48 Hours or Less
Step 1. Control the rate Preserved Ventricular Function
• Diltiazem or Verapamil
or
• Metoprolol (or another beta-blocker) And consider 1 of the following
• Procainamide
• Amiodarone
• Digoxin
Impaired Ventricular Function (EF <40%)
• Diltiazem or
• Digoxin or
• Amiodarone
Step 2. Convert the Rhythm DC Cardioversion and/or Antiarrhythmicsa
Preserved Ventricular Function
Use 1 of the following;
• Amiodarone
• Procainamide
• Ibutilide
• Flecainide
• Propafenone
Impaired Ventricular Function (EF <40%)
• Amiodarone
48 Hours or More or Unknown Duration
Step 1. Control the rate Preserved Ventricular Function
• Diltiazem or Verapamil or
• Metoprolol (or another beta-blocker) Avoid antiarrhythmics for rate control as they may convert the rhythm and cause
embolization.
Impaired Ventricular Function (EF <40%)
• Diltiazem or
• Digoxin or
• Amiodarone
Step 2. Convert the Rhythm† DC Cardioversiona
Urgent Cardioversion 1. Begin IV heparin 2. TEE to rule out atrial clot
3. If no clot, cardioversion within 24 hours 4. If rhythm converts, continue
anticoagulation for 4 more weeks Delayed Cardioversion
1. Anticoagulation with INR 2–3 for at least 3 weeks
2. Cardioversion
3. If rhythm converts, continue anticoagulation for 4 more weeks
†If WPW, DO NOT use AV nodal blocking agents as they may worsen tachycardia 1) DC Cardioversion or
2) Sotalol, Amiodarone, Procainamide, Propafenone, or Flecainide.
Atrial fibrillation or flutter with serious signs and symptoms of
hemodynamic instability requiring immediate treatment?
Synchronized DC cardioversion
Duration of atrial fibrillation or flutter
Atrial fibrillation or flutter with WPW?
YES NO
YES
NO
DC, direct current; WPW, Wolff–Parkinson–White; EF, ejection fraction; IV, intravenous; TEE, transesophageal echocardiogram; INR, international normalized ratio.aPremedicate when possible with a sedative (e.g., diazepam, midazolam, ketamine, and etomidate) and analgesic (e.g., fentanyl and morphine). Perform synchronized cardioversion with 100 J, 200 J, 300 J, 360 J biphasic energy or monophasic equivalent, starting with lowest energy level and increasing if needed. Perform asynchronous cardioversion if delays in synchronized cardioversion with worsening clinical status.
Cardiac Disorders rCardiac Arrhythmias and Conduction Abnormalities 1 4 7
by the QRS complexes. If visible, they generally present as narrow inverted P waves at the end of the QRS complex, commonly described as a “pseudo R” in V1 and/or
“a pseudo S” in lead II. AV nodal re-entrant tachycardia is not associated with any specific diseases, can occur at any age, and is more common in women.
PSVT may also be mediated by an accessory pathway between the atria and ventricles that bypasses the AV node.Manifestaccessory pathways are seen on the sinus rhythm ECG as a delta wave of pre-excitation. The pre-excitation also causes a short PR interval because the accessory pathway does not have the delayed conduc- tion of the AV node. Accessory pathways may conduct antegrade (forming the delta wave) or retrograde.Concealedaccessory AV pathways only conduct retrograde, and are invisible in sinus rhythm. Either of these pathways may mediate anorthodromic re-entrant tachycardiain which the electrical impulse propagates antegrade through the AV node and retrograde (from ventricle to atrium) through the accessory pathway.
The result is a narrow QRS complex tachycardia, typically with inverted retrograde P waves between the QRS and T wave (although the QRS may be wide because of aberrancy, e.g., bundle branch block or fascicular block).
