EKG Review Flashcards
1
Q
The limb leads view the heart from the
A
frontal plane
2
Q
The chest leads view the heart from the
A
horizontal plane, THROUGH the heart, front to back
3
Q
Limb leads are:
A
I, II III, aVR, aVL, aVF
4
Q
On EKG, each small box represents
A
0.04 seconds = 40 ms
5
Q
On EKG, each large box represents
A
0.2 seconds = 200 ms
6
Q
On EKG, one large vertical box represents
A
0.5 mV
7
Q
An upright deflection sees an electrical impulse traveling
A
toward it
8
Q
A negative deflection sees an electrical impulse traveling
A
away from it
9
Q
An EKG spike that is both up and down is called
A
isoelectric
10
Q
In a normal heart, the electrical impulse originates in the
A
SA node
11
Q
Only electrical connection between atria and ventricles
A
AV node
12
Q
Electrical pathway of heart
A
SA node –> AV node –> Bundle of His –> Left and right bundle branches –> Purkinje fibers
13
Q
Why is the left bundle branch unique?
A
It has two fascicles - left anterior and left posterior fascicles
14
Q
After the atria fire, why is there a pause before the QRS complex?
A
To allow the ventricles to fill?
15
Q
The PR interval means
A
The time is takes for the electrical impulse to get through the AV node
16
Q
Q wave is
A
The first negative deflection after the PR interval
17
Q
T wave is
A
Ventricular repolarization
18
Q
11 steps to interpreting EKGs
A
Rate Rhythm Electrical axis P wave configuration PR interval QRS interval QRS complexes ST segments T waves U waves QT duration
19
Q
Where do leads I and aVL “look?”
A
High left lateral wall LV
20
Q
Where do leads II, III and aVF “look?”
A
Inferior wall
21
Q
Where does V1 “look?”
A
RV
22
Q
Where do leads V2-V3 “look?”
A
Interventricular septum
23
Q
Where do leads V4-V6 “look?”
A
Left lateral wall of LV
24
Q
When the left atrium is enlarged, usually due to LV dysfunction, or possibly hypertension or mitral valve disease, the terminal portion of the P wave becomes
A
negative and broad, also with left atrial enlargement
25
When the P wave becomes wide and notched in the inferior leads, including II, III and AVF, then what other pathology is present?
Left atrial enlargement
26
Right atrial enlargement is manifested by
Peaked, tall appearing p waves located in the inferior II, III, AVF
27
The right atrium depolarizes in what direction?
Directly toward II, III, AVF
28
If it looks like it would hurt to sit on the P wave in lead II, what pathology is likely?
Right atrial enlargement
29
First degree AV block means
PR interval >200ms
30
Third degree (complete) AV block occurs when
P waves do not conduct through AV node;
| Atrial and ventricular activity are completely independent of each other
31
The hallmark of RBBB is called
RSR'
32
If the QRS wis wide, do what next?
Measure the PR interval; if short, there could be aberrant AV conduction
33
Most common cause of inappropriate shock by ICD
Afib
34
Patient manipulation of pacemaker, either accidentally or deliberately, resulting in diaphragmatic pacing
Twiddler's syndrome
35
Types of pacemakers
A, V, AV
36
Asymmetric T-wave inversion is often present with
Left ventricular hypertrophy
37
Symmetric T wave inversion is often seen with
Ischemia
38
The presence of prominent U waves suggests
Hypokalemia
39
The presence of inverted U waves may suggest
Myocardial ischemia
40
QT range
330-430 ms in general
41
Prolonged QT can lead to what pathology
Torsades (aka polymorphic ventricular tachycardia)
42
What electrolyte abnormalities prolong the QT interval
Hypomagnasemia
Hypokalemia
Hypocalcemia
43
What electrolyte abnormality can shorten the QT
Hypercalcemia if severe
44
Common medications that prolong the QT
Class IA antiarrhythmics including quinidine, procainimide, disopyramide
Class III antiarrhythmics including sotalol, amiodarone
Erythromycin-type medications
TCAs including amitriptyline
Many others
45
EKG effects of hypokalemia
Prominent U waves
| QT lengthening
46
EKG effects of hyperkalemia
Peaked T waves
Progressive blunting of the P wave until P disappears
Widened QRS leading to vfib/asystole
47
EKG effects of hypomagnasemia
QT lengthening
48
EKG effects of hypercalcemia
Shortened QT
49
EKG effects of hypocalcemia
QT lengthening
50
T/F: A younger patient normally has more voltage on their EKG.
True
51
Fastest way to diagnose left ventricular hypertrophy
Nelson's criteria: If the sum of the deepest S wave inV1 or V2 and the tallest R wave in V5 or V6 is greater than 45mm (for <35 years of age) and 35mm (for >45 years of age)
52
Leads V1 and V2 lie directly over the
RV
53
In the presence of RVH, expect to see large upright deflections in what leads?
