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1
Q

HIS DEBS as arrythmogenic factors

A

H=Hypoxia—->COPD, PE
I=Ischemia and Irritability—->infarction, inflammation, infection
S=Sympathetic stimulation—->hyperthyroidism, CHF, nervousness, exercise
D=Drugs—->quinidine
E=Electrolyte disturbances—->Ca, Mg
B=Bradycardia—-> sick sinus syndrome
S=Stretch—-> enlargement and hypertrophy

2
Q

Normal biphasic wave of P in which leads?

A

Lead III and V1

3
Q

Normal septal Q wave in which leads?

A

Lead I, aVL, V5, V6 (rarely in inferior leads + V3, V4)

4
Q

Normal QT interval over RR interval ratio?

A

40%

5
Q

2 steps checking axis of QRS

A

1) Lead I and aVF (if both positive=normal range)

2) Lead with most equal biphasic QRS (perpendicular)

6
Q

2 common causes for sustained ectopic rhythm

A

Digitalis toxicity, beta-agonists from inhaler therapies

7
Q

4 Qs for arrhythmias

A

Q1: Are normal P wave present? including right axis
Q2: QRS wide or narrow? (3格界定)
* Q1 and Q2 decide the arrhythmia is ventricular or supraventricular (atrial or junctional).
Q3: What’s the relationship b/t P and QRS? (one-to-one=atrial origin)
Q4: Is the rhythm regular or irregular?

8
Q

5 types of sustained supraventricular arrythmias

A
  1. PSVT=AVNRT (AV nodal reentranttachycardia)
  2. A flutter
  3. A fibrillation
  4. MAT (multifocal atrial tachycardia)
  5. PAT (paroxysmal atrial tachycardia)=ectopic atrial tachycardia
9
Q

PSVT HR

A

150-250 bpm

10
Q

3 leads to check the retrograde P wave in PSVT

A

Lead II, III, V1 (pseudo-R’)

11
Q

Common causes of A fib

A
  1. Mitral valve disease
  2. CAD
  3. Hyperthyroidism
  4. PE
  5. Pericarditis
  6. Long-lasting HTN
12
Q

2 irregular rhythm of supraventricular arrhythmia

A

A-fib, MAT

13
Q

Define MAT (multifocal atrial tachycardia) and when is it commonly seen

A

> 3 different P wave morphologies

Severe lung disease

14
Q

Pattern of PAT (paroxysmal atrial tachycardia). Can it be slowed down by carotid message as in PSVT?

A

a warm-up or cool-down period

No or mild slowing.

15
Q

Rules of malignancies that PVCs may cause life-threatening arrhythmias

A
  1. Frequent PVCs
  2. > 3 PVCs in a row
  3. Multi form PVCs
  4. R-on-T phenomenon
  5. Any PVC occurring in the setting of an AMI
16
Q

2 common conditions that accelerated idoventricular rhythm seen

A
  1. AMI

2. Early hours following reperfusion

17
Q

How does Torsades de pointes occur?

A

A PVC falling during the elongated T wave

18
Q

Electrolytes that cause TdP?

A

Hypo-Ca, hypo-Mg, hypo-K

19
Q

ABX that cause TdP?

A

Erythromycin, quinolones, levofloxacin

20
Q

Can supraventricular beat have a wide QRS?

A

Yes.
An early PAC occurs–> run through LBB (RBB still in refractory period)–> RBB receives conduction from LBB–> wide, bizarre QRS that looks like a PVC. (aberrant conduction)

21
Q

Clinical clues to ddx VT and PSVT:

  1. Which is more common in a diseased heart?
  2. Which can be terminated by carotid massage?
  3. Which is commonly a/w AV dissociation?
  4. Cannon A wave may be seen?
A
  1. VT
  2. PSVT
  3. VT
  4. VT
22
Q

What happen to AV node in AV dissociation?

A

Constantly refractory by impulses from above and below

23
Q

EKG clues to ddx VT and PSVT:

  1. P always followed by QRS?
  2. Fusion beats may be seen?
  3. Initial deflection may in opposite direction of the normal QRS?
A
  1. PSVT
  2. VT
  3. VT
24
Q

When does Ashman phenomenon occur?

A

It’s a wide, aberrant conduction of supraventricular beat after a QRS complex that is preceded by a long pause.
Bundle branches anticipate another long pause following this beat and repolarize slowly–> before completion of repolarization, another supraventricular impulse passes through AV node, but the conduction is blocked along the normal pathways–> wide, bizarre QRS (looks like a PVC)

25
Q

Which arrhythmia is the best setting for Ashman phenomenon?

A

A Fib

26
Q

How to check AV block?

A

Relationship of P and QRS

27
Q

Def of first-degree AV block

A

PR> 0.2 sec (5小格)

28
Q

Does first-degree AV block a block?

A

No, only a delay

29
Q

Def of Mobitz type I second-degree AV block (or Wenchebach block)

A

Progressive lengthening of each successive PR until one P fails to conduct through AV node (漸行漸遠)
* Block in AV node, usually transient and benign

30
Q

Def of Mobitz type II second-degree AV block

A

Conduction is an all-or-nothing phenomenon w/o progressive lengthening of PR
* Block in His bundle, usually serious

31
Q

Which rhythm can be suppressed: PVC or ventricular escape rhythm?

A

PVC

32
Q

Which rhythm can be life-saving: PVC or ventricular escape rhythm?

