Cardiology - Part 1

Front 1

Which coronary artery supplies the SA node?

Back 1

The sinoatrial node is supplied by the SA nodal artery, which may arise from the RCA (60%) or LCA (40%)

Front 2

Describe dominance of circulation

Back 2

The artery that supplies the posterior interventricular artery determines coronary dominance.
Right-dominant circulation: PIV and at least one posterolateral branch arise from RCA (80%)
Left-dominant circulation: PIV and at least one posterolateral branch arise from LCx (15%)
balanced circulation (5%)

Front 3

Where does venus blood from the heart drain?

Back 3

Most venous blood from the heart drains into the RA

Front 4

Layers of the heart

Back 4

endocardium
myocardium
epicardium (visceral pericardium)
pericardial space
parietal pericardium

Front 5

What is the main difference between semilunar valves and atrioventricular valves?

Back 5

Semilunar valves have no subvalvular apparatus
Atrioventricular valves have chordae tendinae and papillary muscles

Front 6

Describe the pathway that impulses travel through the conduction system of the heart?

Back 6

SA node -> AV node -> bundle of his -> LBB/RBB -> purkinje fibres

Front 7

How are impulses carried from the right atrium to the left atrium?

Back 7

Bachmann's bundle

Front 8

Describe effect of sympathetic nerves on the cardiovascular system

Back 8

Innervate SA node, AV node, ventricular myocardium, and vasculature
-SA node fibers (beta-1) increase HR
-Cardiac muscle fibers (beta-1) increase inotropy and cardiac output
-Stimulate of beta1 and beta2 receptors in vasculature causes vasodilation

Front 9

What is the normal interval for P wave, PR, QRS, and QT

Back 9

P - 0.12
PR - 0.12-0.2
QRS - < 0.12
QT - <0.46 or 1/2 R-R

Front 10

What does 1 small square and 1 large square represent on an ECG

Back 10

1 mm (1 small square) = 40 msec
5 mm (1 large square) = 200 msec

Front 11

What features are necessary for normal sinus rhythm

Back 11

P wave precedes each QRS; QRS follows each P wave
P wave axis is normal (positive in leads I, and aVF)
Rate between 60-100

Front 12

What makes a normal axis on ECG

Back 12

-30 to 90 degrees (i.e. positive QRS in leads I and aVF)

Front 13

Criteria for left ventricular hypertrophy on ECG

Back 13

S in V1 + R in V5 or V6 > 35 mm
R in aVL > 11 mm

Front 14

Criteria for right ventricular hypertrophy on ECG

Back 14

right axis deviation
R/S ratio > 1 in lead V1

Front 15

Criteria for left atrial enlargement on ECG

Back 15

Biphasic P wave with negative terminal component of the P wave in lead V1
P wave > 120 msec, notched in lead II

Front 16

Criteria for right atrial enlargement on ECG

Back 16

P wave > 2.5 mm in height in leads II, III, or aVF

Front 17

Describe the typical sequential changes of evolving MI

Back 17

1st - hyperacute T waves
2nd - ST elevation in the leads facing the infarcted area (usually 3-5 hours)
3rd - significant Q waves (> 40 msec or > 1/3 of QRS) (hours to days post infarct)
4th - inverted T waves (1 day to weeks)

Front 18

What defines significant ECG changes for STEMI

Back 18

J point = the junction between the QRS complex and the ST segment
Need ST elevation at least 1 mm in 2 adjacent limb leads or at least 1-2 mm in adjacent precordial leads

Front 19

DDx for ST elevation

Back 19

Acute STEMI, ventricular aneurysm, LBBB, acute pericarditis, Vasospastic (prinzmetal's) angina

Front 20

ECG changes in hyper and hypokalemia

Back 20

hyperkalemia - tall peaked T waves, loss of P waves and widening of QRS, sine wave pattern
hypokalemia - ST segment depression, prolonged QT, U waves

Front 21

ECG changes in hyper and hypocalcemia

Back 21

hypercalcemia - shortened QT interval
hypocalcemia - prolonged QT interval

Front 22

ECG changes in pericarditis

Back 22

Early - diffuse ST segment elevation +/- PR segment depression, upright T waves
Late - Isoelectric ST segment, flat or inverted T waves

