INTRODUCTION — Coronaviruses are important human and animal pathogens. At the end of 2019, a novel coronavirus was identified as the cause of a cluster of pneumonia cases in Wuhan, a city in the Hubei Province of China. It rapidly spread, resulting in a global pandemic. The disease is designated COVID-19, which stands for "coronavirus disease 2019" [1]. The virus that causes COVID-19 is designated "severe acute respiratory syndrome coronavirus 2" (SARS-CoV-2); previously, it was referred to as 2019-nCoV.
Understanding of COVID-19 is evolving rapidly. Interim guidance has been issued by the World Health Organization and the United States Centers for Disease Control and Prevention [2,3]. Links to these and other related society guidelines are found elsewhere. (See "COVID-19: Epidemiology, virology, and prevention", section on 'Society guideline links' and "COVID-19: Clinical features", section on 'Society guideline links'.)
This topic will discuss the epidemiology, prevalence, evaluation, diagnosis, and management of arrhythmias and conduction system disease in patients with COVID-19. Clinical presentation, diagnosis, and management of other cardiac presentations (eg, acute coronary syndrome, heart failure, etc) and noncardiac manifestations of COVID-19 are discussed in detail elsewhere:
●(See "COVID-19: Epidemiology, virology, and prevention".)
●(See "COVID-19: Clinical features".)
●(See "COVID-19: Diagnosis".)
●(See "COVID-19: Management in hospitalized adults".)
●(See "COVID-19: Management of the intubated adult".)
●(See "COVID-19: Myocardial infarction and other coronary artery disease issues".)
●(See "COVID-19: Evaluation and management of cardiac disease in adults".)
●(See "COVID-19: Clinical manifestations and diagnosis in children".)
●(See "COVID-19: Infection prevention for persons with SARS-CoV-2 infection".)
●(See "COVID-19: Questions and answers".)
Community-acquired coronaviruses, severe acute respiratory syndrome (SARS) coronavirus, and Middle East respiratory syndrome (MERS) coronavirus are discussed separately. (See "Coronaviruses" and "Severe acute respiratory syndrome (SARS)" and "Middle East respiratory syndrome coronavirus: Virology, pathogenesis, and epidemiology".)
EPIDEMIOLOGY — Patients with COVID-19 may be at increased risk of certain arrhythmias. Factors such as severity of illness and taking specific medications for COVID-19 treatment may increase the risk of developing an arrythmia.
Incidence and prevalence — The prevalence of arrhythmias and conduction system disease (and cardiovascular disease in general) in patients with COVID-19 varies from population to population [4]. The vast majority of patients presenting with a systemic illness consistent with COVID-19 will not have symptoms or signs of arrhythmias or conduction system disease. Patients may be tachycardic (with or without palpitations) in the setting of other illness-related symptoms (eg, fever, shortness of breath, pain, etc).
The following observations have been reported from various cohorts:
●QTc prolongation – Among 4250 patients with COVID-19 from a multicenter New York cohort, 260 (6.1 percent) had QTc >500 milliseconds at the time of admission [5]. However, in another study of 84 patients who received hydroxychloroquine and azithromycin, the baseline QTc was 435 milliseconds before taking these medications [6].
●Atrial fibrillation – In a large United States registry of nearly 31,000 patients hospitalized with COVID-19, 5.4 percent developed new-onset atrial fibrillation (AF) during their index hospitalization [7]. In a separate meta-analysis of 19 observational studies with 21,653 patients hospitalized with COVID-19, the prevalence of AF was 11 percent. AF was higher in patients with severe versus non-severe COVID-19 (19 versus 3 percent) [8].
●Out-of-hospital cardiac arrest – Two studies suggest an increase in the risk of out-of-hospital cardiac arrest during the pandemic. In a study from Italy, there was a nearly 60 percent increase in the rate of out-of-hospital cardiac arrest during the peak of the 2020 COVID-19 pandemic (when compared with the same time frame from 2019) [9]. In a study from France, there was a 52 percent increase in the cumulative incidence of out-of-hospital cardiac arrest during a two-month period between February and April 2020 compared with 2019 [10]. These observations could be related to COVID-19 infections, stress related to the pandemic, or delays in seeking medical attention by those with cardiac symptoms.
