ࡱ> ! #` bjbjmm 7(t& 5: brady) REGULARITY Regular vs irregular may need a caliper; analyze type of irregularity RHYTHM Sinus: sinus P waves in front of QRS complexes in a 1:1 fashion P WAVES Sinus: upright in I, II, aVF, V3-V6 LAE: terminal negativity in V1 e" 1x1 mm; Pe" 3mm wide and bifid RAE: initial positivity in V1 e" 1mm tall; II, III, aVF tall peaked Ps Not sinus: P wave morphology not c/w sinus; PR too short or too long Review causes of abnormal Ps (including limb lead reversal) P-R INTERVALS Normal: 0.12-0.20 s (3-5 little boxes) < 0.12 s: sympathetic activation; preexcitation (WPW); steroids > 0.20 s: 1o AV block (age; drugs; inferior MI; cardiomyopathies) Irregular: analyze rhythm for 2o or 3o AV block QRS COMPLEXES WIDTH Normal ( 0.11 s (< 3 little boxes) Wide e" 0.12 s (e" 3 little boxes): review 6 major causes of wide QRS: ventricular rhythm; RBBB; LBBB; WPW; paced; nonspec. IVCD AXIS Normal: QRS( in I, ( in II LAD: QRS( in I, ( in II (age; LVH; IMI; LAFB) RAD: QRS( in I, ( in II (young; RVH/PHTN; ASD; lat. MI; LPFB) AMPLITUDE High voltage: LVH; young; thin; abnormal amplification Low voltage (5 mm limb leads; (10 mm chest leads: ( ventricular muscle mass (remote MIs, infiltrative processes) ( resistance/impedance (obese, emphysema, anasarca, sclerod.) Electrical alternans: frequently due to large pericardial effusion PROGRESSION Normal: QRS( in V1; ( in V5 or 6; R/S ratio increases from V1(V4-5 If QRS is upgoing in V1: review causes (RBBB, BiV, WPW, VT, RVH, PMI) PATHOL Qs Width e" 0.03 s (1 mm) and/or depth e" S! of QRS amplitude in e" 2 neighboring leads: probable MI (possibly remote) ST SEGMENTS ST elevation: review causes (always consider acute MI) ST depression: ischemia; strain; nonspecific ST: the smoothest segment in the ECG (all notches are suspicious for Ps) T WAVES Usually follow the QRS axis; usually ( in aVR and V1; maybe ( in III or aVL Upright in most leads; if narrow based or peaked: consider hyperkalemia Flat, bifid or notched: consider hypokalemia, drugs, CNS, LQTS Inverted: ischemia, injury, strain, lytes, drugs, CNS, catecholamines QT INTERVALS Normal QTc: males ( 0.44 s; females ( 0.46 s Prolonged: review causes (metabolic, drugs, CNS, catecholamines) Littmann 08/01/2011 P WAVES I. SINUS P WAVES - Upright in at least 8 of 12 leads - Never inverted in I, II, aVF, V3-V6 - Always inverted in aVR - May be inverted or biphasic in V1, V2, III or aVL Left atrial enlargement (LAE) or LA hypertrophy, scarring: risk factor for atrial fibrillation V1: terminal negativity e" 1x1 mm (sensitive but not specific) Lead I or II: P wave is wide (e" 2.5 mm) and bifid (specific but not sensitive) 1st degree A-V block (prolonged PR) Right atrial enlargement (RAE): risk factor for atrial flutter V1: initial upgoing component e" 1 mm tall (specific but not sensitive) II, III, aVF: tall and peaked Ps (2.5 mm tall or S! of QRS height in 2 of 3 leads) (sensitive but not specific) Flat line in lead I and inverted P, QRS in aVL: strongly suggestive of emphysema II. NON-SINUS P WAVES P wave morphology is not consistent with sinus (including inverted P in lead I) Apparent sinus tachycardia with long or very short PR intervals Ectopic atrial rhythm (P wave morphology abnormal both in limb leads and in chest leads) Atrial tachycardia with 2:1 A-V conduction (twice as many Ps as is apparent) Atrial flutter with 2:1 A-V conduction (twice as many Ps as is apparent; use halving method or block down the AV node to find hidden flutter waves) Paced atrial rhythm (pacer spikes; QRS usually also paced; rate regular at 60 or 70) Retrograde P waves (AV junctional rhythm; idioventricular rhythm; ventricular paced rhythm; reentrant SVT): P waves follow the QRS complexes; Ps are ( in II-III-aVF and ( upright in V1 Dextrocardia (both P and QRS ( in I; QRS progression is reversed in chest leads) R-L arm lead reversal (lead I as above but normal QRS progression in chest leads) R arm - R leg lead reversal (P ( in lead I; and flat line in lead II) Artifact (Parkinsonian tremor [limb leads] and HFOV [chest leads] may mimic atrial flutter) Differential diagnosis of inverted P waves in lead I (in order of likelihood): Limb lead reversal (R-L arm or R arm - R leg as described above) Ectopic atrial rhythm or atrial tachycardia with 2:1 A-V conduction Dextrocardia (QRS too is inverted in I; QRS progression is reversed in chest leads) Atrial paced rhythm (usually QRS is also paced) III. CANT FIND P WAVES If ventricular rhythm is irregular: probable atrial fibrillation If ventricular rhythm is regular: Slow and narrow: AV junctional escape rhythm Slow and wide: junctional escape with bundle branch block vs ventricular escape rhythm Fast and narrow: SVT Fast and wide: probable ventricular tachycardia Rate is normal: QRS narrow QRS wide - accelerated AV junctional rhythm (rare) - accelerated idioventricular rhythm (rare) - sinus rhythm with 1o AV block - ventricular paced rhythm (search for Ps hidden in the preceding Ts) (atrial activity may be atrial fibrillation) P-R INTERVALS I. NORMAL - P-R interval is measured from the onset of the P to the onset of the QRS - Normal P-R: from 0.12 0.20 s (between 3 and 5 little boxes) - May be normal up to 0.22 s with sinus bradycardia