GEMC- Cardiovascular Board Review Session 1- Resident Training

Project: Ghana Emergency Medicine Collaborative
Document Title: Cardiovascular Board Review for www.EMedHome.com
Author(s): Joe Lex, MD (Temple University School of Medicine)
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Cardiovascular
Board Review for
www.EMedHome.com
Joe Lex, MD, FACEP, MAAEM
Professor of Emergency Medicine
Department of Emergency Medicine
Temple University School of Medicine
Philadelphia, PA USA
3

This Review Will Cover…
1. Cardiopulmonary Arrest / SIDS
2. Congenital Abnormalities
3. Disorders of Circulation
Arterial
Venous
4. Disturbances of Rhythm
Ventricular
Supraventricular 4

5. Diseases of the Myocardium
Cardiac Failure
Cardiomyopathy
CHF
Coronary Syndromes
Myocardial Infarction
Myocarditis
Ventricular Aneurysm 5

6. Disease of the Pericardium
Pericardial tamponade
Pericarditis
7. Endocarditis
8. Hypertension
9. Tumors
10.Valvular disorders
6

Today – Part One
1. Cardiopulmonary Arrest / SIDS
2. Congenital Abnormalities
3. Disorders of Circulation
Arterial
Venous
4. Disturbances of Rhythm
Ventricular
Supraventricular 7

Cardiopulmonary Arrest
Abrupt cessation of pump function
in heart
No palpable pulse
Unconscious and not breathing
May be expected outcome to
serious illness
May be possible to reverse
9

Cardiopulmonary Arrest
Shockable
Ventricular tachycardia
Ventricular fibrillation
Non shockable
Asystole
Pulseless electrical activity (PEA)
10

Primary Causes
Coronary heart disease
Present in 60-70%
Autopsy: 30% had recent MI
Cardiomyopathy
Cardiac rhythm disturbances
Hypertensive heart disease
Congestive heart failure
11

When Does It Occur?
Most likely to occur in first few
hours after awakening from sleep
More likely to occur in winter rather
than summer
12

Other Causes: Noncardiac
Trauma
Non-trauma bleeding
Gastrointestinal
Aortic rupture
Intracranial hemorrhage
Overdose
Pulmonary embolism
13

Recognizing Arrest
International Liaison Committee
on Resuscitation (ILCOR)
Diagnose cardiac arrest in all
casualties who are unconscious
and not breathing normally
Carotid artery palpation no longer
gold standard
14

Various Guidelines
Resuscitation Guidelines
BLS: Basic Life Support
ALS: Advanced Cardiac Life
Support
PALS: Pediatric Advanced Life
Support
NRP: Neonatal Resuscitation
Program
15

Cardiopulmonary Resuscitation
Start as soon as possible, interrupt
as little as possible
 benefit  chest compressions
Proper CPR  survival
Tracheal intubation: no  survival
Assisted ventilation may 
outcome
Prehospital intubation  survival
16

Automated External Defibrillator
AED: they’re automated, not
automatic
Diagnoses shockable rhythm
Tells operator to shock
ILCOR recommends universal sign
to identify location
17

ACLS Drugs
Medications included in guidelines
Not shown to  survival to hospital
discharge from out of hospital
cardiac arrest (OHCA)
Includes epinephrine, atropine,
amiodarone
18

ACLS Drugs
Vasopressin: does not improve or
worse outcomes
Possible benefit in those with
asystole especially if used early
Epinephrine: appears to improve
short term outcomes such as return
of spontaneous circulation (ROSC)
19

ACLS Drugs in ET Tube
Lidocaine: rarely used
Epinephrine
Atropine: no longer recommended
for PEA
Naloxone
20

Chain of Survival
21
1. Early recognition and call for help
- To prevent cardiac arrest
2. Early CPR
- To buy time
3. Early Defribilation
- To restart the heart
4. Post resuscitation care
- To restore quality of life

Chain of Survival
Early recognition
Each minute untreated arrest 
survival ~10%
Early CPR
Blood and oxygen to vital organs
Early defibrillation
Only known effective therapy
Early advanced care
22

Survival from Cardiac Arrest
Initial emergency care by
ambulance  ROSC ~15%
Defibrillation in <5 min  ~30%
23

Therapeutic Hypothermia
Cooling after cardiac arrest with
return of spontaneous circulation
(ROSC) but without return of
consciousness improves outcomes
Target temperature of 32–34 °C
(90–93 °F)
Death rates in hypothermia group
 35%
24

3.1.1 Sudden Infant
Death Syndrome
25

SIDS
Sudden Infant Death Syndrome
aka SUDI: sudden unexpected
death in infancy
aka cot death or crib death
Not predicted by medical history
Unexplained after thorough
forensic autopsy and detailed death
scene investigation
26

SIDS
Cause: unknown, many theories
Prenatal associations:
Maternal age: teenage mothers at
greatest risk
Delayed / poor prenatal care
Maternal smoking
27

SIDS
Postnatal associations:
Low birth weight
Exposure to tobacco smoke
Prone sleeping position
No breastfeeding
Room temperature too high or low
Excesses of bedding, clothing, soft
sleep surfaces, stuffed animals
28

Differential Diagnosis
Infant botulism
Long QT syndrome (<2%)
Helicobacter pylori infections
Shaken baby syndrome / other
nonaccidental trauma
Overlying
29

Caring for Survivors
Family-centered / team-oriented
Provide personal, compassionate,
individualized support to families
Respect social, religious, cultural
diversity
Notify primary care physician
Identify / report child maltreatment
30

3.2 Congenital
Abnormalities of the
Cardiovascular System
31

Congenital Heart
Disease (CHD)
32

Noncyanotic Defects
Ventricular septal defect 20 – 25%
Atrial septal defect 5 – 10%
Patent ductus arteriosus 5 – 10%
Coarctation of aorta 8%
Pulmonic Stenosis 5 – 8%
Aortic Stenosis 5%
33

Cyanotic: Terrible T’s
Tetralogy of Fallot 10%
Transposition of Great
Arteries
5%
Tricuspid Atresia 1 – 2%
Total anomalous
pulmonary venous return
1%
Truncus Arteriosus <1%
34

Typical Presentations
Cyanosis
Shock
Heart Failure
35

Present with Cyanosis
Tetralogy of Fallot (to 12 weeks)
Transposition of the great arteries
Tricuspid atresia
TAPVR
Truncus arteriosus
Pulmonary atresia
Hypoplastic right or left heart
All others birth to 2 weeks36

Present with Shock
Coarctation of aorta
Aortic stenosis from 1st week on
37

Present with Heart Failure
Ventricular septal defects
Patent ductus arteriosus from 4
weeks on
38

Some Clues
Central cyanosis with minimal
respiratory distress (“comfortably
blue”): suggests CHD rather than
pure pulmonary problem
39
Cornelia Csuk (Wikipedia)

Some Clues
Worsening cyanosis with crying
suggests cardiac rather than purely
pulmonary etiology
40

