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Cardiology > Exam 1 ECG's Galore > Flashcards

Exam 1 ECG's Galore Flashcards

1
Q

P wave

A 
Atrial depolarization (phase 0) 
Normal = 0.06 -0.11 sec
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2
Q

Q wave

A

First negative deflection of QRS complex

Pathologic when in leads I, V1-3

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3
Q

R wave

A

First positive deflection of QRS complex

Increases in amplitude from right to left

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4
Q

S wave

A

First negative deflection following an R wave

Decreases in amplitude from right to left

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5
Q

T wave

A 
Ventricular repolarization (phase 3) 
Should be in concordance with QRS complex
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6
Q

U wave

A

Usually not seen - may be related to electrolyte disturbances

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7
Q

QRS complex

A

Ventricular depolarization from start to finish

Normal = 0.07-0.11 sec

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8
Q

PR interval

A

Depolarization of atria and ventricles

Normal = 0.12-0.20 sec

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9
Q

QT interval

A

Ventricular depolarization and repolarization
Beginning of Q wave to end of T wave
Increases in length as heart rate decreases

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10
Q

ST segment

A

Ventricular plateau phase (phase 2)
Varies with heart rate
Generally isoelectric
Best indicator of ischemia

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11
Q

J point

A

Point where QRS joins ST segment

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12
Q

Degrees of Normal Axis

A

+30 to +100

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13
Q

Left atrial abnormality

A

P wave > 0.12 sec (3 small boxes)
Notched P wave in lead II
Wide, deep terminal P wave forces in V1
Left atrium depolarizes late

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14
Q

Right atrial abnormality

A

P wave > 0.12 sec (3 small boxes)
P waves tall and peaked in lead II and V1
Right atrium depolarizes late

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15
Q

Right ventricular hypertrophy (RVH)

A

Right axis deviation
Commonly have right atrial abnormality
Tall R waves in right leads
Deep S waves in left leads

ST depression with upward convexity and inverted T waves in right leads

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16
Q

Left ventricular hypertrophy (LVH)

A

Left axis deviation
Commonly have left atrial abnormality
Tall R waves in left leads

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17
Q

Right bundle branch block (RBBB)

A

Wide QRS ( >0.12 sec)
rsR’ pattern in V1
Deep, broad S wave in V6

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18
Q

Left bundle branch block (LBBB)

A

Wide QRS ( >0.12 sec)
Broad, slurred R wave in V6 with late peak
QS in V1

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19
Q

Left anterior fascicular block (LAFB)

A

Left axis deviation
Small Q in I and AVL
Small R in II, III, AVF
Normal QRS duration

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20
Q

Left posterior fascicular block (LPFB)

—rare—

A

Right axis deviation
Small Q in II, III, AVF
Small R in I and AVL
Normal QRS duration

NO EVIDENCE OF RVH

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21
Q

First degree AV block

A

PR interval > 0.20 sec (1 big box)

Generally benign

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22
Q

Second degree AV block description

A

Grouped QRS complexes - one or more (not all) atrial impulses fail to reach the ventricles, WITH NO PREMATURITY

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23
Q

Second degree AV block type I (Wenckebach)

A

PR interval progressively lengths until AV conduction is lost

Grouped QRS complexes, leads to periodicity, sometimes one is dropped

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24
Q

Second degree AV block type II

uncommon but bad

A

PR interval DOES NOT LENGTHEN

May drop QRS complexes but cannot predict where (no periodicity)

Almost always preceded by BBB

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25
Q

Third degree AV block

A

Wide QRS complexes

P rate &raquo_space;» QRS complex rate

Atrial rates (P rates) are faster than ventricular rates QRS rates)

NO ATRIAL IMPULSES REACH THE VENTRICLES

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26
Q

AV dissociation

A

Rates of the atria and ventricles are SIMILAR (even though the rhythms are independent)

Narrow QRS complexes = using normal conduction pathway

p waves may enter QRS complex

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27
Q

Subendocardial ischemia

A

ST segment depression

may have inverted T waves

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28
Q

Transmural ischemia

A

ST segment elevation
May have tall peaked (hyperacute) T waves
May have elevated J point

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29
Q

Myocardial Infarction - general rules of thumb for ECG (acute vs. old)

A

QRS changes most helpful

ACUTE = ST elevation = STEMI = current of injury

OLD = pathologic Q waves = NECROSIS

EVOLVING = gradually losing ST elevation and developing Q waves

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30
Q

Anterior MI

A

Q waves in V1-3

Left anterior descending of LCA

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31
Q

Lateral MI

A

Q waves in I, AVL

Left anterior descending of LCA

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32
Q

Inferolateral or posterolateral MI

A

Q waves in V4-6

Left anterior descending of LCA

33
Q

Inferior MI

A

Q waves in II, III, AVF
Right coronary artery (90% of the time)
May be characterized by AV block

34
Q

Posterior MI

A

R waves progressively get bigger in V1-3
Mirror image of anterior MI
Left circumflex of LCA

35
Q

Ventricular pre-excitation

A

MUST HAVE SHORT PR INTERVAL (<0.12 sec) AND DELTA WAVES

QRS usually > 0.10 sec

Conduction via Kent bundle

36
Q

Atrial prematures

A

Occur early in cycle
Abnormally shaped P waves
P wave may superimpose on T wave

MOST COMMON CAUSE OF A PAUSE ON AN ECG IS A NON-CONDUCTED ATRIAL PREMATURE

May have…
Normal QRS or aberrant
Compensatory pause or not

37
Q

Junctional prematures (supraventricular prematures)

A

Arise in AV junction = VERY SHORT PR

P waves may be absent, follow, or precede QRS
QRS usually narrowing (if no BBB present)

