c Cardiology and Cardiovascular Surgery Mark Dam, Shiying Liu and Michael Ward. chapter editors Doreen Ezeife and Nigel Tan, associate editors Stnen Wong, EBM editor Dr. Chi-Ming Chow, Dr. Andrew Dueck and Dr. Anna Woo, staff editors With contributions from Dr. Young Kim

Basic Anatomy Review .. 2 Coronary Circulation Cardiac Anatomy

Differential Diagnoses of Common Presentations . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 Chest Pain Syncope Local Edema Generalized Edema Palpitations Dyspnea

Cardiac Diagnostic Tests .................. 5 Electrocardiography (ECG) Basics Approach to ECGs

Rate Rhythm Axis Intraventricular Conduction Abnormalities Hypertrophy and Chamber Enlargement Ischemia/! nfarction Miscellaneous ECG Changes

Other Cardiac Diagnostic Tests Cardiac Biomarkers Ambulatory ECG Echocardiography Stress Testing

Nuclear Cardiology Cardiac Catheterization and Angiography Contrast-Enhanced CT Coronary Angiography Magnetic Resonance Imaging (MRI)

CARDIAC DISEASE Arrhythmias ........................... 12 Mechanisms of Arrhythmias Bradyarrhythmias AV Conduction Blocks Supraventricular Tachyarrhythmias Pre-Excitation Syndromes Ventricular Tachyarrhythmias Electrophysiology (EPS) Studies Electrical Pacing Implantable Cardioverter Defibrillators (ICDs) Catheter Ablation

Ischemic Heart Disease (IHD) ............. 22 Chronic Stable Angina Acute Coronary Syndromes (ACS)

Unstable Angina (UA)/Non-ST Elevation Ml (NSTEMI) ST-Eievation Myocardial Infarction (STEMI)

Treatment Algorithm for Chest Pain Sudden Cardiac Death Coronary Revascularization

Percutaneous Coronary Intervention (PCI) Coronary Artery Bypass Graft (CABG) Surgery Off Pump Coronary Artery Bypass (OPCAB) Surgery

Toronto Notes 2011

Heart Failure. . . 32 Congestive Heart Failure (CHF) Sleep-Disordered Breathing

Cardiac Transplantation ................. 35 Ventricular Assist Devices (VADs)

Myocardial Disease ..................... 36 Myocarditis Dilated Cardiomyopathy (DCM) Hypertrophic Cardiomyopathy (HCM) Restrictive Cardiomyopathy (RCM)

Valvular Heart Disease .................. 40 Infective Endocarditis (IE) Rheumatic Fever Choice of Valve Prosthesis Summary of Valvular Disease

Pericardia! Disease ...................... 44 Acute Pericarditis Pericardia! Effusion Cardiac Tamponade Constrictive Pericarditis

VASCULAR DISEASE Peripheral Arterial Disease ............... 46 Acute Arterial Occlusion/Insufficiency Chronic Arterial Occlusion/Insufficiency

Hypertension .. FM35

Pulmonary Hypertension ............... R16

Carotid Artery Disease ................ NS21

Aortic Disease ......................... 48 Aortic Dissection Aortic Aneurysm

Peripheral Venous Disease .. 51 Deep Venous Thromboembolism Superficial Thrombophlebitis Varicose Veins Chronic Venous Insufficiency Lymphedema

Common Medications ................... 54

Landmark Cardiac Trials ................. 57

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59

Cardiology and CV Surgery Cl

C2 Cardiology and CV Surgery 1'oroDio 2011

Basic Anatomy Review Coronary Circulation

Dillltol8

conventional arterial supply to the heart arises from the right and left coronary arteries, originating from the root of the aorta (see Figure I)

right coronary artery (RCA) acute marginal branches atrioventricular (A V) nodal artery posterior Interventricular artery (PIV) = posterior descending artery (PD)

Left main coronary artery (LCA): two major branches left anterior descending artery (LAD)

- septal branches - diagonal branches

left drcumfleJ: artery (I.Cx) - obtuse marginal branches

dominance of drculatlon right-dominant circulation: PIV and at least one posterolateral branch arise from RCA (8096) Left-dominant circulation: PIV and at least one posterolateral branch arise from LCx (1596) balanced cin::ulation: dual supply ofposteroinferior LV from RCA and LCx (596)

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

most venous blood from the heart drains into the RA through the coronary a:lnns, although a small amount drains through Th.ebesian veins into all four chambers, contributing to the physiologic R-L shunt

Laft IDDI' dncending (LAD)

Aare 1. Anatomy of tile Coronary Arterl11 (llgld: alterlor oblque pro)ecGon)

I SVI!ol8 I

l '- --% .... ' \ .... 10 I 'u ., lA ('"LV- .,_- !Ill "'- MV-

D \ I. ,.,..

Legend: AV-IICirticiiM LA -kilt lllrn LV -left'llllllricle I I

Carotid Pul"

JVPWIWform Cardiae

so 40 R . _. =,_

llaat l > Soundl .

Q a 'A 0.8 lime(secl

Flg1re Za. Cardiac Cycle

PIN- milrlll valva

c Anll .... 211011

s, s,

QRS AblaJt I-Alii II A brillion Camoll-3ft! dep l'elltblodt tv_..: Tra.pd eii.Mbd JVP Card II: r....-: xdlant anly, llbsarty dMclnt

ECG

l'rl!rrirrtyd8Qrt. runn.urs 1191

Flgere 2b. Canllac Cycle. JVP Pulle and Cai'GIId Pllsa

'IbroDlo Nota 2011 Buic Anatomy Review

Cardiac Anatomy layen of the heart

endocardium myocardium epicardium =visceral pericardium pericardia! space parietal pericardium

"Y&lves tricuspid valve (TV): separate.. RA and RY pubrulDic valve (PV): separates RY and pulmonary artery (PA) mitral valve (MV): separates LA and LV aortic valve (AV): separates LV and ucending aorta

oonchu:tion aydem impulses travel from: SA AV bundle: of His LBB/RBB -+ Purkinje fibres SA node governs pacemaking control anterior-, middle- and posterior-internal nodal tracts carry impulses in the right atrium and

along Ba.chmann's bundle In the left atrium atrial impulses converge at the AV node

the AV node is the only conducting tract from the atria to the ventricles because of electrical isolation by the annulus fibrosis (except when accessory pathways are present)

the bundle of His bifurcates into left and right bundle bl'llllCbes (LBB and RBB) LBB further splits into anterior and posterior fascicles RBB and fasdclt:s ofLBB give o1fPurkinje fibres which conduct impulses into the ventricular

myocardium canllovascular lnncmdio.n

lfiiiP8thet:lc nerves innervate the sinoatrial node (SAN), atroventricular node (AVN), ventricular

myocardium and vasculature SAN (pl) fibres increase pacemaking activity (chronotropy) cardiac muscle fibres increase contractllity (inotropy) to help increase cardiac output stimulation of IH- and IJ2-receptora in the W:1.etal and coronary c.ln:ulation causes

vasodllatation parasympathetic nenes

Innervate the SAN, AVN, atrial myocardium but few vascular beds basal vagal tone dominates the tonic sympathetic stimulation of the SAN and AVN

resulting in slowing of pacemaking activity and condw:tion (ie. reduced chronotropy and drmnotropy)

parasympathetic& have very little impact on total peripheral vascular resistance

- Middle 1rlct

- Posteriorlrlle:t

Figun 3. Conduction Systam of the Heart

lknlla aiHII

Cl Ytulg M. IGm 2010

Cardiology and CV SUJ'8ery C3

C4 Cardiology and CV Surgery Differential Diagnose5 of Common Presentations Toronto Notes 2011

Differential Diagnoses of Common Presentations Note: bold text indicates most common, underlined text indicates life threatening

Chest Pain Pulmonary

pneumonia pulmonary embolism (PEl pneumothorax/hemothorax, tension pneumothorax empyema pulmonary neoplasm bronchiectasis TB

Cardiac Ml/angina myocarditis pericarditis/Dressier's syndrome cardiac tamJonade

Gastrointestin esophageal: spasm, GERD, esophagitis, ulceration,

achalasia, neoplasm, Mallory-Weiss syndrome PUD gastritis pancreatitis biliary colic

Mediastinal lymphoma thymoma

Vascular dissecting aortic aneurysm

Surface structures costochondritis rib fracture skin (bruising, shingles) breast

Syncope Hypovolemia Cardiac

structural or obstructive causes myocardial disease (e.g. acute coronary syndrome) aortic stenosis hypertrophic cardiomyopathy (HCM) cardiac tamponade/constrictivt: pericarditis

arrhythmias (sc:c: arrhythmia section) Respiratory

massiyePE pulmonary hypertension hypoxia hypercapnia

Neuio1ogic stroke/TIA (esp. vt:rtebrobasilar insufficiency) migraine seizure vuovagal

Metabolic anemia hypoglycemia

Drugs antihypertensives antiarrhythmics beta-blockers, CCBs

Psychiatric panic attack

Local Edema Inflammation/infection Venous or lymphatic obstruction

thrombophlebitis/deep vein thrombosis chronic lymphangitis venous insufficiency filariasis

Generalized Edema Increased hydrostatic pressure

increased fluid retention cardiac causes e.g. CHF hepatic causes e.g. cirrhosis renal causes e.g. acute and chronic renal failure

vasodilators (especiallyCCBs) refeeding edema

Decreased oncotic pressure hypoalbuminemia

Hormonal hypothyroidism exogenous steroids pregnancy estrogens

Palpitations Cardiac

arrhythmias (PAC, PVC, SVT, VT) mitral valve prolapse valvular heart disease J:m>ertrophic obstructive cardiomyqpatby

Endocrine thyrotoxicosis pheochromocytoma hypoglycemia

Systemic fever anemia

Drugs tobacco, caffeine, alcohol, epinephrine, ephedrine,

aminophylline, atropine Psychiatric

panic attack

Dyspnea Cardiovascular

acuteMI CHF/LV failure aortic stenosis/mitral stenosis cardiac elevated p onary venous pressure

Respiratory airway disease

asthma COPD exacerbation upper airway obstruction (anaphylaxis, foreign body,

mucus plugging) parenchymal lung disease

ARDS pneumonia interstitial lung disease

pulmonary vascular disease pulmonary embolism pulmonary HTN pulmonary vasculitis

pleural disease pneumothorax

pleural effusion Neuromuscular and chest wall disorders

C-spine injury polymyositis, myasthenia gravis, Guillain-Barre syndrome kyphoscoliosis