V1, V2
54
Common causes of left atrial enlargement
HTN
| Malformations/distortions of mitral valve
55
Common causes of right atrial enlargement
COPD
Pulmonary HTN
Asthma
56
Rare cause of right atrial enlargement
ASD/VSD
57
The mass of the myocardium depolarizing determines the ______ of the wave inscribed on the EKG
Amplitude/voltage
58
Peaked P waves in II, III, and/or AVF indicate
Right atrial enlargement
59
How to diagnose left atrial enlargement in V1
one box down and one box wide
60
Where should you look for a double humped P wave in diagnosing left atrial enlargement?
II, III, AVF (have to be separated by one another with one small box)
61
What does a double humped P wave mean?
Left atrium large and depolarizing after right atrium
62
Common causes of left ventricular hypertrophy
Uncontrolled HTN
Obesity
Valvular issues including regurgitation
Less common - HOCM
63
Nelson's criteria for identifying LVH
Add the voltage of the S wave in V1 or V2 (whichever is greater) to the voltage of the tallest R wave in V5 or V6.
If the total >45mm, LVH present. >35mm for pts >45
64
Quick criteria for identifying left ventricular enlargement
If AVL QRS > 15 mm
65
Common causes of right ventricular enlargement
Lung disease
| Pulmonary emboli
66
Most common reason for a prominent R wave in V1-V2
Prior posterior wall MI
67
Why is the P wave normally inverted in AVR?
Because the electrical impulse is traveling away from it
68
No discernible P waves prior to QRS complexes
| Pathology:
Junctional rhythm, originates within the AV node
| Usually <60 bpm
69
Definition of normal sinus rhythm
P followed by QRS every time
70
Define wandering atrial focus
Sinus arrhythmia where P wave morphologies are different
71
Increased automaticity in the atria is called
PAC - premature atrial contraction
| P waves will not have the same morphology as normal P waves, for example may deform the T wave
72
Increased automaticity/impatient focus that originates in the ventricle is called
PVC, preventricular contraction
| PVC is wide compared to normal QRS
73
Types of arrhythmias
1. Increased automaticity/impatient focus
| 2. Reentrant phenomenon/Reentrant loop
74
Atrial flutter, definition
Reentry loop in atria
75
Possible locations of supraventricular tachycardias
AV node, atria
76
Common causes of multifocal atria tachycardia (3)
Lung disease
Theophylline toxicity
Hypoxemia
77
Average BPM of atrial flutter with 2:1 conduction
150
78
Average range of AV nodal reentrant tachycardia
160-200
79
Upper limit of normal QRS duration
120ms
80
Definition of paroxysmal atrial tachycardia, PAT
Ectopic atrial focus usurping the SA node
81
Common arrhythmia in digoxin toxicity
PAT
82
Most common ventricular arrhythmia
PVCs
83
Definition of unifocal PVC
Arises from the same location in the ventricle every time
84
Definition of bigeminal PVC
PVC that occurs every other beat
85
Short bursts of consecutive PVCs
Salvos of v-tach
86
Management of torsades
1. Magnesium sulfate - decreases calcium influx
1-2gm IV over 1-2 min, repeat in 5-15min; then 1-2gm/hr (3-10mg/min) drip
Danger of hypermagnesemia → depressed neuromuscular function and respiratory drive, so monitor closely
Supplement with K+
2. Isoproterenol - Increases HR / AV conduction
2-8 mcg/min
Target HR > 90 bpm
3. Overdrive Pacing - Atrial > Ventricular pacing
Goal HR 90-120
Note: Not a treatment for TdP, but useful in maintaining sinus rhythm
4. Defibrillation / synchronized cardioversion - Patient in extremis
5. Lidocaine (a class Ib antiarrhythmic drug) shortens the QT interval and may be effective especially for drug-induced torsades de pointes.
*AVOID amiodarone and procainamide, which may worsen prolonged QT
87
SVT with abberancy aka
Wide SVT
SVT with LBBB
SVT with RBBB
SVT with accessory pathway ie WPW
88
First step in evaluating wide SVT
Though shalt not attempt to interpret an EKG without looking at a patient's prior tracings.
89
Most common way to distinguish aberrantly conducted SVT with V-tach
Locate the AV dissociation
| Are ventricles firing without atrial input? --> vtach
90
Narrow complex tachycardia >150 suggests
AV nodal reentry tachycardia
91
EKG pearl
Narrow complex tachycardia is always supraventricular in origin
92
EKG Commandments
I. Part A: Thou shalt not overinterpret the EKG
Part B: Thou shalt not underinterpret the EKG
II. Beware the mischievous EKG machine or, in these more advanced times, the computer. Don't even think of allowing the computer to interpret the EKG for you. If you do, you do so at your own peril.
III. Beware the treacherous technician or the grubby medical student. They mean no harm, but they can inadvertently misplace leads or improperly adjust the settings, resulting in the creation of faulty data.
IV. Thou shalt not attempt to interpret an EKG without a patient's prior tracings, if you can get your hands on one. Looking at an old EKG will make your interpretation of the new one easier and more likely accurate.
