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ACLS Rhythms for the ACLS Algorithms
A p p e n d i x 3
Posterior division
Anterior division
Purkinje fibers
Sinus node
Bachmann’s bundle
AV node
Bundle of His
Right bundle branch
Left bundle branch
Internodal pathways
1. Anatomy of the cardiac conduction system: relationship to the ECG cardiac cycle. A, Heart: anatomy of conduction system.
B, P-QRS-T complex: lines to conduction system. C, Normal sinus rhythm.
A
The Basics
B
AVN
P
Q
S
R
Absolute Refractory Period
Relative Refractory Period
Ventricular Repolarization
PR
PR
QT Interval
T
Ventricular P Depolarization PR
C Normal sinus rhythm
- Ventricular Fibrillation/Pulseless Ventricular Tachycardia
Defining Criteria per ECG
Clinical Manifestations Pulse disappears with onset of VF Collapse, unconsciousness Agonal breaths ➔ apnea in <5 min Onset of reversible death
Common Etiologies Acute coronary syndromes leading to ischemic areas of myocardium Stable-to-unstable VT, untreated PVCs with R-on-T phenomenon Multiple drug, electrolyte, or acid-base abnormalities that prolong the relative refractory period Primary or secondary QT prolongation Electrocution, hypoxia, many others
Recommended Therapy Comprehensive ECC algorithm, page 10; VF/pulseless VT algo- rithm, page 77
Early defibrillation is essential Agents given to prolong period of reversible death ( oxygen, CPR, intubation, epinephrine , vasopressin ) Agents given to prevent refibrillation after a shock causes defibrillation (lidocaine, amiodarone, procainamide, β -blockers) Agents given to adjust metabolic milieu (sodium bicarbonate, magnesium)
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Coarse VF
Fine VF
The Cardiac Arrest Rhythms
Pathophysiology Ventricles consist of areas of normal myocardium alternating with areas of ischemic, injured, or infarcted myocardium, leading to chaotic pattern of ventricular depolarization
Rate/QRS complex: unable to determine; no recognizable P, QRS, or T waves Rhythm: indeterminate; pattern of sharp up (peak) and down (trough) deflections Amplitude: measured from peak-to-trough; often used subjectively to describe VF as fine (peak-to- trough 2 to <5 mm), medium-moderate (5 to <10 mm), coarse (10 to <15 mm), very coarse (>15 mm)
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- Asystole
Defining Criteria per ECG Classically asystole presents as a “flat line”; any defining criteria are virtually nonexistent
Rate: no ventricular activity seen or ≤6/min; so-called “P-wave asystole” occurs with only atrial impulses present to form P waves Rhythm: no ventricular activity seen; or ≤6/min PR: cannot be determined; occasionally P wave seen, but by definition R wave must be absent
QRS complex: no deflections seen that are consistent with a QRS complex
Clinical Manifestations Early may see agonal respirations; unconscious; unresponsive No pulse; no blood pressure Cardiac arrest
Common Etiologies (^) End of life (death)
Ischemia/hypoxia from many causes Acute respiratory failure (no oxygen; apnea; asphyxiation) Massive electrical shock: electrocution; lightning strike Postdefibrillatory shocks
Recommended Therapy Comprehensive ECC Algorithm, page 10; Asystole Algorithm, page 112
Always check for DNAR status Primary ABCD survey (basic CPR) Secondary ABCD survey
