Dysrhythmia Interpretation and Management/EKG

Automaticity
Cardiac muscle can generate its own electrical activity
Cardiac cycle
Two activities:
1. Electrical (caused by automaticity)
1a. Depolarization = active –> stimulates contraction
1b. Repolarization = resting

2. Mechanical (muscular) = contraction
2a. Systole-contraction
2b. Diastole-relaxation

Depolarization process
Leads to systole/contraction

• Na+ outside, K+ inside
• Change cell permeability
• Na+ enters, K+ exists
• Ca2+ slowly enters cells
• ATP needed to move electrolytes back to resting state

Cardiac Conduction Pathway
Begins in SA node (60-100 bpm) → Atrial contraction
→ AV node (60-80 bpm) → Bundle of His → L and R Bundle branches → Ventricles (Purkinje fibers) (15-40 bpm)
Interpreting the EKG steps
1. Determine the heart rhythm
2. Measure the heart rate
3. Examine the P waves
4. Examine the P to QRS ratio
5. Measure the PR interval
6. Examine the QRS complex
7. Interpret the rhythm
P wave
• Represents electrical firing from SA node
• Atrial depolarization
• Not to exceed 3 boxes high
PR segment/interval
• Atrial depolarization/delay in AV node
• Results from short pause in electrical conduction as the wave of depolarization slows down while traveling through AV junction

• Normal: 0.12-0.20 second
• < 0.12 seconds = Impulse from AV junction • > 0.20 seconds = First-degree AV block

QRS complex/interval
• Ventricular depolarization
1. Q wave = First negative (downward) deflection after P wave
2. R wave = First positive (upward) deflection after P wave
3. S wave = Negative waveform after R wave
• Not everyone has traditional QRS

• Normal: 0.06-0.10 seconds (narrow complex)
• Wider complex = Further away from SA node

Pathologic Q waves
• ≥ 1 box (0.04 seconds) in width
• More than 1/4 of R wave amplitude
Indication of myocardial infarction/tissue death and necrosis (In an acute MI, you won’t see the Q wave until tissue has been necrotic)
ST Segment
• Look for depression or elevation
• ST elevation = Myocardial injury
• ST depression = Reciprocal changes, digoxin, and ischemia
T wave
• Ventircular repolarization
• Follows QRS complex
• Bigger than P wave, but no greater than 5 small boxes high

• Peaked T wave = Hyperkalemia
• Inverted T wave = Ischemia in myocardium

QT Interval
• Beginning of QRS complex to end of T wave
• Normal: 0.32-0.50 seconds
• >0.40-0.45 = Look at drugs that prolong QT interval causing escape rhythms/beats (i.e. amiodarone); longer when HR is slower
U Wave
• Sometimes after T wave
• Unknown origin
• May be normal or hypokalemia
Normal Sinus Rhythm
Normal Sinus Rhythm
• Regular rhythm
• Rate: 60-100 bpm
• Normal P wave
• P wave before each QRS
• Normal PR, QRS, and QT
Sinus Dysrhythmia
• Sinus rhythm
• Rate varies with respirations
• Inspire = Increase
• Expire = Decrease
• Rarely affects hemodynamic status
• Speeds up, slows down, speeds up, etc.
Sinus Tachycardia
Sinus Tachycardia
• Sinus rhythm
• Rate: 100-150 bpm
• Causes: Stimulants, exercise, fever, alterations in fluid status
• N/I: Assess for s/s of low cardiac output
Sinus Bradycardia
Sinus Bradycardia
• Sinus rhythm
• Rate: <60 • Causes: Vagal maneuvers (i.e. bearing down, icing), ischemia, elevated intracranial pressure (ICP), and athletes (normal) • Produces various hemodynamic responses
Sinus Arrest or Exit Block
Sinus Arrest or Exit Block
• Sinus node fails to initiate impulse
• Causes: Vagal responses, heart disease, drugs that slow HR
• HR can be normal or slow
• Irregular rhythm
• Decrease cardiac output
Atrial Dysrhythmias: Defintion + causes
• Increased automaticity in the atrium
• Generally have P-wave changes

• Causes:
-Stress
-Electrolyte imbalances
-Hypoxemia
-Atrial injury
-Digitalis toxicity
-Hypothermia
-Hyperthyroidism
-Alcohol
-Pericarditis

