Various treatment options exist for JET but there is no consensus on the best regimen. Treatment is aimed at slowing the ‘JET driven’ heart rate. However, strategies that reduce the JET rate may also reduce the rate of depolarisation of the sinus node, such that restoration of AV synchrony may not be re-established. Reduction in the tachycardia alone can be beneficial as it reduces myocardial workload, but may also allow pacing to restore AV synchrony. Markers of a low cardiac output state - a widening difference between the arterial and venous oxygen saturation, a widening of the central/peripheral temperature difference, and markers of end organ dysfunction (increasing acidosis, lactate) - should be continually monitored.
Analgesia/Sedation
Analgesia and sedation should be considered to minimise global oxygen demand, although judicial use may potentially reduce cardiac output. Despite the tachycardia being driven by a non-physiological ectopic focus, optimising analgesia/sedation will reduce endogenous catecholamine production which in turn will reduce any additional influence that the chronotropic effects may superimpose upon the JET rate. Muscle relaxation should be considered as an adjunct, especially if the desired degree of hypothermia is suspected to induce shivering (see below).
Optimisation of electrolytes and fluids
Hypomagnesaemia, hypokalaemia and hypocalcaemia have been linked with the perioperative onset of JET. (Cardiopulmonary bypass is associated with decreased magnesium levels). Magnesium should be maintained >1.5mmol/L, potassium >4.0mmol/L and ionised calcium >1.2mmol/L. Acidosis and hypovolaemia may contribute to JET although correction with bicarbonate/increased ventilation, or fluid supplementation respectively is not without side effects. Bicarbonate can cause a paradoxical intra-cellular acidosis and imparts a CO2load; increased minute ventilation will induce complex cardiopulmonary interactions and judicious volume supplementation may not be well tolerated by a poorly functioning right ventricle operating at the top of it Starling’s curve/ performance. A red cell transfusion will supplement oxygen carrying capacity.
Modest hypothermia
Modest hypothermia has been shown to reduce the rate of automatic tachycardias such as JET. It also will minimise cellular metabolic activity and may simultaneously reduce endogenous catecholamine release. Although poorly evidenced, titrated degrees of hypothermia may sequentially reduce the JET rate, although there is no correlation between temperature reduction and rate reduction. Antipyretics should be considered, prior to using ice packs, cooling blankets or bladder/gastric irrigation with cold saline. However, hypothermia will increase the systemic vascular resistance which will increase the myocardial stroke work index and may further compromise cardiac output. Shivering will increase cellular metabolic demand. Hypothermia is associated with impaired immunity, impaired healing, deranged coagulation and increased risk of arrhythmias on re-warming. In view of these potential adverse effects, we recommend three target ranges depending upon clinical effectiveness (see flow chart below).
Avoidance of inotropes
The use of inotropic drugs postoperatively is associated with an increased risk of JET due to the increase in cardiac systolic wall stress and heart rate, and may be dose dependent. Dopamine, in particular, has been shown to have a direct arrhythmogenic effect. As far as possible, inotropic support should be kept to a minimum in the immediate postoperative period. In the presence of over-vasodilation from an often co-existing ‘systemic inflammatory response’, the cautious introduction of vasoconstriction may permit a reduction of direct inotropic support. However, this is a potentially dangerous strategy as the dramatically detrimental effects of vasoconstriction causing an elevation in systemic vascular resistance and an increased myocardial workload cannot be overstated.
Antiarrhythmic drugs
All antiarrhythmic drugs are myocardial suppressants. Although many classes of antiarrhythmic drugs have been used in the treatment of JET, amiodarone is widely felt to be the safest and most effective agent. Its mechanism of action is a prolongation of the duration of the action potential and refractory period of all myocardial cells, and non-competitive α- and β-adrenergic inhibition (Vaughan Williams’ class III, and may be considered as having calcium channel blocking and β-blocking effects). However, Amiodarone has potentially serious side effects. It is a negative inotrope, with a slow onset of action and a very long half life. It is also associated with arrhythmias - sinus bradycardia or atrio-ventricular block. Excessive amiodarone can lead to profound bradycardia and has resulted in the need for ECLS. Late sinus bradycardia has been documented following the cessation of amiodarone but is usually transient and easily treated with external pacing. Amiodarone may cause hypothyroidism. We have recently reviewed our experience and usage of amiodarone in Yorkhill to recommend a loading dose of 5mg/kg over 1-4 hours, followed by an infusion of 10 micrograms/kg/min (range 5-15 micrograms/kg/min). In view the potential haemodynamic consequences, the risk:benefit ratio of the need for the loading dose, the rate that this is infused, and the maintenance infusion rate should be agreed by the bedside clinical team (see flow chart).
Esmolol is a short acting beta blocker which reduces the rate of JET by increasing AV block. However, beta blockers may reduce systolic function and esmolol is generally only considered in refractory cases of JET. Its consideration should therefore raise concerns about the need for further support such as ECMO.
Overdrive atrial or atrio-ventricular sequential pacing to restore AV synchrony
Restoration of AV synchrony may be achieved by pacing, higher than the JET rate. Even if the JET rate is successfully reduced by following the proposed algorithm, pacing to restore AV synchrony is still recommended as the addition of atrial systole to ventricular filling will augment the cardiac output. Paradoxically, establishing synchrony may reduce myocardial oxygen consumption even though the external pacing rate will be higher than the therapeutically suppressed JET rate. More contentiously, re-establishing A-V synchrony may protect against further degeneration in cardiac rhythm. Atrial pacing alone may be associated with a long PR interval or even Wenckebach due to the effects of trauma, oedema, drugs and hypothermia on the AV node. This problem will be over-come by ‘AV sequential pacing’ (DDD mode) but results in ventricular pacing with ventricular dysynchrony. The best pacing mode must be determined for the individual patient depending on the presence of AV block and the haemodynamics in each mode.
Extracorporeal life support
JET can be life threatening and all therapeutic strategies may further compromise cardiac output. ECLS has been successfully used in Yorkhill as an artificial haemodynamic support until resolution of the malignant dysrhythmia.