Anxiety/psychosomatic Severeanemia

'IbroDlo Nota 2011 Cardiac Diagnostic Testl

Cardiac Diagnostic Tests Electrocardiography (ECG) Basics

the electrocardiogram (ECG) is a graphic representation of the electrical activity of the heart recorded from the surface of the body

on the ECG graph the horizontal axis represents time

1 mm. (I small square)= 40 msec 5 mm. (I large square) = 200 .l1lllec (at paper speed 25 mmlaec)

the vertical axis represents voltage 1 mm. (I small square) = 0.1 m V 10 mm. (2large squares)= 1 mV (at standard gain setting)

leads standard 12-leadECG

Umb leads: I. II, DI. a VI., aVR. aVF precordial leads: VI-V6 (VI-V2 septal, V3-V 4 anteriol; VS-V6lateral)

additional leads right-sided leads: V3R-V6R (useful in RV infarction and dmrocardia)

lateral = I, a VL, V5, V6; inferior = II, Til, a VF; &ontal = VI-V 4

Approach to ECGs Rate normal = 60-100 bpm (atrial mre: IS0-250 bpm = paroxsyma1 tachycardia, 250-350 bpm = atrial

flutter, >350 bpm = atrial fibrillation regular rhythm

to calculate the rate, divide 300 by number of large squares between 2 QRS complexes (there are 300 large squares in 1 minute: 300 x 200 maec = 60 sec)

or remember 300-150-100-75-60-5()....43 (rate falls in this sequence with the number of additional large squares between QRS)

irregu1a.r rhythm rate = 6 x number ofR-R intervals in 10 seconds (the '"rhythm strips" are 10 second

recordings) types: wandering pacemaker, multifocal atrial tachycardia. atrial fibrillation

atrial escape = 60-80 bpm; Junctional escape = 40-60 bpm; ventricular escape = 20-40 bpm Rhythm regular = R-R interval is the same aaoss the tracing irregular= R-R interval va.rl.es across the tradng

regularly-irregula.r = repeating pattern of varying R-R intervals irregularly irregular = R-R intervals vary erratically

normal sinus rl:rythm (NSR) P wave precedes each QRS; QRS follows each P wave P wave axis is normal (positive in leads I, a VF) rate between 60-100 bpm

Axis mean axis indicates the direction of the mean vector can be determined for any waveform (P, QRS, T) the standard ECG reported QRS axis usually refers to the mean axis of the frontal plane; it

indicates the mean direction of ventricular depolarization forces QRS axis in the horizontal plane is not routinely calculated; it Is directed posteriorly and to the

left the transition from negative to poaltive is usually In lead V3

QRS axis in the frontal plane (see Flgure 5) normal uis: -300 to 90" (i.e. posltive QRS in leads I and II) left axis deviation (LAD): axis 90

Cardiology and CV SUJ'8ery C5

O..nrillw flf DiatiDSiic r .... Cmilc IHrurllllra (T n. CK-MB)- in

-vmptullllllie IIBbl ECG-atrwt. wi11ulnl-. orin

-vmptullllllie IIBbl 811811. or with .... IIM:t.r illqi .. - wi1h lb8la tmilc clllleterizltiant CTA MIIAIM!I

Figura 4. ECG WHeferma 11d Nannll Values

111118 Cllculltianl Examples Practice

....

AJtnuh ta EC&I &IIIIIIIY Rail Rhythn Axis Conducti111 Clwmbar rRIII!IIII&ntfhypatrophy lschami.-'lnhuctian Milcelllneoua

Far mara 111d 'iisit

L8ft Ant. Hemiblack lnlllriorMI WPW RV Pacing N0111111IYariant BIMdlld llillplngm Llad Mispl-mant Endocardial CUIIian dafacl

RVH l..aftl'oat Hamibhx:k PE COPD t..1anll Ml WF'W Dllldracanlill Sapbll Dahn:1a

C6 Cardiology and CV Surgery

Figure 5. Axial Reference System Elldlilld conlliis I+) Bill dispid by 1hi!DI llmiWI. lirpJEstllllei"-J toward the plllitM ol1flllllll rlllllts in Ill upMtd dallection il thatilld. NonriiQRS IIliis is between -30'111d +90'.

Cardiac Diagnostic Teats Toronto Notes 2011

Intraventricular Conduction Abnormalities

Right Bu1dla BI'IIICh Block (RBBBJ Lift Bundl1 B111nch Block (LBBBJ CampiBIB RBBB Ca11platll LIBB QRS duration > 120 msec QRS dLnlion > 1 20 msec Positive ORS in lead V1 (rSR' or occasionally broad R wave] Broad S waves in leads I, VS-6 ( >40 msecl

Broad notched or slurred R waves in leads I, aVI.. and usually V5andV6

Usually secondll'fTWIIW inversion i'lleads V1-2 Deep broad S waves in leads V1-2 Secondlry ST-T changes (-vein leads with broad R WIIWS,

+vein V121 are usually present LBBB usually masks ECG signs Df myocardial inlan:tion

Left Anllriar Fudc:ullr Bloc:k (LAFBI LBft l'oltlriar F.c:ic:ullr Bloc:k (LPFBI Biflldc:ullr Bloc:k (Left Antcrill' Hemibloc:kl {Left Pauiar Hemibloc:kl Left axis deviation (-30" 1D -911"1

Small q and prominent R in leads I and aVL

Small r and prominent S in leads II. IlL and aVF

Right axis deviation ( 11 II" 1D 1811"1 Small r and prominant S i1

leads I and aVL Small q and prominent R in

leads 11,111, and aVF

RBBB pattern Small q and prominent R

The first 60 msec (1 .5 small squares] Dlthe ORS shows the pattern Dl LAFB or LPFB

Bilascicular block refers 1D impaired conduction in two of the three fascicles, most commonly a RBBB and left anterior hemiblock; the appearance on an ECG meets the criteria fur bDih types of blocks

Laft Bundla Right Bundle Lift Ventricular Right Ventricular

lll'lllilt Figura 6. Complete LBBB. RBBB. LVH and RVH (only samples, please see online examples for the full range of waveforms and the text for additional characteristics I Nonspecific Intraventricular Block QRS duration >120 msec absence of criteria for LBBB or RBBB Hypertrophy and Chamber Enlargement left ventricular hypertrophy (LVH)

Sin V1 + Rin V5 orV6 >35 mmabove age40, (>40 mmforage 31-40, >45 mmforage 21-30) RinaVL>llmm Rin I+ Sin III >25 mm additional criteria:

LV strain pattern (ST depression and T wave Inversion in leads I, aVL, V4-V6) left atrial enlargement

right ventricular hypertrophy (RVH) right axis deviation R/S ratio >I or qRin lead VI RV strain pattern: ST segment depression and T wave inversion in leads VI-2

left atrial enlargement (LAE) biphasic P wave with the negative terminal component of the P wave in lead VI ; I20 msec, notched in lead II ("P mitraleD)

right atrial enlargement (RAE) P wave > 2.5 mm in height in leads II, III, or a VF ("P pulmonalea)

Laft Atrial Enlargement Right Atrial Enlargement

mmmm Figura '1. LAE, RAE (only samples, please see online examples and text above for characteristics]

'IbroDlo Nota 2011 Cardiac Diagnoslic Testl

lschamia/lnfrction look fur the anatomic distribution of the following ECG abnormalities (see Table 1) iachemia

ST segment depression T wave l.nversion (most commonly in Vl-V6)

injury tra.nsmura.l (involving the eplcardium) - ST elevation in the leads fadng the area injured/

infarcted; transient ST elevation may occur in patients with coronary artery spasm (e.g. Prinzmetal angina) can be slight or prominent (> 10 mm)

I!Ubendocardial- marked ST depression in the leads facing the affected area; it may be accompanied by enzyme changes and other signs of myocardial infarction; may also occur with angina

Figure I. ECG CIJanu wiUJ lm.ctiun

evolving infarction (ST elevation in contiguous leads = acute MI) typical" sequential changes of evolving myocardial infarction

lilt hyperacute T waves (tall. symmetric T waves) in the leads facing the infarcted area, with

or without ST elevation 2nd

ST elevation (injury pattern) in the leads facing the lnfarcted area usually 1n the first hOUIS post Infarct in acute posterior infarction. there is ST depression in Vl-V3 {reciprocal to ST elevation

in the posterior leads, that are not recorded in the standard 12-lead ECG) 3rd

significant Q waves: >40 msec or >113 of the total QRS (hours to days post-infarct) 4th

inverted T waves (one day to weeks after infarction) this classical sequence, however. does not always occur, e.g.

Q waves of infarction may appear in the very early stages, with or without ST cha.ngea non-Q wave iDfarction: there may be only ST or T changes, despite clinical evidence of

infarction completed infarction

abnormal Q (note that wide Q waves may be found in m and a VL in normal individuals)

duration >40 msec (>30 msec in aVF for inferior Infarction) QIQRS voltage ratio is >3396

abnormal R waves (RIS ratio > 1, duration >40 msec) in VI and more frequently 1n V2 are found in posterior infarction (usually in association with signs of inferior andJor lateral infarction)

Tillie 1. Area af lnflln:tion{O wava}/lllchamia (right daminant aiii'IDmy)

Leltar*rior descending (lAD) Anl!mseplal VI,V2

Circumflex

Anlarior V3, V4 Anlllnllltlnl aVL, V3-t Extensivurariar I, aVL, Vl-t ...... Right verm:le faltsrill" Ml (lillie. with n. Mil Lltlnl lsdatad postarior Ml

II,IILaVF V3R, V4R (right sided chest leads) VI, V2 fptrilant: R WIVII) V5-t VI, V2 fptrilant: R WIVII)

Cardiology and CV SUJ'8ery C7

,,

IIIJ!IIIclllt EC& ClllngM Look for ST It 80

mc from J pam J point - the junction betw8111 th1

QRS eompleot and the ST llllment ST aiiMIIion: lit laut 1 mm il

2 14acant inb lalds, Dr lit least 1-2 rnm in ldjacllll precordilllds

ST prweion: diiWI!IIgpilg Dr harimntlll

Q WIIVI; pllh*9icll if CIIISO!:lsmall mwcl or >3B of the 11111111lRS

,, . .----------------, Q ._ Sepllll depollrimli1111 by the 11ft bundle Seen in leads I, II, Ill, aVL.. VS, Vl5

C8 Cardiology and CV Surgery

.... , ,

'-Vullaae Dafinilion: IDIIII ORS ha9JI in

PIICordillleldl < ID rrm .. d linb lelldii 7 mmoVL): progressive changes whereby P waves flatten and disappear, QRS

widens and may show bizarre patterns, axis shifts left or right, ST sblft wltb. tall T waves hypokalemia (see Figure 10)

ST segment depression, prolonged QT interval., low T wwes, prominent U waves (U> T) enhances the mxic effects of digitalis

hypercalcemia: shortened QT interval hypocalcemia: prolonged QT interval 1-Ji-- .,V\ - .jA, - + -1-L - -L,_ f"IIIIIFI 10. HJPGbli Hypothermia s1nU8 bradycardia when severe, prolonged QRS and QT intervals

... !\.-"

atrial fibrillation with slow venlricular response and other alrlallvenlricular dysrhythmias Osborne J waves (see Figure 11): "bump-like" waves at the junction of the J point and the

STsegmmt

Pericarditis early- diffuse ST segment elevation PR segment depression. upright T waves lllter - iscelectric ST segment, flat or inverted T waves low voltage if chronic coD.St:rictive pericarditis tachycardia Drug Effects digitalis

therapeutic levels may be associated with Kdigitalis dfea- (see Figure 12): !IT downtdoping or "scooping'" T wave depression or inversion QT shortening U waves slowing of ventricular rate in atrial fibrlllation

toxic levels associated with: arrhythmias: paroxysmal atrial tachycardia (PAT) with conduction bWcks, severe

bradycardia in atrial fibrillation, accelerated junctional rhythms, PVCs, ventricular tachyt:ardia (seeArrlJythmiru, C12)