Clue: Give 100% Oxygen
Purely pulmonary: PaO2 should rise
to 250 mm Hg
Cyanotic CHD associated with 
blood flow: PaO2 may occasionally
reach as high as 150 mm Hg
Cyanotic CHD associated with 
blood flow: PaO2 will not rise
>100 mm Hg
41

Clue: Chest X-Ray
Boot-shaped heart: tetralogy of
Fallot
Egg-on-a-string silhouette:
transposition of the great vessels
Snowman-shaped or figure-of-eight
heart: total anomalous pulmonary
venous return (TAPVR)
42

Clue: Chest X-Ray
Boot-shaped heart: tetralogy of
Fallot
43
Source Undetermined

Tet Spell: Cyanosis When Crying
44

Tet Spell: Cyanosis When Crying
45Melimama (Wikimedia Commons)

Narrowing of pulmonary valve
46
Source Undetermined

Ventricular septal defect
47
Source Undetermined

Aorta displaced over VSD
48
Source Undetermined

Treatment for Tet
Place in knee-to-chest position
SVR   R to L shunt across VSD
Supplemental O2 (limited value)
Morphine: 0.1–0.2 mg/kg IV or IM
Fentanyl as alternative
Sodium bicarbonate: 1 mEq/kg IV
 ketamine / propranolol /
phenylephrine
49

Clue: Chest X-Ray
Egg-on-a-string silhouette:
transposition of the great vessels
50
Source Undetermined

Clue: Chest X-Ray
Snowman or figure-of-8 heart: total
anomalous pulmonary venous
return (TAPVR)
51
Source Undetermined

Clue: Chest X-Ray
Snowman or figure-of-8 heart: total
anomalous pulmonary venous
return (TAPVR)
52
Source Undetermined

Patent Ductus Ateriosus
More severe / complex lesions may
not be clinically apparent until
ductus arteriosus begins to close
First several weeks of life
Defects with obstructive lesions of
the pulmonary or systemic
circulations will be unmasked
Present with cyanosis, shock, both
53

Patent Ductus Ateriosus
Preserves blood flow from aorta to
the pulmonary circulation
Or
Preserves blood flow from main
pulmonary artery to systemic
circulation
54

Patent Ductus Arteriosus
55
National Institutes of Health (Wikipedia)

CHDs Requiring Patent Ductus
To preserve blood flow from aorta to
the pulmonary circulation:
Tetralogy of Fallot
Tricuspid atresia
Pulmonary atresia
Hypoplastic right heart syndrome
Transposition of the great vessels
56

CHDs Requiring Patent Ductus
To preserve blood flow from main
pulmonary artery to systemic
circulation:
Severe coarctation of aorta
Severe aortic stenosis
Hypoplastic left heart syndrome
57

Patent Ductus Arteriosus
Prostaglandin E2 is responsible for
keeping ductus patent
NSAIDs can help close a PDA
If beneficial to prevent closure,
administer prostaglandin analog:
alprostadil, misoprostol
History: prostglandins first isolated
from seminal fluid of prostate
58

Prostaglandin E1 Therapy
PGE1 infusion: start at 0.05 to 0.1
µg/kg/min
Apnea common: intubate first
Controlled ventilation will also
help  work of breathing
Other adverse reactions: fever,
seizures, bradycardia, hypotension,
flushing,  platelet aggregation
59

3.3.1 Arterial
60Source Undetermined

3.3.1.1 Arterial
Aneurysm
61
Arcadian (Wikimedia Commons)

Aneurysms
Dilation of arterial wall to >1.5 times
its normal diameter
Larger aneurysm  more likely to
rupture
Once stress on vessel wall
exceeds tensile strength, it
ruptures
62

Aneurysms
True aneurysm: involves all three
layers of arterial wall
Atherosclerotic, syphilitic,
congenital, ventricular
False aneurysm / pseudo-
aneurysm: collection of blood
leaking out of artery, but confined
next to vessel by surrounding tissue
63

Abdominal Aortic Aneurysm
64
Source Undetermined

Disease of aging
Occurrence expected to  as
population of elderly grows
Rare before age 50 years
Average age at diagnosis: 65 to 70
Men >> women
Most common and most important
complication  rupture
65

Normal diameter: 2 cm
AAA: 3 cm
<4 cm: rupture uncommon
>5cm: high risk for rupture
When unruptured, symptoms
vague and nonspecific
Symptomatic usually large and
palpable
66

Signs & Symptoms
Abdominal bruit: ~5 – 10%
Most have normal femoral pulses
Rupture often first manifestation
CLASSIC TRIAD: pain, BP,
pulsatile abdominal mass
BP inconsistent, often late finding
Contained retroperitoneal bleed
67

Signs & Symptoms
Syncope (10%)
Flank / back / abdominal pain
Common misdiagnosis: kidney stone
GI bleed from aortoduodenal fistula
Extremity ischemia from thrombus
embolization
Shock
Sudden death
68

Aorto-Enteric Fistula
AAA erodes into GI tract
Usually 3rd or 4th portion duodenum
AKA Aorto-duodenal fistula
Hematemesis, melenemesis, melena,
or (if rapid transport) hematochezia
History aortic graft placement
greatly  clinical suspicion
69

Other Findings
Periumbilical ecchymosis  Cullen
Flank ecchymosis  Grey Turner
70
Source Undetermined Source Undetermined

Diagnosis: Radiograph
May be picked up incidentally on
plain x-ray  eggshell calcification
Not sensitive or specific
71

Diagnosis: Ultrasound
Virtually 100% sensitive
Measurement of aortic diameter
accurate and reproducible
Relatively inexpensive
Requires no contrast agents or
radiation exposure
Performed at bedside
CANNOT determine rupture
72

73
Source Undetermined

74
Source Undetermined

Diagnosis: CT
Virtually 100% accurate
Less subject to technical problems
and interpretation errors
IV contrast desirable, not essential
Better than US at retroperitoneal
bleeds
75

Diagnosis: CT
76
Source Undetermined

Ruptured = Unstable
Large bore IV access x 2
Type & Cross 6 Units PRBC
Volume controversial: permissive
hypotension vs aggressive
resuscitation
Get to operating room as soon as
possible
50% mortality
77

Post-Op Complications
Graft infection: local vs general
Most common: inguinal portion of
aortofemoral graft
Aortoenteric fistula: discussed
above
Pseudoaneurysm
Endoleak: blood flow outside graft
lumen but within aneurysm sac
78

3.3.1.2 Aortic
Dissection
79
Source Undetermined

Definition
Tear of aorta intimal lining with
expanding blood collection 
forces layers apart  false lumen
Death due to  blood supply to
other organs, cardiac failure
Rupture uncommon
Aneurysm dissection RARE
80

Epidemiology
Men > women
Incidence  with age
Hypertension in most patients
History cardiac surgery in ~18%
Bicuspid aortic valve in ~14%
Atherosclerosis rarely involved at
dissection site
May have positive family history
81

Epidemiology
82
CardioNetworks (Wikimedia Commons)

Epidemiology
Uncommon <40 years
Other: stimulant use, exertion,
trauma
High-speed deceleration injury
usually causes traumatic aortic
rupture  different disease
83

