back to basics: cardiology review i michael froeschl, md frcpc assistant professor of medicine
TRANSCRIPT
Back To Basics:
Cardiology Review I
Michael Froeschl, MD FRCPC
Assistant Professor of Medicine
F R O E S C H L
Overview
1. CADa. Atherosclerosis
b. Stable Obstructive CAD
c. Unstable CAD: Acute Coronary Syndrome
2. ECG/Arrhythmiaa. Review
b. Bradydysrhythmias
c. Tachydysrhythmias
3. Syncope
NB: Key Feature Questions
Learn how to answer them!
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1. Two Concepts
1. Ischemia: Tissue oxygen demand exceeds tissue oxygen supply
2. Infarction: Tissue necrosis secondary to tissue ischemia
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1. Supply-Demand Mismatch
↓ Supply
Coronary obstruction Microvascular
obstruction ↓ Perfusion pressure ↓ PaO2 ↓ Hemoglobin
↑ Demand
↑ Heart Rate ↑ Contractility ↑ Wall Tension
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1. CAD
Obstructive CAD
ACS
Atherosclerosis
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1a. Atherosclerosis Targets
Mode-of-Life Issues
Smoking Diet Exercise Alcohol Stress
Medical Issues
Dyslipidemia Hypertension Diabetes Mellitus Obesity
INTERHEART, Lancet 2004
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1a. Atherosclerosis Targets
“Vascular Protection”
1. ASA
2. Statins
3. ACE-Inhibitors or ARBs
4. Beta-Blockers
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1b. Stable Obstructive CAD
Usual manifestation is Angina Pectoris:
(“strangling”) chest pain secondary to myocardial ischemia
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1b. Stable Obstructive CAD: DX
1. Clinical assessment in all Chest Pain
Sqeezing retrosternal Brought on by stress Relieved by rest or NTG
Patient (age, gender, vascular risk) Physical exam and basic blood work
3/3: Typical anginal CP2/3: Atypical anginal CP0-1/3: Non-anginal CP
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1b. Stable Obstructive CAD: DX
2. Testing in some (for diagnosis and prognosis)
a. Functional Assessment (“stress test”) Exercise ECG Dipyridamole Perfusion Scan Dobutamine Echocardiogram
b. Anatomical Assessment Coronary Angiography (conventional, CT)
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1b. CCS Angina Severity Scale
I Ordinary activity does not cause angina; angina only with increased activity
II Slight limitation of ordinary activity (> 2 blocks level, > 1 flight of stairs)
III Marked limitation of ordinary activity (< 2 blocks level, < 1 flight of stairs)
IV Inability to carry out any activity without discomfort; symptoms may be present at rest
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1b. Stable Obstructive CAD: MX
Vascular Protection (ASA, statin, ACE-I/ARB)
Beta-Blocker (non-DHP CCB if not tolerated)
NTG Address Risk Factors Possibly Revascularize (PCI or CABG)
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1c. Acute Chest Pain
Management:
ABC Vitals IV, O2, Monitor
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1c. Acute Chest Pain: DDX
1. Myocardial Ischemia2. PE3. Aortic Dissection4. Pneumothorax5. GI Rupture6. Other (pericarditis, pneumonia,
GERD/PUD/gastritis, MSK, skin)
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1c. Acute Myocardial Ischemia
↓ Supply
Coronary obstruction Microvascular
obstruction ↓ Perfusion pressure ↓ PaO2 ↓ Hemoglobin
↑ Demand
↑ Heart Rate ↑ Contractility ↑ Wall Tension
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1c. Acute Coronary Syndrome
Definition: myocardial ischemia due to acute coronary insufficiency
90% due to plaque rupture, thrombus +/- spasm
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1c. Two Manifestations of ACS
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1c. Two Manifestations of ACS
Complete Coronary Occlusion
No blood flow beyond
Transmural ischemia
ST-elevation on ECG
Localizes
Reciprocates
Threatened Coronary Occlusion
Decreased blood flow
Subendocardial ischemia
ST-depression or normal
Not localizing
No reciprocal ST ↑
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1c. ACS
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49M with chest pain X 1 hour:
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1c. STEMI
ABC; Vitals; IV, O2, Monitor HX, O/E, ECG: STEMI Acute reperfusion therapy (ART): lytics vs
PPCI ASA, NTG, BB (if safe), clopidogrel, anti-
coagulation (UFH), morphine
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1c. STEMI
Contraindications to Lytics:
90-min assessment CP ECG +/- Reperfusion Arrhythmia
1. Hemorrhagic stroke ever2. Ischemic stroke < 3 mos3. Intracranial AVM4. Intracranial malignancy5. Head trauma < 3 mos6. Active bleeding 7. Aortic dissection
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1c. NSTE ACS
ABC; Vitals; IV, O2, Monitor HX, O/E, ECG: NSTE ACS ASA Risk Stratify (HX, PE, ECG, TNT) Treat accordingly
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Risk Assess
High Interm Low
HX Ongoing CP
CP>20 min resolved
New/progrCCS
3-4
O/E ↓BP, S3, MR, rales
N N
ECG ST↓
trans ST↑
T inv N
TNT >0.1 0.01-0.1 <0.01
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TX High Interm Low
Admit? Yes Yes No
RX ASA
NTG
BB
clopidogrel
-coag
GP 2B3A-I
ASA
NTG
BB
clopidogrel
-coag
ASA
NTG SL
BB
IX Coronary Angio
Inpt stress Outpt stress
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1c. Complications Post-MI
Recurrent ischemia HF/shock Arrhythmia Mechanical Thromboembolic Pericarditis Depression
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1c. Prognosis Post-MI
