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Project: Ghana Emergency Medicine Collaborative
Document Title: Cardiovascular Board Review for www.EMedHome.com
Part 2
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
Page 4
Part Two 5. Diseases of the Myocardium
Cardiac Failure
Cardiomyopathy
CHF
Coronary Syndromes
Myocardial Infarction
Myocarditis
Ventricular Aneurysm 4
Page 5
3.5 Acquired
Diseases of the
Myocardium
5 Patrick J. Lynch (Wikimedia Commons)
Page 6
3.5.1.1 Cor
Pulmonale
6
Mariana Ruiz (Wikipedia)
Page 7
Cor Pulmonale
Cor = heart
Pulmonale = of the lungs
In other words, pulmonary heart
disease
Also known as “right heart failure”
7
Page 8
Cor Pulmonale
Chronic: right ventricle
hypertrophy
Adaptive response to long-
term in pressure
Acute: right ventricle dilatation
Stretching of ventricle in
response to acute in
pressure 8
Page 9
Acute Cor Pulmonale
Massive pulmonary embolization
Exacerbation of chronic cor
pulmonale
9
Page 10
Chronic: Many Causes 1
COPD
Primary pulmonary hypertension
Asthma
Recurrent pulmonary embolism
Loss of lung tissue following
trauma or surgery
End stage pneumoconiosis
10
Page 11
Chronic: Many Causes 2
Sarcoidosis
T1-4 vertebral subluxation
Obstructive sleep apnea
Altitude sickness
Sickle cell anemia
Bronchopulmonary dysplasia (in
infants)
11
Page 12
Signs & Symptoms 1
Shortness of breath on exertion
At rest when severe
Wheezing
Chronic wet cough
Ascites
Pedal edema
Prominent neck and facial veins
12
Page 13
Signs & Symptoms 2
Hepatomegaly
Abnormal heart sounds
Bi-phasic atrial response on EKG
due to hypertrophy
13
Page 14
Chest X-Ray
Right ventricular hypertrophy
Right atrial dilatation
Prominent pulmonary artery
Peripheral lung fields: vascular
markings
Changes of COPD
14
Page 15
Chest X-Ray Right
ventricular
hypertrophy
Right atrial
dilatation
Prominent
pulmonary
artery
Peripheral
lung fields:
vascular
markings
(COPD) 15
Source Undetermined
Page 16
ECG RVH
Right axis deviation
Prominent R wave in lead V1
Inverted T waves in right precordial
leads
Large S in I, II and III
Large Q in lead III
Tall peaked P waves (P pulmonale)
in II, III and aVF 16
Page 17
ECG P pulmonale
Peaked P waves in inferior leads >2.5
mm (P pulmonale)
Absent R waves in right precordial
leads (SV1-SV2-SV3 pattern) 17
Source Undetermined Source Undetermined
Page 18
What We Need to Know 1
Sildenafil = Revatio® = Viagra®
PDE5 inhibitor
Relaxes arterial wall
pulmonary arterial resistance and
pressure workload of
right ventricle symptoms
Beware of using nitrates
refractory hypotension
18
Page 19
What We Need to Know 2
Epoprostenol = PGI2 = Flolan®
Delivered by pump: very short T½
Sudden cessation rebound
pulmonary hypertension
Dyspnea, dizziness, etc.
Potent platelet inhibitor major
bleed risk
19
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3.5.1.2 High Output
Cardiac Failure
20
Page 21
High Output Failure
Term is misnomer
Many conditions: heart is normal,
can generate cardiac output
Underlying problem: in systemic
vascular resistance threatens
arterial blood pressure activation
of neurohormones salt and
water retention by kidney
21
Page 22
High Output: Causes 1
Chronic severe anemia
Large AV fistula
22 Source Undetermined
Page 23
High Output: Causes 2
Multiple small arteriovenous shunts
e.g. Paget's disease of bone
Some severe hepatic or renal
disorders
Hyperthyroidism
Beriberi
23
Page 24
High Output: Causes 3
Acutely in septic shock, especially
Gram-negative bacteria
24 Source Undetermined
Page 25
High Output Failure
Many high output states are
curable conditions
Untreated leads to systolic failure
Since associated with peripheral
vascular resistance, use of
vasodilator therapy may aggravate
the problem
25
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3.5.1.3 Low Output
Cardiac Failure
26
Page 27
Low Output Cardiac Failure
cardiac output but normal
demand for blood
Manifestations of impaired
peripheral circulation and
vasoconstriction
Most forms of heart disease
Covered in Section 3.5.3:
Congestive Heart Failure
27
Page 28
3.5.2
Cardiomyopathy
28
Page 29
Cardiomyopathy
Literally “heart muscle disease”
Measurable deterioration of myocardial function
Usually leads to heart failure
Most common form: dilated
Common symptoms: dyspnea and peripheral edema
At risk for dysrhythmias, sudden cardiac death
29
Page 30
Extrinsic Causes
Primary pathology: outside
myocardium itself
Most cardiomyopathies are
extrinsic
Most common cause: ischemia
30
Page 31
Intrinsic Causes
Not due to identifiable external
cause
Causes can be found for most
31
Page 32
Signs & Symptoms
Can mimic virtually any form of
heart disease
Chest pain: common
Severe cases associated with heart
failure, arrhythmias, and systemic
embolization
32
Page 33
Dilated Cardiomyopathy
Ventricular dilatation and global
myocardial dysfunction (<40%)
Usually present with biventricular
failure, e.g. fatigue, dyspnea,
orthopnea, ankle edema
2-year survival = 50%
Progressive cardiogenic
shock or sudden cardiac
death 33
Page 34
Dilated Cardiomyopathy
Ischemic: following massive
anterior MI due to extensive
myocardial necrosis and loss of
contractility
Non-ischemic: most are idiopathic
ECG usually abnormal, but no
features unique to DCM
34
Page 35
Non-Ischemic Cardiomyopathy
HOCM
Restrictive
Dilated
Myocarditis
Tako-Tsubo
35
Source Undetermined
Page 36
Restrictive Cardiomyopathy
Least common
Occurs in advanced stages of
myocardial infiltrative disease
Hemochromatosis,
amyloidosis, sarcoidosis, etc.