●In-hospital cardiac arrest – In a single-center United States study of 700 patients admitted with COVID-19 (11 percent in the intensive care unit), nine patients experienced cardiac arrest, although only one patient had a shockable rhythm of torsades de pointes (eight patients had PEA/asystole) [11]. In a separate cohort of 136 Chinese patients with severe pneumonia due to COVID-19, and who experienced in-hospital cardiac arrest and attempted resuscitation, most arrests were deemed respiratory in origin, and the initial rhythm was non-shockable in the vast majority of patients (asystole in 90 percent, pulseless electrical activity in 4 percent) [12]. Return of spontaneous circulation (13 percent), survival to 30 days (3 percent), and survival with intact neurologic function (1 percent) were extremely low in this critically ill cohort.
●Ventricular ectopy and tachycardia – In 143 patients admitted to a single center, nonsustained VT occurred in 15.4 percent, premature ventricular contractions in 28.8 percent, ventricular fibrillation 1.4 percent, and sustained ventricular tachycardia occurred in 0.7 percent [13].
●Bradyarrhythmias – In 143 patients admitted to a single center, complete atrioventricular block occurred in 1.4 percent and sinus arrest in 0.7 percent [13].
Potential risk factors — These may include the following:
●The presence of cardiovascular complications in the setting of COVID-19 infection, such as myocardial injury or myocardial ischemia. (See "COVID-19: Myocardial infarction and other coronary artery disease issues" and "COVID-19: Evaluation and management of cardiac disease in adults".)
●More severe infection and mechanical ventilation can predispose to AF and other atrial arrythmias [8,14]. The presence of hypoxia, shock (septic or cardiogenic), or evidence of widespread systemic inflammation can predispose to arrhythmia [15]. (See "COVID-19: Management of the intubated adult".)
●The presence of electrolyte disturbances (eg, hypokalemia) may predispose to the development of arrhythmias. (See "Clinical manifestations and treatment of hypokalemia in adults", section on 'Cardiac arrhythmias and ECG abnormalities' and "Hypomagnesemia: Clinical manifestations of magnesium depletion", section on 'Cardiovascular'.)
●Therapies that prolong the QT interval may increase the risk of polymorphic VT. (See 'Patients with polymorphic ventricular tachycardia (torsades de pointes)' below.)
●Remdesivir may be a risk factor for bradycardia [16-19]. However, several large randomized trials of remdesivir did not report bradycardia as an adverse event [20-23]. (See "COVID-19: Management in hospitalized adults", section on 'Remdesivir'.)
●The presence of fever, which can unmask cardiac channelopathies such as Brugada syndrome and long QT syndrome in susceptible patients [24,25]. (See 'Brugada syndrome' below and "Brugada syndrome: Clinical presentation, diagnosis, and evaluation" and "Congenital long QT syndrome: Epidemiology and clinical manifestations".)
Outcomes
●Mortality post-cardiac arrest – Mortality after cardiac arrest is extremely high and may be even higher in the setting of COVID-19. A national registry study from France compared 30-day mortality rates for patients with and without COVID-19 who had out-of-hospital cardiac arrest and subsequent admission to an intensive care unit [26]. In this study, 127 patients with confirmed COVID-19 had a 100 percent 30-day mortality, compared with 96.5 percent of such patients without COVID-19. A separate study from a hospital in rural Georgia showed that 63 patients with COVID-19 who experienced an in-hospital cardiac arrest had a 100 percent in-hospital mortality [27]. The latter study did not have a COVID-19 negative control group.
●AF and mortality – Studies are mixed as to whether AF and new-onset AF are associated with all-cause mortality among hospitalized patients with COVID-19 [7,28]; in such patients, AF has not been shown to be associated with adverse major cardiac events.
In a large United States registry of nearly 31,000 patients hospitalized with COVID-19 from 120 institutions, 5.4 percent developed new-onset AF during their index hospitalization, and new-onset AF was associated with a higher rate of death (45.2 versus 11.9 percent) and major adverse cardiac events (23.8 versus 6.5 percent) [7]. However, after adjusting for patient comorbidities, new-onset AF was nonsignificantly associated with a higher risk of death (hazard ratio [HR] 1.10, 95% CI 0.99-1.23) and was not associated with major adverse cardiac events (HR 1.31 95% CI 1.14-1.50).
On the other hand, in a cohort of 9564 patients hospitalized with COVID-19 from New York with propensity score matching of 1238 pairs of patients with and without and AF, in-hospital mortality was higher in patients with AF: 54 versus 37 percent (relative risk [RR] 1.46, 95% CI 1.34-1.59) [28]. In a propensity-score-matched analysis of 500 patients, patients with new-onset AF had worse outcomes compared with those with a history of AF (55 versus 47 percent [RR 1.18, 95% CI 1.04-1.33]). A strength of this study was the use of propensity score matching, which better balanced the comorbidities in the AF cases and non-AF control groups, leading to more reliable mortality risk ratios. However, generalizability of this single-center study may be lower than that of the multicenter registry described above [7].