Asystole: agonal complexes too slow to make this rhythm “PEA”
ACLS Rhythms for the ACLS Algorithms
- Sinus Tachycardia
Defining Criteria and ECG Features
Rate: >100 beats/min Rhythm: sinus PR: ≤0.20 sec QRS complex: normal
Clinical Manifestations None specific for the tachycardia
Symptoms may be present due to the cause of the tachycardia (fever, hypovolemia, etc)
Common Etiologies Normal exercise
Fever Hypovolemia Adrenergic stimulation; anxiety Hyperthyroidism
Recommended Therapy
No specific treatment for sinus tachycardia
Never treat the tachycardia per se Treat only the causes of the tachycardia Never countershock
Pathophysiology None—more a physical sign than an arrhythmia or pathologic condition
Normal impulse formation and conduction
Sinus tachycardia
ACLS Rhythms for the ACLS Algorithms
3. Stable wide-complex tachycardia: unknown type
DC cardioversion or Procainamide or Amiodarone
DC cardioversion or Amiodarone
4. Stable monomorphic VT and / or polymorphic VT
Confirmed SVT
Confirmed stable VT
Wide-complex tachycardia of unknown type
Attempt to establish a specific diagnosis
- 12-lead ECG
- Esophageal lead
- Clinical information
Treatment of stable monomorphic and polymorphic VT (See stable VT: monomorphic and polymorphic algorithm)
Unstable patient: serious signs or symptoms
- Establish rapid heart rate as cause of signs and symptoms
- Rate-related signs and symptoms occur at many rates, seldom <150 bpm - Prepare for immediate cardioversion (see algorithm)
Unstable
Preserved cardiac function
Ejection fraction <40% Clinical CHF
Monomorphic ventricular tachycardia
Polymorphic ventricular tachycardia
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A
B2 One-Way Block
D
D (^3)
C3 Slow Conduction
C 1
D
B1 C
C
Muscle Fiber
Purkinje Fiber
A — Normal impulse comes down Purkinje fibers to join muscle fibers. B — One impulse (B 1 ) encounters an area of one-way (unidirectional) block (B 2 ) and stops. C — Meanwhile, the normally conducted impulse (C 1 ) has moved down the Purkinje fiber, into the muscle fiber (C 2 ); and as a retrograde impulse, moves through the area of slow conduction (C 3 ). D — The retrograde impulse (D 1 ) now reenters the Purkinje and muscle fibers (D 2 ); and keeps this reentry cycle repeating itself multiple times (D 3 ).
- Reentry Tachycardia Mechanism
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Recommended Therapy Control Rate
Evaluation Focus: Treatment Focus:
1. Patient clinically unsta- ble? 2. Cardiac function impaired? 3. WPW present? 4. Duration ≤48 or >48 hr? 1. Treat unstable patients urgently 2. Control the rate 3. Convert the rhythm 4. Provide anticoagulation
Normal Heart Impaired Heart
Diltiazem or another calcium channel blocker or meto- prolol or another β-blocker
Digoxin or diltiazem or amio- darone
Impaired Heart
If ≤48 hours: — DC Cardioversion or amiodarone If >48 hours: — Anticoagulate × 3 wk, then — DC cardioversion, then — Anticoagulate × 4 more wk
Normal Heart
- Atrial Fibrillation/Atrial Flutter (continued)
Atrial fibrillation
Atrial flutter
If ≤48 hours: — DC cardioversion or amiodarone or others If >48 hours: — Anticoagulate × 3 wk, then — DC cardioversion, then — Anticoagulate × 4 wk or
IV heparin and TEE to rule out atrial clot, then DC cardioversion within 24 hours, then Anticoagulation × 4 more wk
TEE indicates transesophageal echocardiogram.
