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Flashcards in Cardiology Deck (89):
1

most common cause of pathologic sinus bradycardia

fibrotic replacement of the sinus node associated with aging

2

Causes of pathologic sinus bradycardia

-fibrotic replacement with aging
-damage secondary to infarction or cardiac surgery
-infiltrative processes (sarcoidosis, amyloidosis)
-increased vagal tone secondary to Valsalva maneuver or vomiting
-Medications (B-blockers, CCB's)
-Genetic diseases (rare)

3

Characterized by a dropped QRS complex with no change in preceding PR intervals, suggestive of His-Purkinje disease

Mobitz type 2 second-degree AV block

4

Occurs when two or more nonconducted P waves occur for each QRS complex

-Advanced second-degree heart block
or
-High grade heart block

5

Occurs when there is no relationship between P waves and the QRS escape rhythm

Third-degree heart block

6

Pathologic location of third-degree heart block

His bundle or below

7

Reversible causes of complete heart block

-medications (BB, CCB's, digoxin)
-Lyme disease

8

This type of infarction is more likely to have permanent conduction defects because of larger infarct sizes

Anterior MI

9

This type of infarction may have only transient heart block that resolves after a few days

Inferior MI

10

If persistent post-MI heart block develops:

-increased in hospital mortality from ventricular arrhythmias and cardiogenic shock
-decision to place permanent pacemaker should be made after a few days

11

Indications for permanent pacemaker

-symptomatic sinus bradycardia (HR < 40 bpm) or sinus pauses
-symptomatic complete heart block or second-degree heart block (type 1 or 2)
-Asymptomatic complete heart block or advanced second-degree heart block
-Afib with pauses > 5 seconds
-Alternating bundle branch block

12

How to place a pacemaker in asynchronous mode

-reprogram the pacemaker
-place a magnet over the pacemaker

13

Bradyarrhythmias arise from three sites

-SA node
-AV node
-Infranodal (His-Purkinje system)

14

Chronotropic incompetence

inability to raise sinus rate appropriately in response to exercise

15

SA block (first degree)

-fixed delay between the depolarizing SA node and the depolarization exiting the node and propagating as a P wave
-delay is fixed and cannot be detected on surface EKG

16

SA block (second degree) - Type I (Wenckebach)

-progressive delay between SA nodal depolarization and exit of the impulse to the atrium
-manifests as a progressive shortening of the P-P interval until there is a pause, reflecting an SA node impulse that was blocked form exiting the node

17

SA block (second degree) - Type II

-constant P-P interval with intermittent pauses
-pauses represent an SA node impulse that was blocked form exiting the node
-duration of the pause is a multiple of the basic P-P interval

18

SA block (third degree)

-demonstrates no P-wave activity, no impulses exit the sinus node
-surface EKG is indistinguishable from sinus arrest - no sinus node activity

19

First degree AV block

-PR interval prolonged ( > 200 ms)
-ventricular rate = atrial rate

20

Second degree AV block (Mobitz I-Wenckebach)

-progressive PR interval prolongation followed by a single blocked P wave and a nonconducted QRS complex

21

Second degree AV block (Mobitz I-Wenckebach) location of block

-within AV node superior to bundle of His

22

Second degree AV block (Mobitz II)

-regular P waves with intermittent nonconducted QRS complexes in the absence of atria premature complexes
-resulting RR interval spanning the nonconducted complex is exactly double the conducted RR intervals

23

Second degree AV block (Mobitz II) location of block

-AV block below the bundle of His
-high propensity to progress to more advanced forms of AV block

24

How to determine AV block with a ratio of 2:1

-cannot differentiate with 2:1 conduction
-must use longer rhythm strips, maneuvers, and intracardiac recordings
-widened QRS supports Mobitz Type II but lacks certainty

25

Third degree (complete) AV block

-independent atrial and ventricular activity with an atrial rate that is faster than the ventricular rate

26

Ventricular rhythm location and block location with :

Third degree (complete) AV block + Narrow QRS

-Junctional escape rhythm
-usually block in AV node

27

Ventricular rhythm location and block location with:

Third degree (complete) AV block + Wide QRS

-Ventricular escape rhythm
-block in His bundle or below

28

How long should anticoagulation be continued after atrial fibrillation ablation?

