There may a 1:1 relationship between atria and ventricular activity with a short RP interval, or atrioventricular dissociation with slower atrial than ventricular rates if the AV node is unable to conduct from the ventricles to the atria.The differential diagnosis of JET includes other forms of supraventricular tachycardia, most commonly atrioventricular nodal reentrant tachycardia (AVNRT). These can be distinguished using adenosine. The response to adenosine in JET is a temporary loss of conduction to the atria leading to continuation of the tachycardia but with atrioventricular dissociation. In contrast, administration of adenosine in AVNRT will usually terminate the arrhythmia. The diagnosis can be conclusively proven by performing an invasive electrophysiological study. Treatment
Treatment is aimed at slowing the rate by correcting acidosis, correcting electrolytes (especially magnesium and calcium), cooling the patient, and antiarrhythmic medications. Occasionally pacing of the atrium at a rate higher than the JET may allow improved cardiac function by allowing atrial and ventricular synchrony.Medications used to treat JET include beta-adrenoceptor blockers such as propranolol,  calcium channel antagonists such as verapamil, and antiarrhythmics such as flecainide, amiodarone, and propafenone. Amiodarone is frequently used in the short term in children experiencing JET following heart surgery, although propanolol, flecainide and propafenone are more commonly recommended for long term use due to the frequency of side effects associated with amiodarone.In those who experience recurrent episodes of JET, an alternative to long term medical therapy is catheter ablation.
Using treatments for other kinds of pulmonary hypertension in patients with these conditions can harm the patient and wastes substantial medical resources.High-dose calcium channel blockers are useful in only 5% of IPAH patients who are vasoreactive by Swan-Ganz catheter. Unfortunately, calcium channel blockers have been largely misused, being prescribed to many patients with non-vasoreactive PAH, leading to excess morbidity and mortality. The criteria for vasoreactivity have changed. Only those patients whose mean pulmonary artery pressure falls by more than 10 mm Hg to less than 40 mm Hg with an unchanged or increased cardiac output when challenged with adenosine, epoprostenol, or nitric oxide are considered vasoreactive. Of these, only half of the patients are responsive to calcium channel blockers in the long term.A number of agents have recently been introduced for primary and secondary PAH. The trials supporting the use of these agents have been relatively small, and the only measure consistently used to compare their effectivity is the "six-minute walk test". Many have no data on mortality benefit or time to progression. Vasoactive substances
Many pathways are involved in the abnormal proliferation and contraction of the smooth muscle cells of the pulmonary arteries in patients with pulmonary arterial hypertension. Three of these pathways are important since they have been targeted with drugs — endothelin receptor antagonists, phosphodiesterase type 5 (PDE-5) inhibitors, and prostacyclin derivatives. Prostaglandins
Prostacyclin (prostaglandin I2) is commonly considered the most effective treatment for PAH. Epoprostenol (synthetic prostacyclin) is given via continuous infusion that requires a semi-permanent central venous catheter.