AOA Cardiology
Review
Part 1: Myocardial
Infarction
Objectives
• Work through a typical cardiac patient
case presentation
• Review acute myocardial infarction from
risk factors, symptoms, diagnosis,
treatment, and complications
• Understand mechanism of major drugs
used to treat HTN and MI
Case presentation
• A 62yo Caucasian Male presents in the
ED with the chief complaint of chest pain
and difficulty breathing
• What more do you want to know?
Symptoms
• Patient describes a sensation
of “crushing heaviness” at his
sternum “like an elephant is
sitting on my chest” 10/10
• It has been going on for the
last half hour and started after
dinner
• He has had this sensation
before but usually it occurred
when he was mowing the lawn
or raking leaves and always
went away with rest and some
Bayer Aspirin
• Nothing seems to make it
better or worse
• The patient denies any nausea
or vomiting
• States that he feels a little
sweaty and that he just can’t
seem to catch his breath,
however he admits that he
may just be anxious and overly
concerned as to what is
causing his pain.
• The patient also states that his
left shoulder is a little sore but
that may be due increased
activity
• He has also had a
nonproductive cough for 3
days but no fevers, chills, or
night sweats
Medical History
PMHx: The patient has struggled with
obesity for most of his adult life. Five
years ago he started watching what he
eats after his doctor told him that his
blood sugar was too high. He tries to
remember to take his “water pill” and
baby aspirin every day but admits that
usually he is just too busy with work to
remember to do so.
FamHx: Mother died at age 72 of cancer
Father had heart attack and age 43
but lived until the age of 78
One younger brother with COPD
Older sister with diabetes
Has two sons (42 and 37, both healthy
as far as he knows)
Social: lives at home with wife, works full
time
20 pack year history of smoking,
quit two years ago
Drinks EtOH socially at holiday
parties, no other drug use
Medications:
Baby ASA daily
“Water pills” - thinks its HCTZ for some
elevated blood pressures he had 4
years ago, have not been rechecked
since
Claritin for allergies
Glucosaimine/Chondrioitin for joint pain
Differential Diagnosis
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Myocardial Infarction
Angina
Aortic Dissection
GERD
Pulmonary Embolism, Pneumonia
Muscle Strain, Costochondritis
Panic Attack, Anxiety
What do You Want to do Now?
• VS: HR: 156 BP: 164/98
RR: 35 O2: 98%
• CXR: Clear lung fields, no
cardiomegaly or
pneumonia
• Cardiac Enzymes:
Troponin and CK-MB
• EKG: ST elevations in
V2, V3, and V4
• Sublingual nitroglycerin =
minimal pain relief
STEMI Alert!!!!
• ED resident calls STEMI Alert and cath lab
is notified for possible PTCA
• Patient given morphine for pain and
sublingual nitro 2 more times at five
minute intervals
• Cardiology is consulted and patient started
on heparin, ASA, β-blocker, statin, and
given sublingual nitrate for home use. Also
started on ACEi for renal protection
Ischemic Heart Disease
Usually secondary to coronary artery disease (atherosclerosis)
1. Subintimal thickening causes occlusion of lumen
2. Early fatty streaks progress to plaque formation (LDL oxidization,
foam cells, fibrous cap)
3. Any damage to the endothelial cell layer exposes the vessel to
the coagulation cascade and further thrombus formation
Myocardial oxygen consumption/demand depends on HR, BP and
contractility
When vessels of heart are diseased, they are maximally dilated in order
to maintain adequate perfusion of the heart (cardiac myocytes
maximally extract O2 from blood)
Tachycardia increases O2 deliver to tissue, however also decreases
time in diastole → less filling time, less perfusion time
CAD Spectrum
• Stable Angina – Predictable chest pain; usually brought on by
exertion, psychological stress, cold weather, or heavy meals;
relieved by rest and sublingual nitro. Usually < 10min. No changes
on EKG or elevation of cardiac enzymes.
