During cardiac arrest, provision of high-quality CPR and rapid defibrillation are of primary importance and drug administration is of secondary importance.
A resuscitation drug, administered by a peripheral venous route, should be administered by bolus injection and followed with a 20-mL bolus of IV fluid.
Briefly elevating the extremity during and after drug administration may recruit the benefit of gravity to facilitate delivery to the central circulation, although the evidence to support such an effect has not been evaluated.
Most in-hospital cardiac arrests should take place in an intensive care unit. As a result, many patients may already have a central IV catheter in place. If central IV access is not in place, an appropriately trained provider may attempt such access if it doesn’t interfere with high-quality CPR (especially compressions).
If IV or IO access cannot be established, epinephrine, vasopressin, and lidocaine may be administered by the endotracheal route during cardiac arrest.
The optimal endotracheal dose of most drugs is unknown, but typically the dose given by the endotracheal route is 2 to 2½ times the recommended IV dose.
Dilute the dose in 5 to 10 mL of sterile water (or normal saline) and inject the drug as a rapid spray (aerosolized) directly into the endotracheal tube.
Whenever anyone in cardiac arrest fails to respond to initial efforts, providers should consider potential reversible causes, which may be recalled as the Hs and Ts (see Table 1).
Table 1: Treatable Causes of Cardiac Arrest: The H's and T's
Open table in a new window
Note: Although providers identify ventricular fibrillation (VF) and pulseless VT (pVT), the rhythm analysis detects VF or VT; the determination that the VT is pulseless is a clinical assessment.
The keys to management pf VF/pVT arrest are:
- Immediate delivery of high-quality CPR until defibrillator is available and after each shock
- rapid defibrillation
- if the VF/pVT is refractory to shocks, then vasopressors and antiarrhythmics are delivered as needed.
- Providers should search for and treat reversible causes if cardiac arrest fails to respond
Attempted defibrillation with an AED
- When the initial rhythm check reveals VF/VT, the AED will typically prompt rescuers to charge the device (if it doesn’t do so automatically), quickly “clear” the victim for shock delivery, and then deliver a shock.
- Resume CPR (beginning with chest compressions) immediately after shock delivery, without a rhythm or pulse check, and and continue for 2 minutes before the next rhythm check.
Attempted defibrillation with a manual defibrillator
- When the initial rhythm check reveals VF/VT, the first provider resumes CPR while the second provider charges the defibrillator. After this first rhythm analysis and shock, the defibrillator is ideally charged to the correct subsequent dose before the next rhythm check so if VF/VT persists at the next rhythm check, the shock can be delivered without delay.
- Once the defibrillator is charged, CPR is paused to “clear” the patient for shock delivery.
- After the patient is “clear,” the second provider gives a single shock as quickly as possible to minimize the interruption in chest compressions (“hands-off interval”).
- The first provider resumes CPR beginning with compressions immediately after shock delivery (without a rhythm or pulse check) and continues CPR for 2 minutes.
- After 2 minutes of CPR the sequence is repeated, beginning with a rhythm check.
The provider giving chest compressions should switch at every 2-minute cycle to minimize fatigue.
Defibrillators (using Biphasic Truncated Exponential, Rectilinear biphasic, or monophasic waveforms) are recommended to treat atrial and ventricular arrhythmias.
Based on their greater success in arrhythmia termination, defibrillators using biphasic waveforms (Biphasic Truncated Exponential or Rectilinear biphasic) are preferred to monophasic defibrillators for treatment of both atrial and ventricular arrhythmias.
In the absence of conclusive evidence that 1 biphasic waveform is superior to another in termination of VF, it is reasonable to use the manufacturer’s recommended energy dose for the first shock. If this is not known, defibrillation at the maximal dose may be considered.
It is reasonable that selection of fixed versus escalating energy for subsequent shocks be based on the specific manufacturer’s instructions.
The value of VF waveform analysis to guide management of defibrillation in adults with in-hospital and out-of-hospital cardiac arrest is uncertain.
