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Intraoperative bradycardia (heart rate less than 60 beats per minute) is a common but sometimes dire occurrence in anesthesia care when mismanaged. In study published in 1990, bradycardia occurred in 18.9% of 17,201 patients having general anesthesia with volatile drugs. Bradyarrhythmias usually occur from combinations of:
- primary cardiac disease (ischemic heart disease or a new acute problem such as an acute coronary syndrome)
- acute illness (hypovolemia, hypoxemia, metabolic acidosis) or electrolyte disturbances (hypokalemia, hypomagnesaemia)
- surgical (vagal) stimulation
- drugs including beta blockers or fentanyl
The Advanced Cardiac Life Support (ACLS) algorithm for the treatment of symptomatic bradycardia includes the restoration of adequate Airway-Breathing-Circulation (A-B-Cs), followed intravenous atropine, epinephrine, or a pacemaker. When anesthesia professionals ignore the A-B-Cs and utilize non-ACLS medications such as glycopyrrolate or ephedrine to treat life-threatening bradycardia, tragic outcomes can result.
We’ll look at four cases of intraoperative bradycardia management. The first two closed cases illustrate how erroneous treatment of low heart rates led to patient deaths:
Case 1:
A 60-year-old man walks into a hospital for an ERCP (endoscopic retrograde cholangiopancreatography) for gallstones. He has a history of hypertension. His BMI=32. The procedure is performed in the prone position. The anesthesiologist sedates the patient with propofol, fentanyl, and midazolam, without an airway tube. Twenty-five minutes into the procedure, the heart rate drops to 30 beats per minute, the blood pressure drops to 87/50, and the oxygen saturation is 96%. The anesthesiologist treats with 0.4 mg of IV glycopyrrolate (Robinul). Four minutes later, the heart rate is still 53 beats per minute, but the blood pressure has now decreased to 50/25. The patient’s breathing is labored. The anesthesiologist treats with 25 mg of IV ephedrine. Five minutes later, the oxygen saturation and blood pressure are unobtainable, and the heart rate is down to 22 beats per minute. Now twelve minutes after the initial bradycardia, the anesthesiologist at last flips the patient supine, intubates the trachea, injects epinephrine 1 mg IV, and begins CPR/chest compressions. Pulse and blood pressure return, but after the delayed treatment for the abnormal vital signs, the patient suffers permanent anoxic brain damage.
Case 2:
A 50-year-old female walks into a surgery center for an elective cervical spine epidural steroid injection. The procedure is performed in the prone position. The anesthesiologist sedates her with lidocaine 20 mg, propofol total dose 75 mg, fentanyl 100 mcg, and ketamine 25 mg. The injection is done successfully. As the patient is being moved from the operating room table to the gurney and turned supine, the heart rate drops to 35 beats per minute. The blood pressure is unobtainable. The patient is unresponsive. The anesthesiologist treats with 0.4 mg glycopyrrolate and 10 mg of ephedrine IV. Pulses are absent, so CPR/chest compressions are initiated. The patient is intubated. One mg of epinephrine IV is injected 8 minutes after the onset of the bradycardia. The pulses return, and the patient is transferred to the ICU, but she suffers permanent anoxic brain damage and is eventually transferred to a chronic nursing care inpatient facility.
In anesthetic disasters such as these, the duration of brain hypoxia is critical. If something goes wrong during anesthesia and surgery and the flow of oxygen to the brain is cut off, an anesthesia practitioner has about five minutes to treat it. Brain cells start dying within five minutes after the oxygen supply disappears, and brain hypoxia can rapidly cause severe brain damage or death.
In contrast to Cases 1 and 2, Cases 3 and 4 illustrate the successful and appropriate use of glycopyrrolate and ephedrine to manage less significant bradycardias:
Case 3:
A healthy 30-year-old male presents for tonsillectomy. General anesthesia is induced with propofol 250 mg, fentanyl 100 micrograms, and rocuronium 40 mg, and an endotracheal tube is inserted. Five minutes after induction, the heart rate drops to 55 beats per minute (bpm), and the blood pressure falls to 80/50. The anesthesiologist treats with glycopyrrolate 0.2 mg IV. The heart rate rises to 72, and the blood pressure rises to 100/60.
Case 4:
A healthy 44-year-old female presents for laparoscopic cholecystectomy. General anesthesia is induced with propofol 200 mg, fentanyl 100 micrograms, and rocuronium 40 mg, and an endotracheal tube is inserted. Ten minutes after induction, the heart rate drops to 55 beats per minute, and the blood pressure falls to 80/50. The anesthesiologist treats with ephedrine 10 IV. The heart rate rises to 72 and the blood pressure rises to 100/60.
