c

Cardiology and Cardiovascular SurgeryMark 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 KimBasic 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 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

Toronto Notes 2011

Cardiology and CV Surgery Cl

C2 Cardiology and CV Surgery

1'oroDio

2011

Basic Anatomy ReviewCoronary Circulation conventional arterial supply to the heart arises from the right and left coronary arteries, originating from the root ofthe aorta (see Figure I) right coronary artery (RCA) acute marginal branches atrioventricular (AV) 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

dominance ofdrculatlon

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

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)

10 I.,_-

%. ' ..I SVI!ol8 IDillltol8

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

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CardII: r....-: xdlant anly, llbsarty dMclnt l'rl!rrirrtyd8Qrt. runn.urs 1191

Flg1re Za. Cardiac Cycle

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

'IbroDlo Nota 2011

Buic Anatomy Review

Cardiology and CV SUJ'8ery C3

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

lknlla

- Middle1rlct- Posteriorlrlle:t

aiHII

Cl Ytulg M. IGm 2010

Figun 3. Conduction Systam of the Heart

C4 Cardiology and CV Surgery

Differential Diagnose5 of Common Presentations

Toronto Notes 2011

Differential Diagnoses of Common PresentationsNote: 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

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

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

Palpitations Cardiac arrhythmias (PAC, PVC, SVT, VT) mitral valve prolapse valvular heart disease J:m>ertrophic obstructive cardiomyqpatby Endocrine thyrotoxicosis pheochromocytoma hypoglycemia Systemic

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

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

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

'IbroDlo Nota 2011

Cardiac Diagnostic Testl

Cardiology and CV SUJ'8ery C5O..nrillw flf DiatiDSiic r.... Cmilc IHrurllllra (Tn. CK-MB)- in -vmptullllllie IIBbl ECG-atrwt. wi11ulnl-. orin -vmptullllllie IIBbl 811811. or with IIM:t.r illqi.. - wi1h lb8la tmilc clllleterizltiant

Cardiac Diagnostic TestsElectrocardiography (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. aVI., aVR. aVF precordial leads: VI-V6 (VI-V2 septal, V3-V4 anteriol; VS-V6lateral) additional leads right-sided leads: V3R-V6R (useful in RV infarction and dmrocardia) lateral =I, aVL, V5, V6; inferior =II, Til, aVF; &ontal =VI-V4

....

CTA

MIIAIM!I

Figura 4. ECG WHeferma 11d Nannll Values

Approach to ECGsRate

111118 Cllculltianl Examples

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 bpmRhythm 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, aVF) rate between 60-100 bpm

Practice

....AJtnuh ta EC&I &IIIIIIIY Rail Rhythn Axis Conducti111

Clwmbar rRIII!IIII&ntfhypatrophy lschami.-'lnhuctian

Milcelllneoua

Far mara

111d

'iisit

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 ofventricular depolarization forces QRS axis in the horizontal plane is not routinely calculated; it Is directed posteriorly and to theleft 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

L8ft Ant. Hemiblack lnlllriorMI WPW

RV Pacing

N0111111IYariant

RVH l..aftl'oat Hamibhx:k PE

dafacl

BIMdlld llillplngm Llad Mispl-mant Endocardial CUIIian

COPD

t..1anll Ml WF'W Dllldracanlill

Sapbll Dahn:1a

C6 Cardiology and CV Surgery

Cardiac Diagnostic Teats

Toronto Notes 2011

Intraventricular Conduction AbnormalitiesRight Bu1dla BI'IIICh Block (RBBBJ

CampiBIB RBBB QRS duration >120 msec Positive ORS in lead V1 (rSR' or occasionally broad Rwave] Broad Swaves in leads I, VS-6 (>40 msecl Usually secondll'fTWIIW inversion i'lleads V1-2

Lift Bundl1 B111nch Block (LBBBJ Ca11platll LIBB QRS dLnlion >120 msec Broad notched or slurred Rwaves in leads I, aVI.. and usuallyV5andV6

Deep broad Swaves in leads V1-2

Figure 5. Axial Reference System Elldlilld conlliis I+) Bill dispid by 1hi!DIllmiWI. lirpJEstllllei"-J toward the plllitM

Secondlry ST-T changes (-vein leads with broad RWIIWS, +vein V121 are usually present LBBB usually masks ECG signs Df myocardial inlan:tion

ol1flllllll rlllllts in Ill upMtd dallection il thatilld. NonriiQRS IIliis is between -30'111d +90'.