A

Ventricular escape rhythm

33
Q

Def of third-degree AV block

A

Presence of AV dissociation in which ventricular rate is slower than sinus or atrial rate

34
Q

Leading cause of third-degree AV block

A

Degenerative disease of conduction system

35
Q

A common cause of reversible complete heart block

A

Lyme disease: block located in AV node, narrow-QRS junctional escape rhythm

36
Q

Which AV block(s) requires permanent pacemaker?

A

Mobitz type II heart block and third-degree

37
Q

Can different degrees of AV block coexist?

A

Yes

38
Q

Why QRS is wide in BBB? (>3格)

A

Delayed depolarization

39
Q

What does ST and T look like in BBB?

A

Similar change as in secondary repolarization abnormalities in ventricular hypertrophy (ST: depression, T: inversion)

40
Q

What’s ‘critical rate’ in BBB?

A

The ventricles conduct normally at slow HR, but above a certain rate, BBB develops. This certain HR is critical rate.

41
Q

When doesn’t criteria of ventricular hypertrophy apply?

A

Presence of BBB

42
Q

What does hemiblock change on EKG

A

Axis dev

43
Q

Left anterior hemiblock axis and vector direction

A

-30 to -90 degrees

Depolarization: inferior-to-superior, R-to-L

44
Q

Left posterior hemiblock axis and vector direction

A

+90 to +180 degrees

Depolarization: superior-to-inferior, L-to-R

45
Q

What’s incomplete BBB?

A

Morphologies of LBBB or RBBB but QRS normal

46
Q

What’s the bypass pathway name in WPW syndrome?

A

Bundle of Kent (can be L or R sided b/t atrium and ventricle)

47
Q

Why QRS is wide in WPW syndrome?

A

Premature activation–> a fusion beat (small region of myocardium depolarize first)

48
Q

2 most common tachyarrhythmias seen in WPW syndrome

A

PSVT, A fib

49
Q

Route of narrow-QRS of PSVT in WPW syndrome

A

PAC down AV node–> ventricle–> bundle of Kent–> atrium–> ventricle

50
Q

Route of wide-QRS of PSVT in WPW syndrome

A

Atrium–> bundle of Kent–> ventricle–> AV node–> atrium

51
Q

What’s the worst scenario A fib causes in WPW syndrome

A

VF

52
Q

3 stages of MI

A
  1. Peaks and inverts–> hyperacute T wave
  2. STE and merges with T
  3. New Q
53
Q

Difference of T in MI and hypertrophy

A

Symmetric T in MI, asymmetric T in hypertrophy

54
Q

What does a changing T mean

A

Ischemia

55
Q

What does a changing ST mean

A

Injury

56
Q

What does it mean if the STE persists after MI?

A

Formation of a ventricular aneurysm

57
Q

What does a pathologic Q mean?

A

Irreversible myocardial cell death–> unable to conduct an electrical current–> electrical forces direct away from the area

58
Q

Which lead normally has a deep Q?

A

aVR (thus, not helpful in assessing MI)

59
Q

Which supplies the AV node mostly: RCA or LCX?

A

RCA

60
Q

Leads for inferior infarct and artery

A

II, III, aVF, RCA

61
Q

Lateral infarct and artery

A

I, aVL, V5, V6, LCX

62
Q

Anterior infarct and artery

A

V1-V6, LAD

63
Q

Posterior infarct and artery

A

Reciprocal changes in anterior leads esp V1, RCA

64
Q

Anterolateral infarct artery

A

LCA

65
Q

When does poor R wave progression occur?

A
  1. Anterior infarction
  2. RVH
  3. Chronic lung disease
66
Q

Why check posterior MI in case of inferior MI confirmed?

A

Same blood supply

67
Q

How to differentiate tall R in V1 in RVH and posterior MI?

A

R axis dev

68
Q

Conditions that result in STE

A
  1. MI (mostly transmural)
  2. Prinzmetal’s angina
  3. J point elevation (benign early repolarization, esp V4)
  4. Acute pericarditis
  5. Acute myocarditis
  6. Hyper-K
  7. PE
  8. Brugada syndrome
  9. Hypothermia
69
Q

Conditions that result in STD

A
  1. Typical angina

2. Non-Q wave infarction

70
Q

When does ‘rule of appropriate discordance’ apply?

A

Normal LBBB (QRS and J point are in different directions)= if they’re in same direction, something wrong!

71
Q

What is ‘modified Sgarbossa criteria’ for?

A

Dx AMI in the setting of LBBB (new/old)

72
Q

CIs to stress testing

A
  1. Any acute systemic illness
  2. Severe aortic stenosis
  3. Uncontrolled CHF
  4. Severe HTN
  5. Angina at rest
  6. Presence of a significant arrhythmia
73
Q

Drugs that prolong QT (6)

A
  1. Anti-arrhythmic Class IC and III
  2. TCAs
  3. Phenothiazines (ex. methylene blue, anti-psychotics)
  4. Erythromycin
  5. Quinolone ABX
  6. Antifungals
74
Q

How to treat inherited long QT (3)

A
  1. Beta-blockers
  2. Implantable defibrillator
  3. Restricted from competitive sports (adrenalin bursts)
75
Q

EKG change in acute pericarditis (in large effusion)

A

Diffuse STE and flattened/inverted T (low voltage, electrical alternans)

76
Q

Why electrical alternans occur

A

Large effusion allows the heart to rotate freely w/in the sac that changes the axis every time it beats

77
Q

EKG change in a nonmassive PE

A

Normal or sinus tachycardia

78
Q

Definitive Rx for Brugada syndrome

A

ICD

79
Q

Most common ventricular arrhythmia in Brugada syndrome

A

Polymorphic ventricular tachycardia (resembles TdP)