II. TOO SHORT (< 0.12s) Causes If the sinus rate is fast (sinus tachycardia): probably due to adrenergic activation (fever, shock, thyrotoxicosis, beta-adrenergic agonists) If the sinus rate is normal: Congenital small AV node High dose corticosteroids Ventricular preexcitation (WPW): delta wave; widened QRS; abnormal QRS If the sinus rate is very slow: consider isorhythmic AV dissociation (junctional escape rhythm with sinus P waves marching through) III. TOO LONG (> 0.20s): 1o AV block - If you cant find P waves, search for P waves hidden in preceding T waves - P-R intervals may be up to 600 ms long (15 mm!) Causes Left atrial enlargement Advanced age Degenerative or atherosclerotic conduction system disease Connective tissue disease (ankylosing spondylitis; HLA-B27) Inferior MI Medications: (-blocker, verapamil, diltiazem, digitalis Myocarditis (including Lyme disease) Aortic valve endocarditis (paravalvular abscess) Cardiomyopathies IV. VARIABLE Progressive prolongation of P-R intervals: type I 2o AV block (Wenckebach periodicity) Random: 3o AV block Occasionally P-R intervals may vary with fluctuating vagal/adrenergic tone usually this is associated with marked sinus arrhythmia (OSA, autonomic dysfunction) QRS COMPLEXES I. QRS WIDTH (DURATION) - Normal: ( 0.11 s (< 3 little boxes) - Wide: e" 0.12 s (3 little boxes or wider) Ventricular rhythms no P waves before QRS complexes usually regular if rate is ~70, consider pacemaker rhythm: search for pacer spikes < 60/min: ventricular escape (usually 35-40/min)  why? Sinus arrest or AV block 60-120/min: accelerated idioventricular rhythm (reperfusion arrhythmia; cocaine; lytes; ICU) e" 125/min: ventricular tachycardia with ventricular rhythms, the QRS morphology and ST-Ts should not be further analyzed Right bundle branch block (RBBB) rSR pattern in V1; R both taller and wider than R the QRS complexes are usually upgoing in V1 usually wide S waves in left leads bifascicular block: RBBB + left anterior or posterior fascicular block RBBB does not affect the initial QRS forces: search for pathologic Q waves RBBB does not affect the ST segments in the lateral leads: search for possible ischemia expected (secondary) repolarization pattern: ST-T usually ( in V1; often ( in V2, V3 as well Left bundle branch block (LBBB) left leads (I, aVL and V5 or V6) are predominantly upgoing V1 V3: the QRS is predominantly downgoing slow upslope and notch in left leads absence of Q waves in most of the left leads in general, the QRS and ST-T cannot be analyzed in LBBB, but: pathologic Q waves in the inferior leads may signify remote inferior MI pathologic Q waves in several lateral leads may signify remote anterior MI ST segment elevation concordant with the QRS complex may signify acute STEMI T-wave inversion concordant with QRS complex (Ts ! in V1-V3) may signify ischemia expected (secondary) repolarization pattern: ST-T axis opposite to QRS axis Wolff-Parkinson-White (WPW) pattern ventricular preexcitation short P-R intervals (( 0.11s) delta waves usually does not fit either bundle branch block pattern V1 may be either upgoing or downgoing (upgoing in ~60%) RV paced rhythm (indication: bradycardia) I, aVL looks like LBBB all chest leads (including V5 and V6) are downgoing II, III, aVF are downgoing BiV paced rhythm (indication: CHF and LBBB) QRS in lead I starts down; QRS in V1 usually upgoing search for pacer spikes and clinical correlation (does the patient have a pacemaker?) Nonspecific intraventricular conduction delay (IVCD) does not fit any of the above frequently coexists with LAE, 1o AV block, atrial fibrillation several causes: review the company it keeps Causes of IVCD LVH with QRS widening: when LVH criteria are present periinfarction block: when pathologic Q waves are present hyperkalemia: when narrow-based peaked T waves are present hypothermia: when Osborne waves, bradycardia, ST-T abnormalities, long QT are present drug toxicities: when QT prolongation is present (TCA: deep S in I; tall R in aVR) infiltrative heart disease and connective tissue disease (e.g., amyloidosis, PSS) An algorithmic approach to the differential diagnosis of wide complex rhythms Are there P waves in front of the QRS complexes? no P waves; rate slow or fast ( probable ventricular rhythm (escape or VT) no P waves; rate normal: ( consider paced rhythm P waves present: ( review QRS morphology in V1 QRS predominantly upgoing in V1 is morphology c/w RBBB? ( RBBB if not: is this WPW? ( WPW if not: is this a paced rhythm? ( BiV pacemaker if not: nonspecific IVCD ( review causes of IVCD QRS predominantly downgoing in V1 is morphology c/w LBBB? ( LBBB if not: is this WPW? ( WPW if not: is this a paced rhythm? ( RV pacemaker if not: nonspecific IVCD ( review causes of IVCD II. QRS AXIS Lead I Lead II - Normal axis ( ( - Left axis deviation ( ( - Right axis deviation ( ( Causes of left axis deviation Advanced age LVH Inferior MI (loss of inferior forces) Left anterior fascicular block (LAFB); diagnostic criteria: left axis deviation > - 45o leads I and aVL ( but start with a narrow Q (qR) leads II, III, aVF ( but start with a small r (rS) QRS may be slightly widened but < 0.12s Causes of right axis deviation Young age RVH, pulmonary