EVALUATION — In most available reports, the specific cause of palpitations or type of arrhythmia have not been specified. Hypoxia and electrolyte abnormalities, both known to contribute to the development of acute arrhythmias, have been frequently reported in the acute phase of severe COVID-19 illness; therefore, the exact contribution of COVID-19 infection to the development of arrhythmias in asymptomatic, mildly ill, critically ill, and recovered patients is not known [29].
Cardiovascular testing
ECG — Most patients in whom COVID-19 is suspected and, in particular, patients with severe disease or in whom QT-prolonging medications will be used, should have a baseline electrocardiogram (ECG) performed at the time of entry into the health care system [30]. Ideally, this would be a 12-lead ECG, but a single- or multi-lead ECG from telemetry monitoring or multiple lead positions from a hand-held ECG device may be adequate in this situation to minimize staff exposure to the patient [31]. This will allow for documenting baseline QRS-T morphology should the patient develop signs/symptoms suggestive of myocardial injury or an acute coronary syndrome. Additionally, the baseline ECG allows for documentation of the QT (and corrected QTc) interval. Importantly, QTc will need to be monitored if QT-prolonging therapies are initiated to reduce the risk of acquired long QT syndrome. (See "Acquired long QT syndrome: Clinical manifestations, diagnosis, and management" and 'Patients receiving therapies that prolong the QT interval' below.)
Continuous ECG monitoring — In the absence of documented cardiac arrhythmias, suspected myocardial ischemia, or other standard indications, continuous ECG monitoring is not required. However, as part of infection control mechanisms for patients with established or suspected COVID-19 infection, many hospitals are utilizing continuous ECG monitoring (in conjunction with automated blood pressure readings and oxygen saturation monitors) in lieu of standard vital sign checks by nursing staff. This practice reduces the number of clinical staff interacting with the patient, thereby reducing the risk to health care workers and preserving personal protective equipment.
Transthoracic echocardiography — While some patients may develop cardiac manifestations, including myocardial injury, an initial transthoracic echocardiogram is not necessary for all patients. Providers may consider using a point-of-care ultrasound for a focused exam. (See "COVID-19: Evaluation and management of cardiac disease in adults".)
DIAGNOSIS OF ARRHYTHMIAS — Arrhythmias are most commonly diagnosed from a combination of vital signs and review of the ECG, ideally a 12-lead ECG, but a rhythm strip can also be used. Tachycardias present with a pulse greater than 100 beats per minute, while most bradyarrhythmias present with a pulse less than 50 to 60 beats per minute.
●The most common arrhythmia overall in patients with COVID-19 is sinus tachycardia, but the most likely pathologic arrhythmias include atrial fibrillation, atrial flutter, and monomorphic or polymorphic VT.
●The differentiation between various tachycardias based on regularity (ie, regular or irregular) and QRS width (ie, narrow or wide QRS complex) requires only a surface ECG. (See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation" and "Wide QRS complex tachycardias: Approach to the diagnosis".)
●Bradyarrhythmias, including sinus pauses or high-grade heart block with slow escape rhythms, have not typically been seen but can be identified using a surface ECG if present. (See "Sinus node dysfunction: Clinical manifestations, diagnosis, and evaluation" and "Second-degree atrioventricular block: Mobitz type II" and "Third-degree (complete) atrioventricular block".)
The diagnosis of acquired long QT syndrome can be made in a patient with sufficient QT prolongation on the surface ECG in association with a medication or other clinical scenario (ie, hypokalemia or hypomagnesemia) known to cause QT prolongation. Ideally, the diagnosis is made following review of a full 12-lead ECG, but sometimes a single-lead rhythm strip is adequate if a full 12-lead ECG cannot be obtained. Acquired QT prolongation is typically reversible upon removal of the underlying etiology, such as discontinuation of an offending medication or correction of electrolyte derangements. (See 'Management' below.)
Overall, the average QTc in healthy persons after puberty is 420±20 milliseconds. In general, the 99th percentile QTc values are 470 milliseconds in postpubertal males and 480 milliseconds in postpubertal females [32]. A QTc >500 milliseconds is considered highly abnormal for both males and females.
MANAGEMENT
Patients with polymorphic ventricular tachycardia (torsades de pointes) — All patients with torsades de pointes (TdP) should have an immediate assessment of the symptoms, vital signs, and level of consciousness to determine if they are hemodynamically stable or unstable.