"regularization" of ventricular rate in atrial fibrillation due to a junctional rhythm and AV dissociation

amiodarone, quinidine, phenotbiaziru:s, bicyclic antidepressants, antipsychotics, some antihistamiD.es, some antibiotics: prolonged QT interval, U waves

12. Atrial Fllrillation. IT a .. ga duatD Digitalis ("diaitalis aHacr)

Pulmonary Disorders cor pulmonale (often secondary to COPD)

low voltage, RAD, poor R wave progression RAE and RVH with strain multifocal atrial tachycardia (MAT)

massive pulmonary embolism (PE) sinU8 tachycardia and atrial fi.brlllatlon/atrial flutter are the most common arrhytbmlas RAD, RVH with strain - most specific sign is SIQ3T3 (Sin I. Q and inverted T wave in rm

'IbroDlo Nota 2011 Cardiac Diagnostic Testl

Cardiac Biomarkers provide diagnostic and prognomc infonnati.on and identify increased risk of mortality in acute

coronary syndromes Tallie 2. CM!Iac Enzyna

lllnllal EIMIIId DDx at Elnlllal Tropanin Tropanil T 1-2 days

1day 3days Myocardial inlllrctian. mytJcarditis. pericllllitis. ITU!IClllar dysbaphy, Cll'dilc dalirlll:ian. ale.

check troponin I at presentation and 8h later creatine kinase-MB (CK-.MB, depends on local laboratory protocol)

new CK-MB elevation can be wed to diagnose reinfarction, troponin cannot other biomarkers of cardiac disease:

AST and LDH also increased in myocardial infarction (low specificity) BNP and NT -proBNP - secreted by ventricles in response to increased end-diastolic pressure

and volume DDx: CHF. AF. PE, COPD exacerbation, pulmonary hypertension

Ambulatory ECG indications fur outpatient management: palpitations, syncope, antiarrhythmic drug monitoring,

and arrhythmia surveillance in patients with docwnented or potentially abnormal rhythms. surmllance of non-sustamed arrhythmias that c::an lead to prophylactic intervention

available technologies Holter monitor

battery operated, continually records up to 3 leads hn symptoms remrded by patient on Holter clock fur mrrelation with ECG findings

continuous loop recorder (diagnostic yield 66-8396) worn continuously and can record data before and after patient activation fur

symptomatl.c episodes (usually worn fur 2 weeks) external and implantable devices

external devices can be tran.stelephonically downloaded implantable loop recorder (ll.R) -implanted subcutaneously to the right or left of the

sternum; triggered by placing an activator aver it; anterograde and retrograde recording time is programmable; cannot be tran8telephonically downloaded; left in place for 14 to 18montlu

Echocardiography Transthoracic Echocardiogrephy (TTE) ultrasound beams are directed across the chest wall to obtain images of the heart indications: evaluation ofleft ventricular ejection fraction (LVEF), wall motion abnormalities,

myocardJal ischemia and compllcations of MI, chamber sizes, wall thickness, valve mozphology, pranmal great vessels. pericardia! effusion. unexplained hypotension, murmurs, syncope, congenital heart disease

use with Doppler, which is used to quantify degree of valvular stenosis or regurgitation Trensoeaophageal Echocardiography (TEE) ultrasound probe inserted into the esophagus to allow fur better resolution of the heart and its

structures better visualization of posterior structures, such as left atrium, mitral and aortic valves,

interatrialaeptum invasive procedure, used to complement transthoracic echocardiography indications: intracardiac thrombi, tumours, valvular vegetations (infective endocarditis),

aortic dissection, aortic atheromas, prosthetic valve function, shunts, technically inadeqwrte transthoracic studies

use with Doppler, which is used to quantify degree of valvular stenosis or regurgitation Stress Ec:hocardlography echocardiography in combination with either physiologic (exercise treadmill or bike testing) or

pharma.cologic (dobutamine infusion) stress validated in demonstrating myocardial ischemia and 8S8e&Sing viability provides i.nfonnation on the global left ventricular .reaponse to exercise regional wall motion is analyzed at rest and with stress used for valvular heart disease evaluation

Cardiology and CV SUJ'8ery QJ

"' T111p00ln T (HJ!y rap.fui!Gnl

Figure 1 3. Cardiac EnQII'Ia

u. .... .,..llllrilnli: ..... ina. E'lllllllllld ,......_., ACIII.,._ (UIBj N1111004; 350;641-64 .. Pro!plc:IM. rlllbrDd Clllnlad 1rilll. nlllillwih IQitl Minll1fliii1181W8 llak-ucblad. lniiMnllll: Allllll1lllt iad" lllllr.niiBII d ii-IPe ....... ptpidilll'llbnclild .-.!. a.-: TIIIIIDdld!IIQII .. dtDIII colt cl 1l8lln.m. llldl: Mlllilll1inaiDIIDirga- sllnr il1111 iiDw6on Pf wlallillft'4ll'ld wil11111 c:allniiiJCiq) 18.0 w. 11.0 - 1111 iniiMnti:ll PIP l$541 D vs. $1l64, p-0.005). lllllftln.1111 meu.nnartof a.-llllrillllic JIIPiill 11tapblllldiUIIM en. IIDI-IIinlll101.w.1Z\p=D.45). c.-...: hi!Bim'MihiiWW... 1BUIIIBII al ii-IPe rninllic ,. ..._ DniM cntllld IIICI8vallll 111111 CUll af lniiDIId.

CIO Cardiology and CV Surgery

...,,

Most CDIIIIIIODiy Ulllll T.-lmill ltnw Tell: PnrtDoall The lkucl PrltDcol - 7 stage test

with each stage lasting 3 minutes. Wdh each IIUCCNSiVIJ llbge, 1he 1relldmll increa- in both speed IJid gredient.

For old individuals or those with limibJd exen:ise capacity: eilher The Modifild Bruce or The Modihd Naughtun l'rotDcol

...,,

Important ContrlindicatiDns ta Exen:ile luling Acute Ml, eartic dissection,

pericerditis, myocarditis, pumanary embalism

Severe AS, arllllilll HTN to exen:iaa adaqulll&ly

...,,

Most lmpartut Prognostic Futort il Exercise luling Sldlpmsian ST ahrVIIIion liload PfiiSII8 compensetion

...,,

Dulal Trudmill Saare Weighted index combining: 1 . TraadmiU IIX8rcise time using

standard Bruce protocol 2. Maximum net ST segment deviation

(dlpmsion or eiiVIItion) 3. Exen:in-inducad angina Provides diagnostic 1nd prognostic information (IIUCh u 1 -y&lr morlllity)

.... ,

Pltients with normal parfusion 51udi81 ltpukstmlhiVIJa incidanca of dalth or nonfatal Ml and are 1hus often spared furth inVIIsive evaluation for assessment of their symptoms.

Cardiac Diagnostic Teats Toronto Notes 2011

Contrast Echocarcl iography contrast agents injected into the bloodstream to improve imaging of the heart conventional agent: agitated saline (contains microbubbles of air) allows visualization of right heart and intracardiac shunts, most commonly patent foramen

ovale (PFO) and sometimes intrapulmonary shunt newer contrast agents are capable of crossing the pulmonary bed and achieving left heart

opacification following intravenous injection; these contrast agents improve visualization of endocardial borders and enhance evaluation of ejection fraction

Stress Testing exercise testing is a cardiovascular stress test using treadmill or bicycle exercise with

electrocardiographic and blood pressure monitoring guidelines for use:

patients with intermediate ( 10-90%) pretest probability of CAD based on age, gender and symptoms

complete RBBB ST depression 10 mmHg from baseline despite an increase in workload,

when accompanied by other evidence of ischemia moderate to severe angina ST elevation (> 1 mm) in leads without diagnostic Q-waves (other than Vl or a VR) increasing nervous system symptoms (e.g. ataxia, dizziness, or near syncope) signs of poor perfusion (cyanosis or pallor) technical difficulties in monitoring ECG or systolic blood pressure patient's desire to stop sustained ventricular tachycardia

Interpretation the most commonly used ECG criteria for a positive exercise test: mm of horizontal or

downsloping ST-segment depression or elevation (at least 60 to 80 msec after the end of the QRS complex)

NUCLEAR CARDIOLOGY myocardial perfusion imaging {MPI) with ECG-gated single photon emission computed

tomography (SPECT), using radiolabelled tracer role in evaluating myocardial viability, detecting ischemia, and simultaneously assessing

perfusion and left ventricular function the degree of severity shown on the scan reveals the likelihood of further cardiac event rates

independent of the patient's history, examination, resting ECG, and stress ECG result often denoted as MIBI scan with reference to radiolabelled tracer user exercise

treadmill test (unless contraindicated) vasodilator stress with intravenous drugs

dipyridamole (Persantine), adenosine act to increase coronary flow by vasodilation of arterioles (the resistance vessels)

images of the heart obtained during stress and at rest 3-4h later fixed defect - impaired perfusion at rest and during stress (infarcted/hibernating) reversible defect - impaired perfusion only during stress (ischemic)

.... , Tracers

ACC/AHA zaaz Guidelines for Use Stabbl angina, baseline ECG abnormalities, post-rwac:IArization assessment. heart h.ilure, patients Ulllble to exercise, preoperative risk assessment for patients undergoing nancanl wrgery.

thalliwn-201 (201Tl, a K analogue) technetiwn-99 (99Tc)-labelled tracer (sestamibi/Cardiolite or hexamibi/Myoview-)

Summary of Stress Testing Exercise ECG

initial evaluation in patients without hard-to-interpret ECGs who are able to exercise Exercise Stress Echo

when ECG is uninterpretable intermediate pre-test probability with normal/equivocal exercise ECG post-ACS when used to decide on potential ef1icacy of revascularization to evaluate the clinical significance of valvular heart disease

'IbroDlo Nota 2011 Cardiac Diagnoslic Testl

Dobutamine Stress Echo in patients unable to aerdse, with the same lndlcatlons as aerdse stress echo to assess tissue viability

o Exeidse Myocardial Perfusion Imaging (MPI) when ECG is uninterpretable intermediate pre-test probability with normal/equivocal exercise ECG in patients with previOUI imaging whose symptoms have changed to diagnose iachemla

Dipyridamclel.Adenosine MPI to diagnose CAD in possible ACS patients with non-diagnostic ECG and negative serum

biomarkers when ECG is uninterpretable due to LBBB or V-paced rhythm in patients unable to aercise, with the same indications as exercise :MPI

Cardiac Catheterization and Angiography o invasive: catheters are introduced peu:utaneously intJJ arterial and venous circulation under

conscious sedation and contrast ia injected arterial access most commonly through the femoral artery. radial approach gaining

favour especJally for obese patients and outpatients dependent on driving and ambulation (occupational requirements)

venous access through the femoral vein or internal jugular vein same day procedure as outpatient

indications for prehospitalization: anticoagulation therapy, renal failure, diabetes, contrast allergy

catheterization permits direct meamrement of intracardiac pn:llllures, transvalvular and mean peak pressure gradients, valve areas, cardiac output, shunt dam. oxygen saturations, and visualization of coronary arteries, cardiac chambers and great vessels

Right Heart Catheterization (Swan-Ganz catheter) right atrial. right ventricular. pulmonary artery pressures are recorded o Pulmonary Capillary Wedge Pressure

obtained by advancing the catheter to wedge into the di.stal pulmonary artery records pressures measured from the pulmonary venous system in the absence of pulmonary venous di&ease, will rdlect left atrial pressure