LV systolic function remains the most important determinant of prognosis post-MI
Usually assessed by means of echocardiogram prior to discharge
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1c. Secondary Prevention: RX
ASA in all Statin in almost all (LDL < 2) ACE-I in most Beta-Blocker NTG if angina Clopidogrel x 1 year post-ACS, post-stent Treat risk factors
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1c. Secondary Prevention: Life
Smoking Diet Exercise Weight Alcohol Stress
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2. ECG = EKG
Identify the study Setting Technical Details Read: rate, rhythm, axis, alphabet Interpret Previous
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2a. Electrical Anatomy
The heart is a pump coordinated and powered by an integral electrical system
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2a. Electrical Anatomy
The SA Node has the steepest slope of spontaneous Phase 4 depolarization and therefore is the dominant pacer
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2a. Electrical Anatomy
Atrial depolarization normally flows from top to bottom and from right to left
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2a. Electrical Anatomy
The AV Node delays then relays electrical activation to the ventricles
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2a. Electrical Anatomy
The His-Purkinje System conducts electrical activation to all areas of both ventricles
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2a. Electrical Anatomy
Three phases of ventricular depolarization:
1. Septum LR(atrial repolarization
occurs simultaneously)
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2a. Electrical Anatomy
2. Depolarization of both ventricles simultaneously from endocardium to epicardium
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2a. Electrical Anatomy
Ventricular repolarization ensues, from epicardium to endocardium
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2a. The 12-Lead ECG
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2a. PQRSTU
PR ST TP
PR QT
Segments
Intervals
QRS
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2a. PQRSTU
PR ST
Segments
Intervals
PR ST TP
PR QT
QRS
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2a. Reading an ECG
1. Rate
2. Rhythm
3. Axis
4. Alphabet
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1. Rate: “Count-Off” Method
Start300
150100
7560 Normal Rate = 60-100 bpm
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2. Rhythm
Normally, the sinus node controls the entire heart
This is known as “Normal Sinus Rhythm” (NSR):- P wave axis is normal (0-90°)- Each P is followed by a QRS- Each QRS is preceded by a P
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3. QRS Axis
1. If QRS + in I AND II, QRS axis is normal2. If QRS not + in I AND II, you must
calculate QRS axis3. To do so, use leads I and aVF to identify
the 90°-quadrant4. Then use the isoelectric lead to quantify
QRS axis (to nearest 30°)
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4. Alphabet
P waves PR (segments and intervals) QRS (Qs, height, width) ST segments T waves QT interval
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Arrhythmia = Dysrhythmia
1. Slow
2. Fast
3. Normal rate
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2b. Bradydysrhythmias
1. Sinus Node Sinus brady, pause, arrest, block
2. “AV Node” 2° AVB (Type I and Type II) 3° AVB
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2b. AV Block
Nodal 1° AVB2° AVB I 3° AVB
Infra-Nodal 2° AVB II 3° AVB
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2b. AV Block
Nodal AVB is more benign because:- Causes are often functional (as opposed to
infranodal block which is almost always structural)
- If progression to CHB, nodal escapes available
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90F presents with fatigue:
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2c. Tachydysrhythmia
SVT NCTWCT
VT WCT
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2c. NCT
Regular Irregular
AVN-Indep AVN-Dep AF
ST AVNRT MAT
AFL AVRT AFL/AT +
AT variable block
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75F to ER with palpitations:
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25F to ER with palpitations:
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72M without symptoms:
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2c. Atrial Fibrillation: 2 Issues
Symptoms
Rate Control
(BB, CCB, dig)
vs
Rhythm Control
(e.g. amiodarone)
Stroke Risk (CHADS2)
CHF/LVEF <= 35% = 1
Hypertension = 1
Age > 75 = 1
Diabetes = 1
Stroke (embolic) = 2
2 = OAC1 = ASA or OAC0 = ASA
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2c. WCT
VT
AV Dissociation
Fusion/Capture Beats
Bizarre QRS Axis
Wide QRS
QRS Concordance
DDX
SVT + Aberrancy Accessory Pathway Pacemaker Bundle Branch Block Metabolic
derangement
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66M prior MI with palpitations:
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2c. Torsades de Pointes
Polymorphic VT due to a long QTc (often with a characteristic appearance)
Causes: Congenital Acquired
1. Electrolyte disturbances (Hypo K, Ca, Mg)2. Drugs (antipsychotics, antidepressants, antibiotics,
antiarrhythmics)3. Other
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3. Syncope
PumpObstructionArrhythmia
FluidHypovolemia
PipesSubclavian StealVBIMigraine
NeurocardiogenicCSHVasovagalSituational
Questions?