James K. Takayesu
SINUS ARRHYTHMIA
Some variation in the sinoatrial (SA) node discharge rate is common; however, if the variation exceeds 0.12 second between the longest and shortest intervals, sinus arrhythmia is present. The electrocardiogram (ECG) characteristics of sinus arrhythmia are (a) normal sinus P waves and PR intervals, (b) 1:1 atrioventricular (AV) conduction, and (c) variation of at least 0.12 second between the shortest and longest P-P interval (Fig. 4-1). Sinus arrhythmias are affected primarily by respiration and are most commonly found in children and young adults, disappearing with advancing age. Occasional junctional escape beats may be present during very long P-P intervals. No treatment is required.
FIG. 4-1. Sinus arrhythmia.
PREMATURE ATRIAL CONTRACTIONS
Premature atrial contractions (PACs) have the following ECG characteristics: (a) the ectopic P wave appears sooner (premature) than the next expected sinus beat; (b) the ectopic P wave has a different shape and direction; and (c) the ectopic P wave may or may not be conducted through the AV node (Fig. 4-2). Most PACs are conducted with typical QRS complexes, but some may be conducted aberrantly through the infranodal system, typically with a right bundle branch block (RBBB) pattern. When the PAC occurs during the absolute refractory period, it is not conducted. Since the sinus node is often depolarized and reset, the pause is less than fully compensatory. PACs are associated with stress, fatigue, alcohol use, tobacco, coffee, chronic obstructive pulmonary disease (COPD), digoxin toxic-ity, coronary artery disease, and may also occur after adenosine-converted paroxysmal supraventricular tachycardia (PSVT). PACs are common in all ages, often in the absence of significant heart disease. Patients may complain of palpitations or an intermittent “sinking” or “fluttering” feeling in the chest.
FIG. 4-2. Premature atrial contractions (PACs). A. Ectopic P′ waves (arrows). B. Atrial bigeminy.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
1. Discontinue precipitating drugs (alcohol, tobacco, or coffee) or toxins.
2. Treat underlying disorders (stress or fatigue).
3. PACs that produce significant symptoms or initiate sustained tachycardias can be suppressed with agents such as β-adrenergic antagonists (eg, metoprolol 25–50 milligrams PO three times daily), usually in consultation with a follow-up physician.
SUPRAVENTRICULAR BRADYARRYTHMIAS
SINUS BRADYCARDIA
CLINICAL FEATURES
Sinus bradycardia occurs when the SA node rate becomes slower than 60 beats/min. The ECG characteristics of sinus bradycardia are (a) normal sinus P waves and PR intervals, (b) 1:1 AV conduction, and (c) atrial rate slower than 60 beats/min. Sinus bradycardia represents a suppression of the sinus node discharge rate, usually in response to three categories of stimuli: (a) physiologic (vagal tone), (b) pharmacologic (calcium channel blockers, β-blockers, or digoxin), and (c) pathologic (acute inferior myocardial infarction [MI], increased intracranial pressure, carotid sinus hypersen-sitivity, hypothyroidism, or sick sinus syndrome).
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Sinus bradycardia usually does not require specific treatment unless the heart rate is slower than 50 beats/min and there is evidence of hypoperfusion.
1. Transcutaneous cardiac pacing is the only Class I treatment for unstable patients.
a. Attach the patient to the monitor leads of the external pacing device.
b. When placing transcutaneous pacing pads, place the anterior pad over the left lateral precordium and the posterior pad at the level of the heart in the right infrascapular area. Do not use multifunction pacing defibrillation pads unless the patient is unconscious as they cause a lot of discomfort.
c. Slowly increase the pacing output from 0 mA to the lowest point where capture is observed, usually at 50 to 100 mA, but may be up to 200 mA. A widened QRS after each pacing spike denotes electrical capture.
d. If needed, administer a sedative, such as lorazepam, 1 to 2 milligrams IV or an opiate, such as morphine, 2 to 4 milligrams IV for pain control.
2. Atropine is a Class IIa treatment for symptomatic bradycardia. The dose is 0.5 milligram IV push, repeated every 3–5 minutes as needed up to a total of 3 milligrams IV If given via endotracheal tube, increase the dose by 2–2.5 times over the IV dose. Slow administration or lower doses may cause paradoxical bradycardia. Atropine may not be effective in cardiac transplant patients since the heart is den-ervated and has no vagal stimulation.
