My Achy Breaky Heart

Source: The only EKG book you’ll ever need by Malcolm S. Thaler 9th ed 2019
The Heart Basics
I. Anatomy & Physiology
a. A muscle made up of cardiac muscle (unique)
i. Picture of different types of muscles; describe why cardiac muscle is different
b. 4 chambers
i. 2 upper: atria (atrium)
ii. 2 lower: ventricles
c. 4 valves
i. 2 semilunar: atrial, pulmonary
ii. 2 (what are these called?): tricuspid (mitral) & bicuspid
iii. Pictures, please
d. Coronary Arteries/Aorta
i. How the arteries come off the aorta
ii. How the heart feeds itself
iii. Name the arteries
e. Systole & Diastole
i. Systole: contraction
ii. Diastole: relaxation
II. Electrophysiology
a. Types of cells
i. Pacemaker cells: the source of electricity in the heart
1. About the width of a single spider web strand
2. Depolarize spontaneously continuously
a. Each depolarization initiates one complete cycle of cardiac contraction and
relaxation (one heartbeat)
3. Location
a. High up in the right atrium: the sinoatrial (SA)/sinus node
i. Intrinsic beat: 60-100 bpm
ii. Highly sensitive to the autonomic nervous system
1. Easily accelerates d/t catecholamines (norepi/epi) from sympathetic NS
2. Easily decelerates d/t vagal stimulation and the parasympathetic NS
4. Interesting tidbit
a. Transplanted hearts cannot be stimulated from vagal stimulation since the nerves
are cut; therefore, donor hearts usually beat about 100bpm
ii. Electrical conducting cells: the pathway the electricity follows to depolarize
1. Long and thin; function as wires in an electrical circuit— “electrical highway”
2. Purkinje system: the ventricular conducting fibers
3. Bachman’s bundle: the conductive pathway that branches off the sinus node into the
left atrium to allow for rapid activation of the left atrium from the right.
a. Branches off the sinus node and across the intra-atrial septum but is fairly
anatomically variable based on the patient.
iii. Myocardial cells: the cells that contract in the heart (cause the heart to pump)
1. Largest of the cardiac cells
2. Contain a large amount of contractile proteins actin and myosin
a. Define actin and myosin
 My Achy Breaky Heart
Source: The only EKG book you’ll ever need by Malcolm S. Thaler 9th ed 2019
b. Cardiac cells’ “insides” are negatively charged, while their “outsides” are positively
charged
i. Achieved through the membrane pumps that distribute ions—K+, Na-, Cl- Ca++)
ii. Talk about the pumps
iii. When depolarization reaches the myocardial cell, the cell releases Ca++ within the cell,
which causes it to contract. This is called excitation-contraction coupling
1. The released calcium causes the actin and myosin to interact—this chemical reaction
causes the cell to contract.
c. Depolarization
i. In order for the heart to pump, the cells depolarize.
1. This occurs spontaneously in pacemaker cells and in other cells is initiated by the
arrival of an electrical impulse (the pacemaker cells) causing the positive cells to
cross the membranes.
d. Repolarization
i. The cardiac cells then restore their resting polarity (negativity) by the pumps resetting
the ions to their respective locations
e. Action potential
i. One electrical cycle of depolarization and repolarization from a single cell produces a
tracing called an action potential
ii. Each action potential stimulates another in the neighboring cell, which continues until
the entire heart is depolarized
iii. After depolarization, pacemaker cells have a negative action potential where it is
impossible to stimulate it into another contraction. After reaching this negative level
(usually -60mV), the voltage gradually rises until it reaches a threshold for sudden
depolarization and resumes the cycle again.
The EKG waves
I. Voltage
a. The waves seen on an EKG are the passing of electricity among the myocardial cells
i. The electricity that passes in the electrical conducting cells is too small to register
ii. 3 characteristics:
1. Duration (measured in fractions of a second)
2. Amplitude (measured in millivolts mV)
3. Configuration (the shape and appearance of the wave)
II. P waves (atrial depolarization)
a. The sinus node fires spontaneously (not visible on EKG) and depolarization spreads
outward in the atrial myocardium
b. EKG records a small burst of electrical activity (P wave) that records the depolarization of
the atria myocardium from start to finish
i. The right atrium begins to depolarize first/finishes before the left
1. First part of P wave represents rt. Atrial depolarization
2. Second part of P wave represents lt. atrial depolarization
III. The Pause
a. Healthy hearts have an electrical ‘gate’ junction between the atria and ventricles, the AV
(atrioventricular node)
i. The AV node slows the conduction b/t slows the conduction down/pauses it, but only for
a fraction of a second (usually about 1/10th of a second).