Diffuse myocardial infiltration leads
to low voltage QRS complexes
No specific ECG findings 36
Page 37
Peripartum Cardiomyopathy
Symptoms and signs of heart
failure that present initially during
last 3 months of pregnancy or first 5
months postpartum
Clinically identical to dilated CM
Complain of chest pain, palpitations
May be in CHF: rales, dyspnea,
cardiomegaly, +S3
37
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Peripartum Cardiomyopathy
ECG left ventricular hypertrophy
NSST-T wave changes
Echocardiography: all 4 chambers
enlarged, left ventricular systolic
function
preload & afterload, contractility
If pregnant: hydralazine, labetalol
Mortality ~2% 38
Page 39
3.5.2.1 Hypertrophic
Cardiomyopathy
39
Page 40
Hypertrophic Cardiomyopathy
Leading cause of sudden cardiac
death in young athletes
Frequently asymptomatic until
sudden cardiac death
Prevalence 0.2 – 0.5% of general
population
40
Page 41
Mechanism
Asymmetric septal hypertrophy
(~2/3)
Aortic stenosis & HTN have
symmetric hypertrophy
Dynamic outflow obstruction
At rest ~25%
Can be provoked in ~70%
If obstruction HOCM 41
Page 42
Symptoms
Dyspnea most common
Chest pain
Palpitations
Lightheadedness
Fatigue
Syncope
Sudden cardiac death
42
Page 43
Findings: Murmur 1
Murmur similar to aortic stenosis
Classically, murmur is loudest at
left parasternal edge, 4th intercostal
space, rather than aortic area
43
Page 44
Findings: Murmur 2
HCM murmur in intensity with
any maneuver that volume of
blood in left ventricle
Stand abruptly
Valsalva
Amyl nitrite murmur by
venous return to heart
44
Page 45
ECG Findings
LVH precordial voltages, non-
specific ST / T-wave abnormalities
45 Source Undetermined
Page 46
ECG Findings
Asymmetric hypertrophy
“dagger Q-waves” infero-lateral
46
Source Undetermined
Page 47
Management
Beta-blockers & calcium channel
blockers: slow heart rate, improve
diastolic function
Amiodarone: reduces ventricular
dysrhythmias
47
Page 48
3.5.3 Congestive
Heart Failure
48
Page 49
Types of Failure
Systolic dysfunction: failure of
ventricular contractility
AHA / ACC: left ventricular
ejection fraction <40%
Diastolic dysfunction: failure of
diastolic ventricular relaxation
high filling pressures
1/3 – ½: some renal insufficiency
49
Page 50
Left-Sided Heart Failure
Left ventricle does not pump
enough blood backs up into
lungs, causing pulmonary edema
LV heart failure eventually causes
right-sided heart failure
50
Page 51
Left-Sided Heart Failure
rate of breathing tachypnea
work of breathing
Rales or crackles: initially in lung
bases fluid in alveoli (pulmonary
edema
Cyanosis: late, severe
51
Page 52
Left-Sided Heart Failure
Laterally displaced apex beat
Gallop rhythm: from blood flow
or intra-cardiac pressure
Murmur can be cause (e.g. aortic
stenosis) or result (e.g. mitral
regurgitation) of heart failure
52
Page 53
Extra Heart Sound
Occurs soon after the normal two
“lub-dub” heart sounds (S1 and S2)
Associated with heart failure
Occurs at beginning of diastole,
~0.12 to 0.18 seconds after S2
Mnemonic ken-TUC-ky, with “ky”
representing S3
53
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Right-Sided Heart Failure
54
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Right-Sided Heart Failure
Right ventricle does not pump
enough blood backs up into
body systemic edema
Nocturia common: leg fluid returns
to circulation when flat
If severe: ascites, hepatomegaly
Possible jaundice, coagulopathy
55
Page 56
Peripheral Edema & Anasarca
56 Source Undetermined Source Undetermined
Page 57
Right-Sided Heart Failure
Jugular venous pressure: marker of
fluid status
Can be accentuated by eliciting
hepatojugular reflux
If right ventricular pressure
parasternal heave
Signifies compensatory in
contraction strength
57
Page 58
Jugular Venous Distention
58 Source Undetermined
Page 59
Biventricular Failure
Left + right + pleural effusions
Dull to percussion + breath
sounds at bases
Pleural veins drain both into both
systemic and pulmonary venous
system
If unilateral: usually right sided
59
Page 60
Radiographic Findings
60
The radiological signs of heart failure:
• Fluid in lung fissures
• Kerley B lines
• Prominent upper lobe pulmonary arteries
• Fluid in the lung interstitium
• Large heart
• Pleural effusion
Page 61
Radiographic Findings
Cardiomegaly
large heart
61
Source Undetermined
Page 62
Radiographic Findings
Cephalization =
upper lobe
blood diversion
Occurs when
PAWP 12-18
mmHg
62 Source Undetermined
Page 63
Radiographic Findings
Kerley B lines:
short parallel
lines at lung
periphery
Interlobular
septa: usually
<1 cm
PAWP 18–25
MMHg 63
Source Undetermined
Page 64
Radiographic Findings
Bat wing =
central
interstitial
edema
PAWP >25
mmHg
64
Source Undetermined
Page 65
B-Natriuretic Peptide
From distended ventricles
>500 pg/mL: highly associated with
heart failure (LR = 8.1)
100-500 pg/mL: indeterminate (LR
= 1.8)
<100 pg/mL: highly unlikely (LR =
0.13)
65
Page 66
Acute Management 1
Immediate therapeutic goals
Improve respiratory gas exchange
Maintain adequate arterial
saturation
left ventricular diastolic pressure
Maintain adequate cardiac and
systemic perfusion
66
Page 67
Acute Management 2
Noninvasive positive pressure
ventilation (NIPPV)
Continuous (CPAP) or inspiratory /
expiratory (BiPAP)
Recruit collapsed alveoli
functional residual capacity
improve oxygenation
work of breathing 67
Page 68
Acute Management 3
Result: left ventricular preload
and afterload by intrathoracic
pressure
More rapid restoration of normal
vital signs and oxygenation
Fewer intubations
68
Page 69
Management: Nitroglycerin 1
Lower doses: venodilation
preload
Higher doses: arteriolar dilation
blood pressure
afterload
69
Page 70
Management: Nitroglycerin 2
Sublingual 400 mcg x 3
Total 1200 mcg in 10 minutes
Good bioavailability
Start IV 50 – 80 mcg/min
Can go to 200 – 300 mcg / min for
BP control
70
Page 71
Management: Loop Diuretic
Furosemide standard
In volume overload: plasma
volume, preload, pulmonary
congestion
Diuresis unnecessary in low
plasma volumes
71
Page 72
Management: Morphine
