A rapid response event was initiated by the bedside nurse for a patient with new-onset fatigue, lightheadedness, and substernal pain at rest. On prompt arrival of the rapid response team, the patient’s telemetry showed that he was gradually getting bradycardic to 50-60 beats per min (bpm). He was a 70-year-old male with a known history of coronary artery disease, hyperlipidemia, type 2 diabetes, and hypertension. He was admitted earlier for a syncopal event that was currently being evaluated.
Temperature: 98.2 °F, axillary
Blood Pressure: 100/52 mmHg
Heart Rate: 51 bpm – regular rhythm ( Fig. 10.1 )
Respiratory Rate: 22 breaths per min
Pulse Oximetry: 94% oxygen saturation on room air
Focused Physical Examination
The patient was an elderly male in moderate distress, altered, pale, and diaphoretic grabbing the center of his chest. Appropriate personal protective equipment was established, and the patient was examined. A cardiac exam showed normal heart sounds with no murmurs. He had an elevated jugular vein distention. His lung exam showed minimal bibasilar crackles. His abdomen was soft, non-tender, and non-distended. His extremities were warm to the touch, and no peripheral edema was noted. Capillary refill was <2 s.
A cardiac monitor and pacing pads were attached immediately to the patient. Then, a 1000 mL of normal saline fluid bolus was started. One dose of 2 mg IV morphine was administered because of severe pain. A stat electrocardiogram (EKG) was obtained, which showed sinus bradycardia with elevated ST segments in leads II, III, and aVF concerning for an inferior wall myocardial infarction. A stat page was sent to interventional cardiology for review of the EKG. Troponin levels, complete blood count, comprehensive metabolic panel, and lactate level were obtained. The patient’s hemodynamics deteriorated during the rapid response event, and his heart rate dropped to the mid-30s, with blood pressure dropping to 82/50 mmHg. Atropine 0.5 mg was administered per advanced cardiac life support (ACLS) protocol, and transcutaneous pacing was initiated, which improved the BP to 102/59 mmHg. Cardiology was consulted, and the patient was immediately sent to the cardiac catheterization lab for possible percutaneous coronary intervention and from there to the intensive care unit for further care.
Second-degree atrioventricular (AV) block in the setting of inferior myocardial infarction.
Bradycardia – Heart Block After Myocardial Infarction
The cardiac conduction system is discussed in detail in Chapter 9 . The sinoatrial (SA) node is the cardiac pacemaker, and following atrial activation, the electrical impulse reaches the AV node. The AV nodal depolarization is mediated by a slow calcium-mediated action potential which slows down the conduction speed. The impulse passes to the Bundle of His and then to the ventricles through the right and left bundle branches from the AV node. In the setting of myocardial infarction, certain parts of electrical conduction systems get ischemic ( Table 10.1 ). The right coronary artery is the source of the blood supply to both the SA and AV nodes. Occlusion of this artery would cause ischemia and dysfunction of both these critical checkpoints in the cardiac impulse pathway. This AV nodal dysfunction is exacerbated by the enhanced release of acetylcholine from the inferoposterior myocardium in the setting of ischemia, which can result in the progression of bradycardia to heart block.
|Segment of the conduction pathway||Blood supply|
|SA Node||60% by the right coronary artery; 40% by left circumflex artery|
|AV Node||90% by the right coronary artery; 10% by the left circumflex artery|
|His Bundle||Right coronary artery (AV nodal branch)|
|Main Left Bundle Branch||Left anterior descending artery with some collateral flow from the right coronary artery or left circumflex artery|
|Left Posterior Fascicle||AV nodal branch and septal branches of the left anterior descending artery|
|Left Anterior Fascicle||Left anterior descending artery with some contribution from right coronary artery and left circumflex artery|
|Right Bundle Branch||Septal perforators from the left anterior descending artery with some contribution from right coronary artery and left circumflex artery|
Definition and Diagnosis
Bradycardia is defined as a resting heart rate <60bpm. This heart rate can be asymptomatic if adequate compensatory mechanisms are present. However, in the absence of adequate compensatory mechanisms, it can produce lightheadedness, syncope, exertional intolerance, dyspnea, and fatigue. Bradycardia may be pathologic or physiologic (details available in Chapter 9 ). Bradycardia is one of the most common arrhythmic complications of inferior wall myocardial infarction ( Table 10.2 ). It is crucial to differentiate the transient events from those likely to progress to irreversible or high-degree AV block.