Cardiovascular 2: Cardiac Rhythms Portal
This portal is a reference for common cardiac rhythms and is not a detailed or complete rhythm interpretation section. For a complete review of cardiac rhythms, see American Heart Association resources and other ECG references.
Base rhythm recognition on careful ECG and rhythm interpretation within the context of total patient assessment. Simple rhythm classification is based on heart rate. Accordingly, rhythms are divided into bradyrhythmias, tachyrhythmias, and rhythms that do not generate a pulse. Rhythm is then further defined based on the origin (pacemaker) for the beats and the conduction of the exciting impulse through the myocardial tissue. CALS providers should be able to recognize the rhythms contained in this portal.
Bradyarrhythmias
Sinus Node Dysfunction
- Sinus Pause or Arrest
- Sinoatrial Exit Blocks (First-, Second-, and Third-Degree)
- Bradycardia-Tachycardia Syndrome
AV Conduction Disturbance
- First-Degree AV Block
- Second-Degree AV Block—Types I and II
- Third-Degree (Complete) AV Block
Tachyrhythmias
Premature Complexes
- Premature Atrial Complexes
- AV Premature Junctional Complexes
- Premature Ventricular Contractions
Tachycardias
- Sinus Tachycardia
- Atrial Fibrillation
- Atrial Flutter
- Paroxysmal Supraventricular Tachycardias
- AV Nodal Reentrant Tachycardias
- AV Reentrant Tachycardias
- Sinus Node Reentrant Tachycardias
- Non-Reentrant Atrial Tachycardias (including MAT)
- Preexcitation (Wolff-Parkinson-White) Syndrome
- Non-Paroxysmal Junctional Tachycardias
- Ventricular Tachyarrhythmias
- Ventricular Tachycardia
- Torsades de Pointes
- Accelerated Idioventricular Rhythm
Rhythms that do not generate a pulse
- Ventricular Flutter/Fibrillation
- Pulseless Ventricular Tachycardia
- Asystole
- Pulseless Electrical Activity
Bradyrhythmias
Sinus Node
Dysfunction
The
sinoatrial (SA) node is normally the dominant cardiac pacemaker because
its intrinsic discharge rate is the highest of all potential cardiac
pacemakers. In adults, the normal sinus rate under basal conditions is
60 to 100 beats per minute (bpm).
Etiology
Most cases of SA node
dysfunction are due to idiopathic degeneration or pharmacologic agents
(eg, digoxin, beta blockers, calcium channel blockers, amiodarone).
Diagnoses
- Sinus Pause or Arrest – Sinus node intermittently fails to produce an impulse. ECG manifestation is a prolonged period (> 3 sec) of atrial asystole.
- SA Exit Blocks
- First-Degree SA Exit Block – This denotes a prolonged conduction time from the SA node to the surrounding atrial tissue. This cannot be recognized on the surface ECG but needs invasive intracardiac recordings.
- Second-Degree SA Exit Block – This denotes intermittent failure of sinus impulses to conduct into the atrial tissue. ECG shows intermittent absence of P waves.
- Third-Degree (Complete) SA Block – There is a lack of SA nodal activity. On the ECG, this arrhythmia looks similar to sinus arrest. Intracardiac recordings can distinguish between the two.
- Bradycardia-Tachycardia Syndrome – Periods of atrial tachycardias are followed by prolonged sinus pauses, or there is alternating bradycardias and tachycardias.
Treatment
Permanent pacemaker is the definitive treatment for significant
(symptomatic) sinus node dysfunction.
AV Conduction
Disturbances
The
specialized conducting system normally ensures synchronous conduction
of each sinus impulse from the atria to the ventricles. To evaluate the
clinical significance of a conduction abnormality, it is important to
determine:
- site of conduction disturbance
- risk of progression to complete heart block
- stability of a distal pacemaker
Etiology
Increased
vagal tone, electrolyte abnormalities, drug effects (beta blockers,
calcium channel blockers, digoxin), MI (especially inferior), acute
infections (viral myocarditis, acute rheumatic fever, infectious
mononucleosis), sarcoidosis, amyloidosis, and neoplasms (cardiac
mesotheliomas) are among the causes for AV conduction abnormalities.
