ekg exam 2

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ekg exam 2
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  1. how is the P wave measured
    from the beginning of the P wave until the start of the PR segment. It is also measured from the isoelectric line to the highest point of the P wave
  2. what is the normal amplitude and duration of a P wave
    • amplitude: 0.5-2.5mm
    • duration: <0.11 seconds
  3. what are the abnormal amplitudes and duration of a P wave
    • amplitude >2.5 like RAE
    • amplitude <0.5mm hyperkalemia
    • duration >0.12 seconds like LAE
  4. how is the QRS complex measured
    from the beginning of the Q(or R if no Q) to the end of the complex. Also measured from the isoelectric line to the top of the R wave and from the isoelectric line to the bottom of the S wave.
  5. when is the Q wave defined as "significant"
    if > than 1/3 the depth of the R wave or > 1 small box wide
  6. what is the normal amplitudes and durations of the QRS complex
    • 0.05 seconds to 0.10 (0.12) seconds
    • wide variations in amplitude
    •    - upper limits
    •        - 30 in lead II
    •        - 30 in V1 to V6
  7. what are the abnormal amplitudes and duration of the QRS complex
    • QRS duration >0.12 seconds (BBB)
    • between 0.10 and 0.12 seconds (pBBB)
    • total amplitude (voltage) < 5mm (0.5mv)
    • total amplitude >30mm
    • significant Q waves
  8. how is the PR interval measured
    from the beginning of the P wave to the beginning of the Q wave (R wave if there is no Q)
  9. what is the normal duration of the PR interval
    0.12 to 0.20 seconds
  10. what are the abnormal durations of a PR interval
    • duration > 0.20 (prolonged)-- AV block, meds
    • duration < 0.12 (shortened)-- low atrial focus, accessory pathway (WPW,LGL)
  11. how is the QT interval measured
    from the beginning of the QRS complex to the end of the T wave
  12. what is the normal QT interval
    • based on gender and HR
    • QTc=QT√ of the RR interval
    • useful rule of thumb: QT should be half of RR
    • QTC for males: <0.42; females: <0.43
  13. what is the abnormal QT interval
    • >0.43: delayed repolarization
    • <0.3: short QT syndrome or electrolyte imbalance
  14. an impaired impulse through one or more of the divisions of the conduction system distal to the bundle of HIS, it is defined as a QRS > 0.12 seconds (3 small boxes), and is recognized by an R, R′ in specific leads of a 12 lead EKG
    BBB
  15. A QRS between 0.10 and 0.12 is defined only as a what
    • intraventricular conduction delay (IVCD, pBBB, BBB)
    • If it can't be determined which bundle is involved, it is labeled as non-specific
  16. what are the etiologies of a RBBB
    • idiopathic degenerative conduction system disease
    • ischemic heart disease
    • cardiomyopathy
    • massive PE
    • RVH
    • normal variant
  17. what is the ECG criteria for a RBBB
    • QRS duration > 0.12 in any lead
    • RSR' in V1-V3 (any one or more)
    • wide S wave in V4-V6 (any one or more)
    • ST depression in V1 and V2
    • inverted T wave in V1 and V2 (discordant T wave)
    • if RSR' and QRS <0.12 then incomplete BBB or IVCD
  18. diagnosing a RBBB is by seeing what
    a slurred S wave in leads I and V6

