Toronto Notes 2011 - Cardiology_and_Cardiovascular_Surgery

Download Toronto Notes 2011 - Cardiology_and_Cardiovascular_Surgery

Post on 30-Nov-2015




7 download




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 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, 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 traCl4 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 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 (, 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 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, 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 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 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 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! 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, PToronto 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)!., pToronto 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, pToronto 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. CoroniiV lltery disease {61HO'Yo) 2. HTN 3. Idiopathic {often in the fonn of dilated cardiomyopathy) 4. Valvul.-{e.g_ AI., AR and MRI 5. Alcohol {may CMJSB dilllllld cardiomyopathy) Preclpillntll of llllut hilur1 HEART FAILED Hypertension (common) fndocerditir,/snvironmsnt {e.g_ hset WliVel Anemia humlltic h..n diull11 and othlr valwlar disease Thyrotoxicosis Failure to take meds {very common) Antlythmia {common) lnfectionlischemi.tlnfllrction (common) Lung problems {PE, pneumonia. COPD) Endocrine (pheochromocytomlr, hyperaldosteronism) Di11111ry ildiscrwtions {common) .... ' , 9J-----------------. Mnsurlng NT11f8 BNP BNP is 158C1'818d by ventricles due to LV llnlll:h end Wlll1llnlion. Cardiomyocytn semll BNP priCIIISOI that is claaved iniD proBNP. After secretion into ventricles. proBNP is cl811'18d into the IIC!ive C-111nninal portion end the inar:tive NT-proBNP portion. Nf.tlroBNP levlls (pa/lal.) Ag1 HF wry liklly 450 50-75 >900 >75 >1800 Umillllions - Age, body habitus, renal function. pulmonary 1111bolism C34 Cardiology and CV Surgery Heart Failure Toronto Notes 2011 It' F...,_ -' Hrl hilun1 gn CXR HERB-8 Heart enlarvament (cardiothcncic ndio >0.50) Pleural Effusion Ra-diSlribution (alveolar Kerley &-tine Bronchiollll"llivllolar culling SIIIId llllllt Fliln in Mlb? ..111M 1997; 277:1712-19 1ba beslliDilgs far dlllding incrnsed 111111 pli!SUI! 1111 llliqlpllic radinilldian.. "lbe betlliDilgs far dellc:ting ct,Rinctian 1111111 lllnllllllllllpicll irnpulsl, llliqlpllic ltwavesllfl.B88 011111 lllae1nlclrdiognm.. "Oiulaic dysfooc1ian is litlicuiiD dillpSI but iliSIOCillad wilh alMIId bbod 111111U11 during hell! .... , .. .----------------. C ... llllic Tr..ment-' CHF ACE inhibi1Dr5* Beta blockers* Aldonlronuntagonim* (if IIYirl CHF) Diurvtic lnotropa Antiarrythmic Anticoagulant * = Mortality Benflfit .... , , Mllllcllllons Contralndlcmd In CHF NSAJDS -may increese BP Clanl/ID antilllhythmics Metformin - Cll in severe HF Thiazolidinedionas- increase cGMP phosphodiestel'lllse (e.g. sildllllllfil) with basalina low BP Acute Treatment of Pulmonary Edema treat acute precipitating factors (e.g. ischemia. arrhythmias) L - (furosemide) 40-500 mg IV M -morphine 2-4 mg IV- decreases anxiety and preload (venodilation) N- nitroglycerin- topica1/IV/SL 0- oxygen P- positive airway pressure (CPAP/BiPAP)- decreases preload and need for ventilation P - position - sit patient up with legs hanging down unless patient is hypotensive in ICU setting or failure ofLMNOP, other interventions may be necessary nitroprusside (IV) hydralazine (PO) sympathomimetics dopamine - low dose: selective renal vasodilation (high potency D1 agonist) - medium dose: inotropic support (medium potency agonist) - high dose: increases SVR (low potency agonist), which is undesirable dobutamine - selective inotrope agonist) and arterial vasodilator antagonist) phosphodiesterase inhibitors (milrinone) - inotropic effect and vascular smooth muscle relaxation (decreased SVR), similar to dobutamine - adverse effect on survival when used as long-term oral agent consider PA catheter to monitor pulmonary capillary wedge pressure (PCWP) if patient is unstable or a cardiac etiology is uncertain (PCWP > 18 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 Management Conservative 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 Toronto Notes 2011 Heart Failure/Cardiac Transplantation 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 withdrawn 6. 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 1 c and 2c prevention of sudden cardiac death prior MI, optimal medical therapy, LVEF C36 Cardiology and CV Surgery REMATCH Trill 1>1111 Jlicnc 1999; 67:723-730 lncallld III1MI al 23'1. 111. 8'li. LVAD VI. 1111di:llll111111Q111Ef11 ol belllfaiknlf!Br 2 Helllmlll VAD ha 1 biqic: lll.lla,1llillbv does not require 10110"tmm l9rlr rilk al irQction. Cardiac TranaplantationJMyocardial Diseue Toronto Notes 2011 infection leading cause of morbidity and mortality after cardiac transplantation risk peaks early during the first few months after transplantation and then declines to a low persistent rate allograft coronary artery disease approximately 50% develop graft CAD within 5 years of transplantation the most common cause of late death following transplantation malignancy develop in 15% of cardiac transplant recipients second most common cause of late death following transplantation cutaneous neoplams most common, followed by non-Hodgkin's lymphoma and lung cancer immunosuppressive medication side effects (prednisone. cyclosporine., Prognosis the Heart Failure Survival Score (HFSS) uses 7 prognostic variables - ischemic cardiomyopathy; resting heart rate. LVEF, mean BP, QRS > 120ms, serum Na, peak V02 -to stratify patients into low, medium, and high risk categories; one-year survival rates without transplant for these three strata were 88, 60, and 35%, respectively Ventricular Assist Devices (VADs) works to unload the ventricle while maintaining its output; also results in decreased myocardial oxygen consumption, permitting recovery of the myocardium that is not irreversibly injured can support the left (LVAD), right (RVAD) or both ventricles (BiVAD) indications bridge to transplantation postoperative mechanical support when unable to separate from cardiopulmonary bypass despite inotropic and Intra-Aortic Balloon Pump (IABP) support IABP is a catheter based device inserted into the aorta via the femoral artery that decreases myocardial 0 2 demand and increases blood flow to coronary arteries postoperative cardiogenic shock Myocardial Disease Definition of Cardiomyopathy (CMP) intrinsic or primary myocardial disease not 2 to congenital, hypertensive, coronary, valvular, or pericardia! disease functional classification: dilated, hypertrophic or restrictive LV dysfunction 2 to MI often termed "ischemic cardiomyopathy", but is not a true cardiomyopathy (Le. primary myocardial disorder) since the primary pathology is CAD Myocarditis Definition inflammatory process involving the myocardium ranging from acute to chronic; an important cause of dilated cardiomyopathy Etiology idiopathic infectious viral (most common): coxsackie B, echovirus, poliovirus, HIY, mumps bacterial: S. aureus, C. perfringens, C. diphtheriae, Mycoplasma, Rickettsia fungi spirochetal (Lyme disease - Borrelia burgdorftn) Chagas disease (Trypanosoma cruzi), toxoplasmosis toxic: catecholamines, chemotherapy; cocaine hypersensitivity, eosinophilic: drugs (antibiotics, diuretics, lithium, clozapine), insect/snake bites systemic diseases: collagen vascular diseases (SLE, RA, others), sarcoidosis, autoimmune other: giant cell myocarditis, acute rheumatic fever Signs and Symptoms constitutional symptoms acuteCHF chest pain - due to pericarditis or cardiac ischemia arrhythmias systemic or pulmonary emboli sudden death Toronto Notes 2011 Myocardial Disease Investigations