The patient with visible pre-excitation (delta wave and short PR interval) in sinus rhythm and with palpitations (usually from paroxysmal orthodromic re-entrant tachycardia) is said to haveWolff–Parkinson–White syndrome(WPW). Patients with WPW are also prone to arrhythmias with antegrade conduction through the accessory pathway. These includeantidromic re-entrant tachycardia, in which the excitation prop- agates antegrade through the accessory pathway and retrograde through the AV node.
Atrial arrhythmias (including atrial fibrillation) may also conduct antegrade through the accessory pathway. The short refractory period of the accessory pathway may allow very rapid conduction of impulses to the ventricles, resulting in rapid “pre-excited atrial fibrillation” with ventricular rates up to 300 beats per minute, often resulting in hemodynamic instability requiring urgent intervention. Rapid conduction of atrial fibrillation through an accessory pathway may also induce ventricular fibrillation (VF).
This is thought to be the pathogenesis of the rare sudden death that is associated with WPW.
Treatmentof PSVT aims at aborting the re-entrant rhythm by blocking con- duction through the AV node with vagal maneuvers (Valsalva, carotid massage, face immersion in cold water [diving reflex]) or adenosine given as a 6 mg IV bolus (t1/2 approximately 10 seconds). A second 12-mg dose can be given after 1 to 2 minutes if the first was ineffective, and a third dose of 12 or 18 mg can be given if needed. If these treatments fail, the AV nodal blocking agents beta-blockers, calcium channel blockers, or digoxin should be used. Patients with WPW and pre-excited atrial fibrillation or flutter must be rapidly treated with direct current cardioversion or class IA, IC, or III drugs (e.g., procainamide, flecainide, and amiodarone), which slow myocardial con- duction and prolong the refractory period, and not AV nodal blocking agents especially when the accessory pathway has a short anterograde refractory period capable of rapid ventricular conduction (Algorithm 20.6).
Ectopic atrial tachycardia occurs when there is automaticity at a single focus out- side the sinoatrial (SA) node. A P wave precedes each QRS as in sinus tachycardia, but the P wave axis is altered. When increased automaticity occurs at three or more different atrial sites, which may include the SA node, it is termedmultifocal atrial tachycardia, with the alternating foci causing at least three P wave morphologies on ECG. Both can be seen in cases of digitalis toxicity (which causes increased automaticity), severe cardiopulmonary disease, hypokalemia, hyperadrenergic states, and as a side effect of theophylline.
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Treatmentincludes AV nodal blocking agents and removal of inciting agents/
factors.
Ventricular Tachycardias
The two main tachyarrhythmias arising from the ventricles areVFandVT. VT may be monomorphic, if the QRS morphology is fixed, or polymorphic, if the QRS complex is variable. Polymorphic VT is more like VF than monomorphic VT in that it results in chaotic ventricular activation, often with hemodynamic instability, possibly leading to cardiac arrest and sudden death. Also like VF, it is more likely to occur in the setting of acute ischemia, infarct, or acute heart failure.
Monomorphic VT results from re-entrant electrical impulses within the ventri- cles or from a focal ventricular site with frequent spontaneous action potentials that propagate to the remainder of the ventricles. VT is characterized on ECG by a wide QRS complex (>0.12 seconds), and a rate usually between 100 and 200 beats per minute (although it may be higher). VT that lasts<30 seconds is termednonsustained VT(NSVT), and sustained VT (just termedVT) if it lasts>30 seconds. The most common setting for monomorphic VT is in healed myocardial infarction. It occurs less commonly in acute ischemia and infarct. Importantly, monomorphic VT may occur in the absence of structural heart disease. The “idiopathic VTs” do not have a poor prognosis and may not cause hemodynamic instability, emphasizing the need to assess and treat the patient’s condition, and not solely the ECG.
An important specific type of polymorphic VT istorsades de pointes,which is poly- morphic VT associated with prolongation of the QT interval (in sinus rhythm) from numerous causes, including (a) drugs (especially tricyclic antidepressants, antipsy- chotics, certain antiarrhythmics, macrolides, and fluoroquinolone; see Web site in Algorithm 20.5); (b) electrolyte abnormalities (hypokalemia, hypomagnesemia, and hypocalcemia); and (c) congenital long QT syndromes. Torsades de pointes appears on ECG as a characteristic pattern of oscillating amplitude of the QRS, or “twisting,”
around the baseline. Torsades de pointes is generally symptomatic but may be nonsus- tained. If prolonged, hemodynamic instability, syncope, and/sudden death may result.
