ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

COVID-19: Arrhythmias and conduction system disease

COVID-19: Arrhythmias and conduction system disease
Literature review current through: Jan 2024.
This topic last updated: Nov 08, 2023.

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 continuously. 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".)

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]. In a global case series of 4526 hospitalized patients with COVID-19, 827 (18.3 percent) had any arrhythmia and 509 (11.2 percent) had atrial fibrillation, most of whom did not have a known prior history of arrhythmia [9]. However, there may be selection bias with this study, as many of the sites did not send information on all admitted COVID-19 patients.

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) [10]. 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 [11]. 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) [12]. 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) [13]. 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 [14]. A more recent analysis from the COVID-19-Associated Hospitalization Surveillance Network of over 8600 hospitalizations for COVID-19 found that ventricular tachycardia occurred 0.9 percent of the time [15].

Bradyarrhythmias – In 143 patients admitted to a single center, complete atrioventricular block occurred in 1.4 percent and sinus arrest in 0.7 percent [14].

Postural orthostatic tachycardia syndrome (POTS) – Several case series have described an increased incidence of POTS in those with persistent symptoms following acute illness (“long COVID”) [16-21] (see "Postural tachycardia syndrome"). Other case series have suggested an increased rate of POTS after COVID-19 vaccination [22,23]. However, a large cohort study of more than 280,000 patients who received the COVID-19 vaccination and more than 12,000 who developed a COVID-19 infection found that the risk of POTS and related syndromes within 90 days of exposure was more than five-fold higher for those who developed infection than those who received vaccination (odds ratio 5.35, 95% CI 5.1-5.7) [24].

Inappropriate sinus tachycardia – Inappropriate sinus tachycardia has been similarly noted in case reports in those with persistent symptoms after infection [25]. (See "Sinus tachycardia: Evaluation and management".)

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 [8,26]. The presence of hypoxia, shock (septic or cardiogenic), or evidence of widespread systemic inflammation can predispose to arrhythmia [27]. (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 [28-31]. However, several large randomized trials of remdesivir did not report bradycardia as an adverse event [32-35]. (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 [36,37]. (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 [38]. 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 [39]. 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 [7,40]; 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) [40]. 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 [41].

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 [42]. 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 [43]. 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.

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 [44]. 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 [45], 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 "Sustained monomorphic ventricular tachycardia in patients with structural heart disease: Treatment and prognosis".)

(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 [46]. However, patients may still be treated with chloroquine or hydroxychloroquine [6,47], which are structurally similar to quinidine and have QT-prolonging effects by blocking activation of the potassium channel IKr (hERG/Kv11.1) [41,48-50]. 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 [48].

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 [51]. 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 [52]. 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 [53-55].

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 [56]. 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) [57]. 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.

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 [58]. 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 [59].

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 [48]. (See "Brugada syndrome or pattern: Management and approach to screening of relatives", section on 'High-risk patients'.)

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 [41,60-64].

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.

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 [61]. 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".)

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) [41,63,65] (see "Adult basic life support (BLS) for health care providers" and "Adult basic life support (BLS) for health care providers", section on 'Resuscitation of patients with COVID-19 or similar illness'):

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 [66,67].

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) [65,68]. 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 [69].

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

Evaluation – 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.)

Cardiovascular testing – 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.)

Polymorphic VT 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 therapies that prolong the QT – These patients should have a baseline QTc value, and a 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. (See 'Arrhythmia-related procedures' above.)

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 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.)