- First-Degree AV Block
Description
The pacemaker is usually in the SA node. Therefore, when the pacemaker is normal, the shape of the P waves is normal. All pacemaker impulses are conducted through the AV node, but because of a slow conduction, the PR interval exceeds the upper limit of normal (0.20 second or 1 large square). The heart rate and rhythm are not affected.Diagnosis
- Normal P waves
- PR interval > 0.2 sec
- PR interval > 0.24 is almost always due to AV node delay.
Treatment
• Usually asymptomatic and requires no therapy.
- Second-Degree AV Block
Type I (Wenckebach’s Phenomenon)
Description
Second-Degree AV Block Type I (Wenckebach’s phenomenon) occurs at the level of the AV node. This frequently is due to an increase in parasympathetic tone or drug effect, such as from digitalis, beta blockers, or calcium channel blockers. Wenckebach’s phenomenon manifests as having a regular atrial rhythm, but an irregular ventricular rhythm, with progressive elongation of the PR interval with shortening of the R to R interval and with the R to R interval that brackets the non-conductive P wave as being < two times a normal cycle.Diagnosis
- QRS complexes in regular groupings
- Pause following dropped P is less than fully compensatory (< 2 RR intervals).
- PR interval lengthens until P is dropped.
- QRS complexes are usually of normal width, resembling that of a normal cardiac rhythm.
Treatment
- Usually the ventricular rate is adequate and the patient is asymptomatic; hence, observation is sufficient.
- For symptomatic blocks, atropine or pacemaker may rarely be required.
- Further therapy is defined in Vol III—CV10, Bradycardia.
Type II
Description
Second-Degree AV Block Type II occurs below the AV node, with the block occurring either at the bundle of HIS (uncommonly) or in the bundle branches (most commonly). The PR intervals tend to be of equal length, but there can be more than one non-conducted P wave in a row. Type II second-degree block is associated with organic lesions in the conduction pathway and is rarely due just to increased parasympathetic tone or drug affect. Therefore, this block has:
- poorer prognosis
- greater chance of developing a third-degree heart block
Most of these blocks are at the level of the bundle branches. The PR interval may be normal or prolonged. To drop a beat, the patient needs to have a complete block of one bundle, either the right or the left, and intermittent interruption of the conduction in the contralateral bundle. Therefore, Type II second-degree block is usually associated with a wide QRS complex. When the block is at the bundle of HIS, the QRS complex is not wide since the ventricular conduction is not disturbed or blocked.
Diagnosis
- PR intervals are constant for the conducted P waves.
- Usually just one P wave in a row is dropped, but there can be more than one non-conducted P wave in a row.
- QRS complexes are usually prolonged and resemble a bundle-branch-block configuration.
Treatment
- Pacemaker is usually mandatory due to the risk of progression to complete block.
- Note: Atropine should be used only with caution as this can exacerbate the degree of block by accelerating the sinus rate.
- Further therapy is defined in Vol III—CV10, Bradycardia.
- Third-Degree (Complete) AV Block
Description
Third-Degree AV Block can be at the level of the AV node, bundle of HIS, or the bundle branches. The distinction is important since pathogenesis, treatment, and prognosis vary depending on the anatomical level of the block.When the block is at the AV node, a junctional escape pacemaker frequently initiates the ventricular depolarization. The QRS complex is a narrow complex with a stable rate and rhythm of 40 to 60 bpm. This is because the block is above the bundle bifurcation. This location of third-degree block is common with inferior MIs, toxic drug effects (from digitalis or Inderal), or from damage to the AV node. This is usually transient, and the prognosis is good.
Third-degree blocks at the infranodal level most often are due to blocks involving both bundle branches. This indicates extensive infranodal conduction symptom disease, often from coronary disease, which is frequently associated with an extensive anterior wall MI. These usually do not result just from increased parasympathetic tone or from drug effects. The only remaining natural escape mechanism for pacing the heart is the ventricle distal to the blockage. This is an unstable rhythm with an intrinsic rate < 40 bpm and a high frequency of developing asystole. These complexes are wide in nature.