Controversial: central sympatholytic
that releases vasoactive histamine
causes peripheral vasodilation
72 Vaprotan (Wikimedia Commons)
Page 73
Management: ACE Inhibitor
Controversial: good afterload
Enalaprilat IV (0.625 – 1.25 mg)
Captopril sublingual (12.5 – 25 mg)
No good, large studies
Some sources say “theoretically
harmful”
73
Page 74
3.5.4 Coronary
Syndromes
74
Page 75
Acute Coronary Syndromes
Continuum or progression of
coronary artery disease from
myocardial ischemia to necrosis
Stable angina unstable angina
acute myocardial infarction
75
Page 76
Classic Presentations
76 J. Heuser (Wikipedia) J. Heuser (Wikipedia)
Page 77
3.5.5 Ischemic
Heart Disease
77
Page 78
Classic Presentations
Stable Angina
Transient, episodic chest
discomfort that is predictable and
reproducible
Familiar symptoms occur from a
characteristic stimulus
Improve with rest or sublingual
nitroglycerin within few minutes
78
Page 79
Classic Presentations
Unstable Angina
New onset
Occurs at rest or with frequency
Severely limiting
Lasts longer than a few minutes
Resistant to meds that previously
relieved the symptoms
79
Page 80
Classic Presentations
Acute Myocardial Infarction
Retrosternal chest discomfort
lasting > 15 minutes
Dyspnea, diaphoresis, light-
headedness, palpitations, nausea
and/or vomiting
Radiation to arms, shoulders, neck
probability of ischemia
80
Page 81
Atypical Presentations
More common in elderly
History of angina often absent
Epigastric discomfort / indigestion
or nausea and vomiting
Shortness of breath
Syncope or confusion
Fatigue, dizziness, or generalized
weakness 81
Page 82
Atypical Presentations
So-called “Silent MI” vague
~12.5% of all MIs
Worse prognosis than “classic”
Suspect in elderly, diabetics, those
with spinal cord injuries or disease,
alcoholics
82
Page 83
Risk Factors, Major
Cigarette smoking
Hypertension
Diabetes Mellitus
Hypercholesterol
Hypercoagulability
Family history of
CAD at < 55 in first
degree relative
Prior history of
CAD
PVD
Carotid
arteriosclerosis
83
Page 84
Risk Factors, Other
Male sex
Advanced age
Methamphetamine use
Cocaine use
Obesity
Inactive Lifestyle
Post-menopause
84
Page 85
Factors Predicting AMI
History ischemic heart disease
Chest pain / discomfort worse than
usual angina
Pain
similar to a prior AMI
lasts longer than an hour
radiates to jaw / neck / shoulder / arm
85
Page 86
Diagnosis
Normal initial EKG / troponin does
NOT rule out MI
History: most important tool
Suspect history: admit “ROMI”
Typically ≤ 25%of ROMI have
discharge diagnosis of “Acute MI”
Improvement after nitroglycerin /
antacid dose NOT rule in / out
86
Page 87
EKG
Most important adjunctive
diagnostic test
Initial EKG diagnostic in only ~25-
50%
Normal / non-diagnostic initial
EKG does not rule out ACS
87
Page 88
NSTEACS
Non-ST-elevation acute coronary
syndrome (NSTEACS)
Non-ST-elevation myocardial
infarction (NSTEMI)
Unstable angina (UA)
Differentiation may be retrospective
based on cardiac biomarkers
88
Page 89
NSTEACS
Non-ST-elevation acute coronary
syndrome (NSTEACS)
Main ECG abnormalities
ST segment depression
T wave flattening or inversion
89
Page 90
Causes of ST Depression
Myocardial
ischemia /
NSTEMI
Reciprocal
change in STEMI
Posterior MI
Digoxin effect
Supraventricular
tachycardia
Hypokalemia
RBBB
Right ventricular
hypertrophy
LBBB
Left ventricular
hypertrophy
Ventricular paced
rhythm 90
Page 91
Causes of T Wave Inversion
Normal in children
Persistent
juvenile T wave
pattern
Myocardial
ischemia /
infarction
Bundle branch
block
Ventricular
hypertrophy
(‘strain’ patterns)
Pulmonary
embolism
Hypertrophic
cardiomyopathy
intracranial
pressure
91
Page 92
Ischemic T Wave Inversions
Ischemia: contiguous leads based on
anatomical location of area of
ischemia / infarction:
Inferior = II, III, aVF
Lateral = I, aVL, V5-6
Anterior = V2-6
92
Page 93
Ischemic T Wave Inversions
Dynamic inversions with acute
myocardial ischemia
93
Source Undetermined
Source Undetermined
Page 94
Ischemic T Wave Inversions
Fixed inversions follow infarction, usually in association with pathological Q waves
94
Source Undetermined
Source Undetermined
Page 95
Biphasic T Waves
Two main causes:
Hypokalemia
Myocardial ischemia
Waves go in opposite directions:
Hypokalemic: go then
Ischemic: go then
95
Page 96
Biphasic T Waves
Due to hypokalemia: then
96
Source Undetermined
Page 97
Biphasic T Waves
Due to ischemia: then
97
Source Undetermined
Page 98
Biphasic T Waves: Wellens’
Inverted / biphasic T waves in V2-3
Patient presents with ischemic
chest pain
Highly specific for critical stenosis
of left anterior descending artery
98
Page 99
Biphasic T Waves: Wellens’
Type 1 Wellens’ T-waves: deeply
and symmetrically inverted
99
Source Undetermined
Page 100
Biphasic T Waves: Wellens’
Type 2 Wellens’ T-waves: biphasic,
with initial deflection positive and
the terminal deflection negative
100 Source Undetermined
Page 101
Flattened T Waves
Non-specific
Dynamic or in contiguous leads:
think ischemia
Generalized: think electrolyte
abnormality, like hypokalemia
101 Source Undetermined
Page 102
Inverted U Wave
Infrequently recognized but specific
sign of myocardial ischemia
102 Source Undetermined
Page 103
TIMI Risk Score 1
Thrombolysis In Myocardial Infarction
Assesses risk of death and
ischemic events in patients with
unstable angina or a non-ST
elevation myocardial infarction
103
Page 104
TIMI Risk Score 1
1. Age >= 65
2. ASA use in last 7 days
3. 2 angina episodes in last 24hrs
4. ST changes 0.5mm on admit EKG
5. serum cardiac biomarkers
6. Known CAD: stenosis 50%
7. 3 risk factors for CAD: cigarette
smoking, hypertension, HDL < 40,
diabetes, family history 104
Page 105
TIMI Risk Score
14 day risk: all-cause mortality, new or recurrent MI, or ischemia requiring urgent revascularization
0 or 1 = 4.7% risk
2 = 8.3% risk
3 = 13.2% risk
4 = 19.9% risk
5 = 26.2% risk
6 or 7 = 40.9% risk 105
Page 106
NSTEACS
50% of UA patients will show
evidence of myocardial necrosis
based on cardiac serum markers
such as troponin T or I and creatine
kinase isoenzyme (CK)-MB
