GEMC- Cardiovascular Board Review Session 2- Resident Training

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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2

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

http://www.emedhome.com/

Part Two 5. Diseases of the Myocardium

Cardiac Failure

Cardiomyopathy

CHF

Coronary Syndromes

Myocardial Infarction

Myocarditis

Ventricular Aneurysm 4

3.5 Acquired

Diseases of the

Myocardium

5 Patrick J. Lynch (Wikimedia Commons)

http://commons.wikimedia.org/wiki/File:Heart_myocardium_diagram.jpg

3.5.1.1 Cor

Pulmonale

6

Mariana Ruiz (Wikipedia)

http://en.wikipedia.org/wiki/Cor_pulmonalemediaviewer/File:Right_Ventricular_hypertrophy.svg

Cor Pulmonale

Cor = heart

Pulmonale = of the lungs

In other words, pulmonary heart

disease

Also known as “right heart failure”

7

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

Acute Cor Pulmonale

Massive pulmonary embolization

Exacerbation of chronic cor

pulmonale

9

Chronic: Many Causes 1

COPD

Primary pulmonary hypertension

Asthma

Recurrent pulmonary embolism

Loss of lung tissue following

trauma or surgery

End stage pneumoconiosis

10

Chronic: Many Causes 2

Sarcoidosis

T1-4 vertebral subluxation

Obstructive sleep apnea

Altitude sickness

Sickle cell anemia

Bronchopulmonary dysplasia (in

infants)

11

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

Signs & Symptoms 2

Hepatomegaly

Abnormal heart sounds

Bi-phasic atrial response on EKG

due to hypertrophy

13

Chest X-Ray

Right ventricular hypertrophy

Right atrial dilatation

Prominent pulmonary artery

Peripheral lung fields: vascular

markings

Changes of COPD

14

Chest X-Ray Right

ventricular

hypertrophy

Right atrial

dilatation

Prominent

pulmonary

artery

Peripheral

lung fields:

vascular

markings

(COPD) 15

Source Undetermined

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

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

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

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

3.5.1.2 High Output

Cardiac Failure

20

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

High Output: Causes 1

Chronic severe anemia

Large AV fistula

22 Source Undetermined


Multiple small arteriovenous shunts

e.g. Paget's disease of bone

Some severe hepatic or renal

disorders

Hyperthyroidism

Beriberi

23


Acutely in septic shock, especially

Gram-negative bacteria


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

3.5.1.3 Low Output

Cardiac Failure

26

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

3.5.2

Cardiomyopathy

28

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

Extrinsic Causes

Primary pathology: outside

myocardium itself

Most cardiomyopathies are

extrinsic

Most common cause: ischemia

30

Intrinsic Causes

Not due to identifiable external

cause

Causes can be found for most

31

Signs & Symptoms

Can mimic virtually any form of

heart disease

Chest pain: common

Severe cases associated with heart

failure, arrhythmias, and systemic

embolization

32

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

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

Non-Ischemic Cardiomyopathy

HOCM

Restrictive

Dilated

Myocarditis

Tako-Tsubo

35

Source Undetermined

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

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

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

3.5.2.1 Hypertrophic

Cardiomyopathy

39

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

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

Symptoms

Dyspnea most common

Chest pain

Palpitations

Lightheadedness

Fatigue

Syncope

Sudden cardiac death

42

Findings: Murmur 1

Murmur similar to aortic stenosis

Classically, murmur is loudest at

left parasternal edge, 4th intercostal

space, rather than aortic area

43

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

ECG Findings

LVH precordial voltages, non-

specific ST / T-wave abnormalities


ECG Findings

Asymmetric hypertrophy

“dagger Q-waves” infero-lateral

46

Source Undetermined

Management

Beta-blockers & calcium channel

blockers: slow heart rate, improve

diastolic function

Amiodarone: reduces ventricular

dysrhythmias

47

3.5.3 Congestive

Heart Failure

48

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

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


rate of breathing tachypnea

work of breathing

Rales or crackles: initially in lung

bases fluid in alveoli (pulmonary

edema

Cyanosis: late, severe

51


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

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

Right-Sided Heart Failure

54


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

Peripheral Edema & Anasarca

56 Source Undetermined Source Undetermined


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

Jugular Venous Distention


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

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


Cardiomegaly

large heart

61

Source Undetermined


Cephalization =

upper lobe

blood diversion

Occurs when

PAWP 12-18

mmHg



Kerley B lines:

