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SA Node
primary pacemaker
60-100 bpm
located in the right atrium
Atrioventricular (AV) Node
slows the impulse to allow ventricular filling (“atrial kick” provides 1/3 of total ejected volume)
Bundle of His and Purkinje Fibers
impulse moves down the right/left bundle branches into the Purkinje fibers, triggering ventricular contraction
Systole
depolarization
electrical stimulation
mechanical contraction
systole/diastole
Diastole
repolarization
electrical relaxation
mechanical relaxation
systole/diastole
Autonomic Control of Heart
HR is regulated by ANS, comprising sympathetic (adrenergic) stimulation
Sympathetic (adrenergic) Stimulation
Positive chronotropy (increased heart rate)
Positive dromotropy (increased AV Node conduction)
Positive inotropy (increased force of myocardial contraction)
Vascular effect: constriction of peripheral blood vessels, increased bp
Parasympathetic Stimulation
Negative chronotropy: decreased heart rate
Negative dromotropy: decreased AV conduction
Contractility: decreased force of atrial myocardial contraction
Decreased sympathetic stimulation dilates arteries, lower bp
Obtaining ECG and Electrode Placement
Preparation: Washing the application area with soap and water, and clipping excess hair, reduces skin impedance and enhances electrode conductivity.
Preventing Artifact: Poor electrode adhesion causes artifact—distorted, irrelevant waveforms that obscure accurate electrical capture
Normal Variations of ECG
Because of these different viewpoints, a normal rhythm tracing will inherently look different across different leads, such as lead I compared to lead II or lead III
Identifying Changes in ECG
A change in the waveform can indicate an actual alteration in how the electrical impulse originates or is conducted, or it may simply result from changing the lead being viewed
Comprehensive Assessment of ECG
To accurately assess the heart and identify exactly where, when, and what abnormalities are occurring, healthcare providers must evaluate the ECG from every lead, not just a single view
P Wave
atrial depolarization
PR Interval
time for sinus stimulation to AV node conduction (0.12-0.20 sec)
QRS Complex
ventricular depolarization
<0.12 sec
ST Segment
early ventricular depolarization (monitored for ischemia)
T Wave
ventricular repolarization
QT Interval
total time for ventricular depolarization and repolarization
Determining Heart Rate Method 1: Regular Rhythms
accurate for regular rhythms
count number os small boxes within an RR interval and divide number 1500 by that number
Ex. 1500/10= 150 bpm
Determining Heart Rate Method 2: Irregular Rhythms
6 second method
alternative for irregular rhythms (less accurate)
count number of RR intervals within a 6 sec strip and multiply number by 10
Ex. 7 RR intervals x 10= 70 bpm
you must count the RR intervals, not QRS complexes because it might lead to an inaccurate high calculated high heart rate
Determining Atrial rate
Methods can also be used to calculate the atrial rate by measuring the PP interval instead of the RR interval
Simple 6 Step Pathway
rate, rhythm, P waves, RR interval, PR interval, QRS complex, ST segment and QT/QTc
Simple 6 Step Pathway: Rate
Count QRS complexes in a 6 sec strip and multiply by 10, or use box methods
Decide: bradycardia (<60), normal (60-100), or tachycardia (>100)
Simple 6 Step Pathway: Rhythm
Regular vs irregular
Measure RR intervals across the strip
If RR distances are equal (or vary <1 small box) its regular
If they vary its irregular
Simple 6 Step Pathway: P Waves
Are P waves present and consistent in shape?
Are there more P waves than QRS, fewer, none?
Simple 6 Step Pathway: PR Interval
Measure form the start of P to start of QRS
Is it within 0.12-0.20 secs, shorter or prolonged?
Ask: is the pr integral constant or does it change beat to beat
Simple 6 Step Pathway: QRS Complex
Measure the width
Is it narrow (<0.12 secs) or wide (>0.12 secs)
Narrow: supraventricular origin
Wide: ventricular origin or conduction delay
Simple 6 Step Pathway: ST Segment and QT/QTc
ST: is it isoelectric, elevated, or depressed?
