The Refractory Period in Cardiac Physiology

Scenario: After surviving a sudden cardiac arrest at home, a 68-year-old man was admitted to the cardiac intensive care unit (ICU). Pertinent history includes hypertension, atrial fibrillation (AF), and nonischemic heart failure with a functional ejection fraction of 35%. The patient was intubated in the field, and mechanical ventilation was started upon his hospital arrival. The initial level of high-sensitivity troponin T was 0.31 ng/L (normal <14 ng/L). It was decided to stabilize him before taking him to the cardiac catheterization laboratory to assess coronary perfusion to rule out myocardial ischemia as a cause of the cardiac arrest. The nurses noted that the patient had frequent premature ventricular contractions (PVCs) during monitoring. Shown below are 2 separate rhythm strips in leads II and V1 with an accompanying arterial blood pressure waveform. Panel A was recorded approximately 3 minutes before panel B. Panel B was recorded 15 hours after ICU admission.Panel A: Atrial fibrillation with 1 PVC associated with a dampened arterial blood pressure waveform. Panel B: Atrial fibrillation that deteriorates into VF after a PVC occurs close to the end of the T wave; there is an immediate loss of arterial blood pressure. Possible prior septal wall myocardial infarction based on qR pattern in V1 and changes in ST-T wave in both leads suggestive of acute myocardial ischemia.The cardiac cycle is made up of both an absolute and a relative refractory period. This period represents the end of the cardiac cycle and is when potassium and sodium are shifting back into (potassium) and out of (sodium) the cardiac cells as the heart prepares for another cycle. During the absolute refractory period (early to mid T wave) a premature beat cannot elicit another beat because the cardiac cells have not fully recovered. This is an important protective mechanism in normal physiologic conduction. In panel A, the PVC occurs well after the end of the T wave.However, during the relative refectory period (mid to end of the T wave), because the cardiac cells are "hyperpolarized," a premature beat of sufficient stimuli can initiate depolarization. Unlike the absolute refractory period, the relative refractory period is a vulnerable part of the cardiac cycle, thus, a PVC (or pacemaker impulse) during this part of the cardiac cycle sets the stage for a reentry mechanism that can lead to ventricular tachycardia (VT) and/or VF. In patients with AF, rapid and irregular ventricular activation is hypothesized to create conditions that might enable the occurrence of VT/VF when an R-on-T type PVC occurs. In panel B, an R-on-T type PVC (best seen in lead II) occurs in the relative refectory period that initiates VF. R-on-T type PVCs were first described by Smirk in 1949. Patients are more susceptible to ventricular arrhythmias when acute ischemia is present and/or they have had a prior myocardial infarction. Both are potential factors in this scenario and may have been the cause of the cardiac arrest at home.The code team should be called immediately, followed by advanced cardiac life support. Atrial fibrillation is one of the most common supraventricular arrythmias, affecting 1% to 2% of the population; however, the association of AF and lethal ventricular arrythmias is not entirely clear. Patients in the ICU are vulnerable to proarrhythmic conditions, such as electrolyte imbalance and QT-prolonging drugs and treatments (eg, ventilatory support, total parenteral nutrition, and diuretics), making R-on-T PVCs a concern. These factors should be assessed carefully and treated as indicated. Patients with hypertension and heart failure often have AF and frequent PVCs, which may place them at higher risk for R-on-T events, especially when proarrhythmic factors are present; thus, continuous ECG monitoring should be maintained. The patient was successfully resuscitated but died 2 days later following a complex clinical course.