    leads V1 and V2 should have increased R:S ration and some semblance of an RSR' or QR' complex
  19. what are the etiologies of a LBBB
    • idiopathic degenerative conduction system disease
    • CAD/ischemic heart disease
    • dilated cardiomyopathy
    • aortic stenosis
    • HTN/LVH
    • hyperkalemia
    • MI
    • normal variant
  20. what are the ECG criteria for a LBBB
    • QRS duration > 0.12 in any lead
    • high voltage S waves in V1-V3 (any one or more)
    • tall R wave in V4-V6, I and aVL (any one or more)
    • slurred notch in any of the above (vice true RSR')
    • ST depression in V5, V6, I and aVL
    • inverted T wave in V5, V6, I and aVL (T wave discordance)
    • if RSR' and QRS <0.12 then "incomplete" BBB or IVCD
  21. explain the P wave, PRI, QRS, and characteristics of a RBBB
    • P wave: before each QRS, identical
    • PRI: 0.12 to 0.20 seconds
    • QRS: >0.12 seconds
    • characteristics: RSR' in V1
  22. explain the P wave, PRI, QRS, and characteristics of a LBBB
    • P wave: before each QRS, identical
    • PRI: 0.12 to 0.20 seconds
    • QRS: ≥ 0.12 seconds
    • characteristics: RR' in V5
  23. an ECG containing a LBBB can not be evaluated for what
    • ischemia or infarction
    • ventricular hypertrophy
    • ST/T wave changes (except concordance)
  24. what are the common diagnostic criteria for a complete LBBB
    • QRS duration ≥ 120 msec
    • broad, notched R waves in lateral precordial leads (V5 and V6) and usually leads I and aVL
    • small or absent initial r waves in right precordial leads (V1 and V2) followed by deep S waves
    • absent septal q waves in left-sided leads
    • prolonged instrinsicoid deflection (>60 msec) in V5 and V6
  25. what are the common diagnostic criteria for a complete RBBB
    • QRS duration ≥ 120 msec
    • broad, notched R waves (rsr', rsR', or rSR' patterns) in right precordial leads (V1 and V2)
    • wide and deep S waves in left precordial leads (V5 and V6)
  26. what are the etiologies of left anterior hemiblock (LAFB)
    • acute MI
    • HTN
    • aortic stenosis
    • dilated cardiomyopathy
    • consider LAD as source
  27. what are the ECG criteria for LAFB
    • left axis deviation
    • normal or slightly widened QRS (<0.12)
    • S wave larger than R wave in II, III, aVF
    • qR or R wave in lead I
    • rS wave in lead III (probably II and aVF)
    • Q1S3
  28. what are the etiologies of a left posterior hemiblock (LPFB)
    • rare
    • acute MI
    • consider RCA as source
  29. what are the ECG criteria of a LPFB
    • right axis deviation
    • normal or slightly widened QRS (<0.12)
    • q wave in lead III
    • s wave in lead I
    • S1Q3
  30. what are the different bifascicular blocks
    • RBBB+anterior hemiblock
    • RBBB+posterior hemiblock
    • anterior hemiblock+posterior hemiblock = LBBB
    • RBBB+ LAFB+LPFB= third degree AV block