Left Heart Catheterization systolic and end-diasto1ic pressure tracings recorded; left ventricular size, wall motion

and ejection fraction can be assessed by injecting contrast Into the left ventricle (left ventriculography)

cardiac output (measured by the Pick oxygen method or the indicator dilution method) Coronary Angiography

Cardiology and CV Surgery Cll

,, ,

liellltlwlly 1111 &peclllclty Ill Vll'loul 111Mtlldq Exarcila ECG (Sn 611; Sp 71) Stms (Sn 71; Sp 881 PET -..inu!Sn 81; Sp 82) MIBI acannllg (Sn BB; Sp 77)

coronary vasculature accessed via the coronary ostium ..... 1 conttaindicated with severe renal failure (due to contrast agent toxicity), must check renal status ,}---------,

1-......... 2 -lnflnlplcal

- AnllrDipical i - Anllnlllllal

Figure 1 4. Coronary Angiogram Sclllmltic {RCA = right coronary artBry, AM = acuta marginal. LAD = left antariar dascending, OM = obtuse marginal! Prognosticators o angiograpbic variables may provide valuable information regarding lesion severity, complexity,

locatl.on and progno!lis

ACCIAHA 2002 .._ .. lllllld .. lndlml- fur c-ay Ana-..., Disebling (CCS c:luses Ill end M

chronic llllble enain diiPite medical tharapy

critaia on clilir:ll essmment or nor.-ilvaiva Wli1;

SUdden cardiac dlllllh. ..-icu vanbi1D1r arrhythmia. or CHF

Uncartlin dilpsis or prognosisaftar non-invuive tailing

lllllbilily to IRiarvo nor.-inv1111iva liSting

"

c__,- Gold standlrd far localizing nl q111ntifyilg CAD.

,.--------------. Hamodynlmicaly significant llanosis is dllil'lld q 711'1 or more narrowing Gf1he dilnllblr.

Cl2 Cardiology and CV Surgery Cardiac Diagnostic Tests/ Arrhythmias Toronto Notes 2011

Diagnostic Catheterization outcomes related to complications for diagnostic catheterization should be < 1% procedure related complications: vascular injury, renal failure, stroke, MI

mortality rate 0.1-0.2% inadequate diagnostic procedures should occur in far fewer than 1% of cases provocative pharmacological agents can be used to unmask pathology

fluid loading may unmask latent pericardia! constriction afterload reduction or inotropic stimulation may be used to increase the outflow tract

gradient in hypertrophic cardiomyopathy coronaryvasoreactive agents (e.g. methylergonovine, acetylcholine) a variety of pulmonary vasoreactive agents in primary pulmonary hypertension (e.g. oxygen,

calcium channel blockers, adenosine, nitric oxide, or prostacyclin)

Contrast-Enhanced CT Coronary Angiography fast ECG-synchronized multi-slice CT image acquisition in the heart has enabled non-invasive

imaging of the coronary arterial tree often used to assess coronary artery and previous graft stenosis/viability that could not be seen

during coronary angiography sensitivity= 85%, specificity= 90% for the diagnosis of obstructive coronary disease with

>50% stenosis

Magnetic Resonance Imaging (MRI) offers high spatial resolution, eliminates the need for iodinated contrast, and does not involve

exposure to ionizing radiation valuable in assessment of congenital cardiac anomalies, abnormalities of the aorta, and

assessment of viable myocardium

CARDIAC DISEASE

Arrhythmias Mechanisms of Arrhythmias

(I} Alterations in Impulse Fonnation 1his can occur due to: A. Abnonnal Automaticity

automaticity is a property of certain cardiomyocytes to depolarize themselves to their threshold voltage so as to spontaneously generate action potentials in a rhythmical fashion

under normal circumstances, only cells at the specialized conduction system (SAN, A VN and ventricular conduction system) exhibit natural automacity and are thus pacemaking cells - the automaticity of these pacemakers can either become abnormally increased or decreased

cells in the myocardium outside the conduction system in disease (e.g. post-MI ventricular ischemia) may inappropriately acquire the property of automaticity and contribute to abnormal depolarization. If these ectopic generators depolarize at a rate that is greater than the SAN, they assume pacemaking control and become the source of abnormal rhythm

automaticity can be influenced by: neurohormonal tone (sympathetic and parasympathetic stimulation) abnormal metabolic conditions (hypoxia, acidosis, hypothermia) electrolyte abnormalities drugs (e.g. digitalis) local ischemia/infarction other cardiac pathology

this mechanism is responsible for the accelerated idioventricular rhythm and ventricular tachycardia that often occurs 24 to 72 hours post myocardial infarction

'IbroDlo Nota 2011

B. Trigcred Adtrily due to AftcrdepoJ.arizations There are two types of triggered activity: 1. Early AfterdepolarhatioM

occur in the conten action potential prolongation consequence of the membrane potential becoming more positive during repolarization result in self-maintaining depolarizing oscillations of action potential, generating a

ta.chyarrhythmia. basis for the degeneration of QT prolongation. either congenital or acquired. into Torsades

de Pointe& 2. Delayed Afterdepolarizaons

occur after the action potential has fully repolarized, but before the next usual action potential. thus called a delayed afterdepolarization

commonly occurs in situations of high intracellular calcium (digitalis intoxication, ischemia) or during enhanced catecholamine stimulation

(II) Alterations in Impulse Conduction 'Ibis can occur due to: A. Re-Entry C1rcuit8 (see Figure 15 for detailed descrl.ptl.on)

the presence of self-sustaining re-entry circuit causes rapid repeated depolarizations in a region of myocardium

e.g. myocardium that has infarcted and become ischemic will consist of non-excitable and partially excitable zones which will promote the fOrmation of re-entry circuits

Rgurt 15. Mecllanlun of Reentry Requii'8B both unidirectional block (11and slowed ratrugrada cDnlbction (21. When an action potential raachas a division in the conduction path (anywhara in the myacardiuml, the impulse proceeds II'Ound and stirrdates dstal rnyocmdium. If the action patantial propagatas through a block (rafractary tissual in 1ha retrograde dirac-tian but nllt in 1ha foTward diraction,. unidiFICtianal block is p111S1nt 111. This can occur as a rasult af calular dysfunction with changes in cellwar refractoriness. Slowed retrograde conduction of the action potential'lllrough B (datted lne) encounters excitable tissue in A because these myacytes have had sufficient time to repolarise by this time paint. and now the impulsa is free to excite A again thus generating a raantJy circuit.

B. Conduction Block ischemia, fibrosis, trauma and drugs can cause transient, permanent, unidirectional or

bidirectional block most common cause of block is due to refractory myocardium (cardiomyocytes are in

refractory period or zone of myocardium unexcitable due to fibrosis) if block OCCill'll along the specialized conduction system, distal zones of the conduction

system can assume pacemaking control conduction block can not only lead ro bxadyaudia, but also tachyc:ardl.a when impaired

conduction leads to re-entry phenomenon C. Bypua 'lradl

normally the only conducting tra

Cl4 CardiologyandCVSurgery

....

Bnulyanhythmias Examples

lin Arrhytbmi1 Normal P W.V., 1111riatian of !he P-P int8rval by > 120 msec due to lllll'(ing rate of SA node ......... ry SA": Seen moru oftun in young lldulb

{

'IbroDlo Nota 2011

AV Conduction Blocks 1st Degree AV Block prolonged PR interval (>200 msec) frequently found o..mong otherwise healthy adults no treatment required

2nd Degree AV Block some of tbe atrial impulses are not conducted to the ventricles c:an describe block by ratio ofP waves to# of QRS (e.g. 2: l, 3: l, 4:1 increases in severity) second degree AV block is further subdivided into:

Type I (Mobitz I) 2nd Degree AV Block a gradual prolongation of the PR interval precedes the fallw:e of conduction of a P wave

(Wenc:kebach phenomenon) AV block ls usually in AV node (proximal)

- triggers (usually reverslble): Increased vagal tone (eg. following surgery), RCA-mediated ischemia

- not an indication fur temporary or permanent pacing

Fiare 17. Secand D11re1 AV llack with Wencklblch l'llllom8lllln (Mabib: I) (4:3 canductian)(I.Hd V1) Type D (MobJtz II) 2nd Degree AV Block.

tbe PR interval is constant; there I& an abrupt failure of conduct:lon of a P wave AVblock is usually distal to tbe AV node (I.e. His bundle) increased risk ofhigh grade or 3rd degree AV block

Figure 1 I. Sacand Dagna AV Black (Mollitz II) (3:2 cand1ctian) (Lead V1) 2:1 AV Block often not possible to determine whether the block is type I or type II prolonged or repeated recordings may clarify the diagnosis

Figure 1 9. 2:1 AV Black (Lead II) 3rd Degree AV Block complete failure of conduction of the supraventricular impulses to the ventricles ventricular depolarization initiated by an escape pacemaker distal to the block QRS can be narrow or wide Ounctional va. ventricular escape rhythm) PP and RR intervals are constant, variable PR intervals no relationship between P waws and QRS complexes (P tltrrJUWl) management (see &ctricalPacing. C21)

Figure 20. Third Degree AV Block (Comp1818 Heart Blo-*) (Lead II)

Cardiology and CV Surgery ClS

"' , 'JWe II (llollllz Ill 'r Typa II AV bla'* ilan indiCIIIian fllr pemwulllt piCina.

C16 CardioloBY aod CV Suqp:ry 10ronto Nota 2011

Figura .Z1 . Abill Flutter wid! V.riabla Block

Supraventricular Tachyarrhythmias Presentation for SVT (and pra-axcltatlon syndromes) symproms can include: palpitations, dizziness, dyspnea. chest discomfort, presyncopelsyncope me;y precipitate congestive heart failure (CHF), hypotension, or ischemia in patients with

underlying disease o untreated tachycardJas can cause cardiomyopathy (rare. potentially reveraJble with treatment of

SVT's) includes supraventricular and ventricular rhythms

Supraventricular Tachyanhythmlu (SVT) tachyarrhythmias that originate in the atria or AV junction this term is used when a more specific diagnosis of mechanism and site of origin cannot be made characterlzed by narrow QRS, unless there is pre-existing BBB or aberrant ventr:icul.ar

c:onductl.on (abnormal conduction due to a change in cycle length) Sinus Tachycardia sinus rhythm with rate> 100 bpm o occurs in normal subjects with increased sympathet1.c tone (exerc.l.se, emotions, pain), alcohol

use, caffeinated beverages, drugs (e.g. beta-adrenergic agonists, anticholinergic drugs, etc.) etiology: fever, hypotension, hypovolemia. anemia, thyrotoxicosis, heart failure, MI. shock,

pulmonary embolism, etc. treatment: treat underlying disease; consider beta-blocker if symptomatic, CCB if beta-blockers

contraindicated Premature Beats o premature atrial contraction {PAC. Figure 25)

ectopic supraventricular beat originating in the atria P wave morphology of the PAC usually ditrera from that of a normal sinus beat

junctlanal premature beat ectopic supraventricular beat that originates in the vicinity of the AV node P wave is usually not seen or an inverted P wave is seen and me:y be before or closely follow

the QRS compleJ: treatment uauall.y not required

Atrial Flutter rapid, :regular atrial depolarization from a maao re-entry drcuit within the atrium (molt

commonly the right atrium) atrial rate 250-350 bpm, usually 300 bpm AV block UBUally occurs; it may be fixed (2:1, 3:1,4:1, etc.) or variable etiology: CAD, thyrotoxicosis, MV disease. cardiac swgery, COPD, pulmonary embolism,

pericarditis ECG: sawtooth flutter wava (most common type of flutter) in inferior leads (II, m, a VF);

narrow QRS (unless aberrancy) in atrial flutter with 2:1 block, carotid sinus massage (first check for bruits), Valsalva maneuver

or adenosine may decrease AV conduction and bring out flutter waves o treatment

acute: if unstable (e.g. hypotension, CHF, angina): electrical cardioversion if stable