Convert Rhythm
ACLS Rhythms for the ACLS Algorithms
- WPW (Wolff-Parkinson-White) Syndrome
Pathophysiology The prototypical pre-excitation syndrome: congenital mal-
formation; strands of conducting myocardial tissue between atria and ventricles When persistent after birth strands can form an accessory pathway (eg, bundle of Kent)
Defining Criteria and ECG Features
Key: QRS complex is classically distorted by delta wave
(upwards deflection of QRS is slurred)
Rate: most often 60-100 beats/min as usual rhythm is sinus Rhythm: normal sinus except during pre-excitation tachycardia PR: shorter since conduction through accessory pathway is faster than through AV node P waves: normal conformation QRS complex: classically distorted by delta wave (upwards deflection of QRS is slurred)
Clinical Manifestations A person with WPW may never have symptoms
People with WPW have same annual incidence of atrial fibrillation as age- and gender-matched population Onset of atrial fibrillation for WPW patients, however, poses risk of rapid ventricular response through the accessory pathway This rapid ventricular response can lead to all signs and symptoms of stable and unstable tachycardias
Common Etiology The accessory pathway in WPW is a congenital malformation
ACLS Rhythms for the ACLS Algorithms
Common Etiologies
Recommended Therapy
If specific diagnosis unknown, attempt therapeutic/diagnostic maneuver with
Vagal stimulation
Adenosine... THEN
Defining Criteria and ECG Features
Key: position of the P wave; may show antegrade or retrograde propagation because origin is at the junction; may arise before, after, or with the QRS
- Junctional Tachycardia
Rate: 100 -180 beats/min Rhythm: regular atrial and ventricular firing PR: often not measurable unless P wave comes before QRS; then will be short (<0.12 secs) P waves: often obscured; may propagate antegrade or retrograde with origin at the junction; may arise before, after, or with the QRS QRS complex: narrow; ≤0.10 secs in absence of intraventricular conduction defect
Clinical Manifestations Patients may have clinical signs of a reduced ejection fraction because augmented flow from
atrium is lost Symptoms of unstable tachycardia may occur
Digoxin toxicity Acute sequelae of acute coronary syndromes
Preserved heart function: β -Blocker Calcium channel blocker Amiodarone NO DC cardioversion!
If impaired heart function: Amiodarone NO DC cardioversion!
Pathophysiology Area of automaticity (automatic impulse formation) develops in the AV node (“junction”)
Both retrograde and antegrade transmission occurs
Junctional tachycardia: narrow QRS complexes at 130 bpm; P waves arise with QRS
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Supraventricular tachycardia
Junctional tachycardia
Multifocal atrial tachycardia
Sinus rhythm (3 complexes) with paroxysmal onset (arrow) of supraventricular tachycardia (PSVT)
Rhythmic Algorithm No. 2: Narrow-Complex Tachycardias
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- Multifocal Atrial Tachycardia
Rate: >100 beats/min; usually >130 bpm Rhythm: irregular atrial firing PR: variable P waves: by definition must have 3 or more P waves that differ in polarity (up/down), shape, and size since the atrial impulse is generated from multiple foci QRS complex: narrow; ≤0.10 sec in absence of intraventricular conduction defect
Clinical Manifestations Patients may have no clinical signs Symptoms of unstable tachycardia may occur
Common Etiologies Most common cause is COPD (cor pulmonale) where pulmonary hypertension places increased strain on the right ventricle and atrium Impaired and hypertrophied atrium gives rise to automaticity Also digoxin toxicity, rheumatic heart disease, acute coronary syndromes
Recommended Therapy If specific diagnosis unknown, attempt therapeutic/diagnostic maneuver with Vagal stimulation Adenosine... THEN
Preserved heart function: β -blocker Calcium channel blocker Amiodarone NO DC cardioversion! If impaired heart function: Amiodarone Diltiazem NO DC cardioversion!
Pathophysiology Areas of automaticity (impulse formation) originate irregularly and rapidly at different points in the atria
Defining Criteria and ECG Features If the rate is <100 beats/min, this rhythm is termed “wan- dering atrial pacemaker” or “multifocal atrial rhythm” Key: By definition must have 3 or more P waves that differ in polarity (up/down), shape, and size since the atrial impulse is generated from multiple foci.