The primary goal of pharmacologic therapy during cardiac arrest is to facilitate restoration and maintenance of a perfusing spontaneous rhythm. The α-adrenergenic vasoconstrictive effects can improve coronary perfusion pressure and myocardial perfusion, as well as cerebral perfusion.
The timing of drug administration for VF/pVT or Asystole/PEA cardiac arrest is based on the consensus of experts (see Table 2).
Table 2: Timing and sequence of drug administration during cardiac arrest—the knowns and unknowns.
Open table in a new window
The alpha-adrenergic effects of epinephrine can improve the diastolic (relaxation) pressure in the aorta and ultimately improve coronary perfusion pressure. Although epinephrine has not been shown definitively to improve survival with favorable neurological outcome, it has been shown to increase 30-day survival and survival to hospital discharge.
We recommend that epinephrine be administered to patients in cardiac arrest.
On the basis of protocols used in clinical trials, it is reasonable to administer 1 mg every 3-5 minutes.
The optimal timing of epinephrine, particularly in relation to defibrillation when cardiac arrest is due to a shockable rhythm, is not known.
With respect to timing, for cardiac arrest with a shockable rhythm, It may be reasonable to administer epinephrine after initial defibrillation attempts have failed.
Based on the consensus of experts, epinephrine is administered every 3-5 minutes during resuscitation. In practical terms, that means it is typically administered during every other 2-minute period of CPR when VF/pVT persists despite delivery of shocks and high-quality CPR.
High-dose epinephrine is not recommended for routine use in cardiac arrest.
Vasopressin may be considered in a cardiac arrest but offers no advantage as a substitute for epinephrine in cardiac arrest.
In IHCA, the combination of intra-arrest vasopressin, epinephrine, and methylprednisolone and post- arrest hydrocortisone may be considered; however, further studies are needed before recommending the routine use of this therapeutic strategy.
When VF/pVT persists despite shocks and epinephrine, either amiodarone of lidocaine may be administered.
The principal objective of antiarrhythmic drug therapy in shock-refractory VF/pVT is to facilitate the restoration and maintenance of a spontaneous perfusing rhythm in concert with the shock termination of VF.
Do not compromise the quality of CPR or timely defibrillation to establish vascular access to enable drug administration.
Amiodarone or lidocaine may be considered for VF/pVT that is unresponsive to defibrillation. These drugs may be particularly useful for patients with witnessed arrest, for whom time to drug administration may be shorter.
The routine use of magnesium for cardiac arrest is not recommended in adult patients (Class III: No Benefit; LOE C-LD). Magnesium may be considered for torsades de pointes (ie, polymorphic VT associated with long-QT interval).
Recommendations for the use of antiarrhythmic medications in cardiac arrest are based primarily on the potential for improvement in short-term outcome.
If the next rhythm check indicates that no shockable rhythm is present, look for an organized rhythm on the defibrillator screen.
When a rhythm check in a patient in cardiac arrest reveals an organized rhythm, perform a pulse check.
- If a pulse is detected and an adequate blood pressure confirmed, post–cardiac arrest care should be initiated immediately (see Part 8, Post-Cardiac Arrest Care)
- If the pulse is absent (eg, PEA) or the rhythm is asystole, resume CPR immediately, beginning with chest compressions, and provide care that is consistent wth the Asystole/PEA (right) branch of the cardiac arrest algorithm (see Figure 2).
The key to treatment of cardiac arrest associated with Asystole or PEA is
- delivery of high-quality CPR
- epinephrine administration as soon as possible and then every 3-5 minutes (typically during every other 2-minute period of CPR)
- Identification and treatment of reversible causes (see Table 1, above)
First Rhythm analysis:
- When the first rhythm check in an patient in cardiac arrest reveals a nonshockable rhythm, resume CPR immediately, beginning with chest compressions, and treat the patient according to the Asystole/PEA (right) branch of the Adult Cardiac Arrest Algorithm (see Figure 2), beginning at box/step 10. Continue CPR for 2 minutes before the rhythm check is repeated.
