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Cardio Block > EKG Interpretation 1 and 2 > Flashcards

EKG Interpretation 1 and 2 Flashcards

1
Q

What are the 6 goals of EKG evaluation?

A
  1. diagnose arrhythmia
  2. diagnose conduction blocks
  3. evaluate chamber enlargement
  4. ischemia
  5. electrolyte disturbance
  6. non-cardiac disease manifestations
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2
Q

Where is the SA node located and what is its inherent conduction rate?
What does it initiate?
What wave on the EKG is associated with it?

A

It is in the upper-posterior RA.
It depolarizes at 60-100 bpm.
It initiates atrial systole (squeezing blood into the ventricles)
It corresponds to the P wave on the EKG (SA to AV node)

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3
Q

Where is the AV node located and what is its inherent conduction rate?
What does it initiate?
What does it correspond to on the EKG?

A

Located near the inferior interatrial septum.
It has inherent conduction of 40-60bpm.
In sinus conduction, it serves as a delay to allow time for blood to enter ventricles before initiating ventricular systole.
AV node correlates to PR segment on the EKG

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4
Q

What are the conduction fibers of the ventricle called?

What does their depolarization correspond to on the EKG?

A

His bundles and Purkinje system (LBB and RBB)
Left bundle divides into left anterior and left posterior and is supplied by LAD artery.
Corresponds to QRS complex on the EKG

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5
Q

What is occurring in the heart during:

  1. P wave
  2. PR segment
  3. QRS wave
  4. T wave
  5. U wave
A
  1. atrial depolarization (SA to AV) or P’ if its an ectopic atrial site to AV
  2. Delay at AV node (due to Ca not Na)
  3. ventricular depolarization- LBB and RBB
  4. ventricular repolarization
  5. delayed repolarization (seen in hypokalemia)
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6
Q

What is the paper speed for EKG?
What is each “little box”?
What is each “large box”?
What are the axis of the paper?

A

25mm/s
Each little box is 1mm and 40 msec and each large box is 5mm and 200 msec
Horizontal : time
Vertical : voltage (each 10mm is 1 mV)

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7
Q

What are the limb leads? What plane do they look at the heart from?

A

I, II, III, AVF, AVL, AVR and they look at the heart from the frontal plane

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8
Q

What are the precordial leads and what plane do they look at the heart from?

A

V1-V6 and they look at the heart from the vertical plane (front to back)

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9
Q

If an impulse is traveling toward a lead, what will be the direction of the deflection on the EKG?

A

+

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10
Q

What are the 8 steps for reading an EKG?

A
  1. Name
  2. Rate
  3. Rhythm
  4. Axis
  5. Intervals
  6. hypertrophy
  7. infarctions
  8. important patterns
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11
Q

How do you calculate rate?

A

Find a QRS on a dark black line from a large box.
300, 150, 100, 75, 60, 50
If below 50, use the 3 second marks to figure out how many peaks were in 6 seconds and multiply by 10.
OR count the number of peaks on the rhythm strip of the sheet (10 seconds) and multiply by 6

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12
Q

What is the inherent conduction rate of:

  1. ventricle
  2. junctional rhythm
  3. normal sinus rhythm
  4. sinus tachycardia
  5. supraventricular/ventricular tachycardia
  6. Flutter
  7. Fibrillation
A
  1. 20-40 bpm
  2. 40-60 bpm
  3. 60-100 bpm
  4. 100-150 bpm
  5. 150-250 bpm
  6. 300 integers (300, 150, 100)
  7. 350+
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13
Q

What is “normal sinus rhythm?

A

regular rate of 60-100 bpm.

P wave with the same morphology preceding each QRS complex

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14
Q

Describe bradycardia with idioventricular rhythm.

A

It goes at a rate of 20-40 bpm with no P waves and wide QRS. This is because there is no SA node, AV node stimulation or His/bundle branch. Instead of depolarizing at the same time, the ventricle will depolarize more slowly.

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15
Q

What is junctional rhythm?

A

The “pacemaker” is the AV junction instead of the SA node so the rate will be 40-60 bpm.
There will be no P waves because there is simultaneous depolarization of atria and ventricle
Low in junction: P wave inverted/ after QRS
High in junction: P wave inverted before QRS

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16
Q

What are 5 common causes for the heart switching to junctional rhythm?