Front 23

ECG changes in massive PE

Back 23

Sinus tachycardia and AF/atrial flutter most common
RAD, RVH with strain - most specific sign is S1Q3T3 (S in I, Q and inverted T wave in III)

Front 24

Troponin I and troponin T peak? Duration elevated? DDx of elevation

Back 24

Peak 1-2 days. Elevated up to 2 weeks.
DDx - MI, CHF, AF, acute PE, myocarditis, chronic renal insufficiency, sepsis, hypovolemia

Front 25

DDx for sinus bradycardia

Back 25

Increased vagal tone or vagal stimulation
Vomiting
Myocardial ischemia or infarction
Sick sinus syndrome
Increased ICP
Hypothyroidism
Drugs (beta-blocker, CCB)

Front 26

What is a first degree AV block

Back 26

Prolonged PR interval (>200 msec)

Front 27

What is a second degree AV block

Back 27

Some of the atrial impulses are not conducted to the ventricles
Type I - gradual prolongation of the PR interval precedes the failure of conduction of a P wave (Wenckebach). AV block is usually in the AV node.
Type II - PR interval is constant; there is an abrupt failure of conduction of a P wave. AV block usually distal to the AV node

Front 28

Which AV blocks require permanent pacing

Back 28

second degree type II AV block is an indication for permanent pacing due to increased risk of high grade or third degree AV block

Front 29

What is a third degree AV block

Back 29

Complete failure of conduction of the supraventricular impulses to the ventricles. Ventricular depolarization initiated by an escape pacemaker distal to the block. No relationship between P waves and QRS ("P waves marching through")

Front 30

DDx of sinus tachycardia

Back 30

Fever, hypotension, hypovolemia, anemia, thyrotoxicosis, CHF, MI, shock, PE, etc.

Front 31

What is atrial flutter? What causes it?

Back 31

Rapid, regular atrial depolarization from a macro re-entry circuit within the atrium (most commonly right atrium).
Atrial rate 250-350 bpm.
AV block usually occurs; it can be fixed or variable.

Front 32

Treatment of atrial flutter

Back 32

Acute: if unstable (eg. hypotension, CHF, angina) use electrocardioversion.
If stable use rate control: beta-blocker, diltiazem, verapamil or digoxin or chemical cardioversion: amiodarone, type I antiarrythmics

Front 33

Symptoms of atrial fibrillation

Back 33

Palpitations, fatigue, syncope, and may precipitate or worse heart failure

Front 34

What causes atrial fibrillation?

Back 34

Single circuit re-entry and/or ectopic foci act as aberrant generators producing atrial tachycardia

Front 35

What is the CHADS2 score used for?

Back 35

CHADS2 predicts risk of stroke in non-valvular atrial fibrillation by looking at risk factors.

Front 36

Whats are the components of the CHADS2 score?

Back 36

Congestive heart failure (1)
Hypertension (1)
Age > 75 (1)
Diabetes (1)
Stroke/TIA prior (2)

Front 37

Appearance of atrial fibrillation on ECG

Back 37

No organized P waves due to rapid atrial activity
Irregularly irregular ventricular response and narrow QRS

Front 38

Describe the management of atrial fibrillation

Back 38

RACE
Rate control - beta-blockers, ditiazem, verapamil
Anti-coagulation - ASA, warfarin, dibigitran (depending on risk via CHADS2 score)
Cardioversion (electrical) - if AF > 24h require anticoagulation first
Etiology - treat underlying cause

Front 39

What is the treatment of AV nodal re-entrant tachycardia?

Back 39

Acute: valsalva or carotid massage, adenosine is first choice if unresponsive to vagal maneuvers
Long term: beta-blocker, diltiazem, digoxin

Front 40

What is carotid massage?

Back 40

Carotid massage is actually a constant pressure directed posteriorly against the carotid artery for 5-10 seconds. Always listen for bruits before palpation.

Front 41

Define pre-excitation syndromes

Back 41

Referes to a subset of supraventricular tachycardias, mediated by an accessory pathway, which can lead to ventricular pre-excitation

Front 42

Describe Wolff-Parkinson-White Syndrome

Back 42

Congenital defect where an accessory conduction tract (bundle of kent; can be right or left atrium) abnormally allows early electrical activation of part of one ventricle. Impulses travel at a greater conduction velocity across the bundle of kent thereby effectively bypassing AV node.