Subsequent rhythm analysis:When a rhythm check in a patient in cardiac arrest reveals no shockable rhythm, look for an organized rhythm on the monitor screen. If an organized rhythm is present,perform a pulse check.
- If a pulse is detected and an adequate blood pressure confirmed, post–cardiac arrest care should be initiated immediately (see Part 8, Post-Cardiac Arrest Care).
- If the pulse is absent (eg, PEA) or the rhythm is asystole, resume CPR immediately, beginning with chest compressions, and continue for 2 minutes before the rhythm check is repeated.
If the patient who presented with Asystole/PEA cardiac arrest ever demonstrates a “shockable” rhythm (VF/VT), treat the patient according to the VF/pVT (left) side of the Adult Cardiac Arrest algorithm (see Figure 2).
- If the patient received epinephrine during the previous 2 minutes of CPR, join the algorithm at step 7, delivering a shock and immediately resuming CPR, beginning with compressions.
- If the patient did not receive epinephrine during the previous 2 minutes of CPR, join the algorithm at step 5, delivering a shock and immediately resuming CPR, beginning with compressions.
The provider performing chest compressions should switch every 2 minutes.
Epinephrine administration can improve aortic diastolic (relaxation) pressure and improve coronary perfusion. If the myocardium is better perfused, administration of a shock may be more likely to eliminate VF/VT.
We recommend that epinephrine be administered to patients in cardiac arrest.
On the basis of protocols used in clinical trials, it is reasonable to administer 1 mg every 3-5 minutes.
Post-hoc analysis from a recent out-of-hospital cardiac arrest trial of epinephrine administration demonstrated an association of earlier epinephrine administration for arrest associated with Asystole/PEA and survival.
With respect to timing, for cardiac arrest with a non- shockable rhythm, it is reasonable to administer epinephrine as soon as feasible.
Vasopressin may be considered in cardiac arrest but offers no advantage as a substitute for epinephrine in cardiac arrest.
During each 2-minute period of CPR recall the H’s and T’s to identify factors that may have caused the arrest or may be complicating the resuscitative effort; treat those conditions as soon as possible.
The association of PEA with hypoxemia makes placement of an advanced airway theoretically more important than during VF/pulseless VT and might be necessary to achieve adequate oxygenation or ventilation.
PEA caused by severe volume loss or sepsis may benefit from administration of empirical IV/IO crystalloid.
PEA caused by severe blood loss may benefit from a blood transfusion.
When pulmonary embolism is presumed or known to be the cause of cardiac arrest, empirical fibrinolytic therapy can be considered.
If tension pneumothorax is clinically suspected as the cause of PEA, initial management includes needle decompression.
Echocardiography can be used to guide management of PEA because it provides information about:
- intravascular volume status
- cardiac tamponade
- mass lesions (tumor, clot)
- left ventricular contractility
- regional wall motion.
See “Part 10: Special Circumstances of Resuscitation” for management of toxicological causes of cardiac arrest.
Monitoring both provider performance and patient physiologic parameters during CPR is essential to optimizing CPR quality.
Although no clinical study has examined whether titrating resuscitative efforts to physiologic parameters during CPR improves outcome, it may be reasonable to use physiologic parameters (quantitative waveform capnography, arterial relaxation diastolic pressure, arterial pressure monitoring, and central venous oxygen saturation) when feasible to monitor and optimize CPR quality, guide vasopressor therapy, and detect ROSC.
Ultrasound (cardiac or noncardiac) may be considered during the management of cardiac arrest, although its usefulness has not been well established.
If a qualified sonographer is present and use of ultrasound does not interfere with the standard cardiac arrest treatment protocol, then ultrasound may be considered as an adjunct to standard patient evaluation.