V. Be cautious of the pernicious patient. That means to be cautious of artifacts that might appear on the EKG as a result of the patient hiccuping, coughing or shaking.
93
The delay that occurs between atrial and ventricular activation occurs where?
Within the AV node itself
94
First degree AV block (PR>200 ms) might be normal in
a well trained athlete
95
Common causes of first degree AV block
```
BB
CCB
Clonidine
Aging
Ischemic heart disease
Less common: athletes, amyloid, sarcoid, hemachromatosis
```
96
Three types of second degree AV block
Mobitz I
Mobitz II
High grade AV block
97
Untreated Mobitz II can lead to
Complete heart block
98
Definition of high grade AV block
Multiple P waves needed to produce a QRS complex
99
When a QRS occurs in a patient with 3rd degree/complete heart block, it is the result of
Escape mechanism firing below the AV node
100
Why are certain escape rhythms (occurring below the AV node) narrow, and others wide?
If the escape focus is high, is the Bundle of His, the QRS is likelier to be narrow. If the escape focus is low, in the bundles or ventricular myocardium is usually involved, lending to a wider QRS complex
101
In RBBB, the first upright R wave in V1, which is smaller than the second upright R wave, is caused by
Depolarization of the intraventricular septum
102
In RBBB, the downward S wave in V1 represents
Depolarization of the left ventricle
| S wave is down bc impulse traveling away from V1, V2
103
In RBBB, R' wave is caused by
Depolarization of RV
104
Additional finding to remember in RBBB other than RSR'
Slurred terminal S wave in V6 representing late right ventricular activation
105
Difference between incomplete and complete RBBB
QRS >120 ms
106
Hemiblocks can only occur in the
Left bundle, because the left bundle is composed of two separate pathways aka fascicles
If both fascicles are blocked --> LBBB
107
Left anterior fascicular block is noted by
QRS normal in duration (<120ms)
Left axis deviation
Q wave in AVL
108
Left posterior fascicular block is noted by
QRS normal in duration (<120ms)
Right axis deviation
Q wave in lead I
109
Where can Q waves be normal?
V4-V6, if small;
| Pathological Q waves are always wide and deep
110
Q waves in II, III, AVF indicate
Previous inferior wall MI
111
Q waves in I and AVL indicate
Previous lateral wall MI
112
A bifascicular block is defined by
RBBB with one of the left fascicular blocks
113
Define trifascicular block
First degree AV block with RBBB and LAFB, or RBBB and LPFB
114
Define the ST segment
End of QRS to beginning of T wave
| ST segment normally travels horizontally on the baseline of the EKG
115
T wave inversion with upright QRS suggests
Myocardial ischemia;
| Symmetric T wave inversion is more ominous than asymmetric
116
Persistent ST elevation might be a sign of
Aneurysm
117
Leads V1 and V2 are looking at what sections of the heart
RV and through to the posterior wall of the left side of the heart
118
What leads are used to diagnose a LV posterior MI?
V1 and V2
119
Acute posterior wall MIs appear with:
ST depression with upright T waves in V1, V2
| *Whatever happens in the backside of the heart will be seen in reverse
120
EKG Pearl
Posterior wall infarctions often come with concurrent inferior and sometimes lateral wall MIs
121
Artery most likely to infarct without EKG changes
Left circumflex artery
| Known as the electrocardiographic blind spot
122
Q waves are normal in
AVR
123
If you suspect an old anteroseptal myocardial infarction, do what to check?
Move the V leads down an intercostal space and repeat the EKG;
If the Q waves are still present in V1-V3, there is an old anteroseptal infarct
124
Rhythms that originate in the AV node are defined as
Junctional rhythms
125
PAILS pneumonic for reciprocal changes
```
Posterior goes to anterior
Anterior goes to inferior
Inferior goes to lateral
Lateralgoes to septal
Septal goes to posterior
```
126
U waves on EKG, think
Hypokalemia
127
Explain the QTU prolongation in hypokalemia
QT prolongation occurs not as a result of lengthening of of the time interval from the beginning to QRS to the end of the T wave, but because of the addition of a prominent U wave at the end of the T-wave.
128
Progression of prolonged QT leads to
Torsades des pointes
129
MOA spironolactone
Potassium sparing diuretic
130
Besides peaked T waves, what are other signs of hyperkalemia on EKG?
Flattening P waves
| PR interval lengthening
131
Progression of QRS widening leads to
Ventricular fibrillation
132
What do you see on an ekg with hypocalcemia?
Lengthening of time between QRS and T waves
133
What do you see on an ekg with hypercalcemia?
Shortening of QT interval (beginning of Q to beginning of T)
134
Severe hypomagnesemia on ekg manifests as
Torsades des pointes
135
EKG findings in pericarditis are ST elevations in every lead except
AVR
136
Class IA antiarrhythmic drugs
Quinidine
Procainamid
Disopyramide
--Prolong QT
137
What is Schamroth's sign?
Sign of significant lung disease:
Flattening of P, QRS and T waves in lead I;
S waves in lateral precordial leads (V5, V6)