Diagnosis of non-ST elevation
myocardial infarction
106
Page 107
NSTEACS: Treatment
Oxygen: evidence unclear
Nitroglycerin: vasodilate coronary
arteries, blood flow to heart
Antiplatelet agent: aspirin /
clopidogrel to reduce progression of
clot formation
Anticoagulant: heparin,
unfractionated or LMWH
107
Page 108
3.5.6 Myocardial
Infarction
108
Page 109
EKG for STEMI
amplitude R and T waves
(“giant” R / “hyperacute” T)
1st change to occur in evolving MI
Transient finding: may resolve by
presentation
109
Source Undetermined
Page 110
EKG for STEMI
amplitude R “giant” R waves
110 Source Undetermined
Page 111
EKG for STEMI
ST usually earliest recorded sign
± reciprocal changes
Initial up-sloping portion of ST
segment usually convex or flat
(horizontally or obliquely)
Q waves: represent myocardial
necrosis but not severity of infarct
Inverted T waves 111
Page 112
Other Causes of ST 1
Early repolarization
Acute pericarditis: all except aVR
Pulmonary embolism: V1 and aVR
Hypothermia: V3-V6, II, III and aVF
Hypertrophic cardiomyopathy: V3-5
Hyperkalemia: V1-V2 (V3)
112
Page 113
Other Causes of ST 2
Acute neurologic events: all leads,
primarily V1-V6
Acute sympathetic stress: all leads,
especially V1-V6
Brugada syndrome
Ventricular aneurysm
Cardiac contusion
113
Page 114
Other Causes of ST 3
Left ventricular hypertrophy
Idioventricular rhythm including
paced rhythm
114 Source Undetermined
Page 115
Early Repolarization 1
ST segment elevation without
underlying disease
Probably has nothing to do with
actual early repolarization
Commonly seen in young men
115
Page 116
Early Repolarization 2
Characteristics
Upward concave elevation of RS-T
segment with distinct or
“embryonic” J waves
Slurred downstroke of R waves or
distinct J points or both
RS-T segment elevation in
precordial leads
116
Page 117
Early Repolarization 3
Characteristics
Rapid QRS transition in precordial
leads with counterclockwise rotation
Persistence of these characteristics
for many years
Absent reciprocal ST depression
Large symmetrical T waves
117
Page 118
Early Repolarization 4
Generalized concave ST elevation in
precordial (V2-6) and limb leads (I, II,
III, aVF) 118
Source Undetermined
Page 119
Early Repolarization 5
J-point notching evident in inferior
leads (II, III and aVF)
119
Source Undetermined
Page 120
Early Repolarization 6
J-point notching evident in inferior
leads (II, III and aVF)
120
Source Undetermined
Page 121
Early Repolarization 7
Prominent, slightly asymmetrical T
waves that are concordant with main
vector of QRS complexes 121
Source Undetermined
Page 122
Early Repolarization 8
Descending limb of T wave is straighter
and slightly steeper than ascending
limb 122
Source Undetermined
Page 123
Early Repolarization 9
Descending limb of T wave is straighter
and slightly steeper than ascending
limb 123
Source Undetermined
Page 124
Specific
Infarcts
124
Page 125
125
Effects of Myocardial Ischemia,
Injury, and Infarction on the ECG
Page 126
126
Patrick J. Lynch (Wikipedia)
Page 127
Left Main Occlusion
Widespread horizontal ST
depression, most prominent in
leads I, II and V4-6
ST elevation in aVR ≥ 1mm
ST elevation in aVR ≥ V1
127
Page 128
Left Main Occlusion
Widespread ST depression, most
prominent in lateral leads (V4-6, I, aVL)
ST elevation > 1mm in aVR 128
Source Undetermined
Page 129
Left Main Occlusion
Widespread ST depression, most
prominent in lateral leads (V4-6, I, aVL)
ST elevation > 1mm in aVR 129
Source Undetermined
Page 130
Left Main Occlusion
Widespread ST depression, most
prominent in lateral leads (V4-6, I, aVL)
ST elevation > 1mm in aVR 130
Source Undetermined
Page 131
Left Main Occlusion
Widespread ST depression, most
prominent in lateral leads (V4-6, I, aVL)
ST elevation > 1mm in aVR 131
Source Undetermined
Page 132
132
Patrick J. Lynch (Wikipedia)
Page 133
Anterior STEMI
Occlusion of left anterior
descending artery (LAD)
Worst prognosis infarct size
ST segment with Q wave
formation in precordial leads (V1-6)
± high lateral leads (I and aVL)
Reciprocal ST in inferior leads
(mainly III and aVF)
133
Page 134
Anterior STEMI: Hyperacute
134
Source Undetermined
Source Undetermined
Page 135
Anterior STEMI: Acute
135
Source Undetermined
Source Undetermined
Page 136
Anterior STEMI: Acute
Q waves in V1-2
Reduced R wave height (Q-wave
equivalent) in V3-4
136
Source Undetermined
Page 137
Anterior STEMI: Tombstone
137 Source Undetermined
Page 138
Anterior STEMI: Tombstone
Proximal LAD large infarction with
poor LV ejection fraction
High likelihood of cardiogenic shock
and death 138
Source Undetermined
Page 139
STEMI: High Lateral
Occluded 1st diagonal branch (D1)
of LAD isolated ST in I, aVL
Occlusion of circumflex artery
ST in I, aVL, V5-6
139
Page 140
140
Patrick J. Lynch (Wikipedia)
Page 141
STEMI: High Lateral
ST elevation primarily localized to
leads I and aVL
Associated with reciprocal ST
depression and T wave inversion in
inferior leads
141
Page 142
STEMI: High Lateral
Occluded 1st diagonal branch (D1)
of LAD isolated ST in I, aVL
142
Source Undetermined
Page 143
STEMI: Lateral
Supplied by branches of LAD and
left circumflex (LCx) arteries
Usually as part of larger territory
infarction, e.g. anterolateral STEMI
Lateral extension of anterior,
inferior or posterior MI indicates
large territory of myocardium at risk
worse prognosis
143
Page 144
STEMI: Lateral
Isolated lateral STEMIs uncommon
Lateral STEMI as a stand-alone MI
is indication for emergent
reperfusion
144
Page 145
STEMI: Inferior 1
~80% dominant RCA
~18% dominant LCx
Rare: “type III” or wraparound LAD
concomitant inferior and anterior
ST elevation
145
Page 146
STEMI: Inferior 2
40-50% of all MIs
In general, more favorable
prognosis than AMI
~40% have concomitant right
ventricular infarction
Severe hypotension in
response to nitrates
Worse prognosis 146
Page 147
STEMI: Inferior 3
~20% develop significant
bradycardia due to 2o or 3o AV
block
in-hospital mortality (>20%)
May be associated with posterior
infarction
Worse prognosis due to area
of myocardium at risk
147
Page 148
STEMI: Inferior 4