Epidemiology
Exception: congenital heart
disease, giant-cell arteritis, Ehlers-
Danlos or Marfan’s syndrome,
>40% Marfan’s  aortic dissection
Women with Marfan’s at risk during
pregnancy
84

Marfan’s Syndrome
Noted in 5–9%
of people with
aortic dissection
85
BQmUB2010144 (Wikimedia Commons)

Classification
Anatomic classification important
for diagnosis and therapy
Stanford classification
Type A  ascending: ~60%
More lethal
Type B  descending: ~40%
Acute if <2 weeks duration
About 2/3 are acute
86

Symptoms
Pain in >90% of patients
Painless  implies chronic
Usually excruciating
Occurs abruptly
Most severe at onset
Typically described as “sharp”
more than “tearing” or “ripping”
87

Symptoms: pain
Anterior chest: think ascending
aorta
Neck and jaw: think aortic arch
Interscapular: think descending
thoracic aorta
Lumbar / abdomen: think below
diaphragm
88

Symptoms
Pain migration consistent with
propagation
Occurs in <20%
Onset often accompanied by
visceral pain symptoms: nausea,
vomiting, diaphoresis, severe
apprehension, lightheadedness
89

Blood Pressure
Variable at presentation
Proximal: ~35% BP, ~25% BP
Distal: ~70% BP, ~5% BP
Severe BP  grave prognosis
Associated with severe aortic
insufficiency, pericardial tamponade,
rupture
90

Blood Pressure
Pseudohypotension: false BP
Involvement of brachiocephalic
artery supplying right arm
Involvement of left subclavian
artery supplying left arm
91

93
brachiocephalic
artery supplies
right arm
Rob Swatski (Flickr)

left subclavian
artery supplies
left arm
94Rob Swatski (Flickr)

Aortic Insufficiency
Occurs in half to two-thirds of
ascending aortic dissections
Aortic insufficiency murmur audible
in one-third of proximal dissections
May be inaudible if BP
95

Myocardial Infarction
1–2% of dissections
Involves coronary arteries
RCA > LCA
Inadvertently treat with lysis 
>70% mortality
97

Diagnosis
Difficult, often missed
D-dimer <500 mcg/mL MAY be
able to rule out (not definitive)
Wide mediastinum on chest x-ray:
moderate sensitivity, low specificity
Up to 20%  normal chest x-ray
Calcium sign suggestive
98

Wide Mediastinum
99
Source Undetermined

Calcium Sign

Computerized Tomography
Noninvasive
Requires peripheral vein injection
of iodinated contrast
Sensitivity 96 – 100%
Specificity 96 – 100%
Poorly identifies site of intimal tear
101

102
Source Undetermined

103
Source Undetermined

MRI
Current gold standard
Sensitivity = 98%, specificity = 98%
Locates intimal tear, secondary
tears, involved branch vessels
Non-invasive test, no iodinated
contrast material
Disadvantage: not always
available, time consuming
104

Transesophageal Echo (TEE)
Sensitivity ~98%, specificity ~97%
Relatively non-invasive: patient
swallows echocardiography probe
Especially good to evaluate aortic
insufficiency, coronary artery
involvement
106

Transesophageal Echo (TEE)
107
Source Undetermined

Aortogram
No longer “gold standard”
108
Source Undetermined

Management
Stanford type A (ascending aortic):
surgical management
Stanford type B (uncomplicated
distal aortic): medical management
109J. Heuser (Wikipedia)

Management
Presenting as hypertensive
emergency  strict blood pressure
control
Target mean arterial pressure
(MAP) of 60 to 75 mmHg
Also:  shear-force dP/dt (force of
blood ejection from left ventricle)
110

Management
1st line treatment: beta-blocker
Rapidly acting, titratable parenteral
agent preferred
Esmolol, propranolol, labetalol
Do NOT use vasodilators alone 
cause reflex tachycardia
May be used as supplement to
control BP
111

Risk of Death
25% in first 24 hours
50% in first 48 hours
75% in first week
90% in first month
112

3.3.1.3 Arterial
Thromboembolism
113
Source Undetermined

Peripheral Arterial Disease
Defined as ankle-brachial index
(ABI) of <0.9
Prevalent in ~15% over age 70
Risk factors: diabetes, tobacco use
Acute occlusion  irreversible
changes in peripheral nerves and
skeletal muscle tissue in 4 – 6 hrs
114

ABI = SBP arm / SBP leg
Normal >0.9; <0.4  critical
Cuff inflated proximal to artery in
question
90% sensitive, 98% specific for
hemodynamically significant leg
artery stenosis (i.e. >50% occlusion
in major leg arteries)
115

“Six Ps": pain, pallor, poikilothermia
(coldness), pulselessness,
paresthesias, and paralysis
Pain earliest symptom, may  with
limb elevation
Mottling, splotchiness, cool
temperature also common
 distal pulse unreliable finding
116

Claudication  cramplike pain,
ache, tiredness brought on by
exercise and relieved by rest
Reproducible, resolves within 2
to 5 minutes of rest
Acute limb ischemia pain not well
localized, not relieved by rest or
gravity
117

Claudication 
cramplike pain,
ache, tiredness
brought on by
exercise and
relieved by rest
118
NHLBI (Wikipedia)

Most common cause acute arterial
occlusion: thromboembolic disease
Differential diagnosis: vasculitis,
Raynaud disease, thromboangiitis
obliterans, blunt or penetrating
trauma, or low-flow shock states
(sepsis)
119

Acute Arterial Occlusion
Stabilize
Fluid resuscitation, pain control
Dependent positioning can 
perfusion pressure
ECG,  echocardiography to
assess for conditions associated
with embolism
120

Give aspirin
Unfractionated heparin: 80 U/kg
bolus, 18 U/kg//hr
Definitive treatment in consultation
with vascular surgeon and
interventional radiologist
Preferred: catheter-directed
embolectomy
121

Reperfusion injury after
revascularization can cause
myoglobinemia, renal failure,
hyperkalemia, and metabolic
acidosis
122
Source Undetermined

Chronic Arterial Occlusion
If no immediate limb threat and no
co-morbidities: discharge on
aspirin (75 milligrams daily)
Close vascular surgical follow-up
123
Source Undetermined

3.3.2.1 Venous
Thromboembolism
Covered in another
section, but…
124

Phlegmasia cerulea dolens
Literally: painful blue edema
Uncommon severe form of DVT
Extensive thrombotic occlusion of
major and collateral extremity veins
Sudden severe pain, swelling,
cyanosis, edema
High risk of massive pulmonary
embolism, even when treated
125

Phlegmasia cerulea dolens

3.4 Disturbances of
Cardiac Rhythm
127

Sinus Rhythm
Rate: 60 – 100 beats / minute
Rhythm: regular with 1:1
relationship of P to QRS
PR interval: 0.12 – 0.20 seconds
QRS complex: 0.06 – 0.10 seconds
P waves upright in Leads I, II, AVF
128

