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The top of the adult range is the end that tracks with harm: in the VISION cohort a maximum intraoperative heart rate above 100 beats per minute was associated with myocardial injury, myocardial infarction and 30-day mortality, and a separate cohort analysis found the definition of intraoperative tachycardia with the strongest predictive power for death and infarction was a heart rate of at least 100 sustained for at least 30 minutes.
The bottom of the range is far less frightening than residents expect — in the same VISION analysis a minimum intraoperative heart rate below 55 beats per minute was associated with less myocardial injury and lower mortality, and a retrospective analysis of time spent above 90 beats per minute found no association with myocardial injury at all, so a slow rate with a good pressure is a number to explain rather than a number to chase.
Most intraoperative bradycardia in a healthy adult is drug or reflex rather than disease: in a multivariable analysis of adult surgical records the strongest predictor was the absence of anticholinergic premedication, with propofol induction and neuraxial blockade adding risk, and neostigmine-glycopyrrolate reversal is itself a dose-dependent cause of both bradycardia and tachycardia in the same patient.
Glycopyrrolate and atropine both raise heart rate, but glycopyrrolate protects better against neostigmine-induced bradycardia while producing less initial tachycardia, fewer arrhythmias and less junctional rhythm, whereas intravenous atropine produces the more marked and more immediate tachycardia — which is why glycopyrrolate is the routine partner for neostigmine and atropine is what you reach for when you need rate right now.
Esmolol is a cardioselective beta-1 blocker with rapid onset and a short duration of action, which is exactly why it suits a heart rate you want under control within minutes and are willing to hand back afterwards; its main tolerability cost is hypotension, and that hypotension is itself rapidly reversible.
Labetalol antagonises alpha-1 as well as beta-1 and beta-2 receptors, so it lowers blood pressure and peripheral resistance with a less pronounced fall in heart rate than a pure beta-blocker, while metoprolol is the longer-acting beta-1 choice — and POISE is the reason nobody starts a beta-blocker on the morning of surgery, because extended-release metoprolol cut myocardial infarction from 5.7% to 4.2% but raised stroke from 0.5% to 1.0% and death from 2.3% to 3.1%.
The heart rate moved and the blood pressure did not — what does that combination tell you that either number alone does not?
Before you treat this rate, what have you actually excluded: light anaesthesia, hypovolaemia, pain, hypercarbia, fever, the surgeon pulling on something?
How long do you want this effect to last? Now pick the drug whose duration matches that answer.
If you slow this heart and the blood pressure follows it down, what is your next move — and do you have it drawn up?