(1) rate control: beta-blocker, diliiazem, verapamJl, or digoxin (2) chemical cardioversion: sotal.ol, amiodarone. type I antiarrbythmics or

electrical cardioversion anticoagulation guidelines same as for patients with AF (see Alrlal Ftbrlllatlon, C17) long-term: antiarrhythmic:&, catheter radl.ofrequency (RF) ablation (success rate dependent

on site of origin of atrial flutter)

Multlfocal Atrial Tachycardia (MAT) irregular rhythm caused by presence of 3 or more atrial foci (may mimic AF) atrial rate 100-200 bpm; at least 3 distinct P wave morphologies and PR intervals vary, some P

waves may not be conducted o occurs more commonly in patients with COPD, and hypoxemia; less commonly in patients with

hypokalemia, hypomagnesemia. sepsis, theophylline or digital.la toxicity treatment: treat the underlying cause; CCBs may be used (e.g. diltiazem, verapamil),

beta-blockers may be contraindicated because of severe pulmonary disease no role for electrical cardioversion, antiarrhythmics or ablation

'IbroDlo Nota 2011

Atrial Fibrilllltion (Af) most common sustained arrhythmia incidence lnaeases with age (10% of population >80 years old) symptoms: palpitations, fatigue. syncope and may precipitate or worsen heart failure may be associated with thromboembolic events (4%/year In nonvalvular AF) IDitlation

9lng].e circuit re-entry and/or ectopic fod act as aberrant generatois producing atrial tachycardia {350-600)

impul&e& then conduct irregularly acro&S the atrial myocardium to give rise to fibrillation in some cases, ectopic foci have also been mapped to the pulmonary vein ostia and can be ablatEd

maiutnaoce the tachycardia causes atrial structural and electropbysl.ol.oglcal remodelling changes that

further promote AF; thus the longer the patient is in AF, the more difficult it is to convert back to sinus rhythm

the AV node Irregularly filters incoming atrial impulses producing an Irregular ventricular

response of 75 Ilia ballS Slnia'TIA. (flill')

AFonECG

8.5-1 8.2

aspirin 81-325 daly caurradin (INR 2-3) caurradin IINR 2-3)

no organized P waves due to zapid atrial activtty {350-600 bpm) causing a cbaotlc fibrillatory baseline

Irregularly Irregular ventricular response (typically 100-lSObpm), narrow QRS {unless aberrancy or previous BBB)

wide QRS compleus due to aberrancy may occur following a long-short cycle sequence ("Ashman phenomenonj

loss of atrial contraction. thus no wave seen In ]VP, no S4 on auscultation

Figure 22. Abill Fibrillllion (Laad II) Management (adapted &om ACC/AHAJESC pidelinal006) Major objectiftl {RACE) 1. Rate control: beta-blockers, diltiazem, verapamil (in patients with heart allure: digoxin,

amiodarone) 2. Anti-coaguhn:ion: prevmt thromboembolism

assess stroke risk: determine CHADS2 score in patients with nonvalvular AF if no risk factors. ASA 81-325 mg dafly I moderate risk factor, ASA or warfarin (INR2.0-3.0, target 2.5) moderate risk factors or any high risk factor (prior stroke. TIA or embolism. mitral

stenosis, prosthetic valve), warfarin 3. Cardioversion {electrlcal)

if AF 24-48 hrs, anticoagulate fur 3 weeks prior and 4 weeks after cardioversion if patient unstable (hypotensive, active angina due 1D tachycardia, uncontrolled heart failure),

should cardiovert immediately 4.Etiology

HTN, CAD, valvular disease, pericarditis, cardiomyopathy, myocardlti&, ASD, following surgery. PE. COPD, thyrota:ncosls, SSS (Sick Sinus Syndrome), alcohol ("holiday heart")

may present in young patients without demonstrable disease ("lone .AF") and in the elderly without underlying heart

CIS Carcliolosrand CV Surgery A:rrhythmiu 1'oroDio 2011

lnlllllec '2 ......... lbcb .. l'dl*lllll ....... sn61Tr.-.II!MricAt?lcb CGdrn !31:al0081111 llldy: Ccdnn Syarlllic lllwilw.l ACTs will llrillfirlltmllll m limy rt lllnlla II' tJniaJt ilchMTi: au.:t. II'IIIMIIDI: Lqtam ... ltiM!Ga wluil --Dibrnl: lllllnllll. .... dad!, rn,acardll imtlins. llldl: aiJ!Ib!ctt 11111111al ma (OR 0.68, MO.M-0.115). ildlaric lllnlla ((1110.53, !IS0.41 -ILIB). 1111 r,Qnil: lridi 181:1[11 0.48.115'10.25 - 0.10). lhlfUIIII fiUigrbtttfilren:e in flld a 111nvfwnnllpiin I Ill 1.18, 1M 1..20 -3.28). ........ wufarin enWcra. bU - na118Gite rill!: d lillllily II' nu1llly 1111 llf'li. s9fl1811 imlcranillilmlnlllgl rill 1111 PlniiiDid " bnit fir IIIHo!QIIiPiflll-

.... ' , .. lhe cntid llllltiGB i1111lually a cOIIIbml prenura diral:lad pollariorly against 1hl CIIV!id artav for 5-10 11conds.. Nwr{lliltlln for bnihl .... palpation.

Additio1111l Management Pointa Regarding Atrial Fibrillation recent studies of patienb with atrial fibrillation suggest that there is no difference in long-term

survival when treating patients with a rhythm-control ver8118 rate-control strategy however, many patients with a significant underlying structural heart lesion (e.g, acute MI.

history of congestive heart fallure), valvular lesions (mitral stenosis, mitral regurgitation, aortic stenosls), hypertrophic cardlomyopathy, cardJ.ac amyloid. other cardiomyopathies, pericardial disease, congenital heart lesions) will not tolerate atrial fibrillation well (since many dependent on atrial kick.) and these patients should be cardiaverted (chemical or electrical) as soon as possible

Newly Discovered AF anticoagulants may be benefi.dal ifhigb. risk for stroke lf the episode is self limited and not associated with severe symptoms. no need for

antlar.rhythmic drugs lf AF persists, 2 options:

1. rate control and anticoagulation {as indicated above) 2. cardioversion (as above)

Recurrent AF/Pennanant AF lf episodes are brief or minimally symptomatic, antiarrhythmic drug may be avoided; rate

control and anticoagulation are appropriate patients who have undergone at least one attempt to restore sinus rhythm may remain in AF

after recurrence: permanent AF may be accepted (with rate control and antithrombotics as indicated by CHADS2 score) in certain clinical situations

if symptoms are bothersome or episodes are prolonged, antiarrhythmic drugs should be used no or minimal heart disease: ftecainide, pmpafenone or sotalol LV dysfunction: amiodarone CAD: beta-blockers. amiodarone

AV Nodal Re-Entrant Tachycardia (AVNRT) re-entrant clrcuit using the dual pathways (Cut conducting beta fibres and slow conducting

alpha fibres) within or near the AV node; often found in the absence of structural heart disease; cause is commonly idiopathic, although familial AVNRT has been reported

sudden onset and offset fast resuJar rhythm; rate 150-250 bpm usually initiated by a supraventricular or ventricular premature beat AVNRT accounts for 60-7096 of all paroxysmal SVTs retrograde P waves may be seen but are usually lost In the QRS complex treatment

acute: Valsalva or carotid massage. adenosine is first choice if UDreSponsive to vagal maneuvers; if no response, try metoprolol, digoxin, diltiazem; electrical cardiaversion if patient hemodynamically unstable (hypotension, angina or CHF)

long-term: lst line: beta-blocker, diltiazem, digoxin, 2nd: anti-arrhythmic d.nJw! (flecainide. propafenone), 3rd: catheter ablation

2. An alrial pranlllura bllllt (APBJ llflar 11narmlll deponing bllld conducu through A

(ainCII npallrilad) but nat B (still rafractury -11111 proUina unidirec:tiallll block)

lha i11110181nMIIa along A and n111ChB1 the diltlll and of B which hu now npalarilad, allowing

18?rogl'lfle coiiiM:Iian to IIS!IIblish a18811?ry circuit i E

1. for AVNRT: Praunce of fulllld algw tnll:ll in AV node

F'ra Z1 Macllani1111 far AV Nollll A..&try

12 :::E i 0

'IbroDlo Nota 2011

Pre-Excitation Syndromes refer to a subset of supraventricular tachyarrbythmiu, mediated by an accasory pathway, which

c:an lead to vmtricular pre-excitation Wolff-Parkinson-White fWPW) Syndrome congenital defect present in 1.5-2/1000 of the general population an accessory conduction tract (Bundle of Kent; can be in 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 since the ventricles are a.ctivated earlier, the ECG shows early wntricu1ar depolarization in the

furm of initial slurring of the QRS complex - the so called delta wave atrial impulses that conduct to the ventricles through both the Bundle of Kent and the normal

AV nodeJHis-Purkinje system generate 11 broad "fusion complex" ECG features ofWPW

PR Interval 200 bpm) and the QRS complex

widens treatment: electrical cardioversion. IV procainam!de or IV amiodarone

do not use drugs that &low AV node conduction (digoxin, beta blockers) as this may cause preferential conduction through the bypass tract and then precipitate VF

long-term: ablation of bypass tract when possible AV ReEntnmt Tachycardia (AVRT) re-entrant loop via accessory patbwa.y and normal conduction system initiated by a premature atrial or ventricular complex orthodromic AVIIT: stimulus from a premature romplatravds up the bypass tmct 0/ID A) and

down the AV node (A to V) with narrow QRS complex (no delta wave because stimnlus travels tluough normal conduction system)

comprille& 95 percent of the reentrant tachycardias associated with WPW syndrome antidromic AVRT: more rarely the stimnlus goes up the AV node (V to A) and down the bypass

tract (A to V); wide and abnormal QRS as ventricular activation is only via the bypass tract treatment

acute: similar to AVNRT acept avoid long-acting AV nodal blockers, e.g. digoxin and verapamil

long-term: for recurrent arrhythmias, ablation of the bypass tract Is recommended drugs such as flecalnide and procainamide can be used

Ventricular Tachyarrhythmias Premature Ventricular Contraction (PVC) or Ventricular Premature Beat (VPB) QRS width >120 msec, no preceding P wave, bimrre QRS morphology origin: LBBB pattern = RV site; RBBB pattern = LV site PVCs may be benign but are usually signifi.c:ant in the following situations:

consecutive = VT) or multiform (varied origin) PVC falling on the T wave of the previous beat ("Ron T phenomenonj: may precipitate

ventricular tachycardia or VF Accelerated ldloventrlculer Rhythm ectopic ventricular rhythm with rate 50-100 bpm more frequently occurs in the presence of sinus bradytardia, and is easily overdriven by a faster

supraventricular rhythm frequently OCCill'll in p11tientll with acute myocardial infarction or other types ofheart disease

(cardiomyopathy. hypertensive. valvular) but it does not affect prognosis and does not usually require t:reat:ment

CardiologyandCVSuqery Cl9

a.d.tK.nl Can IDiilll in rVIt

or laft ha.t

,, I J ..