In intubated patients, failure to achieve an End-Tidal CO2 of greater than 10 mm Hg by waveform capnography after 20 minutes of CPR may be considered as one component of a multimodal approach to decide when to end resuscitative efforts, but it should not be used in isolation.
ECPR refers to venoarterial extracorporeal membrane oxygenation during cardiac arrest, including extracorporeal membrane oxygenation and cardiopulmonary bypass. These techniques require adequate vascular access and specialized equipment.
There is insufficient evidence to recommend the routine use of Extracorporeal CPR for patients with cardiac arrest. (2019 ACLS)
Extracorporeal CPR may be considered for selected patients as rescue therapy when conventional CPR efforts are failing in settings in which it can be expeditiously implemented and supported by skilled providers.
The mainstays of restoring acid-base balance during cardiac arrest includes the restoration of oxygen delivery with high-quality CPR and appropriate ventilation with oxygen.
Routine use of sodium bicarbonate is not recommended for patients in cardiac arrest.
In some special resuscitation situations, such a spreexisting metabolic acidosis, hyperkalemia, or tricyclic antidepressant overdose, administration of sodium bicarbonate can be beneficial (see Part 10: Special Circumstances in Resuscitation).
If sodium bicarbonate is administered, whenever possible, bicarbonate therapy should be guided by the bicarbonate concentration or calculated base deficit obtained from blood gas analysis or laboratory measurement. To minimize the risk of iatrogenically induced alkalosis, do not attempt complete correction of the calculated base deficit.
The precordial thump may be considered for termination of witnessed monitored unstable ventricular tachyarrhythmias when a defibrillator is not immediately ready for use , but should not delay CPR and shock delivery.
There is insufficient evidence to recommend for or against the use of the precordial thump for witnessed onset of asystole.
Once there is return of spontaneous circulation, providers begin post-cardiac arrest care, focusing on support of :
- Neurologic function, including Targeted Temperature Management
- Circulation, including treatment of possible acute coronary occlusion (ie, ST-elevation myocardial infarction), arrhythmias andshock, and support of fluid balance
- Oxygenation and Ventilation
For further information, see Part 8: Post-Cardiac Arrest Care.
The final decision to stop resuscitative efforts can never rest on a single parameter, such as duration of resuscitative efforts.
In the out-of-hospital setting, cessation of resuscitative efforts in adults should follow system-specific criteria under direct medical control (see Part 3: Ethical Issue in Resuscitation).
- Electrocardiographic (ECG) and rhythm information should be interpreted within the context of total patient assessment.
- Errors in diagnosis and treatment are likely to occur if treatment decisions neglect clinical evaluation and are based solely on rhythm interpretation.
- Evaluate the patient’s symptoms and clinical signs, including ventilation, oxygenation, heart rate, blood pressure, level of consciousness, and signs of inadequate organ perfusion.
- When an arrhythmia causes a patient to be unstable (vital organ function is acutely impaired or cardiac arrest is ongoing or imminent), immediate intervention is indicated.
- When an arrhythmia is causing symptoms (e.g. palpitations, lightheadedness, or dyspnea) but the patient is stable and not in imminent danger, more time is available to decide on the most appropriate intervention. In both unstable and symptomatic cases make an assessment as to whether the arrhythmia itself is causing the patient to be unstable or symptomatic. Tachycardias, for example, can be a compensatory response to another patient condition (such as hemorrhage or sepsis) at which treatment should instead be directed.
- It is critically important to determine the cause of the patient’s instability in order to properly direct treatment.
- In general, sinus tachycardia is a response to other factors and, thus, it rarely (if ever) is the cause of instability in and of itself.
The goals of management of bradyarrhythmias in adults are to rapidly identify and treat patients who are hemodynamically unstable or symptomatic due to the bradyarrhythmia. Drugs (beginning with atropine) or, when appropriate, pacing may be used to control unstable or symptomatic bradycardia.