Unstable patients — Patients with sustained TdP usually become hemodynamically unstable, severely symptomatic, or pulseless and should be treated according to standard resuscitation algorithms [33], including cardioversion/defibrillation (algorithm 1 and algorithm 2 and algorithm 3). Initial treatment with antiarrhythmic medications, with the exception of intravenous (IV) magnesium, is not indicated for hemodynamically unstable or pulseless patients. A full discussion of the standard approaches to basic life support and advanced cardiac life support is presented separately. (See "Adult basic life support (BLS) for health care providers" and "Advanced cardiac life support (ACLS) in adults".)
Stable patients — Patients with TdP who are hemodynamically stable on presentation may remain stable or may become unstable rapidly and without warning. As such, therapy should be promptly provided to most patients. A stable patient is one who typically shows no evidence of hemodynamic compromise but may have frequent, repetitive bursts of TdP. This patient should have continuous monitoring and frequent reevaluations due to the potential for rapid deterioration as long as the TdP persists. (See "Acquired long QT syndrome: Clinical manifestations, diagnosis, and management", section on 'Initial management'.)
Patients with other arrhythmias — The management of other arrhythmias in the setting of COVID-19 infection is no different from the routine management of these conditions without COVID-19 infection. Please refer to the following topics for management:
Atrial fibrillation and other supraventricular tachycardias:
●(See "Overview of the acute management of tachyarrhythmias".)
●(See "Atrial fibrillation: Overview and management of new-onset atrial fibrillation".)
●(See "Overview of atrial flutter".)
●(See "Atrioventricular nodal reentrant tachycardia".)
●(See "Treatment of arrhythmias associated with the Wolff-Parkinson-White syndrome".)
●(See "Focal atrial tachycardia".)
Monomorphic VT:
●(See "Wide QRS complex tachycardias: Approach to management".)
●(See "Ventricular tachycardia in the absence of apparent structural heart disease".)
Conduction system disease:
●(See "Sinus node dysfunction: Treatment".)
●(See "Third-degree (complete) atrioventricular block".)
●(See "Second-degree atrioventricular block: Mobitz type II".)
●(See "Temporary cardiac pacing".)
Patients receiving therapies that prolong the QT interval — Hydroxychloroquine and chloroquine are two medications that can cause acquired long QT syndrome (LQTS). (See "Acquired long QT syndrome: Definitions, pathophysiology, and causes".)
Neither hydroxychloroquine nor chloroquine are recommended for treatment of COVID-19; additionally, in June 2020, the US FDA revoked its emergency use authorization for these agents in patients with severe COVID-19, noting that the known and potential benefits no longer outweighed the known and potential risks [34]. However, patients may still be treated with chloroquine or hydroxychloroquine [6,35], which are structurally similar to quinidine and have QT-prolonging effects by blocking activation of the potassium channel IKr (hERG/Kv11.1) [29,36-38]. Other medications with QT-prolonging effects may be tried for COVID-19 (table 1). In addition, both chloroquine and hydroxychloroquine are metabolized by CYP3A4, so other medications that inhibit this cytochrome could raise plasma levels [36].
Monitoring for QT prolongation — As in patients without COVID-19, among patients with COVID-19, the baseline QTc value should be obtained prior to administering any drugs with the potential to prolong the QT interval [39]. When patients are receiving any QT-prolonging medications, a dynamic discussion of the benefits and risks of these medications should be ongoing based on the baseline risk (including baseline QTc, electrolyte levels, etc), perceived or actual benefit of therapy, and development of significant QT prolongation or TdP. A systematic review of 14 studies showed that about 10 percent of patients developed a QTc interval ≥500 ms or change of >60 ms while taking hydroxychloroquine or chloroquine [40]. Data from various cohort studies of patients with COVID-19 treated with one or more QT prolonging drugs suggest a modest increase in QTc (20 to 30 milliseconds) in most patients, although the response in an individual patient may be more profound [41-43].
Patients with COVID-19 who have a baseline QTc interval ≥500 milliseconds (with a QRS ≤120 milliseconds) are at increased risk for significant QT prolongation and polymorphic VT [44]. In such patients, as with any patient at risk for acquired LQTS, efforts should be made to correct any contributing electrolyte abnormalities (eg, hypocalcemia, hypokalemia, and/or hypomagnesemia), with a goal potassium of close to 5 mEq/L. Even in those with a normal QT interval, there should be a review and discontinuation of any QT-prolonging medications that may not be essential to the immediate care of the patient (eg, proton pump inhibitors, etc) (table 1) [45]. The diagnosis and treatment of acquired long QT syndrome are discussed separately. (See "Acquired long QT syndrome: Definitions, pathophysiology, and causes" and "Acquired long QT syndrome: Clinical manifestations, diagnosis, and management".)
