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EKG Flashcards

1
Q

Side of small boxes

A

0.04 s

1 mm

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2
Q

Large box size

A

0.20s

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3
Q

What is the best method for checking rate on an irregular rhythm?

A

6 second rule

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4
Q

What are the 4 ways to determine rate?

A

1500/small boxes
300/large boxes
300, 150, 100, 75, 60, 50
6 second rule

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5
Q

When you are looking at P waves, which two leads are best?

A

V1 and Lead 2

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6
Q

If all the P waves don’t match what should you be thinking about?

A

Wandering pacemaker or multifocal atrial tachycardia

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7
Q

What is the normal amplitude of P waves?

A

<2.5 mm (lecture 1 says <2mm)

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8
Q

What are you thinking about if the P wave is greater than 2mm?

A

Atrial hypertrophy

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9
Q

What are you thinking about if there is not a P for every QRS and vice versa?

A

Irregular rhythm, escape or premature beats

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10
Q

If there are no P waves what should you be thinking about?

A

Escape rhythms, A. Fib, ventricular rhythms, or sinus arrest

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11
Q

What does it mean if the T wave is peaked?

A

Hyperkalemia

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12
Q

What does it mean if the P wave is flat?

A

Hypokalemia

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13
Q

What do U waves indicate?

A

Hypokalemia + decrease in Mg

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14
Q

If the PR interval is not normal, what should you be thinking about?

A

Blocks or WPW

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15
Q

If the QRS interval is wider than 0.12s what should you be thinking of?

A

BBB, V. Fib, or hyperkalemia

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16
Q

QT interval should be….?

A

Less than half the R-R interval

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17
Q

What is the J point?

A

Where the QRS complex ends and the TS segment begins

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18
Q

Hypercalcemia will show up how on an EKG?

A

Shortened QT interval

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19
Q

Hypocalcemia will show up how on an EKG?

A

Prolonged QT/ST

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20
Q

What is the infarction triad?

A

Ischemia (reversible)
Injury
Necrosis (irreversible)

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21
Q

What is a strain pattern?

A

A pressure overload that leads to sustained delayed repolarization of the St segment (down-sloping)
Best seen in V5 and V6

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22
Q

What is the Rule of 35?

A

Determining hypertrophy (left ventricular hypertrophy)
Measure the DEEPEST S wave in V1 or V2
+
Measure the TALLEST R wave in V5 or V6

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23
Q

What determines an ST elevation?

A

An increase of 1 mm in two are more CONTINUOUS leads

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24
Q

What are some causes of RAH?