If bradycardia produces signs and symptoms of instability (eg, acutely altered mental status, ischemic chest discomfort, acute heart failure, hypotension, or other signs of shock that persist despite adequate airway and breathing), the initial treatment is atropine.
If bradycardia is unresponsive to atropine, intravenous (IV) infusion of β-adrenergic agonists with rate-accelerating effects (dopamine, epinephrine) or transcutaneous pacing (TCP) can be effective while the patient is prepared for emergent transvenous temporary pacing if required.
Figure 4: Adult Bradycardia With a Pulse Algorithm
Bradycardia is defined as a heart rate <60/minute, but symptomatic bradycardia generally is <50/minute. Bradycardias include sinus bradycardia and sinus rhythms with heart block; but can also occur with any rhythm (such as atrial fibrillation) for which the rate is inappropriately slow.
The Bradycardia Algorithm (see Figure 4) focuses on management of clinically significant bradycardia (ie, bradycardia that is inappropriate for the clinical condition).
- Focus initial evaluation on signs of increased work of breathing (tachypnea, intercostal retractions, suprasternal retractions, paradoxical abdominal breathing) and oxyhemoglobin saturation as determined by pulse oximetry (Box 2).
- If oxygenation is inadequate or the patient shows signs of increased work of breathing, provide supplementary oxygen.
- Attach a monitor to the patient, evaluate blood pressure, and establish IV access.
- If possible, obtain a 12-lead ECG to better define the rhythm.
- While initiating treatment, evaluate the patient’s clinical status and identify potentially reversible causes.
- Identify signs and symptoms of poor perfusion and determine if those signs are likely to be caused by the bradycardia (Box 3).
- If the signs and symptoms are not due to bradycardia, reassess the underlying cause of the patient’s symptoms.
- Signs and symptoms of bradycardia may be mild; asymptomatic or minimally symptomatic patients do not necessarily require treatment (Box 4) unless there is suspicion that the rhythm is likely to progress to symptoms or become life-threatening (eg, Mobitz type II second-degree AV block in the setting of acute myocardial infarction [AMI]).
- If the bradycardia is suspected to be the cause of acute altered mental status, ischemic chest discomfort, acute heart failure, hypotension, or other signs of shock, timmediate treatment is needed.
Atropine remains the first-line drug for acute symptomatic bradycardia.
- Recommended atropine dose for bradycardia: 0.5 mg IV every 3 to 5 minutes to a maximum total dose of 3 mg.
- Doses of atropine sulfate of <0.5 mg may paradoxically result in further slowing of the heart rate.
- Atropine administration should not delay implementation of external pacing for patients with poor perfusion.
- Use atropine cautiously in the presence of acute coronary ischemia or MI; increased heart rate may worsen ischemia or increase infarction size.
- Atropine will likely be ineffective in patients who have undergone cardiac transplantation because the transplanted heart lacks vagal innervation.
NOTE: Providers should not rely on atropine in type II second-degree or third-degree AV block or in patients with third-degree AVmblock with a new wide-QRS complex where the location of block is likely to be in non-nodal tissue (such as in the bundle of His or more distal conduction system). These bradyarrhythmias are not likely to be responsive to reversal of cholinergic effects by atropine and are preferably treated with transcutaneous pacing (TCP) or β- adrenergic support as temporizing measures while the patient is prepared for transvenous pacing (see Figure 4, Box 6).
Transcutaneous pacing is painful in conscious patients, and, it is at best a temporaizing measure. Whether it is effective or not (ie, achieving inconsistent capture), prepare the patient for transvenous pacing and obtain expert consultation.
It is reasonable for healthcare providers to initiate transcutaneous pacing in unstable patients who do not respond to atropine.
Immediate pacing might be considered in unstable patients with high-degree AV block when IV access is not available. If the patient does not respond to drugs or transcutaneous pacing, transvenous pacing is probably indicated. See Figure 4, Box 6.
