is based mainly on the ECG. However, some features of the clinical history can be key:
Pulmonary disease and cardiovascular risk factors are often associated with AF and atrial arrhythmias.
AVNRTs/AVRTs are more typical in patients under 40 years old.
A wide QRS tachycardia should be considered VT unless otherwise proven. VT should be suspected in patients with ventricular dysfunction, structural or valvular heart disease, myocardial scar due to a prior myocardial infarction, and in the post‐infarct patient.
Polymorphic VT associated with a normal QT interval is more typical in the setting of acute myocardial ischemia. When associated with an acquired prolonged QT, drugs or magnesium depletion (as in cases of torsade des pointes) are underlying causes.
Physical examination
In the ICU setting, this should focus on signs of hemodynamic compromise, which may require urgent cardioversion.
In wide QRS tachycardia, signs of underlying cardiomyopathy (cardiomegaly, diastolic or significant systolic murmur, abnormal findings in the ECG such as bundle branch block or abnormal repolarization) make the diagnosis of VT highly probable.
In wide QRS tachycardia, a pounding sensation in the neck is more often related to AVNRT. This finding is produced due to simultaneous contraction of the atrium and ventricle – when the AV valve is closed – that propels venous flow backwards.
Useful clinical decision rules and calculators
The ECG criteria for VT diagnosis are:
Absence of typical right or left bundle branch block (RBBB/LBBB) morphology.
Extreme axis deviation (‘northwest axis’): QRS is positive in aVR and negative in I and aVF.
Very broad complexes: ≥160 milliseconds in LBBB morphology and ≥140 milliseconds in RBBB morphology.
AV dissociation: variable PR interval with P and QRS complexes at different rates; this is highly specific.
Capture/fusion beats.
Positive or negative concordance throughout the precordial leads.
Brugada’s sign: the distance from the onset of the QRS complex to the nadir of the S wave is >100 milliseconds.
Josephson’s sign: notching near the nadir of the S wave.
RSR complexes with a taller ‘left rabbit ear’: this is the most specific finding in favor of VT. This is in contrast to RBBB, where the right rabbit ear is taller.
Laboratory diagnosis
List of diagnostic tests
Potassium has a pronounced effect on both conduction and automaticity, with even small variations of its concentration. Consequently, of all the electrolytes, disturbed potassium metabolism accounts for the vast majority of clinical arrhythmias (e.g complete AV block, VF).
Calcium, magnesium, and sodium affect the action potential and induce experimental arrhythmias (MAT or torsade des pointes, in case of magnesium) but at concentrations which are unphysiologic.
Concentration of digoxin should be monitored, especially in patients with depressed renal function.
Imaging modalities
Transthoracic echocardiogram should be performed in patients with unexplained ventricular arrhythmias in order to rule out structural heart disease. Urgent echocardiogram should be performed in case of sudden hemodynamic worsening or uncontrolled arrhythmias.
Algorithm 15.2Diagnostic algorithm for narrow QRS tachycardia
(Adapted from Tracy & Boushahri 2014)
Algorithm 15.3Diagnostic algorithm for wide QRS tachycardia
(Adapted from Tracy & Boushahri 2014)
Potential pitfalls/common errors made regarding diagnosis of disease
A wide complex tachycardia of ventricular origin can be misdiagnosed as SVT with aberrant conduction. Administration of verapamil in cases of diagnostic uncertainty may result in profound hemodynamic deterioration.
Atrial flutter with a variable degree of AV block and MAT are often misdiagnosed as AF. This usually happens because the ECG shows irregular ventricular response and this is automatically taken as AF.
Treatment
Treatment rationale
Bradyarrhythmias
Treat any reversible causes. When causing significant hemodynamic compromise:
Acute treatment with one of the following:
Atropine: 0.5 mg IV, repeated if necessary every 3–5 minutes to a total dose of 3 mg. This is more effective in sinus node dysfunction or in block at the level of the AV node. It is unlikely to be effective when block is at or below the bundle of His, or in transplanted hearts (lack vagal innervation).
Isoprenaline: 10–20 μg IV, repeated according to clinical response, followed by an infusion at 1–4 μg/min.
Do not delay treatment with transcutaneous pacing or a chronotropic agent in order to give atropine/isoprenaline. If these agents are ineffective, consider temporary pacing.
If pacing is delayed or not available, start infusion of one of the following:
Dopamine: 2–10 μg/kg/min, titrated according to clinical response.
Epinephrine: 2–10 μg/min, titrated according to clinical response.
In the presence of bradycardia and hemodynamic compromise, look for myocardial infarction or poor ventricular function.
Tachyarrhythmias
Severe hemodynamic compromise induced by any tachyarrhythmia should be treated with emergent electric DC cardioversion.
Sedation is indicated when tolerated.
Synchronize shocks with the QRS complex except in cases of cardiac arrest due to VF. Biphasic waveform (100–200 J energy) is preferable than monophasic (200–400 J). Pads placed anterior to posterior provide greater efficacy.
Atrial fibrillation
Reversion to sinus rhythm
Electric DC cardioversion: as previously indicated.
Pharmacologic cardioversion: within 48 hours after onset in clinically and hemodynamically stable patients.
