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Cardiology

Cardiology

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CARDIOLOGY
Dr. A. WooStephen Juvet, Daniel Kreichman and Manish Sood, chapter editorsKatherine Zukotynski, associate editor 
BASIC CLINICAL CARDIOLOGY EXAM
 . . . . . .
2
Cardiac HistoryFunctional Classification of Cardiovascular DisabilityCardiac Examination
CARDIAC DIAGNOSTIC TESTS
. . . . . . . . . . . . .
6
ECG Interpretation - The BasicsHypertrophy and Chamber EnlargementIschemia/InfarctionMiscellaneous ECG Changes Ambulatory ECG (Holter Monitor)Echocardiography (2-D ECHO)Coronary AngiographyCardiac Stress Tests and Nuclear CardiologyTests of Left Ventricular (LV)Function
 ARRHYTHMIAS
 . . . . . . . . . . . . . . . . . . . . . . . . . . .
12
Mechanisms of Arrhythmias Altered Impulse Formation Altered Impulse ConductionOther Etiologic FactorsClinical Approach to Arrhythmias BradyarrhythmiasConduction DelaysTachyarrhythmiasSupraventricular Tachyarrhythmias (SVT’s)Ventricular Tachyarrhythmias (VT’s)Pre-excitation SyndromesPacemaker IndicationsPacing Techniques
ISCHEMIC HEART DISEASE
 . . . . . . . . . . . . . . . .
19
Background Angina Pectoris Acute Coronary SyndromesUnstable Angina/Non ST Elevation Myocardial Infarction (MI) Acute ST Elevation MISudden Death
HEART FAILURE
 . . . . . . . . . . . . . . . . . . . . . . . . . .
27
Compensatory ResponsesSystolic vs. Diastolic DysfunctionSleep-Disordered BreathingHigh-Output Heart Failure Acute Cardiogenic Pulmonary EdemaCardiac Transplantation
MCCQE 2002 Review NotesCardiology C1
CARDIOMYOPATHIES
 . . . . . . . . . . . . . . . . . . . . .
32
Dilated Cardiomyopathy (DCM)Hypertrophic Cardiomyopathy (HCM)Restrictive Cardiomyopathy (RCM)Myocarditis
 VALVULAR HEART DISEASE
 . . . . . . . . . . . . . . .
36
Infective Endocarditis (IE)Rheumatic Fever  Aortic Stenosis (AS) Aortic Regurgitation (AR)Mitral Stenosis (MS)Mitral Regurgitation (MR)Mitral Valve ProlapseTricuspid Valve DiseasePulmonary Valve DiseaseProsthetic Valves
PERICARDIAL DISEASE
 . . . . . . . . . . . . . . . . . . .
45
 Acute PericarditisPericardial EffusionCardiac TamponadeConstrictive Pericarditis
SYNCOPE
 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
47EVIDENCE-BASED CARDIOLOGY 
 . . . . . . . . . . .
48
Congestive Heart Failure (CHF)Ischemic Heart Disease (IHD) Atrial Fibrillation (A fib)
COMMONLY USED CARDIAC
 . . . . . . . . . . . . . . .
49MEDICATIONS
ß-blockersCalcium Channel Blockers (CCB) Angiotensin Converting Enzyme (ACE) Inhibitors Angiotensin II BlockersDiureticsNitrates Anti-Arrhythmic Anti-Platelet
REFERENCES
 . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
52
 
C2Cardiology MCCQE 2002 Review Notes
BASIC CLINICAL CARDIAC EXAM
CARDIAC HISTORY 
coronary artery disease: chest pain (CP) (location, radiation, duration, intensity, activities associated with onset; alleviating factors (associated with rest, NTG)
heart failure: fatigue, presyncopeleft-sided symptoms: decreased exercise tolerance, shortness of breath on extertion (SOBOE)/chest pain on exertion (CPOE)right-sided symptoms: paroxysmal nocturnal dyspnea (PND)/orthopnea, SOB at rest, ascites,
 Arrhythmia: presyncopal/syncopal episodes, palpitations
Baseline function: exercise tolerance (# flights of stairs/blocks), need for nitroglycerin (NTG), symptoms during low impact activities/daily activities (combing hair, showering) or at rest
FUNCTIONAL CLASSIFICATION OF CARDIOVASCULAR DISABILITY 
Table 1. Canadian Cardiovascular Society (CCS) Functional Classification
ClassFunctionI
ordinary physical activity does not cause angina; angina only with strenuous or prolonged activity
II
slight limitation of physical activity; angina brought on at > 2 blocks on level (and/or by emotional stress)
III
marked limitation of physical activity; angina brought on at
2 blocks on level
IV 
inability to carry out any physical activity without discomfort; angina may be present at rest
Table 2. New York Heart Association (NYHA) Functional Classification
ClassFunctionI
ordinary physical activity does not evoke symptoms (fatigue, palpitation, dyspnea, or angina)
II
slight limitation of physical activity; comfortable at rest; ordinary physical activity results in symptoms
III
marked limitation of physical activity; less than ordinary physical activity results in symptoms
IV 
inability to carry out any physical activity without discomfort; symptoms may be present at rest
CARDIAC EXAMINATION
General Examination
Skin – peripheral vs. central cyanosis, clubbing, splinter hemorrhages, Osler’s nodes, Janeway lesionsbrownish-coloured skin – hemochromatosis
Eyes – conjunctival hemorrhages, Roth spots, emboli, copperwire lesions, soft/hard exudates
Blood Pressure (BP)
should be taken in both arms with the patient supine and upright
be wary of calcification of the radial artery in the elderly as it may factitiously elevate BP (Osler’s sign)
orthostatic hypotension - postural drop > 20 mm Hg systolic or > 10 mm Hg diastolicincreased HR > 30 bpm (most sensitive - implies inadequate circulating volume)patient unable to stand - specific sign for significant volume depletion
pulse pressure(PP) (PP = systolic BP (SBP) - diastolic PB (DBP))wide PP: increased cardiac output (CO) (anxiety, exercise, fever, thyrotoxicosis, AR, HTN),decreased total peripheral resistance (TPR) (anaphylaxis, liver cirrhosis, nephrotic syndrome, AVM)narrow PP: decreased CO (CHF, shock, hypovolemia, acute MI, hypothyroidism, cardiomyopathy),increased TPR (shock, hypovolemia), valvular disease (AS, MS, MR), aortic disease (e.g. coarctation of aorta)
pulsus paradoxus (inspiratory drop in SBP > 10 mmHg ): cardiac tamponade, constrictive pericarditis, airway obstruction, superior vena cava (SVC) obstruction, COPD (asthma, emphysema)
The Arterial Pulse
remark onrate, rhythm, volume/amplitude, contouamplitude and contour best appreciated in carotid arteries
pulsus alternans - beat-to-beat alteration in PP amplitude with cyclic dip in systolic BP; due to alternating LV contractile force (severe LV dysfunction)
pulsus parvus et tardus – slow uprising of the carotid upstroke due to severe aortic stenosis (AS)
pulsus bisferiens – a double waveform due to AS + AR combined
spike and dome pulse – double carotid impulse due to hypertrophic obstructive cardiomyopathy (HOCM)
 