QT: roughly < half the RR interval
If clearly prolonged, think QTc prolongation and risk of torsades
Normal Sinus Rhythm (NSR) ECG Characteristics
Ventricular and atrial rate: 60-100 bpm
Ventricular and atrial rhythm: regular
QRS shape and duration: usually normal, may be regularly abnormal
P wave: normal, consistent shape, always before QRS
PR interval: consistent, 0.12 to 0.20 secs
P:QRS ratio: 1:1
Management Strategies for NSR
Normal electrical conduction from SA node
No medical management required
Represents health heart function
Sinus Bradycardia
occurs when SA node creates an impulse slower than normal rate
Sinus Bradycardia Causes
Metabolic needs (sleep, athletic training, and hypothyroidism)
Vagal stimulation (vomiting, suctioning, and severe pain)
Meds (calcium channel blockers (nifedipine, amiodarone) and beta blockers
Idiopathic sinus node dysfunction
Increased intracranial pressure
Coronary artery disease
Sinus Bradycardia ECG Characteristics
Ventricular and atrial rate: <60 bpm
Ventricular and atrial rhythm: regular
QRS shape and duration: usually normal, may be regularly abnormal
P wave: normal, consistent shape, before QRS
PR interval: consistent, 0.12 to 0.20 secs
P:QRS ratio: 1:1
Sinus Bradycardia Management Strategies
Identify Causes and Symptoms
No clinical instability/causative factors
Resolve causative factors prevent vagal stimulation, withhold beta blockers
monitor
Clinical instability
Administer atropine 0.5 mg IV bolus (repeat every 3-5 mins, max 3 mg)
If unresponsive to atropine
Emergency transcutaneous pacing or dopamine, isoproterenol, or epinephrine
Sinus Tachycardia (ST)
sinus node creates an impulse faster than normal rate
Sinus Tachy Causes
Physiologic or psychological stress (acute blood loss, anemia, shock, hypervolemia, hypovolemia, heart failure, pain, hypermetabolic states, fever, exercise, and anxiety)
Meds that stimulate sympathetic response (catecholamines, aminophylline, atropine), stimulants (caffeine and nicotine), and illicit drugs (amphetamines, cocaine, ecstasy)
Inappropriate Sinus Tachy
Enhanced automaticity of the SA node
Innate ability of cardiac cells to initiate an electrical impulse
Postural Orthostatic tachycardia Syndrome (POTS)
Tachycardia w/o hypotension and by presyncopal symptoms like palpitations, lightheadedness, weakness, and blurred vision with sudden postural changes
Sinus Tachy ECG Characteristics
Ventricular and atrial rate: >100 bpm (often <120 bpm)
Ventricular and atrial rhythm: regular
QRS shape and duration: usually normal, may be regularly abnormal
P wave: normal, consistent shape, before QRS (may be buried in T wave)
PR interval: consistent, 0.12 to 0.20 secs
P:QRS ratio: 1:1
Sinus Tachy Management Strategies
identify and abolish cause
Vagal Maneuvers: Valsalva, carotid massage, coughing, cold stimulus
Adenosine: Interrupts tachycardia
Hemodynamic instability: Synchronized cardioversion
stable/persistent: Beta blockers, calcium channel blockers, catheter ablation
Premature Atrial Complex (PAC)
electrical pulse starts in the atrium before the next normal impulse of the sinus node
usually seen w/tachycardia
Causes of PAC
Caffeine, alcohol, nicotine, stretched atrial myocardium (hypervolemia), anxiety, hypokalemia, hypermetabolic states, or atrial ischemia, injury, or infarction
PAC ECG Characteristics
Ventricular and atrial rate: depends on underlying rhythm
Ventricular and atrial rhythm: irregular, early P waves, shorter PP interval, noncompensatory phase
QRS shape and duration: early QRS usually normal, may be abnormal or absent
P wave: early, different shape, or hidden in T wave; others consistent
PR interval: early PR shorer but normal (0.12-).2 secs)
P:QRS ratio: usually 1:1
PAC Management Strategies
Infrequent PACs (<6 mins); no treatment necessary. Monitor
Frequent PACs (>6 mins): medical management → treat underlying cause (Reduce caffeine intake, Correct hypokalemia)
Atrial Fibrillation (A-Fib)
can result from diverse pathophysiological etiologies
results from abnormal impulse formation that occurs when a structural or electrophysiologic abnormalities alter atrial tissue causing a rapid, uncoordinated twitching of atrial musculature