ECG: non-specific ST-T changes conduction defects bloodwork increased CK, troponin, LDH, and AST with acute myocardial necrosis increased WBC, ESR, ANA, rheumatoid factor, complement levels blood culture, viral titres and cold agglutinins for Mycoplasma CXR: enlarged cardiac silhouette echo: dilated, hypokinetic chambers, segmental wall motion abnormalities myocardial biopsy Management supportive care restrict physical activity treatCHF treat arrhythmias anticoagulation treat underlying cause if possible Prognosis usually self-limited and often unrecognized, many recover sudden death in young adults may progress to dilated cardiomyopathy few may have chronic myocarditis Table 13. Summary Table for CH F and Myocardial Disease SYSTOLIC HEART FAIWRE DIASTOLIC HEART FAIWRE Dilalad Cardiomropallly Idiopathic, infectious (e.g. myocarditis), alcohol, fllmiial, collagen vascular disease, etc. Secondary CauHs Coronary artery disease, Ml, diabetes, vnlar (e.g. AR, MR) Hypallnlphic Cardiomyopathy Genetic disorder affecting cardiac sarcomeres (most common cause of sudden cardiac death il young athletes) Rasbictive Caniomyopallrr Amyloidosis, sarcoidosis, sderoderrna. h111110clromatosis, Fab!J's. Pompe's Disease, Loefller's, etc. SacandiiJ Causes Hypertension. diabetes, valvular {e.g. AS), post-MI, transiently by ischemia, etc. Dilated Cardiomyopathy (DCM) Definition unexplained dilation and impaired systolic function of one or both ventricles Etiology idiopathic (presumed viral or genetic) -50% ofDCM alcohol familial uncontrolled tachycardia (e.g. persistent atrial fibrillation) collagen vascular disease: SLE, PAN, dermatomyositis, progressive systemic sclerosis infectious: viral (coxsackie B, HIV), Chagas disease, Lyme disease, Rickettsial diseases, acute rheumatic fever, toxoplasmosis neuromuscular disease: Duchenne muscular dystrophy, myotonic dystrophy, Friedreich's ataxia metabolic: uremia, nutritional deficiency (thiamine:, selenium, carnitine) endocrine: hyper/hypothyroidism, DM, pheochromocytoma peripartum toxic: cocaine, heroin, organic solvents drugs: chemotherapies (doxorubicin, cyclophosphamide), anti-retrovirals, chloroquine, clozapine, TCA radiation induced Signs and Symptoms may present as CHF systemic or pulmonary emboli arrhythmias sudden death {major cause of mortality due to fatal arrhythmia) Cardiology and CV Surgery C37 .... , , M-iof Risks Factars hr DCM Alcohol, cocaine, family history and obesity. C38 Cardiology and CV Surgery ..... , Allnonnal Lalli in DCM High 8NP High Cr High LFTa low Bicarb lowNa Myocardial Diseue Toronto Notes 2011 Investigations bloodwork: CBC, electrolytes, Cr, bicarbonate, BNP, CK, troponin, LFfs, TSH, TIBC ECG: variable ST-T wave abnormalities, poor R wave progression, conduction defects (e.g. BBB), arrhythmias (non-sustained VT) CXR: global cardiomegaly (globular heart), signs of CHF, pleural effusion echocardiography: chamber enlargement. global hypokinesis, depressed LVEF, MR and TR, mural thrombi endomyocardial biopsy: not routine, used to rule out a treatable cause angiography: in selected patients to exclude ischemic heart disease Management treat underlying disease: e.g. abstinence from EtOH treat CHF: see Heart Failure. C32 thromboembolism prophylaxis: anticoagulation with warfarin indicated for: AF, history of thromboembolism or documented thrombus LVEF Toronto Notes 2011 Myocardial Disease Management avoid factors which increase obstruction, including volume depletion and strenuous exertion treatment ofHOCM (with LVOT obstruction) medical agents: beta-blockers, disopyramide, verapamil (only in patients without resting or provocable obstruction) avoid nitrates, diuretics and ACEI as they decrease outflow tract diameter and worsen symptoms patients with drug-refractory symptoms surgical myectomy septal ethanol ablation dual chamber pacing treatment of ventricular arrhythmias: amiodarone or ICD first-degree relatives of patients with HCM should be screened annually during adolescence (physical, ECG, 2D echo), then serially every 5 years Prognosis potential complications: AF, VT, CHF, sudden death (most common cause ofSCD in young athletes) major risk factors for sudden death (consider lCD placement) history of survived cardiac arrest/sustained VT family history of multiple premature sudden deaths other factors associated with increased risk of sudden cardiac death syncope non-sustained VT on ambulatory monitoring marked ventricular hypertrophy (maximum wall thickness mrn) abnormal BP in response to exercise (in young patients with HCM) Restrictive Cardiomyopathy (RCM) -------------------Definition impaired ventricular filling with usually intact systolic function in a non-dilated, non-hypertrophied ventricle 2 to myocardial abnormality (stiffening, fibrosis and/or decreased compliance) usually with intact systolic function initially Etiology infiltrative: amyloidosis, sarcoidosis non-infiltrative: scleroderma, idiopathic myocardial fibrosis storage diseases: hemochromatosis, Fabry's disease, Gaucher's disease, glycogen storage diseases endomyocardial endomyocardial fibrosis, Loeffler's endocarditis or eosinophilic endomyocardial disease radiation heart disease carcinoid syndrome (may have associated TV or PV dysfunction) Clinical Manifestations CHF (usually with preserved LV systolic function), arrhythmias elevated JVP with prominent x and y descents, Kussmaul's sign S3, S4, MR, TR thromboembolic events Investigations ECG: low voltage, non-specific, diffuse ST-T wave changes non-ischemic Q waves CXR: mild cardiac enlargement echo: LAE, RAE; specific Doppler finding with no significant respiratory variation cardiac catheterization: increased end-diastolic ventricular pressures endomyocardial biopsy: to determine etiology (especially for infiltrative RCM) Management exclude constrictive pericarditis treat underlying disease: control HR, anticoagulate if atrial fibrillation supportive care and treatment for CHF, arrhythmias heart transplant: might he considered for CHF refractory to medical therapy Prognosis depends on etiology Cardiology and CV Surgery C39 C40 Cardiology and CV Surgery Valvular Heart Disease Toronto Notes 2011 Valvular Heart Disease Infective Endocarditis (IE) see Infectious Diseases. ID14 AHA 2007 guidelines recommend IE prophylaxis only for patients with prosthetic valve material, past history of IE, certain types of congenital heart disease or cardiact transplant recipients who develop valvulopathy only for the following procedures dental respiratory tract procedures on infected skin/skin stru.ctures/MSK structures + not GI/GU proudura specifically Rheumatic Faver see Pediatrics, P57 Prognosis acute complications: myocarditis (DCM/CHF), conduction abnormalities (sinus tachycardia, AF), valvulitis (acute MR), acute pericarditis (not constrictive pericarditis) chronic complications: rheumatic valvular heart disease - fibrous thickening, adhesion, calcification of valve leaflets resulting in stenosis/regurgitation, increased risk of IE thromboembolism onset of symptoms usually after 10-20 year latency from acute carditis of rheumatic fever mitral valve most commonly a1fected Choice of Valve Prosthesis ........ C..i:ll ,.. .. bllflrlllllctq ........ ..... Tabla 14. Mechanical Valva vs. Bioprosthatic Valva Etdlells E. Glnns V, Shldowilz S. Bel C. SiJ S. JS.SIIIf8mu.lll8811; 131101:6K-'104. Dljiii1NIIII Mldicinl, TGRHlbl Haspilll, ON. c-a. Bhled CIOIS taetionaiiiUdy. Mil: 1 Z4 PlllieniJ uurrmulmy canioloa clnic.l'llilnll wmmminld fllr: I) nunu DVII the right cliMcle 2) nunu loudest llsecurat rigli imollaiiJliC13) llducad i1lllllity of S2 4) !educed volume 11111e Cldlldse 51 deiiYI!d Clllllidi4JSinlll . .... l'ldilnll Wllllllllllinld by blindld iwalligllm, and the Cliliclllllllmi'illiDII findings Will compnl fD finlilgs on !l6slquant Modellle" --lllnlllil-dlfinld 'IIM-25 ITIT1Hq. Rllulll: Abearafla nunu DVII the rigli cBvicle 1\ild out aortic stlllotis wflile affla 4 111Cii1Bd in lllltic s11nosis Cam:lllianl: lled!idlllehnitJBI C8111CCU!It81y rula in and rula out rnodarlll _, - lllnosil. Machanical Vllva BiDprostllllic Valva o Good durability o Less prefi!IT!d in small acrtic root (stl!lloticl o Increased risk of thromboembolism (1 anticoagulation with coumadin o Target INR aortic valves: 2.1h!.D mitral valves: 2.5-3.5 o Increased risk of hemonhage: 1-2"1Vyear o Limited long-term durability (milralToronto Notes 2011 Valvular Heart Disease Cardiology and CV Surgery C41 Summary of Valvular Disease Table 15. Valvular Heart Disease AS Etiology click Congenital (bicuspid, unicuspid valve), calcification (wear and tear), rheumatic disease Aortic valve area: N=34 cm2 s, s, s, Mild AS 1.5 to 3 cm2 Anas Nader 2009 Moderate AS 1 .0 to 1 .5 cm2 Severe AS < 1.0 cm2 Critical AS 40 yrs (male) or >50 yrs (female) Treatment Avoid exertion, fever (increased LA pressure), treat AF and CHF, increase diastolic filling time (beta-blockers, digitalis) Surgery if: NYHA class III-IV CHF and failure of medical therapy (usually MVA < 1 .2 cm2) Invasive Options Percutaneous balloon valwloplasty: young rheumatic pts and good leaflet morphology, asymptom pts with mod-sev MS, new-onset AF. pulmon HTN Contraindication: Left atrial thrombus, moderate MR Open Mitral Commissurotomy: If mild calcif + leaflet/chordal thickening - restenosis in 50% pts in 8 yrs Valve replacement: mod-sev calcif and sev scarred leaflets AR Etiology Supravalvular: aortic root disease (Marian's, atherosclerosis and dissecting aneurysm, connective tissue disease) Valwlar: congenital (bicuspid AV. large VSD), IE s, s, Acute Onset: IE, aortic dissection, trauma, failed prosthetic valve Pathophysiology s, Anas Nader 2009 Volume overload -+ LV dilatation -+ increased SV, high sBP and low dBP -+ increased wall tension -+ pressure overload -+ LVH (low dBP -+ decreased coronary perfusion) Symptoms Usually only becomes symptomatic late in disease when LV failure develops Dyspnea, orthopnea, PND, syncope, angina Physical Exam Waterhammer pulse, bisleriens pulse, femoral-brachial sBP > 20 (Hill's test wide pulse pressure), hyperdynamic apex, displaced PM I, heaving apex Auscultation: early decrescendo diastolic murmur at LLSB (cusp) or RLSB (aortic root), best heard sitting, leaning forward, on full expiration, soft S1, absent S2, S3 (late) Investigations ECG: LVH, LAE CXR: LVH, LAE, aortic root dilatation Echo/TTE: quantffy AR, leaflet or aortic root anomalies Cath: ff >40 yrs and surgical candidate-to assess for ischemic heart disease Exercise testing: hypatension with exercise Treatment Asymptomatic: serial Echos, afterload reduction (e.g. ACEis, niledipine, hydralazine) Symptomatic: avoid exertion, treat CHF Surgery if: NYHA class III-IV CHF. LVEF C42 Cardiology and CV Surgery Valvular Heart Disease Toronto Notes 2011 Table 15. Valvular Heart Disease (continued) TS Etiology Rheumatic disease, congenital, carcinoid, fibroelastosis; usually accompanied by MS Pathophysiology Increased RA pressure -+ right heart failure -+ decreased CO and fixed on exertion Symptoms Peripheral edema, fatigue, palpitations Physical Exam s, S, OS s, Anas Nader 2011 Prominent a waves in JVP, +ve abdominojugular reflex, Kussmaul's sign, diastolic rumble 4th left intercostal space Investigations ECG: RAE CXR: dilatation of RA without pulmonary artery enlargement Echo: diagnostic Treatment Preload reduction (diuretics) Surgery if: usually only ff other surgery needed (e.g. MVR) Surgical Options Valve Replacement: -If severely diseased valve - Bioprosthesis preferred PS click Etiology Usually congenital, rheumatic disease (rare), carcinoid Pathophysiology s, s, s, Increased RV pressure -+ Anas Nader 2009 RV hypertrophy -+ right heart failure Symptoms Chest pain, syncope, fatigue, peripheral edema Physical Exam Systolic murmur at 2nd LICS accentuated by inspiration, pulmonary ejection click. right-sided S4 Investigations ECG: RVH CXR: prominent pulmonary arteries enlarged RV Echo: diagnostic Treatment Balloon valvuloplasty if severe symptoms Surgical Options Percutaneous or open balloon valwloplasty Mitral Valve Prolapse Etiology TR Etiology RV dilatation, IE (IV drug use), rheumatic disease, congenital (Ebstein anomaly), carcinoid Pathophysiology s, RV dilatation -+ TR -+ further RV dilatation -+ right heart failure Symptoms Peripheral edema, fatigue, palpitations Physical Exam s, s, Anas Nader 2009 cv waves in JVP. +ve abdominojugular reflux, Kussmaul's sign, holosystolic murmur at LLSB accentuated by inspiration, left parastemallift Investigations ECG: RAE, RVH, AF CXR: RAE, RV enlargement Echo: diagnostic Treatment Preload reduction (diuretics) Surgery if: usually only ff other surgery needed (e.g. MVR) Surgical Options Annuloplasty, i.e. repair (rarely replacement) PR Etiology Pulmonary HTN, IE, rheumatic disease, tetralogy of Fallot (post-repair) Pathophysiology s, s, s, Increased RV wlume -+ increased wall tension -+ Anas Nader 2009 RV hypertrophy -+ right heart failure Symptoms Chest pain, syncope, fatigue, peripheral edema Physical Exam diastolic murmur at LLSB, Graham Steell (diastolic) murmur 2nd and 3rd LICS increasing with inspiration Investigations ECG: RVH CXR: prominent pulmonary arteries ff pulmonary HTN; enlarged RV Echo: diagnostic Treatment Rarely requires treatment; valve replacement ff severe Surgical Options Pulmonary valve replacement Myxomatous degeneration of chordae; thick. bulky leaflets that crowd orifice; Marian's syndrome; pectus excavatum, straight back syndrome, other MSK abnormalities; 'IbroDlo Nota 2011 15111 LV IIIII 1 s\ IZ Figure 33. Hemodynamics Df Aortic -TIME Stenosis across the aortic valva res!Ms in the generation af a significant pressure gradient between the laft ventricle and the aorta and a aascendo-(Jecrescendo munnur during systolic contraction. The stenosis decreases the i ntllnsity af aortic valve closure hance dimirishing S2. "" Ill "\ / \ 'SII81 j I "' li ,. \ .!. i II I ll = 151 I II I, J II I H ; I II _)) ......... Valvular Heart Diseaae ,. Lvr\ I \. ADIIIIC 81 \ PRESSURE 'j l \ DROP = . ' ill "'i \ 151 .' , r H I I I II I HEART I 1111 SOUNDS: II sz Figure 34. HemiMipllllllcs of Aortic Ragu.,;tmo. nME Regurgitation across the aortic valve during diastnle causes tha aortic pressure to rapidly decrease and a decrescendo munnur can be heard at the onset of diastole I after S2 is audible). The presence af regurgitant blood from the aorta incraasas laft-ventricular and-(Jiastolic volume. (\ I ' ) \ I i 1 I I, I I I I I 1. I I / i --!...1 \_ ..... -TIME HURr I I I IIII 11111111 Ill SGUNDS: Sl SZ OS Sl sz Figure 3&. Hemodynamics Df Mitral Stenosis CardioloBf and CV Surgery C43 110 LV I LA - 1 TALL WAVE : r \1: / \ t'X. II 10 __ )' l IEART SOUNDS: I Sl SZ TIME Figura 35. Hemodynllllllcs of Acnl Mitral Regurgitation During systolic contraction, blood 111!1Urgitates from the I aft ventricle into tha 111ft a1rium across tha incompetent mitral valve resulting in an audible holosystolic munnur batwean S1 and S2. The portion af left ventricular end diastolic volume that regurgitates into the 111ft a1rial myocardium inaeases laft a1rial preSSII"es resulting in a tal V-wava. Cl iii E I;! ::i I!' 0 Fir.rt nota that tha 111ft atrial pressure exCBBds the 111ft ventriwar pressure during diastole dua to mitral stenosis and 1he consequent generation af a pressure gradient across the left atrium and left ventricle. In diastola, the stenotic mitral valve opens which cotTBiponds to the opening snap (OS) and the paBSige of blood across tha rritral stanosis results in an audible dacrescendo munnur. Laft a1rial contraction prior to S1 inCT1111SB& tha preSSII"B gradient resulting in accantuation of tha munnur before S 1 is audible. C44 Cardiology and CV Surgery Pericardial Disease Toronto Notes 2011 ..... , , Acull PeriCinltil Chest Pain