Wide complex tachycardias (except clear sinus tachycardia with aberrancy) should initially be assumed to be VT, and the urgency of treatment should depend on assess- ment of the patient and the hemodynamic situation. Distinguishing VT from SVT with a wide QRS is therefore of secondary importance. Mistaken diagnosis of “SVT with aberrancy” can result in mistreatment. The differential diagnosis of wide com- plex tachycardia is threefold: (a) VT, (b) SVT with aberrancy (typical bundle branch or fascicular blocks or atypical aberrancy), and (c) pre-excited supraventricular rhythm (including atrial fibrillation) in which case the ECG in sinus rhythm will typically feature a delta wave.
Algorithm 20.5 shows the ECG criteria that favor VT. Also, old ECGs should be examined for bundle branch blocks or ventricular pre-excitation syndromes. As previously mentioned, if the diagnosis of the wide complex rhythm is uncertain, it should be assumed to be VT, and treatment should proceed according to the patient’s condition.
NSVT may occur in the setting of acute ischemia, and evaluation and treatment should be focused on the ischemia. Direct pharmacologic treatment (e.g., lidocaine and amiodarone) of NSVT in ischemia/infarct is not advisable. In the patient not suffering from active ischemia, NSVT is frequently asymptomatic and has little prognostic utility for malignant arrhythmia, especially in the absence of structural heart disease
Cardiac Disorders rCardiac Arrhythmias and Conduction Abnormalities 1 4 9
and ventricular dysfunction. Symptomatic NSVT may be treated pharmacologically, primarily to relieve symptoms.
Sustained VT generally causes symptoms by impairing CO, resulting in hypoten- sion, loss of consciousness, and possibly cardiac arrest. It may also deteriorate into VF.
Treatmentof symptomatic VT with a detectable pulse issynchronousdirect cur- rent cardioversion (with sedation or anesthesia in the awake patient) or, if the VT is well tolerated, with an antiarrhythmic drug (such as procainamide, amiodarone, or lidocaine). Patients with hemodynamically compromising, pulseless monomorphic or polymorphic VT usually require immediate treatment with asynchronous defibrilla- tion (see section “Cardiac Arrest”), followed by antiarrhythmic drugs if necessary.
Sustained torsades de pointes with hemodynamic collapse also requires asyn- chronous cardioversion. Treatment of torsades de pointes aims at correcting any under- lying electrolyte abnormalities and stopping any drugs known to prolong the QT inter- val. Torsades de pointes is likely to recur if the inciting factors cannot be eliminated immediately. Magnesium sulfate given at 1 to 2 mg IV may have utility, particularly in hypomagnesemic patients. Lidocaine or phenytoin may also be suppressive. Torsades de pointes is frequentlybradycardia dependent,and temporary pacing or isoproterenol infusion may be used to increase the HR and prevent recurrences.
VFis the result of chaotic electrical currents within the ventricles, preventing coordinated contractions. VF on ECG has a chaotic appearance without any discernible QRS complex. Untreated VF rapidly results in death. VF may be preceded by VT and is most commonly seen in patients with acute myocardial infarction.
Treatmentis immediate asynchronous electrical defibrillation, followed by antiar- rhythmic drugs when a stable rhythm returns (see section “Cardiac Arrest”). Also see treatment Algorithm 20.3.
B R A D Y A R R H Y T H M I A S
Bradycardia, defined as a HR of less than 60 beats per minute, occurs from (a) SA node dysfunction or (b) disturbances of the AV conduction system. Clinically significant bradycardia occurs when there is inadequate CO, generally associated with hypoten- sion, and which may manifest as any or all of presyncope, syncope, fatigue, confusion, depressed level of consciousness, chest pain, shock, or congestive heat failure. Acute treatment aims at restoring adequate CO and identifying the underlying rhythm and its cause.