3. Epinephrine, 2–10 micrograms/min IV, or dopa-mine, 3–10 micrograms/kg/min IV, may be used if external pacing is not available.
4. Internal pacing will be required in the patient with symptomatic recurrent or persistent sinus bradycardia due to sick sinus syndrome.
5. Isoproterenol, 2–10 micrograms/min IV infusion, may be effective but carries a risk of increased myo-cardial oxygen demand.
SUPRVENTRICULAR TACHYARRYTHMIAS
SINUS TACHYCARDIA
CLINICAL FEATURES
The ECG characteristics of sinus tachycardia are (a) normal sinus P waves and PR intervals and (b) an atrial rate usually between 100 and 160 beats/min. Sinus tachycardia is in response to three categories of stimuli: (a) physiologic (pain or exertion), (b) pharmacologic (sympathomimetics, caffeine, or bronchodilators), or (c) pathologic (fever, hypoxia, anemia, hypovolemia, pulmonary embolism, or hyperthyroidism). In many of these conditions, the increased heart rate is an effort to increase cardiac output to match increased circulatory needs.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Diagnose and treat the underlying condition.
SUPRAVENTRICULAR TACHYCARDIA
CLINICAL FEATURES
Supraventricular tachycardia (SVT) is a regular, rapid rhythm that arises from impulse reentry or an ectopic pacemaker above the bifurcation of the His bundle. The reentrant variety is the most common (Fig. 4-3). Patients often present with acute, symptomatic episodes termed paroxysmal supraventricular tachycardia (PSVT). Atrioventricular nodal reentrant tachycardia (AVnRT) can occur in a normal heart or in association with rheumatic heart disease, acute pericarditis, MI, mitral valve prolapse, or preexcitation syndromes. In patients with atrioventricular bypass tracts (AVRT), reentry can occur in either direction, usually (80–90% of patients) in a direction that goes down the AV node and up the bypass tract producing a narrow QRS complex (orthodromicconduction). In the remaining 10% to 20% of patients, reentry occurs in the reverse direction (antidromic conduction). Ectopic SVT usually originates in the atria, with an atrial rate of 100–250 beats/min and may be seen in patients with acute MI, chronic lung disease, pneumonia, alcohol intoxication, or digoxin toxicity
FIG. 4-3. Reentrant supraventricular tachycardia (SVT). A. Second (*) initiates run of PAT. B. SVT, rate 286.
There is a high incidence of tachyarrhythmias in patients with preexcitation syndromes including PSVT (40–80%), atrial fibrillation (10–20%), and atrial flutter (about 5%). All forms of preexcitation are caused by accessory tracts that bypass part or all of the normal conducting system, the most common form being Wolff-Parkinson-White (WPW) syndrome (Fig. 4-4). The ventricles are activated by an impulse from the atria sooner than would be expected if the impulse were transmitted down the normal conducting pathway. This premature activation causes initial fusion beat morphology with slurring of initial QRS complex, causing the pathognomonic delta wave. Among patients with WPW-PSVT, 80% to 90% will conduct in the orthodromic direction and the remaining 10% to 20%) will conduct in the antidromic direction. ECG findings of atrial fibrillation or flutter with antidromic conduction down the bypass tract show a wide QRS complex that is irregular with a rate faster than 180–200 beats/min (see Atrial Fibrillation below).
FIG. 4-4. Type A Wolff-Parkinson-White syndrome.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
1. Perform synchronized cardioversion in any unstable patient (eg, hypotension, pulmonary edema, or severe chest pain).
2. In stable patients, the first intervention should be vagal maneuvers, including:
a. Valsalva maneuver: While in the supine position, ask the patient to strain for at least 10 seconds. The legs may be lifted to increase venous return and augment the reflex.
b. Diving reflex: Have the patient immerse the face in cold water or apply a bag of ice water to the face for 6–7 seconds. This maneuver is particularly effective in infants.
c. Carotid sinus massage: Auscultate to ensure that there is no carotid bruit and massage the carotid sinus against the transverse process of C6 for 10 seconds at a time, first on the side of the non-dominant cerebral hemisphere. This should never be done simultaneously on both sides.
3. Administer adenosine, 6 milligrams rapid IV bolus, into a large vein followed by a 20-mL normal saline rapid flush. If there is no effect within 2 minutes, give a second dose of 12 milligrams IV Most patients experience distressing chest pain, flushing, or anxiety lasting less than 1 minute. Ten percent of patients may experience transient atrial fibrillation or flutter after conversion. This is first-line treatment for WPW-associated SVT with a narrow QRS complex (ortho-dromic conduction) but is ineffective in cases of anterograde conduction over an accessory pathway. Adenosine may induce bronchospasm in asthmatics requiring treatment with bronchodilators.