The following caveats and observations may be relevant to the ECG diagnosis of acquired LQTS during the COVID-19 pandemic:
●The best method to obtain the QT interval is with a 12-lead ECG, but to reduce exposure to staff, this may not always be feasible.
● A single-lead ECG may underestimate the QT interval, and there should be an attempt to use a multiple-lead telemetry system to monitor the QT interval. There is no clear guidance regarding the optimal approach to monitor outpatients with COVID-19 who are receiving QT-prolonging medications.
●Ambulatory ECG monitoring technologies, including the use of mobile or wearable technologies (eg, mobile cardiac outpatient telemetry), have been reported as reliable alternatives when the demand exceeds capacity for standard telemetry monitoring [46]. In one study of 100 patients during the COVID-19 pandemic, in which a single-lead ECG was recorded using a smartwatch in three different locations (left wrist, left ankle, left lateral chest wall), 94 percent of patients were able to obtain an accurate QT interval which correlated to the 12-lead ECG [47].
A specific protocol for medication-related QT prolongation monitoring in patients with COVID-19 is provided below:
●One protocol has been published from the Mayo Clinic, using the same QTc cutoffs as above [48]. If two to three hours after a dose of a QT-prolonging agent, the QTc increases to ≥500 milliseconds or if the change in QT interval is ≥60 milliseconds, there should be a reevaluation of the risk of TdP versus benefit of the medication, and the following steps should be taken:
•Recognition that there is an increased risk of TdP.
•Discontinuation of all other QT-prolonging medications.
•Correction of all electrolyte abnormalities.
•Place the patient on continuous telemetry, with consideration of a wearable defibrillator or placement of external defibrillator patches.
•If TdP develops, then QT-prolonging medications should be stopped.
●Another protocol proposes an ECG at baseline and again at four hours after administration of QT-prolonging medication only if there is congenital or acquired long QT syndrome, patients are already taking other QT-prolonging medications, or patients have structural heart disease or bradycardia [36]. Another ECG can be completed one to three days later. For most others, an ECG or other QTc interval-monitoring method can be done 24 hours after starting the medication. If the QTc increases to ≥500 milliseconds, if the change in QT interval is ≥60 milliseconds, or if ventricular ectopy develops, this protocol recommends cardiology consultation.
Brugada syndrome — Because there is an increased risk of ventricular arrhythmias in the setting of fever in those with Brugada syndrome, aggressive fever reduction with acetaminophen is imperative. High-risk patients, such as those with a spontaneous type 1 pattern ECG and prior syncope, might consider going to an emergency department if they have fever that cannot be promptly lowered with acetaminophen [36]. (See "Brugada syndrome: Prognosis, management, and approach to screening", section on 'Treatment'.)
IMPORTANT INFORMATION FOR PROVIDERS CARING FOR COVID-19 PATIENTS — In addition to providing the best possible care for each patient, infection control to limit transmission is an essential component of care in patients with suspected or documented COVID-19 [29,49-53].
Inpatient care and consultation — The approach to caring for hospitalized patients with documented or suspected COVID-19 differs slightly, with the intent to reduce exposure to (and spread of) COVID-19 to health care providers. In general, the number of persons interacting directly with the patient and the time spent in the room should be minimized. Social distancing should be maintained, with both the patient and other members of the health care team.
The following steps, when possible, will minimize exposure of personnel and limit the use of personal protective equipment (PPE):
●For stable new admissions, the patient should be seen in person by the attending physician and at most one house officer or advanced practitioner (when applicable).
●For stable patients on daily rounds, one person on the primary care team should enter the room to conduct the needed physical exam, with the rest of the team participating from outside the room via video chat or telephone.
●Routine arrhythmia consultations, particularly in stable patients with ECG evidence documenting a specific arrhythmia or conduction disorder, can be completed without entering the patient's room by reviewing the available records and ECG monitoring data.
●Consider placing all patients on telemetry with concerns of arrhythmias, thereby reducing the need for in-room vital signs.
●Utilize rooms with windows in the door to assist with monitoring patients from outside of the room. Patients can be contacted by telephone for routine matters without requiring entry into the room.
