AAA PA: Lab & Diagnostic Testing > Module 2c: Electrocardiogram > Flashcards

Module 2c: Electrocardiogram Flashcards

(54 cards)

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1
Q

What are the rhythm rules of a first-degree heart block?

A

Rate: depends on underlying rhythm
Regularity: Regular
P Wave: Normal
P:QRS: 1:1
PRI: >0.20sec
QRS: Normal
Grouping: None
Dropped: None

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2
Q

What are the rhythm rules of a Mobitz I second-degree heart block?

A

(Wenckebach)
Rate: depends on underlying rhythm
Regularity: Regularly irregular
P Wave: Present
P:QRS: Variable 2:1, 3:2, 4:3, 5:4, etc
PRI: Variable
QRS: Normal
Grouping: Present & variable
Dropped: Yes
(AV Fatiguing)

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3
Q

What are the rhythm rules of a Mobitz II second-degree heart block?

A

Rate: depends on underlying rhythm
Regularity: Regularly irregular
P Wave: Normal
P:QRS: Variable X:X-1, 3:2, 4:3, 5:4
PRI: Normal
QRS: Normal
Grouping: Present & variable
Dropped: Yes
(often have bundle branch block too, nonreversible)

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4
Q

What are the rhythm rules of a third-degree heart block?

A

Rate: dissociated sinus & escape rhythm Regularity: Regular (P & QRS rate different)
P Wave: Present
P:QRS: Variable X:X-1, 3:2, 4:3, 5:4
PRI: Variable no pattern
QRS: Normal or wide
Grouping: None
Dropped: None
(no A-V or V-A conduction)

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5
Q

What are the rules of right bundle branch blocks?

A
  1. QRS >=0.12sec
  2. Slurred S waves in I & V6
  3. rSR’ pattern V1 (bunny ears) - not always present
    • QR’ or qR’ in V1 s/ RBBB correlated w/ old/new infarc
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6
Q

What are the rules of a Left bundle branch block?

A
  1. QRS >=0.12
  2. Broad R waves I, aVL, & V6
  3. Broad S wav V1 may have smaller r wave
  4. Lack septal Q waves in I & V6
    - V1 “W”, V6 “M”
    Larger area of heart, more uncoordinated squeeze
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7
Q

What is an Intraventricular Conduction Delay?

A
  • A catch all block that does not match LBBB or RBBB
  • Localized Not >=0.12 sec wide - frequent
  • Generalized QRS >=0.12 sec, not all characteristics LBBB & RBBB
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8
Q

What is a Hemiblock?

A
  • Fascicular block
  • Left anterior Hemiblock (LAF)
  • Left posterior hemiblock (LPF)
  • Bifasicular: RBBB w/ LAF or LPF
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9
Q

What are the aspects of paced rhythms?

A
  • Five letter code: 1st 3 letters indicate pacemaker function
  • Sensing: rate of firing (over or under)
  • Capture: electrical current cause heart depolarize - want to use lowest voltage possible
  • Failure: under/absent pacing
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10
Q

What are the measurements indicated by ECG boxes?

A
  • Small box: 0.04 sec, 1mm,
  • 2 large boxes: 10mm, 1mV
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11
Q

What are the types of myocardial damage?

A

ischemia -> injury -> infarction

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12
Q

What is myocardial ischemia? How does it show up on an ECG?

A
  • Diminished blood flow to myocardium (hypoxia)
  • Not necessarily lead to infarction
  • Symmetrical T wave inversion s
  • Horizontal or down-sloping ST depressions
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13
Q

What is myocardial injury? How does it show up on an ECG?

A
  • Elevated cardiac troponin above 99th percentile upper reference limit of assay & indicates acute injury
  • Troponin elevation may/may not be associated w/ ischemic sx
  • Elevation ST s also indicates ACUTE injury
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14
Q

What is myocardial infarction? How does it show up on an ECG?