ST in leads II, III and aVF
Progressive development of Q
waves in II, III and aVF
Reciprocal ST in aVL (± lead I)
148
Page 149
STEMI: Inferior 5
149
Source Undetermined
Page 150
150
Patrick J. Lynch (Wikipedia)
Page 151
STEMI: Inferior from RCA
ST in lead III > lead II
Reciprocal ST in lead I
Signs of right ventricular infarction
STE in V1 and V4R
151
Page 152
STEMI: Inferior from RCA
ST in lead III > lead II
Reciprocal ST and T wave
inversion in aVL
152
Source Undetermined
Page 153
STEMI: Inferior from RCA
ST in lead III > lead II
Reciprocal ST and T wave
inversion in aVL
153 Source Undetermined
Page 154
154
Patrick J. Lynch (Wikipedia)
Page 155
STEMI: Inferior from LCx
ST in lead II = lead II
Reciprocal ST and T wave
inversion in I or aVL
Q wave in III, aVF
155 Source Undetermined
Page 156
Right Ventricular Infarct
Isolated RV infarct rare
Complicates ~40% of inferior
STEMIs
Poor RV contractility preload
sensitive
Nitrates severe hypotension
Treat with fluid loading
156
Page 157
Right Ventricular Infarct
ST in V1
Only standard ECG lead that
looks directly at the right ventricle
ST in lead III > lead II
Lead III more “rightward
facing” than lead II
Must do right-sided leads
157
Page 158
Right Ventricular Infarct
158
V1R V2R
V3R
V4R V5R
V6R
Arcadian (Wikimedia Commons)
Page 159
Right Ventricular Infarct
ST in V1
ST in lead III > lead II
159 Source Undetermined
Page 160
Right Ventricular Infarct
Right-sided leads
ST in lead III > lead II
ST throughout right-sided leads
V3R-V6R
160 Source Undetermined
Page 161
Posterior Infarct
Accompanies 15-20% of STEMIs,
usually inferior or lateral
Isolated posterior MI (3-11%)
Lack of obvious ST means
diagnosis often missed
Isolated posterior infarct is
indication for emergent
coronary reperfusion
161
Page 162
Posterior Infarct
Suggested by changes in V1-3
Leads look at internal surface of
posterior myocardium
Horizontal ST depression
Tall, broad R waves (>30ms)
Upright T waves
Dominant R wave (R/S ratio > 1) in
V2 162
Page 163
Posterior Infarct
ST becomes ST
Q waves become R waves
Terminal T-wave inversion
becomes an upright T wave
163 Source Undetermined
Page 164
Posterior Infarct
Same EKG flipped upside down
Now looks like typical STEMI
Also with posterior leads
164 Source Undetermined
Page 165
Posterior Infarct
Same EKG flipped upside down
Now looks like typical STEMI
Also with posterior leads
165
Source Undetermined
Page 166
Posterior Infarct: Leads
166
Scapula
V7 V8 V9
Source Undetermined
Page 167
Posterior Infarct
Posterior extension of inferior or
lateral infarct implies much larger
area of myocardial damage
risk of left ventricular dysfunction
and death
167
Page 168
Posterior Infarct
Tall, broad R waves (>30ms)
Upright T waves
Dominant R wave (R/S ratio>1) in
V2
168
Source Undetermined Source Undetermined
Page 169
Posterior
Tall, broad
R waves
(>30ms)
Upright T
waves
Dominant R
wave (R/S
ratio>1) V2
169 Source Undetermined
Page 170
Posterior Infarct
Same patient, posterior leads V7 –
V9
170
Source Undetermined
Page 171
Posterior Infarct
171
Source Undetermined Source Undetermined
Page 172
Q-Waves: Normal
Depolarization of interventricular
septum (“septal Qs”)
Lateral leads I, aVL, V5 and V6
172
Page 173
Q-Waves: Pathologic
Electrical signal passes through
stunned or scarred myocardium
Deflection amplitude of 25% or
more of subsequent R wave
>0.04 s (40 ms) wide, >2 mm
amplitude
173
Page 174
Q-Waves: Pathologic
Deflection amplitude of 25% or
more of subsequent R wave
>0.04 s (40 ms) wide, >2 mm
amplitude
174 Source Undetermined
Page 175
Initial EKG Useful for…
… screening
… risk stratification
… establishing criteria that
determine which therapeutic
interventions will be employed
175
Page 176
Serial EKGs
Nondiagnostic EKG but concern for
possible ongoing ischemia
Capture ischemic changes
Demonstrate stability
Detect silent ischemia
ST segment trend-monitoring
MAY improve detection
176
Page 177
Serum Biomarkers
177
Source Undetermined
Page 178
Serum Biomarkers
Proteins that leak from injured
myocardial cells through damaged
cell membranes into bloodstream
Troponin T / I
CK-MB
Obsolete: serum glutamic
oxaloacetic transaminase (SGOT)
/ lactate dehydrogenase (LDH)
178
Page 179
Serum Biomarkers: Troponin
179
Ayacop (Wikimedia Commons)
Page 180
Serum Biomarkers: Troponin
Marker for all heart damage, not
just AMI
Tachycardia, CHF, myocarditis,
pericarditis, defibrillation, contusion
in ~40% of patients with critical
illnesses such as sepsis
Severe GI bleed: mismatch
between myocardial oxygen
demand and supply 180
Page 181
Serum Biomarkers: Troponin
Type I MI: coronary artery
occlusion
Type II MI: low flow state leading
to troponin leakage
DIFFERENT PATHOLOGIES
DIFFERENT TREATMENTS
NOT ALWAYS OBVIOUS
181
Page 182
Serum Biomarkers: Troponin
Marker Rise
(hrs)
Peak
(hrs)
Remains
Elevated
Troponin T 6 12 – 18 10 – 14 days
Troponin I 6 12 – 18 7 – 10 days
CK-MB 4 – 10 20 <2 days
Myoglobin 2 – 3 4 – 24 <1 day
182
Page 183
Serum Biomarkers: Others
CK-MB: serum levels of two
variants of enzyme phospho-
creatine kinase
Isoenzymes CKM and CKB
Myoglobin: primary oxygen-
carrying pigment of muscle tissues
Very nonspecific for cardiac
damage 183
Page 184
Serum Biomarkers: Others
Marker Rise
(hrs)
Peak
(hrs)
Remains
Elevated
Troponin T 6 12 – 18 10 – 14 days
Troponin I 6 12 – 18 7 – 10 days
CK-MB 4 – 10 20 <2 days
Myoglobin 2 – 3 4 – 24 <1 day
184
Page 185
Use of Serum Markers
Admit / discharge decisions based
primarily on history and clinical
presentation
Marker detection requires sufficient
myocardial cell damage AND
enough time for markers to be
released into serum
185
Page 186
Use of Serum Markers
Initial markers have low sensitivity
for detecting ischemia, cannot be
used to reliably diagnose or exclude
ACS
No single determination of one
serum biomarker reliably identifies
or excludes AMI within <6 hrs of
symptom onset
186
Page 187
Use of Serum Markers
This is a moving target
High sensitivity troponins MAY
change everything (or may not)
Should we call them “Low
Specificity Troponins” instead?