    • may be intermittent or rate related
    • compare old EKG
  31. which bifascicular block usually progresses to a complete heart block
    RBBB+LPFB
  32. what are the etiologies of LAE
    • valvular heart disease (MS, MR, AS, AR)
    • LVH
    • HCM or HOCM
    • HTN
  33. what is the ECG criteria for a LAE (P-mitrale)
    • a notched P wave in any lead (lead II)
    •    - >0.11 wide or peaks >0.04 apart
    • diphasic P in V1
    •    - terminal portion of P wave ≥ 1mm deep and ≥ 0.04 wide (P terminal force)
  34. what are the etiologies of RAE
    • valvular heart disease (TS, PS, MR, MS)
    • COPD
    • pulmonary HTN
    • PE
  35. what is the ECG criteria for RAE (P-pulmonale)
    • tall, peaked P wave in any lead
    •    - ≥ 2.5mm
    • most prominent in leads I, II, aVF
    • biphasic P in V1 with initial force > terminal force
  36. describe what LAE (P-mitral) will look like on lead II and lead V1
    • lead II: broad and notched (>0.12 secs)
    • V1: inverted
  37. describe what RAE (P pulmonale) will look like on lead II and lead V1
    • lead II: peaked (greater than 3mm)
    • lead V1: upright
  38. describe what combined atrial hypertrophy will look like on lead II and lead V1
    • lead II: may be both peaked and broad
    • lead V1: biphasic ("peaked" and "broad")
  39. what are the etiologies of LVH
    • HTN
    • valvular disease (AS, AR, MR, HCM)
    • coarctation of the aorta
    • patent ductus arteriosus
    • acromegaly
  40. what are the false positives of LVH
    • thin chest wall
    • S/P radical mastectomy
    • LBBB
    • acute MI
    • LAFB
    • WPW
  41. what are the different criterias for LVH
    • scott criteria
    • Estes criteria
    • cornell voltage
    • cornell voltage duration
  42. explain scott criteria
    • normal duration QRS (<0.12)
    • sum of S in V1 or V2 + R in V5 or V6 > 35mm (use deepest in V1/V2 and tallest in V5/V6)
    • R wave in aVL > 11mm (supportive)
  43. explain cornell voltage and cornell voltage duration
    • cornell voltage: R aVL + S V3 > 20mm (F), > 25mm (M)
    • cornell voltage duration: cornell voltage X QRS duration in ms
  44. what are the etiologies of RVH
    • COPD
    • pulmonary HTN
    • valvular disease (MS, MR, TR, PS)
    • PE
    • chronic left HF
    • ASD, VSD
    • tetralogy of fallot
  45. what is the RCH criteria of RVH
    • RAD(must have)
    • normal QRS duration
    • reversal of R wave progression
    • may have strain pattern in V1 and V2
    • must not have a BBB
  46. what do "normal" Qs indicate
    activation of the intraventricular septum. they will therefore appear in the leads that "look" left
  47. describe septal Qs
    • they are normal in I, aVL, V5 and V6(left or lateral leads)
    • Small Qs are also generally innocent in lead III and lead V1 if no other abnormality is seen
  48. when are Q waves significant
    if they are > 1 box in width (longer than 0.04 msec) OR larger than 1/3 of the R wave
  49. what do significant Q waves indicate
    MI or obstructive septal hypertrophy (IHSS)
  50. in transmural MI, significant Q waves (1box wide of 1/3 the R) appear where
    in the leads "looking at" the areas of infarction: (ie, II, III, aVF for inferior MI; I aVL and V5-V6 for lateral infarct; etc)
  51. in idiopathic hypertrophic subaortic stenosis, the Qwaves tend to appear where
    in the same leads in which normal "septal" Qs are seen-- because the pathology is thickening of the septum
  52. significant Q waves of IHSS (idiopathic hypertrophic subaortic stenosis) are almost accompanied by what
    evidence of marked left ventricular hypertrophy
  53. for Q wave summary, explain the causes of Q waves, septal Q waves, what makes them significant, and HOCM(IHSS)
    • causes: septal, infarction, IHSS
    • septal: I, aVL, V5-V6, occasionally inferior leads
    • significant:
    •    - Q > 1/3 of R
    •    - Q > 1 box wide
    •    - Not in lead III
    • HOCM(IHSS): increased "septal" Qs, evidence of LVH
  54. deviation of the ST segment from the baseline can indicate what
    • infarct or ischemia
    • periocarditis
    • electrolyte abnormalities
    • ventricular strain
  55. how is the ST elevation or depression generally measured
    at a point 2 boxes beyond the QRS complex
  56. when is an ST depression considered significant
    if the segment is at least 1 box below baseline, as measured two boxes after the end of the QRS.

    as with infarcts, the location of the ischemia is reflected in the leads in which the ST depression occurs
  57. what are the etiologies of ST depression
    • ischemia
    • hypothermia
    • hypokalemia
    • tachycardia
    • subendocardial infarct
    • reciprocal ST elevation
    • ventricular hypertrophy
    • BBB
    • digitalis
  58. what is an ST elevation usually attributed to
    impending infarction, but can also be due to pericarditis or vasospastic (variant) angina
  59. in ST elevation, how is the height of the segment measured
    at a point 2 boxes after the end of the QRS complex
  60. when is the ST elevation considered significant
    if it exceeds 1mm in a limb lead or 2mm in a precordial lead
  61. what are the etiologies of an ST elevation
    • infarction
    • vasospastic (Prinzmental angina)
    • pericarditis
    • early repolarization