(Left Antcrill' Hemibloc:kl

Left Anllriar Fudc:ullr Bloc:k (LAFBI LBft l'oltlriar F.c:ic:ullr Bloc:k (LPFBI Biflldc:ullr Bloc:k {Left Pauiar Hemibloc:kl Left axis deviation (-30" 1D -911"1 Right axis deviation ( 11 II" 1D 1811"1 RBBB pattern Small q and prominent Rin Small r and prominant S i1 Small q and prominent Rleads I and aVL Small r and prominent Sin leads II. IlL and aVF leads I and aVL Small qand prominent Rin leads 11,111, and aVF 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

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 characteristicsI

lll'lllilt

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 aVF ("P pulmonalea) Laft Atrial EnlargementRight Atrial Enlargement

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

mmmm

'IbroDlo Nota 2011

Cardiac Diagnoslic Testl

Cardiology and CV SUJ'8ery C7

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

,,IIIJ!IIIclllt EC& ClllngM

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 occurwith angina

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 1mm il 2 14acant inb lalds, Dr lit least 1-2 rnm in ldjacllll precordilllds ST prweion: diiWI!IIgpilg Drharimntlll Q WIIVI; pllh*9icll if CIIISO!:lsmall

11111111lRS

mwcl or >3B of the

,,..----------------,Q. _

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

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 75IliaballS

4.1).5.9 (mod) 8.5-1 8.2

caurradin (INR 2-3) caurradin IINR 2-3)

Slnia'TIA. (flill')

AFonECG 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)

Milllill*l-m.ITrial N1112002; 3U:1B33af3.5 ,an. .....,:QQprilllls(irMIIIQI70"A 61lmU.IIIv.tai-Mthllrill1libli1111ionanl lii#J rilltItlllralllll' d!Bit ............ IIIIa cU:inn dlllniiiiDI:bn. crligmin iblear ildq

IIWr:RWIIonilld.

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) ifAF 24-48 hrs, anticoagulate fur 3 weeks prior and 4 weeks after cardioversion ifpatient 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 8511111!11iiM Mill' llllllcllnl1art lillllltlhm dalceII Vf >95'1. "Mrt tlmiwle vr iliiiiiW no IIIUcllnlhiWIdiaa

VT

Exbwna axis daviati111

Clplure or flllilll QIIS widlh >140 msa:

vr vr vrVT

vr May suggast: vr vr (polymalplic)

_..willl

Torsadea de Polntes a variant of polymorphic VT that occun In patients with baseline QT prolongation- "'twisting ofthe 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 ifhemodynamic compromise

'IbroDlo Nota 2011

Cardiology and CV Surgery Clt

Figura 27. Tarud da PailtalVentricular 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 ofsudden death refer to ACLS algorithm for complete therapeutic guldellnes

r 'fFigura Zl. v..bic..ar Fir..lltian

J

L,.

,; 1

'":1

Electrophysiology (EPS) Studies invasive test fur the investigation and treatment of cardiac rhythm disorders using iotn!cardi.ac catheters provide detailed analysis ofthe arrhythmia mechanism and precise site oforigin when ECG data are nondiagnostic or unobtainable bradyarrhytbmias: define the mechanisms ofsinus 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 ofa bradyarrhythmia or tachyanhythmia in the setting ofheart: diseasePacemaker 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 biventrlcularTallie 5. Pacemakar Nonaclature1'111111111 I

CllanOr paced0 = Nana A= AlrUn v= v.ntri:IIJ D= lklai(A+V)

I'DIIIIal I ChltM lensed0 = None A= Atriun v= Ventricle D=Dual (A+V)

1'111111111. Reapcnae tD 1181'11ing0 =None I= lnhlitad T= Tri!prad

I'DIIIIIIIIVPnlpnmability 0 =None R= Rata rnoct.da1im

Tactryanhythmia como!

S =Shock D= Dual (P+SI

0 = NIIIB P = Paca

examples ofcommonly used pacemakers 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 ofsinus rhythm and normal AV ronduction, provides physiologic pacing

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; 147:25162 Studr: Mela-!Mw of 12 RCTs used for lmpilnllbll CltdiMIW llllillillltDr (ICDI mcy, 5RCTs IUid 48 DbseMdilllll Allfiesfor 111d 21 RCTs1nd 43 DbnmliDI'III sludiesfor Sllely rMiw. 8516 b' ICDeflicq 26 840