short parallel

lines at lung

periphery

Interlobular

septa: usually

<1 cm

PAWP 18–25

MMHg 63

Source Undetermined


Bat wing =

central

interstitial

edema

PAWP >25

mmHg

64

Source Undetermined

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

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

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

Acute Management 3

Result: left ventricular preload

and afterload by intrathoracic

pressure

More rapid restoration of normal

vital signs and oxygenation

Fewer intubations

68

Management: Nitroglycerin 1

Lower doses: venodilation

preload

Higher doses: arteriolar dilation

blood pressure

afterload

69

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

Management: Loop Diuretic

Furosemide standard

In volume overload: plasma

volume, preload, pulmonary

congestion

Diuresis unnecessary in low

plasma volumes

71

Management: Morphine

Controversial: central sympatholytic

that releases vasoactive histamine

causes peripheral vasodilation

72 Vaprotan (Wikimedia Commons)

http://commons.wikimedia.org/wiki/File:Morphine_vial.JPG

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

3.5.4 Coronary

Syndromes

74

Acute Coronary Syndromes

Continuum or progression of

coronary artery disease from

myocardial ischemia to necrosis

Stable angina unstable angina

acute myocardial infarction

75

Classic Presentations

76 J. Heuser (Wikipedia) J. Heuser (Wikipedia)

http://en.wikipedia.org/wiki/Myocardial_infarctionmediaviewer/File:AMI_pain_back.png

http://en.wikipedia.org/wiki/Myocardial_infarctionmediaviewer/File:AMI_pain_front.png

3.5.5 Ischemic

Heart Disease

77


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


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


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

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

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

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

Risk Factors, Other

Male sex

Advanced age

Methamphetamine use

Cocaine use

Obesity

Inactive Lifestyle

Post-menopause

84

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

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

EKG

Most important adjunctive

diagnostic test

Initial EKG diagnostic in only ~25-

50%

Normal / non-diagnostic initial

EKG does not rule out ACS

87

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

NSTEACS

Non-ST-elevation acute coronary

syndrome (NSTEACS)

Main ECG abnormalities

ST segment depression

T wave flattening or inversion

89

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

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

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


Dynamic inversions with acute

myocardial ischemia

93

Source Undetermined

Source Undetermined


Fixed inversions follow infarction, usually in association with pathological Q waves

94

Source Undetermined

Source Undetermined

Biphasic T Waves

Two main causes:

Hypokalemia

Myocardial ischemia

Waves go in opposite directions:

Hypokalemic: go then

Ischemic: go then

95

Biphasic T Waves

Due to hypokalemia: then

96

Source Undetermined

Biphasic T Waves

Due to ischemia: then

97

Source Undetermined

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


Type 1 Wellens’ T-waves: deeply

and symmetrically inverted

99

Source Undetermined


Type 2 Wellens’ T-waves: biphasic,

with initial deflection positive and

the terminal deflection negative


Flattened T Waves

Non-specific

Dynamic or in contiguous leads:

think ischemia

Generalized: think electrolyte

abnormality, like hypokalemia


Inverted U Wave

Infrequently recognized but specific

sign of myocardial ischemia


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

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

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

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

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

3.5.6 Myocardial

Infarction

108

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

EKG for STEMI

amplitude R “giant” R waves


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

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


Acute neurologic events: all leads,

primarily V1-V6

Acute sympathetic stress: all leads,

especially V1-V6

Brugada syndrome

Ventricular aneurysm

Cardiac contusion

113


Left ventricular hypertrophy

Idioventricular rhythm including

paced rhythm


Early Repolarization 1

ST segment elevation without

underlying disease

Probably has nothing to do with

actual early repolarization

Commonly seen in young men

115


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


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


Generalized concave ST elevation in

precordial (V2-6) and limb leads (I, II,

III, aVF) 118

Source Undetermined


J-point notching evident in inferior

leads (II, III and aVF)

119

Source Undetermined


J-point notching evident in inferior

leads (II, III and aVF)

120

Source Undetermined


Prominent, slightly asymmetrical T

waves that are concordant with main

vector of QRS complexes 121

Source Undetermined


Descending limb of T wave is straighter

and slightly steeper than ascending

limb 122

Source Undetermined


Descending limb of T wave is straighter

and slightly steeper than ascending

limb 123

Source Undetermined

Specific

Infarcts

124

125

Effects of Myocardial Ischemia,

Injury, and Infarction on the ECG

126

Patrick J. Lynch (Wikipedia)

http://en.wikipedia.org/wiki/Left_coronary_arterymediaviewer/File:Coronary_arteries.png

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

Left Main Occlusion

Widespread ST depression, most

prominent in lateral leads (V4-6, I, aVL)