A
  1. hypoxia
  2. ischemia
  3. digitalis toxicity (Digoxin OD)
  4. electrolyte abnormality (hypokalemia)
  5. chronic lung disease
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17
Q

What is the difference between sinus bradycardia and wandering atrial pacemaker?

Who are these conditions usually seen in?

A

Sinus bradycardia is still conducting from the SA node, just slower. All the P waves will look the same and be followed by QRS.

Wandering atrial pacemaker- different ectopic pacemakers in the atrium are firing to the AV node so the P waves will look different. They will still all be followed by QRS

Both can be normal and seen in young healthy athletes

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18
Q

What is multifocal atrial tachycardia?

What 3 pathological states might you see MAT in?

A

Three different P wave morphologies followed by a QRS complex at a rate greater than 100 bpm (below 100 it is wandering atrial pacemaker).

  1. chronic lung disease
  2. coronary artery disease
  3. congestive heart failure
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19
Q

Describe the waveform of sinus tachycardia.

A 
It has a rate between 100 and 150 bpm due to conduction from the SA node. 
It has the same morphology P followed by QRS
I can be due to:
1. exercise 
2. infection
3. MI
4. PE
5. sepsis 
6. obesity 
7. hyperthyroidism
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20
Q

Describe the rate of paroxysmal supraventricular tachycardia.

What are the 2 major types?

What is the rhythm?

A

PSVT has a regular rhythm between 150-250bpm originating in the atria.

  1. AVNRT- av node reentry tachycardia
  2. AVRT- AV reciprocating tachycardia (associated with WPW)
    PSVT usually involves a reentry pathway that has been triggered by a premature atrial contraction.
    This results in delayed conduction to ventricles and wide QRS
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21
Q

What is atrial tachycardia?

  1. HR
  2. Rhythm
  3. P wave
  4. PR interval
  5. QRS
A

Regular rhythm that is fast because of a reentry pathway in the atria at a focus other than the SA node.
P wave is different from SA node P wave, but is regular and conducts 1:1 with the ventricle.

  1. 150-250
  2. regular
  3. abnormal P before each QRS
  4. <.12
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22
Q

What is the cause of atrial flutter?
What is the rate?
What determines ventricular contraction?
What can cure atrial flutter?

A
  1. Reentry pathway in the atrium that causes the atria to have a rate that is an integer of 300.
  2. 300, 150, 100, 75
  3. The AV node determines the ventricular contraction and fires in a 2:1 or 4:1 blocking some of the atrial conduction
  4. cured by ablation (cryo or radiofreq)
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23
Q

If the HR is 150, what should one view as the prime reason?

A

Atrial flutter with a 2:1 block rather than a sinus tachycardia

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24
Q

What is the rhythm of atrial fibrillation due to?
What is the rate of atrial contraction?
What is the ventricular rate?
What does the waveform look like?

A

It is due to multiple reentry pathways in the atria that cause irregular rate over 350.
AV node blocks most impulses and leads to a ventricular contraction rate of 60-140.
It looks irregularly irregular because there is no coordination between atrial and ventricular contraction.
No P waves, bc the chaos in the atrium can’t sustain contraction

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25
Q

What is the regular rate of a ventricular tachycardia?
What is characteristic about the waveform?
What is the cause?

A

120-220 bpm and the QRS waves are really wide because the ventricle has to depolarize itself by reentry instead of using conduction pathways.

It is caused by hypoxia, hypokalemia, ischemia

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26
Q

What is ventricular fibrillation?
What does the waveform look like?
What is the treatment?

A

V fib is pulseless, chaotic contraction of the ventricle caused by ischemia or hypoxia.
It looks like a “bag of works”
The patient needs to be shocked out of it.

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27
Q

What is a premature beat?

What are the 2 kinds?

A

Irregular beats that occur when another focus takes over as the pacemaker for a beat and then returns to SA conduction.
PAC - premature atrial contraction
PVC or VPB- premature ventricular contraction (ventricular premature beat)

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28
Q

What is bigeminy?

A

When a premature beat occurs at a fixed rhythm.