4. In patients with narrow-complex SVT (orthodro-mic conduction) and normal cardiac function, cardioversion may also be achieved with the following second-line agents:
a. Calcium-channel blockers: Diltiazem, 20 milligrams (0.25 milligram/kg) IV over 2 minutes, or vera-pamil, 0.075–075.0 milligram/kg (3–10 milligrams) IV over 15 to 60 seconds with a repeat dose in 30 minutes, if necessary. Verapamil may cause hypotension that can be prevented by pre-treatment with calcium chloride or gluconate (500–1000 milligrams).
b. Beta-blockers: Esmolol, 500 micrograms/kg IV bolus, metoprolol, 5 milligrams IV, or pro-pranolol, 0.1 milligram/kg divided in 3 doses given 2 minutes apart.
c. Digoxin, 0.4 to 0.6 milligram IV.
5. Patients with wide-complex SVT (antidromic conduction across accessory pathway) should be approached as presumed ventricular tachycardia (VT; see Ventricular Tachycardia) unless there is a known history of WPW syndrome. Patients with this type of tachycardia are at risk for rapid ventricular rates and degeneration into ventricular fibrillation (VF); therefore, agents that preferentially block the AV node such as β-blockers, calcium channel blockers, and digoxin should not be used. Treat stable patients with procainamide, 17 milligrams/kg IV over 30 minutes up to 50 milligrams/kg, or until 50% QRS widening is noted (contraindicated in patients with myasthenia gravis since it may increase weakness).
ATRIAL FLUTTER
CLINICAL FEATURES
Atrial flutter is a rhythm that originates from a small area within the atria. ECG characteristics of atrial flutter are (a) a regular atrial rate between 250 and 350 beats/min; (b) “sawtooth” flutter waves directed superiorly and most visible in leads II, III, and aVF; and (c) AV block, usually 2:1, but occasionally greater or irregular (Fig. 4-5). One-to-one conduction may occur if a bypass tract is present. Carotid sinus massage or valsalva maneuvers are useful techniques to slow the ventricular response by increasing the degree of AV block, which can unmask flutter waves in uncertain cases. Atrial flutter is seen most commonly in patients with ischemic heart disease as well as congestive heart failure (CHF), acute MI, pulmonary embolus, myocarditis, blunt chest trauma, and digoxin toxicity. Atrial flutter may be a transitional arrhythmia between sinus rhythm and atrial fibrillation. Consider anticoagulation in patients with an unclear time of onset or duration longer than 48 hours before conversion to sinus rhythm due to increased risk of atrial thrombus and embolization.
FIG. 4-5. Atrial flutter.
EMERGENCY DEPARTMENT CARE
The treatment is the same as atrial fibrillation and is discussed below.
ATRIAL FIBRILLATION
CLINICAL FEATURES
Atrial fibrillation (Afib) occurs when there are multiple, small areas of atrial myocardium continuously discharging in a disorganized fashion. This results in loss of effective atrial contraction and decreases left ventricular (LV) end-diastolic volume, which may precipitate CHF in patients with impaired cardiac function. The ECG characteristics of Afib are (a) fibrillatory waves of atrial activity, best seen in leads V1? V2, V3, and aVF, and (b) an irregular ventricular response, usually between 170 and 180 beats/min in patients with a healthy AV node (Fig. 4-6). Afib may be paroxysmal (lasting for less than 7 days), persistent (lasting for more than 7 days), or chronic (continuous). Afib can be idiopathic (lone Afib) or may be found in association with longstanding hypertension, ischemic heart disease, rheumatic heart disease, alcohol use (“holiday heart”), COPD, and thyrotoxicosis. Patients with LV dysfunction who depend on atrial contraction may suffer acute CHF with Afib onset. Rates of greater than 300 beats/min with a wide QRS complex are concerning for a preexcitation syndrome such as WPW (Fig. 4-7). Patients with Afib who are not anticoagulated have a yearly embolic event rate as high as 5% and a lifetime risk greater than 25%. Conversion from chronic Afib to sinus rhythm carries a 1% to 5% risk of arterial embolism; therefore, anticoagulation for 3 weeks is required before cardioversion in patients with Afib for longer than 48-hour duration and in those patients with an uncertain time of onset who are not on anticoagulation therapy.