 My Achy Breaky Heart
Source: The only EKG book you’ll ever need by Malcolm S. Thaler 9th ed 2019
1. This is to allow the atria to finish contracting before the ventricles contract
2. The pause allows the atria to completely empty themselves into the ventricles before
the ventricles contract.
3. AV also heavily influenced by the autonomic nervous system
IV. Ventricular Depolarization
a. Depolarizing waves “escape” the AV node and sweep rapidly down the ventricular
conducting system
i. Bundle of His
ii. Bundle branches
iii. Terminal Purkinje fibers
b. Bundle of His: emerges from the AV node and divides into lt. and rt. bundle branches
c. Bundle Branches
i. Rt. bundle branch: carries current down the right side of the septum all the way to the
apex of the rt. ventricle
ii. Lt. bundle branch divides into three fascicles
1. Septal fascicle: depolarizes the interventricular septum in a lt.-rt. direction
2. Anterior fascicle: depolarizes the anterior wall of the lt. ventricle
3. Posterior fascicle: depolarizes the posterior part of the ventricle
d. Purkinje Fibers: the branching off of the bundle branches to deliver electrical current into
the myocardium
e. Depolarization of the ventricles causes the QRS complex
i. Significantly larger because there is more muscle mass in the ventricles than the atria
ii. Earliest part QRS complex: depolarization of the interventricular septum (Q wave)
iii. R & S: depolarization of both rt and lt ventricle
1. Mostly represents lt ventricle; lt ventricle has 3x the muscle mass as the rt.
V. Parts of the QRS
a. Q: the first deflection downward (nl. amplitude is no more than 0.1 mV)
i. Indicates septal depolarization
1. The septum (the wall of muscle separating the lt. and rt. ventricles) depolarizes first
and left to right
2. The septal fascicle of the left bundle branch delivers the depolarization wave to the
rest of the ventricles
b. R: the first deflection upward
i. A second upward deflection is called R’ (R-prime)
ii. Indicates the rest of the ventricular myocardium depolarizing (R+S)
c. S: the first downward deflection following an upward deflection
d. Therefore, you can be missing any of these parts and the wave can be a QRS, RS, QR, R,
etc. wave.
VI. Ventricular repolarization
a. There is another “pause” between the QRS and T waves; this is caused by the refractory
period where it is impossible to stimulate the ventricular cells into depolarizing (the
negative action potential).
b. The T-wave represents the repolarization of the ventricles, meaning they will be ready to
depolarize once more
c. Atrial repolarization also creates a wave, but it is hidden by the QRS complex.
VII. Why do the waves look different?
 My Achy Breaky Heart
Source: The only EKG book you’ll ever need by Malcolm S. Thaler 9th ed 2019
a. The waves look different based on where you are ‘standing’ (think 3 blind men touching
an elephant). Each electrode is viewing the depolarization/repolarization through a
different lens, which means it will look different based on if the cells are depolarizing
toward the electrode or away from it.
i. Toward: positive deflection then negative deflection
ii. Away: negative deflection followed by a positive deflection (QRS is upside down)
VIII. Measuring the waves
a. The “straight line” is the isoelectric line
b. PR: beginning of the P wave to the beginning of the QRS complex (measures end of atrial
depolarization to the start of ventricular depolarization)
i. Normal range: 0.12-0.2 seconds
c. QRS: beginning of the QRS complex to the end of the complex
i. Normal range; 0.06-0.1
d. QT: measured from the beginning of the QRS complex to the end of the T wave (measures
the time from the beginning of ventricular depolarization to the end of ventricular
repolarization)
i. Lasts for 40% of the cardiac cycle (from R wave to R wave)
ii. Greatly affected by the heart rate (slow HR=longer QT; rapid HR=shorter QT)
e. ST: end of the QRS complex to the beginning of the T wave (measures time between
depolarization and repolarization of the ventricles)
EKG Interpretation
I. Heart Rate
a. Distance between a small square is 0.04 seconds
b. Distance in a large square is 0.2 seconds; 5 large squares=1 second
c. 3 step method:
i. Find an R wave that falls on a heavy line (edge of a large square)
ii. Count the number of large boxes between R waves
iii. Divide that number by 300
iv. For greater accuracy, count the number of small squares and divide by 1500.