C YOII'III M.Kim ZD11

Figu111 24. Acceuary pathway caniiiUGiian in WPW causes 8llly venbiciAr actintian lllna tD tiJa appe .. nca al 1 daltB wave {llurred gpstrelre of tha DRS) a tha ECG Wore unll canduction occurs acraa the AVN

l'nlmature VenbiciW CGntractiCII !PVC)

Pr .. urtura Alrial ConiiKiion (PAC) NDIB: Thil dilgrlm 111D show& rr..tedT--

Figu111 ZS. PVC (with bigaminy pattern) 11'111 PAC

C20 Carcliolosrand CV Surgery 1'oroDio 2011

'' , Arrl!rlllnlll IIIII llay l'rMIIIt U I 1M4t lUll 'lllchyoanla Vantriculllr illl:hyaldill SVT with ab..-.nt conduction (1'111

rell18d) SVTwith prwuilting BBB or

nlllllp8cific iltmlnlric.ar condulrtiDn d8tilct

AV cordlction through a bypaN tnllrt in Wf'W plllianb wring .. lllrilll tachywlhythmia (a.g. lllrilll flllt8r, atrialllll:hyaldia)

AniDIImic AVRT il Wf'W pdanbl

Venb'ic:ular Tac:hycardia (VT) 3 or more consecutive ectopic ventricular complexes (Figure 26)

rate >100 bpm (usually 14{)..200) ventricular flutter: if rate >200 bpm and complexes resemble a sinusoidal pattern '"8U8tal.ned vr if it lasts longer than 30 sec ECG characteristics: wide regular QRS tachycardia (QRS usually >140 msec);

AV dJssodatlon; bizarre QRS pattern. Also favour Ih ofVT: left axl.s or right am deviation, nonspecific intraventricular block pattern, monophasic or bipbasic QRS in Vl with RBBB, QRS concordance in Vl-V6

occasionally during VT supraventricular impulses may be conducted to the ventricles genenrting QRS complexes with normal or aberrant supraventricular morphology ("ventricular capture") or sUDUilatl.on pattern ("fusion complexes")

m.onomorplW: VT identical complaes with uniform morphology more common than polymorphic VT typically result from Intraventricular re-entry drcuit potential causes: chronic infarct scarring, acute MI/isdtemia, cardiomyopathies, myocarditis,

arrbythmogenic right ventricular dyapluia, idiopathic, drugs (e.g. cocaine), electrolyte disturbances

polymorphic VT compleus with constantly changing morphology, amplltude, and polarity more frequently aasodated with hemodynamic instability due to faster rates (typically

200-250 bpm) vs. monomorphic VT potential causes: acute myocardial infarction, severe or silent ischemia, and predisposing

facoors fur QT prolongation (see below in Torsades de Pointes) treatment

sustained VT (loDger than 30 seconds) is an emergency, requiring immediate treatment hemodynamic compromise - electrical cardioversion no hemodynamic compromise- electrical cardioversion, lidocaine, amlodarone, type Ia

agents (procainamide, quinidine)

F'1111r1 26. Ventricullr Tachycanla(MDDomurphic) Tabla 4. Wida Camplax Tachycanlia: Cluaa fDr Diffarallilling VT n. SVT with Abarrancy*

PresBJiir.l S\'llpbml Hislay a! CAD and praviaus Ml Plft&cal xlm

Cslllllll y WIIV8I YariableS1

c.utid sinus IIIIIS\111111!/Dnosile tllminltalardlytlmia

Nat helplul vr VT vr SVT""

AV clssacidian Clplure or flllilll QIIS widlh > 1 40 msa: Exbwna axis daviati111

(left or rVt sLperior axis) Fositive ORS CliiCOrdln:e

(A WIV8 ICI'OII chast: llllds) Nagltiw QIIS concordance

{S WIIV8 acroa chest leads) Axis an11ythmia

"H 1111i111t >8511111!11iiM Mill' llllllcllnl1art lillllltlhm dalce II Vf >95'1. "Mrt tlmiwle vr iliiiiiW _..willl no IIIUcllnlhiWI diaa Torsadea de Polntes

vr vr vr VT vr May suggast: vr vr (polymalplic)

a variant of polymorphic VT that occun In patients with baseline QT prolongation- "'twisting of the points" (Figure 27)

looks like usual VT acept that QRS complexes "rotate around the baseline" changing their axis and amplitude

vmtricular rate greater than 100 bpm. usually 150-300 bpm etiology: patients with prolonged QT intervala are predisposed

congenital long QT syndromes drugs- e.g. Class lA (quinidine), Class Ill (sotal.ol), phenothia.zl.nes (TCAs), erythromycin.

quinolones, antlhistam.ines electrolyte distw:bances - hypokalemia, hypomagnesemia nutritional defidend.es causing above electrolyte abnormalities

treatment IV magnesium, temporary pacing, isoproterenol and correct underlying cause of prolonged QT, electrical cardioversion if hemodynamic compromise

'IbroDlo Nota 2011

Figura 27. Tarud da Pailtal Ventricular Abrlllatlon (VAb) chaotic ventricular arrhythmia, with very rapid irregular ventricular fibrillatory waves of

varying morphology {Pigure 28) terminal event, unless advanced cardiac life-support (ACLS) procedures are promptly init:i..ed

ID maintain vent:ilation and cardiac output. and electrical defi.brillation is carried out most frequent cause of sudden death refer to ACLS algorithm for complete therapeutic guldellnes

J L,. ,; 1 r 'f '":1 Figura Zl. v..bic .. ar Fir..lltian

Electrophysiology (EPS) Studies invasive test fur the investigation and treatment of cardiac rhythm disorders using iotn!cardi.ac

catheters provide detailed analysis of the arrhythmia mechanism and precise site of origin when ECG

data are nondiagnostic or unobtainable bradyarrhytbmias: define the mechanisms of sinus node dysfunction and localize site of AV

conduction block. tachyarrhythmias: map fur possible ablation or to assess indudbllity of ventricular tachycardia

Electrical Pacing the decision to implant a pacemaker usually is based on symptoms of a bradyarrhythmia or

tachyanhythmia in the setting of heart: disease Pacemaker Indications SA node dysfunction (most common): symptomatic bradyt:ardia hemodynamic instability

common manifestations include: syncope. near syncope. transient Ught:headed:nes. or severe fatigue

SA node dysfunction is commonly caused by: intrinsic disease within the sinus node (e.g, idiopathic degeneration, fibrosis, ischemia, or surgical trauma), abnormalities in autonomic nervous system function. and drug effects

AV nodal-infranodal block: Mobitz II, complete heart block Pacing Techniquea temporary: transvenous (jugulaJo subclavian. femoral) or eDernal pacing permanent: transvenous iniD RA, apex ofRV or both

can sense and pace atrium, wntricle or both new generation: rate responsive. able to respond to physiologic demand biventrlcular

Tallie 5. Pacemakar Nonaclature 1'111111111 I I'DIIIIal I CllanOr paced ChltM lensed 0 = Nana 0 = None A = AlrUn A= Atriun v = v.ntri:IIJ v = Ventricle D = lklai(A+V) D =Dual (A+V)

1'111111111. Reapcnae tD 1181'11ing 0 =None I= lnhlitad T = Tri!prad

examples of commonly used pacemakers

I'DIIIIIIIIV Pnlpnmability 0 =None R = Rata rnoct.da1im

Tactryanhythmia como! 0 = NIIIB P = Paca S =Shock D = Dual (P+SI

VVI: single lead in ventricle. pacemaker inhibited in response to a sensed beat in ventricle; protect patient from bradycardia

DDD: separate leads in atrium and ventricle; pace atrium if atrium does not contract; once an atrial event has occurred (whether paced or native) device will ensure that ventricular contraction follows; device is inhibited in the presence of sinus rhythm and normal AV ronduction, provides physiologic pacing

Cardiology and CV Surgery Clt

C22 Cardiology and CV Surgery Arrhythmiu/lschem.ic: Heart Disease (IHD) Toronto Notes 2011

................... c.d ..... t.AIUII wilb Lllt'IIIIMidu .,.. o,M:tilll AnnllllemMed21X11; 1 47:25162 Studr: Mela-!Mw of 12 RCTs used for lmpilnllbll CltdiMIW llllillillltDr (ICDI mcy, 5 RCTs IUid 48 DbseMdilllll Allfiesfor 111d 21 RCTs1nd 43 DbnmliDI'III sludies for Sllely rMiw. 8516 b' ICDeflicq 26 840 far ..r.ty IIYiiiW Ylitb 11ft Wll1lricUir ljac:tian hlction Qllntlllle Cardiomler Delldllw implllrotian. Aklllle martll!y lllllllvne eveJ'G a.ulll: ICDs radUCid morlllly by 20'Jo 11 =44.4\IMI!grnlnt nMb:lian (54\l in suddan Clldi.: dlllh 1Q. 37\. 63%; hid I rab:ed relltiw risk rl 0.54 fur ll.ggse mllltJIIy - RCTs (CI 0.43 D.58.11=60.4llj.llltM of success of lCD n,lllllllian were 99\ ta 98.8% 99.3'11j willla 1 .2\ (CI O.B 1.5\1 clwa ofperiirnpllllllltian COIIII*Itialls!pel'100patient-yam)WIII'II: 1.4(CI 1.5(CI1.31.811ead prablllrl; O.i (CI 0.5 0.111 ilflmt sill irlaclian; and 19.1 (CI 1U 22.01 il1l!llllllPiJII dilclllrgls il RCTI111111111'1tSofU(CI4.5-5.3Iilllfiiii'Dilril il DbaaMIIilllll ftldiiS. ICDs 11e saltllld &lleciNe in rWilg morlllly il aclil ]lltilra l'lilll LV iYIIaic dylb1cliDn. but cany l!irP'i1311rilb of inlpJIIIIJirilla 6sdi1JQ8I.IiiiNncls RCTsllld Dlialrvatioraln.danwthatirnp!Md risk lll'ltilicllion of pllim lillY Utlw impiiMI lllll:amlld llll!CIIIIImsa Milts.