    • measure: 2mm beyond QRS
    • significant: 1mm limb lead
    •                  2mm chest lead
  62. where is the T wave normally upright, inverted, and variable
    • upright: I, II, and V3-V6
    • inverted: aVR
    • variable: III, aVL, aVF, and V1-V2
  63. when would T waves normally be abnormal
    • in ventricular hypertrophy
    • LBBB
    • chronic pericarditis
    • electric abnormality
  64. why would T waves be peaked and tall, inverted, or flattened
    • tall, peaked: hyperkalemia if generalized, infarct if localized
    • inverted: evolving infarct, chronic pericarditis, conduction block, ventricular hypertrophy, acute cerebral disease
    • flattened: non-specific
  65. why would a U wave be enlarged
    • electrolyte abnormality (such as hypokalemia)
    • severe CAD
    • drug effects
  66. this is CP die to ischemia of the heart muscle, generally due to obstruction of the coronary arteries
    angina
  67. which type of angina is when there is CP or discomfort that typically occurs with activity or stress, it usually begins slowly and gets worse over the next few minutes before going away, it goes away with meds or rest, but may happen again with additional activity or stress
    stable angina
  68. which type of angina usually occurs without cause, lasts longer than 15-20 minutes, responds poorly to nitro and can occur along with symptoms of low cardiac output
    unstable angina
  69. which type of angina is associated with CP due to spasm of the coronary arteries
    variant or Prinzmetals angina
  70. lack of adequate oxygen supply to the myocardial muscle tissue to meet its demand, and is usually caused by inadequate blood flow to the coronary arteries is known as what
    ischemia
  71. an ST depression represents what
    • subendocardial myocardial ischemia
    • it is a dire warning sign and should be managed aggressively
    • often associated with T wave inversion
  72. cellular death and tissue necrosis that represents a permanent loss of myocardium and subsequent loss of function is known as what
    infarct
  73. ST elevation represents what in ischemia and infarction
    • acute transmural myocardial injury
    • it is severe and progressive
    • it occurs in areas of necrosis

    by the time ST elevation occurs, there has been a transmural deprivation of oxygen/blood flow from the epicardium to the endocardium
  74. why would T wave Δs be present
    • may be hyperacute early (tall, peaked)
    • may be flattened
    • may invert
    • may persist for days, months or years after an infarct
  75. describe the evolution of a hyperacute MI
    • tall, peaked T wave
    • suggestive, but not diagnostic of MI
    • may proceed clinical symptoms
    • not generalized (only in leads "looking at" MI)
  76. describe the evolution of an acute MI
    • ST segment elevation
    • Q waves
  77. describe the evolution of an old or aged undetermined MI
    • ST segment returned to baseline or slightly elevated
    • Q waves remain (likely forever)
  78. in reciprocal changes, if you have an ST elevation in leads II, III, and aVF, any ST depression would be seen where
    I, aVL, and any of the V leads
  79. what is highly sensitive as an indicator of an acute MI
    reciprocal changes (ST depression seen in the opposite leads from an ST elevation)
  80. if you have an inferior MI, what med do you not want to give (or if given use very cautiously)
    nitro
  81. this is a genetic disease that is characterized by abnormal ECG findings, it has an increased risk of sudden cardiac death, and has a loss of function of the sodium channels
    Brugada syndrome
  82. what can Brugada syndrome show on an ECG
    • RBBB
    • persistent ST elevation in leads V1, V2, and V3
    • prolonged PR interval
  83. if there is a death by a sudden onset of V-Tach or V-fib, what do you want to expect was the cause and how do you test for it
    Brugada syndrome

    genetic testing
  84. how is brudgada syndrome treated
    ICD (implantable cardioverter defibrillator)
  85. this is an easy to identify cardiac syndrome which indicates a critical high grade occlusion of the proximal LAD. Id not identified and properly treated, the mean time from onset of symptoms to extensive anterior wall MI is 8.5 days
    Wellens syndrome
  86. how does Wellens syndrome present on an ECG
    • progressive, symmetrical, deep T wave inversion in chest leads V2 and V3. The slope of the T waves are generally 60°-90° (or tall, diphasic, t waves)
    • little or no enzyme elevation
    • no loss of precordial R waves
    • angina CP
  87. this is a dangerous or deadly ventricular arrhythmia caused by dysfunctional ion channels, it is one-half the length of the cardiac cycle, and it is congenital
    Long QT syndrome
  88. what can cause lengthening of the QT interval
    • a variety of medications that block ion channels
    • certain types of cardiac pathology or metabolic conditions