II. Identify Dysrhythmias
a. Are normal P waves present, and is the axis nl? (positive in lead II, negative in aVR)
i. P waves normal/present: origin of arrhythmia is in the atria
ii. No P waves: dysrhythmia originates below atria (AV node or in ventricles)
iii. P waves abnormal/present: atrial activation but atrial focus rather than SA node or
retrograde activation from the AV node/ventricles
b. Are the QRS complexes narrow (<0.12) or wide (>0.12)?
i. Narrow complex: depolarization is occurring on normal pathways (most efficient and
takes the least amount of time, so it results in narrow complexes)
ii. Wide complex: depolarization initiated in the ventricular myocardium and spreads much
slower (wider complexes)
c. Questions 1 & 2 help us identify if the arrhythmia is ventricular or supraventricular
(atrial or junctional) in origin
d. What is the relationship between P waves and the QRS?
i. 1:1=sinus or atrial origin
ii. Depolarization independently from one another=AV dissociation (dangerous)
e. Is the rhythm regular or irregular
 My Achy Breaky Heart
Source: The only EKG book you’ll ever need by Malcolm S. Thaler 9th ed 2019

Arrhythmias/dysrhythmias Overview
I. Basics
a. Arrhythmia and dysrhythmia mean the same thing (like EKG vs ECG)
i. “any disturbance in the rate, regularity, site of origin, or conduction of the cardiac
electrical impulse” (p.104)
b. Normal sinus rhythm (originates in the sinus node): 60-100bpm
II. Clinical Manifestations
a. May be discovered incidentally (pt. showing no symptoms)
b. Palpitations: an awareness of your own heartbeat.
i. Patients may feel their heart accelerate/decelerate or pause
c. Light-headedness and/or syncope
i. Occurs when arrhythmias compromise the cardiac output
d. Chest pain (angina)
e. Sudden cardiac death
III. Arrhythmia Causes (HIS DEBS)
a. Hypoxia: when the heart is deprived of oxygen, it becomes irritable.
i. Lung disorders often precipitate cardiac arrhythmias (COPD, acute PEs)
b. Ischemia and Irritability: MIs, angina, myocarditis
c. Sympathetic Stimulation: increasing of the sympathetic tone for any reason can cause
arrythmias (d/t hyperthyroidism, HF, anxiety, exercise, etc.)
d. Drugs: both prescribed and illicit. Antiarrhythmics are a common culprit, ironically.
e. Electrolyte disturbances: imbalances in K+, Ca--, Mg can all cause arrhythmias.
f. Bradycardia: very slow heart rates seem to be predisposed to arrhythmias. A common one
is bradytachycardia syndrome (sick sinus syndrome)
g. Stretch: enlargement/hypertrophy of the chambers (d/t HF, cardiomyopathy, valvular
disease) can cause arrhythmias
5 types of arrhythmias
I. Sinus origin: still originating from the sinus node but is too fast, too slow, or irregular
a. Sinus tachycardia (>100bpm) & bradycardia (<60bpm)
i. Can be normal or pathologic
1. Exercise=HR>100; highly fit athletes usually have HR<60 normally
2. May also be caused by disease processes (such as hyperthyroidism) or medications
(beta-blockers, CCB, opioids)
3. Bradycardia is the most commonly seen rhythm change in the early stages of an
acute MI
4. Bradycardia can also cause an enhanced vagal tone and cause healthy individuals to
pass out.