hypertension, COPD, secundum ASD Lateral MI (loss of lateral forces) Left posterior fascicular block (LPFB); diagnostic criteria: right axis deviation > +100o leads II, III, aVF ( but start with a narrow Q (qR) leads I and aVL ( but start with a small r (rS) all other causes of right axis deviation have been excluded (isolated LPFB is exceedingly rare; it is a combined clinical and ECG diagnosis) III. QRS AMPLITUDE High voltage  probable left ventricular hypertrophy (LVH); criteria: S in V1 plus R in V5-6 (whichever is the larger) e" 35 mm sensitive but not specific; the larger the sum the more specific S-V1 + R-V5 e" 35 mm R in aVL e" 13 mm specific but not sensitive R-aVL e" 13 mm R in I plus S in III e" 27 mm intermediate sensitivity-specificity R-I + S-III e" 27 mm LAE, LAD, ST-T abnormalities (strain pattern): LVH more likely QRS voltages may be higher in normal young and thin individuals unexplained high voltage: check amplification (r/o 20 mm/mV) Low voltage: QRS amplitude ( 5 mm in all limb leads; ( 10 mm in all chest leads; causes: decreased muscle mass: remote MIs; infiltrative processes (amyloidosis, hypothyroidisms) increased tissue resistance or skin impedance: obesity; emphysema; pericardial effusion; anasarca; scleroderma unexplained low voltage: check amplification (r/o 5 mm/mV) Variable voltages respirophasic: extensive diaphragmatic excursions (diaphragm. paralysis, severe COPD) electrical alternans (every other beat taller): suggestive of large pericardial effusion electrical pseudo-alternans: bigeminal PVCs, intermittent WPW IV. R WAVE PROGRESSION IN CHEST LEADS Normal QRS progression in chest leads: - QRS predominantly downgoing in V1 - QRS predominantly upgoing in V5 or V6 - There is a gradual increase in the R/S ratio from V1 ( V4 QRS predominantly upgoing in V1 (R/S ratio > 1) differential diagnosis: QRS wide e" 0.12 sQRS narrow ( 0.11 sRBBB ( V1: rSR RVH ( T negative in V1 (strain) ( right axis deviation ( deep S waves in V5-V6 ( V1 may start with narrow Q (qR) ( clinical picture (emphysema)VT ( fast; V1 not c/w RBBB ( typically no consistent P-QRS relationshipPosterior MI ( T upright in V1 (mirror image) ( inverted Ts in lateral leads ( inverted Ts in inferior leads ( clinical picture (chest pain)WPW ( short PR; delta wave; V1 not c/w RBBBSubtle preexcitation ( short or short-normal PR ( subtle delta waveBiV paced ( pacer spikes in front of QRS complexesV1-V3 lead reversal ( R wave regression from V1 to V3 ( computer may read it anterior MI ( P wave biphasic in V3Normal variant ( no other signs of RVH, MI, WPWQRS predominantly downgoing in V5 and V6 QRS narrow QRS wide - emphysema - paced rhythm - RVH - WPW - LAFB - VT - lateral MI Regression of R/S ratio in chest leads Possible anterior MI Severe emphysema, RVH Morbid obesity RBBB Dextrocardia Incorrect electrode placement V. PATHOLOGIC Q WAVES - Width: e" 0.03s - Depth: e" S! of QRS amplitude - Needs to be present in at least 2 neighboring leads Myocardial infarction Qs develop in second or third phase II-III-aVF inferior RCA (or LCX) V1-V4 anteroseptal LAD V1-V6 (( I, aVL) extensive anterior LAD V3-V6 (( I, aVL) lateral LCX I, aVL, V2 high lateral LAD-diagonal-1 Noninfarction Q waves LBBB WPW LVH Infiltrative processes (amyloidosis, scleroderma, cardiac metastases) Cardiomyopathies PE Hyperkalemia ST SEGMENTS I. ST SEGMENT ELEVATION - Normal ST segment: at baseline (same level as the PR segment) - Subtle ST segment elevation is frequently seen in V1-V3, especially in men; may be normal - The ST segment is the smoothest segment in the ECG; all notches are suggestive of P waves - The cause of ST elevation must always be evaluated in the clinical context - In patients with chest pain, acute MI should always be considered first Causes of ST elevation Ischemia, injury, infarction (i - i - i ) Characteristics: chest pain; ST( localized to a wall/vascular distribution; Q waves Acute or recent MI: hyperacute: no Q, T(; subacute: R(, T(; later: pathologic Qs Prinzmetal angina: like hyperacute MI but transient; no associated Q or T wave changes Cardiac trauma (contusion, stab wound, GSW): persistent ST( but no progression of T, Q Subacute cardiac rupture: progressive ST elevation in Q wave leads LV aneurysm: persistent ST elevation in Q wave leads ST elevation in aVR with diffuse ST depression elsewhere: possible left main obstruction Myocarditis Following high-energy cardioversion Acute adrenergic stress: pressors, inotropes, emotional stress; frequently present in ICU Secondary ST elevation Characteristics: wide QRS complexes or LVH; mirror image of ST depression LBBB: coved, elevated ST-Ts in leads with downgoing QRS complexes WPW: as above Paced rhythm: as above LVH: upward concave ST elevation and upright Ts in V1-V2 (mirror image strain) Terminal notching of the QRS complex followed by hammock-shaped ST elevation Heart rate fast - pericarditis: diffuse ST elevation; depressed PR segments (esp. in II) HR normal - early repolarization: triphasic QRS with terminal notch; upright Ts; normal QT HR slow - hypothermia: Osborn wave; prolonged QT; shivering artifact Early repolarization variant: early repolarization-type ST( followed by inverted Ts usually seen in AA males with LVH, and with acute