  1. World Health Organization. Director-General's remarks at the media briefing on 2019-nCoV on 11 February 2020. Available at: http://www.who.int/dg/speeches/detail/who-director-general-s-remarks-at-the-media-briefing-on-2019-ncov-on-11-february-2020 (Accessed on February 12, 2020).
  2. Centers for Disease Control and Prevention. 2019 Novel coronavirus, Wuhan, China. Information for Healthcare Professionals. https://www.cdc.gov/coronavirus/2019-nCoV/hcp/index.html (Accessed on June 19, 2022).
  3. World Health Organization. Novel Coronavirus (2019-nCoV) technical guidance. https://www.who.int/emergencies/diseases/novel-coronavirus-2019/technical-guidance (Accessed on June 19, 2022).
  4. Kochi AN, Tagliari AP, Forleo GB, et al. Cardiac and arrhythmic complications in patients with COVID-19. J Cardiovasc Electrophysiol 2020; 31:1003.
  5. Richardson S, Hirsch JS, Narasimhan M, et al. Presenting Characteristics, Comorbidities, and Outcomes Among 5700 Patients Hospitalized With COVID-19 in the New York City Area. JAMA 2020; 323:2052.
  6. Chorin E, Dai M, Shulman E, et al. The QT interval in patients with COVID-19 treated with hydroxychloroquine and azithromycin. Nat Med 2020.
  7. Rosenblatt AG, Ayers CR, Rao A, et al. New-Onset Atrial Fibrillation in Patients Hospitalized With COVID-19: Results From the American Heart Association COVID-19 Cardiovascular Registry. Circ Arrhythm Electrophysiol 2022; 15:e010666.
  8. Li Z, Shao W, Zhang J, et al. Prevalence of Atrial Fibrillation and Associated Mortality Among Hospitalized Patients With COVID-19: A Systematic Review and Meta-Analysis. Front Cardiovasc Med 2021; 8:720129.
  9. Coromilas EJ, Kochav S, Goldenthal I, et al. Worldwide Survey of COVID-19-Associated Arrhythmias. Circ Arrhythm Electrophysiol 2021; 14:e009458.
  10. Baldi E, Sechi GM, Mare C, et al. Out-of-Hospital Cardiac Arrest during the Covid-19 Outbreak in Italy. N Engl J Med 2020; 383:496.
  11. Baldi E, Sechi GM, Mare C, et al. COVID-19 kills at home: the close relationship between the epidemic and the increase of out-of-hospital cardiac arrests. Eur Heart J 2020; 41:3045.
  12. Bhatla A, Mayer MM, Adusumalli S, et al. COVID-19 and cardiac arrhythmias. Heart Rhythm 2020; 17:1439.
  13. Shao F, Xu S, Ma X, et al. In-hospital cardiac arrest outcomes among patients with COVID-19 pneumonia in Wuhan, China. Resuscitation 2020; 151:18.
  14. Cho JH, Namazi A, Shelton R, et al. Cardiac arrhythmias in hospitalized patients with COVID-19: A prospective observational study in the western United States. PLoS One 2020; 15:e0244533.
  15. Woodruff RC, Garg S, George MG, et al. Acute Cardiac Events During COVID-19-Associated Hospitalizations. J Am Coll Cardiol 2023; 81:557.
  16. Kanjwal K, Jamal S, Kichloo A, Grubb BP. New-onset Postural Orthostatic Tachycardia Syndrome Following Coronavirus Disease 2019 Infection. J Innov Card Rhythm Manag 2020; 11:4302.
  17. Miglis MG, Prieto T, Shaik R, et al. A case report of postural tachycardia syndrome after COVID-19. Clin Auton Res 2020; 30:449.
  18. Shouman K, Vanichkachorn G, Cheshire WP, et al. Autonomic dysfunction following COVID-19 infection: an early experience. Clin Auton Res 2021; 31:385.
  19. Goodman BP, Khoury JA, Blair JE, Grill MF. COVID-19 Dysautonomia. Front Neurol 2021; 12:624968.
  20. Larsen NW, Stiles LE, Shaik R, et al. Characterization of autonomic symptom burden in long COVID: A global survey of 2,314 adults. Front Neurol 2022; 13:1012668.
  21. Blitshteyn S, Whitelaw S. Postural orthostatic tachycardia syndrome (POTS) and other autonomic disorders after COVID-19 infection: a case series of 20 patients. Immunol Res 2021; 69:205.
  22. Park J, Kim S, Lee J, An JY. A case of transient POTS following COVID-19 vaccine. Acta Neurol Belg 2022; 122:1081.
  23. Reddy S, Reddy S, Arora M. A Case of Postural Orthostatic Tachycardia Syndrome Secondary to the Messenger RNA COVID-19 Vaccine. Cureus 2021; 13:e14837.
  24. Kwan AC, Ebinger JE, Wei J, et al. Apparent Risks of Postural Orthostatic Tachycardia Syndrome Diagnoses After COVID-19 Vaccination and SARS-Cov-2 Infection. Nat Cardiovasc Res 2022; 1:1187.