Multifocal atrial tachycardia: narrow-complex tachycardia at 140 to 160 bpm with multiple P-wave morphologies (arrows)
Defining Criteria and ECG Features
Key: Regular, narrow-complex tachycardia without P-waves, and sudden, paroxysmal onset or cessation, or both
Note: To merit the diagnosis some experts require capture of the paroxysmal onset or cessation on a monitor strip
- PSVT (Paroxysmal Supraventricular Tachycardia)
Rate: exceeds upper limit of sinus tachycardia (>120 beats/min); seldom <150 beats/min; up to 250 beats/min Rhythm: regular P waves: seldom seen because rapid rate causes P wave loss in preceding T waves or because the origin is low in the atrium QRS complex: normal, narrow (≤0.10 sec usually)
Clinical Manifestations Palpitations felt by patient at the paroxysmal onset; becomes anxious, uncomfortable
Exercise tolerance low with very high rates Symptoms of unstable tachycardia may occur
Common Etiologies Accessory conduction pathway in many PSVT patients
For such otherwise healthy people many factors can provoke the paroxysm, such as caffeine, hypoxia, cigarettes, stress, anxiety, sleep deprivation, numerous medications Also increased frequency of PSVT in unhealthy patients with CAD, COPD, CHF
Recommended Therapy
If specific diagnosis unknown, attempt therapeutic/diagnos- tic maneuver with
Vagal stimulation
Adenosine... THEN
Preserved heart function: AV nodal blockade — β -Blocker — Calcium channel blocker — Digoxin DC cardioversion Parenteral antiarrhythmics: — Procainamide — Amiodarone — Sotalol (not available in the United States) Impaired heart function: DC cardioversion Digoxin Amiodarone Diltiazem
Pathophysiology Reentry phenomenon (see page 260) : impulses arise and recycle repeatedly in the AV node because of areas of unidirectional block in the Purkinje fibers
ACLS Rhythms for the ACLS Algorithms
Sinus rhythm (3 complexes) with paroxysmal onset (arrow) of supraventricular tachycardia (PSVT)
ACLS Rhythms for the ACLS Algorithms
Long baseline QT interval
- Correct abnormal electrolytes
Therapies: any one
- Magnesium
- Overdrive pacing
- Isoproterenol
- Phenytoin
- Lidocaine
Normal baseline QT interval
- Treat ischemia
- Correct electrolytes
Medications: any one
- β -Blockers or
- Lidocaine or
- Amiodarone or
- Procainamide or - Sotalol
Polymorphic VT
- Is baseline QT interval prolonged?
Normal baseline QT interval
Prolonged baseline QT interval (suggests torsades)
Torsades de pointes
PR QT
Prolonged baseline QT interval
QT
Normal baseline QT interval
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- Monomorphic Ventricular Tachycardia (Stable)
Rate: ventricular rate >100 bpm; typically 120 to 250 bpm Rhythm: no atrial activity seen, only regular ventricular PR: nonexistent P waves: seldom seen but present; VT is a form of AV dissociation (which is a defining characteristic for wide-complex tachycardias of ventricular origin vs supraventricular tachy- cardias with aberrant conduction) QRS complex: wide and bizarre, “PVC-like” complexes >0.12 sec, with large T wave of opposite polarity from QRS
Clinical Manifestations
Common Etiologies An acute ischemic event (see pathophysiology) with areas of “ventricular irritability” leading to PVCs PVCs that occur during the relative refractory period of the cardiac cycle (“R-on-T phenomenon”) Drug-induced, prolonged QT interval (tricyclic antidepressants, procainamide, digoxin, some long-acting antihistamines)
Recommended Therapy Normal Heart
Pathophysiology Impulse conduction is slowed around areas of ventricular injury, infarct, or ischemia These areas also serve as source of ectopic impulses (irritable foci) These areas of injury can cause the impulse to take a circular course, leading to the reen- try phenomenon and rapid repetitive depolarizations
Impaired Heart
Amiodarone or Lidocaine then DC cardioversion if persists
Defining Criteria per ECG Key: The same morphology, or shape, is seen in every QRS complex Notes: 3 or more consecutive PVCs: ventricular tachycardia VT <30 sec duration ➔ non-sustained VT VT >30 sec duration ➔ sustained VT
Monomorphic VT can be asymptomatic, despite the widespread erroneous belief that sus- tained VT always produces symptoms Majority of times, however, symptoms of decreased cardiac output (orthostasis, hypoten- sion, syncope, exercise limitations, etc) are seen Untreated and sustained will deteriorate to unstable VT, often VF
Monomorphic ventricular tachycardia at rate of 150 bpm: wide QRS complexes (arrow A) with opposite polarity T waves (arrow B)
B
A
Any one of following parenteral antiarrhythmics: Procainamide Sotalol Amiodarone Lidocaine