3.4.1 Cardiac
Dysrhythmias
129

Premature Atrial Contraction
Extra beat
Originates outside sinus node from
ectopic atrial pacemaker
Usually interspersed throughout
underlying rhythm
Underlying rhythm is usually sinus
130

Ectopic P wave
Upright in Lead II
Appears earlier than next expected
sinus beat
Has different configuration than
normal P wave
May or may not be conducted
through AV node
131

QRS complex usually normal
May be widened due to aberrant
conduction
QRS generally followed by
noncompensatory pause
SA node reset  returning sinus
beat occurs ahead of schedule
132

133
Source Undetermined

Most frequent cause of EKG pause
Can be normal variant
Can be caused by drugs or
underlying disease
Can precipitate supraventricular
tachycardia, atrial fibrillation, atrial
flutter
134

135
Source Undetermined

Asymptomatic: no treatment
indicated
Frequent or symptomatic: correct
underlying cause
136

Sinus Tachycardia
Rate: >100 beats / minute (usually
<160 beats / minute)
137

Sinus Tachycardia
Newborn: 110 – 150 bpm
2 years: 85 – 125 bpm
4 years: 75 – 115 bpm
6 years+: 60 – 100 bpm
138

Sinus Tachycardia
P-wave hidden in T-wave
139
Source Undetermined

Sinus Tachycardia
“Camel hump” appearance
140
Source Undetermined

Sinus Tachycardia
“Camel hump” appearance
141
Source Undetermined
Arpingstone (Wikimedia Commons)

Sinus Tachycardia
Common causes
Drugs
Fever
Hyperthyroid
Pulmonary
embolism
Hypovolemia
Anemia
Hypoxia
Pain
Anxiety:
diagnosis of
exclusion
142

Sinus Tachycardia
Treatment: fix underlying cause
Acute myocardial infarction: may
be useful to treat “inappropriate”
tachycardia with beta-blocker to
slow heart rate
Cocaine toxicity: may be helpful to
treat with benzodiazepine
143

Sinus Bradycardia
Rate: <60 beats / minute
144

Sinus Bradycardia
145
Source Undetermined

Sinus Bradycardia
Common causes
Acute inferior wall
MI
Vasovagal event
(e.g. vomiting)
 vagal tone (e.g.
athlete)
Vagal stimulation
(e.g. pain)
Hypothermia
Hypothyroidism
Brainstem
herniation
Myocarditis
Sick sinus
syndrome
146

Sinus Bradycardia
Common causes,
pharmacologic
Beta-blocker
Calcium-channel
blocker
Digoxin
Amiodarone
Opiate
Central alpha-2
agonist (clonidine,
dexmedetomidine)
GABA-ergic agent
(barbiturate,
benzodiazepine,
baclofen, GHB)
Organophosphate
poisoning
147

Sinus Bradycardia
Treat if symptomatic
Shock
Hypotension
Short of breath
Chest pain
 mentation
PVCs in acute myocardial infarction148

Sinus Bradycardia
Atropine 0.5-1mg q5 minutes prn
Total: 0.03 – 0.04 mg/kg
Acute myocardial infarction: may
worsen ischemia, precipitate
dysrhythmia
Mobitz II and 3°AV Block with
wide complex: atrial rate AV
block ventricular rate, BP
149

Sinus Bradycardia
Atropine ineffective in patient with
heart transplant
Atropine dose <0.5mg can be
parasympathomimetic
Produce further  in heart rate
150

Sinus Bradycardia
Transcutaneous pacing (TCP)
Treatment of choice if no response
to atropine or severe symptoms
May need analgesic / sedative
Transvenous pacing
Persistent symptomatic
bradycardia
More about pacing in Part 3
151

Sinus Bradycardia
Dopamine 5-20 mcg/kg/min
No response to atropine and / or
TCP not readily available
Epinephrine 2-10 mcg/min
Particularly useful if significant
hypotension
152

Sinus Bradycardia
Isoproterenol 2-10 mcg/min
Only in low doses as last resort
Significant negative effects
 myocardial oxygen consumption
Peripheral vasodilatation
Serious dysrhythmias
153

3.4.1.1 Ventricular
Dysrhythmias
154

Premature Ventricular Contractions
Abnormal QRS complexes and T
waves occurring in another
underlying rhythm
155
Source Undetermined

Six characteristics:
1. Occur earlier than expected
normal QRS (premature)
2. Wider than normal QRS, usually
≥0.12 sec
3. Bizarre QRS morphology
156

4. No preceding P wave: retrograde
conduction occasionally causes
inverted P wave after QRS
5. ST and T deflection opposite that
of QRS: generally followed by
compensatory pause
6. SA node not reset, so next P
wave occurs at usual time
157

Bigeminy: every other beat PVC
Trigeminy: every 3rd beat PVC
Quadrigeminy: every 4th beat
Couplet: 2 consecutive PVCs
Triplet: 3 consecutive PVCs
158

Common Causes
Hypokalemia
Hypomagnesemia
Cardiomyopathy
Hyperthyroidism
Myocardial
Infarction
Hypoxia
CHF
Mechanical:
catheter in RV
Myocardial
contusion
159

Common causes: Drugs
Alcohol / tobacco / caffeine
Cocaine
Digitalis or quinidine toxicity
Most common dysrhythmia seen
with digitalis toxicity
Methylxanthines: theophyline
160

Treatment
No symptoms  no treatment
May be normal variant
Correct underlying cause
Pull back central line
Deflate Swann balloon to avoid
floating in to outflow track
161

Escape PVCs associated with
bradycardia
Treat with atropine: lidocaine may
suppress existing functioning
rhythm
162

Associated with acute MI or ischemia
 treatment controversial
CONSIDER: frequent (> 30/hr),
multiform / multifocal or associated
with runs of ventricular tachycardia
Occur in couplets
R-on-T phenomenon during
ventricular depolarization
163

Associated with acute MI or ischemia
Treat underlying ischemia /
infarction: oxygen, nitroglycerine,
morphine, ASA, fibrinolytic therapy
If these measures fail, most experts
say watchful waiting, but a few
advocate treatment
164

Pharmacologic agent: lidocaine
1 – 1.5mg/kg bolus, then 2 – 4
mg/min drip. May repeat boluses
0.5 – 0.75mg/kg every 5 – 10
minutes as needed to maximum
total 3mg/kg
165

Pharmacologic agent if lidocaine
ineffective: procainamide
15 – 18 mg / kg IV until…
…favorable response noted
…QRS widens 50% >original width
…hypotension develops
…total 17mg / kg administered
166

Pharmacologic agent: magnesium
sulfate
Decreases frequency of PVCs
1 – 2 grams slow IV push over 1 –
2 minutes followed by infusion of 1
– 2 gms/hr
167

Ventricular Tachycardia
168
Source Undetermined

Three or more consecutive PVCs
occurring at a rate >100 / minute
Non-sustained: 3 ventricular beats
for maximum 30 seconds
Sustained: lasts >30 seconds (less
if treated by electrocardioversion
within 30 seconds)
169

Monomorphic VT: all ventricular
beats have same configuration
Polymorphic VT: ventricular beats
have a changing configuration and
heart rate is 100-333 bpm
Biphasic VT: ventricular
tachycardia with a QRS complex
that alternates from beat to beat
170