b. Sinus arrhythmia
i. NSR that is slightly irregular
ii. Normal phenomenon: seen when the heart varies with inspiration and expiration
(insp=accelerate, exp=decelerate)
c. Sinus arrest, asystole, escape beats
i. Sinus arrest: the sinus node stops firing (also known as a sinus exit block)
ii. Asystole: “flat-lining”; prolonged electrical inactivity
 My Achy Breaky Heart
Source: The only EKG book you’ll ever need by Malcolm S. Thaler 9th ed 2019
iii. Escape beats: “rescue beats” that occur when the sinus node does not initiate
depolarization—most common type of escape beat is junctional (see below for more
information on junctional beats)
II. Ectopic rhythms: electrical activity originates from a focus other than the sinus node
a. Occurs because there is enhanced automaticity in a non-sinus node site
i. Disorder of impulse formation (new impulses are formed and take over the heart)
b. Common causes: digitalis toxicity, beta adrenergic stimulation (from inhalers used to treat
asthma/COPD), caffeine, alcohol, and stimulants (cocaine, meth)
III. Reentrant arrhythmias: electrical activity is trapped in a certain part of the heart
a. Disorder of impulse transmission
i. A wave of depolarization is blocked/transmits more slowly, which allows a wave of
depolarization from another area of the heart to reenter the circuit, causing a racetrack
effect (reentry loop)
ii. Depolarization is sent in all directions, overwhelms the sinus node, and this loop begins
to run the heart
b. Reentry loops can be of varying sizes and affect various areas of the heart
IV. Conduction blocks: the electrical activity starts in the sinus node, but encounters blocks
and delays
V. Preexcitation syndromes: the heart essentially “short circuits” by following alternate
conduction circuits
Non-sinus pacemakers
I. Types of Pacemakers
a. Sinus pacemaker: 60-100 bpm
b. Atrial pacemakers: 60-75bpm
c. Junctional pacemakers (located near the AV junction): 40-60bpm
d. Ventricular pacemakers: 30-45bpm
II. Junctional Rhythms
a. No P wave (originates at the AV node, so atria do not depolarize)
b. May occasionally see a retrograde P wave (inverted)
i. Depolarization originates at the AV node, so the P wave is inverted
Supraventricular Arrhythmias
I. Basics
a. “SVT” is not a rhythm itself, but rather a group of rhythms that originate in the atria/AV
node but are not sinus rhythm.
b. Any arrhythmia that originates above the ventricle, i.e., in the atria or the AV node
II. Atrial and Junctional Premature Beats (PACs/PJCs)
a. PACs produce a P wave with a different contour and beat early (prematurely)
i. Because the beat originates somewhere other than the SA node, the beat looks different
than the other P waves
b. PJCs don’t usually produce P waves, but retrograde P waves can be seen occasionally
c. Usually conducted normally in the ventricles, so the QRS complex will be narrow
III. Sustained supraventricular arrhythmias:
a. AV nodal reentrant tachycardia (paroxysmal supraventricular tachycardia)
b. Atrial flutter
c. Atrial fibrillation
d. Multifocal atrial tachycardia and wandering atrial pacemakers
 My Achy Breaky Heart
Source: The only EKG book you’ll ever need by Malcolm S. Thaler 9th ed 2019
IV. AV nodal reentrant tachycardia (paroxysmal supraventricular tachycardia)
a. Onset usually precipitated by a PAC or PJC and terminates abruptly
b. Can be elicited by alcohol, caffeine, excitement, or anxiety
c. May occur in perfectly healthy hearts with no underlying cardiac disease
d. Rhythm is regular and beaths between 150-250bpm
e. Usually driven by a reentrant circuit looping in the AV node
f. Can be interrupted through carotid massage, the Valsalva maneuver, squatting
i. Baroreceptors in the carotid arteries can be fooled into thinking BP is rising by applying
gentle pressure externally to the carotid artery.
ii. The baroreceptors in the carotid arteries influence vagal input to the heart.