A
  • Irreversible damage
  • Myocardium non-viable (dead) –> scar forms
  • Infarcted are cannot depolarize or contact
  • Q-waves on ECG tracing
  • LV thickest & > blood supply, often involved in MI
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15
Q

What is chronic coronary disease and acute coronary syndrome?

A
  • Chronic Coronary Disease: entire spectrum of stable CAD - sx stable & typically predictable (chest pain w/ walking)
  • Acute Coronary Syndrome: acute myocardial ischemia caused by abrupt reduction coronary blood flow - new, severe, accelerating sx, require urgent eval/tx
    • STEMI (ST elevation in 2 contiguous leads) NSTEMI, Unstable Angina
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16
Q

What are the Coronary Arteries?

A

Aorta
- LCA (LM)
- LAD: diagonal branches: septum & anterior LV
- Cx: obtuse marginal branches
- (Posterior descending): posterior, inferior LV
- RCA:
- Marginal branches: RV
- Posterior descending (70-80%) posterior, inferior LV

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17
Q

What vessels supply the electrical system of the heart?

A
  • AV nodal branch
    • 70-80% pts: off posterolateral branch RCA
    • 10-15% pts off LCx
  • SA nodal artery: off Right coronary in 60% ppl
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18
Q

What are the cardiac conduction abnormalities associated with an MI?

A
  • Sinus bradycardia
  • AV block:
  • Bifasicular block (LAFB + RBBB)
  • LBBB
  • Presence of conduction d/o indicate large area at risk, extensive MI or severe CAD
  • Most conduction d/o are reversible w/ reperfusion therapy
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19
Q

How is sinus bradycardia associated with MI?

A
  • Frequent in acute inferior STEMI esp 1st hrs after occlusion, (3x more common than in anterior MI)
  • caused by depressed automatism
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20
Q

How does AV block present in MI?

A
  • Frequent acute inferior STEMI from RCA occlusion
  • associated w/ inferior STEMI: usually temporary, benign, & nearly always resolves w/ reperfusion therapy
    (SA also more frequent in inferior STEMIs)
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21
Q

How do bifasicular block associated with MI?

A
  • New LAFB & RBBB may be the result of LM lesion or proximal LAD lesion
  • Bifasicular block in the setting of an acute anterior MI is a warning possible impending progression to complete heart block
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22
Q

How is LBBB associated with MI?

Study These Flashcards
A
  • NEW LBBB
  • In the proper clinical setting, consider a STEMI equivalent (presume it is a new if no prior ECG)
  • Blood supply to Left bundle is of dual origin (LAD + either RCA or LCx depending on coronary artery dominance)
  • Severe 2 or 3 vessel dz likely present for LBBB to develop
23
Q

What is the coronary artery distribution on ECG? (Contiguous leads)

Study These Flashcards
A
  • High Lateral (LCx or diagonal): I, aVL
  • Lateral (LCx or diagonal): V5, V6
  • Inferior (RCA or LCx): II, III, aVF
  • Anteroseptal (LAD): V1, V2
  • Septal (LAD): V3, V4
24
Q

How does MI appear in the QRS complex?