Front 43

Appearance of Wolff-Parkinson-White syndrome on ECG

Back 43

PR interval <120
"delta wave" - slurred upstroke of the QRS (fusion of bundle of kent and normal pathway)
Widening of QRS complex

Front 44

Which drugs should be avoided in Wolff-Parkinson-White syndrome

Back 44

Drugs that slow AV node conduction (digoxin, beta-blockers) should be avoided as this may cause preferential conduction through the bypass tract and then precipitate VF.

Front 45

Clinical clues to differentiate between VT and SVT

Back 45

History of CAD and previous MI - more likely VT
Variable S1 - more likely VT
Carotid sinus massage/adenosine terminates arrhythmia - more likely SVT

Front 46

ECG clues to differentiate between VT and SVT

Back 46

AV dissociation - VT
QRS width > 140 msec - VT
Extreme axis deviation - VT

Front 47

Describe torsades de pointes

Back 47

A variant of polymorphic VT that occurs in patients with baseline QT prolongation. Looks like a sine wave.

Front 48

Etiology of torsades de pointes

Back 48

Congenital long QT syndrome
Drugs - class IA and class III
Electrolyte disturbance - hypokalemia, hypomagnesemia

Front 49

Treatment of torsades de pointes

Back 49

IV magnesium, temporary pacing, isoproterenol and correct underlying cause of prolonged QT, electrical cardioversion

Front 50

What are the most important pathogenetic mechanisms in ischemic heart disease?

Back 50

Atherosclerosis and thrombosis

Front 51

Describe the pathophysiology of atherosclerosis

Back 51

Endothelial injury from htn, DM, smoking, dyslipidemia, RA
Monocyte recruitment, enhanced LDL permeability
Monocytes enter into initial space and differentiate into macrophages - LDL is converted to oxidized LDL
Macrophages uptake OX-LDL to become foam cells
Fibrous cap on plaque forms

Front 52

Describe the Canadian Cardiovascular Society (CCS) classification of Angina

Back 52

Class I - Angina with strenuous, rapid or prolonged activity
Class II - Angina brought at > 2 blocks or > 1 flight of stairs
Class III - < 2 blocks, < 1 flight of stairs
Class IV - inability to carry out any physical activity without discomfort. Angina may be present at rest.

Front 53

Define chronic stable angina

Back 53

Symptom complex that results from an imbalance between oxygen supply and demand in the myocardium

Front 54

Factors that decrease myocardial oxygen supply

Back 54

Decreased luminal diameter: atherosclerosis, vasospasm
Decrease duration of diastole: tachycardia
Decreased hemoglobin: anemia
Decreased SaO2 hypoxemia
congenital anomalies

Front 55

Factors that increase myocardial oxygen demand

Back 55

Increased heart rate
Increased contractility
Increased wall stress: myocardial hypertrophy, aortic stenosis

Front 56

What are the 3 major precipitants of unstable angina

Back 56

3 E's: Exertion, emotion, eating

Front 57

Typical signs and symptoms of unstable angina

Back 57

Retrosternal chest pain, tightness, or discomfort radiating to left (+/- right) shoulder/arm/neck/jaw, associated with diaphoresis, nausea, anxiety

Front 58

Define Levine's sign

Back 58

Clutching fist over sternum when describing chest pain

Front 59

Which drugs should beta-blockers not be combined with

Back 59

Verapamil/diltiazem combined with beta-blockers may cause symptomatic sinus bradycardia or AV block

Front 60

What is the effect of beta-blockers and CCB in treatment of chronic stable angina

Back 60

Increase coronary perfusion and decrease demand (HR, contractility) and BP (afterload)

Front 61

Define variant (Prinzemtal's angina)

Back 61

Myocardial ischemia secondary to coronary artery vasospasm, with or without atherosclerosis
Uncommonly associated with infarction or LV dysfunction
Typically ST elevation on ECG
Treat with nitrates and CCB

Front 62

What are the most compelling features that increase likelihood of MI

Back 62

ST segment elevation
New Q wave
Chest pain radiating to both right and left arm simultaneously
Presence of S3
Hypotension

Front 63

What are the most compelling features that decrease likelihood of MI

Back 63

Normal ECG
Pleuritic chest pain
Pain reproduced on palpation
Sharp or stabbing chest pain
Positional chest pain

Front 64

Define acute coronary syndrome

Back 64

ACS includes the spectrum of unstable angina, NSTEMI, and STEMI

Front 65

What percent of MI's are unrecognized or "silent"? Which patients is this most common in?