FIG. 4-6. Atrial fibrillation.
FIG. 4-7. Atrial fibrillation in Wolff-Parkinson-White syndrome.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
1. Treat unstable patients with synchronized cardioversion (50–100 J).
2. Stable patients with Afib for longer than 48 hours should be anticoagulated with heparin (80 units/kg IV followed by an infusion of 18 units/kg/h IV) before cardioversion. Consider a transesophageal echocardiogram to rule out atrial thrombus before cardioversion.
3. Control rate with diltiazem. Administer 20 milligrams (0.25 milligram/kg) IV over 2 minutes followed by a continuous IV infusion, 5–15 milligrams/h, to maintain rate control. Give a second dose of 25 milligrams (0.35 milligram/kg) in 15 minutes if the first dose fails to control rate. Alternative rate control agents for patients with normal cardiac function include verapamil, 5–10 milligrams IV; metoprolol, 5–10 milligrams IV; and digoxin, 0.4–4.0 milligram IV Treat patients with preexcitation syndromes (eg, WPW) with procainamide, 17 milligrams/kg IV, over 30 minutes up to 50 milligrams/kg or until 50% QRS widening is noted. Avoid β-adrenergic or calcium channel blockers (ie, verapamil) due to the risk of causing degeneration to VF
4. In patients with impaired cardiac function (EF <40%), use amiodarone, 5 milligrams/kg IV over 30 minutes, followed by 1200 milligrams over 24 hours (contraindicated in patients with iodine or shellfish allergy; increased risk of rhabdomyolysis if coadministered with simvastatin) or digoxin 0.4–4.0 milligram IV.
5. Patients with Afib for shorter than 48 hours may be chemically or electrically cardioverted in the emergency department. Use amiodarone, ibutilide (see comments for atrial flutter), procainamide, flecain-ide, or propafenone in patients with normal cardiac function. Ibutilide is dosed at 0.01 milligram/kg IV up to 1 milligram, infused over 10 minutes. A second ibutilide dose may be given if there is no response in 20 minutes. Ibutilide should not be administered to patients with known structural heart disease, hypoka-lemia, prolonged QTc intervals, hypomagnesemia, or CHF because of the possibility of provoking torsades de pointes. Monitor for 4–6 hours after giving ibutilide. Patients with impaired cardiac function may be cardioverted with amiodarone or electrically.
MULTIFOCAL ATRIAL TACHYCARDIA
CLINICAL FEATURES?
Multifocal atrial tachycardia (MAT) is defined as at least three different sites of atrial ectopy. The ECG characteristics of MAT are (a) three or more differently shaped P waves; (b) changing P-P, PR, and R-R intervals; and (c) atrial rhythm usually between 100 and 180 beats/min (Fig. 4-8). Because the rhythm is irregularly irregular, MAT can be confused with atrial flutter or atrial fibrillation (Afib). MAT is found most often in elderly patients with decompensated COPD, but it also may be found in patients with CHF, sepsis, methylxan-thine toxicity, or digoxin toxicity
FIG. 4-8. Multifocal atrial tachycardia (MFAT).
EMERGENCY DEPARTMENT CARE AND DISPOSITION
1. Treat the underlying disorder.
2. Specific antiarrhythmic treatment is rarely indicated. Rate control may be achieved with verapamil, 5–10 milligrams IV, or diltiazem, 10–20 milligrams IV in patients with acute COPD or CHF exacerbations.
3. Magnesium sulfate, 2 grams IV over 60 seconds, followed by a constant infusion of 1–2 grams/h, may decrease ectopy and convert MAT to sinus rhythm in some patients.
4. Replete potassium levels to greater than 4 mEq/L to increase myocardial membrane stability.
JUNCTIONAL RHYTHMS
CLINICAL FEATURES
In patients with sinus bradycardia, SA node exit block, or AV block, junctional escape beats may occur, usually at a rate between 40 and 60 beats/min, depending on the level of the rescue pacemaker within the conduction system. Junctional escape beats may conduct retro-gradely into the atria, but the QRS complex usually will mask any retrograde P wave (Fig. 4-9). When alternating rhythmically with the SA node, junctional escape beats may cause bigeminal or trigeminal rhythms. Sustained junctional escape rhythms may be seen with CHF, myocarditis, acute MI (especially inferior MI), hyperkalemia, or digoxin toxicity (“regularized Afib”). If the ventricular rate is too slow, myocardial or cerebral ischemia may develop. In cases of enhanced junctional automaticity, junctional rhythms may be accelerated (60–100 beats/min) or tachycardic (>100 beats/min), thus overriding the SA node rate.
