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EKG Deck Flashcards

1
Q

Why do different leds record different electrical currents coming from the heart?

A

Different leads record at different positions on the body, each records current at different vecotr angles

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2
Q

If a positive current (aka depolarization) is travelling toward a lead…..

EKG will show

A

there will be a positive deflection

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3
Q

If a positive current (aka depolarization) is travelling away from a lead…..

EKG will show

A

there will be a negative deflection

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4
Q

If a negative current (aka depolarization) is travelling away from a lead…..

EKG will show

A

there will be a positive deflection

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5
Q

Where are all the locations of the 12 leads of an EKG?

A
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6
Q

What are the four main events in ventricular depolarrization?

A
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7
Q

What are some of the features of sequences withing the cardiac cycle?

A

Long PR interval – abnormality in AV nodal function

Long QRS duration – abnormality in bundle branch function

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8
Q

Wat are two defining features of serial cardiac cycles?

A

rate and rhythm

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9
Q

Two types of ectopic beats?

A
  • Ectopic beats – premature or extra heart beat
    • Atrial ectopic beats – morphology of ectopic beat is similar to the normal heart beats
    • Ventricular ectopic beats – morphology of ectopic beat is vastly different compared to the normal heart beat (i.e. elongated and elevated QRS complex)
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10
Q

Two types of anomalities of serial cardiac cycles?

A

ectopic

arrhythmias

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11
Q

what are EKG paper dimensions?

A
  • Small box = 1mm x 1mm = 0.04sec x 0.04sec = 40ms x 40ms
  • Big box = 5mm x 5mm = 0.20sec x 0.20sec = 200ms x 200ms
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12
Q

Three ways to measure heart beat from EKG paper?

A

count off, six second, and divsion method

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13
Q

The “Count Off” Method

A
  • The “Count Off” Method – used with regular rhythms
    • HR = 60s / (0.2 x number of big boxes)
    • Start at an R wave and count off to next R wave
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14
Q

The Six Second Method

A
  • The Six Second Method – used with irregular rhythms
    • HR = number of R-R intervals in six seconds x 10
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15
Q

The Division Method

A
  • The Division Method – used with rapid and regular rhythms
    • HR = 1,500 / mm distance between R-R intervals
    • HR = 60,000 / ms between R-R intervals
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16
Q

What are normal intervals on the EKG?

  • r-r
  • p-r
  • qrs
A
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17
Q

What do EKG axis and horizontal/transition analysis indicate?

A

Provides information on ventricular size, conduction, hypertrophy, and damage

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18
Q

What vector directions indicate normal, left, and right ventricular dominance?

A
  • Ventricular dominance
    • Normal – between -30 degrees and +90 degrees
    • Left axis deviation – anything more negative than -30 degrees
      • Left ventricular hypertrophy
    • Right axis deviation – anything more positive than +90 degrees
      • Right ventricular hypertrophy
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19
Q

Calculating the QRS Frontal Plane Axis

Isoelectric method?

A
  • Find the isoelectric lead and draw a line
  • Find a lead perpendicular to the line
  • Place vector in the direction with positive deflecting leads
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20
Q

Calculating the QRS Frontal Plane Axis

Interpolation method?

A
  • If no isoelectric lead is present, place vector in the quadrant defined by leads I and aVF
  • Narrow down with other leads whose perpendiculars divide up the quadrant of interest
  • Interpolate to within 15 degrees
21
Q

Horizontal Plane Transitions

What does it look at?

A

Transitions examines ventricular dominance in the horizontal plane by observing the “transition” from negative QRS to positive QRS when moving from V1 to V6

22
Q

Horizontal Plane Transitions

Method?

A
  • If V1 is negative, look at leads towards V6 to find the FIRST isoelectric-looking lead (may be between two leads if one lead is more negative and following lead is more positive)
    • If V1 is positive, you cannot calculate the transition because the isoelectric point falls outside the scope of the pericordial leads (simply note that there are anterior forces)
  • Normally, the isoelectric lead will fall between V2 and V5, but NOT the actuall V2 or V5 lead.
  • If the isoelectric point is V1 or V2, the perpendicular of the transition lead has more anterior forces (the perpendicular points more anteriorly than normal)
  • If the isoelectric point is V5 or V6, the perpendicular of the transition lead has more posterior forces (the perpendicular points more posterior than normal)
23
Q

What does a bundle branch block mean in terms of depolarization?