Friction Rub ECG Chanv-s ..... , , Ewn'sSign llronchill brelltiJing and dulmss to percussion at til& lower lllgla of til& left scapula in periclrdilll ellusion due 1D affusion compressing I aft lower lobs of lung. Pericardial Disease Acute Pericarditis Etiology of Pericarditis/Pericardia! Effusion idiopathic is most common: usually presumed to be viral infectious viral: Coxsackie virus A, B (most common), echovirus bacterial: S. pneumoniae, S. aureus TB fungal: histoplasmosis, blastomycosis post-MI: acute (direct extension of myocardial inflammation, 1-7 days), Dressler's syndrome (autoimmune, 2-8 weeks) post-cardiac surgery (e.g. CABG), other trauma metabolic: uremia (common), hypothyroidism neoplasm: Hodgkin's, breast, lung, renal cell carcinoma, melanoma collagen vascular disease: SLE, polyarteritis, RA, scleroderma vascular: dissecting aneurysm other: drugs (e.g. hydralazine), radiation, infiltrative disease (sarcoid) Signs and Symptoms diagnostic triad: chest pain, friction rub, and ECG changes pleuritic chest pain - alleviated by sitting up and leaning forward pericardia! friction rub- may be uni-, bi- or triphasic fever, malaise Investigations ECG: initially diffuse elevated ST segments depressed PR segment, the elevation in the ST segment is concave upwards -+ 2-5 days later ST isoelectric with T wave flattening and inversion CXR: normal heart size, pulmonary infiltrates echo: assess pericardia! effusion Treatment treat the underlying disease anti-inflammatory agents (high dose NSAIDs/ ASA, steroids if severe or recurrent); analgesics Prognosis complications: recurrence, atrial arrhythmia, pericardia! effusion, tamponade, constrictive pericarditis Pericardial Effusion Etiology transudative (serous) CHF, hypoalbuminemia/hypoproteinemia, hypothyroidism exudative (serosanguinous or bloody) causes similar to the causes of acute pericarditis may develop acute effusion secondary to hemopericardium (trauma, post-MI myocardial rupture, aortic dissection) physiologic consequences depend on type and volume of effusion, rate of effusion development, and underlying cardiac disease Signs and Symptoms may be asymptomatic or similar to acute pericarditis dyspnea, cough extra-cardiac (esophageal/recurrent laryngeal nerve/tracheo-bronchial/phrenic nerve irritation) ]VP increased with dominant Y descent arterial pulse normal to decreased volume, decreased pulse pressure auscultation: distant heart sounds rub Investigations ECG: low voltage, flat T waves CXR: cardiomegaly, rounded cardiac contour echo (procedure of choice): fluid in pericardia! sac pericardiocentesis: definitive method of determining transudate vs. exudate, identify infectious agents, neoplastic involvement Treatment mild: frequent observation with serial echocardiograms, treat underlying cause, anti-inflammatory agents for inflammation severe: may develop cardiac tamponade Toronto Notes 2011 Perlcardial Diaeaae Cardiac Tamponade --------------------------------------Etiology major complication of rapidly accumulating pericardia! effusion; cardiac tamponade is a clinical diagnosis any cause of pericarditis but especially trauma, malignancy, uremia, idiopathic, proximal aortic dissection with rupture Pathophysiology high intra-pericardia! pressure -+ decreased venous return -+ decreased diastolic ventricular filling -+ decreased CO -+ hypotension and venous congestion Signs and Symptoms tachypnea, d}'lipnea, shock, muffled heart sounds pulsus paradoxus (inspiratory fall in S}'litolic BP >10 mmHg during quiet breathing) JVP "xD descent only, absent Y descent hepatic congestion/peripheral edema Investigations ECG: electrical alternans (pathognomonic variation in R wave amplitude), low voltage echo: pericardia! effusion, compression of cardiac chambers (RA and RV) in diastole cardiac catheterization Treatment pericardiocentesis - echo- or ECG-guided pericardiotomy avoid diuretics and vasodilators (these decrease venous return to already under-filled RV -+ decrease LV preload-+ decrease CO) fluid administration i.e. saline load may temporarily increase CO treat underlying cause Constrictive Pericarditis Etiology chronic pericarditis resulting in fibrosed, thickened, adherent, and/or calcified pericardium any cause of acute pericarditis may result in chronic pericarditis major causes are idiopathic, post-infectious (viral, TB), radiation, post-cardiac surgery, uremia, MI Signs and Symptoms dyspnea, fatigue, palpitations abdominal pain may mimic CHF (especially right-sided HF) ascites, hepatosplenomegaly, edema increased ]VP, Kussmaul's sign (paradoxical increase in JVP with inspiration), Friedreich's sign (prominent Y descent) BP usually normal (and usually no pulsus paradoxus) precordial examination: pericardia! knock (early diastolic sound) see Table 16 for differentiation from cardiac tamponade Investigations ECG: non-specific: low voltage, fiat T wave, AF CXR: pericardia! calcification, effusions echo/CT/MRI: pericardia! thickening cardiac catheterization: equalization of end-diastolic chamber pressures (diagnostic) Treatment medical: diuretics, salt restriction surgical: pericardiectomy (only if refractory to medical therapy) prognosis best with idiopathic or infectious cause and worst in post-radiation with death resulting from heart failure Table 1 &. Differentiation of Constrictive Pericarditis n.. Cardiac Tamponade Charac:terillic COIIIIrictive Pericarditis Tamponade M Y>Y Y>Y Kussmaurs sign Present Absent Pulsus paradoxus UncolllllOn /lJwsys Pericardia! knock Present Absent Hypotension Variable Severe Cardiology and CV Surgery C4S ..... , _._ ______________ Classic quartet of bmponade: hypotansion, incraased JVP, tachyclll'dia, pulsus paradoxus. ..... , _._ ______________ DDx PuiiiUI Plll'ldoxul Con5trictiv j)llricarditis Sw.. obstructive pumonary diusa (a.v.llllhm) Tension Pneumothorax Pulmonary embolus Cllllioguic ahock C46 Cardiology and CV Surgery Peripheral Arterial Disease Toronto Notes 2011 .... Dilfllrentill of Claudicdan V.scular Atherosclerotic disease Vasculitis (e.g. Buerver's dis-. Takayasu's lllteritist Dillbelic neuropathy Venous disease (e.g. DVT. varicou vain& I Popliteal entnlpment syndrome Neurospinll disease (e.g. spinal atenosist dystrophy MSK Osteoarthritis Rhematoid arthritirlconnective tiaau& di- Remota ll'lluma VASCULAR DISEASE Peripheral Arterial Disease Acute 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 Etiology embolus cardiac embolus (80-90%): history of MI Toronto Notes 2011 Peripheral Arterial Disease Chronic Arterial Occlusionnnsufficiency --------Etiology predominantly due to atherosclerosis: primarily lower extremities with symptoms related to the location of obstruction Risk Factors major: smoking, DM, hyperhomocysteinemia minor: HTN, hyperlipidemia, family history, obesity, sedentary lifestyle, male gender Clinical Features claudication 1. pain with exertion: usually in calves or any exercising group 2. relieved by short rest: 2 to 5 minutes, and no postural changes necessary 3. reproducible: same distance to elicit pain, same location of pain, same amount of rest to relieve pain pulses may be absent at some locations, bruits may be present signs of poor perfusion: hair loss, hypertrophic nails, atrophic muscle, skin ulcerations and infections, slow capillary refill, prolonged pallor with elevation and rubor on dependency, venous troughing (collapse of superficial veins of foot) other manifestations of atherosclerosis: CVD, CAD, impotence, splanchnic ischemia Differential Diagnosis osteoarthritis (OA): worse at night and varies day-to-day neurogenic claudication: due to spinal stenosis or radiculopathy; pain very similar but relieved by longer rest and postural changes varicose veins: localized pain, typically less severe, after exercise and never at rest; related to the presence and site of varices inflammatory processes: Buerger's disease, Takayasu's arteritis