1. Right carotid: affects sinus node vagal input
iii. Left carotid: affects AV vagal input
g. If massage, Valsalva, etc. do not work, adenosine is the next level of treatment
i. Avoid this medication in patients with bronchospastic lung disease
ii. Second line therapies: BB, CCB, electrical cardioversion
V. Carotid Massage Directions
a. Auscultate for carotid bruits prior to massage (do not massage if there is evidence of
carotid disease)
i. Lie pt. flat, extend the neck, and rotate the head slightly away
ii. Palpate carotid artery and apply gentle pressure for 10-15 seconds. Press as firm as
would be required to compress a tennis ball
iii. Never compress both arteries simultaneously
iv. Start on the right side, but if it fails, try the left
VI. Atrial flutter
a. Usually occurs in patients with underlying pathology
i. Seen most often generated by a reentrant circuit that runs around the annulus of the
tricuspid valve
b. Regular rhythm with an atrial rate of 250-350 bpm
c. Flutter waves create a saw-toothed pattern in leads II & III
d. The number of atrial impulses overwhelms the AV node (AV node doesn’t have time to
repolarize before the next impulse hits)
i. Causes an AV block—the node blocks a number of the atrial impulses
1. Most common is 2:1; for every 2 flutter waves, 1 produces a QRS
e. Carotid massage can increase the degree of the block (2:1 to 4:1); this makes it easier to
identify the sawtooth pattern
i. Massage will not terminate the rhythm as it originates above the AV node
f. When measuring the degree of the block, there is always a P wave hidden within the QRS
complex; count the number of P waves and add one.
g. Disease processes associated with A-flutter:
i. HTN, obesity, diabetes mellitus
ii. Electrolyte imbalance, alcohol use/intoxication
iii. Drug abuse (meth and cocaine especially)
iv. Pulmonary disease (COPD, PEs)
v. Thyrotoxicosis
vi. Underlying cardiac conditions (congenital and acquired) such as atrial septal defect
(ASD), rheumatic valvular disease, CAD, and CHF
 My Achy Breaky Heart
Source: The only EKG book you’ll ever need by Malcolm S. Thaler 9th ed 2019
VII. Atrial fibrillation
a. Most common and clinically significant sustained arrhythmia; often seen in:
i. Elderly
ii. Underlying cardiovascular d/o
1. HTN, metabolic syndrome, mitral valve disease, CAD
iii. Alcoholism & obesity
iv. Obstructive sleep apnea
v. PEs thyrotoxicosis, pericarditis (less common)
b. Symptoms
i. Palpitations, chest pain
ii. SOB, dizziness
iii. Occasionally asymptomatic
c. Atrial heart rate may be upwards of 500bpm; unable to identify true P waves
d. “multiple tiny reentrant circuits whirl around in a totally unpredictable fashion”
e. AV nodes allows impulses to pass through at variable intervals, creating an irregularly
irregular ventricular rate usu. b/t 120-180bpm
f. The multitude of P waves creates an “undulating baseline” of fibrillation waves
g. Carotid massage might slow the ventricular rate, but is rarely used
h. Treatments
i. Rate and/or rhythm control
1. Rhythm control may occur through antiarrhythmics or ablation
ii. Anticoagulants
1. Pts. in chronic a-fib are at high risk of systemic embolization
2. Quivering atria are an ideal place for blood to coagulate
3. Pts. are placed on anticoagulants if high risk for embolization
4. If unable to tolerate anticoagulants (high risk bleeder, falls, etc.), physicians may
insert a left atrial appendage device to prevent clots from forming in the lt. atrium.
VIII. Multifocal atrial tachycardia & wandering atrial pacemakers
a. Irregular rhythm with 100-200bpm
b. Results from random firing of several ectopic atrial foci
c. If HR<100, called a wandering atrial pacemaker
d. Commonly seen in pts. with sever lung disease, but can be seen in healthy hearts
e. Rarely requires treatment; carotid massage has no effect on it
f. Irregular, but still has easily identifiable P waves
i. Different than sinus arrh.: pt. must exhibit at least 3 P-wave morphologies
IX. Paroxysmal atrial tachycardia (ectopic atrial tachycardia)
a. Usually seen in normal hearts or digitalis toxicity
b. Regular rhythm 100-200bpm; results from either enhanced automaticity of an ectopic
atrial focus or from a reentrant circuit in the atria
i. Automatic type more common; may see irregularity when the PAT begins and
terminates
ii. Reentrant form also called atypical atrial flutter and starts abruptly from a PAC
c. Carotid massage might slow PAT mildly, but virtually no effect
X. AV reciprocating tachycardia
a. Caused by reentrant loops that reciprocates b/t the atria and ventricles (usu. seen in WPW)
 My Achy Breaky Heart
Source: The only EKG book you’ll ever need by Malcolm S. Thaler 9th ed 2019
Ventricular Arrhythmias
I. Premature Ventricular Contractions
a. The most common type of ventricular arrhythmia; QRS is wide and bizarre
1. Ventricular depolarization does not follow normal conduction pattern
2. For a beat to be called a PVC, it needs to measure 0.12 seconds in most leads
3. Usually followed by a compensatory pause, but it can occure between two normally
conducted beats without a pause; these are called interpolated PVCs.