A

left and right ventricles depolarize separately

24
Q

How is a bundle branch block identified on the EKG?

A
  • QRS > 0.12 seconds or 3 small boxes
  • Last 0.4 seconds determine the terminal vector
25
Q

How is a right bundle branch block identified on the EKG?

  • What is the terminal vector like?
  • Which venticle vector is unmasked?
  • Can you read left ventricular hypertrophy with an RBB?
  • Can you read infarct with an RBB?
A
  • RBBB – terminal vector is anterior and rightward
    • Because RV is contracting later, the LV vector is unmasked because the summation of the vectors is no longer superimposed
    • Cannot read LVH
    • Can read infarct
26
Q

How is a left bundle branch block identified on the EKG?

  • What is the terminal vector like?
  • Can you read left ventricular hypertrophy with an LBBB?
  • Can you read infarct with an LBBB?
A
  • LBBB – terminal vector is posterior and leftward
    • LV vector is abnormal, so cannot read hypertrophy or infarct
27
Q

What direction is the T-wave for BBB?

A
  • In BBBs, the T wave always points in the opposite direction of the summative QRS vector
28
Q

What does ventricular hypertrophy mean?

A
  • Ventricular hypertrophy – too much left or right ventricular muscle
29
Q

What does LVH do the QRS vector?

What does RVH do to the QRS vector?

What happens to the T-wave in ventricular hypertrophy?

A
  • LVH alters the magnitude of the summative QRS vector (normal summative QRS vector already points leftward)
    • S (V1 OR V2) + R (V5 OR V6) ≥ 35mm
    • R in aVL ≥ 11 mm
  • RVH alters the direction of the QRS vector (very abnormal for RV to be hypertrophied)
    • Right axis shift + anterior forces
  • In VH, the T wave always points in the opposite direction of the summative QRS vector
30
Q

What is a myocardial infarction scar?

A
  • Myocardial infarction scar – death of a large segment of left ventricular muscle
31
Q
  • How can you detect a past MI on an EKG?
  • Acute MIs?
A
  • Past MI indicated if Q wave ≥ 0.04 seconds or ≥ 0.01 mV (1 little box) on two or more contiguous leads
  • Acute MIs have distinctive ST-T elevations
32
Q
  • What leads and coronary arteries are associated with the inferior and inferiorposterior?
A
  • RCA: inferior and inferoposterior
    • Leads II, III, aVF
33
Q

What leads and coronary arteries are associated with the anteropseptal, septal, anterior, and anterolateral?

A
  • LAD: anteroseptal, septal, anterior, anterolateral
    • Precordial leads V1-6
34
Q

What leads and coronary arteries are associated with the lateral, anterolateral, and high lateral?

A
  • LCx: lateral, anterolateral, high lateral
    • Leads I, aVL, and precordial leads V5-6
35
Q

Define ischemia and infarction of the heart.

A
  • Ischemia – temporary with no muscle death
  • Infarction – persistent with muscle death and scar formation
36
Q

In ischemia of the heart, how long doe EKG abnormalities and chest pain last? What kind of change do you see with ischemia?

A
  • Ischemia – temporary with no muscle death
    • EKG abnormalities/CP last for less than 20 minutes
    • ST depression – transient
37
Q

How long do EKG abnormalities and chest pain last in infarction? What are the two types and how do they appear in the EKG?

A
  • EKG abnormalities/CP lasts for more than 20-30 minutes
  • Two Types:
    • Non-ST elevation MI (NSTEMI) usually presents with ST depression
    • ST elevation MI (STEMI) – the junction (J point) of the ST segment is above baseline
38
Q

If you see elevated ST segments in:

  • V1 - V4, what does that indicate?
  • II, III, aVF?
A
  • Elevated ST segments:
    • V1-V4 = anterio-septal
    • II, III, aVF = inferior wall
39
Q

What is the MI progression in an EKG from normal → acute → hours → days 1-2 → days later → weeks later?

40
Q

How does pericarditis appear in the EKG?