Diagnosis
- No relation between P waves and QRS complexes
- Usually wide QRS complexes with rate of < 40 unless the block is at the AV node
Treatment
- Pacemaker is required when the block is below the level of the AV node or the patient is symptomatic due to the resulting bradycardia.
- Further therapy is defined in Vol III—CV10, Bradycardia.
Tachyarrhythmias
Premature Complexes
- Premature Atrial Complexes
Description
A premature atrial complex (PAC) is a premature beat, initiated in one area of the atria other than the SA node. This causes the atria to depolarize in a different direction and gives rise to a P wave different in configuration than the sinus P wave. The QRS complexes are normal but the SA node’s cycle is reset, causing the next P wave to arrive earlier than expected.Etiology
PACs can be found in > 60% of normal people and are increased in settings of infection, myocardial ischemia, drug toxicity, and with excessive tobacco and caffeine use.Diagnosis
- Early, different-looking, upright P wave
- Sum of pre- and post-PAC PP interval is < two PP intervals.
Treatment
- PACs are usually asymptomatic, and no therapy is indicated.
- If the PACs cause symptoms, beta blockers or calcium channel blockers may be used.
- AV Premature Junctional Complexes
Description
An AV premature junctional complex (PJC) is a premature beat initiated in an area around the bundle of HIS. It depolarizes the atria in a backward direction, producing an inverted premature P wave. Conduction travels to the ventricles through the normal pathways, producing a normal QRS with a ventricular pause following it. The SA node is reset, and the next P wave arrives earlier than expected.Etiology
May be seen in cardiac disease or digitalis intoxication.Diagnosis
- Early normal appearing QRS with no visible P or an inverted P preceding or following the QRS.
- Noncompensatory pause following the PJC
Treatment
- Resembles treatment of PACs.
- Premature Ventricular Contractions
Description
A premature ventricular contraction (PVC) is a premature beat initiated in one area of the ventricles that depolarizes one ventricle and then with delay depolarizes the other ventricle through an abnormal conduction pathway in the ventricular myocardium. This produces a bizarre looking QRS complex 0.12 sec or greater with a compensatory pause following it. Usually the atria do not get depolarized or the P wave occurs after the PVC, sometimes being seen in the T wave of the PVC. PVCs may occur singly or in bigeminy or trigeminy (two sinus beats followed by a PVC). Two successive PVCs are termed couplets, while three or more are considered ventricular tachycardia.Etiology
PVCs occur in > 60% of normal people and may occur in > 80% of people with previous MI.Diagnosis
- Early, wide, and bizarre looking QRS complex ≥ 0.12 sec
- Compensatory pause following the PVC
- No ectopic P wave
Treatment
- Usually asymptomatic but may need beta blockers if PVCs cause symptoms.
Tachycardias
Tachycardias refer to arrhythmias with three or more complexes
at rates
> 100 bpm. They occur more often in diseased hearts. In a
hemodynamically
stable patient, attempt to determine the origin and mechanism of the
tachycardia.
Information obtained from the ECG includes:
- Presence, frequency, morphology, and regularity of P waves and QRS
- Relationship between atrial and ventricular activity
-
Comparison of the QRS morphology during sinus rhythm and during the
tachycardia - Response of carotid sinus massage or other vagal maneuvers
- Sinus Tachycardia
Description
In adults, sinus tachycardia denotes a rate > 100 bpm. The rate does not usually exceed 200 and is a physiologic response to stress or tachycardia-causing stimulus.Etiology
Fever, volume depletion, anxiety, exercise, thyrotoxicosis, shock from any source, and medications are among the causes of sinus tachycardia.Diagnosis
- P waves with sinus contour preceding each QRS
Treatment
- Direct toward the underlying cause.
