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Abstract 17124: Severe Bradycardia in Critically Ill Patients With COVID-19
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Cardiac manifestations of severe Covid19 infection are still poorly understood. From January to May 2020, 113 consecutive patients were admitted in intensive care units for severe Covid19 and 10 out of them presented an episode of bradycardia.
Patients had a median age of 63 years, 6/10 were men, 7/10 were under mechanical ventilation for severe acute respiratory distress syndrome and 4/10 received a veno-venous extracorporeal membrane oxygenation. All bradycardias were due to sinus node bradycardia with a median heart rate of 36 bpm (range 10 - 45 bpm). For 6 patients, bradycardia was persistent and 3 required continuous isoprenaline infusion (Figure, patient A). Bradycardia was sudden for 4 patients and required brief resuscitation maneuvers for one (Figure, patient B)
.
Patients had normal baseline ECG and echocardiography, except for two patients who were under beta-blockers. For those two patients beta blockers were interrupted several days before bradycardia. A comprehensive review of patient’s files ruled out bradycardia due to drug-drug interactions, myocarditis, hyperkalemia, hypoxia or vagal physical stimulation. Holter ECG was performed for 7 patients: 3 recordings evoked vagal hyperactivity (low mean heart rate and elevated pNN50 / RMSSD, Figure Patient A), 3 others cardiac dysautonomia (SDNN<100ms, Figure Patient B).
Amongst these 10 patients, 5 were discharged from ICU among which 2 returned home and five died from covid-19 associated multiple-organ failure. None of them required temporary or permanent cardiac pacing.
To conclude, sinus bradycardia occurred commonly in severe Covid19 infection. This highlights the need to monitor cardiac rhythm. Even if the pathophysiology remains unclear, cardiac dysautonomia and vagal hyperactivity could be hypothesized rather than an intrinsic sinus node disease.
Ovid Technologies (Wolters Kluwer Health)
Title: Abstract 17124: Severe Bradycardia in Critically Ill Patients With COVID-19
Description:
Cardiac manifestations of severe Covid19 infection are still poorly understood.
From January to May 2020, 113 consecutive patients were admitted in intensive care units for severe Covid19 and 10 out of them presented an episode of bradycardia.
Patients had a median age of 63 years, 6/10 were men, 7/10 were under mechanical ventilation for severe acute respiratory distress syndrome and 4/10 received a veno-venous extracorporeal membrane oxygenation.
All bradycardias were due to sinus node bradycardia with a median heart rate of 36 bpm (range 10 - 45 bpm).
For 6 patients, bradycardia was persistent and 3 required continuous isoprenaline infusion (Figure, patient A).
Bradycardia was sudden for 4 patients and required brief resuscitation maneuvers for one (Figure, patient B)
.
Patients had normal baseline ECG and echocardiography, except for two patients who were under beta-blockers.
For those two patients beta blockers were interrupted several days before bradycardia.
A comprehensive review of patient’s files ruled out bradycardia due to drug-drug interactions, myocarditis, hyperkalemia, hypoxia or vagal physical stimulation.
Holter ECG was performed for 7 patients: 3 recordings evoked vagal hyperactivity (low mean heart rate and elevated pNN50 / RMSSD, Figure Patient A), 3 others cardiac dysautonomia (SDNN<100ms, Figure Patient B).
Amongst these 10 patients, 5 were discharged from ICU among which 2 returned home and five died from covid-19 associated multiple-organ failure.
None of them required temporary or permanent cardiac pacing.
To conclude, sinus bradycardia occurred commonly in severe Covid19 infection.
This highlights the need to monitor cardiac rhythm.
Even if the pathophysiology remains unclear, cardiac dysautonomia and vagal hyperactivity could be hypothesized rather than an intrinsic sinus node disease.
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