ST elevation > 1mm in aVR 128

Source Undetermined

Left Main Occlusion




Source Undetermined

Left Main Occlusion




Source Undetermined

Left Main Occlusion




Source Undetermined

132



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

Anterior STEMI: Hyperacute

134

Source Undetermined

Source Undetermined

Anterior STEMI: Acute

135

Source Undetermined

Source Undetermined

Anterior STEMI: Acute

Q waves in V1-2

Reduced R wave height (Q-wave

equivalent) in V3-4

136

Source Undetermined

Anterior STEMI: Tombstone


Anterior STEMI: Tombstone

Proximal LAD large infarction with

poor LV ejection fraction

High likelihood of cardiogenic shock

and death 138

Source Undetermined

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



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

STEMI: High Lateral

Occluded 1st diagonal branch (D1)

of LAD isolated ST in I, aVL

142

Source Undetermined

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

STEMI: Lateral

Isolated lateral STEMIs uncommon

Lateral STEMI as a stand-alone MI

is indication for emergent

reperfusion

144

STEMI: Inferior 1

~80% dominant RCA

~18% dominant LCx

Rare: “type III” or wraparound LAD

concomitant inferior and anterior

ST elevation

145

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

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

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

STEMI: Inferior 5

149

Source Undetermined

150



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



Reciprocal ST and T wave

inversion in aVL

152

Source Undetermined




inversion in aVL


154



STEMI: Inferior from LCx

ST in lead II = lead II


inversion in I or aVL

Q wave in III, aVF


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


ST in V1

Only standard ECG lead that

looks directly at the right ventricle


Lead III more “rightward

facing” than lead II

Must do right-sided leads

157


158

V1R V2R

V3R

V4R V5R

V6R

Arcadian (Wikimedia Commons)

http://commons.wikimedia.org/wiki/File:Illu_thoracic_cage.jpg


ST in V1




Right-sided leads


ST throughout right-sided leads

V3R-V6R


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

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

Posterior Infarct

ST becomes ST

Q waves become R waves

Terminal T-wave inversion

becomes an upright T wave


Posterior Infarct

Same EKG flipped upside down

Now looks like typical STEMI

Also with posterior leads


Posterior Infarct

Same EKG flipped upside down

Now looks like typical STEMI

Also with posterior leads

165

Source Undetermined

Posterior Infarct: Leads

166

Scapula

V7 V8 V9

Source Undetermined

Posterior Infarct

Posterior extension of inferior or

lateral infarct implies much larger

area of myocardial damage

risk of left ventricular dysfunction

and death

167

Posterior Infarct

Tall, broad R waves (>30ms)

Upright T waves

Dominant R wave (R/S ratio>1) in

V2

168


Posterior

Tall, broad

R waves

(>30ms)

Upright T

waves

Dominant R

wave (R/S

ratio>1) V2


Posterior Infarct

Same patient, posterior leads V7 –

V9

170

Source Undetermined

Posterior Infarct

171


Q-Waves: Normal

Depolarization of interventricular

septum (“septal Qs”)

Lateral leads I, aVL, V5 and V6

172

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

Q-Waves: Pathologic

Deflection amplitude of 25% or

more of subsequent R wave

>0.04 s (40 ms) wide, >2 mm

amplitude


Initial EKG Useful for…

… screening

… risk stratification

… establishing criteria that

determine which therapeutic

interventions will be employed

175

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

Serum Biomarkers

177

Source Undetermined

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

Serum Biomarkers: Troponin

179

Ayacop (Wikimedia Commons)

http://commons.wikimedia.org/wiki/File:Troponin_1YV0.png


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


Type I MI: coronary artery

occlusion

Type II MI: low flow state leading

to troponin leakage

DIFFERENT PATHOLOGIES

DIFFERENT TREATMENTS

NOT ALWAYS OBVIOUS

181


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

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

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

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


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


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

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

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

Coronary Artery CT

Very controversial

A work in progress

Zealots on both sides

Something MAY emerge in next

few years

190

Radionuclide Scanning

191

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

Technetium (99mTc) sestamibi

Active chest pain + nondiagnostic

EKG 100% sensitive / 83-92%

specific

Pain-free patient: 65% sensitive

193

Thallium 201 scintigraphy

194

Source Undetermined

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

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

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

Treatment

198

Treatment

IV (NS)

cardiac monitor

pulse

oximeter

Oxygen

Antiplatelet

agents

Anticoagulant

therapy

Nitroglycerin

Morphine

Beta-blocker

Reperfusion

therapy

ACE-I 199

Treatment

IV (NS)