A 
Pulmonary HTN 
Congenital heart disease 
Tricuspid or pulmonary valve disease 
Pulmonary Embolism 
Seen with RVH
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25
How do the P waves differ between RAH and LAH?
The different between left and right atrial hypertrophy is that the RAH if initial component of diphasic P wave is larger in lead V1 LAH if terminal component of diphasic P wave is larger in lead V1 Basically where is in the P wave in lead V1 is it larger, beginning or end?
26
Why is Left ventricular Hyptertrophy most common?
Systemic HTN
27
What continuous leads are you looking in for anterior infarction?
Anterior = V3, V4
28
What leads are you looking at for septal infarction?
Septal = V1 + V2
29
What leads are you looking in for inferior infarction?
2, 3, +aVF
30
What leads are you looking at for lateral infraction?
1 + aVL + V5 + V6
31
Which lead is not used to determine infarction?
aVR
32
Where are you most likely going to see a RBBB?
Wide QRS + Broad S wave in 1, V5, V6
33
What are you likely to see on the EKG with LBBB?
``` Wide QRS + Broad R wave in lead 1, aVL, and V5 or V6 + Deep S wave in V1 and V2 ```
34
What causes the “scooped out” ST segments?
Digitalis
35
What is the difference on the EKG between sinus arrest and sinus block?
Both are bradycardic due to the pause The arrest has a change in RR interval in attempts to compensate The block has preserved RR interval, as if there was no pause
36
What are you looking for in order to dx Wolff-Parkinson-White?
Delta wave in the QRS complex
37
What are you looking for on the EKG with PE?
SINUS TACH IS THE MC FINDING S1Q3T3 Large S in Lead 1 Large Q in Lead 3 (with inverted T wave)
38
What is Brugada Syndrome?
Syncope with sudden death Frequently inherited Looking for RBBB with ST elevation in V1-V3 Treated with cardioverter-defibrillator
39
Wellens Syndrome
Unstable angina, stenosis of the proximal left anterior descending (LAD) —> anterior wall infarction V2, V3 T wave inversion Little to no ST elevation
40
Long QT syndrome
May be genetic, medication induced, or related to medical conditions, asymptomatic to syncope, seizure or sudden death Longer than 0.44s typically considered abnormal
41
What will you see with RBBB?
Wide QRS Broad S wave in Lead 1, V5, V6 RR’ commonly seen
42
What will you see with LBBB?
Wide QRS Broad R wave in 1, aVL, and V5 or V6 Deep S in V1 and V2
43
What is your method?
1) Rhythm 2) Rate 3) Waves 4) Intervals 5) Axis 6) Hypertrophy 7) ST elevation/depression (+—> location) 8) Blocks (left or right) 9) Electrolytes 10) Pacemakers 11) Zebras
44
What can an EKG tell you?
``` Rate Rhythm Where impulse originates Conduction pathways how much electricity is being conducted to the ECG leads (high or low voltage) ```
45
What does an EKG NOT tell you?
cardiac output hemodynamic status pulse (only confirmatory for STEMI or NSTEMI)
46
What does parasympathetic activity do to the heart?
increase HR
47
What does a vagal maneuver do to HR?
decrease HR
48
What rhythms are irregular?
``` sinus arrhythmia wandering pacemaker multifocal atrial tachycardia A. fib V. fib ```
49
How long should the AT interval be?
half the distance to R-R interval (or else it might be prolonged)
50
Why are there PVCs?
the ventricular automaticity can be irritated by low oxygen levels, hypokalemia, and injury/inflammation/infarction
51
At what point do PVCs become V. Tach?
if there are 3+ in a row or 6+ in a minute
52
What causes multifocal PVCs?
severe cardiac hypoxia because several locations in the ventricles are irritated WARNING (this PVCs will all look different)
53
How does the treatment differ between organized rhythm from unorganized rhythm?
organized? cardiovert | unorganized? defibrillation
54
Why is there V. tach?
ischemic heart disease myocardial scar from previous MI can cause an ectopic electrical focus hemodynamic compromise
55
What causes Tarsades de Pointes?
two competitive, irritable foci in the ventricular myocardium d/t: -hypokalemia -hypomagnesemia -hypocalcemia -medications that block potassium channels including anti-HTN, antibiotics, and anticonvulsants -congenital long QT syndrome
56
Why does V. fib happen?
cardiac arrest there is no coordinated electrical activity in the heart no squeezing of the ventricles
57
Why do first degree heart blocks occur?
increased vagal tone (athletes) medications (antiarrhythmics) MI electrolyte disturbance
58
Which second degree heart block is more dangerous?
``` type 2 (mobitz type 2) regular with irregularity ```
59
Mobitz type 1 has which type of rhythm?
irregularly regular
60
Why do we care about axis deviation?
physical movement of the heart hypertrophy (toward) infarction (away)
61
What is the difference between physiological left axis and pathologic?
Physiological left axis: 0- -45 (common in athletes and obese pts) Pathological left axis: -45 - -90 (disease process, suggests left anterior hemiblock, pts are 4 times more likely to arrest with a hemiblock and chest pain"
62
What causes RAH?
right atrial hypertrophy - pulmonary HTN - congenital heart disease - tricuspid or pulmonary valve disease - PE - seen with RVH
63
What causes left atrial dilation?
volume overload or pressure
64
What causes LAH?
HTN AMI mitral or aortic valve stenosis LVH
65
What causes LVH?
more common due to systemic HTN increased pressure or volume found in mitral and aortic stenosis, cardiomyopathy, HTN
66
Can an EKG every rule out an MI?
NO
67
What are the EKG signs of ischemia? (stable angina)
inverted T wave or ST depression
68
Q wave
necrosis usually dx of MI significant if 1 mm wide or 1/3 amp of the QRS complex
69
Which leads would confirm a lateral MI?
lead 1 + AVL + V5 + V6
70
Which leads would confirm an inferior MI?
lead 2, lead 3, and AVF
71
Which leads would confirm a septal MI?
V1 + V2
72
Which leads would confirm an anterior MI?
v3 + v5
73
Posterior infarct
opposite side of anterior Tall R waves in V1 - V3 ST depression

EKG (1 decks)

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