4. Isolated PVCs are rarely a cause for treatment
b. Ratios of PVCs
i. Bigeminy: 1:1 PVC and normal beat
ii. Trigeminy: 2:1 PVC to normal beat (every third beat is a PVC)
c. If PVCs constitute more than 10% of the hearbeats, it can cause the heart to restructure
itself and lead to dilated cardiomyopathy.
i. Can be treated medically or with ablation therapy
d. Circumstances in which PVCs pose an increased risk for triggering ventricular
tachycardia, ventricular fibrillation, or death are called the rules of malignancy
i. Frequent PVCs
ii. Runs of consecutive PVCs (esp. 3+ in a row)
iii. Multiform PVCs (the PVCs vary in site of orgin and so does their appearance)
iv. PVCs falling on the T wave of the previous beat (“R on T” phenomenon)
v. PVCs post acute MI
II. Ventricular Tachycardia (VT)
a. Officially defined as a run of 3+ PVCs
b. Sustained VT (lasting more than 30 seconds) and VT assoc. with hemodynamic instability
are medical emergencies and require immediate treatment
c. May be monomorphic (each beat looks the same) or polymorphic (beats look different)
i. Polymorphic VT assoc. with acute coronary ischemia, infarction, electrolyte imbalances,
and prolonged QT intervals
ii. Monomorphic VT seen often with healed infarctions; the scar tissue provides an area of
reentrant tachycardia
d. The development of sustained ventricular tachycardia post MI within the first 6 weeks
post infarct is associated with a high 1 year mortality rate.
e. Post MI patients are at a higher risk of developing VT, especially in the first 48 hrs.
III. Torsade de Pointes
a. “twisting of the points”
b. Unique form of VT seen in pts. with prolonged QT intervals
c. Causes of prolonged QT
i. Congenital
ii. Electrolyte disturbances (esp. low Ca++, Mg, K+)
iii. Develops during an MI
iv. Pharmacology (antiarrhythmics, tricyclic antidepressants, phenothiazines, antifungals,
antihistamines + abx [erythromycin, azithromycin, quinolones])
IV. Ventricular Fibrillation (VF)
a. Only seen in dying hearts
b. Most frequently seen arrhythmia in adults who experience sudden death
c. Coarse VF (EKG is jerky/spasmodic) vs. fine VF (gentle ripple)
 My Achy Breaky Heart
Source: The only EKG book you’ll ever need by Malcolm S. Thaler 9th ed 2019
d. No cardiac output; medical emergency
e. VT can degenerate into VF if not treated
f. VF precipitants
i. MI/myocardial ischemia
ii. Heart failure
iii. Hypoxemia/hypercapnia
iv. Shock/hypotension
v. Electrolyte imbalances
vi. Overdoses of stimulants
V. Accelerated Idioventricular Rhythm
a. Benign; seen after reperfusion of an acute infarction
b. Represents a ventricular escape focus; rarely is it sustained
c. Usually between 50-100 bpm; if <50 bpm, called “idioventricular rhythm”
Conduction Blocks
I. Basics
a. Definition: “any obstruction or delay of the flow of electricity along the normal pathways
of electrical conduction
b. Can occur anywhere in the conduction pathway
i. Sinus node block: electricity is conducted from the sinus node, but it is immediately
blocked and not transmitted to the atrial tissues. The EKG shows a pause in the normal
cardiac cycle.