Implantable Cardioverter Defibrillators (ICDs) sudden cardiac death (SCD) usually results from ventricular fibrillation (VFib), sometimes

preceded by monomorphic or polymorphic ventricular tachycardia (VT) ICDs detect ventricular tachyarrhytlunias and are highly effective in terminating VT NFib and

in aborting SCD several studies demonstrate mortality benefit vs. antiarrhythmics in 2 prevention (AVID,

CASH,CIDS) benefit fur 1 o prevention of SCD in patients with ischemic and non-ischemic cardiomyopathy,

depressed left ventricular ejection fraction (LVEF), prolonged QRS see Heart Failure, C32 for current treatment recommendations

Catheter Ablation Techniques radiofrequency (RF) energy: a low-voltage high-frequency form of electrical energy (similar to

cautery). RF energy produces small, homogeneous, necrotic lesions approximately 5-7 mm in diameter and 3-5 mm in depth

Indications paroxysmal SVT

A VNRT: accounts for more than half of all cases accessory pathway (orthodromic reciprocating tachycardia): 30% of SVT

re-entrant rhythm, with an accessory AV connection as the retrograde limb corrected by targeting the accessory pathway

atrial flutter: flutter focus in RA atrial fibrillation: potential role fur pulmonary vein ablation ventricular tachycardia: commonly arises from the right ventricular outflow tract and less

commonly originates in the inferoseptalleft ventricle near the apex (note: majority of cases of VT are due to scarring from previous MI and cannot be ablated)

Major Complications approximately 1% of patients death: 0.1-0.2% cardiac: high grade AV block requiring permanent pacemaker, tamponade, pericarditis vascular: hematoma, vascular injury, thromboembolism, TIA/stroke pulmonary: pulmonary embolism

Ischemic Heart Disease (IHD) Epidemiology most common cause of cardiovascular morbidity and mortality atherosclerosis and thrombosis are the most important pathogenetic mechanisms male:female ratio= 2:1 with all age groups included (Framingham study), 8:1 for age 70 peak incidence of symptomatic HID is age 50-60 (men) and 60-70 (women) for primary prevention of ischemic heart disease, please see Family Medicine, FM17

Tabla &. Risk Factors for Atharosclerotic Heart Disease Mljar Rislr: FIU:bn Smoking Diabetes mellitus {DM) Hypsrbn&ion (HlN) Ftrnily history (FHx) Dl Ml

Fim degree male rei alive

Toronto Notes 2011 Ischemic Heart Disease (IHD)

HTN Hypercholesterolemia Cigaratl8s Endothelial injury Macrophage influx --------+Foam calls Dlcidized LDL ... Flllty slruaks 4Jid core

Growth -----------+AthertJIIIil ..

Lumen murowilg Ruplln

Figure 29. Pathophysiology of Atherosclerosis

Chronic Stable Angina Definition

Endothelial damage i- Cytoki1as Smooth mu8Cie Fibror cap

CalcffiCIIIion symptom complex resulting from an imbalance between oxygen supply and demand in the

myocardium factors influencing supply

luminal diameter (most important factor) duration of diastole (important fur coronary artery perfusion) hemoglobin Sa02

factors influencing demand heart rate contractility wall stress

Etiology and Pathophysiology decreased myocardial oxygen supply

atherosclerosis, vasospasm tachycardia (decreased duration of diastolic coronary perfusion) anemia hypoxemia congenital anomalies

increased myocardial oxygen demand tachycardia hyperthyroidism (increased contractility, increased HR} myocardial hypertrophy, aortic stenosis

Signs and Symptoms typical: retrosternal chest pain, tightness or discomfort radiating to left ( right) shoulder/arm/

neck/jaw, associated with diaphoresis, nausea, anxiety predictably precipitated by the "3 E's: Exertion, Emotion and Eating brief duration, lasting< 10-15 minutes and typically relieved by rest and nitrates Levine's sign: clutching :fist over sternum when describing chest pain anginal equivalents: dyspnea, acute left ventricular failure, flash pulmonary edema

Clinical Assessment history, physical and directed risk factor assessment labs: Hb, fasting glucose, fasting lipid pro:file ECG (at rest and during episode of chest pain if possible) CXR (suspected heart failure, valvular disease, pericardia! disease, aortic dissection/aneurysm,

or signs or symptoms of pulmonary disease) stress testing (see Cardiac Diagnostic Tests, CS} or angiography echocardiography

to assess systolic murmur suggestive of aortic stenosis (AS), mitral regurgitation (MR) and/ or hypertrophic cardiomyopathy (HCM)

to assess LV function in patients with Hx of prior Ml, pathological Q waves, signs or symptoms of congestive heart failure (CHF)

Cardiology and CV Surgery C23

..... , ,

Chronic stable angi1111 is most often due to a fixed siBnosis clllll8d by an atheroma. Acuts coronary syndromaa ara tha mutt of

.... , ,

Can.dian Cardion_.., ICCSI hnctillnal C._lilic1tian Df Anatn Cllst 1: ordinary physical ectivity

(walking, climbing stairs) does not CllllH angina; angina with rtnnuous, rapid, or prolonged ectivity.

Clla II: slight limitation Df on!ilary activity: angina brought m > 2 blocks on level or climbing > 1 flight of stair11 or by emotional rlnll.

Cllss Ill: marked limitation of ordillllry ectivity: engi1111 brought on at

C24 Cardiology and CV Surgery Ischemic Heart Disease (IHD) Toronto Notes 2011

Optilllllhllcallhlpy with ....... Pl:lt. Stllilel:aranuy .._COURAGE Trill NU.f2007; 356:1503-16 l1udr. lllncloniled. CCIII1IIIed iilll'oitll me11ian l'llldltim 2287 petimll MID llld alijeclive IYidara gf llrjiCII"dill ia:larillllld 19iblt lllhllcoronll'f lll8ly disa11a. 1...-. l'llierQwellllllldonilld 111 IIIC8ive inllnsivl phnllcolagic llllrepy lll1d lillllytl iniiMOOan Mil orl'oitllout pen:ibreu COI'OOIIV inlllwrDln (Fa). l'limlryou1comewulkue mollllily IIIII nonfllll mvoCIIIill inlln:lioa (MQ. Secondlly lllk:ome hid llllillianil mmtJ alllrab, Ml111d lapiiJimlior1 fDJ ualllbla 11911 willlliiQIIivB bilnltkm. llelulll:n..wunoliQnifil:lrt._cein prinwy (ooqJSIId hmnllllio: 1.05; 01 Slmldll'f IMI:Oines (hmrd ratio: 1.05; P=0.62) bltwean the PCIIIId iiiiMitioiiPJPL The PCI P4> hill liJtler Ales of '-CI.IIIrimlion 114.6Y81Q alfvlkM-11p (lllmd lllie 0.60, P

Toronto Notes 2011 Ischemic Heart Disease (IHD)

Acute Coronary Syndromes (ACS) Definition coronary atherosclerosis with superimposed thrombus on ruptured plaque: other causes of unstable angina:

coronary thromboembolism (e.g. infective endocarditis, intracavitythrombus, paradoxical embolism) or cholesterol embolism

severe coronary vasospasm coronary dissection increased demand can also contribute (e.g. tachycardia, anemia)

Spectrum of ACS unstable angina (UA)/non-ST elevation myocardial infarction (NSTEMI) ST elevation myocardial infarction (STEMI) sudden cardiac death

Investigations history and physical

note that up to 30% of Mis are umecognizc:d or "silent" due: to atypical symptoms - more common in women, DM, elderly, post-heart transplant (because of denervation)

ECG,CXR labs

serum cardiac biomarkers for myocardial damage (repeat 8 hours later) (see Cardiac Biomarkers, C9)

CBC, INR/aPTT, electrolytes and magnesium, creatinine. urea, glucose, serum lipids draw serum lipids within 24-48 hours because values are unreliable from 2 to 48 days post-MI

Unstable Angina (UA)/Non ST Elevation Ml (NSTEMI) Definition syndrome of acute plaque rupture and thrombosis with incomplete or transient vessel occlusion unstable angina is clinically defined by any of the following:

accelerating pattern of pain: increased frequency, increased duration, with decreased exertion, decreased response to treatment

angina at rest new onset angina angina post-MI or post-procedure (e.g. percutaneous coronary intervention [PCI], coronary

artery bypass grafting [ CABG]) NSTEMI is clinically defined by the presence of 2 of 3 criteria:

symptoms of angina/ischemia rise and fall of serum markers of myocardial necrosis evolution of ischemic ECG changes (without ST elevation or new LBBB)

acute phase ofUAJNSTEMI risk of progression to MI or the development of recurrent MI or death is highest in the early

period at 1 to 3 months after the acute phase. most patients resume a clinical course similar to that

in patients with chronic stable coronary disease majority of NSTEMis do not result in the development of Q waves

ST Elevation Myocardial Infarction (STEMI) Definition syndrome of acute plaque rupture and thrombosis with total coronary occlusion resulting in

myocardial necrosis STEMI is clinically defined by new ischemic ECG changes plus one or both of ischemic

symptoms and elevated cardiac enzymes ECG criteria (see Approach to ECGs, CS)

ST elevation in 2 contiguous leads mm in limb leads or nun in precordial leads) or new BBB (either LBBB or RBBB)

Acute Management of STEMI after diagnosis of STEMI is made, do not wait for results of further investigations before

implementing reperfusion therapy goal is tore-perfuse artery: thrombolysis (EMS-to-needle) within 30 minutes or primary PCI

(EMS-to-balloon) within 90 minutes (depending on capabilities of hospital)

Cardiology and CV Surgery C25

llllii!'IW Bm. I ..,_..illllfln:llll7 JWA 1 118; 2lllt1 Z56-63 The -.,st r.tures 11111 inc:lelse lhe llllllillaad a1 111m sr...-IIMtion.-n-. c11111 ]llin lldiJting 1o bath the riilt 11111 111ft ann sindlneollly, pre-al111 S3111d The -.,st r.tures 11111 decrease lhe lcllillaad al Ill 111 nDmlll ECG "11011. pluilic c:lllll!plin, an or Sllbllilg cllalt plil.llld positillnll dl8lt plin.

TIM I Rillk far UNNSTEMI a..t.lllb 1'11111 lilblriell ri8: fdDrs fur CAD ICooMI CAD ISIInolis Aspirinu. inplll7da\'J RKint IS24 hrl-. angina ST-segrrert dellillion 0!:0.5 mm iiiCIIIIId Clldlc rnmbll II& TDIIII'oilll qi0Q11Phy CAD COIOfiiUY lf1lly llseue NSTIMI nan STIIgllllnllllvllian myaclllill inflln:tian TM 1ilurilalylil in myac:ardilll irOn:tion UA =II!SIIIIIe.,P .lAMA 2UOO; 284:m-842

lf11.tmtnt of NSTEMI IIEMDAN Enolll!larin Morphine Ot Nitnd

C26 Cardiology and CV Surgery Ischemic Heart Disease (IHD) Toronto Notes 2011

a.m lllflldi. NfJM 2006; 354:1417-811 Studr. Pros,ective. 11llllorrized. controlled nUiiclntrllrill. l'ilil* 20,419 prtients (ITIIIW IQll 60 11- 11111el with Simi wiD W81111C.'1181Uad to llllargo lbilat,'sis. l'llierQW81111111doniledto IIICIINt litMr IIIJlllllrin or Wligld bald lllillclioniiJd hlplrin in llddililn 1nd lllndlld thapiel. DIDin: Dedi oroomntnorntal Ml ll diJyl pasiMit. a-11111: ThecaufOIIeprinlryaull:ame IJCQIII8I( ""' altai in tile IIIOXI()Irin compll1d witli those wllo received lllfnlctioalled hq)uin (UI WI. 12.1)!., p

Toronto Notes 2011 Ischemic Heart Disease (IHD)

Diqnolis STlMI: lie tr111tment t STEMI: on&&! of pain

C28 Cardiology and CV Surgery Ischemic Heart Disease (IHD) Toronto Notes 2011

..... , , .. Resting LVEF is a useful progno5tic factor.