Monomorphic VTach
171
Source Undetermined

Polymorphic VTach
172
Source Undetermined

Bidirectional VTach
173
Source Undetermined

P waves: usually absent
If present: retrograde or not related to
QRS (AV- dissociation)
QRS complexes: wide (≥ 0.12 sec)
and may be bizarre
174

± Fusion beat: cross between
bizarre QRS and normal QRS
Pathognomonic for ventricular
tachycardia
175
Source Undetermined

± Capture beat: atrial impulse
penetrates AV node from above to
stimulate (“capture”) ventricles
QRS looks normal: ventricular
conduction via normal pathway
Rare
Pathognomonic for ventricular
tachycardia
176

177
Source Undetermined

Deflection of ST segment and T
wave is generally opposite that of
QRS complex
Rate: >100 bpm, usually 150 – 200
Rhythm: generally regular, but
beat-to-beat variation may occur
178

QRS axis: generally constant
Monomorphic: QRS complexes
look the same
Polymorphic: QRS complexes have
varying morphology
Current therapeutic modalities
based on this classifications
179

Wide Complex Tachycardia
180
Source Undetermined

V-Tach vs. Aberrant SVT
1. Ventricular tachycardia vs.
2. SVT with aberrant conduction due
to bundle branch block vs.
3. SVT with aberrant conduction due
to WPW
Assume ventricular tachycardia
Unstable  synchronized
cardioversion
181

PROBABLY V-TACH
Age >35  PPV 85%
Structural heart disease
Ischemic heart disease
Previous MI
Cardiomyopathy
FHx sudden cardiac death 182

MAYBE ABERRANCY
Prior ECG  bundle branch block
with identical morphology
Prior ECG  evidence of WPW
Patient has history of similar
successfully terminated with
adenosine or vagal maneuvers
183

Stable  procainamide or
amiodarone
Both convert SVT or V-Tach
Procainamide contraindicated with
cyclic anti-depressant overdose
Adenosine may initially slow either
rhythm, but it may recur
184

Stable  procainamide or
amiodarone
Drug therapy fails synchronized
cardioversion
185

EKG suggests V-Tach
Absence typical RBBB / LBBB
morphology
Extreme axis deviation: QRS
positive in aVR, negative in I + aVF
Very broad complexes: >160ms
AV dissociation: P and QRS
complexes at different rates
186

EKG suggests V-Tach
Fusion beats: sinus and ventricular
beat coincide to produce hybrid
complex
Capture beats: sinoatrial node
transiently ‘captures’ ventricles in
midst of AV dissociation to produce
a QRS complex of normal duration
187

± Fusion beat: cross between
bizarre QRS and normal QRS
Pathognomonic for VT
188
Source Undetermined

Pathognomonic for VT
189
Source Undetermined

EKG suggests V-Tach
Positive or negative concordance
throughout chest leads
Leads V1-6 show entirely positive
(R) or entirely negative (QS)
complexes, with no RS complexes
seen
190

EKG suggests V-Tach
RSR’ complexes with taller left
rabbit ear
Most specific finding in favor of VT
In RBBB, right rabbit ear is taller
193

Verapamil accelerates heart rate,
drops blood pressure and does not
convert rhythm
Adenosine can convert
catecholamine-induced VT to sinus
(very rare)
CANNOT use adenosine to
distinguish VT from SVT
aberrancy 194

Torsades de Pointes
AKA Polymorphic ventricular
tachycardia (PVT)
195
Source Undetermined

Torsades de Pointes
“Twisting of the points”
QRS complexes “twist” around the
isoelectric line
Must be evidence of both PVT
and QT prolongation
Rate: usually 200-240
196

Torsades de Pointes
Causes: drugs
Class IV antidysrhythmics:
quinidine, procainamide
Class I-C: propafenone, flecainide
Tricyclic antidepresssants
Droperidol / haloperidol
Phenothiazines
197

Torsades de Pointes
Drug combinations: e.g.
terfenadine + ketoconazole or
erythromycin
Other causes: hypomagnesemia,
hypokalemia
198
Source Undetermined

Torsades de Pointes
During short runs, “twisting” may
not be apparent
Bigeminy in patient with known
prolonged QT may herald imminent
TdP
TdP with heart rate >220 beats /
minute more likely to degenerate
into ventricular fibrillation
199

Ventricular Flutter
200
Source Undetermined

Ventricular Flutter
Extreme ventricular tachycardia
Loss of organized electrical activity
Rapid, profound hemodynamic
compromise
Usually short lived due to
progression to ventricular fibrillation
Treat as ventricular fibrillation
201

Ventricular Flutter
Continuous sine wave
No identifiable P waves, QRS
complexes, or T waves
Rate usually > 200 beats / min
ECG looks identical when viewed
upside down!
202

Ventricular Fibrillation
204
Source Undetermined

Most common: fine or coarse
zigzag pattern without discernible P
waves, QRS complexes or T waves
Sometimes looks like ventricular
tachycardia
Patient without pulse, unresponsive:
treatment same
205

Most important shockable
cardiac arrest rhythm
Ventricles attempt to contract at
rates of up to 500 / minute
Ventricles unable to contract in
synchronised manner  immediate
loss of cardiac output
206

Heart no longer effective pump
Invariably fatal without ACLS
Prolonged ventricular fibrillation:
coarse VF  fine VF  asystole
Due to progressive depletion of
myocardial energy stores
207

Treatment: DEFIBRILLATE
IMMEDIATELY
3 successive “stacked” shocks,
checking only the monitor between
shocks
Start with 200J
If persistent, defibrillate again with
200-300J and then 360J
208

If defibrillation unsuccessful, start
ACLS
Look for reversible causes (H’s &
T’s)
209

Reversible Causes
5 H’s
Hypovolemia
(most common)
Hypoxemia
Hydrogen ions
(acidosis)
Hyperkalemia /
Hypokalemia
Hypothermia
5 T’s
Tablets (drugs)
Tamponade
(cardiac)
Tension
pneumothorax
Thrombosis,
coronary
Thrombosis,
pulmonary
210

Persists despite treatment of
reversible cause  give anti-
fibrillatory drug
Amiodarone or procainamide
Lidocaine as last resort
Continue shocks every 30 – 60
seconds while meds being drawn
Defibrillate with 360J after each drug
dose
211

Pulseless Electrical Activity
212
Source Undetermined

Electrical activity other than V-Tach
or V-Fib without pulse
Electromechanical dissociation
(EMD)
Idioventricular rhythms
Ventricular escape rhythms
Bradyasystolic rhythms
THIS IS CARDIAC ARREST
213

Often occur in association with 5
H’s and 5 T’s
214

Causes: same as ventricular
fibrillation and pulseless ventricular
tachycardia
Treatment: ACLS
CPR, intubation, start an IV
Search for and treat underlying cause
215

Hypoxia: ventilate 100% oxygen
Hypovolemia: administer fluid bolus
Hypothermia: check core body
temperature, warm prn
Hydrogen ions: bicarbonate for
suspected severe acidosis
Hyperkalemia: seek EKG changes
216