Premature Atrial Contractions (PAC)
Premature Atrial Contractions (PAC)
• Early beats initiated by atrium
• P waves and PR interval may vary
• Non-compensatory pause
• P wave may be found in T wave
Blocked Premature Atrial Contractions
Blocked Premature Atrial Contractions
• Pause noted on rhythm strip
• Premature P wave
• May alter cardiac output
Wandering Atrial Pacemaker
Wandering Atrial Pacemaker
• SA node not fully in control; May give some beats but mostly ectopic (outside stimuli)
• Varying configurations of P waves (since different areas of atrium)
• At least 3 different looking P waves must be seen
• HR < 100 • PR interval varies • Irregular rhythym
Multifocal atrial tachycardia (MAT)
Multifocal atrial tachycardia (MAT)
• Similar to wandering atrial pacemaker but faster (>100 bpm)
Paroxysmal atrial tachycardia (PAT, PSVT)
Paroxysmal atrial tachycardia (PAT, PSVT)
• Without warning, sudden onset of very fast tachycardia
• HR 150-250 bpm
• Regular rhythm
• P waves (if present) may merge in T waves
• AV block
• Ectopic foci in atria rapidly fluttering
• QRS complex is normal
• Hemodynamic effects vary
• S/S: Sudden onset palpitations, racing heart
• Tx:
1. Adenosine (blocks atrial beats for 6 seconds so SA can reset as primary pacemaker)
2. Beta blockers (slow down heart rate)
Atrial flutter
Atrial flutter
• Ectopic foci in atria, heart disease
• Classic “sawtooth” pattern
• Atrial rate fast and regular (250-350 bpm) with AV block
• Degree of conduction varies; may be 3 P waves: 1 QRS complex
Atrial fibrilation
Atrial fibrilation
• Erratic impulse formation in atria
• No discernible P wave
• Irregular R-R intervals*
• Aberrant (normal) ventricular conduction can occur
• Results in loss of atrial kick = decreased cardiac output, pooling blood
• High risk for pulmonary or systemic emboli
• New onset patients feel weak, lightheaded
• Maintain with anticoagulants
Junctional (Nodal) Rhythms
Junctional (Nodal) Rhythms
• Regular rhythm
• PR interval low end of normal
• P-wave changes – May be absent or retrograde (because stimulus from AV node)
• Normal rate: 40-60 bpm
• Decreased CO possible
Junctional tachycardia
Junctional tachycardia
• Rate 60-100 bpm for accelerated junctional rhythm
• Rate 100-150 bpm for junctional tachycardia
Premature junctional contractions (PJC)
Premature junctional contractions (PJC)
• P-wave changes
• PR interval shorter than normal (because closer to ventricle)
• Usually noncompensatory pause
• QRS complex that is irregular with the rest of the waves and changing P waves
Ventricular dysrhythmias + causes
Ventricular dysrhythmias + causes
• Impulses initiated from lower portion of heart (i.e. Bundle of His)
• Depolarization occurs, leading to abnormally wide QRS complex
• Ectopic and escape beats
• Common causes:
1. Myocardial ischemia, injury, and infarction
2. Low potassium or magnesium
3. Hypoxemia
4. Acid-base imbalances
Premature ventricular contractions (PVCs)
Premature ventricular contractions (PVCs)
• Wide and bizarre beats
• Compensatory pause
• Patterns:
-Bigeminy and trigeminy
-Couplets and triplets
• Uniforcal vs multifocal (depends on morphology)
• QRS complex >0.10 second
• Irregular rhythm (d/t early beats and compensatory pause)
• Absent P waves
• Assess and treat cause:
1. Hypoxia
2. Ischemia
3. Electrolyte imbalance
• May need antiarrhythmic agents
Ventricular tachycardia
Ventricular tachycardia
• Rapid, life threatening
• Three or more PVCs in a row
• Fast rate (>100 bpm)
• Initiated by ventricles
• Wide QRS, no P waves before each beat
• Usually regular
• May or may not have a pulse –> Treat pulseless same as v-fib
• Significant loss of cardiac output
• Hypotension
• Tx: Cardioversion w/ external defibrilator or medications
Ventricular fibrilation
Ventricular fibrilation
• Chaotic pattern
• No discernible P, Q, R, S, or T waves
• Coarse versus fine
• No cardiac output; life threatening
• Emergent defibrilation
Idioventricular rhythm
Idioventricular rhythm
• Hallmark = Very slow
• Escape from Purkinje fibers
• Rate: 15-40 bpm
• Regular rhythm
• Wide QRS interval
• No P waves
Accelerated idioventricular rhythm
• Same as idioventricular rhythm
• Rate > 40 bpm
• Hemodynamic effects correspond to heart rate
Ventricular standstill (asystole)
• No P, Q, R, S, T waveforms
• Assess in two leads (EKG may be off)
• No cardiac output
• Death
Pulseless electrical activity (PEA)
• EKG rhythm but no pulse
• Causes: H’s & T’s
H’s & T’s
H:
1. Hypoxia
2. Hypovolemia
3. Hypothermia
4. H+ ions (acidosis)
5. Hypokalemia or hyperkalemia

T:
1. Tablets (overdose)
• Tamponade (cardiac)
• Tension pneumothorax
• Thrombosis (coronary)
• Thrombosis (pulmonary)

Atrioventricular blocks (AVB)
• Block of conduction from atria to ventricles
• Causes:
1. Coronary artery disease
2. Myocardial infarction (eg inferior wall)
3. Infections
4. Enhanced vagal tone
5. Drug effects (eg digoxin toxicity)
Normal EKG intervals
• PR interval = 0.12-0.20 seconds
• QRS <0.12 seconds (0.06-0.10 seconds) • QT interval = 0.32-0.50 seconds