Dopamine infusion may be used for patients with symptomatic bradycardia, particularly if associated with hypotension, in whom atropine may be inappropriate or after atropine fails.
Begin the dopamine infusion at 2-10 mcg/kg per minute and titrate to patient response.
Epinephrine infusion may be used for patients with symptomatic bradycardia, particularly if associated with hypotension, for whom atropine may be inappropriate or after atropine fails.
Begin the infusin at 2 to 10 mcg per minute.
Isoproterenol is a beta-adrenergic agent with beta-1 and beta-2 effects, resulting in an increase in heart rate and vasodilation. The recommended adult dose is 2 to 10 mcg/min by IV infusion, titrated according to heart rate and rhythm response.
The goal of therapy for tachycardia is to rapidy identify and treat patients who are hemodynamically unstabe or symptomatic due to the arrhythmia. Cardioversion or drugs or both may be used to control unstable or symptomatic tachycardia.
Management of patients with symptomatic tachyarrhythmias is summarized in the algorithm (see Figure 5).
If the tachycardic patient is unstable with severe signs and symptoms related to a suspected arrhythmia (eg, acute altered mental status, ischemic chest discomfort, decompensated heart failure, hypotension, or other signs of shock), immediate cardioversion should be performed (with prior sedation in the conscious patient).
In select cases of regular narrow-complex tachycardia with unstable signs or symptoms, a trial of adenosine before cardioversion is reasonable to consider.
The principles of management of tachyarrhythmias is requires identification of the unstable patient and determining if the tachycardia is narrow-complex or wide-complex tachycardia, has a regular or irregular rhythm, and, for wide complex tachycardia, whether the QRS morphology is monomorphic or polymorphic.
Figure 5: Adult Tachycardia With a Pulse Algorithm
The first step in the management of any tachycardia is to determine if the patient’s condition is stable or unstable (Figure 5, Box 3).
- If the patient is unstable, proceed with immediate cardioversion (see Therapy for Regular Wide-Complex Tachycardias, below)
- If the patient is stable, continue evaluation by determining if rhythm is regular (vs irregular)
The most common forms of wide- complex tachycardia are:
- VT or VF
- SVT with aberrancy
- Pre-excited tachycardias (associated with or mediated by an accessory pathway)
- Ventricular paced rhythms
Determine if the rhythm is regular or irregular.
- A regular wide-complex tachycardia is likely to be VT or SVT with aberrancy.
- An irregularly irregular wide-complex tachycardia with uniform QRS complexes from beat-to-beat may be atrial fibrillation with aberrancy. Conversely an irregular wide complex tachycardia in which QRS complexes differ in their appearance (morphology) between beats could be pre-excited atrial fibrillation (ie, atrial fibrillation using both the AV node and an accessory pathway for antegrade conduction), or polymorphic VT/torsades de pointes.
- Consider the need for expert consultation when treating wide-complex tachycardias.
An unstable patient with a wide-complex tachycardia should be presumed to have VT, and immediate synchronized cardioversion should be performed (Figure 5, Box 4 and see Electrical Cardioversion, above).
- If the patient becomes unstable proceed with synchronized cardioversion.
- Deliver an unsynchronized higher-dose defibrillation shock if the arrhythmia deteriorates to VF or a polymorphic or irregular VT is present, preventing synchronization of the shock.
If the patient is stable:
- obtain a 12-lead ECG (Boxes 6 and 7) to further evaluate the rhythm and help establish a diagnosis.
- consider the need to obtain expert consultation.
If the etiology of the rhythm cannot be determined, the rate is regular, and the QRS is monomorphic, IV adenosine is relatively safe for both treatment and diagnosis.
- If the wide-complex tachycardia proves to be SVT with aberrancy it will likely be transiently slowed or converted by adenosine to sinus rhythm.
- If the wide-complex tachycardia is VT there will be no effect on rhythm (except in rare cases of idiopathic VT), and the brevity of the transient adenosine effect should be reasonably tolerated hemodynamically.