Study These Flashcards
A
  • “Drowning in negativity”
  • Parts of QRS become negative
    • Q waves develop
    • R waves dec in size
    • Preexisting Q waves get deeper
25
How do Q waves appear in MI? Why?
- **Electrically dead scar tissue** produces pathologic Q wavs - **Delayed sign of MI**usually hrs-d develop - Reperfused early, **stunned myocardium may recover** & pathologic Q may disappear, but usually persist - Q eaves must be present **2 contiguous leads** to be significant - Pathologic: Acute/old MI - Insignificant: Normal ECGs in some leads
26
What are the clues for determining if Q waves are pathologic or insignificant?
- Clue 1: Are Q waves new in appropriate clinical setting (angina) - Clue 2: Pathologic Q wavs **deeper & wider** than normal - Pathologic: >=0.04sec or >1/4 entire QRS amplitude, V1-V3, present two contiguous leads = current/prior MI - Normal: <0.04 sec, V5, V6, I, aVL - Clue 3: Q wave progression V4-V6. Normal: depth inc, infarct: dec - Clue 4: compare to previous ECG
27
How do R waves change in MI?
- Normally: R/S ratio inc V1-V6 - If amp not inc V1-V3 or dec consider anterior wall MI
28
How do preexisting Q waves change with an MI?
- Q wave gets deeper - Significant if **>25% of R wave**
29
What is the time frame of STEMI ECG changes?
- min-hr: Hyperactive T wave - 0-12hr STE - 1-12hrs: Q wave developing - 2-5d: STE w/ T inversion - wk-mo: T recovery - Permanent: persistent STE Reperfusion w/i 12hr - Terminal T inversion, later terminal T inversion, symmetric T wave inverion then normal in d-wks
30
What are the causes of ST elevation?
- Acute Ischemia (STEMI) - Coronary artery spasm (Prinzmetal's) - Pericarditis; myocarditis; Takutsubo's - Normal variant (early repolarization) - LVH w/ secondary repolarization
31
How do you differentiate between pericarditis and STEMI?
- Hx & PE (pleuritic chest pain, positional, recent viral illness = pericarditis) Pericarditis will have... - Diffuse STE (unless multivessel CAD) - Flat or concave STE (middle sag down) - aVR w/ PRE & reciprocal ST depression
32
What is T wave morphology?
- Except for V1, T normally positive - Symmetric T wave inversion = ischemia - Asymmetric inversion = ventricular hypertrophy with strain
33
What is important about ST & T wave changes (Summary)?
- Symmetric T inversion = ischemia - Horizontal ST depression = ischemia - Downsloping/sagging ST depression = maybe ischemia - Downsloping ST depression with asymmetric T inversion most likely LVH or RVH w/ strain - RBBB, LBBB, PVCs, & WPW all cause ST depression & T wave inversion so interpretation for ischemia limited in these situations
34
What are the cardiac myocyte action potential phases? (movement of electrolytes)
35
What does hyperkalemia do to the heart?
- Tall peaked T w/ narrow base (mod hyperkalemia) - Widened QRS w/ tall T wave (mod-severe hyperkalemia) - Loss of P wave (severe hyperkalemia) - **Risk of Cardiac Arrhythmia** - **Sensitivity & specificity of ECG changes for hyperkalemia are POOR** - Clinical cues: renal failure, adrenal dz, ACEi/ARBs, K+ sparing diuretics - Action potential: Cardiomyocyte membrane becomes partially depolarize, closer to threshold, inc excitability, reduction in conduction velocity
36
What does hypokalemia do to the ECG?
- Inc P wave amplitude - Prolongation PRI - ST depression & T wav flattening/inversion - **Prominent U waves** (best seen V2-V3) - Apparent long QT i due to fusion T & U wav
37
What is the importance of the QT interval?
- Slow HR: long QT - Fast HR: short QT - QTc: corrected QT interval based on HR of 60 - Normal QTc: - Male: 350-450ms - Females: 360-460ms - **any values >500mc generally significant & at inc risk arrhythmias** - Est QT: 1/2 RR interval
38
How does calcium affect the ECG?
- Hypercalcemia: shortening QT interval - Hypocalcemia: lengthening of QT interval
39
How does hypermagnesemia affect the ECG?
- Sinus bradycardia - P wave flattening - Prolonged PR - Widened QRS - AV block - Prominent T (rare)