Hot topic over next few years, but
will not be tested
187
Page 188
Diagnosing MI: WHO – 2000
Myocardial cell death
Markers of myocardial cell death
recovered from blood samples
Evidence of myocardial ischemia (ST-
T segment changes)
Loss of electrically functioning cardiac
tissue (Q waves)
Reduction / loss of tissue perfusion
Cardiac wall motion abnormalities
Pathology
Biochemistry
EKG
Imaging
188
Page 189
Two-Dimensional Echo
Detects regional wall motion
abnormalities that occur with AMI
Abnormality starts on 1st beat
Cannot distinguish ischemia, acute
infarction and old infarction
Operator-dependent
Not readily available
189
Page 190
Coronary Artery CT
Very controversial
A work in progress
Zealots on both sides
Something MAY emerge in next
few years
190
Page 191
Radionuclide Scanning
191
Page 192
Technetium (99mTc) sestamibi
Tracer taken up by myocardium in
proportion to blood flow
Bound to six methoxy-isobutyl-
isonitrile (MIBI) ligands
Detects perfusion defects and
hypokinesia
192
Page 193
Technetium (99mTc) sestamibi
Active chest pain + nondiagnostic
EKG 100% sensitive / 83-92%
specific
Pain-free patient: 65% sensitive
193
Page 194
Thallium 201 scintigraphy
194
Source Undetermined
Page 195
Thallium 201 scintigraphy
Reversibly taken up by normally
perfused cells
Areas of uptake indicate regions
of severe ischemia or infarction
≤6hrs of infarct 100% sensitive,
80% specific for AMI
Cannot distinguish new from old
195
Page 196
Stress Testing
Recommended by American
College of Cardiology and
American Heart Association
Treadmill test: sensitivity 73-90%,
specificity 50-74% (Modified Bruce
Protocol)
Nuclear test: sensitivity 81%,
specificity 85-95%
196
Page 197
Chest Pain Evaluation Unit
Safe, effective alternative to routine
admission for low-intermediate risk
patients with chest pain
Protocols vary but usually involve
serial studies (EKGs, markers) and
selective stress testing for
evaluation of risk stratification
197
Page 199
Treatment
IV (NS)
cardiac monitor
pulse
oximeter
Oxygen
Antiplatelet
agents
Anticoagulant
therapy
Nitroglycerin
Morphine
Beta-blocker
Reperfusion
therapy
ACE-I 199
Page 200
Treatment
IV (NS)
cardiac
monitor
pulse oximeter
Oxygen
Antiplatelet
agents
Anticoagulant
therapy
Nitroglycerin
Morphine
Beta-blocker
Reperfusion
therapy
ACE-I 200
Page 201
IV / Monitor / Pulse oximetry
201
Page 202
Treatment
IV (NS)
cardiac monitor
pulse
oximeter
Oxygen
Antiplatelet
agents
Anticoagulant
therapy
Nitroglycerin
Morphine
Beta-blocker
Reperfusion
therapy
ACE-I 202
Page 203
Oxygen
Low flow (2-4L) by nasal cannula
High flow associated with
mortality and infarct size
203
Page 204
Treatment
IV (NS)
cardiac monitor
pulse
oximeter
Oxygen
Antiplatelet
agents
Anticoagulant
therapy
Nitroglycerin
Morphine
Beta-blocker
Reperfusion
therapy
ACE-I 204
Page 205
Antiplatelet Agents: Aspirin
Irreversibly acetylates platelet
cyclo-oxygenase,
Rapid onset: within 60 minutes
205
Page 206
Antiplatelet Agents: Aspirin
325mg on arrival unless
contraindicated
Chew to maximize bioavailability
mortality, infarct size, and rate of
reinfarction
Maximal benefit if given within 4
hours of chest pain onset
NNT to save one life = 40 206
Page 207
Antiplatelet Agents: ADP
Clopidogrel / prasugrel / ticagrelor
platelet aggregation by inhibiting
ADP platelet activation
Second-line therapy for patients
who cannot take ASA
Less effective than ASA due to
delayed onset
207
Page 208
Antiplatelet Agents: ADP
Clopidogrel
Onset 2 – 3 hours
Can speed up by forced doses
Safety profile: similar to ASA
risk of CV events in patients with
UA or NSTEMI AND early
noninvasive approach is planned
208
Page 209
Clopidogrel & CABG
Clopidogrel treatment 7 days
before CABG: major bleeding
Prasugrel: even more bleeding
Ticagrelor: less bleeding
Urgent CABG likely within 7 days:
argument for omitting
thienopyridines during initial
management of ACS
209
Page 210
Clopidogrel & CABG
Clopidogrel / prasugrel / ticagrelor
are all ADP receptor antagonists
A stands for “adenosine”
What happens when we give our
patients adenosine for SVT?
210
Page 211
Clopidogrel & CABG
ST 1 mm in aVR: strong
predictor severe LMCA / 3VD
requiring CABG
Discuss with interventionalist /
thoracic surgeon use of clopidogrel
ST <1mm in aVR: negligible risk
severe LMCA / 3VD requiring
CABG
Thienopyridine can be safely given 211
Page 212
Antiplatelet Agents: G2B3A
Abciximab / eptifibatide / tirofiban
Glycoprotein (GP) IIb/IIIa receptor
antagonists
Block final common pathway for
platelet aggregation
Indications: prior to PCI
Discuss with interventional
cardiologist 212
Page 213
Treatment
IV (NS)
cardiac monitor
pulse
oximeter
Oxygen
Antiplatelet
agents
Anticoagulant
therapy
Nitroglycerin
Morphine
Beta-blocker
Reperfusion
therapy
ACE-I 213
Page 214
Anticoagulant Therapy
Unfractionated heparin
Low molecular weight heparin
Direct thrombin inhibitors
214
Page 215
Anticoagulant Therapy
Unfractionated heparin and
enoxaparin result in similar
outcomes at one year post MI
215
Melissa Wiese (Wikimedia Commons)
Page 216
Heparin
Heparin + ASA more effective than
either alone
Indicated in high risk patients with
ACS (AMI/UA)
incidence of DVT, reinfarction,
nonhemorrhagic CVA, and
formation / embolization of LV
thrombus in AMI
216
Page 217
Unfractionated Heparin
May be useful in unstable angina
by rate of subsequent transmural
infarction
Preferred by cardiologists taking
patients to cath lab because can be
turned off
217
Page 218
Unfractionated Heparin
No reperfusion: bolus 50 – 70
U/kg to maximum of 5000 U, then
IV drip 12 U/kg per hour
Fibrinolysis: bolus 60 – 100 U/kg to
maximum of 4000 U, then IV drip
12 U/kg per hour
PCI: bolus 50 – 70 U/kg to
maximum of 5000 U
218
Page 219
Low Molecular Weight Heparin
Acceptable in patients <75 years
without significant renal dysfunction
recurrent angina, AMI, need for
urgent revascularization, mortality
rate
Preferred agent in absence of renal
failure or planned CABG within 24
hours
219
Page 220
Low Molecular Weight Heparin
bleeding than unfractionated
heparin with equivalent or better
antithrombotic effects
Simple administration and dosing
Limited blood monitoring
More predictable anticoagulation
effect
220
Page 221
Low Molecular Weight Heparin
No reperfusion: no load,
1 mg/kg every 12 hours