- Atrial Fibrillation
Description
One theory of atrial fibrillation (AF) formation suggests that multifocal ectopic foci in the atria fire repeatedly at rates between 350 to 650 bpm causing quivering of the atria rather than contractions. Sporadic impulses permeate to the ventricles, causing an irregularly irregular ventricular rate.Etiology
Usually seen in patients with cardiovascular disease like rheumatic heart disease, hypertensive CVD, chronic lung disease, or thyrotoxicosis. AF is common in the geriatric population.Diagnosis
- No discrete P waves on surface ECG (fibrillatory waves seen)
- Ventricular response irregularly irregular
Treatment
- In acute AF, precipitating factors such as infection, CHF, thyrotoxicosis, and pulmonary embolism should be sought and treated.
- In unstable patients, electrical cardioversion (at least 100J) is the treatment of choice.
- Slowing of ventricular response can be achieved by beta blockers and calcium channel blockers (or digitalis for patients with preserved LV function). In patients with CHF, digitalis, diltiazem, or amiodarone are recommended.
- If the rhythm is very rapid wide-complex atrial fibrillation or flutter, a pre-excitation syndrome may be present. Administration of standard agents (beta blockers, calcium channel blockers) may block the normal pathway and allow for disastrously rapid conduction down the accessory pathway. If immediate cardioversion is not required, pharmacological treatment of these patients includes IV amiodarone or procainamide.12
- Patients with AF for more than 48 hours should be anticoaugulated to INR of at least 1.8 or exclude atrial thrombus by transesophageal echocardiogram.
- Pharmacologic cardioversion and catheter ablation are other modes of treatment for chronic AF.
- Further therapy is defined in Vol III—CV8, Tachycardia.
- Atrial Flutter
Description
One theory of atrial flutter formation suggests that one ectopic focus in the atria depolarizes at a regular rate of 220 to 350 bpm. These flutter waves replace the P waves and display a saw tooth configuration. The refractoriness of the AV node prevents the ventricles from responding to all the flutter waves and produces 2:1, 3:1, 4:1, or a variable ventricular rate.Etiology
Most often seen in patients with organic heart disease. Over the long-term, atrial flutter can convert to atrial fibrillation.Diagnosis
- Flutter waves replace P waves (saw tooth configuration). These flutter waves may not be evident on routine ECG but are often best viewed on lead V1.
- Ventricular response may be 1:1, 2:1, 3:1, 4:1, or may vary. A common pattern in a patient who has not received therapy is to have a 2:1 conduction with a ventricular rate of approximately 150.
Treatment
- The goal is to convert to normal sinus rhythm if possible or to control the ventricular rate.
- Treatment modalities are similar to treatment of AF.
- If the rhythm is very rapid wide-complex atrial fibrillation or flutter, a pre-excitation syndrome may be present. Administration of standard agents (beta blockers, calcium channel blockers) may block the normal pathway and allow for disastrously rapid conduction down the accessory pathway. If immediate cardioversion is not required, pharmacological treatment of these patients includes IV amiodarone or procainamide.12
- Overdrive atrial pace termination is sometimes used.
- Further therapy is contained in Vol III— CV8, Tachycardia.
- Paroxysmal Supraventricular Tachycardia
Paroxysmal supraventricular tachycardias (PSVTs) are atrial tachycardia, most of which are caused by reentry. The reentrant circuit may involve the SA node, atria, AV node, or an AV bypass tract. When such a tract also conducts antegrade, it is called Wolff-Parkinson-White (WPW) syndrome. (See Preexcitation Syndrome in the following pages of this portal.) In the absence of WPW syndrome, reentry through the AV node or a concealed bypass tract make up more than 90% of all PSVTs. In most cases, QRS complexes are normal.
- AV Nodal Reentrant Tachycardia
Description
In AV nodal reentrant tachycardia there is functional dissociation of two discrete conduction pathways around the AV nodal region (called dual AV nodal physiology). These two pathways differ in conduction velocity and refractory periods and are termed “slow” and “fast” pathways based on their conduction velocities. Conduction proceeds antegrade down the slow pathway with retrograde conduction up the fast pathway. Atrial and ventricular excitation occurs concurrently with every tachycardia circuit.Etiology
No age or disease predisposition has been found.Diagnosis
- Regular narrow QRS complex tachycardia at rates of 120 to 250 bpm.