Normal beat, premature beat, normal beat, premature beat

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29
Q

What is sinus arrhythmia?

A

variation in rhythm with respiration but it is really small and not clinically significant

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30
Q

What is meant by axis?
What is the normal axis?
What is LAD (left axis deviation)?
What is RAD (right axis deviation)?

A

The estimate of the angle of the hearts primary electrical vector.
Normal = -30 to 90
LAD = 90 ( more positive)

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31
Q

What gives you the correct axis?

A

the isoelectric lead (QRS height with equal positive and negative deflection)

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32
Q

Lead I protects the _____ axis. If QRS is negative in lead I then there is a _____________.

A

Right, right axis deviation

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33
Q

Lead II protects the _____ axis. If QRS is negative in lead II, then there is a ___________________.

A

left, left axis deviation

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34
Q

If lead I and lead II both have negative deflections, the patient has __________________________.

A

Extreme right or left deviation

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35
Q

If I and AVF are both positive, the axis is _________.

A

Normal

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36
Q

What leads tell you the axis is normal?

A

+ deflection of lead I and AVF

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37
Q

What are 9 causes of right axis deviation?

A
  1. infants/ tall thin adults
  2. RV hypertrophy
  3. chronic lung disease
  4. anterolateral myocardial infarct
  5. left posterior hemiblock
  6. PE
  7. WPW syndrome with left sided accessory
  8. atrial septal defect
  9. ventricular septal defect
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38
Q

What are 6 causes of left axis deviation?

A
  1. left anterior hemiblock
  2. emphysema
  3. hyperkalemia
  4. WPW with a right sided accessory
  5. tricuspid atresia
  6. ostium primum ASD
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39
Q

After you identify a right or left axis deviation, what do you do?

A

Find the most isoelectric lead. 90 degrees to that will be the direction of the impulse (perpendicular to the isoelectric lead)

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40
Q

What is the normal PR interval?
What is the PR interval?
Where does it begin? end?

A

The PR interval is the time between atrial and ventricular depolarization (slow conduction through the AV node).
It starts at the BEGINNING of the P wave to the beginning of the QRS complex.

It is 0.12-0.2 seconds (3-5 small blocks on the EKG)

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41
Q

What does a PR interval less than 0.12sec suggest?

What are the 3 major symptoms the patient will present with?

A

a pre-excitation syndrome where there is an accessory pathway conducting to the ventricles faster than the normal SA-AV node pathway.

Patients present with shortness of breath, palpitations and chest pain

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42
Q

What are the two major syndromes associated with short PR interval (below 0.12)?

A
  1. Wolf-Parkinson-White (WPW) where the bundle of Kent creates a delta wave indicating pre-excitation of the ventricle.
  2. Lown-Ganong-Levine which has an accessory pathway NOT associated with a delta wave due to the fact that it merges with the his-purkinje bundle below the AV node.
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43
Q

Why doesn’t Lown-Ganong-Levine syndrome have a delta wave despite the fact that it is a pre-excitation syndrome?

A

The accessory pathway meets up with the His-Purkinje bundle below the AV node

44
Q

Describe the waveform of a first degree heart block.

By itself, first degree heart blocks are __________, however they are clinically significant in the context of ______ and ________.

A

The PR segment is greater than 0.20 (delayed).
There is a P for every QRS.

By itself, first degree heart block is benign, but it is clinically significant when associated with MI (indicative of recurrent ischemia) and endocarditis (perivalvular abscess).

45
Q

What does a first degree heart block mean in the context of a person who has a myocardial infarction?

A

It means there is recurrent ischemia

46
Q

What does a first degree heart block mean in the context of a person with aortic valve endocarditis?

A

It is indicative of a perivalvular abscess that must be surgically removed.
The aortic valve is near the AV node so this is why the abscess would cause the first degree block

47
Q

What are the two types of second degree heart block?
How do they differ in waveform and location of block?
Which is more likely to progress to complete block and need a pacemaker?