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 1o 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

far ..r.ty IIYiiiW Ylitb 11ft Wll1lricUir ljac:tian hlction Qllntlllle Cardiomler Delldllwimplllrotian. Aklllle martll!y lllllllvne eveJ'G a.ulll: ICDs radUCid morlllly by 20'JonMb:lian (54\l in suddan Clldi.: dlllh 1Q. 37\. 63%; hid I rab:ed relltiw risk rl 0.54 fur ll.ggse mllltJIIy1 1 =44.4\IMI!grnlnt

Catheter AblationTechniques 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

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. -

Indications paroxysmal SVT AVNRT: 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 DiseaseMljar Rislr: FIU:bn Milar Risk Factan Male, pos1menopausal female

SmokingDiabetes mellitus {DM)

Hypsrbn&ion (HlN) Ftrnily history (FHx) Dl MlFim degree male rei alive hill liJtler Ales of '-CI.IIIrimlion 114.6Y81Q alfvlkM-11p (lllmd lllie 0.60, P18 indicates likely cardiac etiology) mechanical ventilation as needed rarely used, but potentially life-saving measures: intra-aortic balloon pump (IABP) left or right ventricular assist device (LVAD/RVAD) cardiac transplant

Long Term ManagementConservative Meuura 1. Symptomatic measures: oxygen in hospital, bedrest, elevation of head of bed 2. Lifestyle measures (grade B evidence): diet, exercise, DM control, smoking cessation, decrease alcohol consumption, patient education, sodium and fluid restriction 3. Multidisciplinary heart failure clinics (grade B evidence): for management of individuals at higher risk, or with recent hospitalization Pharmacological Therapy I. Vuodilators a. ACEis: standard of care - slow progression of LV dysfunction and improve survival all symptomatic patients functional class II-IV (grade A) all asymptomatic patients with LVEF 5.2 mmol/L

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C llllic Tr..ment-' CHF ... ACE inhibi1Dr5* Beta blockers* Aldonlronuntagonim*(if IIYirl CHF) Diurvtic lnotropa Antiarrythmic Anticoagulant

* = Mortality Benflfit

....

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Mllllcllllons Contralndlcmd In CHF NSAJDS -may increese BP Clanl/ID antilllhythmics Metformin - Cll in severe HF Thiazolidinedionas- increase ed.ma cGMP phosphodiestel'lllse (e.g. sildllllllfil) with basalina low BP

Toronto Notes 2011

Heart Failure/Cardiac Transplantation

Cardiology and CV Surgery C35

5. lnotropes: digoxin improves symptoms and decreases hospitalizations, no effect on mortality indications: patient in sinus rhytlun and symptomatic on ACEI (grade A), or CHF and atrial fibrillation (grade B) patients on digitalis glycosides may worsen if these are withdrawn6. Anti-arrhythmic drugs: for use in CHF with arrhythmia can use amiodarone, beta-blocker, or digoxin (grade B)

7. Anticoagulants: warfarin for prevention of thromboembolic events prior thromboembolic event or atrial fibrillation (grade B), presence of LV thrombus on echo possible benefit in other patients with LVEF 130 ms, LVEF 150 ms, high diuretic requirement lCD: mortality benefit in 1c and 2c prevention of sudden cardiac death prior MI, optimal medical therapy, LVEF Y PresentUncolllllOn

Y>YAbsent/lJwsys

Pericardia! knockHypotension

PresentVariable

AbsentSevere

C46 Cardiology and CV Surgery

Peripheral Arterial Disease

Toronto Notes 2011

VASCULAR DISEASE Peripheral Arterial DiseaseAcute Arterial Occlusionnnsufficiency-------------

Definition acute occlusion/rupture of a peripheral artery urgent management required: >6 hours results in irreversible ischemia and myonecrosis lower extremity> upper extremity; femoropopliteal > aortoillac

....Dilfllrentill of ClaudicdanV.scular Atherosclerotic disease

Vasculitis (e.g. Buerver's dis-.Takayasu's lllteritist

Venous disease (e.g. DVT. varicou Popliteal entnlpment syndromevain&I

Dillbelic neuropathy

Neurospinll disease (e.g. spinalatenosist dystrophy

Etiology embolus cardiac embolus (80-90%): history of MI 0.4 cm/yr symptoms, comorbidities (HTN, COPD, dissection), smoking elective AAA repair mortality 2-5%; elective TAA repair mortality 5.5 em or >2x normal lumen size) ascending thoracic aortic aneurysms symptomatic, enlarging, diameter >5.5 em or >2x normal lumen size, >4.5 em and aortic regurgitation (annuloaortic ectasia); em in Marfan syndrome contraindications: life expectancy