Mild sinus bradycardia (heart rate 50 to 60 bpm) in a stable patient, without hypotension, typically resolves and is inconsequential. Severe sinus bradycardia with hemodynamic instability requires rapid intervention. At times these episodes are symptoms of underlying problems such as myocardial ischemia or hypoxia. In Cases 1 and 2, treatment with glycopyrrolate and ephedrine delayed the appropriate treatments of A-B-C management, atropine, and epinephrine, and preventable adverse outcomes ensued.
The Royal College of Anaesthetists in the United Kingdom studied 24,172 patients having general anesthesia with volatile drugs, and found that:
- Severe bradycardia (heart rate less than 30/minute) occurred in 1 in 450 (0.22%) of all anesthesia cases.
- 155 of 881 intraoperative cardiac arrests (17.6%) had a bradycardia before cardiac arrest.
- Severe bradycardia occurred in 1 in 180 (0.55%) of laparoscopic cases.
- Bradycardia progressing to cardiac arrest during insufflation for gynecological laparoscopy, requiring chest compressions, occurred in about 1 in 4,500 cases.
- 25 cases of bradycardia-associated cardiac arrest occurred during gynecological surgery. The cause was judged as insufflation/pneumoperitoneum in 15 cases (60%), anesthesia drugs in 7 cases (28%) and severe hypoxemia, major hemorrhage, and sick sinus syndrome for one case each.
- Bradycardia caused by vagal stimulation alone and progressing to cardiac arrest is very rare and occurred in about 1 in 50,000 cases. For all cardiac arrests associated with bradycardia, 74% survived to hospital discharge.
The treatment for significant bradycardia is guided by the ACLS ADULT BRADYCARDIA ALGORITHM:
The first priorities are to assure adequate oxygenation and ventilation, i.e. AIRWAY-BREATHING-CARDIAC status (A-B-C). If persistent bradycardia is causing hypotension, the pharmacologic treatment is atropine 1 mg IV, with a repeat dose every 3-5 minutes. Secondary pharmacologic treatment is epinephrine or dopamine IV. If medications fail to return the heart rate to normal, the application of a pacemaker is indicated.
THE STANFORD EMERGENCY MANUAL is available for free on the internet, and lists this algorithm for Bradycardia Heart Rate < 50 in the operating room:
Note the sequence of treatment:
- Confirm adequate oxygenation and ventilation
- Atropine 0.5 – 1 mg IV every 3 minutes
- If atropine ineffective, epinephrine 5 – 10 micrograms IV
- Consider dopamine infusion of 5 – 20 mcg/kg/min
- Consider epinephrine infusion of 0.02 – 0.3 mcg/kg/min
- If stable: consider glycopyrrolate 0.2 – 0.4 mg IV
What’s absent from these bradycardia algorithms for unstable patients?
Glycopyrrolate and ephedrine.
Glycopyrrolate is an anticholinergic drug used by almost no one but anesthesia professionals. According to the PDR (Prescribers’ Digital Reference), glycopyrrolate is indicated “for use as a preoperative antimuscarinic to reduce salivary, tracheobronchial, and pharyngeal secretions; reduce gastric acid production and acidity (aspiration prophylaxis); and to block vagal inhibitory reflexes during intubation and induction of anesthesia,” and “for the treatment of cardiac arrhythmias (e.g., bradycardia) that occur intraoperatively and are drug-induced or are associated with visceral traction stimulation of vagal reflexes.”
Glycopyrrolate should increase heart rate in a stable bradycardic patient. But other than anesthesia providers, no one uses glycopyrrolate to treat bradycardia. In an ACLS protocol, atropine is the anticholinergic drug of choice. Cardiologists, internists, and emergency room doctors use atropine. If an anesthesiologist utilizes glycopyrrolate for an unstable patient and the patient’s bradycardia does not improve and/or the patient suffers a complication, that anesthesiologist is subject to criticism for not following the standard of care for acute symptomatic bradycardia.
In the past, glycopyrrolate was an important anticholinergic anesthetic medication administered along with neostigmine to reverse neuromuscular block. Sugammadex is now a more selective and superior drug for reversing neuromuscular block, and the neostigmine-glycopyrrolate combination is a slower, less reliable alternative—old school pharmacology destined for infrequent use.