AFib Risk factors
Alcohol use disorder, diabetes, exercise, family history, female sex, heart failure, hyperthyroidism, hypotension, MI, obstructive sleep apnea, smoking, obesity
Paroxysmal A-Fib
Sudden onset w/termination that occurs randomly or after an intervention; lasts <7 days but may recur
Persistent Afib
Continuous, lasting >7 d
Long Standing Persistent Afib
Continuous, lasting >12 mo
Permanent Afib
Persistent but decision has been made not restore or maintain sinus rhythm
Nonvalvular
Absence of moderate to severe stenosis or mechanical heart valve
Afib ECG characteristics
Ventricular and atrial rate: 300-600 bpm; usually 120-200 bpm in untreated afib
Ventricular and atrial rhythm: highly irregular
QRS shape and duration: usually normal, may be regularly abnormal
P wave:no discernible P waves; irregular undulating waves that vary in amplitude and shape are seen and referred to as fibrillatory or f waves
PR interval: can not be measured
P:QRS ratio: many:1
Afib Management Strategies: Stroke Prevention
Antithrombotic drugs: warfarin, DOACs, Factor Xa inhibitors, prescribed via CHA2DS2-VASc risk assessment
Alternative: left atrial appendage occlusion (LAAO) (WATCHMAN for nonvalvular AF)
Afib Management Strategies: rate Control
Resting ventricular rate <80 bpm
Meds: beta blockers or non-dihydropyridine channel blockers
Afib Management Strategies: Rhythm Conversion
Pharmacologic cardioversion: Flecainide, doferilide, amiodarone
Electrical cardioversion: used to restore sinus rhythm
Requirement: if arrhythmia >48 hrs, anticoagulation or TEE
Afib Management Strategies: Surgical/Advanced Therapies
Options: catheter ablation, maze or mini-maze procedures, convergent procedure
Indication: for rhythms unresponsive to meds or electrical cardioversion
Atrial Flutter
Occurs due to a conduction deficit in the atrium and causes a rapid, regular atrial impulse at a rate between 250 and 400 bpm
Saw tooth on ekg
Atrial Flutter ECG Characteristics
Ventricular and atrial rate: 250 and 400 bpm; ventricular rate usually ranges between 75 and 150 bpm
Ventricular and atrial rhythm: atrial rhythm regular, ventricular rhythm regular but may be irregular due to change in AV conduction
QRS shape and duration: usually normal, may be regularly abnormal
P wave: saw-toothed shape; referred to as F waves
PR interval: difficult to determine due to F waves
P:QRS ratio: 2:1, 3:1, 4:1
Management Strategies for Atrial Flutter
Vagal maneuvers or trial admin of adenosine (IV rapid admin followed by 20 mL saline flush and elevation of arm) to terminate tachycardia or visualize flutter waves
Treated w/antithrombotic therapy, rate control, and rhythm control similarly to afib
Electrical cardioversion is often successful in converting to sinus rhythm
Afib differences from A flutter
Chaotic irregular rhythm, no P waves, irregular RR intervals
Causes: Hypertension, heart failure, valve disease
Symptoms: Palpations, fatigue, SOB
Treatment: Rate control, rhythm control, anticoagulation
A flutter differences from A fib
Rapid regular sawtooth pattern, flutter waves
Causes: Similar to afib, Pulmonary disease
Symptoms: Often similar to afib
Treatment: Cardioversion, ablation, rate control, anticoagulation
Junctional Rhythm
no p waves
Occurs when AV node becomes pacemaker of the heart
inverted p wave
Junctional Rhythm ECG Characteristics
Ventricular and atrial rate: 40-60 bpm
Ventricular and atrial rhythm: regular
QRS shape and duration: usually normal, may be abnormal
P wave: absent before QRS (inverted esp. Lead II) or after QRS
PR interval: consistent, <0.12 sec (if P is before QRS)
P:QRS ratio: 1:1 or 0:1
Management Strategies for Junctional Rhythm
Monitor for signs of reduced cardiac output
Treatment same as sinus bradycardia
Atropine or pacing may be considered
Emergency pacing may be needed
Atrioventricular Nodal Reentry Tachycardia (AVNRT)
Benign non-life threatening arrhythmia goal is to alleviate symptoms and improve quality of life
Aim of therapy is to break reentry of the impulse
AVNRT ECG Characteristics