or chronic cocaine use Electrolyte abnormalities, drug effects Hypercalcemia: coved ST( and absence of Ts in anteroseptal leads (STs are probably Ts) Digitalis: scooped ST( in anteroseptal leads; mirror image of scooped ST( in lateral leads Hyperkalemia: ST( in anteroseptal leads; narrow-based peaked Ts; Brugada pattern Na-channel blocker toxicity (including TCA, cocaine): Brugada pattern Miscellaneous Acute CNS disorder (SAH, ICH, trauma): QT frequently prolonged Brugada syndrome: V1-2: rSR, coved ST(, T( (high take-off ST( followed by T() Pseudo-ST elevation Atrial flutter: regular SVT at ~150/min; flutter waves may mimic ST( Artifact: ST( changes from cycle to cycle (ST( does not respect the cardiac cycle) II. ST SEGMENT DEPRESSION Horizontal or downsloping ST( with upright Ts ( probable ischemia someone stepped on the ST segment may be diffuse or localized diffuse ST depression with ST elevation in aVR: possible left main obstruction ST depression during PSVT is not diagnostic Downsloping ST( with inverted Ts ( probable LV strain usually in association with LVH LVH, strain and chest pain: ECG not very useful Upsloping ST( (J point () ( nonspecific ST usually back to baseline 2 mm after the end of QRS causes: anemia, metabolic abnormalities, MVP, normal variant Scooped ST( ( digitalis or hypercalcemia - usually seen in left leads (I, V5-V6) - QT interval may be shortened - may be associated with other markers of digitalis effect: bradycardia, 1o AV block, atrial fibrillation with slow ventricular response, digitalis-toxic tachyarrhythmias T WAVES I. NORMAL - T wave axis usually follows the QRS axis - Ts are always inverted in aVR; usually inverted in V1; upright in most other leads - Isolated T wave inversion in lead III is normal - With vertical QRS axis, T wave inversion in aVL is normal - If T axis is normal but T waves are narrow based and peaked: consider hyperkalemia - T waves are usually smooth; sharp notches or shoulders on the upslope or downslope of Ts are suggestive of superimposed Ps (or artifact) II. FLAT, BIFID OR NOTCHED Hypokalemia Drugs (antiarrhythmics) Acute CNS disorder (SAH, CVA, trauma) Liver failure Congenital long QT syndrome III. INVERTED Ischemia localized deep, symmetrical (V-shaped) biphasic (positive-negative) ST segments frequently at baseline (isolated T wave inversion without ST depression) Strain strain pattern: upsloping ST depression followed by non-symmetrical T wave inversion (shallow downslope, rapid upslope) LV strain: seen in left leads (I, aVL, V5-V6) usually in association with LVH RV strain: seen in anterior precordial leads (V1-V3) differential diagnosis includes anterior ischemia Injury and nonspecific diffuse may be shallow may be deep and wide may be associated with QT prolongation causes: ischemia; electrolyte abnormalities; drug toxicity; acute CNS event; catecholamine effect; pulmonary edema; massive PE Cardiac memory seen in pts with intermittent wide complex rhythms: intermittent pacing, LBBB, WPW when the QRS becomes narrow, T waves are inverted in those leads which had downgoing QRS complexes during the wide complex rhythm duration of memory Ts mimics duration of previous Wide complex rhythm frequently associated with prolonged QT The T waves are the most sensitive but least specific markers in the ECG (almost anything can turn them down) QT INTERVALS I. NORMAL QT - The QT interval is measured from the onset of the QRS to the end of the T - Between HRs of 70-100, the T wave should be over by half of the R-R interval - Corrected QT (QTc): measured QT divided by the square root of R-R interval (in seconds) - Male: normal QTc ( 0.44s - Female: normal QTc ( 0.46s II. PROLONGED QT Metabolic abnormalities hypokalemia hypocalcemia hypomagnesemia alkalosis liver failure Drug effects antiarrhythmics (potassium-channel blockers): quinidine, procainamide, disopyramide, sotalol, amiodarone, dofetilide, ibutilide psychotropic agents (phenothiazines, haloperidol, TCAs, SSRIs) antibiotics (microlides, quinolones, azoles) antihistamines cocaine many others, especially in combination Acute CNS disorders subarachnoid hemorrhage CVA, especially thalamic stroke brain tumor closed head injury status epilepticus Acute myocardial injury and/or catecholamine effect ischemia pulmonary edema (usually ~24 hrs after resolution) stress-induced cardiomyopathy (including Tako-Tsubo syndrome) massive PE (-adrenergic agonists (inotropes, inhalers) pheochromocytoma cocaine Congenital long QT syndrome (LQTS) III. SHORT QT - Lower limit of QT is uncertain - QT may appear short with digitalis effect - QT is reported to be short with hypercalcemia - Congenital short QT syndrome: risk of VT/VF SPECIFIC ECG PATTERNS I. ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION (STEMI) Phases Acute ST segment elevation: first upward concave, then upward convex QRS is usually normal initially Ts are upright initially Subacute ST segments turn upward convex T waves start to turn down (inverted) loss of R wave amplitude; development of pathologic Q waves Chronic pathologic Q waves STs are usually back to baseline persistent ST elevation suggests LV aneurysm Ts may or may not return to normal occasional terminal positivity of QRS in infarct leads (especially inferior) pathologic Q waves may disappear over time Time course of ECG progression variable; phases may be skipped ECG progression is modified by reperfusion therapy Localization ECG leads Location of MI Probable culprit II-III-aVF ((V5,V6) inferior RCA (or dominant LCX) Mirror image V1-V2 (R(, ST(, T() posterolateral LCX II-III-aVF, plus V1 and RV4 inferior + RV proximal RCA V1-V4 anteroseptal LAD V1-V6 (( I, aVL) extensive anterior LAD I, aVL, V4-V6 lateral LCX I, aVL, V2 (( mirror image III) high lateral LAD-D1 Frequently missed MIs Posterolateral (LCX) ST depression but upright T waves in V1-V3 (diff dx: ant. ischemia or posterolateral STEMI) later: increased R/S ratio in V1-V2 frequently accompanied by small Q waves or T-wave inversion in inferior or lateral leads High lateral subtle ST( in aVL, V2, sometimes in I mirror image (QRS(, ST( and T() in lead III RV infarct almost always in association with inferior MI ST( in R-sided chest leads; sometimes in V1; rarely in V1-V4 (may mimic anterior STEMI) combination of ST( in inferior leads plus ST( in V1 is highly specific for RV infarct frequently associated with sinus bradycardia or atrial fibrillation with AV block Anterior STEMI without ST elevation J-point depression followed by upsloping STs in the anterior chest leads Very tall (hyperacute) T waves usually taller than the corresponding QRS complexes II. PULMONARY EMBOLISM (PE) - The sensitivity of the ECG to diagnose PE is very low - The specificity of ECG signs suggestive of PE is very low - The ECG signs are only useful if they are not known to be old - The ECG may direct you to consider PE under the appropriate clinical scenario - In patients with suspected or documented PE, the presence of ECG markers suggests hemodynamically significant PE (acute cor pulmonale) - The most important unfavorable prognostic sign is new incomplete or complete RBBB Sinus tachycardia: important company for all other markers SI QIII - TIII pattern: S wave in lead I; Q wave and inverted T in lead III Incomplete or complete RBBB: rSR in V1 T wave inversion in V1-V3: mimics anterior ischemia III. PULMONARY DISEASE PATTERN - May be present in chronic obstructive or restrictive lung disease - One or more markers may be present, in any combination - The sensitivity and specificity are low Negative P and QRS in aVL: specific marker of emphysema Vertical P, QRS and T (from deep diaphragm): lead I may look like a flat line Low voltage in the frontal plane (limb leads) SI - SII - SIII pattern: S waves in all three bipolar limb leads Poor R wave progression in the chest leads Deep S waves in the lateral chest leads IV. VENTRICULAR HYPERTROPHY LVH with strain voltage criteria for LVH left atrial enlargement left axis deviation subtle QRS widening (0.11 - 0.13 s) repolarization abnormality (strain pattern or any other ST-T abnormality) definition of strain pattern: Upward convex ST depression followed by non-symmetrical T wave inversion (shallow downslope, rapid upslope) in leads with upright QRS complexes mirror image strain pattern may cause ST elevation in V1-V2 ECG evaluation for coronary ischemia is limited in the presence of LVH with strain RVH Common but less specific findings right axis deviation right atrial enlargement poor R wave progression in chest leads SI SII - SIII pattern deep S waves in V5-V6 Uncommon finding but highly specific for severe RVH QRS narrow but upgoing in V1 QRS in V1 may start with a narrow Q wave (qR pattern) ST segment depressed and T wave inverted in V1-V2 (strain pattern) V. ST-T PATTERNS T-QT pattern large, sometimes global T wave inversion T waves may be giant negative; occasionally giant positive prolonged QT a stereotypical response to a variety of noxious stimuli usually evolves ~24 hrs after the insult Causes: acute CNS disorders (SAH, CVA, thalamic stroke, brain tumor, status epilepticus) catecholamine effect ((-adrenergic agonist inotropes, inhalers, cocaine, pheochromocytoma) emotional stress (Tako-Tsubo cardiomyopathy) pulmonary edema massive PE Brugada pattern RBBB pattern in V1 (rSR: terminal positivity of QRS complex,-IJKLMPSY4 ; = B C E e h k l m n  ÿãßãßãõããÛõãÍãÂÂ×~h6$h<8 h{hzL0h{hzL05>*hv;:h{h<]h{hzL056hLhzL05h<8hzL05>*hLhzL0h hzL056h hzL056CJaJh4hGN5CJ aJ (h hzL05CJ aJ ehr1-JKL3 4 b B l . q ( NagdzL0$a$gd      B N T V X | r x        - . 1 2 3 9 : ; t u v | } ~  ɿɿɳɩɳɳɟho]h{h Q5>*h{h{56 h QH* h[!h56h{h Q56h Qh<]h{hzL05>* h{hzL0hv;:h{hzL056h<8h[!hhzL0hHM:       + / > $&(.0:>@FTZ\`fhvx󱵱󱠱˱h{hPJ56 jhv;:hPJ jhv;:h<8hh h<856hv;:h6$h[!h jh Q hv;:56h{h Q56ho]h QhLh Q5= )*678BCDHdopq 4bchstz{|޾ŝh1h~56h~ jhPJh h{+Zh{+Z h{+Z56hh jhPJh[!h jhPJ jhPJ hv;:56hv;:h{hPJ56hLhPJ5ho]hPJh{+Z9c=> ijgd $a$gd $da$gd<8p^pgdWiq p^p`gdWiqgdzL0"$&2PZ\^`b,.0Jdzددyrnfbh-h{h-6h h{h-h{h-56h{ho]5>*hWiqhWiq56hWiqho]56 hWiq56 hHM56hWiqh{+hWiq56h{ho]56 h{+56h{+hHM56h{+ho]56ho]hLho]5hh~h{h~56&>Elm#+jvw}~ h 6h6CJaJhHM6CJaJh<86CJaJh=7vh=7v56 jh4hh=7vh456 jh4h{h45>*h6$h=7vhh56h4h?h{h?56h{h-56h-,@FTjp24B~Ff"$8tϽϹ} h6$56h[!hhhSA5 h[!h56hZhSA56 hhSAh h5hZhSA5hSAh0hZ6 h[!h6 h6h0hSA6 h6 hSA5>*h hHM(h h 5CJ aJ ehr1@j~ftRaG2<0 & Fdgdh> & Fdgdh>dgdh>R$%FG_mn12DE»»»»⬤ jh6$CJaJ jh6$h6$CJaJhCJaJh~CJaJh D^h CJaJh6$ h D^h  h D^hZh D^h 56h0h 6 hSA5>*h hhZ hZ56 h56hSA3 ;<Q  . / 0 T [ d  !!!!!;!