FIG. 4-9. Junctional escape rhythm, rate 42.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
1. Isolated, infrequent junctional escape beats usually do not require specific treatment.
2. If sustained junctional escape rhythms are producing symptoms, treat the underlying cause.
3. In unstable patients, give atropine, 0.5 milligram IV every 5 minutes to a total of 2 milligrams. This will accelerate the SA node discharge rate and enhance AV nodal conduction.
4. Use transcutaneous or tranvenous pacing in unstable patients not responsive to atropine.
5. Manage patients with digoxin toxicity as discussed for SVT.
VENTRICULAR ARRHYTHMIAS
PREMATURE VENTRICULAR CONTRACTIONS
CLINICAL FEATURES
Premature ventricular contractions (PVCs) are due to impulses originating from single or multiple areas in the ventricles. The ECG characteristics of PVCs are (a) a premature and wide QRS complex; (b) no preceding P wave; (c) the ST segment and T wave of the PVC are directed opposite the preceding major QRS deflection; (d) most PVCs do not affect the sinus node, so there is usually a fully compensatory post-ectopic pause, or the PVC may be interpolated between two sinus beats; (e) many PVCs have a fixed coupling interval (within 0.04 second) from the preceding sinus beat; and (f) many PVCs are conducted into the atria, thus producing a retrograde P wave (Fig. 4-10). If three or more PVCs occur in a row, patients are considered to have nonsus-tained VT.
FIG. 4-10. Premature ventricular contractions (PVCs). A. Unifocal PVC. B. Interpolated PVC. C. Multifocal PVC.
PVCs are very common, occurring in most patients with ischemic heart disease and acute MI. Other common causes of PVCs include digoxin toxicity, CHF, hypokalemia, alkalosis, hypoxia, and sympathomimetic drugs. Pooled data and meta-analyses have found no reduction in mortality from suppressive or prophylactic treatment of PVCs. Ventricular parasystole occurs when the ectopic ventricular focus fires frequently enough to compete with the SA node and is associated with cardiac ischemia, electrolyte imbalance, and hypertensive or ischemic heart disease.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
1. Stable patients require no treatment.
2. Patients with three or more PVCs occurring in a row should be managed as VT.
3. For hemodynamically unstable patients with PVCs, consider lidocaine 1–1.5 milligrams/kg IV (up to 3 milligrams/kg) unless the patient is allergic to amide anesthetics.
ACCELERATED IDIOVENTRICULAR RHYTHM
CLINICAL FEATURES
The ECG characteristics of accelerated idioventricular rhythm (AIVR) are (a) wide and regular QRS complexes; (b) rate between 40 and 100 beats/min, often close to the preceding sinus rate; (c) most runs of short duration (3–30 beats/min); and (d) an AIVR often beginning with a fusion beat (Fig. 4-11). This condition is found most commonly with an acute MI or in the setting of reperfusion after successful thrombolysis.
FIG. 4-11. Accelerated idioventricular rhythms (AIVRs).
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Treatment is not necessary. On occasion, AIVR may be the only functioning pacemaker, and suppression with lidocaine can lead to cardiac asystole.
VENTRICULAR TACHYCARDIA
CLINICAL FEATURES
Ventricular tachycardia is the occurrence of 3 or more successive beats from a ventricular ectopic pacemaker at a rate faster than 100 beats/min. The ECG characteristics of VT are (a) a wide QRS complex, (b) a rate faster than 100 beats/min (most commonly 150–200 beats/min), (c) a regular rhythm, although there may be some initial beat-to-beat variation, and (d) a constant QRS axis (Fig. 4-12). The most common causes of VT are ischemic heart disease and acute MI. Because of this fact, patients presenting with VT should be considered candidates for urgent revascularization. Other etiologies include hypertrophic cardiomyopathy, mitral valve prolapse, drug toxicity (digoxin, antiarrhythmics, or sympathomimetics), hypoxia, hypokalemia, and hyper-kalemia. In general, all wide-complex tachycardia should be treated as VT regardless of clinical symptoms or initial vital signs. Adenosine appears to cause little harm in patients with VT; therefore, stable patients with wide-complex tachycardia due to suspected SVT with aberrancy (see previous section) may be treated safely with adenosine when the diagnosis is in doubt. Atypical VT (torsade de pointes, or twisting of the points) occurs when the QRS axis swings from a positive to a negative direction in a single lead at a rate of 200–240 beats/min (Fig. 4-13). Drugs that further prolong repolarization—quinidine, disopyramide, procainamide, phenothiazines, and tricyclic antidepressants—exacerbate this arrhythmia.