Arrhythmia-related procedures — In order to minimize the potential exposure of health care personnel to asymptomatic carriers of the virus, elective and nonurgent procedures in patients with symptomatic or asymptomatic infection should be postponed until a later date. A discussion of the reasoning behind the decision to postpone any procedure should be communicated to the patient and documented in the medical record. Conversely, urgent and semiurgent procedures should be performed when the perceived benefits of the procedure to the patient outweigh the risks of resource utilization and health care personnel exposure.
Examples of the types of procedures in each category are as follows [29,49]:
Urgent (substantial risk of decompensation, hospitalization, or death if the procedure is delayed):
●VT ablation for medically uncontrolled electrical storm in a hemodynamically compromised patient.
●Catheter ablation of incessant, hemodynamically significant, severely symptomatic tachycardia (supraventricular VT [SVT]/atrial fibrillation [AF]/atrial flutter) not responding to antiarrhythmic drugs, rate control, and/or cardioversion.
●Catheter ablation for Wolff-Parkinson-White syndrome or preexcited AF with syncope or cardiac arrest.
●Lead revision for malfunction in a pacemaker-dependent patient or implantable cardioverter-defibrillator (ICD) patient receiving inappropriate therapy.
●Generator change in pacemaker-dependent patients who are at elective replacement indicator (ERI) or at device end of life.
●Pacemaker or ICD generator change with minimal battery remaining, depending on specific clinical situations.
●Secondary prevention ICD.
●Pacemaker implant for complete heart block, Mobitz II AV block, or high-grade AV block with symptoms or severe symptomatic sinus node dysfunction with long pauses.
●Lead/device extraction for infection, including patients not responding to antibiotics for endocarditis, bacteremia, or pocket infection.
●Cardiac resynchronization therapy in the setting of severe refractory heart failure in guideline-indicated patients.
●Cardioversion for highly symptomatic atrial arrhythmias or rapid ventricular rates not controlled with medications.
●Transesophageal echocardiogram for patients who need urgent cardioversion.
Semiurgent (those procedures not deemed urgent but should be performed in a timely manner due to the clinical scenario):
●VT ablation for medically refractory recurrent VT.
●SVT ablation in patients with medically refractory SVT, resulting in emergency department visits.
●Cardiac implantable electrical device (CIED) generator replacement for ERI battery status that is not urgent.
●Primary prevention ICD in patients at particularly high risk of life-threating ventricular arrhythmia.
Nonurgent (those procedures that may be delayed for weeks or months):
●Premature ventricular complex ablation.
●SVT ablation.
●AF and atrial flutter ablation in stable patients without heart failure, not at significant risk of getting hospitalized by delaying the procedure, or at high risk for procedure-related complications due to comorbidities.
●Electrophysiology testing to evaluate stable tachyarrhythmias or bradycardia.
●Primary prevention ICD that is not semiurgent.
●Cardiac resynchronization therapy in stable patients.
●CIED upgrade.
●Pacemaker implant for sinus node dysfunction, Mobitz I AV block, other stable non-high-degree AV block, or tachy-brady syndrome in mildly symptomatic patients.
●Pacemaker or ICD generator replacements in patients with >6 weeks of battery remaining.
●Extraction of noninfected devices/leads unless device function is dependent on lead extraction and reimplant.
●Cardioversion for stable arrhythmias with well-tolerated symptoms.
●Left atrial appendage (LAA) closure in patients who can be on anticoagulation.
●Transesophageal echocardiogram for routine assessment of valves or LAA closure devices and cardioversions that can be done after appropriate period of anticoagulation.
●Implantable loop recorder implants.
●Tilt-table testing.
Perioperative cardiac implantable electrical device management — For patients with a CIED undergoing surgery or an endoscopic procedure, it is important to know if the patient is pacemaker dependent, if the patient has an ICD with therapies activated, and the likelihood of electromagnetic interference (EMI) during the procedure (eg, due to electrocautery, etc). In a patient with documented or suspected COVID-19 who is undergoing a procedure with a high likelihood of EMI that could result in pacemaker or ICD malfunction, application of a magnet may be used to suspend antitachyarrhythmia therapy in an ICD or to produce asynchronous pacing in a pacemaker [50]. This allows the patient to safely proceed with the necessary procedure without reprogramming the CIED before and after the procedure, thereby reducing the risk to health care personnel and preserving PPE.
The standard approach to CIED management, which includes in-person reprogramming of the CIED before and after the procedure, is discussed in detail elsewhere. (See "Perioperative management of patients with a pacemaker or implantable cardioverter-defibrillator".)
Cardiac implantable electrical device interrogations — For most patients, the majority of CIED follow-up device interrogations on modern-era devices can be done either in person or remotely. To maintain social distancing during the COVID-19 pandemic, we recommend remote CIED interrogations for the vast majority of stable patients [50].