Ibutilide: more effective but not specifically tested in ICU population:
Patient <60 kg: 0.01 mg/kg IV over 10 minutes.
Patient >60 kg: 1 mg IV over 10 minutes.
May repeat once if arrhythmia does not terminate.
Amiodarone: offers a safer profile: 150 mg IV over 10 minutes, then IV drip 1 mg/min for 6 hours followed by 0.5 mg/min for 19 hours (total 1 g over 24 hours).
Heart rate control
If onset >48 hours ago or in stable patients in whom conversion to sinus rhythm is hardly expected while underlying process is still active (postoperative, sepsis, etc.).
Beta‐blockers as first line:
Metoprolol: 2.5–5.0 mg IV bolus over 2 minutes, up to three doses.
Esmolol: 500 μg/kg IV bolus over 1 minute, then 50–300 μg/kg/min IV.
Calcium‐channel blockers are a good alternative, but must be avoided if pre‐excited AF, heart failure, and reduced ejection fraction:
Verapamil: 0.075–0.15 mg/kg IV bolus over 2 minutes, may give an additional 10.0 mg after30 minutes if no response, then 0.005 mg/kg/min infusion.
Diltiazem: 0.25 mg/kg IV bolus over 2 minutes, then 5–15 mg/h.
Amidarone, a suitable alternative when previous drugs are not tolerated: 300 mg IV over 1 hour, then 10–50 mg/h over 24 hours.
Digoxin: onset of action >1 hour. Use with caution if there is decreased renal function. Use one of the following doses:
0.25 mg IV every 2 hours (up to 1.5 mg in 24 hours).
0.5 mg IV bolus + 0.25 mg IV every 3–4 hours (up to 1.5 mg in 24 hours).
AVNRT/AVRT
Perform vagal‐enhancing maneuvers as first step.
If ineffective, use adenosine: 6 mg IV over 1–3 seconds (may be given IO) followed by rapid flush with 20 mL of saline. If no conversion within 1–2 minutes give 12 mg IV, repeat a second time if necessary (30 mg total; dose should be reduced by 50% when injected through a central venous catheter).
Verapamil and diltiazem (dose regimen as previously described) are also very effective, but adenosine is faster and produces less depression of cardiac function. Use verapamil/diltiazem with caution in case of pre‐excitation as they may accelerate ventricular rate. In patients hemodynamically compromised, amiodarone may be an option.
Atrial tachycardia/MAT
Discontinuation/correction of predisposing factors can be effective itself (mainly electrolyte disturbances in MAT). In case it is not, drugs for heart rate control such as metoprolol or verapamil have been demonstrated to be effective (dose regimen as previously described).
Monomorphic VT
Amiodarone as first line: 150 mg IV over 10 minutes, may repeat every 10 minutes as needed; then IV drip 1 mg/min for 6 hours followed by 0.5 mg/min for 18 hours (maximum cumulative dose 2.2 g over 24 hours).
Lidocaine: more effective in the setting of an acute coronary event: 1–1.5 mg/kg IV, may repeat 0.5–0.75 mg/kg every 5–10 minutes (maximum cumulative dose 3 mg/kg); then IV drip 1–4 mg/min.
Procainamide (but not indicated if QT is prolonged): 15–18 mg/kg over 25–30 minutes or 100 mg given no faster than 50 mg/min, may repeat every 5 minutes (maximum cumulative dose 1 g); then IV drip 1–4 mg/min.
Sotalol (but watch for proarrhythmic effect): 1–1.5 mg/kg (or 100 mg) at a rate of 10–20 mg/min.
Polymorphic VT
Intravenous magnesium can be useful as first step:
Magnesium: 2 g IV over 5–30 minutes, and repeat this dose 10 minutes later if needed. Follow with a continuous infusion of 1 g/h for the next 6 hours.
When QT interval is normal, look for myocardial ischemia.
When QT interval is prolonged (torsade des pointes), correct precipitant factors such as electrolytes or drugs. Ventricular pacing or isoproterenol can be also effective, as QT interval shortens as heart rate rises.
Recurrent VT/VF–electrical storm
Correct the underlying and reversible causes as first step. The most useful drugs in an electrical storm are amiodarone and beta‐blockers. Ventricular pacing or isoproterenol can be useful in cases of channelopathy. In case of VF, DC shock (not synchronized, maximum energy) is the treatment.
Prevention/management of complications
Do not attempt DC cardioversion in the setting of uncorrected hypokalemia or digoxin toxicity (risk of developing resistant VF).
Calcium‐channel blockers: cardiac depression and hypotension. Vasopressors may be required.
Digoxin toxicity (complete AV block, joint tachycardia): in general, effects disappear completely in 2–3 days after digoxin is stopped. In the meantime, transvenous temporary pacing may be required. In extreme cases in which immediate neutralization of digoxin effect is needed, antidigoxin antibodies may be useful.
Adenosine: contraindicated in patients with asthma due to bronchospasm induction. Bronchodilators may be required.
Calcium‐channel blockers, digoxin, and adenosine: may accelerate ventricular rate in pre‐excitation as they shorten the refractory anterograde period of the pathway. Emergent defibrillation or DC cardioversion may be required.