- Retrograde P waves may be absent, buried in the QRS complexes, or appear as distortions at the terminal part of QRS.
Treatment
- Vagal maneuvers like carotid sinus massage or Valsalva may be attempted in patients without hypotension or carotid bruits.
- Adenosine (6 to 12 mg IV) is the initial drug treatment choice.
- In patients with normal left ventricular function, calcium channel blockers (diltiazem, verapamil) or beta blockers (metoprolol, esmolol, atenolol) are considered second choices. Digitalis, amiodarone, procainamide, or sotalol are third choice agents.
- In patients with normal left ventricular function, strongly consider electrical cardioversion in unstable patients or when AV nodal agents are unsuccessful.
- In patients with reduced left ventricular function (EF <40% or CHF), if adenosine IV is not successful in converting the rhythm, DC cardioversion is not indicated. Drug therapies to consider include digoxin, amiodarone, or diltiazem.
- In symptomatic patients with chronic AV nodal reentrant tachycardia, radiofrequency catheter ablation is the treatment of choice.
- Further therapy is defined in Vol III— CV8, Tachycardia.
• AV Reentrant Tachycardia
Description
In AV reentrant tachycardia, the impulse travels antegrade from the atria to the ventricles via the AV node and His-Purkinje system and then retrograde via a concealed bypass tract. The PSVT in this case is similar to WPW syndrome except that the bypass tract cannot conduct in an antegrade direction during sinus rhythm or other atrial tachyarrhythmias. This type of PSVT can be initiated by either an APC or VPC.Etiology
No age or disease predisposition.Diagnosis
- Looks similar to AV nodal reentrant tachycardia.
- Precise diagnosis requires atrial activation mapping.
Treatment
- Similar to AV nodal reentrant tachycardia (See previous pages.)
- Further therapy is defined in Vol III— CV8, Tachycardia.
• Sinus Node Reentrant Tachycardia
Description
This type of PSVT is caused by reentry in the region of the sinus node. It is always initiated by a PAC. These PSVTs are less common that AV nodal reentrant tachycardias or AV reentrant tachycardias and are more often associated with cardiac disease. They are managed like other reentrant PSVTs, but catheter ablation is less successful due to the presence of multiple foci.• Non-Reentrant Atrial Tachycardias (including MAT)
Description
Multifocal atrial tachycardias (MATs) are initiated by multifocal PACs. Hence, the P wave morphology and the PR interval of each vary.Etiology
These are usually manifestations of digitalis intoxication or may be associated with severe cardiac or pulmonary disease. MAT is particularly common after theophylline administration, especially when a toxic level of theophylline has occurred.Diagnosis
- MAT requires three or more consecutive P waves of different morphologies at rates > 100 bpm.
- MAT usually has an irregular ventricular rhythm due to varying AV conduction.
Treatment
- Initial treatment is directed at the underlying disorder (if it can be identified). Digitalis or theophylline may need to be discontinued.
- Vagal stimulation or adenosine IV are used only if needed for diagnosis of the tachycardia.
- DC cardioversion is not to be used in patients with MAT.
- Patients with preserved left ventricular function may be treated with calcium channel blockers IV, beta blockers IV, or amiodarone.
- In patients with reduced left ventricular function (EF <40% or CHF), DC cardioversion is not indicated. Amiodarone is the drug of choice. Diltiazem IV may also be used.
- Catheter ablation may be considered for patients with recurrent episodes of MAT.
- Further therapy is defined in Vol III— CV8, Tachycardia.
- Preexcitation (Wolff-Parkinson-White) Syndrome
Description
The preexcitation syndrome is characterized by rapid conduction of supraventricular impulses to the ventricles through an accessory pathway that bypasses the AV node. The most common form is Wolff-Parkinson-White (WPW). In WPW, the AV bypass tract is called the bundle of Kent.While in normal sinus rhythm, the typical ECG pattern has a short PR interval, slurred upstroke of the QRS, and a wide QRS resulting from a fusion of the activation of the ventricles by the normal His-Purkinje system and the bypass tract.
