Back To Basics: Cardiology Review I Michael Froeschl, MD FRCPC Assistant Professor of Medicine.

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Back To Basics: Cardiology Review I Michael Froeschl, MD FRCPC Assistant Professor of Medicine

Transcript of Back To Basics: Cardiology Review I Michael Froeschl, MD FRCPC Assistant Professor of Medicine.

Page 1: Back To Basics: Cardiology Review I Michael Froeschl, MD FRCPC Assistant Professor of Medicine.

Back To Basics:

Cardiology Review I

Michael Froeschl, MD FRCPC

Assistant Professor of Medicine

Page 2: 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

Page 3: Back To Basics: Cardiology Review I Michael Froeschl, MD FRCPC Assistant Professor of Medicine.

NB: Key Feature Questions

Learn how to answer them!

Page 4: Back To Basics: Cardiology Review I Michael Froeschl, MD FRCPC Assistant Professor of Medicine.

F R O E S C H L

1. Two Concepts

1. Ischemia: Tissue oxygen demand exceeds tissue oxygen supply

2. Infarction: Tissue necrosis secondary to tissue ischemia

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F R O E S C H L

1. Supply-Demand Mismatch

↓ Supply

Coronary obstruction Microvascular

obstruction ↓ Perfusion pressure ↓ PaO2 ↓ Hemoglobin

↑ Demand

↑ Heart Rate ↑ Contractility ↑ Wall Tension

Page 6: Back To Basics: Cardiology Review I Michael Froeschl, MD FRCPC Assistant Professor of Medicine.

F R O E S C H L

1. CAD

Obstructive CAD

ACS

Atherosclerosis

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F R O E S C H L

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

Page 10: Back To Basics: Cardiology Review I Michael Froeschl, MD FRCPC Assistant Professor of Medicine.

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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

Page 37: Back To Basics: Cardiology Review I Michael Froeschl, MD FRCPC Assistant Professor of Medicine.

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2a. Electrical Anatomy

Three phases of ventricular depolarization:

1. Septum LR(atrial repolarization

occurs simultaneously)

Page 38: Back To Basics: Cardiology Review I Michael Froeschl, MD FRCPC Assistant Professor of Medicine.

F R O E S C H L

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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F R O E S C H L

2a. The 12-Lead ECG

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2a. PQRSTU

PR ST TP

PR QT

Segments

Intervals

QRS

Page 42: Back To Basics: Cardiology Review I Michael Froeschl, MD FRCPC Assistant Professor of Medicine.

F R O E S C H L

2a. PQRSTU

PR ST

Segments

Intervals

PR ST TP

PR QT

QRS

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F R O E S C H L

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

Page 45: Back To Basics: Cardiology Review I Michael Froeschl, MD FRCPC Assistant Professor of Medicine.

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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°)

Page 47: Back To Basics: Cardiology Review I Michael Froeschl, MD FRCPC Assistant Professor of Medicine.

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4. Alphabet

P waves PR (segments and intervals) QRS (Qs, height, width) ST segments T waves QT interval

Page 48: Back To Basics: Cardiology Review I Michael Froeschl, MD FRCPC Assistant Professor of Medicine.

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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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F R O E S C H L

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

Page 59: Back To Basics: Cardiology Review I Michael Froeschl, MD FRCPC Assistant Professor of Medicine.

F R O E S C H L

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

Page 60: Back To Basics: Cardiology Review I Michael Froeschl, MD FRCPC Assistant Professor of Medicine.

F R O E S C H L

66M prior MI with palpitations:

Page 61: Back To Basics: Cardiology Review I Michael Froeschl, MD FRCPC Assistant Professor of Medicine.

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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

Page 62: Back To Basics: Cardiology Review I Michael Froeschl, MD FRCPC Assistant Professor of Medicine.

F R O E S C H L

3. Syncope

PumpObstructionArrhythmia

FluidHypovolemia

PipesSubclavian StealVBIMigraine

NeurocardiogenicCSHVasovagalSituational

Page 63: Back To Basics: Cardiology Review I Michael Froeschl, MD FRCPC Assistant Professor of Medicine.

Questions?