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79 Cards in this Set
- Front
- Back
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transverse plane leads |
septal- V1 and V2 anterior- V3 and V4 lateral - V5 and V6 |
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sagittal plane leads |
V2 and aVF |
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frontal leads |
I, II, III, aVR, aVF, aVL |
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normal cardiac action potential durations |
1. atrial depol.- 0 to 80 ms (80 ms) 2. AV delay- 80 to 200 ms (120 ms) 3. septal depol- 200 to 220 ms (20 ms) 4. apical depol- 220 to 230 ms (10 ms) 5. LV depol- 230 to 240 ms (10 ms) 6. late LV depol- 240 to 250 ms (10 ms) 7. vent depolarized- 250 to 350 ms (100ms) 8. vent. repol- 350 to 450 ms (100ms) |
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septal leads |
V1/V2 |
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anterior leads |
V2, V3, V4 |
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lateral leads |
I, aVL, V5, V6 |
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inferior leads |
II, III, aVF |
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what determines intrinsic heart rate? |
rate of P4 depol |
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list the various intrinsic rates of different heart tissue |
SA: 60-100 Atria: 55- 60 AV: 45- 50 His: 40-45 Bundle Branches: 40-45 purkinje fibers: 35-40 ventricle: 30-35
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rule of 300 |
-300/# of large boxes between R-R interv -only works for regular rhythms - 300, 150, 100, 75, 60, 50 |
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10 second rule |
-count number of beats per 10 sec strip, then multiply by 6
-works for irregular rhythms |
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calculated HR |
-60,000ms/R-R interval in ms -60s/R-R interval in s |
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list possible causes of RAD |
-RVH, LPFB, lateral wall MI, dextrocardia, vent. ectopic rhythm (PVC/vtach), normal variation, mechanical (insp/emphysema), RV load (e.g. PE or COPD) |
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list possible causes of LAD |
-LVH, LBBB, LAFB, interior wall MI, vent. ectopic rhythms (PVC/vtach), pacemaker rhythm, mechanical shifts (high diaphragm, expiration, pregnancy, ascitis, abd. mass/tumor) |
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describe normal P wave morphology |
leads I, II, and aVF- positive lead III and aVL- positive or biphasic lead aVR- negative lead V1- biphasic |
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describe possible abnormal P wave morphology |
1. rt. atrial enlargement- incr. P wave amp (esp. II) 2. lt. atrial enlargement- notched appearance lead II 3. inversion in V1- ectopic atrial rhythm 4. PTa elevation- atrial infarct 5. PTa depression- pericarditis |
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normal PR interval |
- 0.12-0.20s -includes wave propagation through SA, L and R atria, AV node, His-Purkinje |
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describe the normal QRS complex |
- 0.08 s to 0.12 s - V1, septal vector, depol. septum L to R |
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describe normal T wave morphology |
- positive in most leads except aVR -V1- pos or negative -negative T wave in lead III (positional or respiratory) |
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possible T wave abnormalities and causes |
- tall peak- hyperkalemia -ischemia/necrosis- T wave inversion -inversion- strain -long T wave- prolonged QT interval |
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features of normal ST segment |
- from end of QRS (J-point) to beginning of T wave - isoelectric, representing phase 2 of AP |
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normal QT interval features |
1. longer QT means longer APD 2. inversely proportional to HR 3. men: <440ms, women <450ms
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why is the QT interval corrected for heart rate |
1. repolarization changes with increasing HR 2. systole stays constant, so diastole is sacrificed at high HR, thus repol becomes shorter 3. Bazet: QTc= QT/SQRT(R-R) |
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normal variants in ST segment |
- lead reversal (QRS negative in lead I) - ST segment drifts/early repol - U wave - incomp RBBB - low voltage QRS |
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normal variant- drifts in ST segments |
-limb leads- elev/depr up to 0.1 mV -ST elev. more common inf. leads -precordial- up to 0.3mV in V2/V3, up to 90% of normal subjects(depression in abnormal) -mag of ST elev. is prop. to QRS magnitude
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features of early LV repol |
- ST elevation w/ prominent J-wave (esp. V4/5/6)
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normal U wave features |
- positive deflection of T wave - best visible in V5/6 - possibly represents purk. fiber repol? - not rare, no clinical significance |
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prominent U wave differential |