Certain situations remain, however, in which an in-person CIED interrogation may be the preferred option, including [29,50]:
●Suspected CIED malfunction, including:
•Inappropriate pacemaker pacing or sensing noted on ECG or telemetry monitoring.
•Failure of ICD to deliver therapy during documented sustained ventricular tachyarrhythmia.
●Clinically actionable abnormality of CIED or suspicion of the device being at or near end of battery life, noted on remote monitoring, telemetry, or ambulatory monitoring.
●ICD shocks, presyncope, or syncope concerning for an arrhythmic event to perform programming changes.
●Untreated sustained ventricular arrhythmias in a patient with an ICD.
●Evaluation of symptoms suspicious for arrhythmia or abnormal device function in patients who are not enrolled in remote monitoring.
●Identified need for reprogramming of the CIED, or ICD patients whose device is delivering auditory or vibratory alerts.
●Assessment of AF in a patient with a stroke and no clear documentation of AF on ECG or telemetry monitoring.
●For CIED patients requiring urgent or emergent magnetic resonance imaging (MRI) scanning, consider performing a computed tomography scan instead if possible (to minimize the need for additional health care provider or device manufacturer representative contact); if not urgent, delay the MRI.
●Patients in the emergency department (or other setting) where remote monitoring is not available. Remote monitoring should be used wherever possible, including the option of asking caregivers to bring the patient's home monitoring equipment to the hospital.
After in-person CIED interrogation is performed, it is important to disinfect any parts of the programmer (eg, the programming wand and cord) that have been in contact with the patient. If available, disposable plastic wand coverings may be used to minimize contamination, and consideration should also be given to using a dedicated interrogation device in all settings with known or suspected COVID-19-positive patients.
To reduce exposure of health care personnel to CIED patients, a doughnut magnet can be used as an alternative to a complete CIED interrogation or reprogramming [51]. When a hospitalized patient has a pacemaker that does not have remote monitoring capabilities, and proper function of the pacemaker is in question, temporary application of a doughnut magnet over the pacemaker is safe to quickly determine whether or not the pacemaker is capable of delivering pacing stimuli that can capture the heart. Magnet application will place the pacemaker in an asynchronous pacing mode. Depending on the manufacturer and programmed settings, this may include changes in the paced rate, which gives evidence of battery status (ie, elective replacement indicator) or whether there is pacemaker capture. In addition, demonstration of ventricular capture should provide basic reassurance that the pacemaker is functional and can avoid the need for a complete pacemaker interrogation. (See "Perioperative management of patients with a pacemaker or implantable cardioverter-defibrillator".)
Patients requiring cardiopulmonary resuscitation (CPR) — In general, basic life support and advanced cardiac life support for patients with COVID-19 should be administered in standard fashion, similar to patients without COVID-19, with the following exceptions (algorithm 1 and algorithm 2) [29,52,54] (see "Adult basic life support (BLS) for health care providers", section on 'Resuscitation of patients with COVID-19' and "Adult basic life support (BLS) for health care providers"):
●Any personnel caring for a patient with suspected or confirmed COVID-19 should wear the appropriate PPE before entering the room: gown, gloves, eye protection, and a respirator (eg, an N95 respirator). If supply of respirators is limited, the United States Centers for Disease Control and Prevention acknowledges that facemasks are an acceptable alternative (in addition to contact precautions and eye protection), but respirators should be worn during aerosol-generating procedures, which includes intubation. The appropriate PPE should all be donned prior to interacting with the patient, even if this leads to a delay in the provision of resuscitative care [55,56].
●The number of people involved in the resuscitation should be kept to a minimum. This typically includes a team leader, anesthesiologist to manage the airway (if the patient is not already intubated), recorder/scribe, and persons to perform chest compressions, defibrillation, and administration of medications (often, these participants can rotate to allow for periods of rest after performing chest compressions).
●In COVID-19 patients who are not yet intubated at the time of cardiac arrest, early intubation should be performed by the provider most likely to achieve success on the first pass, utilizing all readily available technology (eg, video laryngoscopy) to optimize first-pass success. Chest compression can be stopped during intubation, and intubation (with a cuffed endotracheal tube) can be performed prior to the standard two minutes of chest compressions and early defibrillation as a means of controlling the potential spread of airborne droplets.
●If available, mechanical chest compression device may be used in place of manual compressions for adults and adolescents who meet minimum height and weight requirements.
