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1. 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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3. 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

4. Part Two
5. Diseases of the Myocardium
Cardiac Failure
Cardiomyopathy
CHF
Coronary Syndromes
Myocardial Infarction
Myocarditis
Ventricular Aneurysm 4

5. 3.5 Acquired
Diseases of the
Myocardium
5
Patrick J. Lynch (Wikimedia Commons)

6. 3.5.1.1 Cor
Pulmonale
6
Mariana Ruiz (Wikipedia)

7. Cor Pulmonale
Cor = heart
Pulmonale = of the lungs
In other words, pulmonary heart
disease
Also known as “right heart failure”
7

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

9. Acute Cor Pulmonale
Massive pulmonary embolization
Exacerbation of chronic cor
pulmonale
9

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

11. Chronic: Many Causes 2
Sarcoidosis
T1-4 vertebral subluxation
Obstructive sleep apnea
Altitude sickness
Sickle cell anemia
Bronchopulmonary dysplasia (in
infants)
11

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

13. Signs & Symptoms 2
Hepatomegaly
Abnormal heart sounds
Bi-phasic atrial response on EKG
due to hypertrophy
13

14. Chest X-Ray
Right ventricular hypertrophy
Right atrial dilatation
Prominent pulmonary artery
Peripheral lung fields:  vascular
markings
Changes of COPD
14

15. Chest X-Ray Right
ventricular
hypertrophy
Right atrial
dilatation
Prominent
pulmonary
artery
Peripheral
lung fields:
 vascular
markings
(COPD) 15
Source Undetermined

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

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

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

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

20. 3.5.1.2 High Output
Cardiac Failure
20

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

22. High Output: Causes 1
Chronic severe anemia
Large AV fistula
22
Source Undetermined

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

24. High Output: Causes 3
Acutely in septic shock, especially
Gram-negative bacteria
24
Source Undetermined

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

26. 3.5.1.3 Low Output
Cardiac Failure
26

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

28. 3.5.2
Cardiomyopathy
28

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

30. Extrinsic Causes
Primary pathology: outside
myocardium itself
Most cardiomyopathies are
extrinsic
Most common cause: ischemia
30

31. Intrinsic Causes
Not due to identifiable external
cause
Causes can be found for most
31

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

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

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

35. Non-Ischemic Cardiomyopathy
HOCM
Restrictive
Dilated
Myocarditis
Tako-Tsubo
35
Source Undetermined

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

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

38. 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

39. 3.5.2.1 Hypertrophic
Cardiomyopathy
39

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

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

42. Symptoms
Dyspnea  most common
Chest pain
Palpitations
Lightheadedness
Fatigue
Syncope
Sudden cardiac death
42

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

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

45. ECG Findings
LVH  precordial voltages, non-
specific ST / T-wave abnormalities
45
Source Undetermined

46. ECG Findings
Asymmetric hypertrophy 
“dagger Q-waves” infero-lateral
46
Source Undetermined

47. Management
Beta-blockers & calcium channel
blockers: slow heart rate, improve
diastolic function
Amiodarone: reduces ventricular
dysrhythmias
47

48. 3.5.3 Congestive
Heart Failure
48

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

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

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

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

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

54. Right-Sided Heart Failure
54

55. 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

56. Peripheral Edema & Anasarca
56Source Undetermined Source Undetermined

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

58. Jugular Venous Distention
58
Source Undetermined

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

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

61. Radiographic Findings
Cardiomegaly
 large heart
61
Source Undetermined

62. Radiographic Findings
Cephalization =
upper lobe
blood diversion
Occurs when
PAWP 12-18
mmHg
62Source Undetermined

63. Radiographic Findings
Kerley B lines:
short parallel
lines at lung
periphery
Interlobular
septa: usually
<1 cm
PAWP 18–25
MMHg 63Source Undetermined

64. Radiographic Findings
Bat wing =
central
interstitial
edema
PAWP >25
mmHg
64
Source Undetermined

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

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

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

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

69. Management: Nitroglycerin 1
Lower doses: venodilation
 preload
Higher doses: arteriolar dilation
 blood pressure
 afterload
69

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

71. Management: Loop Diuretic
Furosemide standard
In volume overload:  plasma
volume,  preload,  pulmonary
congestion
Diuresis unnecessary in low
plasma volumes
71