ii. AV block: any conduction block between the sinus node and the terminal Purkinje fibers
(includes the AV node and His bundle)
iii. Bundle branch block: a conduction block of one or both of the ventricular bundle
branches; if only part of the left bundle branch is blocked, it is called a fascicular block
or hemiblock
II. AV Blocks
a. Three varieties: first, second, and third degree
b. First degree: If the R is far from P, then you have a first degree
i. Delay in conduction between the AV node or His bundle
ii. Wave of electricity spreads normally from the sinus node to the AV node, but it pauses
in the AV node for >0.2 seconds.
iii. Characterized by a PR interval >0.2 seconds
iv. Every atrial impulse activates the ventricles
v. Common in healthy hearts; treatment is not necessary.
c. Second degree
i. Not every atrial impulse makes it through to activate the ventricles.
ii. 2 types: Mobitz type I (Wenckebach) & Mobitz II
1. Wenckebach: Longer, longer, longer drop, then you have a Wenckebach
a. Due to a block within the AV node
b. Block is variable, and PR interval elongates until one impulse does not active the
ventricles
c. After the beat is dropped, the PR interval shortens and the process begins again.
d. Usually fairly benign
e. Pacemakers are not necessary unless symptomatic (pt. is syncopal)
2. Mobitz type II
 My Achy Breaky Heart
Source: The only EKG book you’ll ever need by Malcolm S. Thaler 9th ed 2019
a. Usually a block below the AV node in the His bundle
b. Some atrial impulses are transmitted, but sometimes a P wave is not followed by
a QRS complex.
c. Ratio of dropped beats is rarely constant
d. Often signifies serious heart disease and may progress to a third degree block.
e. Must have a pacemaker inserted.
3. Third degree
a. No atrial impulses make it through to activate the ventricles
b. Atria and ventricles have two different rates; distance between P waves is
consistent, and distance between QRS complexes is consistent, but not consistent
with each other.
c. Ventricles develop an escape rhythm (30-45bpm)
i. Look wide like PVCs/ventricular tachycardia but will have a rate of 30-45
1. VT will always be faster than the patient’s intrinsic rate
2. Escape beats will always be slower than the patient’s intrinsic rate
d. Fun fact: when a patient develops a 3o block, an EKG will show sinus beats (P
waves) with no QRS following for a period of time before an escape rhythm
appears or normal AV conduction resumes.
e. When this happens for 4 seconds, the patient usually nearly/actually faints—
this is called a Stokes-Adams attack.
f. 3o blocks develop because the conduction system of the heart is degenerating.
g. Requires a pacemaker insertion; medical emergency
h. Almost always permanent (lyme disease can cause a reversible 3o block)
i. Lyme disease heart blocks usually cause a narrow QRS complex junctional
escape rhythm; if you see this rhythm, obtain a lyme titer before inserting a
permanent pacemaker!
III. Bundle Branch Blocks
a. Slowing/blockage of the current flow in the right or left bundle branches
b. Right bundle branch block
i. Right ventricular depolarization occurs after the left ventricle is almost fully depolarized
ii. Depolarization delay causes the QRS complex to be >0.12 seconds
iii. Wide QRS complex assumes a unique shape in ventricular leads
1. V1 & V2 leads (on a 12-lead EKG) [right ventricle]
a. nl. wave: small positive R wave, deep negative S wave
b. RBBB: initial R+S wave plus a new second R wave: R’ (R prime)
c. “rabbit ears”
2. I, aVL, V5 & v6 (left ventricle)
a. late RV depolarization causes late deep S waves
c. Left bundle branch block
i. Wide QRS complex assumes a unique shape in the ventricular leads
1. I, aVL, V5, V6
a. Delayed left depolarization causes marked prolongation of tall R waves
i. May be broad on top or notched (not usually “rabbit ears”)
2. V1 & V2 leads
a. Broad, deep S waves
d. Repolarization
 My Achy Breaky Heart
Source: The only EKG book you’ll ever need by Malcolm S. Thaler 9th ed 2019
i. T waves will flip in either V1- V3 or V5 & V6 (based on which BBB)
1. RBBB: right precordial leads show T-wave inversion/ST depression (similar to
repolarization abnormalities seen in ventricular hypertrophy)
2. LBBB: ST depression/T wave inversion in left lateral leads
e. Most common causes of BBB
i. RBBB: common in healthy hearts
ii. LBBB: rarely seen in normal hearts; usually indicates significant cardiac disease
f. BBB can be intermittent and only appear when a patient reaches a “critical rate”—a
particular heart rate where the normal conduction alters into a block.
i. Rate related BBB can be caused by altered physiology; it is directly related to the time it
takes a particular bundle branch to repolarize.