A
  1. Mobitz I (Wenkebach)- prolonged PR interval that gets longer and longer and then drops a QRS (1,2, drop, 1, 2, drop). Block is in AV node.
  2. Mobitz II - constant prolonged PR (doesn’t get longer and longer like Wenkebach) with sporadic QRS drops. Below the AV node and can progress to complete heart block. Mobitz II needs a pacemaker
48
Q

What are the 6 major causes of second degree heart block? (same for mobitz one and two)

A
  1. aging
  2. endocarditis
  3. restrictive cardiomyopathy
  4. drug toxicity
  5. hyperkalemia
  6. myocarditis
49
Q

What is a third degree heart block? What does the waveform look like?
What will the rate be?

A

A third degree heart block is complete dissociation between the atria and ventricle.
On the waveform there will be no concordance between the P and QRS waves.
Rate will be bradycardia <60bpm

50
Q

If a third degree block occurs high in the AV node, what will the QRS look like? Why?

A

It will still be narrow (normal) because there will be a junctional escape rhythm.

51
Q

If a third degree block occurs low in the AV node, what will the QRS look like? Why?

A

It will be wide because the ventricle is providing the escape rhythm

52
Q

What information can the QRS interval give us?
What is the normal interval for QRS?
When does it begin and when does it end?

A

QRS interval is the time for depolarization of the ventricle. It can give information about bundle branch blocks.
It is normally 0.08 to 0.1 second (2 to 2.5 small squares on the EKG)
QRS interval is from the beginning of Q to the end of S.

53
Q

If the QRS interval is 0.1-0.12 seconds, what is this associated with?

A

Hemiblock or fasicular block (although the interval is the upper limit of normal)

54
Q

Describe the 3 main characteristics you look for in a left bundle branch block on the EKG.

A
  1. QRS wider than 0.12 (three small blocks)
  2. no S wave on lead I
  3. wide QRS and RSR’ on V5 and V6
55
Q

Why is there no S wave on lead 1 in a LBBB?

A

Because depolarization travels down the RBBB then depolarizes across the myocardium to the left. The depolarization is going directly at the + lead 1 so will only show + deflection

56
Q

Why do V5 and V6 show RSR’ in LBBB?

A

Because these leads look at the left side of the heart. When the RV depolarizes it goes from right to left and is + deflection. There is a slight deflection when the RV is done depolarizing before the LV starts depolarizing creating a second + deflection

57
Q

What are 5 most common causes of a LBBB?

A
  1. hypertension
  2. dilated cardiomyopathy
  3. hypertrophic cardiomyopathy
  4. idiopathic/degenerative
  5. coronary artery disease
58
Q

A new LBBB on an EKG is very suggestive of a recent or ongoing _______ because the _______supplies blood to the left bundle.

A

anterior MI because the left bundle is supplied by the LAD artery

59
Q

What are the 3 major things you look for on the EKG when diagnosing a RBBB?

A
  1. Wide QRS of greater than 0.12
  2. broad S wave on lead 1
  3. wide QRS and RSR’ complex on V1
60
Q

Why is there a broad S wave on lead I for a RBBB?

A

depolarization comes down the left bundle and then crosses the myocardium to depolarize the RV.
The wave is moving AWAY from lead I (a left lateral lead) so the deflection will be down (S wave) during RV depolarization.
There is still a large R wave during LV depolarization

61
Q

Why is there an RSR’ wave in lead V1 when there is a RBBB?

A

The first R wave is the depolarization of the left ventricle that is going from left to right toward the RV so it is positive.
As the LV finishes depolarizing there is a slight deflection, followed by a second R wave as the RV depolarizes

62
Q

What are the 3 main causes of RBBB?

A
  1. idiopathic/degenerative
  2. Ischemia
  3. pulmonary disease
63
Q

What is Brugada’s syndrome?

A

RBBB with ST elevation in V1-V3.

These patients are at high risk for sudden cardiac death secondary to V-fib

64
Q

What is a left anterior fascicular block (LAFB)/left anterior hemiblock (LAH)?
What is the QRS complex time?
Where does depolarization begin in this situation?

A

QRS complex between 0.1 and 0.12
The waveform looks like LBBB with left axis deviation (no S wave on lead 1)
Depolarization begins in the right heart and inferior left heart

65
Q

Why is there a large left axis deviation in LAH/LAFB?

A

the wave of depolarization is going upward to depolarize the left side of the ventricle

66
Q

What is a Left Posterior Fascicular Block (LPFB)/Left posterior hemiblock (LPH)?
What is the QRS timing?
Where does depolarization begin?