Are there advantages of glycopyrrolate over atropine? Not important ones. Some studies show it provides a more stable heart rate and is less likely to cause reflex tachycardia (a temporary, rapid increase in heart rate). Unlike atropine, glycopyrrolate does not cross the blood-brain barrier, so it does not cause CNS-related side effects such as sedation or confusion (however CNS complications are not common with atropine either).
Ephedrine is an indirect catecholamine-releasing drug which works by stimulating the output of endogenous epinephrine and norepinephrine. According to the PDR, ephedrine is indicated “for the treatment of clinically important hypotension occurring in the setting of anesthesia.” Under “mechanism of action” the PDR says, “ephedrine is a sympathomimetic amine that acts directly as an agonist at alpha and beta-adrenergic receptors. It indirectly causes the release of norepinephrine from sympathetic neurons. Ephedrine stimulates heart rate and cardiac output and variably increases peripheral resistance resulting in an increase in blood pressure.”
I was taught—and I teach—that because ephedrine indirectly causes the release of norepinephrine from the body’s sympathetic neurons, it is of little use when the patient is already stressed and releasing maximal endogenous epinephrine and norepinephrine. When a patient is acutely ill, injecting pharmacologic doses of epinephrine, norepinephrine, or dopamine will boost catecholamine tone significantly. Attempting to boost catecholamine tone indirectly by administering ephedrine is relatively impotent in an acutely ill patient with significant bradycardia and hypotension. That’s why ephedrine is not included in either algorithm.
Ephedrine is useful during anesthesia care to treat mild hypotension. It’s not indicated when the patient is acutely ill with severe hypotension.
Do your patients a favor: When severe bradycardia with hypotension occurs, follow established algorithms. Assure oxygenation and ventilation, and if your patient remains unstable, treat urgently with atropine and epinephrine.
When your bradycardic patient is crashing, leave the glycopyrrolate and ephedrine ampules in the drug cart.
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Dear sir, the recent ACLS algorithms recommend 1mg of atropine in case of bradycardia. Please clarify if I’m wrong.
Regards
Dr Barani
Dr. Barani,
You are correct. I listed atropine 1 mg IV in the text of the column, but the ACLS algorithm is now updated to show the correct initial dose of atropine as 1 mg. Thanks.
Rick Novak
I think what is missing is the pre operative evaluation of the patient’s exercise tolerance.My sleeping HR is 30 (at time I ran close to a 4 minute mile), my intraop heart rate dropped to 30 and the anesthesiologist, warned beforehand, did nothing and I recovered from surgery uneventfully.
Congratulations to you on near-4-minute miles! Remarkable.
Low resting heart rates prior to anesthesia are a different issue.
When we anesthesiologists administer drugs like propofol, fentanyl, midazolam, sevoflurane, and/or rocuronium for general anesthesia, and the patient then develops acute drop in heart rate, blood pressure, and oxygen saturation, then emergent ABC treatment, followed by ACLS algorithm treatment, is indicated.
Sugamnadex is not without its problems, including severe bradycardia in high doses. And if you’re a cisatracurium user like I am, and you should be, then Prostigmin/Robinul or Mestinon/Robinul ( or Enlon Plus) are your only options. And Nimbex reverses more easily than Zemuron and statistically causes fewer anaphylactic reactions. So let’s get off this rocuronium kick, okay?
I review cases from across the United States, and I can attest that rocuronium is the most often administered non-depolarizing muscle relaxant.
For most cases over one hour, the initial intubating dose of rocuronium has run out (check nerve stimulator for validation), and neither sugammadex nor neostigmine/Robinul are needed.
So what do you think happened in cases 1 and 2?
In case #1, the patient became unstable with low heart rate, low blood pressure, and then low oxygen saturation. More likely than not, the patient’s breathing became obstructed, and hypoventilation led to the deterioration in vital signs. The necessary treatment was ABCs, including flipping the patient over, intubating the patient, and treating the bradycardia with atropine and then epinephrine if necessary. There was far too much delay in the treatment.
In case #2, the patient may have been hypoxic from hyperventilating. Whatever the cause, the anesthesiologist’s acute treatment once again is ABCs, and if bradycardia persists, the algorithm demands atropine followed by epinephrine if necessary.
Hello, thank you for these interesting cases. A couple of questions for clarity. The doses of ephedrine and glyco seem low given the gravity of the scenarios. Turning off the gas and giving a stronger dose of ephedrine or even epi seems more realistic. My second question is were these anesthesiologists doing their own cases or anesthesiologists supervising CRNA’s? Thank you. Johnathan Edwards MD