38
Q

Ventricular prematures

A

Wide, bizarre QRS complexes
No P wave
ST segment slopes away from QRS

Usually have compensatory pause (R-R lengthens)

39
Q

R on T ventricular premature description

A

Grade 5 = REALLY BAD

Repolarization is occurring then a depolarization event occurs and triggers a reentrant ventricular tachycardia

40
Q

Multiform ventricular premature description

A

Grade 3

Varying QRS complexes (some negative, some positive, some different shapes)

41
Q

Left ventricular prematures

A

Usually monophasic R or qR in V1
qS or monophasic QS in V6
Left peak in V1 with greater amplitude

42
Q

Atrial flutter

A

Generally regular with periodicity
Flutter waves make the baseline look like sawtooth
Atrial rate ~300 (QRS rate usually 150ish)

Most common presentation = 2:1 AV conduction

43
Q

Atrial fibrillation

A

Variable baseline = coarse to fine with f waves
IRREGULARLY IRREGULAR
QRS complexes do what they want
Controlled (HR 60-100) vs. uncontrolled (tachycardia)
No p waves

44
Q

Orthodromic AV bypass tachycardia

A

Normalization of QRS and no delta waves
P waves after QRS

Go to ventricles via normal conduction pathway and reenter atria via Kent bundle

45
Q

Antidromic AV bypass tachycardia

–rare–

A

QRS wide
P waves after each QRS
Delta waves present
Slow upslope of QRS

Go to ventricles via Kent bundle and reenter atria via normal conduction pathway

46
Q

AV (reentrant) junctional tachycardia (SVT)

A

P waves USUALLY ABSENT (but can be before or after QRS)

NARROW QRS (conduction through normal pathway)

HR about 200

GETS BACK TO SINUS RHYTHM WITH CAROTID MASSAGE

47
Q

Reentrant ventricular tachyarrhythmia

A

WIDE QRS complexes

Tall R wave in V1
Deep S wave in V6

48
Q

Torsades de pointes

A

QRS complex twists around the baseline

49
Q

R on T reentrant ventricular tachyarrhythmia

A

Premature hits on the end of the T wave&raquo_space; can lead to A fib.

50
Q

Class IA anti-arrhythmic drugs

A

Moderate Na channel blockers

Quinidine, Procainamide, Disopyramide

51
Q

Class IB anti-arrhythmic drugs

A

Mild Na channel blockers

Lidocaine, Mexiletine

52
Q

Class IC anti-arrhythmic drugs

A

Marked Na channel blockers

Flecinide, propafenone

53
Q

Class II anti-arrhythmic drugs

A

Beta Blockers

Metoprolol, atenolol

54
Q

Class III anti-arrhythmic drugs

A

Marked K channel blockers

sotolol, amiodarone, ibutilide

55
Q

Class VI anti-arrhythmic drugs

A

Calcium channel blockers

verapamil, diltiazem

56
Q

AE quinidine

A

cinchonism

57
Q

AE procainamide

A

QT prolongation

58
Q

AE disopyramide

A

significant anticholinergic effects

59
Q

Lidocaine use

A

works only on ventricular arrhythmia’s (no atrial effects)

60
Q

Important fact about class I anti-arrhythmic drugs

A

increase mortality in CHF patients

61
Q

Important fact about beta blockers as anti-arrhythmic drugs

A

ONLY class to reduce mortality in these patients

62
Q

AE of sotolol

A

QT prolongation

63
Q

AE’s of amiodarone

A

pulmonary toxicity
corneal deposits
blue-green skin discoloration

64
Q

2 conditions that cause widened splitting of S2

A

RBBB, pulmonic stenosis

65
Q

2 conditions that cause paradoxical splitting of S2

A

LBBB, aortic stenosis

66
Q

What causes an opening snap to be heard?

A

Stenosis in mitral or tricuspid valve

67
Q

Aortic Stenosis

A

Between S1, S2
Harsh, diamond shape
2nd right ICS

68
Q

Aortic Regurgitation

A

Diastolic decrescendo
3rd/4th ICS
High pitch, blowing

69
Q

Mitral Stenosis

A

Mild = presystolic accentuation
Severe = OS sooner in diastole
Low, rumbling, opening click, Down + up
Apex

70
Q

Mitral Regurgitation

A

Pansystolic
Apex&raquo_space; axilla
Heart failure patients
High pitched, blowing

71
Q

3 determinants of stroke volume

A

ventricular contractility **
EDV/preload
afterload

72
Q

3 factors affecting afterload

A

ventricular outflow tract
aortic valve function
peripheral arterial resistance

73
Q

ANREP Effect

A

relates afterload to contractility

increase in aortic pressure abruptly will have a positive inotropic effect for 1-2 min = true inotropic effect (independent of muscle length)

Metabolic changes: increase sodium + calcium in cytosol cause an increase myocardial contraction

74
Q

Force Frequency Relationship

A

Increased HR progressively enhances the force of ventricular contraction

When stimulation becomes too rapid, force decreases (Decreased heart rate has negative staircase effect)

Opposing factor = ventricular filling time (if it increases then there is more in the ventricle, so contraction is stronger)

Decrease duration of filling a high HR

Relates HR to contractility

75
Q

Most common cause of increased afterload

A

hypertension

76
Q

2 modes of passive regulation of pulmonary circulation

A

distension and recruitment (opening capillaries)

77
Q

2 modes of active regulation of pulmonary circulation

A

hypoxic vasoconstriction and ventilation-perfusion matching

78
Q

Difference in QRS between supraventricular and ventricular arrhythmia’s

A 
Supraventricular = narrow QRS (supra skinny)
Ventricular = wide QRS

Cardiology (3 decks)

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