Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Cardiology > Exam 1 ECG's Galore > Flashcards

Exam 1 ECG's Galore Flashcards

(78 cards)

Start Studying
1
Q

P wave

A 
Atrial depolarization (phase 0) 
Normal = 0.06 -0.11 sec
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Q wave

A

First negative deflection of QRS complex

Pathologic when in leads I, V1-3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

R wave

A

First positive deflection of QRS complex

Increases in amplitude from right to left

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

S wave

A

First negative deflection following an R wave

Decreases in amplitude from right to left

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

T wave

A 
Ventricular repolarization (phase 3) 
Should be in concordance with QRS complex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

U wave

A

Usually not seen - may be related to electrolyte disturbances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

QRS complex

A

Ventricular depolarization from start to finish

Normal = 0.07-0.11 sec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

PR interval

A

Depolarization of atria and ventricles

Normal = 0.12-0.20 sec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

ST segment

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

J point

A

Point where QRS joins ST segment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Degrees of Normal Axis

A

+30 to +100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Left ventricular hypertrophy (LVH)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Right bundle branch block (RBBB)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

First degree AV block

A

PR interval > 0.20 sec (1 big box)

Generally benign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Third degree AV block
Wide QRS complexes P rate >>>> QRS complex rate Atrial rates (P rates) are faster than ventricular rates QRS rates) NO ATRIAL IMPULSES REACH THE VENTRICLES
26
AV dissociation
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
27
Subendocardial ischemia
ST segment depression | may have inverted T waves
28
Transmural ischemia
ST segment elevation May have tall peaked (hyperacute) T waves May have elevated J point
29
Myocardial Infarction - general rules of thumb for ECG (acute vs. old)
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
30
Anterior MI
Q waves in V1-3 | Left anterior descending of LCA
31
Lateral MI
Q waves in I, AVL | Left anterior descending of LCA
32
Inferolateral or posterolateral MI
Q waves in V4-6 | Left anterior descending of LCA
33
Inferior MI
Q waves in II, III, AVF Right coronary artery (90% of the time) May be characterized by AV block
34
Posterior MI
R waves progressively get bigger in V1-3 Mirror image of anterior MI Left circumflex of LCA
35
Ventricular pre-excitation
MUST HAVE SHORT PR INTERVAL (<0.12 sec) AND DELTA WAVES QRS usually > 0.10 sec Conduction via Kent bundle
36
Atrial prematures
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
Junctional prematures (supraventricular prematures)
Arise in AV junction = VERY SHORT PR P waves may be absent, follow, or precede QRS QRS usually narrowing (if no BBB present)
38
Ventricular prematures
Wide, bizarre QRS complexes No P wave ST segment slopes away from QRS Usually have compensatory pause (R-R lengthens)
39
R on T ventricular premature description
Grade 5 = REALLY BAD Repolarization is occurring then a depolarization event occurs and triggers a reentrant ventricular tachycardia
40
Multiform ventricular premature description
Grade 3 Varying QRS complexes (some negative, some positive, some different shapes)
41
Left ventricular prematures
Usually monophasic R or qR in V1 qS or monophasic QS in V6 Left peak in V1 with greater amplitude
42
Atrial flutter
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
Atrial fibrillation
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
Orthodromic AV bypass tachycardia
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
Antidromic AV bypass tachycardia --rare--
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
AV (reentrant) junctional tachycardia (SVT)
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
Reentrant ventricular tachyarrhythmia
WIDE QRS complexes Tall R wave in V1 Deep S wave in V6
48
Torsades de pointes
QRS complex twists around the baseline
49
R on T reentrant ventricular tachyarrhythmia
Premature hits on the end of the T wave >> can lead to A fib.
50
Class IA anti-arrhythmic drugs
Moderate Na channel blockers Quinidine, Procainamide, Disopyramide
51
Class IB anti-arrhythmic drugs
Mild Na channel blockers Lidocaine, Mexiletine
52
Class IC anti-arrhythmic drugs
Marked Na channel blockers Flecinide, propafenone
53
Class II anti-arrhythmic drugs
Beta Blockers Metoprolol, atenolol
54
Class III anti-arrhythmic drugs
Marked K channel blockers sotolol, amiodarone, ibutilide
55
Class VI anti-arrhythmic drugs
Calcium channel blockers verapamil, diltiazem
56
AE quinidine
cinchonism
57
AE procainamide
QT prolongation
58
AE disopyramide
significant anticholinergic effects
59
Lidocaine use
works only on ventricular arrhythmia's (no atrial effects)
60
Important fact about class I anti-arrhythmic drugs
increase mortality in CHF patients
61
Important fact about beta blockers as anti-arrhythmic drugs
ONLY class to reduce mortality in these patients
62
AE of sotolol
QT prolongation
63
AE's of amiodarone
pulmonary toxicity corneal deposits blue-green skin discoloration
64
2 conditions that cause widened splitting of S2
RBBB, pulmonic stenosis
65
2 conditions that cause paradoxical splitting of S2
LBBB, aortic stenosis
66
What causes an opening snap to be heard?
Stenosis in mitral or tricuspid valve
67
Aortic Stenosis
Between S1, S2 Harsh, diamond shape 2nd right ICS
68
Aortic Regurgitation
Diastolic decrescendo 3rd/4th ICS High pitch, blowing
69
Mitral Stenosis
Mild = presystolic accentuation Severe = OS sooner in diastole Low, rumbling, opening click, Down + up Apex
70
Mitral Regurgitation
Pansystolic Apex >> axilla Heart failure patients High pitched, blowing
71
3 determinants of stroke volume
ventricular contractility ** EDV/preload afterload
72
3 factors affecting afterload
ventricular outflow tract aortic valve function peripheral arterial resistance
73
ANREP Effect
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
Force Frequency Relationship
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
Most common cause of increased afterload
hypertension
76
2 modes of passive regulation of pulmonary circulation
distension and recruitment (opening capillaries)
77
2 modes of active regulation of pulmonary circulation
hypoxic vasoconstriction and ventilation-perfusion matching
78
Difference in QRS between supraventricular and ventricular arrhythmia's
``` Supraventricular = narrow QRS (supra skinny) Ventricular = wide QRS ```

Cardiology (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions