Medication Induced Bradycardia

Tags: anesthesia bradycardia labetolol medicine PACU pain

In medicine there is never a playbook about how things are going to unfold and this is especially true when it comes to recovering from surgery and anesthesia. For example, sometimes as nurses we give medications to treat one symptom and unintentionally cause another. G.S. was a perfect example of that.

Table of Contents

Patient Background and Surgical History

G.S. was a 50-year-old male who came to the PACU status-post revision of an AV fistula because of an aneurysm. He was supposed to go home that day but because of an adverse drug reaction he ended up in the ICU overnight. G.S. was not the average patient to begin with; he had some severe chronic blood pressure and kidney issues and was currently awaiting a kidney transplant. The CRNA reported that upon awakening in the OR, G.S. had become so violent that he had caused re-bleeding into the new surgical site and had to be put back to sleep and re-operated on!

Initial PACU Assessment and Vital Signs

G.S. slept for the first 30 minutes after arrival to PACU. His vitals were within normal limits until he woke up and started complaining of pain and his blood pressure began trending upwards. I was told in report that he had high blood pressures during the case requiring medication. His current pressure was 180/91 and his HR 68, so I medicated him as ordered with 10 mg of labetalol IV. The labetalol brought his pressure down nicely but unfortunately after about 30 minutes his heart rate changed abruptly into a sinus bradycardia in the 30s.

Responding to Bradycardia: Interventions and Team Collaboration

Despite his very low heart rate, G.S. was alert and oriented with a stable blood pressure of 110/65. I grabbed atropine to have on hand and called for anesthesia stat. His anesthesiologist was there in minutes and administered him glycopyrrolate 0.2 mg intravenous with no effect. In addition, the anesthesiologist suggested we try atropine 0.5 mg, which I administered, but that also had no effect. The anesthesiologist felt that his heart rate was due to the beta-blocking effect of the labetalol and he stated that he was OK with the patient's heart rate as long as his blood pressure was stable and he remained asymptomatic. An EKG was done showing sinus bradycardia with no ST changes noted. However, as a precaution, a stat cardiology consult was paged out, labs were drawn and sent as ordered by anesthesia, and he was upgraded to ICU status for overnight observation.

Managing Pain Without Compromising Hemodynamics

While waiting for the cardiology consult, G.S. began complaining of a lot of pain. I explained to him that I could not give him narcotics for fear that the medication might drop his blood pressure. I suggested IV Tylenol for pain control to the anesthesiologist and he agreed. The Tylenol was given and it appeared to help G.S.'s pain as he began to drift off to sleep. G.S.'s heart rate was still in the low 30s but his blood pressure remained stable at 105/45.

Escalating Complications: Hypotension and Hyperkalemia

Cardiology returned the page and I briefed them on the patient's status. The plan of care was to continue to monitor the patient and treat with glucagon 1 mg intravenous if he became symptomatic. An EKG was repeated as ordered, with no changes noted. I continued to monitor G.S. closely while he slept. About three hours after G.S.'s initial heart rate went down, I noticed that his blood pressure was now trending downwards to the low 90s mmHg systolic. This made me nervous and although he was still oriented x 3 without any complaints of chest pain, dizziness, or shortness of breath, I knew that it was important to address his blood pressure promptly. Cardiology was made aware and they recommended a 250 mL normal saline bolus, which I initiated immediately, effectively bringing his blood pressure back up above 100 mmHg systolic.

By now G.S.'s lab results were coming back and I was called to the phone for a critical value of potassium 7.7 reported by the laboratory. At this point I was thinking to myself, "What else could possibly go wrong?" To answer my own question, G.S. started complaining of nausea and began vomiting. Once more I jumped into action and medicated G.S. for nausea with Zofran from the standing PACU orders and then notified the cardiologist of the critical potassium level.

Treating Hyperkalemia and Coordinating Nephrology

Cardiology gave me orders and I began the treatment for high potassium, which included albuterol nebulizer 10 mg, insulin 10 units intravenous, and calcium gluconate 1 gram intravenous (dextrose was not ordered because his bedside glucose was 250). Given G.S.'s pre-existing renal complications, managing his electrolyte imbalance was especially critical.

Nephrology was consulted at the request of cardiology and I spoke to the on-call nephrologist who made plans to dialyze the patient that night. Thankfully, G.S.'s nausea improved rapidly with the Zofran and his blood pressure was remaining stable above 110 mmHg systolic. With a ready ICU bed and his hyperkalemia treatment underway, I was finally ready to transport G.S. to the ICU after five hours of intense observation and nursing care in the PACU.

Patient Outcome and Nursing Takeaways

By the time I delivered G.S. to the ICU, his nausea was resolved, his heart rate was trending up into the 50s, and his pain was under control. This case highlights how critical thinking and rapid assessment are essential when managing unexpected adverse drug reactions.

Although the administration of labetalol unintentionally caused G.S.'s extreme bradycardia, with keen observation and good nursing care I was able to help G.S. get through that medication complication safely. Nurses working in post-anesthesia care settings must always be prepared for the unexpected, including medication-induced complications that require swift, multi-disciplinary intervention. He was dialyzed in the ICU overnight, and discharged home the next day without any further complications.