40
How does hypomagnesemia affect the ECG?
- Isolated hypomg rare - Often w/ hypoK, hypoCa, Hypophos - Isolated: **longer P wave duration & QTc** - **Risk of Torsades** - Keep Mg >2
41
What causes right atrial hypertrophy? How seen on ECG?
- Causes: COPD, Pulmonary HTN, Tricuspid valve dz - Best seen: II, III, aVF - P wave peaked - Exceeds 0.25 mV amplitude (2.5 boxes) - "**P pulmonale**"
42
What causes right ventricular hypertrophy?
- Pulmonary HTN - Pulmonary valve stenosis - Pulmonary valve regurgitation - COPD - VSD
43
What causes left atrial hypertrophy? How seen on ECG?
- Mitral regurgitation, HTN, chronic atrial fibrillation, LVH - Best seen II & V1 - II: wider & double peaked P wave - V1: P wave becomes biphasic - Negative part of P wave corresponds to enlarged left atrium - Negative part >0.04 sec "**P mitral**" (LAH: Longer, RAH: height)
44
What is seen on an ECG for severe ventricular hypertrophy?
- **Size of R wave generally reflects amount of myocardial mass** (inc muscle mass - higher amplitude) - Fiber length inc (**ventricular dilation**) wave takes longer, spike is wider - Tall R in V5 or V6 should produce deep S wave in opposite leads V1 & V2 they are mirror images - Sokolow-Lyon (sen <50%, spec 85-90%)
45
What is Sokolow-Lyon Criteria?
- S wave in V1 + R wave in V5 or V6 (taller) = 35 small boxes (LVH is probably present) - Other: aVL R wave >= 11 small boxes LVH likely
46
What is LVH with strain pattern?
- **Downsloping ST-s depressions w/ inverted asymmetric T wave >=0.1mV opposite the QRS axis in a resting ECG** - Indicates: inc LV mass & wall stress (more O2 consumption) - Poor cardiac systolic function - Higher CV risk - Resolution associated w/ improved outcomes - Higher risk SCD, higher incidence HF, higher all cause mortality - LVH + strain = poor prognosis
47
What causes left axis deviation?
- Left anterior fascicular block - Inferior MI - Ventricular paced rhythm - Obesity - LVH: valvular heart dz, CM, systolic HF, longstanding HTN - LAD associated w/ higher risk of all-cause death & major adverse CV events
48
What are the antiarrhythmic classes?
- Class I: Sodium-Channel Blockers - Class II: Beta-blockers - Class III: Potassium channel blockers - Class IV: Calcium Channel blockers
49
What are the Class I: Sodium-Channel Blockers? How do they affect the ECG?
- Prolonged depolarization & slow conduction - 1A: Disopyramide, Quinidine, Procainamide - 1B: Lidocaine & Mexiletine - 1C: Flecainide, Propafenone - Toxicity causes wide QRS & arrhythmia
50
What are the Class II: BB. How do they affect the ECG?
- Depress SA node, AV node & ectopic foci - Inc AV node refractory period to affect AV nodal coduction - Toxicity causes bradycardia - Metoprolol, Toprol XL, Carvedilol, Bisoprolol
51
What are the Class III: Potassium Channel Blockers? How do they affect the ECG?
- Prolong action potential duration & effective refractory periods - Amiodarone, Sotalol * , Dofetilide * , Ibutiliede (IV), Dronedarone (NOT in CHF) - Toxicity: long QT & bradycardia *Require in-hospital monitoring for prolonged QT
52
What are the Class IV: Calcium Channel Blockers? How do they affect the ECG?
- Inc AV node refractory period - CI in HFrEF: negative inotropy - Diltiazem, Verapamil - Toxicity causes bradycardia & hypotension
53
What are the digoxin toxicity ECG findings?
- Sinus **bradycardia** - Afib w/ **slow** ventricular response - Down-sloping ST-T changes **"Salvador Dali mustache"** - **Shortening** QT interval - Atrial or junctional **tachycardia w/ block** - Frequent PACs or PVCs - **Only ~24% of digoxin toxicity ECGs are recognized by clinicians!**
54
How do tricyclic antidepressants affect the ECG?
- Anticholinergic effects cause **sinus tachycardia** - TCA toxic changes due to **Sodium channel blockade** - **Prolonged QRS complex (>160ms predictive of VT/VF)** - **QT prolongation**
AAA PA: Lab & Diagnostic Testing
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