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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
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?
* 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
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?
* LBBB – terminal vector is posterior and leftward * LV vector is abnormal, so cannot read hypertrophy or infarct
27
What direction is the T-wave for BBB?
* In BBBs, the T wave always points in the opposite direction of the summative QRS vector
28
What does ventricular hypertrophy mean?
* Ventricular hypertrophy – too much left or right ventricular muscle
29
What does LVH do the QRS vector? What does RVH do to the QRS vector? What happens to the T-wave in ventricular hypertrophy?
* 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
What is a myocardial infarction scar?
* Myocardial infarction scar – death of a large segment of **left** ventricular muscle
31
* How can you detect a past MI on an EKG? * Acute MIs?
* 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
* What leads and coronary arteries are associated with the inferior and inferiorposterior?
* RCA: inferior and inferoposterior * Leads II, III, aVF
33
What leads and coronary arteries are associated with the anteropseptal, septal, anterior, and anterolateral?
* LAD: anteroseptal, septal, anterior, anterolateral * Precordial leads V1-6
34
What leads and coronary arteries are associated with the lateral, anterolateral, and high lateral?
* LCx: lateral, anterolateral, high lateral * Leads I, aVL, and precordial leads V5-6
35
Define ischemia and infarction of the heart.
* Ischemia – temporary with no muscle death * Infarction – persistent with muscle death and scar formation
36
In ischemia of the heart, how long doe EKG abnormalities and chest pain last? What kind of change do you see with ischemia?
* Ischemia – temporary with no muscle death * EKG abnormalities/CP last for less than 20 minutes * ST depression – transient
37
How long do EKG abnormalities and chest pain last in infarction? What are the two types and how do they appear in the EKG?
* 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
If you see elevated ST segments in: * V1 - V4, what does that indicate? * II, III, aVF?
* Elevated ST segments: * V1-V4 = anterio-septal * II, III, aVF = inferior wall
39
What is the MI progression in an EKG from normal → acute → hours → days 1-2 → days later → weeks later?
40
How does pericarditis appear in the EKG? * What age group would this appear in the differentials for? *
* 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
In hyerkalemia - * What are the changes on the EKG? * What occurs electrophysiologically?
* 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
In hypokalemia - * What are the changes on the EKG? * What occurs electrophysiologically?
* 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
How do EKGs appear in hyperkalemia and hypokalemia?
\*Focus only on hyper and hypokalemia\*
44
What are 5 conditions that cause ST-T wave changes?
* Ischemia/Infraction * Pericarditis * Metabolic abnormalities (Hyperkalemia and hypokalemia) * Also some drugs like digoxin * Conduction and Distubrances * T-wave inversion * Hypertrophy * T-wave inversion
45
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)
* 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
Describe the _EKG changes_ for the following conditions: * Non-occlusive CAD * Stable Angina * Unstable Angina * Non ST-elevation MI (NSTEMI) * ST-elevation MI (STEMI)
* 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
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)
* 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
Describe the _plaque morphology_ for the following conditions: * Non-occlusive CAD * Stable Angina * Unstable Angina * Non ST-elevation MI (NSTEMI) * ST-elevation MI (STEMI)
* 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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