- Continuous ECG recording to provide written documentation is strongly encouraged as close attention to varying responses to treatment may help to diagnose the underlying rhythm even if after the fact.
- Typically, adenosine is administered in a manner similar to treatment of PSVT: as a 6 mg rapid IV push; providers may follow the first dose with a 12 mg bolus and a second 12 mg bolus if the rate fails to convert.
- When adenosine is given for undifferentiated wide-complex tachycardia, a defibrillator should be available.
Adenosine should not be given for unstable or for irregularly irregular or polymorphic wide-complex tachycardias, as it may cause degeneration of the arrhythmia to VF.
Verapamil is contraindicated for wide-complex tachycardias unless known to be of supraventricular origin.
For patients who are stable with likely VT, IV antiarrhythmic drugs or elective cardioversion is the preferred treatment strategy.
Procainamide and sotalol should be avoided in patients with prolonged QT. If one of these antiarrhythmic agents is given, a second agent should not be given without expert consultation. Procainamide should be avoided in patients with prolonged QT and congestive heart failure.
An irregularly irregular narrow-complex or wide-complex tachycardia (meaning the interval between successive beats is variable or chaotic) is most likely atrial fibrillation (with or without aberrant conduction) with an uncontrolled ventricular response. Other diagnostic possibilities include MAT or sinus rhythm/tachycardia with frequent atrial premature beats.
General management of atrial fibrillation focuses on control of the rapid ventricular rate (rate control), conversion of hemodynamically unstable atrial fibrillation to sinus rhythm (rhythm control), or both.
Patients with an atrial fibrillation duration of >48 hours are at increased risk for cardioembolic events, although shorter durations of atrial fibrillation do not exclude the possibility of such events. Electric or pharmacologic cardioversion (conversion to normal sinus rhythm) should not be attempted in these patients unless the patient is unstable.
An alternative strategy is to perform cardioversion following anticoagulation with heparin and performance of transesophageal echocardiography to ensure the absence of a left atrial thrombus;
See the ACC/AHA Guidelines for Management of Patients with Atrial Fibrillation.
Polymorphic (irregular) VT requires immediate defibrillation with the same strategy used for VF.
Pharmacologic treatment to prevent recurrent polymorphic VT should be directed by the underlying cause of VT and the presence or absence of a long QT interval during sinus rhythm.
Long QT interval observed during sinus rhythm (ie, the VT is torsades de pointes):
- stop medications known to prolong the QT interval
- correct electrolyte imbalance and other acute precipitants (eg, drug overdose or poisoning—see Part 12: Cardiac Arrest Associated With Toxic Ingestions)
- polymorphic VT associated with long QT syndrome may be treated with IV magnesium
- polymorphic VT associated with known familial long QT may also be treated with pacing and/or β-blockers
- isoproterenol should be avoided in polymorphic VT associated with known familial long QT
- the addition of pacing or IV isoproterenol may be considered when polymorphic VT is accompanied by bradycardia or appears to be precipitated by pauses in rhythm.
In the absence of a prolonged QT interval, the most common cause of polymorphic VT is myocardial ischemia. In this situation IV amiodarone and beta-blockers may reduce the frequency of arrhythmia recurrence.
Myocardial ischemia should be treated with beta-blockers and consideration be given to expeditious cardiac catheterization with revascularization.
Magnesium is unlikely to be effective in preventing polymorphic VT in patients with a normal QT interval, but amiodarone may be effective.
Other causes of polymorphic VT apart from ischemia and long QT syndrome are catecholaminergic VT (which may be responsive to beta-blockers) and Brugada syndrome (which may be responsive to isoproterenol).
Figure 6: Adult Advanced Cardiovascular Life Support
The American Heart Association requests that this document be cited as follows:
American Heart Association. Web-based Integrated Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care – Part 7: Adult Advanced Cardiovascular Life Support. ECCguidelines.heart.org
© Copyright 2015 American Heart Association, Inc.