If the impulse generating the tachycardia is conducted antegrade (from the atrium to the ventricle) down the normal AV conduction system (referred to as orthodromic AV reentrant tachycardia) and retrograde from the ventricle to the atrium and up the bypass tract, the resulting tachycardia usually has a narrow complex configuration. These rhythms can usually be treated like any other similar arrhythmia. If the tachycardia has a wide QRS complex, the antegrade conduction of the exciting electrical impulse is usually down the accessory pathway from the atrium to the ventricle (antidromic AV reentrant tachycardia). Approach these patients more cautiously. Nodal-blocking drugs (beta blockers, calcium channel blockers, adenosine) can result in loss of competition from the normal pathway and lead to disastrously rapid ventricular responses. This is of most concern in atrial fibrillation and flutter. (See Treatment guidelines that follow.)
Etiology
The etiology of WPW is the congenital presence of the accessory pathway. It is more common in patients with congenital heart abnormalities like Ebstein’s anomaly, but most patients with WPW have no known congenital heart disease.Diagnosis
- Shortened PR interval when in sinus rhythm (<0.12 sec)
- Slurred upstroke of QRS (delta wave) when in sinus rhythm
- Widened QRS and variations in QRS width occur.
- Supraventricular tachycardias are prone to occur.
- The tachycardia may be a narrow or wide QRS complex.
Treatment
- If the tachycardia that occurs in a patient with WPW is a regular narrow QRS complex (orthodromic AV re-entry) tachycardia—not atrial fibrillation or flutter—the antegrade limb of the electrical conduction from the atrium to the ventricle is usually down the AV node/His-Purkinje path. These patients may be treated like any other patients with narrow-complex supraventricular tachycardias.13
- In the acute treatment of patients with wide complex AV reentrant tachycardia associated with WPW, the drug of choice is procainamide IV. The use of beta blockers IV, calcium channel blockers IV, digoxin IV, or adenosine IV should be used only if the diagnosis of WPW with a wide complex tachycardia is secure (ie, ventricular tachycardia can be ruled out).
- Treatment of unstable patients with tachycardia associated with WPW often requires synchronized cardioversion.
- Radiofrequency catheter ablation is the treatment of choice for long-term control of tachycardias associated with WPW.
- Non-Paroxysmal Junctional Tachycardia
Description
Junctional tachycardias originate in an area around the AV junction and are composed of at least 4 to 6 ectopic beats in a row at rates > 100 bpm. Conduction to the ventricles follows normal pathways. The usual junctional escape rate is 30 to 60 bpm. A junctional rhythm with a rate of 60 to 120 bpm is referred to as non-paroxysmal junctional tachycardia.Etiology
Digitalis intoxication is the most common cause but theophylline toxicity, inferior MI, myocarditis (etc) may also cause these.Diagnosis
- Normal appearing QRS
- P waves precede, follow, or are buried in the QRS.
Treatment
- Eliminate underlying cause (ie, stop digitalis or theophylline).
- Drug therapy is usually not indicated or needed and may lead to other side effects or arrhythmias.
- Ventricular Tachyarrhythmias
These originate in an area in the ventricles and are composed of wide (> 0.12 sec) and bizarre ectopic beats in a row. Non-conducted P waves that are not associated with the QRS complexes (AV dissociation) are sometimes observed in ventricular tachycardia and may be a differentiating clue for ventricular tachycardia versus supraventricular tachycardia with aberrancy.