Ventricular and atrial rate {150-250 (atrial)}, {120-200 (ventricular)}
Ventricular and atrial rhythm: regular
QRS shape and duration: usually normal (narrow)
P wave: difficult to discern
PR interval: <0.12 sec (if P before QRS)
P:QRS ratio: 1:1, 2:1
Management Strategies for AVNRT
Alleviate symptoms and improve quality of life
Initial treat: catheter ablation (choice treatment)
Acute management: vagal maneuvers (IV adenosine bolus)
Pharm therapies: IV non-dihydropyridine (CCBs, IV beta blocker, IV digoxin)
Unstable/ refractory causes (Electrical cardioversion)
Premature Ventricular Complex (PVC)
Impulse that starts in the ventricle and is conducted through the ventricles before the next normal sinus pulse
Causes of PVC
Intake of coffee, nicotine, alcohol, cardiac ischemia or infarction, heart failure, tachycardia, digitalis toxicity, hypoxia, acidosis, or electrolyte imbalances (hypokalemia)
PVC ECG Characteristics
Ventricular and atrial rate: depends on underlying rhythm
Ventricular and atrial rhythm: irregular due to early QRS, creates one shorter RR interval
QRS shape and duration: >0.12 sec; bizarre and abnormal (unifocal or multifocal)
P wave:visibility varies (absent, hidden in QRS/T, or before QRS w/different shape)
PR interval: If P before QRS <0.12 sec
P:QRS ratio: 1:1, 0:1
Management Strategies for PVC
Initial treatment: aim to correct underlying cause
Frequent and persistent PVC: may treat w/amiodarone or beta blockers
Note: long term pharmacotherapy is not usually indicated
Ventricular Tachycardia
3 or more PVCs in a row
emergency because pts is nearly always unresponsive
Risk Factors for V-tach
pts w/larger MIs and lower ejection fractions
V-tach ECG Characteristics
Ventricular and atrial rate: Ventricular is 100-200, martial rate depends in underlying rhythm
Ventricular and atrial rhythm: usually regular
QRS shape and duration: 0.12 secs or more, bizarre normal shape
P wave: difficult to detect, so atrial rate/rhythm may be indeterminable
PR interval: very irregular if P waves are seen
P:QRS ratio: difficult to determine but usually more QRS complexes than P waves
V-tach Management Strategies: Stable VT
antiarrhythmic meds (amiodarone) or synchronized cardioversion
12 lead ECG, procainamide, sotalol, lidocaine, antitachycardia pacing
V-tach Management Strategies: Unstable VT
treated as V fib w/immediate defibrillation and CPR
Identify and treat underlying causes
V-tach Management Strategies: Symptomatic monophasic VT
Cardioversion is treatment of choice
V-tach Management Strategies: Long Term
ICD considered for pts w/an ejection fraction less than 35%
V-tach Management Strategies: Torsades de Pointes
Immediate treatment required
Identify causes
Correcting electrolyte imbalances (IV magnesium)
IV isoproterenol pacing if associated w/bradycardia
Ventricular Fibrillation (V-Fib)
Rapid, disorganized ventricular rhythm that causes ineffective quivering of the ventricles
No atrial activity seen
Causes of V-Fib
Acute coronary artery disease, acute MI, untreated Vtach, cardiomyopathy, valvular heart disease, Brugada syndrome, acid-base and electrolyte abnormalities
V-Fib Characteristics
Ventricular and atrial rate: greater than 300 bpm
Ventricular and atrial rhythm: extremely irregular, w/o specific pattern
QRS shape and duration: irregular, undulating waves w/changing amplitudes; no recognizable QRS complexes
Management Strategies for V Fib
Characterized by absence of an audible heartbeat, palpable pulse, and respirations
Immediate electrical defibrillation and CPR are essential for survival
Antiarrhythmic drugs such as amiodarone may be indicated if defib attempts are unsuccessful
Idioventricular Rhythm
impulse starts in conduction system below the AV node
Idioventricular Rhythm ECG characteristics
Ventricular rate: 20 and 40 bpm; if rate exceeds 40, rhythm known as accelerated idioventricular rhythm
Ventricular and atrial rhythm: regular
QRS shape and duration: bizarre, abnormal shape; duration is 0.12 secs or more
Management Strategies of Idioventricular Rhythm
Commonly causes pt to lose consciousness and experience signs of reduced cardiac output