SA node dysfunction occurs in a number of pathophysiologic states seen in the intensive care unit including increased intracranial pressure, prolonged apneic periods in patients with the obstructive sleep apnea/hypopnea syndrome, myocardial infarction advanced liver disease, hypothyroidism, hypothermia, hypercapnia, acidemia, hyper- vagotonia, and certain infections. It may also be due to depression of the sinus node by drugs, including sympatholytics such as beta-blockers and clonidine, the cardios- elective calcium channel blockers verapamil and diltiazem, parasympathomimetics, and antiarrhythmic drugs such as amiodarone. Sick sinus syndrome refers to intrinsic sinus node dysfunction with any of the previously mentioned clinical symptoms asso- ciated with the decrease in CO. An important variant of sick sinus syndrome is sinus bradycardia or prolonged sinus pause occurring after termination of atrial fibrillation or other atrial arrhythmias due to depression of SA node automaticity during the tachyarrhythmia, which may be slow to recover. Syncope is a common presentation of this variant, termed thetachy-brady syndrome.
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Disturbances of the AV conduction system can occur in the atria, AV node, or His–Purkinje system. When there is complete block in any part of the AV conduc- tion system (termedthird-degree AV block), an escape pacemaker generally develops.
When complete blockage occurs in the AV node, the His bundle escape pacemaker generally takes over at a rate of 40 to 60 beats per minute, and is associated with a narrow QRS complex (in the absence of an underlying bundle branch block or other aberrant conduction). Complete heart block distal to the AV node often results in an escape pacemaker originating from the more distal conduction system, usually with a rate between 25 and 45 beats per minute. These fascicular escape rhythms generate a QRS complex consistent with their origin (e.g., if the origin is in the right bun- dle, the QRS has a left bundle branch block pattern). If the conduction system fails, a rhythm from the ventricular myocardium may generate a heart beat, with a wide complex of ventricular origin. Thus, in general, the more distal the escape rhythm, the slower and less reliable it tends to be. Heart block with irregular fascicular escapes may require urgent temporary pacing. The ECG shows AV dissociation with nonconducted P waves that “march” out independently of the ventricular escape rhythm. There are many causes of third-degree heart block including acute myocardial infarction, idio- pathic fibrosis, drug toxicity (e.g., digitalis, beta-blockers, and cardioselective calcium channel blockers), chronic cardiopulmonary disease, congenital heart disease, infiltra- tive diseases (sarcoidosis), infections/inflammatory diseases, collagen vascular diseases, trauma, and tumors.
First-degree AV blockis not trulyblock, but is a PR interval>200 ms. It is in itself generally benign, but may result in symptoms if the degree of AV dyssynchrony is severe.
Second-degree AV blockoccurs when some atrial impulses fail to conduct to the ventricles.Mobitz type I second-degree AV block(Wenckebach block) is character- ized on ECG by a variable (usually progressively prolonging) PR interval culminating in a nonconducted atrial beat. Mobitz I uncommonly progresses to complete heart block. When it does, the escape pacemaker of 40 to 60 beats per minute in the His bundle usually provides an adequate backup rate to maintain CO. Mobitz I block can be caused by drugs such as digoxin, beta-blockers, certain calcium channel block- ers, ischemia (especially of the inferior wall), or in healthy individuals from hyper- vagotonia.
Mobitz type II second-degree AV blockgenerally is due to disease in the His–
Purkinje system and is characterized on ECG by a fixed PR interval with one or more nonconducting atrial impulses. It is more likely to progress to complete heart block than Mobitz 1, sometimes precipitously. The typical escape pacemaker rate of 25 to 45 arises in the more distal His–Purkinje system and has a wide QRS. The escape rhythm may not be sufficient to maintain CO and can progress rapidly to cardiac arrest and death.