-normal variant -acute ischemia -severa aortic insufficiency -K/Mg disturbance |
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T wave fusion w/ U wave |
hypokalemia vs LQT |
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how does ventilation affect normal SA node pacemaking activity |
- varies reflexively with ventilation d/t vagal firing rate variability |
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low voltage QRS features |
- <5mm in limb leads and/or <10mm precordial - diff dx- COPD, effusion, obesity, hypothyroidism -infiltrative/restrictive cardiomyopathy |
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RBBB features |
- QRS > 120ms - rSR' in V1 (also wide QRS in V1) - deep S in I, V5/V6 - RV depol after LV, adds addnl L to R vector |
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incomplete RBBB features |
- QRS 100-120 ms but > 80 ms - delayed conduction, small R wave |
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LBBB features |
- QRS > 0.12 s - rS in V1/V2 - wide R wave in V5/V6 - addnl R to L vector (left and sup.) - deep S in V1 |
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2ndary ST-T wave change associated w/ BBB |
RBBB- ST depr. T inversion in V1, upright in I and V6
LBBB- |
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LAFB features |
- QRS > 0.12s - LAD > 45 w/ no other causes of LAD - Q wave in aVL and I - rS in II, III, and aVF - NO Q wave in inf. leads (R/O inf. MI) - NO R waves > 12mm in aVL or I- means LVH, cannot call LAFB |
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LPFB features |
- QRS 80-120ms - RAD > 90 w/ no other cause of RAD - Q wave in II, III, and aVF -rS complex in aVL and I |
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sinus bradycardia |
- < 60 bpm, normal varient - complexes normal w/ even spacing - P wave morphology consistent w/ SA origin |
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1st degree AV block |
- PR int > 200ms - constant PR int. w/ abnormal duration - 1:1 AV conduction |
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2nd degree AV block |
- no 1:1 conduction relationships - intermittent block - can be type mobitz I (physiologic, wenchebach) or mobitz II (pathologic) |
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mobitz I/wenchebach |
- physiologic NOT pathologic - d/t AV node properties, improves w/ exercise - in young/athletes, d/t high PNS input - gradual prolong of PR, possibly some non-conduction P waves |
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mobtiz II |
- pathologic and infranodal - fixed PR interval - worse w/ SNS stim and exercise - requires pacing |
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complete 3rd degree AV block |
- absence of conduction from atria to ventricles - P-P interval constant, R-R interval constant at different rate - His-Purkinje ectopy |
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general features of tachyarrythmias |
- d/t reentry or automaticity foci - wide QRS > 0.12s OR narrow QRS < 0.12s |
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sinus tach |
- >100 bpm - d/t pain, fever, exercise, etc. - evenly spaced normal complexes w/ normal P wave morphology |
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atrial tachycardia |
- P wave morphology/vector other than SA node - > 100 bpm - narrow P waves indicate septal origin - ectopic rhythm by definition - *appearance could be d/t limb lead reversal* |
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wandering pacemaker |
- 3 or more P wave morphologies - variation in P-R, P-P and R-R intervals |
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atrial flutter |
- P- P 200-250ms - regular R-R interval (e.g. 3:1 AV conduction) - stable reentry - sawtooth esp. in inferior leads - typically macroreentry in RAa |
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atrial fib |
- disorganized atrial activity - irregularly irregular - P- P interval <200ms |
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junctional tachycardia/rhythm |
- AV node/jxn origin - commonly retrograde activation - P wave inverted, may be under or after QRS complex
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AV nodal reentrant tachycardia (AVNRT) |
- dual AVN pathways - simultaneous QRS and P waves - P wave closely follows QRS - e.g. SVT |
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AV reciprocating tachycardia (AVRT) |
- need conduction to both chambers - d/t lack of decremental conduction in AV node OR accessory pathway (e.g. WPW) - can be orthodromic or antidromic |
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wide-complex tachycardia |
- ectopic vent. activation - PVC's ectopic ventricular foci resulting in abn QRS - compensatory pause usually present - time interv. between normal R peaks is multiple of R-R interval |
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ventricular tach |
- ectopic ventricular foci > 100 bpm - poor contractility, syncope, sudden death - WCT |
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ventricular fib |
- disorganized ventric. activation - wide, irregular complexes - syncope, sudden death |
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pre-excitation syndrome (WPW) |