other: popliteal entrapment (e.g. tumour, Baker's cyst), radiation injury, remote trauma Investigations non-invasive ankle-brachial index (ABI) (grade lA recommendation): measure brachial and ankle pressures bilaterally (use highest value) generally, ABI C48 Carcliolosrand CV Surgery Peripheral Arterial DileudAortic Dlleue 1'oroDio 2011 surgical/lnlervelrtional indications: claudication interfering with lifestyle, rest pain. pre-gangrene, gangrene surgical options: endovascular (stentinglangioplasty) or arterial bypass grafts bypass graft sites: aortofemoxal, axlllofemoxal, femoropopliteal, distal arterial graft choices: in situ graft - reversed vein graft, synthetic - polytetrafluoroethylene graft (Gor- or Dacron amputllli.oll! if not suitable for revascularization and persistent serious infections and/or gangrene Prognosis conservative therapy: 60-8096 improve, 20-30% stay the same, 5-1096 deteriorate, 596 will require Intervention within 5 years, 'IbroDlo Nota 2011 Aortic Dlleale DeBakey 'JYpe I: involves aacending and descending aorta, 50% of patients Type TI: ascending aorta only (stops at the innominate artery), 35% of patients 'JYpe TIIA: descending thoraclc aorta only (distal to left subclavian artery and proxlmal to diaphragm), 15% of patients (including Type mB) Type TIIB: Type TIIA plus abdominal aorta Debakey: Type I Type II Dabakey: Type IIA Type 1118 Slanfanl; L- TJPI A ___J Slanfanl; L- TJPI B ___J Figun 31. af ADrtic Diuactian Etiology most common: damage to aortic media (smooth muscle and elastl.c tl.!sue), leading to degenerative/cystic changes due to hypertension other: cystic medial necrosis, atherosclerosis, connective tissue disease (Marfun's, Hhlers-Danlos), congenital conditiom (coan::brtion of aorta, bicuspid aortic valves, patent ductus arteriosus), infeCSO Cardiology and CV Surgery ..... , , t----------------. ACCIAHA 2005 Guidalinas dufinu 1111 AAA when the minimum AP diamatw of bdomilllllaorlll em. ..... , , .. .----------------. Cllulc Triatl of Rupturlcl AAA Pain Hypotension Pulsatile abdominal mass ..... , , ACC/AHA 2005 ....... 1. Men Yl1 with AAA in relative nuld have LVS fDrAAA. 2. Men 60-75 yr1 who hBV&BVer smoked should haV& anubne LVS screenilg fDr AAA. Aortic Disease Toronto Notes 2011 surgical resection of intimal tear, reconstitution of flow through true lumen, replacement of the affected aorta with prosthetic graft. correction of any predisposing factors (e.g. bicuspid aortic valve, PDA, etc.) post-operative complications: renal failure, intestinal ischemia, stroke, paraplegia, persistent leg ischemia, death 2/3 of patients die of operative or post-operative complications Type A:. requires emergent surgery with cardiopulmonary bypass, may require hypothermic circulation for transverse arch dissections, valve replacement and coronary re-implantation for aortic root involvement, initial mortality rate without surgery is 3% per hour for first 24 hours, 30% 1 week, 80% 2 weeks Type B: initially managed medically- 10-20% require urgent operation for complications (expansion, rupture, compromise of branch arteries, refractory H1N, or ongoing pain) with treatment, 60% 5 yr survival, 40% 10 yr survival Aortic Aneurysm ----------------------------------------Definition of Aneurysm localized dilatation of an artery having a diameter at least 1.5 times that of the expected normal diameter of that given aortic segment true aneurysm: involving all vessel wall layers (intima, media and adventitia} false aneurysm: disruption of the aortic wall or the anastomotic site between vessel and graft with containment of blood by fibrous capsule made of surrounding tissue aneurysms can rupture, thrombose, embolize or erode and fistulize Classification thoracic (TAA): ascending, transverse arch, descending thoracoabdominal abdominal (AAA): 90-98% are infrarenal Etiology degenerative atherosclerotic traumatic mycotic (Salmonella, Staphylococcus, usually suprarenal) connective tissue disorder (Marfan syndrome, Ehlers-Danlos) vasculitis infectious (syphilis, fungal) ascending thoracic are associated with bicuspid aortic valve risk factors: smoking, liTN, age > 70, family history Epidemiology incidence 4.7 to 31.9 per 100 000 for AAA and 5.9 per 100 000 forTAA high risk groups 65 years and older male:female = 3.8:1 PVD, CAD, CVD family history of AAA Clinical Features common presentation: due to acute expansion or disruption of wall syncope pain (chest, abdominal, flank, back) hypotension palpable pulsatile mass above the umbilicus, pulsatile abdominal mass in two directions airway or esophageal obstruction, hoarseness (left recurrent laryngeal nerve paralysis), hemoptysis, or hematemesis distal pulses may be intact 75% asymptomatic (discovered incidentally) uncommon presentation partial bowel obstruction ureteric obstruction and hydronephrosis GI bleed (duodenal mucosal hemorrhage, aortoduodenal fistula) aortocaval fistula distal embolization (blue toe) associated diseases hypertension, PVD, CAD, COPD, renal insufficiency most commonly in the abdominal aorta (50% abdominal aorta, 40% thoracic aorta, 10% ascending aorta) Toronto Notes 2011 Aortic: Disease/Peripheral VenoWI Disease Investigations bloodwork: CBC, electrolytes, urea. creatinine, PTT, INR, type and cross abdominal U/S (100% sensitive. up to 0.6 em accuracy in size determination) CT (accurate visualization, size detennination) MRI (accurate visualization, limited access) aortogram Doppler/duplex (r/o vascular tree aneurysms elsewhere) Treatment Conservative cardiovascular risk factor reduction: smoking cessation, HTN control, DM and hyperlipidemia control regular exercise watchful waiting, U/S every 6 months to 3 years depending on size and location Surgical when risk of rupture greater than or equal to risk of surgery (>5.5em) risk of rupture depends on size rate of enlargement >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 C52 Cardiology and CV Surgery Peripheral Venous Diaease Toronto Notes 2011 ', , 9}-----------------, Mignrtorv tl4)elficial1hrombophlebitis is ofbJn a sign of underlying malignancy {"Trouss1181l's disellse"). Etiology infectious: suppurative phlebitis (complication of intravenous cannulation; associated with fever, chills) trauma inflammatory: varicose veins, migratory superficial thrombophlebitis, Buerger's disease, SLE hematologic: polycythemia. thrombocytosis neoplastic: occult malignancy (especially pancreatic) idiopathic Clinical Features most common in greater saphenous vein and its tributaries pain and cord-like swelling along course of involved vein areas of induration, erythema and tenderness correspond to dilated and often thrombosed superficial veins complications simultaneous DVT (up to 20% of cases), pulmonary embolus (rare unless DVT) recurrent superficial thrombophlebitis Investigations non-invasive tests (e.g. Doppler ultrasonography) to exclude associated DVT Treatment conservative bedrest and elevation of limb moist heat, compression bandages, mild analgesic, anti-inflammatory and anti-platelet (e.g. ASA), ambulation surgical excision of involved vein indication: failure of conservative measures (symptoms that persist over 2 weeks) suppurative thrombophlebitis: broad-spectrum IV antibiotics and excision Varicose Veins Definition distention of tortuous superficial veins resulting from incompetent valves in the deep, superficial, or perforator systems distribution: greater saphenous vein and tributaries (most common), esophagus, anorectum, scrotum Etiology primary main factor: inherited structural weakness of valves contributing factors: increasing age, female gender, OCP use, occupations requiring long hours of standing, pregnancy, obesity secondary malignant pelvic tumours with venous compression congenital anomalies - arteriovenous fistulae Epidemiology most common form of venous disorder oflower extremity 10-20% of population Clinical Features diffuse