FIG. 4-12. Ventricular tachycardia.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
1. Defibrillate pulseless VT with unsynchronized cardioversion starting at 100 J. Treat unstable patients who are not pulseless with synchronized cardioversion.
FIG. 4-13. Two examples of short runs of atypical ventricular tachycardia showing sinusoidal variation in amplitude and direction of the QRS complexes: “Le torsade de pointes” (twisting of the points). Note that the top example is initiated by a late-occurring PVC (lead II).
2. Treat hemodynamically stable patients with amio-darone, 150 milligrams IV over 10 minutes with repeated boluses every 10 minutes up to a total of 2 grams. Alternatively, an infusion of 0.5 milligram/min over 18 hours may be given after the initial bolus. Second-line agents include procainamide (in patients without suspected MI or LV dysfunction) and lidocaine.
3. For patients with torsades de pointes: Try overdrive pacing set at 90–120 beats/min to terminate torsades de pointes. Magnesium sulfate, 1–2 grams IV over 60–90 seconds followed by an infusion of 1–2 grams/h, can be effective.
4. Isoproterenol, 2–10 micrograms/min IV infusion, is also in refractory torsades but carries a risk of increased myocardial oxygen demand.
VENTRICULAR TACHYARRHYTHMIAS VERSUS SVT WITH ABERRANCY
Patients with wide-complex tachycardia should be approached as having VT until proven otherwise. Age over 35 years, a history of MI, CHF, or coronary artery bypass grafting strongly favor VT. ECG signs favoring VT include AV dissociation, fusion beats, precordial lead QRS concordance, and a QRS duration longer than 0.14 second.
VENTRICULAR FIBRILLATION
CLINICAL FEATURES
Ventricular fibrillation (VF) is the totally disorganized depolarization and contraction of small areas of ventricular myocardium during which there is no effective ventricular pumping activity. The ECG shows a fine-to-coarse zigzag pattern without discernible P waves or QRS complexes (Fig. 4-14). VF is seen most commonly in patients with severe ischemic heart disease, with or without an acute MI. It also can be caused by dig-oxin or quinidine toxicity, hypothermia, chest trauma, hypokalemia, hyperkalemia, or mechanical stimulation (eg, catheter wire). Primary VF occurs suddenly, without preceding hemodynamic deterioration, and usually is due to acute ischemia or peri-infarct scar reentry. Secondary VF occurs after a prolonged period of hemodynamic deterioration due to LV failure or circulatory shock.
FIG. 4-14. Ventricular fibrillation.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
1. Perform immediate electrical defibrillation (unsy-chronized) at 200 J (biphasic) and 360 J (monopha-sic). If VF persists, do five cycles of CPR, check pulse, and defibrillate again if no pulse is present. Keep defibrillation pads on the patient and in the same location because, with successive counter-shocks, transthoracic impedance decreases.
2. If the initial 2 cycles of CPR and defibrillation are unsuccessful, administer antiarrhythmic treatment using amiodarone, 300 milligrams IV push. Lidocaine is second-line and is dosed at 1.5 milligrams/kg IV followed by 0.75 milligram/kg IV for 2 more doses. Repeat the CPR-defibrillation cycle.
3. If no pulse is present after the third CPR-defibrillation cycle, give epinephrine, 1 milligram IV push, or vasopressin, 40 units IV push (1 time only), followed by a 20-mL normal saline flush and immediate resumption of the CPR-defibrillation cycle.
4. In refractory VF, administer magnesium sulfate, 1–2 grams IV over 60–90 seconds followed by an infusion of 1–2 grams/h.
CONDUCTION DISTURBANCES
ATRIOVENTRICULAR (AV) BLOCK
First-degree AV block is characterized by a delay in AV conduction, manifested by a prolonged PR interval (>0.2 second). It can be found in normal hearts and in association with increased vagal tone, digoxin toxicity, inferior MI, amyloid, and myocarditis. First-degree AV block needs no treatment. Second-degree AV block is characterized by intermittent AV nodal conduction: some atrial impulses reach the ventricles, whereas others are blocked, thereby causing “grouped beating.” These blocks can be subdivided into nodal blocks, which are typically reversible, and infranodal blocks, which are due to irreversible conduction system disease. Third-degree AV block is characterized by complete interruption in AV conduction with resulting AV dissociation.