• Unstable Angina – new onset, changing in severity,
frequency or duration, 10-20 min, occurring at rest. No EKG
changes or elevation of cardiac enzymes
• Non STEMI – Subendothelial infarct
• STEMI – Transmural infarct
(Prinzmetal’s Angina – transient coronary vasospasm occurring at rest,
transient ST elevation but negative cardiac enzymes, Tx with CCB’s or
nitrates)
Risk Factors for CAD and MI
• Diabetes – tight glycemic control DOES NOT prevent
macrovascular complications
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Hypertension – BP> 140/90 x3
Smoking - #1 preventable risk factor
Hyperlipidemia – elevated LDL
Family history – premature CAD in first-degree
male relatives < 45 or female relatives < 55
• Metabolic Syndrome – waist circumference, triglycerides,
HDL, BP, and fasting glucose
Myocardial Infarction
Demographics
• Leading cause of
Symptoms:
Chest “pain” – pressure,
tightness, squeezing,
heaviness, burning
May radiate to neck, jaw,
shoulder, arms
Associated with N/V,
diaphoresis, cough,
dizziness, SOB, Levine
Sign, anxiety
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morbidity and mortality in
USA
1.3 million nonfatal MI/yr
0.5-0.7 million fatalities/yr
Male predilection, ages
40-70
Elderly patients and
diabetics may not present
with typical findings
Pathology of
Acute MI
• Myocytes begin to die within 20-40 minutes of ischemia
• 1st 24hrs: coagulative necrosis begins, contraction bands form, loss
of cross striations and nuclei within myocyte
* Death is due to fatal arrhythmias
• 2-4 days: Acute inflammation, neutrophil emigration secondary to
release of inflammatory cytokines from necrotic myocytes, increased
coagulative necrosis
• 5-10 days: Grossly, the area of infarct has a hyperemic border with
central yellow/brown softening, ingrowth of granulation tissue,
macrophages are present, fibroblasts begin laying down scar
* Death due to myocardial rupture → cardiac tamponade
• 7 weeks: hypertrophic cardiac myocytes are present adjacten to
scar (collagen), collagen is weaker than surrounding heart tissue,
contractions pull on collagen increasing risk for aneurysm formation
Treatment for acute MI
• Nitrates – ↓ preload thus ↓ demand, dilates coronary
arteries, reduces chest pain
• Oxygen – decreases area of ischemic injury
• Morphine - ↓ pain, thus may decrease tachycardia
and O2 demand, also ↓ preload
• Heparin – prevents progression of thrombus, does
NOT ↓ mortality (CI’s do exist)
• Revascularization – Consider thrombolysis or
Percutaneous Transluminal Coronary Angioplasty
Prolonged Treatment for MI
• ASA - ↓ mortality, reduces risk for reocclusion by
preventing platelet aggregation
• Β-blocker – reduces HR, contractility and
afterload thus reducing myocardial O2 demand,
↓ mortality
• ACEi - ↓ mortality, use if no contraindications
• Statins - ↓ risk of further coronary events
• Cardiac Rehabilitation/ Lifestyle Modifications
Complications of MI
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Arrhythmia:
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Recurrent MI
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LV failure → pulmonary edema, (S3, S4, pulmonary rales) → right heart failure
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Cardiogenic Shock: hypotension, tachycardia, hypoxia, JVD, ↓CO, ↑ PCWP
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Aneurysm: can ↓ CO, cause, arrhythmias, mural thrombus formation, rupture (especially
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Rupture: free wall, interventricular septum, papillary muscle
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Early Fibrinous pericarditis: pain worse when lying done or with deep inspiration,
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Dressler’s Syndrome – autoimmune fibrinous pericarditis
most common cause of pre-hospital death in MI, Right Coronary artery
supplies SA and AV node, PVC, PSVT, Vtach, Vfib, sinus tach, sinus brady, asystole can all
occur = treat appropriately
pseudoaneurysms)
better with leaning forward
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Cardiac
Tamponade
Life threatening complication
of MI, aortic dissection,
trauma, etc
Bleeding into pericardial sac →
equalization of pressures in all
four chambers → diastolic
dysfunction
Triad of JVD, muffled heart
sounds, and hypotension
Pulsus paradoxus –
exaggerated decrease in
arterial pressure with
inspiration >10mmHg
Electrical alternans on EKG
Treatment depends on cause –
pericardiocentesis vs.
emergent surgery
Hypertension
• BP > 140/90 x3 separate occasions
• 95% essential/primary HTN
• 5% secondary (Endo, Renal, Meds/Drugs, Iatrogenic)
• Malignant HTN: rapidly progressive, young AA males, causes
markedly ↑ DBP, malignany nephrosclerosis/flea-bitten kidneys,
focal retinal hemorrhages, papilledema
• Hypertensive urgency: BP> 200/110 but no end organ damage
• Hypertensive Emergency: with end-organ damage such as
encephalopathy, renal failure, CHF
Tx: IV labetalol or nitroprusside, decrease BP slowly to decrease
risk of stroke
HTN Treatment
• Lifestyle Modifications (exercise, diet)
• Consider Comorbidities when choosing a
medication
• Often using more than 1 medicine, a
thiazide diuretic should be part of
treatment regimen if not contraindicated to
provide synergy
Thiazides
• Decrease sodium reabsorption via Na/Cl
channel in distal loop of Henle thus
decrease fluid retention
- SE: HyperGLUC (glycemia, lipidemia,
uremia, and calcemia) hypokalemia
- Avoid in diabetics, gout
- Good for patients with osteoporosis
• Loop Diuretics – effective diuretic but do not do much to
lower BP unless etiology is volume overload
ACE Inhibitors
• ↓ angiotensin converting enzyme to
↓vasoconstriction, catecholamine release,
sodium reabsorption, and fluid retention
- Renoprotective = use in diabetics
- Avoid use in patients who already have renal
failure because ACEi can increase CR and K+
- SE: cough (bradykinin), angioedema, teratogenic
(consider switching to ARB if having these symptoms)
* Proven to decrease MORTALITY post MI!