Epinephrine 1 mg every 3–5 min
Atropine NO LONGER
RECOMMENDED (2010 ACLS)
Sodium bicarbonate not
recommended EXCEPT preexisting
metabolic acidosis, hyperkalemia,
tricyclic antidepressant overdose
217

Tablets: history, toxidrome
Tamponade: distended neck veins,
EMBU
Tension pneumothorax: breath
sounds, ease of manual ventilation
Thrombosis, heart: assess EKG
Thrombosis, lungs: EMBU for right
heart strain
218

Asystole / Flatline
CPR
Epinephrine
5 H’s and 5 T’s
Atropine and defibrillation NO
LONG RECOMMENDED
219
Source Undetermined

Supraventricular Tachycardia
Any tachydysrhythmia arising from
above the level of Bundle of His
Often used synonymously with AV
nodal re-entry tachycardia (AVNRT)
Paroxysmal SVT (pSVT): abrupt
onset / offset, characteristically
seen with re-entrant tachycardias
involving AV node such as AVNRT
221

Atrial rate: 120-200 beats / minute
Rhythm: regular
P waves: abnormal, may be hidden
in preceding T wave
If P waves visible: 1:1 P to QRS ratio
QRS: usually narrow, may be wide
due to aberrant conduction
Extra beats: none
222

Can be classified based on site of
origin (SA or AV node) or regularity
(regular or irregular)
Classification based on QRS width
not helpful
Influenced by pre-existing bundle
branch block, rate-related aberrant
conduction, accessory pathways
223

224
Source Undetermined

225
Source Undetermined

Treatment
Vagal maneuvers: may respond
Adenosine: mainstay of treatment
Calcium-channel blocker, beta-
blocker, amiodarone: 2nd line
MAY be effective: procainamide,
amiodarone, sotalol
227

Treatment
Vagal maneuvers: may respond
228

NO LONGER RECOMMENDED
Vasopressors: norepinephrine,
methoxamine, phenylephrine
Cholinergic drugs: edrophonium
DC synchronized cardioversion:
rarely required
Catheter ablation: for recurrent
episodes not amenable to medicine
229

Multifocal Atrial Tachycardia
Form of supraventricular
tachycardia
Irregular rhythm sometimes
mistaken for atrial fibrillation
Originates from many different
atrial sites
Characterized by P waves of
varying shape
230

P waves: 3 morphologies in 1 lead
Atrial rate: 100 – 180 beats/minute
Rhythm: irregularly irregular
PP, PR, and RR intervals vary
QRS complex: normal configuration
Nonconducted (blocked) P waves
frequently present, particularly
when the atrial rate is rapid
231

232
Source Undetermined

Causes
Most common: decompensated
COPD
Sepsis
Theophylline toxicity
Right atrial dilatation (cor
pulmonale)
Hypoxia / hypercarbia
234

Treatment
Correct underlying disease process
Unsuccessful, patient symptomatic:
Calcium channel blocker: slows
ventricular rate,  atrial ectopy
Magnesium:  atrial ectopy
Metoprolol: slows ventricular rate
Digoxin / cardioversion usually
ineffective 235

AV Node + His Bundle =
AV Junction
236
Madhero88 (Wikipedia)

Junctional Premature Contractions
Far less common than PACs/PVCs
From ectopic focus in AV node or
bundle of His ABOVE bifurcation
P wave: different shape / deflection
Usually inverted in II, III, and AVF
Can occur before, during or after
QRS complex
237

When P wave precedes QRS: PR
interval is shorter than normal
QRS complex premature
QRS complex normal shape
Unless aberrant conduction
Usually compensatory pause: SA
node NOT reset so next P wave
occurs at its usual time
238

239
Source Undetermined
Source Undetermined

Causes: digitalis toxicity, coronary
artery disease, congestive heart
failure, acute myocardial infarction
(especially inferior wall)
Treat underlying cause
If precipitate lethal dysrhythmias:
intravenous procainamide
240

Junctional Escape
Sinus intrinsic rate: ~75 beats /
minute
Junctional intrinsic rate: 40 – 60
beats/minute
If sinus too slow, junctional may
take over as “back-up” rhythm
Hence “junctional escape”
241

Junctional Escape
242
Source Undetermined

Junctional Tachycardia
Ectopic pacemaker in AV junction
overtakes sinus node
Rate >100 beats / minute 
junctional tachycardia
243
Source Undetermined

Accelerated Junctional Rhythm
Ectopic AV junction pacemaker too
fast for junctional escape, but too
slow for junctional tachycardia
244
Source Undetermined

Atrial Fibrillation
Uncoordinated atrial activation and
random ventricular depolarization
Rhythm: irregularly irregular
Most common sustained
dysrhythmia;
2% of the general population
5% of people > 60 years old
P waves absent  no PR interval
245

Atrial Fibrillation
Atria discharge electrical impulses
to ventricles
No single impulse depolarizes atria
completely
Atria don’t pump
Occasional impulse gets through to
AV node
246

Atrial Fibrillation
May see small irregular deflections
in the baseline (“f waves”)
Atrial rate: 400 – 700 beats/minute
QRS complexes: normal, unless
aberrant conduction
Ventricular response rate: variable,
generally 160 – 180 beats/minute
247

Atrial Fibrillation
248
Source Undetermined

Atrial Fibrillation

Atrial Fibrillation
If rate >200 beats/minute + wide
QRS complex: think Wolf-
Parkinson-White syndrome with
antegrade conduction through
accessory pathway
If regular, slow ventricular rate:
think digitalis toxicity
No extra beats
250

Atrial Fibrillation: Causes
Ischemic heart
disease
Hypertension
Valvular heart
disease (esp. mitral)
Acute infection
Electrolyte
disturbance
(hypokalemia,
hypomagnesemia)
Thyrotoxicosis
Drugs (e.g.
sympathomimetics)
Pulmonary embolus
Pericardial disease
Acid-base
disturbance
Pre-excitation
syndromes
Cardiomyopathies:
dilated, hypertrophic
Pheochromocytoma251

Atrial Fibrillation: Type
1st detected episode vs. recurrent
Paroxysmal (<7 days): terminated
spontaneously
Persistent (>7 days): sustained or
terminated therapeutically
Permanent (>1 year):
cardioversion failed or not
attempted
252

Atrial Fibrillation: Treatment
Treatment depends on:
Cardiovascular stability
Duration of dysrhythmia
Underlying cause / condition
Presence / absence of accessory
pathway
253

1. Treat underlying condition
2. Determine risk for stroke
High risk for cardiogenic
thromboembolism: cardiac
surgery, AMI, hyperthyroidism,
myocarditis, acute pulmonary
disease
254

Other risks for stroke:
Cardiac: congestive heart failure,
coronary artery disease, elevated
systolic blood pressure
Non-Cardiac: prior stroke or TIA,
hypertension, advanced age,
diabetes
255

Control rhythm: restore and
maintain sinus rhythm
Control rate: allow atrial fibrillation
to continue, control ventricular rate
256