IV. Hemiblock
a. Basics
i. Left bundle branch composed of three fascicles—septa, left anterior, and left posterior.
ii. Right bundle branch does not divide into fascicles; therefore, hemiblocks can only
develop on the left side.
b. Patients can experience a blockage of any of the three fascicles; causes a deviation of the
axis, but does not widen the QRS complex
c. Not going to be something as nurses we address, but just be aware the electricity can act
this way
Preexcitation Syndromes
I. Basics
a. Preexcitation: electrical current from the atria to the ventricles occurs quicker than usual.
i. In preexcitation syndromes, accessory pathways bypass the AV node and arrive at the
ventricles without the AV delay
b. There is an incidence of preexcitation syndromes in about 1% of pts, primarily males
II. Wolff-Parkinson-White (WPW)
a. Bypass pathway can be left or right sided
b. PR interval is shortened (>0.12 seconds)
c. QRS complex is >0.1 seconds and a delta wave is present
i. QRS is widened because of premature ventricular contraction
d. Most of the ventricular myocardium is activated by nl. conduction pathways, but a small
region depolarizes early. (this causes a “slur” in the QRS complex)
e. Accessory pathway travels through the “bundle of Kent”
III. A Short PR Interval without a Delta Wave
a. No single pathway the cells take; may be due to various structural abnormalities or may
simply have an AV node that fires quickly.
IV. Why preexcitation matters
a. WPW usually does not cause many issues but does predispose pts. to tachyarrhythmias.
i. 50-70% of individuals with WPW experience at least one SVT arrhythmia
1. Most common is AV reciprocating tachycardia (AVRT) and Atrial fibrillation
a. A-fib can be devastating; d/t the accessory pathway, the AV node cannot act as
‘gatekeeper’ for all the fibrillation beats
i. Allows the ventricular rate to rise to as much as 300 bpm!
ii. Can then devolve into ventricular fibrillation
Pacemakers
 My Achy Breaky Heart
Source: The only EKG book you’ll ever need by Malcolm S. Thaler 9th ed 2019
I. Indications for pacemakers
a. 3o AV block
b. Symptomatic bradycardia/AV blocks (such as sick sinus syndrome and a-fib)
c. Sudden development of AV blocks + BBB in MI patients (temporary pacers)
d. Recurrent tachycardia
e. Patients that need AV nodal blockers but are unable to take medications without
developing symptomatic bradycardia
II. Equipment
a. Pacemakers are a power source controlled by a microchip and connected to electrodes.
b. Electrodes are placed in the right atrium/ventricle venously
c. Provide an extrinsic source of electricity when the heart’s intrinsic source of electricity
(sinus node) or ability to conduct electrical current is impaired.
III. Types
a. Demand pacer: fires only when the patient’s intrinsic heart rate falls below threshold level.
i. May be single-chamber (electrodes placed in atrium/ventricle only) or dual-chamber
(electrodes in both chambers); dual-chamber also called A-V sequential pacemakers
b. Should see a small spike on the EKG. In a ventricular pacer, the QRS will be wide and
bizarre (similar to a PVC)
c. Left epicardial pacing
i. In patients with impaired LV function, RV electrodes can cause a CHF exacerbation d/t
causing ventricular dyssynchrony (essentially causing a LBBB) and decreasing cardiac
output
ii. To address this risk, a new pacer has type has been developed where in which a third
electrode is threaded into the lateral veins of the left ventricle and allows for left
epicardial pacing. This helps reduce CHF symptoms.
iii. If a patient has reduced LV function and a native LBBB, they may benefit from pacing
electrodes placed in both ventricles (called cardiac resynchronization therapy).
1. Shown to reduce rates of hospitalization and death in patients with class II & III HF.
iv. New pacemakers technology has developed leadless pacemakers.
1. Only can be used for ventricular pacing currently, but working on technology to
develop dual-chamber pacing (as of 2019).