aching, fullness/tightness, nocturnal cramping aggravated by prolonged standing (end of day), premenstrual visible long, dilated and tortuous superficial veins along thigh and leg ulceration, hyperpigmentation, and induration (secondary varicosities) associated esophageal varices ( GI bleed), hemorrhoids, varicocele Brodie-Trendelenberg test (valvular competence test) with patient supine, raise leg and compress saphenous vein at thigh; have patient stand; if veins fill quickly from top down then incompetent valves; use multiple tourniquets to localize incompetent veins Complications recurrent superficial thrombophlebitis hemorrhage: external or subcutaneous ulceration, eczema, lipodermatosclerosis, and hyperpigmentation Treatment largely a cosmetic problem conservative: elevation ofleg and/or elastic stockings surgical: high ligation and stripping of the long saphenous vein and its tributaries, sclerotherapy, endovenous laser therapy (EVLT) Toronto Notes 2011 Peripheral Venoua Disease Prognosis natural history benign, slow with predictable complications almost 100% symptomatic relief with treatment if varicosities are primary good cosmetic results with treatment significant post-operative recurrence, especially with sclerosing agent injection Chronic Venous Insufficiency Definition chronic elevation of deep venous pressure and blood pooling in lower extremities Etiology calf muscle pump dysfunction and valvular incompetence (valvular reflux) due to phlebitis, varicosities, or DVT venous obstruction AV fistulas, venous malformations Clinical Features pain (most common), ankle and calf edema - relieved by foot elevation pruritis, brownish hyperpigmentation (hemosiderin deposits) stasis dermatitis ulceration: shallow, above medial malleolus, weeping (wet), painless, irregular outline signs ofDVT/varicose veins/thrombophlebitis Investigations ambulatory venous pressure measurement (gold standard) Doppler U/S (most commonly used) photoplethysmography Treatment conservative elastic compression stockings, leg elevation, avoid prolonged sitting/standing ulcers: zinc-oxide wraps, split-thickness skin grafts, antibiotics, debridement surgical if conservative measures fall, or if recurrent/large ulcers surgical ligation of perforators in region of ulcer, greater saphenous vein stripping venous bypass if short segment obstruction Lymphedema Definition obstruction oflymphatic drainage resulting in edema with high protein content Etiology primary: Milroy's syndrome secondary infection: filariasis (#1 cause worldwide), post-operative malignant infiltration: axillary, groin or intrapelvic radiation/surgery (axillary, groin lymph node removal): #l cause in North America Clinical Features classically non -pitting edema impaired limb mobility; discomfort/pain; psychological distress Treatment avoid limb injury (can precipitate or worsen lymphedema) skin hygiene daily skin care with moisturizers topical treatment of fungal infection; systemic treatment of bacterial infection external support intensive: compression bandages maintenance: lymphedema sleeve exercise gentle daily exercise of affected limb, gradually increasing ROM must wear a sleeve/bandages when doing exercises massage and manual lymph drainage therapy Prognosis if left untreated, becomes resistant to treatment due to subcutaneous fibrosis cellulitis causes rapid increase in swelling: can lead to sepsis and death Cardiology and CV Surgery C53 _._ ______________ Pittilg edema -+ vucLJar Non-pitting adema -+ lymphatic C54 Cardiology and CV Surgery Common Medications Common Medications Tabla 19. Commonly Used Cardiac Therapeutics Drug Class Examples Madlanism of Action ANGIOTENSIN CONVERnNG ENZYME INHIBITORS (ACEISJ enalapril (Vasotec411J. Inhibit ACE-mediated perindopil (CoversyPJ, conversion of angiotensin I ramipril (AIIacel to angiotensin II (AT II), lisinopril causing peripheral vasodilation and decreased aldDS!EnJne synthesis ANGIOTENSIN II RECEPTOR BLOCKERS (ARBS) II-BLOCKERS candesartan, irbesartan, Block AT II receptors, valsarlan causing similar effects to ACEis HTN. CAD. CHF. post-Ml DM Same as ACBs, although evidence is generally less fur ARB&. Dfta1 used when ACEis are not tolerated. Ill antagonists atnlol, mBIIlprOiol bisoprolol propranolol labetalol, carvedilol acebutalol Block jl-adranargic HTN, CAD, acute Ml, f1Jll2 antagonists aJIIJII2 antagonists 111 antagonists with ISA CALCIUM CHANNa BLOCKERS (CCBSJ Benzothiazepines dillimem Phenylalkylaminas varapamil (non-dihydropyridinesl Dihydropyridi1es lll'llodipine nifl!dipine felodipile (Piendii-J DIUIIETICS Thi12ides hydrochlorthil2ide, chlorthalidone metoiBZOne Loop dUetics furosemide (Lasix411J Aldosterone receptor spironolactone. antagonists eplenerone INDTRDPES digoxin (lanoxinJ recaptors, d8Cillllsing HR, post-MI. CHF (start low BP, contractility, and and go slow!, AF, SVT myocardial oxygen demand, slow conooction 11nugh theAVnode Block smooth muscle and HTN, CAD, SVT, diastolic myocardial calcium dysfunction channels causing effects similar to Also wsodilate Block smooth musde HTN cak:ium channels causing vasodilation Reduce Na reabsorption in HTN (drugs of choice fur theDCT uncomplicated HTNJ Blocks N!VX-AlPase in the CHF. pulmonary or loop of Henle peripheral edema Antagooize aldosterone HTN, CHF. hypokalemia receptors NWIC-ATPase, CHF.AF leading to increased intracellular Na and Ca concantration and inCIIIIISed myocardial contractility. Also slows conduction through the AV node ANTICOAGULANTS Coumarins wlriarin (Coumadin-) Antagooizes vitamin K. Abial fibrilllltion, LV leading to decreased dysfunction, prosthetic synthesis of clotting factors viMs II, VII, IX. and X Side Eflecls Dry cough. 1 0% hypotension. fatigue, hyperkalemia, renal insufficiency, angioedema Similar to ACEis, but do not cause av cough HypOillnsion, fltiiJI&, light headedness. deprassian. bradycardia, hyperkalemia, bronchospasm, impotence, depression of counte11'8gulatory response to hypoglycemia. I!X8cerilation of Raynaud's phenomenon and claudication Hypotension, bradycardia, edema Negative inotrope Hypotension, edema, flushing. headeche, light-headedness Hypotension, hypokalemia, polyuria Hypovolemia. hypokalemic metabolic alkalosis Edema. hyperkalemia, gynecomastia AV lllchyarrhythmias, bnldyanhythmias, blurred or yellow vision (van Gogh syndrome), ano11111ia, neusea and vomitilg Toronto Notes 2011 CalllnindicidiiiiS Bilateral renal artery stenosis, pregnancy, caution i1 decreased GFR SameasACEis Si1us bradycardia, 2nd or 3rd dagree heart block. hypotension, WPW. Caution in asthma, claudication, Raynaud's phenomenon. and Si1us bradycardia, 2nd or 3rd dagree heart block, hypotension, WPW, CHF Severe aortic stenosis and liver failure Sulfa allergy, pregnancy Hypovolemia. hypokalemia Renal insufficiency, hypllkalemia, pregnancy 2nd or 3rd degree AV block. hypoklllemia, WPW Bleedi1g (by far the most Recent surgery or bleeding. impol'llrlt side effect), paradoxical bleeding diathesis. thrombosis, skin necrosis prag1111ncy Heperins unfractionatad heparin low molecular weight heparins {LNIWHsJ: dalteparin, enoxaparin, tinzap!lin Antithrombin Ill agonist. leading to decreased clotting factor activity Acute Ml; when irrmediate Bleadi1g. osteoporosis. hepam. anticoagulant effect needed induced thrombocytopenia Recent surgery or bleeding. bleeding diathesis. thrombocytopenia, renal i1sufficiency (fur LMWHs) (less in LMWHsl Toronto Notes 2011 Common Medications Cardiology and CV Surgery C55 Table 19. Commonly Used Cardiac Therapeutics (continued) Drug Class Examples Meclllnism of Aclian ANTI PLATELETS Salic:ylates Thienopyridine& GPIII:VIIIa THROMBOLYTICS NI111ATES UPID LOWERING AGENTS clopidogral ticlopidine [Ticli!P) eptifibBiide, tirufib111. abciximab alteplase, tenecteplase, straptokinasa nitroglycerin Statins atorvastllin pravestllin (Pravachol), rosuwstatin (Crestor0), simVIIstatin {lllcar), lovastatil (Meracor) Antiarrhythmic& :C56 Cardiology and CV Surgery Common Medications Table 21. Actions of Alpha and Beta Adrenergic Receptors CardiiiVISCullr RllpiratDry 01111111 Ocular ALPHA RECEPTORS Alpha1 Alpha2 Constriction of vascular sroooth muscle Constriction of skin. skeletal muscle and splanchnic vessels Increased myocardial Paipherally act to contractility modulate vessel tone Decreased heart rata Vasoconsbict and dilate; owase Alpha 1 vasoconsbictor activity Pilomotor sroooth muscle cantraction Apocrine consbiction Radial rruscle contraction Gaatnin1111tinll Inhibition Ill myentl!ric Ganitaumuy plexus Anal &phinctllr contraction PragrBJI uterine contraction Penile and seminal vesicle ejaculation Urinary bladder contraction Smooth muscle wall relaxation Metabolic Stimulate gluconeogenesis and glycogenolysis at the liver Fat cell lipolysis Adlp!Bd fnlm tlw Fllliy l'llctice NDIBboli Toronto Notes 2011 Belli BETA RECEPTORS Betll2 Increased myocardial Decreased vascular contractility smooth muscle tone Accelerate SA node Accelerate ectopic pBcemakel$ Ciliary muscle relaxation Stimulation of ranal renin release Fat cell lipolysis Glycogenolysis Bronchodilation Bladder walralaxation Uterine relaxation Gluconeogenesis Table 22. Commonly Used Drugs thl1 Act on Alpha and Beta Adrenergic Receptors ALPHA RECEPTORS BETA RECEPTORS Machlnilm Ill Action Alp.l1 Alphl1 and Alpha2 AlphaZ Bltll1 Bltll1 and BIIIZ BltaZ AGonilt Phenylephrine Epilephrine Clonidine Norepinephrine Isoproterenol Albuterol MethDXIlllline Norepinephrine Dobutamine Epinephrine Terblllaline Altagoailt Prams in Phentolamine Yohimbine Metoprolol Propranolol Butaxamine Phenoxybenzamile Aceilutolol TinlDiol Alprenolol Nadolol Ate nolo I Pindolol Esmolol Carvedilol Adlp!Bd fnlm tlw Fllliy l'llctict N!Ohool: Toronto Notes 2011 Landmark Cardiac Trials Landmark Cardiac Trials Trill lklfl1111c:1 ISCHEMIC HEART DISEASE 4S l.anr:st 1994; 344:1383-89 A to Z: Phase Z J4MA 2004; 292:1307-16 ALIJIAT J4MA 2002; 288:2981-97 ASCOT-LLA lilncet 2003; 361 :114&-58 BHAT J4MA 1982; 247:1707-14 CAPRIE l.anr:st 1996; 348:132&-39 CARE NEJM 1996; 335:1001-9 COURAGE NEJM ZOOS; 358:1887-98 CURE NEJM 2001; 345:494-502 EUROPA l.anr:st 2003; 362:782-88 FRISC II Lancet 1999; 354:701-7 FRISC II Lancet 1999; 354:70S.15 GISSI-3 lilncet 1994; 343:1,, S.22 GUSTO-I NEJM 1993; 329:673-82 HOPE NEJM 2000; 342:154-60 HPS lancet 2002; 360:7-22 ISIS-2 lancet 1988; 2:349-60 ISIS-4 lilnm 1995; 345:669-85 LIPID NEJM 1998; 339:1349-57 OASIS-5 NEJMZ006; 354:1464-76 OPllMAAL l.ancst 2002; 360:752-60 PROVE IT- NEJMZ004; 350:1495-1504 TIMI22 SYNTAX NEJM ZOOS; 360:961-972 TNT NEJM 2005; 352:1425-35 WOSCOPS NEJM 1995; 333:1301-7 Results In patients 111gina or previoos Ml and high total cholesll!llll, simvastatin reduced: all-cause mortality, fatal and nonfatal CDI'Dnary events, need for coronary artary bypass surgery or angioplasty Early of aggressive simvastatin regimen resulted in a trend towards reduced major cardiovascular events In hypertensive patients with Cardiology and CV Surgery C57 C58 Cardiology and CV Surgery Trial HEART FAIWRE A IRE CHARM CIBISII COMET CONSENSUS COPERNICUS I-PRESERVE MERIT-HF RALES SAVE SCD-HeFT SOLVD lRACE V-HeFT II DIABETES CARDS ONTARGET ARRHYTHMIA AFFIRM CAST HYPERTENSION HYVET Landmark Cardiac Trials Toronto Notes 2011 l..ancvt 1993; 342:821-8 Lancvt 2003; Lane 1999; 353:9-13 Lane 2003; 362:7-13 NEJM 1987; 316:1429-35 NEJM 2001; 344:1651-8 NEJM 2008; 359:2456-2467 Lancet 1999; 353:2001-7 NEJM 1999; 341:709-17 NEJM 1992; 327:669-77 NEJM 2005; 352:225-237 NEJM 1991; 32S:293-302 NEJM 1995; 333:1670-6 NEJM 1991; 32S:303-10 Lancet 2004; 264:685-96 NEJM 2008; 358:154759 NEJM 2002; 347:1825-33 NEJM 1989; 321:406-12 NEJM 2008; 358:1887-98 Rnipril commiiiiC8d 3-1 0 day$ aftur Ml and continued fur a m1151 15-monlh period significllllly reduced mortality in patients with non-severe CHF Cand88Brl!n reduced OYlllllll mortlllity, cardiovascular d8Bih and CHF hospitalizations Bisoprolol reduced mortality, cardiovascular death. all-cause hospitalization and CHF hospitalization Carvecilol was associated with a reductioo in all cause mortlllity compared with metoprolol Enalapril reduced mortlllity, death due to prtVeSSion of heart failure Carvecilol il addition to standard trelllment significantly reduced the risk of death or hospitalization in patients with severe CHF In patients with CHF and normal LVEF, treatment with ARB (irbesartllnl did nat if11)1UVe mortality or cardiovascular morbidity compared to placebo MeiDpnllol CR/XL daily in addilioo to optirnJm standard therapy improved survival in clinically stable patients, equaling to prevention of 1 death per 27 patiants 1niBted per 'fllllr In 58\181'8 CHF and LVEF Toronto Notes 2011 References References lllilmic Hlllt U..a Cannon CP., atli.lntBnsivlwrwJs modmltl lipid lllwllrq with llltinslfur IWIII CO!IIIIIry syndmmas.IN 2004;350(15]:141&.504. lindat-1, B, alii. Mnn rJ Mygclnlialllllmage and Inflammation il Relllion to long-Term Mortality in U11513ble CoronJY Arl81y lilee. New England Journal rJ Mlclcina. iml; 343:11391147. at Ill Eplare110111, 1181eetivu in pllianbi wi1h laltwntriwllr dylfunction lflur nnrction.I>EJM 2003; 348(14):130121. llluch, U. et 11. Thrombus Farmlltion on the Alheralicletutic l'lllques: l'lthagenesis and Clrical Coosecpnces. Annlls of Internal Medicine. ZOO I; 134: ZZ4238. Thl Alllrillllsvua6!rimlian Thlrl!ill SUiy lirtUp. eom,.rilon rt CllrOIII1YATIBJY Bypass Slrrllary and Sllllling lor tha Tfllllnlnt of Mulliwllll Dil81st. NIW England Junal rl Madicina. 2001; 344:1 117-1124. TIIJ)ie, A. G. G. and Antrran, E. M.low-Molec:uiiTWeiglrl Hepllrins in the Treltment ol Ai:uleCoronary Syndromes. Arcllioles of Internal Medicine. 2001; 161: 1484-1490. Yeglimriln1, Y., Brlunllain, J. B., Aibri, A, and Stone, P. H. RIMIM' Article: l)Jmble Anginll'eclllris. Nlw Englllld Journal rl Medicine. 21KKl; 342:101114. llll:lelrCinlialogy LeeTH and lloul:ller CA. Nori-ive 11151$ in petiente wi1h dlble coronJY TIBrV di !Reviewi.IN 2!KKl;344:1840.5. Fetlman IW.IIII McNurm. D. MyaciTditis {Review]. NEJM 2000; 343:1388-98 . ..... rill percullneoos coranuy intel\1ilrtion. Cin:ulltion. 2001;103:301 H041. AWAHAZOOZ ml1'llqlmlll!cipltiiiiiJMth ... and non-STgmantiiiiVIIion myocardial inflrc1iln (INaillhle at: httpi/wwl't ICC.CJ19) ACCF/AIIA ZOOI FocUied Update 111 the &idelinesfor the DillgnOiisand Management of lleert Failu11 in AdultJ. Ciralllllim 2009; 119:197721116. AWAHA !Jidllinas furthl m.-gamant rt pltiantl with ST-tlmtion myocardial irrfln:tian: 1 rlpOII ci tha American Collegl of CITdiology/Arrwican HrtAIIociltian Tilt Rlrc;e onl'llclice &idefnee !Cormitt8e to &idainas for tha M1ragernent of Pltianll with Acute Cin:ulltian 2004; 11 O(l]:e8z.292. Antnwl EM at al. Al:.t/AIIA &idalinls for the of Patianll with STaiMtion MyaciTdial HarctiMI surnmuy: A Raport oftlia Amarican College rl C.diology. Ameril:lin He.t Association TIISkFon:e llll'rllctice &idelnes. Cin:ulltion. 2004; 110-588. CCS. ZOO I Canadian cardilll'llc* sociaty con1111u guidalna updata for 1hl1111111gamantand priVInlion ci hllllrtfliU.. Canadian Journal of Cardilklgy. 2001;11(auppE):S.24. GP etal. Clnical Fractice, Diastulic Heertfaii.Jre. NEJM 2004; 351:1097. American Colege ci Cardiology (clinicli guidaliles, ate]. CanllliM C.-di01111SCUIIT Sociaty 2005 Co1118naus Confarance Atarial Daa (Draft). www.thahllllrtorv- Cardiololll' Onina ragimtiCII]. www.hllllrMIIwrepeir.nat-Heut VIM Rrpair Online. Beard JD. Clnunic lowar limb ilchanil. BMJ. Fuchs JA. Atherogenesis 1nd the Medal Mlllagemerrt of Atherosclerosis. In Vuc:W1r Suverv 4th edition, Rollert B. Rutherfunl Ell. 1915. WB. Suiders Co, Toronto. pp 222234. Harrilgton RAet al. AntitiiRIIIDitic Tharapylor CoroniJY Artery lilease: tha Saventh ACCP Conlwca an Antithrontoti: 1111 Tlrrornbolytic ThlniP'f. Cllast. Z004; 126 (3suppl]:513a-584a. May J, Whilll GH, end Hlrlis JP. diMinlida ofand1Mscui1T1111Upias. Adv Slrr1135: 153-72. 