72. Management: Morphine
Controversial: central sympatholytic
that releases vasoactive histamine
 causes peripheral vasodilation
72Vaprotan (Wikimedia Commons)

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

74. 3.5.4 Coronary
Syndromes
74

75. Acute Coronary Syndromes
Continuum or progression of
coronary artery disease from
myocardial ischemia to necrosis
Stable angina unstable angina
acute myocardial infarction
75

76. Classic Presentations
76J. Heuser (Wikipedia)J. Heuser (Wikipedia)

77. 3.5.5 Ischemic
Heart Disease
77

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

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

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

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

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

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

84. Risk Factors, Other
Male sex
Advanced age
Methamphetamine use
Cocaine use
Obesity
Inactive Lifestyle
Post-menopause
84

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

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

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

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

89. NSTEACS
Non-ST-elevation acute coronary
syndrome (NSTEACS) 
Main ECG abnormalities
ST segment depression
T wave flattening or inversion
89

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

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

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

93. Ischemic T Wave Inversions
Dynamic inversions with acute
myocardial ischemia
93
Source Undetermined
Source Undetermined

94. Ischemic T Wave Inversions
Fixed inversions follow infarction,
usually in association with
pathological Q waves
94
Source Undetermined
Source Undetermined

95. Biphasic T Waves
Two main causes:
Hypokalemia
Myocardial ischemia
Waves go in opposite directions:
Hypokalemic: go  then 
Ischemic: go  then 
95

96. Biphasic T Waves
Due to hypokalemia:  then 
96
Source Undetermined

97. Biphasic T Waves
Due to ischemia:  then 
97
Source Undetermined

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

99. Biphasic T Waves: Wellens’
Type 1 Wellens’ T-waves: deeply
and symmetrically inverted
99
Source Undetermined

100. Biphasic T Waves: Wellens’
Type 2 Wellens’ T-waves: biphasic,
with initial deflection positive and
the terminal deflection negative
100
Source Undetermined

101. Flattened T Waves
Non-specific
Dynamic or in contiguous leads:
think ischemia
Generalized: think electrolyte
abnormality, like hypokalemia
101
Source Undetermined

102. Inverted U Wave
Infrequently recognized but specific
sign of myocardial ischemia
102
Source Undetermined

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

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

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

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

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

108. 3.5.6 Myocardial
Infarction
108

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

110. EKG for STEMI
 amplitude R  “giant” R waves
110
Source Undetermined

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

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

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

114. Other Causes of  ST 3
Left ventricular hypertrophy
Idioventricular rhythm including
paced rhythm
114
Source Undetermined

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

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

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

118. Early Repolarization 4
Generalized concave ST elevation in
precordial (V2-6) and limb leads (I, II,
III, aVF)
118
Source Undetermined

119. Early Repolarization 5
J-point notching evident in inferior
leads (II, III and aVF)
119
Source Undetermined

120. Early Repolarization 6
J-point notching evident in inferior
leads (II, III and aVF)
120
Source Undetermined

121. Early Repolarization 7
Prominent, slightly asymmetrical T
waves that are concordant with main
vector of QRS complexes
121
Source Undetermined

122. Early Repolarization 8
Descending limb of T wave is straighter
and slightly steeper than ascending
limb
122
Source Undetermined

123. Early Repolarization 9
Descending limb of T wave is straighter
and slightly steeper than ascending
limb
123
Source Undetermined

124. Specific
Infarcts
124

125. 125
Effects of Myocardial Ischemia,
Injury, and Infarction on the ECG

126. 126
Patrick J. Lynch (Wikipedia)

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

128. Left Main Occlusion
Widespread ST depression, most
prominent in lateral leads (V4-6, I, aVL)
ST elevation > 1mm in aVR 128
Source Undetermined

129. Left Main Occlusion
Widespread ST depression, most
prominent in lateral leads (V4-6, I, aVL)
ST elevation > 1mm in aVR 129
Source Undetermined

130. Left Main Occlusion
Widespread ST depression, most
prominent in lateral leads (V4-6, I, aVL)
ST elevation > 1mm in aVR 130
Source Undetermined

131. Left Main Occlusion
Widespread ST depression, most
prominent in lateral leads (V4-6, I, aVL)
ST elevation > 1mm in aVR 131
Source Undetermined

132. 132
Patrick J. Lynch (Wikipedia)