-2-3 months
-then should be guided by risk stratification (CHADS score) providing anticoagulation as if the ablation did not occur

29

CHADS 2 score 0 anticoagulation choice in AF

Aspirin

30

CHADS 2 score 1 anticoagulation choice in AF

Aspirin or Warfarin

31

CHADS 2 score 2 anticoagulation choice in AF

Warfarin (or other anticoagulants)

32

CHADS 2 score 0 anticoagulation choice in AF if unable to tolerate warfarin

ASA + Plavix
-provides greater stroke reduction than either alone but less effective than Warfarin

33

Cholesterol embolization syndrome

-red-purple to blue discoloration of toes
-livedo reticularis (lace-like purple discoloration of mottled skin)
-signs of systemic illness (elevated WBC with eosinophilia, ESR, fever)

34

Acute interstitial nephritis

-eosinophiluria
-hypersensitivity reaction to medications (B lactam antibiotics, PPI)

35

Acute interstitial nephritis diagnostic stain

Hansel stain

36

First line therapy in patients with unstable angina who have contraindications to B-blockers

Diltiazem

37

Absolute contraindications to B-blockade

-symptomatic bradycardia
-advanced AV block
-SBP < 80
-cardiogenic shock
-pulmonary edema
-symptomatic reactive airway disease

38

CCB contraindicated in acute coronary syndrome

Nifedipine (causes increase in heart rate, and therefore myocardial oxygen demand)

39

Can be used to diagnose supraventricular tachycardias

Adenosine

40

Adenosine mechanism for diangosing SVT's

transiently blocks AV nodal conduction and interrupts the reentrant circuit, thereby terminating AV nodal reentrant trachycardia and AV reciprocating tachycardia but not other supraventricular tachyarrhythmias

41

Adenosine effects on atrial tachycardia and other supraventricular arrhythmias (not AVNRT or AV reciprocating tachycardia)

-slows ventricular rate
or
-have no effect

42

EKG findings when adenosine given in atrial tachycardia

-P waves can be seen in the absence of QRS complexes due to adenosine induced AV block

43

Positive exercise ABI diagnostic for PAD

-decrease in ABI by 20% measured immediately following symptom-limited exercise

44

Valvular lesion BIT

TTE

45

TTE helps identify these factors in valvular lesions

-diagnosis and assessment of valvular disease severity
-identification of coexistant lesions
-diagnosis of pulmonary hypertension
-assessment of ventricular size and function

46

Valvular disease indication for TTE

-symptomatic patients
-systolic murmur grade 3/6 intensity or greater
-Continuous murmur (begins after S1 and extends beyond S2)
-Diastolic murmur

47

Atrial fibrillation usually originates from here

pulmonary veins

48

Atrial fibrillation ablation term

pulmonary vein isolation "PVI"

49

Quinidine class

class IA antiarrythmic

50

Quinidine major side effects

Cinchonism --> tinnitus, blurred vision, dizziness, nausea and vomiting

51

Orthodeoxia

oxygen desaturation in the upright position resolved when supine

52

Orthodeoxia DDx

-LA myxoma
-hepatopulmonary syndrome
-pulmonary AVM's

53

Pathologic Q waves

Old MI

54

Pathologic Q waves (criteria)

> 40 ms (1mm) wide
> 2 mm deep
> 25% of QRS amplitude OR if seen in V1-V3

55

-Acute MI with LBBB
-EKG with notch in upslope of R wave in lead I, aVL or V6

Chapman sign

56

LVH Cornell Criteria

R wave in aVL + S wave in V3
- > 28 mm in males
- > 20 mm in females

57

LVH Modified Cornell Criteria

R wave in aVL > 12 mm

58

LVH Sokolow-Lyon Criteria

S wave in V1 + R wave V5 or V6
- > 35 mm

59

LVH Romhilt-Estes scoring system

-Score = 4 (LVH present with 30-54% sensitivity
-Score > 5 (LVH present with 83-97% specificity)

3 --> Amplitude of largest R or S in limb leads > 20 mm
3 --> Amplitude of S in V1 or V2 > 30 mm
3 --> Amplitude of R in V5 or V6 > 30 mm
3 --> ST and T wave changes opposite QRS without digoxin
1 --> ST and T wave changes opposite QRS with digoxin
3 --> Left atrial enlargement
2 --> Left axis deviation
1 --> QRS duration > 90 ms
1 --> Intrinsicoid deflection in V5 or V6 > 50 ms