  25. Mayuga KA, Fedorowski A, Ricci F, et al. Sinus Tachycardia: a Multidisciplinary Expert Focused Review. Circ Arrhythm Electrophysiol 2022; 15:e007960.
  26. Goyal P, Choi JJ, Pinheiro LC, et al. Clinical Characteristics of Covid-19 in New York City. N Engl J Med 2020; 382:2372.
  27. Lazzerini PE, Boutjdir M, Capecchi PL. COVID-19, Arrhythmic Risk, and Inflammation: Mind the Gap! Circulation 2020; 142:7.
  28. Touafchia A, Bagheri H, Carrié D, et al. Serious bradycardia and remdesivir for coronavirus 2019 (COVID-19): a new safety concerns. Clin Microbiol Infect 2021.
  29. Gubitosa JC, Kakar P, Gerula C, et al. Marked Sinus Bradycardia Associated With Remdesivir in COVID-19: A Case and Literature Review. JACC Case Rep 2020; 2:2260.
  30. Barkas F, Styla CP, Bechlioulis A, et al. Sinus Bradycardia Associated with Remdesivir Treatment in COVID-19: A Case Report and Literature Review. J Cardiovasc Dev Dis 2021; 8.
  31. Gupta AK, Parker BM, Priyadarshi V, Parker J. Cardiac Adverse Events With Remdesivir in COVID-19 Infection. Cureus 2020; 12:e11132.
  32. Wang Y, Zhang D, Du G, et al. Remdesivir in adults with severe COVID-19: a randomised, double-blind, placebo-controlled, multicentre trial. Lancet 2020; 395:1569.
  33. Spinner CD, Gottlieb RL, Criner GJ, et al. Effect of Remdesivir vs Standard Care on Clinical Status at 11 Days in Patients With Moderate COVID-19: A Randomized Clinical Trial. JAMA 2020; 324:1048.
  34. Beigel JH, Tomashek KM, Dodd LE, et al. Remdesivir for the Treatment of Covid-19 - Final Report. N Engl J Med 2020; 383:1813.
  35. Grein J, Ohmagari N, Shin D, et al. Compassionate Use of Remdesivir for Patients with Severe Covid-19. N Engl J Med 2020; 382:2327.
  36. Amin AS, Herfst LJ, Delisle BP, et al. Fever-induced QTc prolongation and ventricular arrhythmias in individuals with type 2 congenital long QT syndrome. J Clin Invest 2008; 118:2552.
  37. Chang D, Saleh M, Garcia-Bengo Y, et al. COVID-19 Infection Unmasking Brugada Syndrome. HeartRhythm Case Rep 2020; 6:237.
  38. Baert V, Beuscart JB, Recher M, et al. Coronavirus Disease 2019 and Out-of-Hospital Cardiac Arrest: No Survivors. Crit Care Med 2022; 50:791.
  39. Shah P, Smith H, Olarewaju A, et al. Is Cardiopulmonary Resuscitation Futile in Coronavirus Disease 2019 Patients Experiencing In-Hospital Cardiac Arrest? Crit Care Med 2021; 49:201.
  40. Mountantonakis SE, Saleh M, Fishbein J, et al. Atrial fibrillation is an independent predictor for in-hospital mortality in patients admitted with SARS-CoV-2 infection. Heart Rhythm 2021; 18:501.
  41. Lakkireddy DR, Chung MK, Gopinathannair R, et al. Guidance for Cardiac Electrophysiology During the COVID-19 Pandemic from the Heart Rhythm Society COVID-19 Task Force; Electrophysiology Section of the American College of Cardiology; and the Electrocardiography and Arrhythmias Committee of the Council on Clinical Cardiology, American Heart Association. Circulation 2020; 141:e823.
  42. Gandhi RT, Lynch JB, Del Rio C. Mild or Moderate Covid-19. N Engl J Med 2020; 383:1757.
  43. Cheung CC, Davies B, Gibbs K, et al. Multi-lead QT screening is necessary for QT measurement: implications for management of patients in the COVID-19 era. JACC Clin Electrophysiol 2020.
  44. Giudicessi JR, Noseworthy PA, Friedman PA, et al. Urgent guidance for navigating and circumventing the QTc prolonging and torsadogenic potential of possible pharmacotherapies for COVID-19. Mayo Clin Proc 2020.
  45. Panchal AR, Berg KM, Kudenchuk PJ, et al. 2018 American Heart Association Focused Update on Advanced Cardiovascular Life Support Use of Antiarrhythmic Drugs During and Immediately After Cardiac Arrest: An Update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2018; 138:e740.
  46. US FDA. Coronavirus (COVID-19) Update: FDA Revokes Emergency Use Authorization for Chloroquine and Hydroxychloroquine. June 15, 2020. https://www.fda.gov/news-events/press-announcements/coronavirus-covid-19-update-fda-revokes-emergency-use-authorization-chloroquine-and (Accessed on June 16, 2020).