- accessory AV pathway, may or may not be congenital - decremental AV conduction, NOT in acces. pw between atria/vent. - delta wave- d/t abn depol of area of ventricle/ slurred QRS - short PR interval d/t delta wave - asymptomatic- WPW pattern -symptomatic- WPW syndrome (palp/dizziness/syncope/hemodyn. compromise) |
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orthodromic vs antidromic AVRT |
orthodromic AVRT- normal conduction sequence, short PR int. w/ narrow complex QRS, rt. side accessory pw
antidromic AVRT - retrograde activation of His bundle, wide complex QRS, lt. side accessory pw |
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paced rhythms |
- ventricular- no His activation, change in vector, wide QRS - vector depends on device location - can't call LAD, Q wave, etc, ONLY paced rhythm |
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left atrial enlargement |
- notched P- wave, more distance to cover - P wave duration > 0.12s - V1- terminal negative deflection 2x amplitude of initial pos. force |
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right atrial enlargement |
- tall P waves esp. in limb leads - P pulmonale- lung disease - normal P wave duration-70 - 130ms
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LVH |
- LAD > 30 - Sokolow criteria (V1 S-wave + R wave in V5/V6 >35mm) - Cornell criteria- (V3 S wave + aVL R wave > 2mV/20mm(women) OR 2.8mV/28mm(men) - aVL/I R wave > 12mm - LV strain- ST segment depression/T wave inversion in V5/V6 -LAE |
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RVH |
- RAD > 110 - R wave > 0.7 mm in V1 - S wave > 0.7 mm in V5/V6 - R/S ratio V1 > 1 - RAE - P pulmonale - vs. RBBB- RBBB will have wide QRS and tall R wave in V1 |
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ST elevation coved vs. concave up |
- coved/convex- bad, indicative of MI - concave up - w/ J point notching- early repol but recent evidence suggests risk for early cardiac death |
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pericarditis |
- diffuse ST elevation in every lead (concave up) - PR depression - not known why - pt. will have positional discomfort- vs MI |
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transmural AMI |
- ST elev. in 2 or more contiguous leads - ST elev > 2mm in precordial leads - ST elev > 1mm in limb leads -involvement of epicardial coronary vessels |
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AMI ECG Progression |
1. normal 2. peaked T wave w/ hyperacute ischemia (not understood, not usually seen) 3. ST segment elevation 4. Q wave formation and loss of R wave 5. T wave inversion **eventually returns to normal except for T wave inversion** |
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antero-lateral AMI |
-reciprocal ST depression and T wave inversion in II, III, aVF - ST elevation in V2, V3, V4 - reciprocal changes in limb leads |
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inferior MI |
- >1mm elevation in II, III, and aVF - ST depression in V1/V2 |
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theories for ST elevation causes |
1. injury current- ischemic cells let in more Na and get more + change, ischemic cells are partially depolarized 2. loss of AP d/t loss of plateau - some epi/endocardium repols faster |
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LV wall aneuryism |
- persistent ST elevation in precordial leads - presence of Q waves and lack of large R waves indicates LV aneuryism NOT MI |
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brugada syndrom |
- RBBB, ST elev./T wave inver. in V1-V3 - structurally normal heart |
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ST depression |
- downsloping- abn., indicates ischemia - upsloping- normal, excercise - horizontal- abn, indicates ischemia - NOT indicative of ischemia - small depression, non- specific T wave abn, biphasic T wave |
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LV strain |
- downsloping ST segment - T wave inversion in lateral leads (V5, V6, I, and aVL)
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digitalis indications |
- coved ST depression in V4-V6, I, and aVL - more diffuse, not contiguous |
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causes of peaked and inverted T waves |
Peaked: hyperkalemia, hyperacute ischemia, intra-cranial hemorrhage
Inverted: ischemia (symmetric), LV strain (asymmetric), CNS- cerebral, stroke (symmetric)
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potassium and T wave abn |
hypo(<2.5):ST depression, diphasic T wave, prominent U wave
mild(5.5-6.5): peaked T wave, prolonged PR segment
moderate(6.5-8.0): loss of P wave, prolonged QRS, ST elev., ectopic beats/escape rhythms
severe(>8.0): progressive QRS widening, sine wave, vfib/asystole, axis deviations, bundle branch and fascicular blocks |
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QT interval abn |
- QTc > 450ms (men); >460ms (women) - LQT1- decr. IKs (KCNQ1) - LQT2 - incr. IKr (KCNH2) - LQT3 - incr INa (SCN5A) |
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causes of acquired LQT |
- abtx (quinolones, macrolides) - antiarryth- class 1a, 1c, and 3 - antipsychotics- risperidone, halidol - tricyclic antidepressants |