Interventions follows ACLS guidelines: identify underlying cause administer IV epinephrine, atropine, and vasopressor meds, and initiate emergency transcutaneous pacing as needed
Ventricular Asystole
Flatline, characterized by absent QRS complexes confirmed in 2 different leads
Ventricular Asystole ECG Characteristics
Characterized by absent QRS complexes confirmed in 2 different leads
Occasionally P waves may be apparent for short duration
Management Strategies for Ventricular Asystole
Fatal w/o immediate treatment
Treated similarly to PEA, focusing in high quality CPR w/minimal interruptions
Rapid assessment to identity reversible causes (Hs and Ts: hypovolemia, hypoxia, hydrogen ion, hypo/hyperkalemia, hypothermia, tension pneumothorax, tamponade, toxins, and thrombosis
Initiation of CPR, intubation, and establishment of IV access are the next recommended actions
Asystole
Appearance: Flat line (slight undulations)
Mechanical Activity: No pulse
P wave and QRS: absent
Management Strategies: CPR, epi/vasopressin
Reversible Causes: Treat underlying cause (if identified)
Pulseless Electrical Activity (PEA)
Appearance: Organized electrical activity (P, QRS present)
Mechanical Activity: No pulse
P wave and QRS: Present, but no pulse
Management Strategies: CPR, Epinephrine/vasopressin, treat H’s and T’s
Reversible Causes: Hs and Ts (hypovolemia, hypoxia, etc.)
1st degree Atrioventricular Block
Occurs when all the atrial impulses are conducted through the AV node into the ventricles at a rate slower than normal
1st degree Atrioventricular block ECG Characteristics
Ventricular and atrial rate: depends on the underlying rhythm
Ventricular and atrial rhythm: depends on underlying rhythm
QRS shape and duration: usually normal but may be abnormal
P wave: in front of the QRS complex; shows snus rhythm, regular shape
PR interval: greater than 0.20 secs; PR interval measurement is constant
P:QRS ratio: 1:1
Management Strategies for 1st degree atrioventricular block
Rarely causes any hemodynamic effect
Management of AV blocks is based on the cause and stability of the patient directed toward increasing heart rate to maintain normal cardiac output
If stable w/o symptoms, no treatment may be indicated, or it may involve decreasing/eliminating the cause (withholding meds)
2nd Degree AV Block Type I (Wenchebach)
benign conduction delay at the AV node
PR interval is prolonged
2nd Degree AV Block Type I (Wenchebach) ECG Characteristics
Ventricular and atrial rate: depends on underlying rhythm, but ventricular rate is lower than the atrial rate
Ventricular and atrial rhythm: PP interval is regular, RR interval gradually shortens until there is another long RR interval
QRS shape and duration: usually normal, may be abnormal
P wave: in front of the QRS complex; shape depends on underlying rhythm
PR interval: becomes longer w/each succeeding complex until there is a P wave not followed by QRS
P:QRS ratio: 3:2. 4:3, 5;4, and so forth
Management Strategies for 2nd Degree AV Block Type I (Wenchebach)
Same general AV block management as 1st degree block based in symptoms and cause
2nd Degree AV Block Type I (Mobitz II)
serious arrhythmia where electrical impulses are intermittently blocked below the AV node (His-Purkinje system), causing unexpected dropped QRS complexes without prior PR interval lengthening
2nd Degree AV Block Type I (Mobitz II) ECG Characteristics
Ventricular and atrial rate: depends on underlying rhythm, but ventricular rate is lower than the atrial rate
Ventricular and atrial rhythm: PP interval is regular, RR interval is usually regular but may be irregular depending on P:QRS ratio
QRS shape and duration: usually abnormal, may be normal
P wave: in front of the QRS complex; shape depends in underlying rhythm
PR interval: constant for those P waves just before QRS complexes
P:QRS ratio: 2:1, 3:1, 4:1, 5:1, and so on
Management Strategies for 2nd Degree AV Block Type I (Mobitz II)
Same general AV block management, but if the block is related to necessary meds or other conditions, permanent pacemaker implantation may be indicated
temporary pacemaker may be necessary for severe symptomatic bradycardia