    *it predisposes the pt to Tosades de Pointes
  89. how is long QT syndrome treated
    beta blockers and ICD (implanted cardioverter defibrillator)
  90. this is an inflammation of the pericardium, it occurs as a complication of infections, immunologic conditions, or heart attack
    pericarditis
  91. what are the S/S of pericarditis
    • CP, radiation to the back and relieved by sitting forward and worsened by lying down
    • dry cough
    • fever
    • fatigue
    • anxiety
    • friction rub
    • diffuse ST-elevation and PR-depression on EKG
  92. what are the etiologies of pericarditis
    • idiopathic
    • viral infection (most common)(coxsackie virus)
    • bacterial infection (TB)
    • immunologic conditions (SLE)
    • MI(Dressler's syndrome)
    • trauma to the heart
    • uremia
    • malignancy
    • S/E of medications
    • radiation induced
    • aortic dissection
    • tetracyclines
  93. how is pericarditis treated
    • NSAIDS
    • steroids
    • colchicines
    • sx
  94. this causes a blockage of the pulmonary artery, usually when a venous thrombus becomes dislodged from its site of formation and embolizes the arterial blood supply of one of the lungs
    PE
  95. what are the S/S of a PE
    • SOB
    • pain in chest during breathing
    • anxiety
    • tachypnea
    • tachycardia
  96. what is virchows triad
    • stasis (lack of movement or immobility)
    • injuries to the vascular endothelium
    • hypercoagulability (meds, pregnancy)
  97. what are the ECG findings for a PE
    • tachycardia
    • anteroseptal and inferior T wave inversion (highly specific)
    • S1Q3T3: sign of acute Cor Pulmonale (rare)
    • right axis deviation
    • transient LPFB
  98. how is a PE treated
    • anticoagulation
    • sx
    • fibrinolytic therapy
  99. this is when the wall (septum) between the two ventricles becomes enlarged and obstructs the blood flow from the L ventricle.
    • hypertrophic (obstructive) cardiomyopathy
    • (also known as asymmetric septal hypertrophy, or idiopathic hypertrophic subaortic stenosis)
  100. besides obstructing blood flow, what else does hypertrophic (obstructive) cardiomyopathy do
    the thickened wall sometimes distorts one leaflet of the mitral valve, causing it to leak
  101. this is the most common inherited heart defect, occurring in one of 500 individuals
    hypertrophic cardiomyopathy
  102. what S/S can occur with hypertrophic cardiomyopathy
    • sudden cardiac death (V fib)
    • dyspnea (most common sx)
    • syncope
    • presyncope
    • angina
    • palpitations
    • orthopnea and PND (paroxysmal nocturnal dyspnea)
    • CHF
    • dizziness
  103. how is hypertrophic cardiomyopathy treated
    • septal ablation
    • ICD (implanted cardioverter defibrillator)
  104. what is the dilemma with LBBB
    approximately 1/2 of pts with LBBB and an acute MI do not have CP. These pts are much less likely to receive appropriate medical therapy or reperfusion therapy than LBBB with CP
  105. in a LBBB, what are the Sgarbossa criteria
    • ST segment elevation of 1mm or more that was in the same direction (concordance) as the QRS complex in any lead-- score 5
    • ST segment depression of 1mm or more in any lead from V1 to V3-- score 3
    • ST segment elevation of 5mm or more that was discordant with the QRS complex (ie associated with a QS or rS complex)-- score 2