Back 65

30% of MI's are "silent" due to atypical symptoms. This is more common in women, DM, elderly, post heart transplant.

Front 66

What investigations should be ordered in acute coronary syndrome

Back 66

ECG
CXR
Troponin/CK
CBC, INR/PTT, lytes and magnesium, creatinine, urea, glucose, serum lipids

Front 67

Treatment of NSTEMI

Back 67

BEMOAN
beta-blocker
enoxaparin
morphine
oxygen
ASA
Nitrates

Front 68

How is NSTEMI clinically defined

Back 68

Presence of 2 of 3 criteria:
Symptoms of angina/ischemia
Rise and fall of serum biomarkers of myocardial necrosis
Evolution of ischemic ECG changes (without ST elevation or new LBBB)

Front 69

Define STEMI

Back 69

Syndrome of acute plaque rupture and thrombosis with total coronary occlusion resulting in myocardial necrosis

Front 70

Describe the role of anti-platelet and anticoagulation therapy in management of NSTEMI

Back 70

ASA 162-325 mg
Clopidogrel 300 mg loading dose, then 75 mg QD in addition to ASA.
Subcutaneous LMWH unless renal failure then use IV unfractionated heparin

Front 71

What anti-platelet and anticoagulation drugs should be given in a STEMI if PCI is planned

Back 71

ASA 162-325 mg
clopidogrel 300 mg loading dose and IV GP IIb/IIIa inhibitor + unfractionated heparin during procedure

Front 72

What anti-platelet and anticoagulation drugs should be given in a STEMI if thrombolysis is planned

Back 72

ASA 162-325 mg
LMWH (enoxaprin) until discharge from hospital; can use unfractionated heparin as alternative because of possible rescue PCI

Front 73

What anti-platelet and anticoagulation drugs should be given in a STEMI if no reperfusion therapy is planned

Back 73

ASA 162-325 mg chewed
LMWH (enoxaprin) until discharge

Front 74

What can be used if beta-blockers are contraindicated or if beta-blockers/nitrates fail to relieve ischemia in ACS

Back 74

Non-dihydropyridine calcium channel blockers (e.g. diltiazem, verapamil)

Front 75

Which patients with acute coronary syndrome is thrombolysis not administered in?

Back 75

Thrombolysis is NOT administered for unstable angina and NSTEMI.
Only for STEMI.

Front 76

What are the absolute contraindications to thrombolysis in STEMI

Back 76

Prior intracranial hemorrhage
Known structural cerebral vascular lesion
Known malignant intracranial neoplasm
Significant closed head or facial trauma (<3 months)
Ischemic stroke (<3 months)
Active bleeding
Suspected aortic dissection

Front 77

What are the relative contraindications to thrombolysis in STEMI

Back 77

Uncontrolled HTN sBP >180, dBP >110
Current anticoagulation
Ischemic stroke > 3 months
Noncompressible vascular punctures

Front 78

When is thrombolysis preferred to PCI in STEMI

Back 78

Onset of pain < 3 hours, catheter team not available in < 1 hour, and no contraindications to thrombolysis

Front 79

When would medical management be used for STEMI (no reperfusion therapy)

Back 79

Onset of pain > 12 hours and patient stable

Front 80

Describe long term management post ACS

Back 80

1. Anti-platelet and anti-coagulation therapy - ASA 81 mg, clopidogrel 75 mg QD (at least one month, 12 months if stent placed)
2. beta-blockers - metoprolol 25-50 mg bid or atenolol 50-100 mg QD. Use CCB if BB contraindicated.
3. Nitrates - symptom relief but do not improve outcome
4. ACEi - if diabetic, CHF, LVEF < 40%, and anterior MI
5. Statins - irrespective of cholesterol level - atorvastatin 80 mg QD
6.

Front 81

Which ACS patients should not receive nitrates?

Back 81

Right-sided MI patients who have become preload dependant.

Front 82

Complications of MI

Back 82

CRASH PAD
Cardiac Rupture
Arrhythmia
Shock
Hypertension/Heart failure
Pericarditis/Pulmonary Emboli
Aneurysm
DVT