SECOND-DEGREE MOBITZ I (WENCKEBACH) AV BLOCK
CLINICAL FEATURES
Mobitz I AV block is a nodal block causing a progressive prolongation of conduction through the AV node until the atrial impulse is completely blocked. Usually, only one atrial impulse is blocked at a time. After the dropped beat, the AV conduction returns to normal and the cycle usually repeats itself with the same conduction ratio (fixed ratio) or a different conduction ratio (variable ratio). Although the PR intervals progressively lengthen before the dropped beat, the increments by which they lengthen decrease with successive beats, causing a progressive shortening of each successive RR interval before the dropped beat (Fig. 4-15). This block is often transient and usually associated with an acute inferior MI, digoxin toxicity, or myocarditis or can be seen after cardiac surgery. Because the blockade occurs at the level of the AV node itself rather than at the infranodal conducting system, this is usually a stable rhythm.
FIG. 4-15. Second-degree Mobitz I (Wenckebach) AV block with 4:3 AV conduction.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
1. Specific treatment is not necessary unless slow ventricular rates produce signs of hypoperfusion.
2. In cases associated with acute inferior MI, provide adequate volume resuscitation before initiating further interventions.
3. Administer atropine, 0.5 milligram IV repeated every 5 minutes. Titrate to the desired heart rate or until the total dose reaches 2 milligrams.
4. Although rarely needed, transcutaneous pacing may be used.
SECOND-DEGREE MOBITZ II AV BLOCK
CLINICAL FEATURES
Mobitz II AV block is typically due to infranodal disease, causing a constant PR interval with intermittent non-conducted atrial beats (Fig. 4-16). One or more beats may be non-conducted at a single time. This block indicates significant damage or dysfunction of the infranodal conduction system; therefore, the QRS complexes are usually wide coming from the low His-Purkinje bundle or the ventricles. Type II blocks are more dangerous than type I blocks because they are usually permanent and may progress suddenly to complete heart block, especially in the setting of an acute anterior MI, and almost always require permanent cardiac pacemaker placement. When second-degree AV block occurs with a fixed conduction ratio of 2:1, it is not possible to differentiate between a Mobitz I (Wenckebach) block and a Mobitz II block.
FIG. 4-16. A. Second-degree Mobitz II AV block. B. Second-degree AV block with 2:1 AV conduction.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
1. Atropine, 0.5–1 milligram IV bolus, repeated every 5 minutes as needed up to 2 milligrams total dose, is first-line treatment for symptomatic patients. All patients should have transcutaneous pacing pads positioned and ready for use in the case of further deterioration into complete heart block.
2. Initiate transcutaneous cardiac pacing (see Sinus Bradycardia above) in patients unresponsive to atropine.
3. If transcutaneous pacing is unsuccessful, initiate transvenous pacing (0.2–20 mA at 40–140 beats/min via a semi-floating or balloon-tipped pacing catheter).
THIRD-DEGREE (COMPLETE) AV BLOCK
CLINICAL FEATURES
In third-degree AV block, there is no AV conduction. The ventricles are paced by an escape pacemaker from the AV node or infranodal conduction system at a rate slower than the atrial rate (Fig. 4-17). When third-degree AV block occurs at the AV node, a junctional escape pacemaker takes over with a ventricular rate of 40–60 beats/min; and because the rhythm originates from above the bifurcation of the His bundle, the QRS complexes are narrow. Nodal third-degree AV block may develop in up to 8% of acute inferior Mis, and it is usually transient, although it may last for several days.
FIG. 4–17. Third-degree AV block.
When third-degree AV block occurs at the infranodal level, the ventricles are driven by a ventricular escape rhythm at a rate slower than 40 beats/min. Third-degree AV block located in the bundle branch or the Purkinje system invariably has an escape rhythm with a wide QRS complex. Like Mobitz II block, this indicates structural damage to the infranodal conduction system and can be seen in acute anterior Mis. The ventricular escape pacemaker is usually inadequate to maintain cardiac output and is unstable with periods of ventricular asystole.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