MCCQE 2002 Review NotesCardiology C3
BASIC CLINICAL CARDIAC EXAM
. . . CONT.
Precordial Inspection
observe for apex beat, heaves, lifts
PrecordialPalpation
apex - most lateral impulse
PMI - point of maximal intensity
location: normal at 5th intraclavicular space (ICS) at midclavicular line (
10 cm from midline), lateral/inferior displaced in dilated cardiomyopathy (DCS)
size : normal is 2-3 cm in diameter, diffuse > 3 cm
duration: normal is <1/2 systole (duration > 2/3 systole is considered sustained)
amplitude (exaggerated, brief - AR, MR, L to R shunt)
morphology (may have double/triple impulse in HOCM)
abnormal impulsespalpable heart sounds (e.g. S1 in MS, P2 = pulmonary artery (PA) pulsation, S3, S4)left parasternal lift (right ventricular enlargement (RVE), left atrial enlargement (LAE) , severe left ventricular hypertrophy (LVH))epigastric pulsation (RVH especially in COPD)thrills (tactile equivalents of murmurs) over each valvular area
Clinical Pearl
Left parasternal lift - DDx - RVH (with pulmonary hypertension (HTN), LAE (secondary to severe MR), severe LVH, rarely thoracic aortic aneurysm. Auscultation - Heart Sounds
S
1
composed of audible mitral (M1) and tricuspid (T1) componentsmay be split in the normal young patient
if S
1
is loudshort PR intervalhigh left atrial (LA) pressure (e.g. early MS)high output states or tachycardia (diastole shortened)
if S
1
is softfirst degree AV block calcified mitral valve (MV) (e.g. late MS)high LV diastolic pressures (e.g. CHF, severe AR)occasionally in MR
if S
1
varies in volumeAV dissociation (complete AV block, ventricular tachycardia (VT))AFib
S
2
normally has 2 components on inspiration: A
2
and P
2
normal splitting of S2 (A2 < P2) should vary with respiration
Exp.Insp.
S
2
 A
2
P
2
normal • increased venous return to right side of heart with inspiration results in delayed closure of pulmonary valve (PV) (widens split) A
2
P
2
 A
2
P
2
 wide fixed splitting• atrial septal defect (ASD)S
2
 A
2
P
2
 widened splitting (delayed RV or early LV emptying)• right bundle branch block (RBBB), pulmonary HTN, MR, ventricular septal defect (VSD)P
2
 A
2
S
2
paradoxical splitting (delayed LV or early RV emptying)• left bundle branch block (LBBB), tight AS, systemic HTN, LV fib, paced rhythm, tricuspid regurgitation (TR), Wolfe Parkinson White (WPW)
soft S
2
aortic (A
2
) or pulomonic (P
2
) stenosis
loud S
2
systemic (A
2
) or pulmonary HTN (P
2
)
soft heart soundslow cardiac outputobesityemphysemapericardial effusion ("muffled" = tamponade)
S3 (see Figure 1): volume overloaded ventricleoccurs during period of rapid ventricular fillinglow frequency - best heard with bell at apexcausesmay be normal in children and young adults (age < 30)LV failure (systolic dysfunction, acute MI)rapid ventricular filling (MR or high output states), RV S
3
(TR, MS, RV failure)DDx - split S
2
, opening snap, pericardial knock, tumour plop
S
4
(Figure 1): pressure overloaded ventricle (decreased capacitance, increased contribution of atrial kick to ejection fraction (EF))occurs during atrial contractionbest heard with bell at apexalways pathological (associated with diastolic dysfunction), ischemia (ventricular relaxation needs ATP),hypertrophy (HTN, AS, HCM), RCM, RV S
4
(pulmonary HTN, PS)DDx - split S
1
, ejection clicks, prolapse clicks

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