A rapid response event was initiated by the bedside nurse for new-onset hypotension and bradycardia. On prompt arrival of the rapid response team, it was noted that the patient was a 65-year-old male with a known history of atrial fibrillation treated with oral metoprolol, who was admitted to the hospital two days before for evaluation and management of uncontrolled tachycardia. The patient had been treated initially with a diltiazem infusion which was later transitioned to oral extended-release formulation earlier in the day. The patient continued to receive his home metoprolol during this hospitalization.
Temperature: 99.6 °F, axillary
Blood Pressure: 70 mmHg palpable systolic, diastolic not obtainable
Heart Rate: 47 beats per min (bpm) – sinus bradycardia on telemetry ( Fig. 9.1 )
Respiratory Rate: 22 breaths per min
Pulse Oximetry: 97% oxygen saturation on room air
Focused Physical Examination
The patient was a middle-aged man lying in bed in no apparent distress. Appropriate personal protective equipment was established, and the patient was examined. The patient was lethargic and would not respond to any verbal commands. However, he would move all four extremities to painful stimuli. His carotid pulse was weak but palpable. His focused cardiac exam showed inaudible heart sounds. Jugular venous distension was not appreciated. His lung and abdominal exams were benign.
A cardiac monitor with transcutaneous pacer pads was attached immediately. The monitor showed sinus bradycardia. A 1000 mL bolus of normal saline was started. A stat dose of 0.5 mg atropine was administered without any improvement in heart rate. Two more doses of 0.5 mg atropine were administered without any response. Stat dose of 2 g IV calcium chloride was administered with resultant improvement in heart rate to 50 bpm. Repeat blood pressure check showed improvement to 84/58 mmHg. Stat electrocardiogram (EKG) was obtained, which showed sinus bradycardia without any ST changes suspicious of acute ischemia. The patient’s mental status also improved with these interventions. Stat labs, including complete blood count, basic metabolic panel, magnesium, troponin, and lactate level, were sent and were all within normal limits. The patient was started on a calcium infusion and transferred to the intensive care unit (ICU) for further management.
Bradycardia because of significant atrioventricular (AV) nodal blockade
Cardiac rhythm is initiated and maintained by the sinoatrial (SA) node, and the electrical impulse generated here passes through the atria to the AV node. AV node is the rate-limiting step in the cardiac conduction pathway and is the major physiological and pharmacological rate control site. The impulse passes from the AV node to the Bundle of His, which lies in the interventricular septum. The electrical pathway splits into right and left bundles that depolarize the two ventricles simultaneously ( Fig. 9.2 ). All the foci in the cardiac conduction pathway can serve as pacemakers for the heart; however, the rate at which they generate the electrical impulses differs. The intrinsic firing rate of the SA node is 60-100 bpm which overrides the much slower atrial foci (60-80 bpm), junctional foci (40-60 bpm), and the ventricular foci (20-40 bpm). Defects in the SA node will allow the next pacemaker with the highest firing rate to take over.
Definition and Diagnosis
Bradycardia is defined as a resting heart rate of <60 bpm in adults. Moreover, 49% of symptomatic bradycardia is caused by disturbances of automaticity/conduction, with the remaining caused by reversible causes. See Table 9.1 for various etiologies of bradycardia.
|Etiology of bradycardia|