cardiac

monitor

pulse oximeter

Oxygen

Antiplatelet

agents

Anticoagulant

therapy

Nitroglycerin

Morphine

Beta-blocker

Reperfusion

therapy

ACE-I 200

IV / Monitor / Pulse oximetry

201

Treatment

IV (NS)

cardiac monitor

pulse

oximeter

Oxygen

Antiplatelet

agents

Anticoagulant

therapy

Nitroglycerin

Morphine

Beta-blocker

Reperfusion

therapy

ACE-I 202

Oxygen

Low flow (2-4L) by nasal cannula

High flow associated with

mortality and infarct size

203

Treatment

IV (NS)

cardiac monitor

pulse

oximeter

Oxygen

Antiplatelet

agents

Anticoagulant

therapy

Nitroglycerin

Morphine

Beta-blocker

Reperfusion

therapy

ACE-I 204

Antiplatelet Agents: Aspirin

Irreversibly acetylates platelet

cyclo-oxygenase,

Rapid onset: within 60 minutes

205

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

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

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

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

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

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

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

Treatment

IV (NS)

cardiac monitor

pulse

oximeter

Oxygen

Antiplatelet

agents

Anticoagulant

therapy

Nitroglycerin

Morphine

Beta-blocker

Reperfusion

therapy

ACE-I 213

Anticoagulant Therapy

Unfractionated heparin

Low molecular weight heparin

Direct thrombin inhibitors

214

Anticoagulant Therapy

Unfractionated heparin and

enoxaparin result in similar

outcomes at one year post MI

215

Melissa Wiese (Wikimedia Commons)

http://commons.wikimedia.org/wiki/File:Syringe_with_insulin_for_a_cat.jpg

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

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

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

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


bleeding than unfractionated

heparin with equivalent or better

antithrombotic effects

Simple administration and dosing

Limited blood monitoring

More predictable anticoagulation

effect

220


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

Nitroglycerin (NTG) 1

Dilates collateral coronary vessels

collateral blood flow to ischemic

myocardium

Has antiplatelet effects

222


infarct size and mortality

myocardial oxygen demand

preload

LV end-diastolic volume

afterload

May myocardial susceptibility to

ventricular dysrhythmias during

ischemia and reperfusion 223


pain and consequently

catecholamine release

224


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


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

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

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

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

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

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

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

Morphine

Adverse Effects

Hypotension / bradycardia

responds to fluid bolus and atropine

Respiratory depression

233

Reperfusion Therapy

Thrombolytic (fibrinolytic) therapy

Percutaneous Coronary

Intervention (PCI)

234

Fibrinolytic

Streptokinase (SK)

Anisoylated Plasminogen

Streptokinase Activator Complex

(APSAC, Eminase, Anisterplase)

Tissue Plasminogen Activator

(TPA, Activase, Alteplase)

Reteplase (RPA, Retavase)

Tenecteplase (TNK) 235

Fibrinolytic

Converts plasminogen to plasmin

lyses fibrin content of acute

intracoronary thrombosis

reperfusion of coronary arteries

infarction size, residual LV

function, survival

236

Fibrinolytic

Shorter time between symptom

onset and administration greater

reduction in mortality

Initiate ideally within 30 minutes of

ED arrival

237

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


Class IIa: treatment likely to benefit

ST elevation

Age >75 years

239


Class IIb: treatment may benefit

ST elevation

Time to therapy >12-24 hours

SBP >180 or DBP >110

240


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

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

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

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

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

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


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


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

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

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

Complications of AMI

251

Dysrhythmias

Prehospital phase associated with

highest incidence lethal dysrhythmia

Ventricular fibrillation greatest in 1st

hour of infarction

252

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

Dysrhythmias: Treatment 2

Initial treatment: optimally manage

underlying ischemia / infarction

Lidocaine vs procainamide vs

amioadarone: your call

254

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

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


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


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

Some Other Complications

Cardiac rupture

Ventricular septal rupture

Papillary muscle dysfunction /

rupture

Mitral regurgitation

LV aneurysm

Thromboembolism

Pericarditis 259

3.5.7 Myocarditis

260

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

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

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

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

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

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

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

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

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

Pharmacologic Causes

In addition to ischemia, cocaine

can cause myocarditis & dilated

cardiomyopathy

Doxorubicin can cause

pericarditis, dysrhythmias,

myocarditis, left ventricular

dysfunction

270

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

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

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

Brugada Syndrome


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

3.5.8 Ventricular

Aneurysm

276

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


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

Source Undetermined

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

Education

GEMC- Cardiovascular Board Review Session 2- Resident Training