Calcium Channel Blockers
• Decrease contractility, decrease afterload via
arteriodilation
- Dihydropyridines: Nifedipine
↓ afterload, less effect on heart itself, can cause reflex
tachycardia so use with a β-blocker to prevent especially post
MI
- Non-dihydropyridines: Verapamil, Diltiazem
Class IV antiarrhytmics, act on cardiac myocytes to decrease
contractility
SE: Cardiac depression, peripheral edema, constipation, prolongation
of PR interval → torsades de pointes
β-blockers
• Metoprolol, Atenolol, Esmolol
Cardioselective = β1 only, ↓ CO, ↓ HR, ↓ MVO2
• Propanolol, Timolol, Labetalol
Noncardioselective = avoid use in patients with COPD
or asthma due to risk of bronchoconstriction
Propanolol may prevent reinfarct and SCD
• Useful in HTN, Angina, SVT, CHF
• Proven to ↓ MORTALITY Post MI! Reduces risk of SCD!
• SE: impotence, bronchoconstriction, bradycardia, AV
block, sedation, mask symptoms of hypoglycemia
Others
• Hydralazine – reduces afterload by
unknown mechanism, does not affect
heart so results in reflex tachycardia (use
with β-blocker)
• Minoxidil – reserved for severe, refractory
HTN, side effects include hypertrichosis,
pericardial effusion, and reflex tachycardia
(use with β-blocker and diuretic)
Side Notes
• Heart Attacks in
KIDS?!?!
• Rare (0.2/100,000)
• Usually associated
with:
1. Kawasaki’s Disease
2. HOCM
3. Congenital anomaly
• “Holiday Heart”
• EtOH
cardiomyopathies and
arrhythmias
associated with
weekend alcohol and
drug use
Take Home Points
• HTN and MI are
common things seen by
physicians, therefore it
is likely that you will
see them on the USMLE
Step 1
• Learn key facts about
the medicines such as
odd side effects, these
will help you save time
on the test
• Most often, the CXR,
other imaging, or EKG
help you confirm your
answer, usually you can
AOA Cardiology
Review
Part 2: Cardiomyopathies
Dilated Cardiomyopathy
• Most common
• Four chambered dilation
and hypertrophy
• Systolic dysfunction
(poor contractility)
• Poor prognosis: death
within 5 years of
symptom onset
Etiology
1. CAD with prior MI
2. Toxic: EtOH, doxorubicin,
adriamycin
3. Infectious: Coxsackie B,
Chagas’ disease, Lyme
disease, HIV
4. Metabolic: beriberi,
uremia, genetic storage
diseases
5. Thyroid Disease
6. Pregnancy
7. Rheum: SLE, scleroderma
8. Idiopathic: 50% of cases
Dilated Cardiomyopathy
Diagnosis
1. Signs and symptoms of Left
and Right CHF
2. Arrhythmias
3. S3, S4, AV valve insufficiency
4. EKG, ECHO, CXR consistent
with heart failure
Treatment
• Digoxin, diuretics,
β-blockers, heart
transplant
• Discontinue
offending agent if
possible
• Anticoagulation due
to ↑ risk of
embolization
• ICD if Vtach or Vfib
Hypertrophic
Cardiomyopathy
Symptoms/Signs
1.
2.
3.
4.
• Autosomal dominant
missense mutation in 1 of 10
genes that encode for protein
of the sarcomere
• Cardiac Myocyte disarray
• Diastolic dysfunction due to
poor left ventricle relaxation
• May have dynamic outflow
obstruction with asymmetric
hypertrophy of IVS
5.
DOE, syncope
Angina, Palpitations,
Arrhythmias
Sudden Cardiac Death
Loud S4, strong apical
impulse, systolic ejection
murmur, no click (valve not
involved)
Murmur decreases with
increased preload or
afterload, decreased
contractility; increases with
Valsalva and standing
Hypertrophic Cardiomyopathy
Diagnosis
• Family history
• ECHO
• Myocardial biopsy
diagnostic
Treatment
• Avoid strenuous exercise
• Β-blockers, CCB if
symptomatic
• Myomectomy has high
success rate for relieving
symptoms
• ICD to prevent SCD
• 5% annual mortality due
to SCD
Restrictive Cardiomyopathy
• Infiltration of
myocardium
• Impaired diastolic
function due to
decreased ventricular
compliance
• Systolic dysfunction
in advanced disease
due to impaired
contractility
Etiology
1. Amyloidosis
2. Sarcoidosis
3. Hemochromatosis
4. Scleroderma
5. Carcinoid Syndrome
6. Idiopathic
Restrictive Cardiomyopathy
Diagnosis
1. ECHO: thickened
myocardium
2. Increased RA, LA with
normal LV, and RV size
3. Bright, sparkled
myocardium in
amyloidosis
4. EKG: low voltage
5. Endomyocardial biopsy
6. Can mimic constrictive
pericarditis
Treatment
1. Treat underlying disorder
2. Digoxin if systolic
dysfunction present
Questions?
hwasserm@neoucom.edu
THANK YOU!