●For a critically ill patient who is already intubated and in the prone position at the time of arrest, CPR may be attempted with the patient prone by performing compressions of usual depth (ie, 5 to 6 cm) with the hands between the scapulae (over the T4-T7 vertebral bodies) [54,57]. Defibrillation may be performed with the pads in the anterior-posterior position. The patient should be turned to the supine position for resuscitation only if able to do so without equipment disconnections that may lead to aerosolization of viral particles [58].
●For out-of-hospital resuscitation efforts, lay rescuers should perform chest compression-only CPR while wearing a face mask or cloth covering. When available, an automated external defibrillator should be applied and used according to the usual protocol. (See "Automated external defibrillators" and "Adult basic life support (BLS) for health care providers", section on 'Defibrillation'.)
Initial treatment with antiarrhythmic medications, with the exception of IV magnesium, is not indicated for hemodynamically unstable or pulseless patients. A full discussion of the standard approaches to basic life support and advanced cardiac life support is presented separately. (See "Adult basic life support (BLS) for health care providers" and "Advanced cardiac life support (ACLS) in adults".)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: COVID-19 – Index of guideline topics".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: COVID-19 overview (The Basics)")
●Basics topic (see "Patient education: COVID-19 vaccines (The Basics)")
SUMMARY AND RECOMMENDATIONS
●The vast majority of patients presenting with a systemic illness consistent with COVID-19 will not have symptoms or signs of arrhythmias or conduction system disease. However, patients in whom arrhythmias may be seen include patients with myocardial injury, myocardial ischemia, hypoxia, shock, electrolyte disturbances, or those receiving medications known to prolong the QT interval. (See 'Evaluation' above.)
●All patients in whom COVID-19 is suspected should have a baseline electrocardiogram (ECG) performed at the time of entry into the health care system. Ideally, this would be a 12-lead ECG, but a single-lead or multi-lead ECG from telemetry monitoring may be adequate in this situation to minimize staff exposure to the patient. Continuous ECG monitoring and echocardiography are not required in all patients but can be used in select situations. (See 'Cardiovascular testing' above.)
●Patients with sustained torsades de pointes (TdP) usually become hemodynamically unstable, severely symptomatic, or pulseless and should be treated according to standard resuscitation algorithms, including cardioversion/defibrillation (algorithm 1 and algorithm 2 and algorithm 3). Patients with TdP who are hemodynamically stable on presentation may remain stable or may become unstable rapidly and without warning. These patients should have continuous monitoring and frequent reevaluations due to the potential for rapid deterioration as long as TdP persists. (See 'Patients with polymorphic ventricular tachycardia (torsades de pointes)' above.)
●Patients receiving QT-prolonging medications should have a baseline QTc value obtained prior to administering the drugs. When patients are receiving any QT-prolonging medications, a dynamic discussion of the benefits and risks of these medications should be ongoing based on the baseline risk (including baseline QTc, electrolyte levels, etc), perceived or actual benefit of therapy, and development of significant QT prolongation or TdP. If the QTc subsequently increases to ≥500 milliseconds or if the change in QT interval is ≥60 milliseconds from the baseline ECG, electrolytes (notably potassium and magnesium) should be corrected to the normal range (if needed), and continuous inpatient ECG telemetry should be maintained, with additional management changes that may include dose adjustment or medication withdrawal. (See 'Patients receiving therapies that prolong the QT interval' above.)
●The approach to caring for hospitalized patients with documented or suspected COVID-19 differs slightly, with the intent to reduce exposure to (and spread of) COVID-19 to health care providers. In general, the number of persons interacting directly with the patient and the time spent in the room should be minimized. Social distancing should be maintained, with both the patient and other members of the health care team. (See 'Inpatient care and consultation' above and 'Arrhythmia-related procedures' above.)
●The approaches to cardiac implantable electrical device (CIED) interrogations and perioperative CIED management are summarized in the text. Strategies to avoid in-person device interrogations should be deployed. (See 'Cardiac implantable electrical device interrogations' above and 'Perioperative cardiac implantable electrical device management' above.)
●In general, basic life support and advanced cardiac life support for patients with COVID-19 should be administered in standard fashion as for patients without COVID-19. However, any personnel caring for a patient with suspected or confirmed COVID-19 should wear the appropriate personal protective equipment (including gown, gloves, eye protection, and a respirator or face mask) before entering the room, the number of people involved in the resuscitation should be kept to a minimum, and early intubation should be performed for patients who are not yet intubated at the time of cardiac arrest. (See 'Patients requiring cardiopulmonary resuscitation (CPR)' above.)