2001. Schnieder FA and Comero1J. AJ.Intermillent claudication: rt the p!Oblem, petient ei'IUI!ion, end therapeutic str111gies. Am J Card 87 (Supplj: 30-130, 2001. Way LW,IIohartyliM, aditon. Cummt Surgicel Diagnosis lid Tnlltmant, 11th aditiln. Mldcal Bookr, 2004. SC, C1marun DE. adi1Dn1. Currarll tharepy in thrncjc and cardiCIVUCUIIr mlllbrl. Mc!irMHlilllr1;, 21104. w-.yECt Zinelblum, P. JDSellhson. M.lhe EvoMng Role ci AndltDry Arrhythrri1 Monitoring in General Clriiclill'nletie. Annals of lntemll Medicine. 130 (10]. 1911. lradilh AH. lllDcton Ai, HL. AWAHA cilical compatanca Sllt8rnant 111 and entlllltDry a naport oflhl AWAHN ACP-ASI'.'I tiSic.forca on cilical compatanca. Ci'cu11ti011. 104:3161-3118. 2001. Krahn, A, Klein, li, Simes, A. Vee, R. loop Recorder Use for Detection ollntermillent Arrhythrriu. Pacilg and Clinical Electrophysiology 27 (5]. 2004. SlriiiWng AllOT!, T. Bardsley, W, Behrenbeck, T, Christian, T., Clements, 1., Edwards, B., Gibbons, R, Mler, T, Oh, J, l'elikb, P., V., Squires, R, Weistlet A. 1 196 Mayo Foundation forMadical Ellucation and Rll88an:h. 71(1): 43-52. 1996. Gibbon dill. &sn:iA Taring &ideilas. JACe. 30 (I ):ZW-315. 1817. El:hll:lldiolnphr Pl131o, E. SUess Et:hDCIIdiog!1phy: A histDrical pqective. AmJ Med. 114;12l-130. 2003. Haatlil, G., Gil as, M. Et:hDCIIdiog!1phy and 1hl gnral plfisician.l'oslgrad Mad. J. IIU;84-88. 2004. Chaitlin, M. ACC/AHA/ASE 2003 Guidalina UpdatB for111a Clinical Applicalim of Echocudiogrlohy: &mnary Articla. Journal rlthi.AmariciJI Sociat.y of Edloclrdiography. 16(10]. 2003. liowd11, R. Khn I. SacchL Uatal R. HisiDry cithl avolub af achocardilgRjllry.lnllrnlltiionli Journal ol Cardiology. 87 (I): 16. 2004. llll:lelrCinlialogy Sahharwal N. Llhiri, A. Role of m,ocardial parfusiOII rist stratiication il suspactlld or known coroniJY artily di Hllrt. 89:1 291 1297. 2003. Baler, G., Zlrat, B. ContriiUin rJ Nuclear Clnliologv to lhgnolii and Prognllliis ol Patian11 wi1h Cornry Arl81y Di111111. Cin:ulation. m. IR Kim, WY, atal. CoronaJY magnetic r..onanceangiographylorllla dfldOII of coronBJY "'"" NEJM. 345(26]:1 BSH 2001. Danias, P.,I!OIIssakis, A. loannidis J. Cardiac imaging Diagnostic [)1118nnanca ci coranary magnatic rasonenca angiography as CIIIJ'Illlld against c0111111111io11a rav A mata-nlylis Joulllll of1ha American Colaga rl Clnliologv 44(2]: 1867-1876. 2004. t:T Milar JM atai.II!Qnoatic of coronary engii!QIIIIhy by &c.- CT. NEJM. 359(22):232436. ZOOS. Schoepf, J., Becker. C., Ohnesorge. B., 'ftlcel K. CT ofCoronuy Artery Disease. Radiology 232:1 &-37. 2004. Sombarg. J. Arrtlytlma Thlnpy.lippincott Wilams & 9(6): 537-542. 2002. Cardiology and CV Surgery C59 C60 Cardiology and CV Surgery References Toronto Notes 2011 CatiVEPS Hayn, D.. Fu1111111, S. Cardiac Pacing: Stnd, Wlllra Wa All, Whn WaAra Going. Joumal oiCardiavucullr 151512004. Zipaa II al. ACC,IAHA Task Farca Raport mr Clinicallntracanliac Bactruphysiolllgicalllld Cathlllllr Ablation l'roc:aUaa. JACC. 26121: 555-513. 1115. Welens, J. CardiiC Anflyt!mias: fur a cure. Journal of tile Ameri:an Colege of Cardii*Jw. 44161: 11551163. 2004. Conti, J. ACC 2005 Anrull Saalion Higillgltt. Criac ArrflythmiiL J011mal al the American Colage of Cartilgy. 451111:1130-1!32. 2005. Kaane, D. NIIW Catheta' Abllltion filrtha T..tmant of Cardiac Anhythmilla. Canliac Bsetrophysiology RIMM. 6:341-348. 2002. Skilnes,A., G.. Krllin, A. Yee, H. Cryallblllion: l'atlntials and l'llllllls.J Cardiavuc 2004. l'llcbt D. Ewlution og Mapping IIIII Allllanic Imaging of Cardiac Arrhy1llriu. Jaumal of Canlowscular Bsetrophysiollgy. 15111. 2004. Zipaa, D. Thayaar in slllclmpllysiology: Joumal altha AmariCUI Collllga of Cardiology. 4317]:1306-1324. 2004. Ryan TJ, fUCIII DP, Gunnar RM, et al. Guidelines for perQjtlneous 11ansum.l lllllioJIIIsty. A re!)Cirt of the American Colege of Cardiolocw!Ameri:an Heart Allocil1ion Task Fan:e on Assaaamant of Dilgnostic and Tllarapeutic C.4iavascul ProcailJRIS 1Subconmt18s on Parcutnous Transum.J Conmaiy Angioplastyl. Cin:uhllion 7812):486-502. 1 B88. Bernstein AD. The NASPWBl f'lc:emabrCode. Tl!lC Heart tlstJ.1991; 18141: 21Hll. Garcia TB ud Miller GT. Arrllyttma llecognition: The Art of ln18rprmtion. 2004. Jo1111 & Blrdll:t Publshars, Sud wry, MA. l'ryst!rNsky EN. Bsetropllysiology and Pacing. In: Textboak of CardiMSCUiar Mlllicile Tlird Ecition, Tapa I EJ, c HM, l'rystawsky EN, Th1111'11S JD, PD Eds 2001. & Wilkins, Phi..._,lil. PA. l'lrcuWI1011 AII ..... IIWI'CI Glidehs for pertWriaws transliminal coronary angioplalty: a raport of1he American Collga of Cardiology/Am HIITI.Associllion Taak Fon:e on Aslessmant of lliagnoltic and llllrlpautic Cardiovascular l'roc:aUaa Subcommitllla on l'a'eullnllous Transliminal Coronary angiopllllllyl. J Am Call Cardioi.12:5Z9-,'i45. 1988. O'Nail W.lban, S., Grin111, C. Tile in irtBMntional cardiology. J011mal al the American College of Cartilgy. 45 !71:11111134. 2005. Bulae at II. AWSCA&IIXjlllrt coliCirl dacumalll AmariCIII Collllga of Cardiology/Sol:illly for Canlilc Angiography and hlrwntions Clinical Explrt Cansnus Document on Cardiac Cathat8rizlltion l.abolltory smldards. Joumal oltha Amari CUI Collllga of Cardiology. 31181:21702214. 2001. Baim, D. New devices for pen:utlneous coronary iltel'lention are bypaas UQeiY obsolete. lippincott Wluns & 593-517. 2004. Sarruys PW 11: al.l'en:ullna1111s C0Jm11V intaMnlion vmus coronary-llllry hypess QI6'G for IBVfi COIIl!Vf l1llrY disaaaa. Nf.JM. 3601101:96112. 2009. Callllnucllu S11J11Y WMY.accJug-The AmariCIII College of lcili:al glidalin111, atcl CartiJgy Online HIITI Valva lllpeir Dnlina AIIIXIndar P and Giangola G. Daap wnws thronilolilllld BITIXIIilm: Diagnosis, p1ophyllxil, end traatmant. AM Vase &rg 13: 3111-27, 1191. Beard JD. Chronic bNar iml iidlarnia. BMJ. 2000;320:854.ai7. Bajar HM. Manual of periJpn1ive care in cardiac 3rd ecltion. Maaclllsetls: lllackw!l Si:ielice tic., 1999. Chang DCH, llllrid TE ads. cara in canliac anedh81i and wrgery. Austin: LJndes Bioance, IM. Coularn C/1 and IIIDI Ill Acute lOrtie abnonmities. Semin Roentgenol36: 148-44, 2001. Crawford ES and Crawfurd JL Tluncollbdominll Aartic Aneurysm. In: Vascular surgary: Principles ud Practica 2nd dian, Vaith F.t Hobson RW, Wluns RA,IIIII Wlion SE Edi 1994. MclirwtHilllne, Trndo. Fui:bs JA. Atlle!agenesis d tile Medical Mngement ol Atlierosclerasis. tl VIKullr 4tll edition, Raber! B. Rutherford Ed. 1995. WB Samders Co. Tcronto. pp222234. FniischiiQ JA. Alldoninal Aortic Aneurysms. In: Vucular Principles and Practice 211d elition, Veith F.! Habson RW, Wiliams RA, and Wison SE Eds 11M. McGnrN-IIilllne, Toronto. Hlllatt JN Jr. Alldoninel aortic ll*rfSm: n11urallistory and IJ8IImant. Heart Dis Stroke 1: 3DU, 1992. Hallatt JN Jr. Managsmant of abdominalaortie lii8Ury11111. Mayu Clin Proc 15: 39H, ZDOO. Hlln llJ, Starr A, lluwin FM.Iustrated handbook II canlilll: New York: Sprirver.llerlag tic. 1996. May J, 'Miill GH, and llarrisJP. The complicatione and d!Mnsida ol111diiWIKlilr tharapiaa. Adv Surg35: 15312. 2001. Pitt MPIIlld RS. The nllturallislory oftllOIICic aortic aneurysm disease: An Mrl'iew. J Canl 27G-a 1997. Powall JT ud Brown LC. Thallllurai!Wry of abdominal aortic uaurysma and llllir risk of r\flllll. Adv &nil 35: 113-85, 2001. Roeen CL end Tracy JA. The of lowwllldl'llmity daap venous thrombosis. Em Mad Clin N Am 11: 88S-112. 2001. Schmieder FA and Comenltl AJ. lntemittent cleudic:alian: of the prabhm, patillrl mlllltion, and therlpeutic strdeQies. Am J Canl871Siqlll: 3[}.130, 2001. Venne S. Smilko PE, et al. Clnician Updall1: Shedd radialarbiries be used laWnely far coronary ulely lrt'Pss grafting? 2004;110:e4D-e46. LW, DohertyGM, lliiDI1. CUrrantSuQicalllagnosis and T1111mlnt II til ICition. Lange Medical BookwT'IIcGIIwIIIL 2004. Yang SC, Cameron DE.IChn. CurNnt1herapy in 1hcncic end caniovaacular madicina. McGraw-Hillnc, 2004.