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AI-Generated response:

What are some alternatives to external pacing in a bradycardic patient?

Answer generated on June 4, 2024

The AI-generated responses are for illustration purposes only and should not be used for medical purposes.

Alternatives to external pacing in a bradycardic patient include pharmacological agents such as atropine, dopamine, and isoproterenol, as well as advanced pacing techniques like biventricular pacing or His bundle pacing.

It is important to note that isoproterenol should be avoided in cases of coronary ischemia due to its potential to increase myocardial oxygen demand while decreasing coronary perfusion.[1-2]

  • Atropine can be administered intravenously at a dose of 0.5 mg, repeated if necessary, to increase heart rate in cases of sinus bradycardia.[1]

  • Dopamine can be used as a continuous intravenous infusion starting at 2 to 10 mcg/kg/minute, titrated up to achieve the desired hemodynamic response, with a maximum of 50 mcg/kg/minute. However, higher infusion rates may lead to vasoconstriction or arrhythmias.[3]

  • Isoproterenol, used off-label for bradycardia, can be administered intravenously at doses of 1-20 mcg/min, but its use is generally limited to the electrophysiology laboratory setting.[2]

  • Biventricular pacing is preferred in patients with AV block and systolic dysfunction, except in cases of Lyme disease where heart block typically resolves with antibiotic therapy.[4]

  • His bundle or left bundle branch pacing is a newer form of physiological pacing that can be considered for more synchronous ventricular contraction.[4]

Additional info

When considering alternatives to external pacing, it's crucial to evaluate the patient's specific clinical scenario, including the underlying cause of bradycardia and any associated cardiac dysfunction. For instance, biventricular pacing is specifically indicated for patients with systolic dysfunction and AV block, providing a more physiological pacing option that can improve cardiac function by preserving the natural sequence of ventricular activation.[4] On the other hand, pharmacological interventions like atropine and dopamine are generally used for acute management of symptomatic bradycardia. These agents work by increasing the heart rate and improving hemodynamic stability but must be used cautiously due to potential side effects such as arrhythmias with dopamine at higher doses.[1][3] Isoproterenol, although effective in increasing heart rate, is limited by its cardiovascular side effects, particularly in patients with coronary artery disease, and is therefore used selectively.[2] Each of these alternatives has its specific indications, mechanisms of action, and safety profiles, which should be carefully considered in the context of the individual patient's condition and response to initial treatments.

References

Reference 1

1.

Patton, Kristen K., Olgin, Jeffrey E. (2022). In Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine (pp. 1312). DOI: 10.1016/B978-0-323-72219-3.00068-2

Treatment of sinus bradycardia is not usually necessary unless cardiac output is inadequate or arrhythmias result from the slow rate. Atropine (0.5 mg intravenously as an initial dose, repeated if necessary) is generally acutely effective; lower doses, particularly given subcutaneously or intramuscularly, can exert an initial parasympathomimetic effect, possibly by a central action. For recurrent symptomatic episodes, temporary or permanent pacing may be needed (seeChapters 64 and 69Chapter 64Chapter 69). Although theophylline and terbutaline can be used to increase the sinus rate, as a general rule, no drugs are available that increase the heart rate reliably and safely during long periods without undesirable side effects.

Reference 2

2.

Kusumoto FM, Schoenfeld MH, Barrett C, et al. Heart Rhythm. 2019;16(9):e128-e226. doi:10.1016/j.hrthm.2018.10.037.

Publish date: September 0, 2019.

; however, there are no clinical trials or observational series data to support or discourage its use in this setting. Because isoproterenol increases myocardial oxygen demand through beta-1 effects while decreasing coronary perfusion attributable to beta-2 effects, it is best avoided in settings where there is concern for coronary ischemia. From a clinical standpoint, it is predominantly used in the electrophysiology laboratory (1-20 mcg/min intravenously) and has only a second-line role in treatment of bradycardia in the setting of resuscitation. A trial of 82 patients presenting with unstable bradycardia refractory to intravenous fluid bolus and atropine randomized to transcutaneous pacing or dopamine at doses of 5 mcg/kg/min, titrated every 2 minutes by 5 mcg/kg/min to a maximum of 20 mcg/kg/min, showed no difference in survival to hospital discharge or serious adverse events. Although sympathetic reinnervation can be observed after long-term follow-up after orthotopic heart transplant, evidence for parasympathetic reinnervation is far less common: 34% versus 11% in 1 series that used heart rate variability response to neck suction to test autonomic responses. In patients with bradycardia associated with symptoms or hemodynamic compromise because of calcium channel blocker overdose, intravenous calcium is reasonable to increase heart rate and improve symptoms. In patients with bradycardia associated with symptoms or hemodynamic compromise because of beta-blocker or calcium channel blocker overdose, glucagon is reasonable to increase heart rate and improve symptoms. In patients with bradycardia associated with symptoms or hemodynamic compromise because of beta-blocker or calcium channel blocker overdose, high-dose insulin therapy is reasonable to increase heart rate and improve symptoms. Because of improvements in heart rate and blood pressure, coupled with low risk of adverse effects, intravenous calcium is often recommended as a first-line therapy if central or reliable peripheral venous access is present. 5.3.2.3 Therapy of Digoxin Mediated Bradycardia Attributable to either SND or Atrioventricular Block In patients with bradycardia associated with symptoms or hemodynamic compromise in the setting of digoxin toxicity, digoxin Fab antibody fragment is reasonable to increase heart rate and improve symptoms.

Reference 3

3.

Elsevier ClinicalKey Drug Monograph

Content last updated: April 4, 2024.

Indications And Dosage Continuous Intravenous Infusion dosage Adults: 2 to 10 mcg/kg/minute continuous IV infusion, initially. Titrate by 5 mcg/kg/minute every 2 minutes until goal hemodynamic response is attained. Max: 50 mcg/kg/minute. However, infusion rates more than 20 mcg/kg/minute may result in vasoconstriction or arrhythmias.

Reference 4

4.

Zimetbaum, Peter, Goldman, Lee (2024). In Goldman-Cecil Medicine (pp. 317). DOI: 10.1016/B978-0-323-93038-3.00051-4

In patients with AV block and systolic dysfunction, biventricular pacing is preferred. The only exception is Lyme disease, in which most cases of heart block resolve within a week of antibiotic therapy (Chapter 296). A newer form of physiologic pacing paces the His or left bundle branch region of the right ventricle (Chapter 54). This type of pacing stimulates the native conduction system and results in more synchronous contraction of the left and right ventricles than occurs with placement of a pacemaker into the apex or wall of the right ventricle. Cardiac neural ablation attempts to improve sinus node and AV node conduction by ablating the parasympathetic ganglia that innervate the sinus and AV nodes. This therapy has been used to treat neurocardiogenic syncope (Chapter 49) and is also being investigated for patients with sinus node dysfunction and varying degrees of AV nodal block.

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