A

QRS complex between 0.1 and 0.12.
The waveform looks like LBBB but with right axis deviation.
Depolarization comes from the right heart and superior part of the left heart. The wave is going away from Lead 1 so there is an S wave (negative deflection)

67
Q

The QTc interval can show abnormalities in what?
It is calculated from the beginning of ____ wave to the ________.
What is the equation?

A

It can show abnormalities in electrolytes that regulate repolarization of the ventricle.
It starts at the beginning of the Q wave and is measured until the end of the T wave.

QTc = (QT interval)/ (sq rt RR interval)

68
Q

What is normal QTc for a man? For a woman?

A 
Man= 0.4 (two large blocks)
Woman= 0.44 (two large blocks, one small block)
69
Q

What is the major problem associated with a prolonged QTc?

A

The patient is at risk for sudden cardiac death from ventricular fibrillation

70
Q

What are the congenital syndromes associated with prolonged QTc?

A
  1. Jervell-Lange-Nielson - AR syndrome associated with deafness
  2. Romano-Ward- AD syndrome
71
Q

What are the acquired factors associated with prolonged QT?

A
  1. decreased Ca, K, Mg
  2. CNS lesion
  3. ischemia
  4. Class IA, IC, III antiarrythmias
  5. erythromycin
  6. phenothiazines
72
Q

What causes a short QTc?

A

hyper Ca, Mg, K

73
Q

What are the voltage criteria for left ventricular hypertrophy?

A
  1. aVL R wave >11mm OR
  2. V4-V6 R wave >25mm (5 large boxes) OR
  3. S wave in V1 + R wave in V5 >35mm OR
  4. S wave in V1 +R wave in V6 >35mm
74
Q

What are the potential causes of LVH?

A

It is a sign of a stiff/non-compliant heart so:

  1. hypertension
  2. constrictive pericarditis
  3. hypertrophic cardiomyopathy
  4. Infiltrative disease of myocardium
75
Q

What are the voltage criteria for right ventricular hypertrophy?

A
  1. R wave in V1 >7 mm

2. R wave in V1+ S wave in V6 >10mm

76
Q

What is RVH a sign of?

A

Increases pulmonary artery pressure due to pulmonary hypertension.

  1. asthma
  2. COPD
  3. PE
77
Q

What waveform is associated with left atrial enlargement (P mitrale)?
What are the 4 major causes of left atrial enlargement?

A

> 1mm wide and >1mm deep P wave on V1

  1. CHF (systolic or diastolic dysfunction)
  2. dilated cardiomyopathy
  3. hypertrophic cardiomyopathy
  4. mitral or aortic valve disease
78
Q

What waveform is associated with right atrial enlargement (P pulmonale)?
What are the causes?

A

Tall P wave >2.5mm in leads II, III, AVF (the inferior leads)

  1. CHF
  2. dilated cardiomyopathy
  3. hypertrophic cardiomyopathy
  4. tricuspid valvular disease
79
Q

What is ST depression indicative of?

A

ST depression describes ischemia indicating decreased blood supply to that region of the heart (specifically to the subendocardial layer of the myocardium).
It is significant if the depression is >1mm (one small box)

80
Q

What are the 4 main causes of ST segment depression?

A
  1. ischemia
  2. LVH with no strain
  3. digitalis (digoxin OD)
  4. benign
81
Q

Why is there no Q wave associated with ischemic ST depression?

A

The ischemia is lack of blood supply to subendocardial layer so there is still enough electrical activity in the tissue to no generate a Q wave.
The cells are damaged enough to lose K+ altering repolarization and depression the ST segment

82
Q

What is a T wave inversion indicative of?

A
  1. ischemia
  2. LVH with strain and abdominal pain
  3. digitalis
  4. CNS hemorrhage
83
Q

What causes the T wave to be inverted in ischemic situations?

A

Usually the ventricle repolarizes from the endocardium out to the epicardium. Therefore, repolarization is positive at all leads generating an upright T wave.
If there is ischemia or infarct, the lead looking at the damaged area will see repolarization moving away from it and the T wave will be inverted.