60

Levine grading scale (heart murmurs)

-Grade I/VI intensity

-only audible on listening carefully some times
-only hear with special maneuvers (valsalva, handgrips)

61

Levine grading scale (heart murmurs)

-Grade II/VI Intensity

-faintly audible but immediately audible with stethoscope on chest
-majority of murmurs; no objective difference between them

62

Levine grading scale (heart murmurs)

-Grade III/VI Intensity

-Loud murmur readily audible but with no palpable thrill

63

Levine grading scale (heart murmurs)

-Grade IV/VI Intensity

-Loud murmur with palpable thrill
-Thrill present (palpable vibration you can feel from severe lesion)

64

Levine grading scale (heart murmurs)

Grade V/VI Intensity

-Loud murmur with a palpable thrill
-audible with only the rim of the stethoscope touching the chest

65

Levine grading scale (heart murmurs)

-Grade VI/VI Intensity

-Loud murmur with palpable thrill
-audible with stethoscope off chest

66

Optimal time period from CVA/TIA to carotid endarterectomy

2 weeks

67

Criteria for diagnosis of stress cardiomyopathy

-ST segment elevation
-transient wall motion abnormalities of the apex and mid ventricle
-absence of obstructive coronary artery disease
-absence of other causes of transent left ventricular dysfuction, such as recent head trauma or myocarditis

68

stress cardiomyopathy prognosis

excellent with resolution of LV dysfunction in several weeks with supportive care (B-blockers and ACE inhibitors)

69

Mechanism of stress cardiomyopathy

catecholamine-mediated myocardial stunning (thought to be most likely)

70

-pleuritic chest pain
-EKG changes: PR segment depression, diffuse ST-segment elevation, and T wave changes

acute pericarditis

71

NSTEMI acute intervention (intermediate TIMI risk score)

-Antiplatelet agents (aspirin and clopidogrel)
-B blocker
-Statin
-Antithrombin therapy (UFH or LMWH)

72

Aortic stenosis (mild criteria)

-Jet velocity < 3m/s
-Mean gradient < 25 mm Hg
-Valve area > 1.5 cm2

73

Aortic stenosis (moderate criteria)

-Jet velocity 3-4 m/s
-Mean gradient 25-40 mm Hg
-Valve area 1.0-1.5 cm2

74

Aortic stenosis (severe criteria)

-Jet velocity > 4m/s
-Mean gradient > 40 mm Hg
-Aortic Valve area < 1.0 cm2

75

Indications for intervention in symptomatic carotid artery stenosis

> 70%

76

Indications for intervention in asymptomatic carotid artery stenosis

60%

77

Annual risk for having a CVA with severe carotid artery stenosis?

0.5% risk annually

78

Acceptable surgeon error rate for carotid endarterectomy

< 3%

79

Timeframe to perform CEA after having a CVA

Within 2 weeks

80

-Upper extremity hypertension
-diminished or delayed femoral pulses
-lower extremity claudication with physical activity

coarctation of Aorta

81

-early systolic click
-grade 2/6 early systolic murmur at upper right sternal border

coarctation of aorta

82

50% of patients with aortic coarctation will also have this condition

bicuspid aortic valve (asymptomatic most of the time)

83

Rhythm greater than 100/min and originates in the ventricles

VT

84

Sustained VT

Lasting for > 30 seconds

85

Coronary dominance

Determined by artery PDA arises from
-80% Right dominant
-10% Left dominant
-10% Codominant

86

treatment for severe, asymptomatic mitral regurgitation with normal left ventricular systolic function but evidence of pulmonary hypertension

mitral valve repair

87

indications for mitral valve replacement surgery

-left ventricular EF < 60%
-left ventricular end-systolic diameter > 40 mm
-severe pulmonary hypertension at rest (pulmonary artery systolic pressure > 50 mm Hg) or during exercise ( > 60 mm Hg)
-new onset A-fib

88

most common cause of late ventricular dysfunction in cardiac transplant patients and should be considered in transplant patients with new-onset heart failure

cardiac allograft vasculopathy

89

contraindications to cilostazol in PAD patients

-heart failure with LVEF < 40%
*contraindication stems from cilostazol's similar pharmacologic action to the inotropic drugs milrinone and inamrinone, which demonstrated increased mortality in heart failure patients with long-term use