  • What age group would this appear in the differentials for?
    *
A
  • Pericarditis
    • Diffuse (meaning present in multiple leads) and widespread ST elevation AND PR segment depression
    • If EKG abnormalities are present in a younger person, this should be on differential because younger individuals do not often have MIs
41
Q

In hyerkalemia -

  • What are the changes on the EKG?
  • What occurs electrophysiologically?
A
  • Hyperkalemia – ECF/blood becomes more + and increases K+ conductance → increased RMP
    • Morphological features: tall-peaked Tw and widened QRS
    • Electrophysiology:
      • Due to more positive membrane potential (-60mV compared to normal -90mV) from increased serum K+ → more Na+ channels are inactivated due to the inactivation gate still being closed → Ca++ dependent depolarization rather than Na+ dependent → slower and wider QRS
      • Faster repolarization because of increased serum K+ (mechanism unknown)
42
Q

In hypokalemia -

  • What are the changes on the EKG?
  • What occurs electrophysiologically?
A
  • Hypokalemia – ECF/blood becomes more (-) and decreases K+ conductance → decreased RMP
    • Lowers RMP (sodium channels are unaffected) → cells are hyperpolarized → longer QT(U) interval
43
Q

How do EKGs appear in hyperkalemia and hypokalemia?

A

*Focus only on hyper and hypokalemia*

44
Q

What are 5 conditions that cause ST-T wave changes?

A
  • Ischemia/Infraction
  • Pericarditis
  • Metabolic abnormalities (Hyperkalemia and hypokalemia)
    • Also some drugs like digoxin
  • Conduction and Distubrances
    • T-wave inversion
  • Hypertrophy
    • T-wave inversion
45
Q

Describe the duration of chest pain and when it would occur for the following conditions:

  • Non-occlusive CAD
  • Stable Angina
  • Unstable Angina
  • Non ST-elevation MI (NSTEMI)
  • ST-elevation MI (STEMI)
A
  • Non-occlusive CAD
    • NO chest pain (CP)
  • Stable Angina
    • CP < 15 minutes (mainly exertional, predictable)
  • Unstable Angina
    • CP < 15 minutes (@ rest and exertional)
  • Non ST-elevation MI (NSTEMI)
    • CP >20-30 minutes
  • ST-elevation MI (STEMI)
    • CP > 20-30 minutes
46
Q

Describe the EKG changes for the following conditions:

  • Non-occlusive CAD
  • Stable Angina
  • Unstable Angina
  • Non ST-elevation MI (NSTEMI)
  • ST-elevation MI (STEMI)
A
  • Non-occlusive CAD
    • Stable pattern +/- ST-T wave abnormalities
  • Stable Angina
    • Transient ST depression or nothing
  • Unstable Angina
    • Dynamic ST changes +/- T wave inversions
  • Non ST-elevation MI (NSTEMI)
    • Persistent ST depression +/- T wave inversions
  • ST-elevation MI (STEMI)
    • ST elevation
47
Q

Describe if Troponin I is released for the following conditions:

  • Non-occlusive CAD
  • Stable Angina
  • Unstable Angina
  • Non ST-elevation MI (NSTEMI)
  • ST-elevation MI (STEMI)
A
  • Non-occlusive CAD
    • No Troponin I
  • Stable Angina
    • No Troponin I
  • Unstable Angina
    • No Troponin I
  • Non ST-elevation MI (NSTEMI)
      • Troponin I
  • ST-elevation MI (STEMI)
      • Troponin I
48
Q

Describe the plaque morphology for the following conditions:

  • Non-occlusive CAD
  • Stable Angina
  • Unstable Angina
  • Non ST-elevation MI (NSTEMI)
  • ST-elevation MI (STEMI)
A
  • Non-occlusive CAD
    • Stable plaque; 50-70% stenosis; no thrombus
  • Stable Angina
    • Stable plaque; 70-90% stenosis; no thrombus
  • Unstable Angina
    • Unstable/ruptured plaque; subtotal occlusion (>90% stenosis); white thrombus (platelet aggregation)
  • Non ST-elevation MI (NSTEMI)
    • Unstable/ruptured plaque; subtotal occlusion (>90% stenosis); white thrombus (platelet aggregation
  • ST-elevation MI (STEMI)
    • Unstable/ruptured plaque; TOTAL occlusion (100% stenosis); red thrombus (fibrin formation)

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