Unstable: immediate synchronized
cardioversion
Sedate if possible
Start with 100J
Last resort if digitalis toxic: start with
10J
Heparinize if >48 hrs or hypertrophic
cardiomyopathy
257

Stable, onset <48hrs: pharmacologic
Control ventricular rate first
Goal <100 beats/minute
Calcium channel blocker: diltiazem
Beta blocker: esmolol, metoprolol
If EF < 40%
Digoxin, diltiazem, amiodarone: will
not further depress cardiac function
258

Stable, onset <48hrs: pharmacologic
Patient takes digoxin: add MgSO4
(2.5gm IV x 20mins, then 2.5gm
infused over 2 hrs)
May slow heart rate even more and /
or convert to sinus rhythm
WPW: amiodarone
Avoid beta blocker, calcium channel
blocker
259

Stable: onset / duration > 48hrs
(higher risk systemic embolization)
No immediate cardioversion if
possible
Cardioversion anticipated in 24 hrs
Consider heparin
Consider cardiology consult for TEE
to exclude atrial clot
260

Atrial Flutter
Rapid atrial rhythm: 250-300/min
Slower ventricular response 2o to
nodal delay
Always occurs with AV block
Not all impulses conducted
Variable conduction 2:1, 3:1, 4:1, etc.
P waves: sawtooth pattern
Called “F” or flutter waves
261

Atrial Flutter
Best seen: inferior leads, V1, V2
PR interval (when present) always
normal
Not every P wave followed by QRS
complex
QRS complexes  normal
configuration
262

Atrial Flutter
Ventricular rate: most common
~150 beats / minute
Depends on degree of block
May be variable
Suspect atrial flutter with 2:1 block
in patients with regular ventricular
rate of 130 – 150 beats / minute
263

Atrial Flutter
Causes: similar to atrial fibrillation
Often associated with post-cardiac
surgery and peri-infarction periods
Usually transitional rhythm between
sinus rhythm and atrial fibrillation
Treatment determined by stability,
duration, accessory pathway
264

Atrial Flutter – 3:1 block
265
Source Undetermined

Atrial Flutter
Treatment: unstable
Sedate (if possible)
Synchronized cardioversion: start
with 50J
Treatment: stable
Vagal maneuvers and adenosine
may be useful to slow rate for
diagnostic confirmation
266

Atrial Flutter
Rate control first
Diltiazem (first choice), verapamil,
esmolol, metoprolol
Digoxin no longer first line
Magnesium may be useful adjuvant
267

Atrial Flutter
Rhythm control second
Procainamide
Synchronized cardioversion
Accessory pathway present
Avoid calcium channel blocker,
beta blocker, digoxin, adenosine
Synchronized cardioversion
Procainamide if stable
268

Pre-Excitation Syndromes
Pre-excitation: early activation of
ventricles due to impulses
bypassing AV node via accessory
pathway
AV node would normally slow this
down
271

WPW: accessory pathway referred
to as Bundle of Kent, or
atrioventricular bypass tract
Accessory pathway can conduct
impulses
anterograde (towards ventricle)
retrograde (away from ventricle)
in both directions
272

Majority of pathways allow
conduction in both directions
Retrograde-only: ~15% of cases
Anterograde-only: very rare
273

Orthodromic (left) Conduction
274
Orthodromic Circular
Tachycardia in a patient with
an accessory pathway
Tom Lück (Wikipedia)

Orthodromic (left) Conduction
275
Tom Lück (Wikipedia)
Source Undetermined

Antedromic (right) Conduction
276
Drj (Ecgpedia)

Antedromic (right) Conduction
277
Drj (Ecgpedia)

WPW in Sinus Rhythm
PR: <120ms
Delta wave: slurring slow rise of
initial portion of QRS
QRS: prolonged >110ms
ST segment and T wave discordant
changes – i.e. in the opposite
direction to the major component of
the QRS complex
278

Pseudo-infarction pattern in up to
70% of patients
Due to negatively deflected delta
waves in inferior / anterior leads
(“pseudo-Q waves”), or as a
prominent R wave in V1-3
(mimicking posterior infarction).
279

Suspect accessory pathway if
ventricular rate > 200/min
Synchronized cardioversion may
be 1st line, regardless of stability
Procainamide prolongs refractory
period of accessory pathway
May be therapy of choice in
hemodynamically stable patient
280

CONTRAINDICATED: calcium
channel blockers, beta blockers,
digoxin, adenosine
All block AV nodal conduction
All can  conduction down
accessory pathway, producing  in
ventricular response  ventricular
fibrillation
281

Lown-Ganong-Levine Syndrome
Accessory pathway (James fibers)
connects atria directly to proximal
His bundle, completely bypassing
AV node
Very short PR interval
Narrow QRS complexes
No evidence of delta waves
282

283
Source Undetermined

3.4.2 Conduction
Disorders
284

Bundle Branch Blocks
Conduction abnormality, not rhythm
disturbance
Ventricles depolarize in sequence
rather than simultaneously
Produces wide QRS complex
285

Bundle Branch Blocks
Incomplete BBB  QRS ranges
from 0.09 – 0.11 seconds
Complete BBB  QRS ≥0.012 sec
ST segment has slope opposite
that of terminal half of QRS
complex
286

Right BBB
288
Source Undetermined
Source Undetermined

Right BBB
Unifasciular
Right ventricle activation delayed
Left ventricle activated normally 
early part of QRS complex
unchanged
Depolarization spreads across
septum from left ventricle
289

Right BBB
Delayed right ventricular activation
produces secondary R wave (R’) in
right precordial leads (V1-3) and
wide, slurred S wave in lateral leads
V-6V-1
290

Right BBB
Also causes 2o repolarization
abnormalities: right precordial leads
show ST depression and T wave
inversion
Isolated RBBB: cardiac axis
unchanged
Left ventricular activation proceeds
normally via left bundle branch
291

Right BBB Criteria
Long QRS >120 ms
RSR’ pattern in V1-3
Wide, slurred S wave in lateral
leads (I, aVL, V5-6)
ST depression, T wave inversion in
right precordial leads (V1-3)
292

Right BBB Criteria
ST depression, T wave inversion in
right precordial leads (V1-3)
293
Source Undetermined

Left BBB
Septum is usually activated left 
right, producing small Q waves in
lateral leads
LBBB: septal depolarization
reversed (right  left)
Impulse spreads first to RV
through right bundle branch and
then to LV through septum
295

Left BBB
This sequence extends QRS
duration to >120 ms
Eliminates normal septal Q waves
in lateral leads
Depolarization direction produces
tall R waves in lateral leads (I, V5-
6) and deep S waves in right
precordial leads (V1-3)
296

Left BBB
Depolarization from right to left
produces tall R waves in lateral
leads (I, V5-6) and deep S waves in
right precordial leads (V1-3) usually
leads to left axis deviation
V6
V1
297