1. Perform transcutaneous cardiac pacing in unstable patients until a transvenous pacemaker can be placed.
2. In stable patients, apply transcutaneous pacing pads. Treat the same as second-degree Mobitz II AV block.
FASCICULAR BLOCKS
Conduction blocks may arise in one or more of the three infranodal conduction pathways. Blockage of either of the left fascicles does not prolong the QRS duration, but will change the QRS axis. Left anterior fascicular block (LAFB) causes left axis deviation while left posterior fascicular block (LPFB) causes right axis deviation. Right bundle branch block (RBBB) will prolong the QRS duration (>0.12 second) and cause a RSR’ in the early precordial leads (V1–2). Bifascicular block denotes a combination of any two of these fascicles, the most notable of which is left bundle branch block (LAFB + LPFB). Trifascicular block denotes the presence of first-degree AV block in the presence of a bifascicular block and is indicative of significant conduction system disease that includes the AV node, thus increasing the risk of Mobitz II or third-degree AV block and the potential need for permanent pacemaker placement.
CONDUCTION ABNORMALITIES THAT CAN CAUSE RHYTHM DISTURBANCES
Brugada syndrome and long-QT syndrome increase the risk of spontaneous VT/VF and require evaluation for implantable cardiac defibrillator placement when diagnosed. Brugada syndrome is a genetic disorder of fast sodium channels causing an RBBB pattern in the early precordial leads (V1–2) with a pathognomonic J-point elevation and saddle-shaped or sloped ST segment (Fig. 4-18). Long-QT syndrome is characterized by a QT interval >470 milliseconds in men and >480 milliseconds in women and may be congenital or acquired, leading to an increased risk of torsades de pointes.
PRETERMINAL RHYTHMS
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity is the presence of electrical complexes without accompanying mechanical contraction of the heart. Potential mechanical causes should be diagnosed and treated, including severe hypovolemia, cardiac tamponade, tension pneumothorax, massive pulmonary embolus, MI, and toxic ingestions (eg, tri-cyclic antidepressants, calcium channel blockers, and β-blockers). In addition, profound metabolic abnormalities such as acidosis, hypoxia, hypokalemia, hyperka-lemia, and hypothermia also should be considered and treated.
FIG. 4-18. Brugada syndrome.
After intubation and initiating CPR, administer epinephrine, 1 milligram IV/IO (1:10,000 solution) every 3–5 minutes. If giving via endotracheal tube, increase the dose 2–2.5 times and follow with several rapid ventilations to disperse the drug. Treatment is guided by rapid identification and treatment of the underlying cause. Use agents with α-adrenergic activity, such as norepinephrine and phenylephrine, to improve vascular tone when indicated. Electrical pacing is not effective.
IDIOVENTRICULAR RHYTHM
Idioventricular rhythm is a ventricular escape rhythm at slower than 40 beats/min with a QRS wider than 0.16 second. It is associated with infranodal AV block, massive MI, cardiac tamponade, and exsanguinating hemorrhage.
After intubation and initiating CPR, treatment includes identifying contributing mechanical factors (eg, aggressive volume resuscitation) and α-adrenergic agents.
ASYSTOLE (CARDIAC STANDSTILL)
Asystole is the complete absence of cardiac electrical activity and carries a grim prognosis. Treatment is the same as that for pulseless electrical activity.
CARDIAC PACEMAKERS AND AUTOMATED INTERNAL CARDIAC DEFIBRILLATORS
Pacemakers, automated internal cardiac defibrillators (AICDs), or combination units may be used in patients with a history of sudden death, heart failure, or cardio-myopathy. Malfunction can occur at any level of the device, including infection or hematoma in the pocket housing the device, lead infection/displacement, failure to pace, failure to sense, overpacing, or inappropriate defibrillation. Most pacemakers will have a magnetic switch which, when triggered by magnet application to the unit, will cause the pacemaker to function in a fixed asynchronous mode.
EMERGENCY DEPATTMENT CARE AND DISPOSITION
1. Evaluation should include an ECG, electrolytes, and a chest radiograph to assess lead position and integrity. Arrangements should be made for electrical interrogation of the unit.
2. Patients with pacing failure may require treatment based on their underlying rhythm and associated symptoms.
3. Patients with overpacing may require magnet application to convert the pacemaker to asynchronous mode pacing at a lower rate.
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th edition, see Chapter 22, “Cardiac Rhythm Disturbances,” by Joseph S. Piktel; Chapter 23, “Pharmacology of Antiarrhyth-mics,” by Brad A. Miller and Elizabeth A. Clements; and Chapter 24 “Pharmacology of Vasopressor Agents” by Brad A. Miller and Elizabeth A. Clements.