Compkmon of Ml CRASH PAD Cardiac Ruplln Anhytlunia Shock Hypertensionllleart failure Pericardilifll'ulmonary emboli AMuryam DVT

Poll-Infarction Risk Slntification r + Hiah Risk !30-35%1 Intermediate/Low-Risk 165-70'5\ Prior Ml CHF + Ruc:ummt ll;cllemia Higll-Risk Arrhy1mia

Non-Invasive Stress T liSting I

l t Ischemia or Poor Functional Sllrtus Cardiac Cathatarization ...----------'

ECHO dorerautirelypost-MI

Figure 31. Post-MI Risk Stratification

Prognosis following STEM I 5-15% of hospitalized patients will die

risk factors infarct size/ severity age co-morbid conditions development ofheart failure or hypotension

post-discharge mortality rates 6-8% within first year, half of these within first 3 months 4% per year following first year risk factors

LV dysfunction residual myocardial ischemia ventricular arrhythmias history of prior MI

Teble 8. Complications of Myocerdiellnferction CampliCition Etiolarw Presentalian Anhythmia t Tachycardia Sinus. AF, VT, VFib Fm48hrs 2_ Bradycll"dia Sinus. AV block Fm48hrs Myacardill Ruptu .. 1.LV free wall Transmural infarction 1-7 days 2. Papillary llll&cla MR) Inferior infarction 1-7 days J_ Ventricular septum(-+ \lSD) Septal infarction 1-7 days SHckfCHF Infarction or ana.trysm Within 48 hours Post-lnfln:t Angina Persistent coronary stenosis Anytime

multivessel disease IIICiftlllt Ml Reoccklsion Anytime Tbrombolmbalism MuraVapicallhrombus 7-10days,

DVT up to 6 months Pail:llditis lnll111111181ory 17 days (Dnlllllr'l synlhml AutoimmWll! 2-aweeks

+ Nonnal Results + No further tasting

at this tine

Tb .. Pr

See.AnfJythmias, C1 2

Surgery Surgery Surgery lnotropes, intra-aortic balloon pump Aggressive medical therapy PCI orCABG See above Anticoagulation

ASA

Toronto Notes 2011 Ischemic Heart Disease (IHD)

Treatment Algorithm for Chest Pain Chilli Pain +

1. Morphina PAN 2. 0, 3. ASA 162-325 mg cllewed 4. Nitroglycurin SL 5. ECG 6. CIWdiac Enzymas

... Initial enzymes normal ST aagment deprassion (UA) STEMI No ischemic ECG cllanges Positiva enzymes with no ECG changes (NSTEMI) Initially traet asperUA/ Obsstve: 1. Beta-blockllr NSTEMI pm --+ 2. EIIOX.IIparin (LMWH) Sari& ECGs and enzymas 3. Morphine pm 4. Oxygan Com;idur

5. ASA [if not alraady given) rspurfu&ion Rucummt pain, 6. Nitroglycarin IV options _____.. serial studies - Ri1kl111"11ifv positive .. .. PCI +

Pain resolves, low risk I I High risk I lhrvmbolysis Serial studies nonnal Hf I GPIIIrlllla intibitor, Post-inWct I Clopidogrel risk-stllllify+< Stress Test Stress Tell + low risk+ L .. +ve J Canlilc Ctheterilation I Stress Test .... "1 Corvnary Revascularization !-VI

Consider other Risk Factor causas of chest pain -ve and lif&-long

lllti-anginal Seal/6pfuuiat Shf8gy in S1fMI, Figure 3D therapy S Post-MI Risk Slnttificlfion. FlgU11131

Figure 32. Treltment Algorithm for Chest Pain AdllptBd tram Cecil fmlllillsotMedir:ine 6th Ed. Andreoli IIIII Clrpelder. p.1011Z0041with pemimian fram ElseYier

Sudden Cardiac Death Definition unanticipated, non-traumatic cardiac death in stable patient, within 1 hour of symptom onset;

ventricular fibrillation is most common cause

Etiology primary cardiac pathology

ischemia/MI LV dysfunction severe ventricular hypertrophy

hypertrophic cardiomyopathy (HCM) AS

long QT syndrome congenital heart disease

Management acute: resuscitate with prompt CPR and defibrillation investigate underlying cause (cardiac catheterization, electrophysiologic studies) treat underlying cause anti-arrhythmic drug therapy: a.miodarone, beta-blockers implantable cardioverter defibrillator (lCD)

Cardiology and CV Surgery C29

C30 Cardiology and CV Surgery Ischemic Heart Disease (IHD) Toronto Notes 2011

Wltrlllll ... IIIII Stlnll Cin:liRm 21lll8; 111;311&1206 Studr: t.lllla-nysis of RCTs lfld obii8Miional studies. 22 ACTs a 34 abeeMiioall sllllles. 1,47011111 182,1)1 pllilntsil RCTs llld allleMitianllllbdnmpecMtfiWD llldniiJI p8!QIIInBOUI CUiamy illaMnion. DNo-EUiilg S1ln1s IDES)-Bale S18IQ IBMSl. Outall: J11Crill iArction (MI), lf'ld llrgatYIR8IIMitUIIrilltion ._..: No4ilnlce in mor11ity-bmd betweea DES w. BMS II ACTs. while e.mtionli stlldillllllawlll iQnificlnttr IIMII in DES-11111ed patieull (lard rllio (HA) 0.78, p

Toronto Notes 2011 Ischemic Heart Disease (IHD)

Operative Issues isolated proximal disease in large coronary arteries (> 1.0-1.5 mm) is ideal for bypass surgery;

small, diffusely diseased coronary arteries are not suitable for bypass surgery arteries with severe stenoses (>50% diameter reduction) are bypassed, except those of small

calibre (

C32 Cardiology and CV Surgery

',, .. Dlchlllllmles Ill Hurt FaiU8 FOIWllrd vs. Backw1rd Lift-sided vs. RictTt-sidad Systolic dysfunction vs. Dilstolic dysfunction Low autput vs. High output

',, .. IIH Ejecdcm FrudDn ta Gnlde LV Dylfnction Grade I (EF (Normal I Grade II (EF = 40-59%1 Grade Ill (EF = 21-39%1 Grade IV (EF

Ischemic Heart Disease (IHD)/Heart Failure Toronto Notes 2011

Procedure OPCAB avoids the use of CPB by allowing surgeons to operate on a beating heart

stabilization devices (e.g. Genzyme Immobilizer) hold heart in place allowing operation while positioning devices (Medtronic Octopus and Starfish system) allow the surgeon to lift the beating heart to access the lateral and posterior vessels

procedure is safe and well tolerated by most patients; however, OPCAB surgery remains technically more demanding

Indications used in poor candidates for CPB who have: calcified aorta, poor LVEF, severe peripheral

vascular disease (PVD), severe COPD, CRF, coagulopathy, transfusion issues (e.g. Jehovah's Witness), good target vessels, anterior/lateral wall revascularization, target revascularization in older, sicker patients

absolute contraindications: hemodynamic instability, poor quality target vessels including intramyocardial vessels, diffusely diseased vessels and calcified coronary vessels

relative contraindications: cardiomegaly/CHF, critical left main disease, small distal targets, recent or current acute MI, cardiogenic shock, LVEF

Toronto Notes 2011 Heart Failure

Diastolic Dysfunction (impaired ventricular filling) at least 1/3 of all HF patients have nonnal systolic function (i.e. nonnal ejection fraction);

prevalence higher in older patients increased LV filling pressures produce venous congestion upstream (ie. pulmonary and

systemic venous congestion) findings: H1N, apex beat sustained, S4, nonnal-sized heart on CXR. LVH on ECG/echo, normal

LVEF causes of decreased compliance:

transient: ischemia (relaxation of myocardium is active and requires ATP) permanent

severe hypertrophy (HTN, AS, HCM) restrictive cardiomyopathy (RCM) MI

High-Output Heart Failure caused by demand for increased cardiac output often exacerbates existing heart failure or decompensates a patient with other cardiac pathology differential diagnosis: anemia, thiamine deficiency (beriberi), hyperthyroidism, A-V fistula or

L-R shunting, Paget's disease, renal disease, hepatic disease Etiologies of Primary Insults consider predisposing, precipitating and perpetuating factors most common causes see sidebar less common causes of CHF

toxic e.g. anthracyclines, radiation, uremia, catecholamines infectious e.g. Chagas' disease (common cause in South America), Coxsackie virus, HIV endocrine e.g. hyperthyroidism, DM, acromegaly infiltrative e.g. sarcoidosis, amyloidosis, hemochromatosis genetic e.g. HCM, Friedreich's Ataxia, muscular dystrophy congenital heart disease metabolic e.g. thiamine deficiency, selenium deficiency peripartum

Precipitants of Symptomatic Exacerbations consider natural progression of disease vs. new precipitant always search for reversible cause see side bar ("HEART FAILED") differential can also be organized as follows:

new cardiac insult/disease: Ml, arrhythmia, valvular disease new demand on CV system: hypertension, anemia, thyrotoxicosis, infection, etc. failure to take medications as prescribed

Tabla 1 2. Signs and Symptoms of Left vs. Right Heart Failure

Law canlilc output (farwanll

Investigations

Lift Failure Fatigue Syncope Sy&temic hypoten&ian Coal extremities Slaw capiiiiiY refill Peripheral cyanosis Pulsus aiiBmans Mitral regurgitatian 83 Dyspnea. orthopnea. PND Cough Crackles

Right Failure Right heart failure can mimic mast Df the symptoms Df forward left heart failure if decreased RV output leads to LV underfilling

Tricuspid regurgitation S3 (right-sidedl Peripheral edema Bevated .NP with AJR and Kussmaul's sign Hepalllmegmy Publllile liwr

identify and assess precipitating factors and treatable causes of CHF blood work: CBC, electrolytes (including calcium and magnesium), BUN, creatinine, fasting

blood glucose, HbAl C. lipid profile, liver function tests, serum thyroid-stimulating hormone, ferritin, BNP. uric add (associated with prognosis ofHF in Seattle HF Score)

ECG: look for chamber enlargement, arrhythmia, ischemia/infarction CXR: cardiomegaly, pleural effusion, redistribution, Kerley B-lines, bronchiolar-alveolar cuffing echocardiography: LVEF, cardiac dimensions, wall motion abnonnalities, valvular disease,

pericardia! effusion radionuclide angiography (MUGA): LVEF myocardial perfusion scintigraphy (thallium or sestamibi SPECT)

Cardiology and CV Surgery C33

...._ \ I 9,}-----------------. NIW Yark Hurt ARecidon INYHAI funeti01111l Cl-ificrion of H.-rt failllnl . a- 1: ordillllry physical activity

does not ceusa symptoms of HF a- II: comfortBble lit nJSt, ordinlll'( physicniiiC!ivity rnults in rymptoms a- ID: marked limitation of ordinary activity: less then ordinary physicniiiC!ivity results in rymptoms a- N: inability to carry out any physicniiiC!ivity without discomfort; rymptoms may be pmsnt at rust

..... ' , .,.-----------------, What ... thl Fi11 Most CDIIIIDIRI C.UielofCHF? 1