Left BBB Criteria
QRS 120 ms
Dominant S wave in V1
Broad monophasic R wave in
lateral leads (I, aVL, V5-V6)
No Q waves in lateral leads (I, V5-
V6; small Q waves allowed in aVL)
Prolonged R wave peak time >60
ms in left precordial leads (V5-6)
298

Left BBB
R waves in lateral leads may be:
‘M’ shaped or notched
299
Source Undetermined

Left BBB
R waves in lateral leads may be:
Monophasic rather than biphasic
300
Source Undetermined

Incomplete Left BBB
Typical LBBB morphology with
QRS duration <120ms
301
Source Undetermined

Atrioventricular Block
Impaired conduction between atria
and ventricles
Normal: SA node sets pace 
impulses travel to ventricles
AV block: message does not reach
ventricles or impaired along way
303

1st Degree AV Block
PR interval >200ms (five small
squares)
“Marked” 1o block: PR > 300ms

1st Degree AV Block
May be normal variant
 vagal tone
Athletic training
Inferior MI
Mitral valve surgery
Myocarditis (e.g. Lyme disease)
Hypokalaemia
305

1st Degree AV Block
AV nodal-blocking drugs: beta-
blockers, calcium channel blockers,
digoxin, amiodarone
306
Source Undetermined

1st Degree AV Block
Does not cause hemodynamic
disturbance
No specific treatment required
307

2nd Degree, Mobitz I
AKA Wenckebach
Progressive prolongation of PR
interval culminating in non-
conducted P wave
PR interval is longest immediately
before dropped beat
PR interval is shortest immediately
after dropped beat
308

P-P interval relatively constant
Greatest increase in P-R interval
typically between 1st and 2nd beats
of cycle
309
Source Undetermined

R-R interval progressively shortens
with each beat of cycle
Wenckebach pattern tends to
repeat in P:QRS groups with ratios
of 3:2, 4:3 or 5:4
310
Source Undetermined

Usually reversible conduction block
at level of AV node
Malfunctioning AV node cells tend
to progressively fatigue until they
fail to conduct impulse
His-Purkinje cells tend to fail
suddenly and unexpectedly (i.e.
producing Mobitz II block)
311

Drugs: beta & calcium channel
blockers, digoxin, amiodarone
 vagal tone (e.g. athletes)
Inferior wall MI
Myocarditis
After cardiac surgery: mitral valve
repair, Tetralogy of Fallot repair
312

Usually benign rhythm
Minimal hemodynamic disturbance
Low risk of progression to 3o block
Asymptomatic: no treatment
Symptomatic: atropine usually
works
Permanent pacing: rarely required
313

2nd Degree, Mobitz II
314
Source Undetermined
Source Undetermined

Mobitz II: Description
Intermittent non-conducted P
waves without progressive
prolongation of PR interval
PR interval in conducted beats
remains constant
P waves at constant rate
315

Mobitz II: Description
RR interval surrounding dropped
beat(s): exact multiple of preceding
RR interval
2x preceding RR interval for
single dropped beat
3x preceding RR interval for two
dropped beats
316

Mobitz II: Mechanism
Usually due to conduction failure at
His-Purkinje system (i.e. below AV
node)
317
Madhero88 (Wikipedia)

More likely then Mobitz I to be due
to structural damage to conducting
system
Typically have pre-existing LBBB or
bifascicular block
Produced by intermittent failure of
remaining fascicle
“bilateral bundle-branch block”
318

In ~75%: conduction block distal to
Bundle of His  broad QRS
complexes
319
Source Undetermined

In ~25%: conduction block within
His Bundle itself  narrow QRS
complexes
320
Source Undetermined

Recall Mobitz I  AV node fatigue
Mobitz II is “all or nothing”
His-Purkinje cells suddenly fail to
conduct supraventricular impulse
May be fixed relationship between
P waves and QRS complexes…
…but may be no pattern to
conduction blockade
321

Mobitz II: Causes 1
Anterior MI: septal infarct with
necrosis of bundle branches
Idiopathic fibrosis of conducting
system
Cardiac surgery close to septum,
like mitral valve repair
Inflammatory conditions: rheumatic
fever, myocarditis, Lyme disease
322

Mobitz II: Causes 2
Autoimmune: lupus, systemic
sclerosis
Infiltrative myocardial disease:
amyloidosis, hemochromatosis,
sarcoidosis
Hyperkalemia
Drugs: beta- & calcium channel
blockers, digoxin, amiodarone
323

Mobitz II: Significance
Much more likely than Mobitz I to
be associated with hemodynamic
compromise, severe bradycardia,
progression to 3rd degree block
Hemodynamic instability can be
sudden and unexpected 
syncope (Stokes-Adams attacks) or
sudden cardiac death
324

Mobitz II: Significance
Risk of asystole: ~35% per year
Mandates admission for cardiac
monitoring, backup temporary
pacing, ultimately insertion of
permanent pacemaker
325
Source Undetermined

3rd Degree / Complete Block
326
Source Undetermined
Source Undetermined

No atrial impulses conducted
Atria and ventricles beat
independently of one another
327
Source Undetermined

328
Source Undetermined

329
Source Undetermined

P waves: normal
PR interval: variable  P waves
not related to QRS complexes
PP interval: regular
RR interval: regular
Perfusing rhythm maintained
by junctional or ventricular escape
rhythm
330

Block can occur at level of AV
node, bundle of His or bundle
branches
QRS complexes: narrow or wide
depending on location of block
Above His bundle  narrow
At or below His bundle  wide
331

End point of either Mobitz I or II
Progressive fatigue of AV nodal
cells 2o to increased vagal tone in
acute phase of inferior MI
Sudden complete conduction
failure throughout His-Purkinje
system 2o to septal infarction in
acute anterior MI
332

High risk of ventricular standstill
and sudden cardiac death
Urgent admission for cardiac
monitoring, backup temporary
pacing, and (usually) insertion of
permanent pacemaker
333

Sinus Node Dysfunction
AKA “sick sinus syndrome”
Abnormality of cardiac impulse
formation AND intra-atrial and AV
nodal conduction
Wide variety / combinations of
bradyarrhythmias and
tachyarrhythmias
Most common in elderly
336

Presenting symptoms may include:
Dizziness
Palpitations
Dyspnea
Fatigue
Lethargy
Syncope
337

Causes: intrinsic
Idiopathic degenerative fibrosis
Ischemia
Cardiomyopathies
Infiltrative diseases: sarcoidosis,
haemochromatosis
Congenital abnormalities
338

Causes: extrinsic
Drugs: digoxin, beta- & calcium
channel blockers
Autonomic dysfunction
Hypothyroidism
Electrolyte abnormalities:
hyperkalemia
339

Diagnosis: documentation of
bradyarrhythmia or tachyarrhythmia
in associated with these symptoms
340
Source Undetermined
Source Undetermined

Treatment: stable
Refer to cardiologist for demand
pacemaker and antidysrhythmic therapy
Treatment: unstable
Bradydysrhythmia  rate stimulation
Atropine, isoproternol, pacemaker
Tachydysrhythma  rate control
Digoxin, beta- or calcium channel blocker
341

GEMC- Cardiovascular Board Review Session 1- Resident Training

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