  47. Borba MGS, Val FFA, Sampaio VS, et al. Effect of High vs Low Doses of Chloroquine Diphosphate as Adjunctive Therapy for Patients Hospitalized With Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Infection: A Randomized Clinical Trial. JAMA Netw Open 2020; 3:e208857.
  48. Wu CI, Postema PG, Arbelo E, et al. SARS-CoV-2, COVID-19, and inherited arrhythmia syndromes. Heart Rhythm 2020; 17:1456.
  49. Traebert M, Dumotier B, Meister L, et al. Inhibition of hERG K+ currents by antimalarial drugs in stably transfected HEK293 cells. Eur J Pharmacol 2004; 484:41.
  50. Nguyen LS, Dolladille C, Drici MD, et al. Cardiovascular Toxicities Associated With Hydroxychloroquine and Azithromycin: An Analysis of the World Health Organization Pharmacovigilance Database. Circulation 2020; 142:303.
  51. https://www.hrsonline.org/hrs-covid-19-task-force-update-april-21-2020 (Accessed on April 22, 2020).
  52. Jankelson L, Karam G, Becker ML, et al. QT prolongation, torsades de pointes, and sudden death with short courses of chloroquine or hydroxychloroquine as used in COVID-19: A systematic review. Heart Rhythm 2020; 17:1472.
  53. Mazzanti A, Briani M, Kukavica D, et al. Association of Hydroxychloroquine With QTc Interval in Patients With COVID-19. Circulation 2020; 142:513.
  54. Voisin O, Lorc'h EL, Mahé A, et al. Acute QT Interval Modifications During Hydroxychloroquine-Azithromycin Treatment in the Context of COVID-19 Infection. Mayo Clin Proc 2020; 95:1696.
  55. O'Connell TF, Bradley CJ, Abbas AE, et al. Hydroxychloroquine/Azithromycin Therapy and QT Prolongation in Hospitalized Patients With COVID-19. JACC Clin Electrophysiol 2021; 7:16.
  56. Roden DM, Harrington RA, Poppas A, Russo AM. Considerations for Drug Interactions on QTc in Exploratory COVID-19 Treatment. Circulation 2020; 141:e906.
  57. https://www.crediblemeds.org/ (Accessed on March 30, 2020).
  58. Chang D, Saleh M, Gabriels J, et al. Inpatient Use of Ambulatory Telemetry Monitors for COVID-19 Patients Treated With Hydroxychloroquine and/or Azithromycin. J Am Coll Cardiol 2020; 75:2992.
  59. Strik M, Caillol T, Ramirez FD, et al. Validating QT-Interval Measurement Using the Apple Watch ECG to Enable Remote Monitoring During the COVID-19 Pandemic. Circulation 2020; 142:416.
  60. Wang NC, Jain SK, Estes NAM III, et al.. Priority Plan for Invasive Cardiac Electrophysiology Procedures During the Coronavirus Disease 2019 (COVID-19) Pandemic. J Cardiovasc Electrophysiol 2020.
  61. https://www.hrsonline.org/hrs-covid-19-task-force-update-april-15-2020 (Accessed on April 16, 2020).
  62. https://www.hrsonline.org/clinical-resources/2011-expert-consensus-statement-perioperative-management-patients-implantable-defibrillators (Accessed on April 02, 2020).
  63. Edelson DP, Sasson C, Chan PS, et al. Interim Guidance for Basic and Advanced Life Support in Adults, Children, and Neonates With Suspected or Confirmed COVID-19: From the Emergency Cardiovascular Care Committee and Get With The Guidelines-Resuscitation Adult and Pediatric Task Forces of the American Heart Association. Circulation 2020; 141:e933.
  64. https://www.england.nhs.uk/coronavirus/wp-content/uploads/sites/52/2020/03/specialty-guide-cardiolgy-coronavirus-v1-20-march.pdf (Accessed on April 16, 2020).
  65. Nolan JP, Monsieurs KG, Bossaert L, et al. European Resuscitation Council COVID-19 guidelines executive summary. Resuscitation 2020; 153:45.
  66. Perkins GD, Morley PT, Nolan JP, et al. International Liaison Committee on Resuscitation: COVID-19 consensus on science, treatment recommendations and task force insights. Resuscitation 2020; 151:145.
  67. Couper K, Taylor-Phillips S, Grove A, et al. COVID-19 in cardiac arrest and infection risk to rescuers: A systematic review. Resuscitation 2020; 151:59.
  68. Brown J, Rogers J, Soar J. Cardiac arrest during surgery and ventilation in the prone position: a case report and systematic review. Resuscitation 2001; 50:233.
  69. Barker J, Koeckerling D, West R. A need for prone position CPR guidance for intubated and non-intubated patients during the COVID-19 pandemic. Resuscitation 2020; 151:135.
Topic 127551 Version 45.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