84
Q

What is indicated by an ST elevation?

What is clinically significant elevation?

A

Ischemia and transmural MI to the heart muscle because of a completely occluded vessel.
Significant elevation is 1mm in limb leads and 2mm in precordial leads

85
Q

What are the 8 potential causes of an elevated ST?

A
  1. MI
  2. early repolarization
  3. acute pericarditis
  4. LBBB
  5. Prinzmental’s angina (vasospasm)
  6. hyperkalemia
  7. hypothermia
  8. LVH
86
Q

What is PERSISTANT ST elevation indiciative of?

A

ventricular aneurysm (bulge) at the site of infarct

87
Q

What physiologically causes the ST segment to elevate on the EKG?

A

Transmural tissue damage due to complete arterial occlusion leaks K+.
Resting potential depends on Kin/Kout.
By increasing Kout, you elevate the ST segment.

88
Q

What happens to the ST segment when the tissue has died?

A

When the tissue dies, no more K+ is leaked and the baseline returns to normal

89
Q

What is a Q wave indicative of?

What is the dimensions on the EKG necessary to determine something as a Q wave?

A

Muscle death due to lack of blood supply.
Dead muscle cannot depolarize so what is detected is the impulse moving away from the lead.

It is pathologic if it is 1 small box wide and deeper than 1/4 of the R wave.

90
Q

A complete occlusion of a blood vessel will cause a ___________ MI that will progress over the next 24 hours to a ________ if untreated.

A

ST elevation MI to a Q wave

91
Q

What enzymes are elevated with muscle injury?

A
  1. Troponin I
  2. Creatinine Kinase
  3. CK-MB fraction
92
Q

What supplies the anterior heart vascularly?
What supplies the lateral heart?
What supplies the inferior heart?
What supplies the posterior heart?

A

Anterior- LAD
Lateral- circumflex
Inferior- RCA
Posterior- PDA (85% off RCA, 15% off circumflex)

93
Q

If there is an occlusion in the left coronary artery, what two branches get affected? What parts of the heart?

A
  1. LAD- anterior heart

2. Circumflex- lateral heart

94
Q

What leads look at the anterior part of the heart?

A

V1-V4
V1, V2 = septal
V3, V4 = anterior

95
Q

What leads look at the lateral part of the heart?

A

I, aVL

96
Q

What leads look at the inferior part of the heart?

A

aVF, II, III

97
Q

What would you see on the EKG for posterior wall MI?

A

Tall R in V1 and ST depression in V1-V2 or II, III, aVF

98
Q

What is R wave progression?

A

R wave should normally get larger as one goes across the precordium (V1-> V6)
If there is no R wave at V1 or V2, suspect an old anterior MI

99
Q

What is early repolarization?

What leads are most commonly affected?

A

It is when repolarization starts early and the T wave begins in the ST segment giving the impression of ST elevation.
It is seen in V2 and V3 and can be up to 1-3mm

100
Q

What does hypokalemia manifest as on the EKG?

A

U wave because delayed repolarization of the ventricles results in an extra repolarization wave

101
Q

What are the 3 major signs of hyperkalemia manifested on the EKG?

A

peaked T waves followed by a short QTc
Wide QRS
Flat or absent P waves

102
Q

What are the 2 ways that PE can usually present on the EKG?

A
  1. Sinus tachycardia

2. Broad S in lead 1 with a Q and inverted T in lead 3 (S1Q3T3)

103
Q

Why does PE cause a broad S in lead I?

A

It causes pulmonary hypertension, which increases the RV work causing RV dilation which presents like a RBBB.

104
Q

How does pericarditis present on the EKG?

A

Diffuse ST elevation and PR depression

105
Q

How does hypothermia present on the EKG?

A

“Osborne waves” which is an upward deflection of the 2nd half of the QRS complex

106
Q

What is the nomenclature for pacemakers?

A
  1. First letter is paced chamber (A, V, Dual)
  2. Second letter is sensed chamber
  3. Third letter is activity (triggered, inhibitory, neither)
  4. rate responsive or not

Ex. VVI- senses and paces ventricle conduction but only fires if there was no ventricular beat in the cycle
DDD- both chambers and can inhibit or trigger

Cardio Block (25 decks)

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