>!X!k!!!!Իԭ񥠥ɖɖɖɖɒ h M5>*h MhZh 56 h D^5hZh 5h"h D^hZ56 h D^h h56h  jh6$hh6$ h D^hZhZh D^h 56 h D^h h~CJaJ60  !X!!!!!"1""""""M#####$gd0$a$gd0 d^gdh> d`gdh> & Fdgdh> & Fdgdh>dgdh>!!!!!!!!"""1">""""""""""""b#c##############$$$$$$$($1$׾ۚۓwwhmhXc6hmhck6 hm6 h05>* hck5>*(h0h05CJ aJ ehr hhh Mh6 h6 hH*hh>* hh0hh0 h056h Mh M56h Mh M5h6$h M.1$5$:$>$G$K$P$V$$$$$$$$$$$$$%%%+%@%z%%%%%%%%&%&&&/&F&U&}&&&&&&&&&欢暖z hH* h5>*h[!hhXchXch5hh[!hh5hXch56hGn hXchck56hXchck5h[!hhXc5h[!hhck5hh>* h>* hck5>*hck hm6hmhck6hmhXc6/$P$$$$$$z%%%%&&&& 'C'J'b'o'''')( & Fgd6$gd & Fgd & FgdGn  & Fgdck & Fgdckgdckgdm&&&& ''B'C'I'J'a'b''''')(N(((((((((( )#)')))))))))))))ἵzrhTh6 h:5>* h5>*(h h 5CJ aJ ehrh h[!hhV4 hg%OH* h 5>* hg%O5>*hg%Oh^Jh0mHsH jbhh0 h6$h6$h6$hhh>* h6hh6 h[!h6))(N(((((( ))))))Z****h+ ,, --- & Fgd'Y & Fgd & Fgdgd $a$gd  & Fgdg%Ogdg%O & Fgd)))***Z*****4+f+h+x++, ,f,,,, --x-------0.8.A.E.....i/////////ŽɵšɹhTh'[ 56 jh h 6h h 6h hThc56 hc5 h'Y5h0hchaAh0h'Yh0y hThhTh56h h5 h[!h6hTh6 jhTh6/-0.\.../i///!0M0s000&1q11B22X3334F4 & Fgd'[  & Fgd'[  & Fgd6$ & Fgd]Y & Fgdc & Fgdc/ 0!0M0N0s0t000V1]1111B2233"3V3X3333<4=4F4J4U4o4p444455͉̈́͝vld\h~hk)5haAhaA5h~hO56hThO56hO haA5 h'[ h'[  jhTh'[ 56hTh'[ 56 hO5hOhO5 h'[ 5h h 6haAh0yh0h'[ h h]Y56h h'[ 56hTh6$56 hc56hTh]Y56#F4p44445755556K6[6667]7788R88 & FgdK8gdK8h^hgdk) & Fgdk) & Fgdk) & Fgd~ & FgdO & FgdO56575N555555556L6[6^6666677]7l777777778888R888888888899ÿͿͿͿͿ~zzszzsz jhy)hy)hewhK856h[!hhK85 h[!h5h0h[!h h[!h56hK8hThK856h<]hk)5 hk)H*hk)h~hk)56hThk)56haA haA5h~hg8F5hg8Fhg8Fhg8F5hg8Fh~5h~-88929R9r9999:4:Q::::::;B;`;m;q;;; & Fgd63hgd63h & Fgd_ & Fgdy) & FgdK8 & FgdK899991929R9i9k9l9q99999999999999999999::+:-:.:3:<:H:K:L:P:Q:R:p:r:s:t:w:::::::::::::::::񾷳 hVBh63hhVBhVB>*hVB h63h5>*h63hhThewhew56hewhg8F jh<]h<]hewhK856hK8h_ jhy)hy)?:::::::::::::: ;;;;;;; ;!;%;4;:;;;@;A;B;_;;;;;;;;<<<<<&<2<ѻᰬѡᬡѻ~vq h05h0h05h0hVBh63h5 h63hH*h63h h63h56 hVBh63h jhVBhVB5hVBh[!h h[!hh63h jhVBhVB5 jhVBh[!h5hVBhVB5hVBh[!h5 h63h6hVBh63h56hVBh[!h56 h[!h6,;; <S<{<<<<<5=R====>>:??X@z@@ hh^h`hgdVB & FgdW & F gdWgd'^^gd'^ & Fgd63hgd63h & Fgd63h & FgdVB2<3<4<5<M<N<R<t<u<{<<<<P=Q=R=X=d=e=f================>>>>>>>"?$?8?:?b?Ϣϔ~hVBhW6 hWh$' hW56 h$'56 hy)5>* h'^5>* jhVBh05h0h05 jhVBh05hVBh05h'^ h63hH* h63h56hVB h05h0 hVB5 jhVBhVB5h63h.b?d?h?j?????@@.@0@H@V@X@x@z@@@@@@@@@AA AAAdA|A~AAAAABB4B8BDBEBtBwB»Ϸ³ϊςϷzvrh6$h0h0hW6hWhW6hj!hyhy5 hy5hy hyhyhVBhy6 hy6h$'hVB hWhWhWhW5 hW5hW hVBhj! hVBhW h0h0 h0hWhVBhW6hVBhVB6,@AABEBBBB5CdCCCCGDDDDE,ETEEEgd>E0 & Fgd0^gd>E0 & Fgd>E0 & F gd>E0 & FgdW^gdy & FgdywBBBBBBBBBBBBB5CbCcCdCCCCCCCCCCC$D.D8DEDGD[D\DuDvDDDDEE+E,E/E1E2ETEWEXEYEEEEEEEEԪĦĦԡįĚĖĦhj!hs h>E05>* h06h\u hg8F6h>E0h>E056 h>E0h0h6$h>E0 h>E0h>E0 h\u6h>E0h>E06 jh>E056 hVB56 h>E056h>E0h06h08EEEEFFF*F,FPFRFbFdFlFrFtFvFFFFFFFGBGRGTGGGG H(H)H*HwlaaahDhDCJaJh6$hXHyCJaJhDhXHy>*CJaJhDhD5CJaJhDhXHy5CJaJ jhDhXHy5CJaJhDhsCJaJhDhs5CJaJ jhDhs5 h6$5hDhs5 hXHyhs h6$56 h\u56 hs56hs jh0!EF:FbFdFFGGHKHHpgggggg $Ifgdszkd$$Ifl0h<' t0644 la $$Ifa$gds & F gds *HEHJHKHjHrHsHHHHHHHHHHHHHHHHHHHHHIIII I/I0IOIWIXIII퍂킬ȼvkh\uhsCJaJhDhXHy>*CJaJhDhfCJaJ jhDhf5CJaJhsCJaJh\uCJaJhDhs5CJaJhshDhXHy5CJaJ jhDhXHy5CJaJhDhDCJaJhDhsCJaJhfCJaJhDhXHyCJaJ&HHHH0IvIIJ{{{{{{ $Ifgdszkdd$$Ifl0h<' t0644 laIIIIIJJJ J J$J'J*J.J4JHJLJMJfJgJJJJJJJJJJJJJJJK KKK5Kǻ˰𠘠njtia𠨠hg8FCJaJhDhg8FCJaJ jhDhg8F5CJaJhg8F5CJaJhg8Fhg8F5CJaJhsCJaJhDCJaJh\uCJaJhDhsCJaJhDhs5CJaJhs jhDhXHy5CJaJhDhDCJaJhDhXHyCJaJ jhDhD5CJaJ&JJ4JgJJ{{{ $Ifgdszkd$$Ifl0h<' t0644 laJJJKXKK{{{{ $Ifgdszkd,$$Ifl0h<' t0644 la5K6K~KKKKKKKKKKKKKKKL LLLL$L,L/L3L>L?LILLLPLSLVLWLaLeLiLlLnLoLzLLLLLLLLM,MNƺѳ hI!5>*hfhI! hI!56h0h0>*h0 h0>*h,hD hD56hDhs5CJaJhDhsCJaJhshDhDCJaJh\uCJaJhDCJaJ jhDhD5CJaJ2KKKK{{ $Ifgdszkd$$Ifl0h<' t0644 laKKKL?LWLoLLLLLL|wwwwwn|ff & FgdI!h^hgd0gd, & F gdDzkd$$Ifl0h<' t0644 la LLLLMM-M,NrNNOZOOOP:PeP{PPPPPP & FgdBr; & F gdBr; & Fgdhh^hgdBr; & F gdhgdI! & FgdI! & Fgd,NN N*N,NJNLNNNNNOOZOnOtOOOOOOOOOOOPPPP P!P9P:PeP{PPPPPPPPPP仴џџ~pџh^Jhf56mHsHhfmHsHhfhBr;56mHsHh^JhBr;mHsHhBr;hBr;56h^JhhmHsH jhBr;h^JhBr;mHsH jhhh\uhBr;hBr;hh6 hh56hhhhhh6 hI!6 h\u6 hh6+PPPPPQYQQRkRRRRRPSSSOTTT U,UPUU & Fgdh[ ` gd)  & F gdI gdI $a$gdI  & FgdBr;PPPPPPQQ9QXQYQ{QQQQQRRRRRRRR S SSSSSOSPSUSͽ͸ͱ򬧢{vnv{d\h (hh[5hh[h) 56 jh6$6 h6$6h~h) 6 h) 56h6$h) 6h6$hI 6h6$hh[6 h,L5 hsL5 h35 hI 56 h+6 h) 6 hg8FhI hg8F hI 6 hI 5>*hy)(hI hI 5CJ aJ ehrhI hy)hBr;56 US_SbScSdSoSwSxSzSSSSSSSSSSSSSSSSSST#T2T3TNTOTgThTTTTTTTT U+U,UOUPUhUUUUUUUUUĿĻh~hS566 h) 56h6$h) 6 h6$hh[h6$hh[6 h+)h+)h+) h+)5hg8F hg8F5h,hh[ jh-T[ jh-T[h>vh-T[6h-T[h (hh[5h (h-T[56UU VMV[VrVVWgWWXXX%YYYZ)ZhZZZ[c[ & Fgd,L & F gd,L & Fgd+ & FgdsL & F gdg8F & Fgdh[ ^ gd)  & F gdh[UUUUUUU V VVVLVMVPVQVZV[VgVhVqVrVuVvVVVVVW WWW!W,W-WfWgWpWtWWWWWWWWWWWWXļļȰīĊ}}hsLh+ h+)5h+)h+)56 hg8Fh) h6$hh[6h6$h,6 hg8F6h,h (h-T[5h (hh[5hh[h-T[h#jh-T[5h#jhh[5h) h,6 h>v6h~h) 6h~hS566 hS5661XX XX#X$XAXBXOXWXZX[X]XdXjXXXXXXXXXXXXXXY$Y%Y.Y/Y:Y;YmYnYYYYYYYYYYZZZZ(ZŽh6$h,L6hsLh (h+5 jh#jh (h#j5h, jh#jh#jh-T[h (h-T[5h (hh[5 h6$hh[h6$hh[6 h+)h+hg8FhsLh+6 jh+h+ h+5 hg8F5hh[2(Z)Z;ZNZgZhZxZyZ~ZZZZZZZZZZZZZZZZZ[ [[[[[[[[9[;[=[>[b[c[d[e[~[[᪠ݙ݇~zsoh4^ h35>*hh&2h35CJaJhsLh,L6 jh (h, h (h, jh (h#j h (h#jh (h6$h,L6hKa jh, jh, jh#j jh#jh,h (h#j5h#jh,Lh (h,L5 h6$h,L+c[d[[[[\R\~\\\]4]j]]]]^Z^^^^^$a$gd+1H^Hgdn ` gdn & F gdn & Fgd+1 & F gd[H^Hgdh&2dgd3[[[[[[[[[[\R\T\_\}\~\\\\\\\\\]]]]]]#]&]']3]4]]]]]]]i^j^^^^^üҭ hnhn hnH*hn jhn56 jhn56 hn56h+1h[6 hq56 h+1h+1h6]zhg8Fh+1h+1h36 jh[56 jh[56 h+156 h[56.