Mobitz II can occur from ischemia (especially anteroseptal infarcts), endocarditis, valvular or congenital heart disease, drugs such as procainamide, disopyramide, and quinidine, or idiopathic progressive cardiac conduction system diseases.
Treatmentof clinically significant bradycardia follows the ACLS algorithm out- lined in Algorithm 20.2, and aims at maintaining adequate CO. Atropine is first-line transient pharmacologic therapy, and is more successful in patients with sinus brady- cardia or block within the AV node, rather than block in the more distal His–Purkinje system. Patients who remain clinically unstable require immediate transcutaneous or transvenous pacing. Reversible causes should be identified. In patients with sinus node dysfunction in which the cause is not reversible, permanent pacing can relieve symp- toms. Permanent pacing is typically indicated in Mobitz II or third-degree AV block.
Cardiac Disorders rCardiac Arrhythmias and Conduction Abnormalities 1 5 1
If symptoms of bradycardia are present in Mobitz I AV block, permanent pacing is indicated.
C A R D I A C A R R E S T
Cardiac arrest refers to the cessation of a detectable noninvasive blood pressure and pulse. Cardiac arrest can be separated into three main types: (a) pulseless electrical activity (PEA), (b) VT and VF, and (c) asystole. All three fall under the overall heading of pulseless arrest outlined in Algorithm 20.3. Treatment of PEA and asystole is similar and centers on identifying reversible causes and pharmacologic intervention. VT and VF are treated with immediate electrical defibrillation. Studies have shown that the most important aspect of resuscitation remains CPR.
Treatment of cardiac arrest in an intensive care unit setting requires a team of nurses and physicians trained in ACLS. Ideally there should be an established and easily identifiable team leader responsible for continuously evaluating the patient’s condi- tion and the ECG, assimilating incoming data, and giving all orders. In addition, there should be a scribe, recording changes in condition, ECG and laboratory data, and therapies delivered. Initial patient evaluation follows the ABCs of cardiac arrest in a coordinated and overlapping fashion, ensuring adequate airway control, breath- ing (i.e., ventilation), and circulation. In nonintubated patients, an oral airway device should be placed and a bag-valve-mask should be used to deliver breaths. Intubation is performed when possible. Cardiopulmonary resuscitation (CPR) should begin imme- diately with chest compressions given at a rate of 100 compressions per minute at 1.5 to 2 inches depth, allowing full chest recoil between compressions. Patients should also be immediately connected to an automated external defibrillator (AED), or a manual defibrillator if an AED is not available. The defibrillator is connected to two pads or paddles placed on the chest wall, with one to the right of the sternum centered on the second intercostal space, and one on the left chest wall centered in the midaxillary line at the fifth intercostal space. IV access should be ensured for delivery of medica- tions and fluids. Peripheral IV access is initially adequate. However, central IV access should be obtained as soon as possible via the femoral vein, subclavian vein, or internal jugular vein. Endotracheal intubation or central IV access should not interfere with CPR. Pulses are best monitored in the femoral artery, but the carotid arteries may be used. Once airway control is established and the patient is connected to an external defibrillator, the cardiac rhythm should be rapidly analyzed (Table 20.1).
Pulseless VT and VF
Confirmed VT and VF with hemodynamic collapse should be treated withimmediate asynchronous defibrillation. Automated AED devices typically deliver escalating bipha- sic shocks at 200, 300, and 360 joules (J). Manual devices may generate monophasic or biphasic waveforms. If a manual biphasic device is used and the devices recommended dose scale is unknown, an initial dose of 200 J should be used, with subsequent shocks at the same or higher doses. If a monophasic device is used, the dose should be 360 J for all shocks. The patient’s rhythm, blood pressure, and responsiveness must be continuously monitored with appropriate adjustment of therapy (e.g., continua- tion/discontinuation of CPR and infusion of new medications). If VT/VF persists or recurs after initial treatment, CPR should be resumed immediately after the first shock is given and continued for 2 minutes along with continuous ventilation via a mask air- way or endotracheal tube. The rhythm and pulse should be reassessed 2 minutes after