Fibrinolysis: loading dose 30 mg IV
bolus, then 1 mg/kg subcutaneously
every 12 hours
PCI: unfractionated preferred
221
Page 222
Nitroglycerin (NTG) 1
Dilates collateral coronary vessels
collateral blood flow to ischemic
myocardium
Has antiplatelet effects
222
Page 223
Nitroglycerin (NTG) 2
infarct size and mortality
myocardial oxygen demand
preload
LV end-diastolic volume
afterload
May myocardial susceptibility to
ventricular dysrhythmias during
ischemia and reperfusion 223
Page 224
Nitroglycerin (NTG) 3
pain and consequently
catecholamine release
224
Page 225
Nitroglycerin (NTG) 4
For chest pain if systolic BP
>90mm Hg
Start with sublingual 0.4mg (400
mcg) q3 – 5 minutes prn pain
1200 mcg in 6 – 10 minutes
Excellent bioavailability (>80%)
Ointment / paste: pretty useless
225
Page 226
Nitroglycerin (NTG) 5
Intravenous: books say start @ 10
– 20 mcg/min and increase by 5 –
10 mcg/min until pain controlled or
SBP by 10%
In real life, start higher
Sublingual: 1200 mcg / 10 min =
120 mcg / min
226
Page 227
Nitroglycerin: Adverse
Hypotension: usually responds to
fluid bolus and leg elevation
Reflex tachycardia: can be
moderated by concomitant use of
beta-blocking agent
Contraindicated in patients taking
PDE5 inhibitors (e.g. sildenafil)
Avoid for 12–24 hours after using
227
Page 228
Beta Blockers (BB)
Potential benefits 1
oxygen demand: heart rate,
blood pressure, contractility
risk of ventricular fibrillation
automaticity, electro-
physiologic threshold for activation,
slowing conduction
228
Page 229
Beta Blockers (BB)
Potential benefits 2
Bradycardia prolongs diastole
coronary diastolic perfusion
remodeling, improves left
ventricular hemodynamic function
left ventricular diastolic function
with a less restrictive filling pattern
229
Page 230
Beta Blockers (BB)
Prefibrinolysis era: mortality benefit
10 – 15% in patients treated with
propranolol, metoprolol, atenolol
Early IV therapy associated with
reduction in infarct size
Reperfusion era: ~40% reduction in
mortality in both STEMI (Q wave) or
non-ST elevation (non-Q wave) MI
230
Page 231
Beta Blockers (BB)
Contraindications
HR <60/min
SBP
<100mmHg
Moderate to
severe LV
dysfunction
Hypoperfusion
Precipitated by
cocaine
PR interval
>0.24 sec
2o or 3o AV
block
Active
bronchospasm
231
Page 232
Morphine
Chest pain despite adequate
treatment with antiplatelet,
anticoagulant, anti-ischemics
pain and anxiety circulating
catecholamines tendency
toward dysrhythmias
both pre and afterload
myocardial oxygen demand
232
Page 233
Morphine
Adverse Effects
Hypotension / bradycardia
responds to fluid bolus and atropine
Respiratory depression
233
Page 234
Reperfusion Therapy
Thrombolytic (fibrinolytic) therapy
Percutaneous Coronary
Intervention (PCI)
234
Page 235
Fibrinolytic
Streptokinase (SK)
Anisoylated Plasminogen
Streptokinase Activator Complex
(APSAC, Eminase, Anisterplase)
Tissue Plasminogen Activator
(TPA, Activase, Alteplase)
Reteplase (RPA, Retavase)
Tenecteplase (TNK) 235
Page 236
Fibrinolytic
Converts plasminogen to plasmin
lyses fibrin content of acute
intracoronary thrombosis
reperfusion of coronary arteries
infarction size, residual LV
function, survival
236
Page 237
Fibrinolytic
Shorter time between symptom
onset and administration greater
reduction in mortality
Initiate ideally within 30 minutes of
ED arrival
237
Page 238
Criteria for Thrombolysis
Class I: treatment benefit established
ST > 0.1mV in two or more
contiguous leads
Time to therapy ≤ 12 hours
Age <75 years
Bundle branch block (old)
obscuring ST segment analysis but
history suggesting AMI 238
Page 239
Criteria for Thrombolysis
Class IIa: treatment likely to benefit
ST elevation
Age >75 years
239
Page 240
Criteria for Thrombolysis
Class IIb: treatment may benefit
ST elevation
Time to therapy >12-24 hours
SBP >180 or DBP >110
240
Page 241
Criteria for Thrombolysis
Class III: not indicated, may be
harmful
ST elevation, time to therapy >24
hours, Ischemic pain resolved
ST depression only
No ST elevation
True posterior MI
Presumed new BBB 241
Page 242
Absolute Contraindications
Any prior cerebral hemorrhage
Known structural CNS lesion
Ischemic stroke within 3 months
(unless TIA < 3 hrs)
Significant closed head / facial
injury within 3 months
Suspicion of aortic dissection
Active bleeding / bleeding disorder 242
Page 243
Relative Contraindications 1
Chronic, severe, poorly controlled HTN or severe HTN on admission (SBP > 180 or DBP > 119)
Traumatic / prolonged (>10min) CPR
Non-compressible vascular punctures
Major surgery or internal bleeding within 3-4 weeks
243
Page 244
Relative Contraindications 2
Any other CNS disease – structural
or functional – not noted above
Pregnancy
Active peptic ulcer
Current use of anticoagulants
Prior exposure / allergic reaction to
SK or anistreplase if using these
agents 244
Page 245
Complications
Systemic bleeding 2 – 10%
Cerebral hemorrhage < 1%
Hypotension 3 – 10%
Allergic phenomena 1.5 – 2%
Usually minor; most common with SK
Reperfusion dysrhythmias ~50%
PVCs, idioventricular rhythms
Failure to open occlusion ~20% 245
Page 246
Percutaneous Coronary Intervention
Angioplasty or stent placement
2000 AHA guidelines
Class I for patients <75 years
with ACS and signs of
cardiogenic shock
Class IIa for patients >75
years
246
Page 247
Percutaneous Coronary Intervention
Benefits
More effective than thrombolysis in
opening occluded arteries
Treats underlying fixed obstructed
coronary artery lesions as well as
relieve the acute thrombosis
Associated with lower incidence of
recurrent ischemia, reinfarction,
intracranial hemorrhage, and death 247
Page 248
Percutaneous Coronary Intervention
Cons
Needs to be implemented 60 – 90
minutes
Not all facilities have PCI available
on 24 hour basis
Performance varies based on
center’s volume and operator’s
experience
248
Page 249
Angiotensin Converting Enzyme Inhibitors
When administered within first 24
hours, incidence of severe
ventricular dysfunction and death
All with AMI should receive ACE-I
Not until 6 hours after initial therapy
has started, patient stable
Too early hypotension
249
Page 250
Angiotensin Converting Enzyme Inhibitors
Captopril 12.5mg PO BID
Lisinopril 5 mg PO qd
Contraindications
ACE-I allergy
Killip Class III or IV heart failure