• Ventricular Tachycardia
Description
Ventricular tachycardia (VT) is defined as a series of three or more ventricular complexes that occur at a rate of 100 to 250 bpm where the origin of activation is within the ventricle. Unsustained VT occurs from 3 beats to 30 sec. Sustained VT occurs for more than 30 sec or when it causes hemodynamic collapse. Monomorphic VT, usually associated with significant heart disease, has a single QRS morphology; whereas polymorphic VT has an ever-changing QRS morphology. Note: Prompt recognition and acute treatment of an episode of VT are critical to prevent morbidity and cardiac arrest.Etiology
Coronary artery disease is the most common cause. Other structural disease like cardiomyopathies, infiltrative diseases, and inflammatory myocardial diseases (systemic lupus erythematosus, rheumatoid arthritis) may predispose to VT.Diagnosis
- Three or more QRS complexes at rate >100
- Widened QRS complexes (>0.12 sec)
- Monomorphic or polymorphic appearance
- ECG findings suggestive of VT over SVT with aberrancy:
- QRS > 0.14 sec
- sinus P waves with AV dissociation
- all positive or negative QRS in precordial leads
Treatment
- For treatment of stable VT, see Vol III—CV8, Tachycardia.
- For treatment of pulseless VT, see Vol III—CV5, VF/Pulseless VT.
• Torsades de Pointes
Description
Torsades de pointes is a specific type of VT characterized by polymorphic QRS complexes that change in amplitude and cycle length giving the appearance of oscillations around the baseline.Etiology
Torsades de pointes (by definition) is associated with a prolonged QT interval. This can result from electrolyte abnormalities (hypomagnesemia, hypokalemia), use of tricyclic antidepressants, use of many antiarrhythmic drugs (quinidine, procainamide, etc), or a congenital long QT syndrome.Diagnosis
- Marked QT prolongation on the patient’s normal ECG (often > 0.60 sec)
- Polymorphic VT with oscillation around baseline
Treatment
- Treatment of underlying cause is mainstay of therapy.
- Magnesium IV can reverse torsades de pointes.
- See Vol III—CV8, Tachycardia Portal.
• Accelerated Idioventricular Rhythm
Also known as slow VT with rates between 60 and 120. This can occur in acute MI or in digitalis intoxication and cardiomyopathies. This rarely causes symptoms and is usually transient. Treatment is rarely necessary.
Rhythms that do not generate a pulse:
- Ventricular Flutter/Fibrillation
Description
Ventricular flutter occurs due to rapid firing of one or more ectopic ventricular foci at a fairly regular rate of more than 150 bpm. VF is recognized by grossly irregular undulations of varying amplitudes, contours, and rates caused by rapid firing of multiple ventricular foci. This is associated with disorganized mechanical contraction, hemodynamic collapse, and sudden death.Etiology
Any structural, toxic, or metabolic derangement that adversely affects the homogeneity of ventricular repolarization can predispose to VF. Patients with ischemic heart disease are most often affected. Other causes include WPW with AF and drugs that can prolong the QT interval (quinidine, tricyclics etc)Diagnosis
- Ventricular flutter resembles a sine wave with no P waves.
- VF can appear as coarse erratic waves or as a fine, virtually flat line with no atrial activity and no QRS complexes.
Treatment
- Immediate unsynchronized cardioversion is the primary therapy for VF and pulseless VT.
- See Vol III—CV5 VF/Pulseless VT.
- Pulseless Ventricular Tachycardia
- Asystole
Description: No electrical activity is present. There is no cardiac output, and no pulse is felt. This may represent an initial or terminal event.
ECG Characteristics
- The QRS complexes are absent.
- No rate or rhythm can be identified.
- P waves may occasionally be identified.
Treatment
- Identify in more than one lead.
- Identify any correctable causes.
- Give 1 mg epinephrine IV.
- For additional information, see Vol III—CV7, Asystole.
- Pulseless Electrical Activity
Description
Electrical activity other than VT, VF, and asystole is present, but no central or peripheral pulse can be felt. PEA is a condition, not a rhythm.ECG Characteristics
- QRS complexes are present, but they vary in appearance.
- Rate varies according to the rhythm.
- Rhythm may be regular or irregular.
- P waves may be present or absent.
Treatment
- Direct management toward treating reversible causes, such as hypoxemia, hypovolemia, cardiac tamponade, tension pneumothorax, shock, or hyperkalemia.See Vol III—CV6, Pulseless Electrical Activity.
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