^^^^^___J_g__7`f`u`x``````````````.a/a*h,hP56h,h+)56h,hMnZ5h,hMnZ56h, hMnZ5>*hMnZhP h+)56 h!T56 h+56 hP56 hMnZ56 hP6 h!T6 h+16 hMnZ6 h+15>*h+1(h+1h+15CJ aJ ehr&^^^_h___7````` a/a=aYaZahaqa{aaa bb & F gdq & FgdP & F gdP & F gd,gd!Tgd+1 bbEbebAcBcXcYcZcacwccccccccc d*d+d9d%e+e~eeeeeeeef fYfffg!g"g@gBgCgIgKg[g\gsg h56 jh6 h6H* h6 hkJ6 h5>*(hh5CJ aJ ehrh hq5 hIY5h"h9d h9d56h,hP hP56 hqhq hq6hq hq560bbbBcYcacpccc+d:ddeUe}e~eeeee fYffgd$a$gdgdqgd9d & Fgd9d & F gd9d & FgdP & F gdP & Fgdqf g)gJgKg\gtgggggggAhhhhhhhi7iCiViiii & FgdOb{ & F gdOb{ & Fgd & F gdgdsgtgggg_h`hdhhhhhhhiiiiij"j#jgjjjjjj(k2k3k;kDkSkTkUkjklkokkkkkkk㿸߱߬{{t hpA_56 h+5>* hpA_5>*(hpA_hpA_5CJ aJ ehrhpA_ h9d6 h+6 hZ6 hZ5>* hZhZ hZ56 jbhOb{h9d hOb{hOb{ hOb{56hZhOb{ h56h+)hhh56+iiij"jNj_jgjjjjjj"kTkkklkkkkkl & Fgd~ & Fgd~ & F gd~gd~gdpA_$a$gdpA_gdZ & F gdZ & FgdOb{kkkkkkkkklllll&l'l/l0lNlOlilklslullllllllllllll m mmm*h\ h\56h+hkJ5h+hpA_5h+hr@5 hr@6 hpA_6h%rh8Shr@hpA_ hr@hr@hpA_hpA_6>l'l0lOlulllllm=mmmmm'n4ndnn H^H`gdO,c ` gdO,cH^Hgd~ & Fgd~ & Fgd~ & Fgd~ & Fgd~ & Fgd~ & Fgd~ & Fgd~ & Fgd~BnPnQnRnSncndnpnqnwnynznnnnnnnnnnnnnnnnnnnnnnnnnnnn o oooo$o%o(o)o0o1o2o9o;o=oPoQoToUoboeofopoqotouoooدΧh h!T hO,c5h%r jhO,c jhO,ch\h\6 jhO,ch\ hO,ch\h\h\>*h~hO,c h\h\h~h\6>*Bnn o)oUouoooo3pWppppqqHqqqHrnr & FgdU) & Fgd~ & Fgd~ & Fgd~ & Fgd~ & Fgd~ & Fgd~H^Hgd~ H^H`gdO,coooooooooooooooooo2p3pVpWpppppppppppppqqqqqqJqKqOqPqsqqqqqqqû÷hkJ hkJhkJh+ jh8S jhkJ jh8Sh8Sh8S6h8S h8Sh8ShU)h8ShO,c6 hU)6h8Sh\5h8ShO,c56h\h\H* h\h\ hO,c5hO,ch  jhO,chO,c2qqq9r>rGrHrQrRrWrXrmrnr s s(s)ssstt* hxhxh7hxh756 hkJ56 h756 hx56 h!T56hxhx56 his6 h76 hx6 hx5>*hU) h8ShU) h%r6 hU)6hxh+h8ShkJ jhkJ.nrr s)sdsss*h7h756hJZ hJZ6 hJZ56hJZh756h:h7 h756-wx*x+xGxWxpxxxx yyyMzQzszzzzzz*{G{}{{h^hgd/m ^ gd/m & Fgd/m & F gd/mgd/m & F gd7{{{|C|P|||| }f}}}}} Q o w (  & Fgdz & F gd & Fgdh^hgd & Fgd6J & Fgd/m & F gd/mgd/mO|P|n|u||||||!}"}e}f}v}}}}}}}}}}}}}}   7 P Q n o        ' ( C E    $[򟙟h;hz5h;h;5h;Uhzh: h56hhy56hJZhyhyh56 jbhhhkJ56 hkJ6hkJhkJh56hishhh565 but QRS < 120 ms) high take-off coved (upward convex) ST elevation in V1 and V2 inverted T waves in V1 and V2 Causes: Brugada syndrome: no underlying structural heart disease; unexplained VF/arrest; endemic in Southeast Asia; familial-sporadic otherwise; except for V1-V2, ECG is usually normal possible Brugada syndrome: no underlying structural heart disease; no h/o VF/arrest but either a family h/o unexplained sudden death or a personal h/o unexplained syncope; Southeast Asian male; except for V1-V2, the ECG is usually normal normal variant: none of the above risk factors (incidental finding); except for V1-V2, the ECG is usually normal severe hyperkalemia: Brugada pattern is associated with very wide QRS, abnormal QRS axis sodium-channel blocker toxicity (including cocaine, TCA): Brugada pattern is associated with very wide QRS, abnormal QRS axis propofol infusion syndrome (with high-dose propofol): QRS narrow; acidosis, rhabdo, ARF, hyperkalemia, hypertriglyceridemia, high risk of VT-VF and sudden death right ventricular pathology or injury Terminal positivity of QRS (terminal notch) and hammock-shaped ST elevation Early repolarization (normal variant) best seen in V4 QRS triphasic (up, down, up again) upward concave ST elevation starts from the upsloping QRS (this may cause a notch) normal, upright T waves QT is normal Hypothermia terminal QRS notch more prominent (Osborn wave or J wave) frequently associated with sinus bradycardia or slow atrial fibrillation marked ST-T abnormalities may be present (both ST( and ST() prolonged QT when rewarming: shivering artifact Pericarditis diffuse ST elevation; ST elevation usually spares aVR and V1 usually associated with sinus tachycardia P-R segments may be depressed (especially in II) or elevated in aVR VI. ELECTROLYTE ABNORMALITIES - The hypers ((K, (Ca) shorten the QT interval - The hypos ((K, (Ca) prolong the QT interval - K abnormalities affect the T waves ((K: narrow Ts; (K: wide Ts) - Ca abnormalities affect the ST segments ((Ca: shorter STs; (Ca: longer STs) Hyperkalemia Common findings, in order of severity: narrow based, peaked T waves (base of Ts pinched down) widened QRS complexes (nonspecific IVCD) axis shift, new fascicular block flattened P waves QRS-T sine wave morphology arrhythmias: junctional rhythm; asystole; AV block; VT; VF Less common findings: anterior ST segment elevation Brugada pattern pathologic Q waves double counting of HR by ECG interpretation software: highly specific for hyperkalemia Hypercalcemia ST segment shortened T waves are inscribed right after the QRS complex may mimic coved ST segment elevation in anterior chest leads may rarely cause a normothermic Osborn wave ECG findings of hypercalcemia usually signify severity of hypercalcemia Hypokalemia nonspecific ST depression (usually upsloping) wide, bifid T waves or T-U complexes prolonged QT/QU intervals wavy ST-Ts (3 waves between QRS complexes: T U P) severe hypokalemia may mimic ischemic ST segment depression Hypocalcemia nice, smooth, normal looking T waves prolonged ST segments T waves are pushed to the right prolonged QT intervals a similar pattern is frequently seen in pts with advanced liver failure, even with normal Ca Chronic renal failure, uremia combination of hyperkalemia and hypocalcemia flat, long ST segment followed by narrow-based, peaked T wave (tent on a desert) slowly upsloping ST segment followed by peaked T wave; QT prolonged     PAGE  PAGE 15 =]^$%Ucpquvw"#:;GHMX  #$FGK򾷰zvh^h^h$56 jh$ jh$h$h!Th$6h!Th^6h$h$56 hkJ56 h$56h$hz56hh:56h:h:hz56hhz56h;hz5hzh;h56.