Hypotension (SBP < 100)
Creatinine > 2.5
Renal artery stenosis
250
Page 251
Complications of AMI
251
Page 252
Dysrhythmias
Prehospital phase associated with
highest incidence lethal dysrhythmia
Ventricular fibrillation greatest in 1st
hour of infarction
252
Page 253
Dysrhythmias: Treatment 1
Treat if exacerbates myocardial
ischemia or could potentially
deteriorate into cardiac arrest
Consider treatment of PVCs if
Frequent (>30 / hour)
Multifocal
Short runs of ventricular tachycardia
Couplets / display R on T
phenomenon 253
Page 254
Dysrhythmias: Treatment 2
Initial treatment: optimally manage
underlying ischemia / infarction
Lidocaine vs procainamide vs
amioadarone: your call
254
Page 255
Heart Failure
Left ventricular failure: congestive
heart failure pulmonary edema
cardiogenic shock
Left ventricle impaired ≥25%
CHF / pulmonary edema
Left ventricle impaired ≥40%
cardiogenic shock
255
Page 256
Conduction Disturbances
AV Blocks: 1o and Mobitz I 2o
Generally due to vagal tone
Rarely progress to complete block
Usually associated with inferior MI
Generally respond to drug therapy:
atropine
256
Page 257
Conduction Disturbances
AV Blocks: Mobitz II 2o
Generally due to destruction of
infranodal conduction tissue
Sudden progression to complete
AV block may occur
Usually associated with anterior MI
Pacemaker indicated
257
Page 258
Conduction Disturbances
Bundle Branch Block
Identifies patients more likely to
develop CHF, AV block, V-Fib
Acute anterior wall MI + new
RBBB high risk of developing
complete AV block and / or
cardiogenic shock
258
Page 259
Some Other Complications
Cardiac rupture
Ventricular septal rupture
Papillary muscle dysfunction /
rupture
Mitral regurgitation
LV aneurysm
Thromboembolism
Pericarditis 259
Page 260
3.5.7 Myocarditis
260
Page 261
Myocarditis
Detected in ~10% of routine
autopsies
Numerous virus (especially
enterovirus), bacteria, fungi
South America: Chaga’s disease
Necrosis and destruction of cardiac
tissues
261
Page 262
Myocarditis
Complaints nonspecific: fever,
fatigue, myalgias, N/V/D
No sign or symptom sensitive or
specific
Unexplained tachycardia common,
but nonspecific
Cardiac exam often unremarkable
262
Page 263
Myocarditis
EKG findings nonspecific: sinus
tachycardia, low electrical activity
May be prolonged corrected Q-T
interval, AV block, acute MI pattern
Cardiac troponin usually
WBC / ESR / CRP: nonspecific
263
Page 264
Differential Diagnosis
Can masquerade as acute MI:
severe chest pain, ECG changes,
cardiac markers, heart failure
Patients with myocarditis usually
young, few risk factors for CAD
ECG abnormalities may extend
beyond distribution of single
coronary artery
264
Page 265
Treatment
Determined by patient's clinical
presentation and severity of
disease
Extends from limitation of activity to
rhythm and CHF treatment, ECMO,
VADs, and eventual cardiac
transplantation
265
Page 266
Chaga’s Disease
Common in Central America
Protozoan Trypanosoma cruzi with
transmission by insect vector
~75% have no cardiac symptoms
Syncope / presyncope in 2/3 who
are seropositive
Antitrypanosomal drugs:
benznidazole and nifurtimox 266
Page 267
Trichinosis
Ingestion of cysts of Trichinella
spiralis in undercooked meat, now
mostly game meats
Myocardial involvement in ~20% of
diagnosed cases, appears 2nd – 3rd
week of illness
Many cardiac and EKG findings
Corticosteroids + anti-helminthic
267
Page 268
Lyme Disease
Spirochete Borrelia burgdorferi
Carditis ~21 days after onset of
erythema migrans
Cardiac complications 4 - 10%
Conduction disturbances; BBB, 1st,
2nd, and 3rd degree heart block;
cardiac arrest; dysrhythmias; left
ventricular dysfunction
268
Page 269
Lyme Disease Treatment
Atropine or isoproterenol to treat
stable heart blocks
Temporary pacemaker often
required in unstable patients
IV penicillin or oral tetracycline can
reverse AV blocks
Erythromycin in kids
Ceftriaxone also effective 269
Page 270
Pharmacologic Causes
In addition to ischemia, cocaine
can cause myocarditis & dilated
cardiomyopathy
Doxorubicin can cause
pericarditis, dysrhythmias,
myocarditis, left ventricular
dysfunction
270
Page 271
Kawasaki Disease
Primarily affects children
~25% have coronary artery
abnormalities, usually several
weeks after symptom onset
Usually reversible: may cause
aneurysm formation or 2o
thrombosis and acute MI
Myocarditis / pericarditis also seen
271
Page 272
Brugada Syndrome
Unpredictable ventricular
dysrhythmias and syncope or
sudden cardiac death
More in < 50 years old
Inherited disorder of Na+ channels
Men > women
Most common in Asian patients
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Brugada Syndrome
No structural heart disease
Consider in children, teenagers,
young adults with unexplained
syncope or symptomatic
palpitations
ECG pattern: ST with “saddle-
back” or coved appearance V1-V3
RBBB often coexists
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Brugada Syndrome
274 Source Undetermined
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Brugada Syndrome
Untreated: 10% mortality / year
Only proven therapy: implantable
cardioverter – defibrillator (ICD)
Quinidine is proposed alternative in
settings where ICD’s are
unavailable or inappropriate (eg:
neonates)
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3.5.8 Ventricular
Aneurysm
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Ventricular Aneurysm
Persistent ST elevation following
acute myocardial infarction
Some ST elevation remains in 60%
of patients with anterior STEMI and
5% with inferior STEMI
Associated with paradoxical
movement of ventricular wall on
echocardiography
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Ventricular Aneurysm
ST elevation >2 weeks after AMI
Most common: precordial leads.
May be concave or convex
Usually associated with well-
formed Q- or QS waves.
Relatively small T-waves
Unlike hyperacute T-waves of AMI
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Ventricular Aneurysm
279
Source Undetermined
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Predispose To
Ventricular arrhythmias and sudden
cardiac death
Myocardial scar tissue is
arrhythmogenic
Congestive cardiac failure
Mural thrombus and embolization
Myocardial rupture and death
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