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

134. Anterior STEMI: Hyperacute
134
Source Undetermined
Source Undetermined

135. Anterior STEMI: Acute
135
Source Undetermined
Source Undetermined

136. Anterior STEMI: Acute
Q waves in V1-2
Reduced R wave height (Q-wave
equivalent) in V3-4
136
Source Undetermined

137. Anterior STEMI: Tombstone
137
Source Undetermined

138. Anterior STEMI: Tombstone
Proximal LAD large infarction with
poor LV ejection fraction
High likelihood of cardiogenic shock
and death 138
Source Undetermined

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

140. 140
Patrick J. Lynch (Wikipedia)

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

142. STEMI: High Lateral
Occluded 1st diagonal branch (D1)
of LAD  isolated ST in I, aVL
142
Source Undetermined

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

144. STEMI: Lateral
Isolated lateral STEMIs uncommon
Lateral STEMI as a stand-alone MI
is indication for emergent
reperfusion
144

145. STEMI: Inferior 1
~80%  dominant RCA
~18%  dominant LCx
Rare: “type III” or wraparound LAD
 concomitant inferior and anterior
ST elevation
145

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

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

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

149. STEMI: Inferior 5
149
Source Undetermined

150. 150
Patrick J. Lynch (Wikipedia)

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

152. STEMI: Inferior from RCA
ST in lead III > lead II
Reciprocal ST and T wave
inversion in aVL
152
Source Undetermined

153. STEMI: Inferior from RCA
ST in lead III > lead II
Reciprocal ST and T wave
inversion in aVL
153Source Undetermined

154. 154
Patrick J. Lynch (Wikipedia)

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

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

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

158. Right Ventricular Infarct
158
V1RV2R
V3R
V4R
V5R
V6R
Arcadian (Wikimedia Commons)

159. Right Ventricular Infarct
ST in V1
ST in lead III > lead II
159
Source Undetermined

160. Right Ventricular Infarct
Right-sided leads
ST in lead III > lead II
ST throughout right-sided leads
V3R-V6R
160Source Undetermined

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

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

163. Posterior Infarct
ST becomes ST
Q waves become R waves
Terminal T-wave inversion
becomes an upright T wave
163
Source Undetermined

164. Posterior Infarct
Same EKG flipped upside down
Now looks like typical STEMI
Also with posterior leads
164Source Undetermined

165. Posterior Infarct
Same EKG flipped upside down
Now looks like typical STEMI
Also with posterior leads
165
Source Undetermined

166. Posterior Infarct: Leads
166
Scapula
V7 V8 V9
Source Undetermined

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

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

169. Posterior
Tall, broad
R waves
(>30ms)
Upright T
waves
Dominant R
wave (R/S
ratio>1) V2
169Source Undetermined

170. Posterior Infarct
Same patient, posterior leads V7 –
V9
170
Source Undetermined

171. Posterior Infarct
171
Source Undetermined Source Undetermined

172. Q-Waves: Normal
Depolarization of interventricular
septum (“septal Qs”)
Lateral leads I, aVL, V5 and V6
172

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

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

175. Initial EKG Useful for…
… screening
… risk stratification
… establishing criteria that
determine which therapeutic
interventions will be employed
175

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

177. Serum Biomarkers
177
Source Undetermined

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

179. Serum Biomarkers: Troponin
179
Ayacop (Wikimedia Commons)

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

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

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

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

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

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

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

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

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

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

190. Coronary Artery CT
Very controversial
A work in progress
Zealots on both sides
Something MAY emerge in next
few years
190

191. Radionuclide Scanning
191

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

193. Technetium (99mTc) sestamibi
Active chest pain + nondiagnostic
EKG  100% sensitive / 83-92%
specific
Pain-free patient: 65% sensitive
193

194. Thallium 201 scintigraphy
194
Source Undetermined

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

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

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

198. Treatment
198

199. Treatment
IV (NS) 
cardiac monitor
 pulse
oximeter
Oxygen
Antiplatelet
agents
Anticoagulant
therapy
Nitroglycerin
Morphine
Beta-blocker
Reperfusion
therapy
ACE-I
199

200. Treatment
IV (NS) 
cardiac
monitor 
pulse oximeter
Oxygen
Antiplatelet
agents
Anticoagulant
therapy
Nitroglycerin
Morphine
Beta-blocker
Reperfusion
therapy
ACE-I
200