^%q#;HX$GX"Wgd/m & Fgd^ & Fgd^gd^ & F gd$ & FgdzKXln!"67:;jkno#/HIsǿǿǷǷǿǷǿǷǰ̨̞̞̞Ṵ̈̌h0]$h/m56 hkJ6hKh/m56hkJh/m6 h/m56 jh/m6 jh/m6 h/m6h/m h/m5>*h!Th/mh^6hkJh^h^6h:h^h!Th^68#0W DZxI4Ysh^hgd/m & Fgd: & Fgd/m ` gd/m & F gd/mgd/msQhch]hgd~ &`#$gd^ & F gd/m & Fgd/mhMOabcſſſŰſh0JmHnHuh" h"0Jjh"0JUh?hjh?hU h/mh+)h+)h0]$h/m56 h/m56 h/m6h/m" & Fgd/m5 01h:p~/ =!"#$`% b$$If!vh55#v#v:Vl t655ab$$If!vh55#v#v:Vl t655ab$$If!vh55#v#v:Vl t655ab$$If!vh55#v#v:Vl t655ab$$If!vh55#v#v:Vl t655ab$$If!vh55#v#v:Vl t655a@@@ NormalCJ_HaJmH sH tH DA@D Default Paragraph FontRi@R  Table Normal4 l4a (k@(No ListHH { Balloon TextCJOJQJ^JaJj@j s Table Grid7:V04 @4 ~Footer  !.)@!. ~ Page Numbert ( -JKL34b>>qr:`Op67zL" # ] # @ x  f  8 x  eV/_`x_t$a'kQnno!9F%Vghu8H9\3V@$JwH 4!r!!!! "6"M"""""S####$!$V$$$#%w%%%&I&&&&'8'U'''''(G(y(z(((()&)3)7)]))))*A*`*j****+L+|++ ,,c,,,-2-O--- .H....*/j/// 0f000001F111111 2H2223X3Y3|333<44444-5g5h5556\6]6^666667757J7K7r777777777 8,8f8|8888 9-9X9n9s9w9{9999999:L:: ;^;;;;;C<<<B===>>C>>>>@?N?e??@Z@@@AABsBBCC[CCCDVDWDrDDDDEEqEEEE'F]FFFFGMGGGGGGGH[HHH*IIIIII"J0JLJMJ[JdJnJJJJK|KK5LLLTLcLxLLM-MMNHNpNqNrNNNNNLOOOP=P>POPgPsPPPPPP4QsQQQQQQ R*R6RIR\RRRR SSASRSZS}S~SSSSTGT^T_TTTTTUU#UBUhUUUUU V0V}VVVVW'WWWWWWXHXhXXXX&YJYYYYZ Z;ZZZ;[a[[[\W\\\/]]]^W^^^__!_i___ `[````aa:aJaca{aaaabb@cDcfc{cccccd:dpddddd6eCe|eeeeYfffffg>g\gdghitiiKjjk^kkkkl(l5lElllmm4mEmmmmnDnxnnooDo}ooooo1pGpepwppppq6qsqqqq!rFr`rrrrs>sUssssPttttttttttttttttt000000000000000000000000000000000000000000000000000000000 0 0 00 0 0 000 0 0 0 0 0 0  0  0  0  0  00 0 0 0 000 0 0 0 0 0 0 00000000000000 0 0 0 0 0 000000 0 0 0 0 0 0 0 0 0 00 0 0 000000 0 0 0 0 0 0 0  0! 0 0" 0# 0$ 0% 0& 0' 0( 0 0) 0* 0+ 0, 0- 0. 0/ 00 01 02 0 03 04 05 06 0 07 08 09 0 0: 0; 0 0< 0= 0>0 0? 0@ 0A 0B 0C 0D00 0 0E 0F 0G 0 0H 0I 0J 0K 0  0L 0M 0N 0O000000 0  0  0  0  0P 0Q 0R 0S0 0 0 0 0 0T 0U 0V 0W00 0 0X0 0Y0 0Z0 0[ 0\ 0] 0 0^0 0_0 0` 0 0a 0b0000000 00 0 0 0 00000 0 00 0000 0 0 00 0 0 000 0 0 0 0 0000000 0 0c 0d 0e 0f 0g 0h00000 00 0i 0j 0k 0l 0m 0 0n 0o 0p 0q 0r 0s 0t0000000000 00 0u 0v 0w 0x 0y 0z 0{ 0| 0} 0 0 0~ 0 0 0 0  0 0 0 0 0  0 0 0 0 0  0 0 0  0 000 0 0 0 0 0 0 0 0 0 0 0 000000000000000000 0 0 0 0 000 0  0 0 0 0 0  0 0 0 0  0 0 0 0 0 0  0 0 0 00000000000000 0  0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 00000000000 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 00000000000 0 0 0 0 0 0 0 0 0 0 0 0 0 0 000000000 0 0 0 000000 0 0 0 0 0 000 0 0 0 0 0 0 0 0 0 00 0 0 0 0 00 0 0 00 0 0 0 0 0 00 0 0 0 0 0 0 0 0 00 0 0 0 0 0 0 0 00 0 0 0 0 00 0 0 0 0 00 0 0 000000 00 0 0 0 0 0 00 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0  0 0@000@000@000@000@0@0@0@0@0@000 Qn""S##444-5g5h55\6]6rDDDDEE-MMNpN;[a[[Do}oot00p|00000000000000T00 00 0000 0 00 00 00G/00000000/0000000P/00000P/00 %%%( !1$&)/59:2<b?wBE*HI5KNPUSUX(Z[^ bsgkBnoqvO|K?BCDFGHJKMNPRTVXY[\^_acfjlmopqstvy{}0 $)(-F48;@EHJJKKLPUc[^bfilnnrw{s@EILOQSUWZ]`bdeghiknruwxz|~A !(!!8@0(  B S  ? [[U[D[ϗ[[ќ[Lݚ[P[J[l[,V[,ߜ[ [|Z[L[l[[\['[[D6[$<[L[dW[[[9[i[-[Z[E[|h[ NSSEE--77666==qEqEEEGG|K|KVVgt     YYKK33EE666==EEEEGG~K~KVVgt 9*urn:schemas-microsoft-com:office:smarttagsplace8 *urn:schemas-microsoft-com:office:smarttagsCity9*urn:schemas-microsoft-com:office:smarttagsState:*urn:schemas-microsoft-com:office:smarttagsStreet;*urn:schemas-microsoft-com:office:smarttagsaddress             %U 999,9{9999tttttttttttttt%U 9,9{9999tttttttttttttt# ` V`x_t$nF%Vu8H9\!!""$!$&'3'8'Q'U'x''''''((:(G(&)7)]))A***+ ,,,-..*/j///1 283Y344S5h5 7K7r777,8f8|88 9X9{99:;;>C>>>@?e?AACCCCWDrDDDEEE'F]FFI!J"JJJK5LxLM-MHNrNP>POPPPPsQ\RRR SSTTTBUUUVVXXZ Z;[a[^!_aa@ccccdd6eCeeeff\gdgbkklElmEmmmoooo1pppqqqFr`rrr>sUssstttttttttttttttttttttttttttt~ VXJLt"05{08 @E0zL01+1h&2V4S56v;:Br;h>SAaAVBDg8F6JPJ^JLwLHMGNNg%O\OP QJY]YZ{+ZMnZ-T[h[<]'^4^ D^pA_O,cXch[!h63hckWiq%ris=7v0yXHy6]z${Ob{9d?ew0z:07",;,LclUxIYJZq <8\e#?h@-~4kJKh/m{^OsL8S2w[`)'Y Mk)\u x__>v0:ZKa~-{+Hy~K8qo]!Tf #jWh^rrU=ms1111 2X3Y33444g5h55\6]6^666t@mtmt#mtmt   !+,-1278ft@ @ @(@8@*,\@2h@>@@F@N@@UnknownGz Times New Roman5Symbol3& z Arial5& zaTahoma?5 z Courier New;Wingdings"1h{f{fq&f.c;f.c;!94dYtYt 2QHX ?2EKG COURSE HANDOUT 2006llittm01llittm01                          Oh+'0 ( H T ` lxEKG COURSE HANDOUT 2006 llittm01Normal llittm012Microsoft Office Word@@t@ߓ+@ߓ+f.c՜.+,0 hp  Carolinas HealthCare System;Yt' EKG COURSE HANDOUT 2006 Title  !"#$%&'()*+,-./0123456789:;<=>?@ABCDEFGHIJKLMNOPQRSTUVWXYZ[\]^_`abcdefghijklmnopqrstuvwxyz{|}~     Root Entry FSB+Data 1TableWordDocument7(SummaryInformation(DocumentSummaryInformation8CompObjq  FMicrosoft Office Word Document MSWordDocWord.Document.89qRoot Entry F@Dy$@Data 1TableWordDocument7(     #" SummaryInformation(DocumentSummaryInformation8CompObjq  FMicrosoft Office Word Document MSWordDocWord.Document.89q՜.+,D՜.+,\ hp  Carolinas HealthCare System;Yt' EKG COURSE HANDOUT 2006 Title4 $,