    score >3= specificity of 90%
  106. explain an ST elevation in aVR in the presence of ischemia
    • no longer able to consider the "11 lead ECG"
    • if you don't look for it, you wont find it
    • subtle
    • highly specific for acute occlusion of the left main coronary artery (LMCA)
  107. explain LMCA occlusion
    • 70% risk of developing cardiogenic shock or dying
    • only effective treatment is rapid PCI (percutaneous coronary intervention) or emergent CABG (Coronary artery bypass graft)
    • no effective medical therapy delays or treats
    • not only STEMI pts, but any ACS with LMCA occlusion
  108. what patterns do you want to look for in aVR in a LMCA occlusion
    • STE in aVR greater than STE in V1
    • STE in aVR with simultaneous STE in aVL
    • STE in aVR >1.5mm
  109. explain VT vs SVT with aberrancy
    • wide QRS tachycardias represent either VT or SVT with aberrant conduction
    • VT and SVT represent vastly different clinical situations as far as etiologies, extent of underlying cardiac disease, tx, and prognosis
  110. what is the 1st step in determining VT vs SVT with aberrancy (in a hemodynamically pt)
    look at V1, look to see if QRS is mainly positive in V1 or mainly negative in V1
  111. if the QRS is positive in VT vs SVT with aberrancy, what does that mean
    • V-tach:
    •    - monophasic R
    •    - QR or RS complex
    •    - R,R' with R taller than R'
    •    --- verification findings in V6
    •    --- QS complex, RS with a deep wide S

    • SVT:
    •    - any triphasic complex
    •      - verification findings in V6
    •      --- any triphasic complex, R to S ration >1
  112. if the QRS is negative in VT vs SVT with aberrancy, what does that mean
    • V-tach:
    •    - wide R wave (>0.04 sec)
    •    - a notched or slurred S wave
    •    - a delayed nadir
    •       - verification findings in V6
    •       - QR or QS

    • SVT:
    •    - RS or QS with ski slope S
    •       - verification findings in V6
    •       - monophasic R wave
  113. what is the supporting evidence for VT, in VT vs SVT with abberancy
    • AV dissociation
    •    - P waves march out, not associated with QRS complex
    •    - Cannon A waves
    • QRS >0.14
    • fusion beats or capture beats
    • concordance across chest leads
    • LAD or ERAD
    • known heart disease
  114. what is the supporting evidence for SVT, in VT vs SVT with aberrancy
    • known BBB
    • QRS <0.14
    • ZOT in chest leads (not concordance)
    • normal axis
  115. what are the different types of pacemakers
    • transcutaneous (temporary)
    • transvenous (temporary)
    • permanent:
    •    ventricular
    •    dual chamber
    •    biventricular
    • ICD/cardioverter
  116. what are the indications for a pacemaker
    • SSS (sick sinus syndrome)
    • bradycardia
    • second degree AV heart blocks
    • third degree AV blocks
    • bifascicular blocks and trifascicular blocks
  117. what are the complications and side effects of pacemakers
    • hemorrhage
    • venous thrombosis
    • pericardial effusion and tamponade
    • pneumothorax
    • infx following the implant procedure
    • erractic pacing or sensing due to migrating leads
  118. this is a small battery powered electrical impulse generator which is implanted in patients who are at risk of sudden cardiac death due to VFIB. The device is programmed to detect multiple cardiac arrhythmias and correct them
    automated implantable cardioverter defibrillator (AICD)
  119. what are the indications for an AICD
    • risk of sudden death from ventricular arrhythmias
    • long QT syndrome, Brugada syndrome
    • in combination with a pacemaker
  120. what are the complications and side effects of an AICD
    • anxiety and depression
    • false alarms (sudden firing of the AICD)
    • failure to recognize or convert rhythm
    • driving restrictions
  121. how can sick sinus syndrome present
    • tachy-brady syndrome
    • SA block/arrest
    • sinus node exit block
    • bradycardia
  122. what are the etiologies of SSS
    • diseases of the SA node
    • insult to the SA node
    • increased parasympathetic tone
    • hypoxia
    • drugs that block the SA node (BBB, CCB, digoxin)
    • cardiomyopathy
    • old age, ASHD (atherosclerotic heart disease), HTN
    • open heart sx, pericarditis, rheumatic heart disease
  123. what is sudden syncope related to heart rate called
    stokes-adams attack
  124. what are the etiologies of sinus node exit block
    • infx
    • acute inferior wall MI
    • meds
    • salicylate toxicity
  125. what are the etiologies of a sinus arrest
    • infx
    • acute inferior wall MI
    • meds
    • salicylate toxicity

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