201. IV / Monitor / Pulse oximetry
201

202. Treatment
IV (NS) 
cardiac monitor
 pulse
oximeter
Oxygen
Antiplatelet
agents
Anticoagulant
therapy
Nitroglycerin
Morphine
Beta-blocker
Reperfusion
therapy
ACE-I
202

203. Oxygen
Low flow (2-4L) by nasal cannula
High flow associated with 
mortality and infarct size
203

204. Treatment
IV (NS) 
cardiac monitor
 pulse
oximeter
Oxygen
Antiplatelet
agents
Anticoagulant
therapy
Nitroglycerin
Morphine
Beta-blocker
Reperfusion
therapy
ACE-I
204

205. Antiplatelet Agents: Aspirin
Irreversibly acetylates platelet
cyclo-oxygenase,
Rapid onset: within 60 minutes
205

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

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

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

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

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

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

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

213. Treatment
IV (NS) 
cardiac monitor
 pulse
oximeter
Oxygen
Antiplatelet
agents
Anticoagulant
therapy
Nitroglycerin
Morphine
Beta-blocker
Reperfusion
therapy
ACE-I
213

214. Anticoagulant Therapy
Unfractionated heparin
Low molecular weight heparin
Direct thrombin inhibitors
214

215. Anticoagulant Therapy
Unfractionated heparin and
enoxaparin result in similar
outcomes at one year post MI
215
Melissa Wiese (Wikimedia Commons)

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

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

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

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

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

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

222. Nitroglycerin (NTG) 1
Dilates collateral coronary vessels
 collateral blood flow to ischemic
myocardium
Has antiplatelet effects
222

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

224. Nitroglycerin (NTG) 3
 pain and consequently
catecholamine release
224

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

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

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

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

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

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

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

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

233. Morphine
Adverse Effects
Hypotension / bradycardia 
responds to fluid bolus and atropine
Respiratory depression
233

234. Reperfusion Therapy
Thrombolytic (fibrinolytic) therapy
Percutaneous Coronary
Intervention (PCI)
234

235. Fibrinolytic
Streptokinase (SK)
Anisoylated Plasminogen
Streptokinase Activator Complex
(APSAC, Eminase, Anisterplase)
Tissue Plasminogen Activator
(TPA, Activase, Alteplase)
Reteplase (RPA, Retavase)
Tenecteplase (TNK)
235

236. Fibrinolytic
Converts plasminogen to plasmin 
lyses fibrin content of acute
intracoronary thrombosis 
reperfusion of coronary arteries 
 infarction size,  residual LV
function,  survival
236

237. Fibrinolytic
Shorter time between symptom
onset and administration  greater
reduction in mortality
Initiate ideally within 30 minutes of
ED arrival
237

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

239. Criteria for Thrombolysis
Class IIa: treatment likely to benefit
ST elevation
Age >75 years
239

240. Criteria for Thrombolysis
Class IIb: treatment may benefit
ST elevation
Time to therapy >12-24 hours
SBP >180 or DBP >110
240

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

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

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

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

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

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

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

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

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

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

251. Complications of AMI
251

252. Dysrhythmias
Prehospital phase associated with
highest incidence lethal dysrhythmia
Ventricular fibrillation greatest in 1st
hour of infarction
252

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

254. Dysrhythmias: Treatment 2
Initial treatment: optimally manage
underlying ischemia / infarction
Lidocaine vs procainamide vs
amioadarone: your call
254

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

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

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

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

259. Some Other Complications
Cardiac rupture
Ventricular septal rupture
Papillary muscle dysfunction /
rupture
Mitral regurgitation
LV aneurysm
Thromboembolism
Pericarditis
259

260. 3.5.7 Myocarditis
260

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

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

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

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

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

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

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

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

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

270. Pharmacologic Causes
In addition to ischemia, cocaine
can cause myocarditis & dilated
cardiomyopathy
Doxorubicin can cause
pericarditis, dysrhythmias,
myocarditis, left ventricular
dysfunction
270

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

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
272

273. 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
273

274. Brugada Syndrome
274
Source Undetermined

275. 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)
275

276. 3.5.8 Ventricular
Aneurysm
276

277. 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
277

278. 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
278

279. Ventricular Aneurysm
279
Source Undetermined

280. Predispose To
Ventricular arrhythmias and sudden
cardiac death
Myocardial scar tissue is
arrhythmogenic
Congestive cardiac failure
Mural thrombus and embolization
Myocardial rupture and death
280

281. 281