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CV wk1 and wk2 > Diagnostic features of EKG - disorders > Flashcards

Diagnostic features of EKG - disorders Flashcards

1
Q

EKG findings of LV hypertrophy

A
  1. Bigger R waves in Left-sided Leads (due to larger muscle mass)
    → I, aVL, V5, V6
  2. T wave can be inverted
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2
Q

EKG findings of Right Ventricular Hypertrophy

A

Big R waves in Right-sided Leads

→ V1,V2

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3
Q

EKG findings of Myocardial ischemia

A

ST depression

T wave inversion - sometimes

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4
Q

EKG findings of ischemia during acute coronary syndrome

A

T wave inversion

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5
Q

What is transmural injury and what are the

EKG findings of transmural injury

A

ST elevation

Note: Transmural injury: death of myocardial tissue that extends from the endocardium to the epicardium as a result of a myocardial infarction.

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6
Q

Coronary artery most responsible for MI seen in inferior Leads

A

inferior Leads are II, III, av1

RCA

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7
Q

Coronary artery most responsible for MI seen in anteroseptal leads

A

anteroseptal: V1-V2

LAD

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8
Q

Coronary artery most responsible for MI seen in anteroapical leads

A

V3-V4

LAD (distal)

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9
Q

Coronary artery most responsible for MI seen in anterolateral leads?

A

V5, V6, I, aVl

CFX

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10
Q

Coronary artery most responsible for MI seen in posterior leads

A

V1-V2

RCA

(note: V1-V2 is also anteroseptal and responsible for LAD)

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11
Q

EKG findings of myocardial injury/infarction

A

Pathological/sizable Q waves
(>1 small box)

  • Q waves in inferior leads (II,III, aVF) are due to inferior infarcts.
  • Q waves in anterior leads (V1-V4) are due to anterior wall infarcts.
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12
Q

Can Q waves differentiate between acute MI and one that happened years ago?

A

No, but ST elevation along with Q wave can

ST elevation can.

  • Acute: see ST elevation
  • Hours: see ST elevation AND ↓ R wave and Q deeper waves
  • Weeks: normal ST and persistent Q waves

(note: Q waves are usually the last ECG findings to develop)

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13
Q

What the the giant upright t waves called that are rarely seen in MI?

A

Hyperacute/peaked T waves

- lasts only a few minutes and rarely caught bc usually people dont have an MI while they are hooked up to an EKG

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14
Q

ECG findings in MI in:
Transmural MI
Subendocardial MI

A

transmural:

  • ST elevation
  • With Q waves

Subendocardial:

  • ST depression (lasting 2/3 days)
  • no Q waves

(note: ST depression may reflect transient ischemia w/o necrosis)

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15
Q

Difference between Stenosis and regurge sounds:

A

Stenosis: hear the sound before the closing of valves
Regurge: hear the sound after closing of the valves

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16
Q

How can you tell if you have a prolonged QT interval? Why is this important?

A

If you look peak to peak, divide in half = if you don’t see the T wave, you have a prolonged QT interval

  • When the QT interval is altered susceptibilities to arrhythmias increase - especially likely with QT prolongation.
17
Q

Causes of prolonged QT interval

A 
hypocalcemia
hypokalemai
hypomagnesemia
hypothermia
Class 1A or 3 anti-arrythmic drugs
Congenital Long QT syndrome
18
Q

How do calcium levels affect the QT intervals?

A

Hypercalcemia shortens the QT interval.
§ The commonest cause is hyperparathyroidism.

Hypocalcemia lengthens the QT interval (is more common)
§ Has many causes (life threatening ventricular arrhythmias)

19
Q

EKG findings of hypokalemia

- what can this cause?

A

Prolonged QT

T wave merging with U wave

  • Hypokalemia is a common cause of arrhythmias.
20
Q

Common causes of hypokalemia?

A

overuse of diuretics and vomiting or diarrhea

21
Q 
EKG findings in:
mild hyperkalemia (5.5-7.5)
A

increased T wave voltages with a distinctive peaked, symmetrical appearance.

22
Q 
EKG findings in:
highish hyperkalemia (7.5-9.0)
A

P waves may flatten and the QRS & T waves widen.

A broad S wave often appears.

23
Q 
EKG findings in:
highhh hyperkalemia (>9.0)
A

sinusoidal pattern appears without P or R waves.

24
Q

most common cause of hyperkalemia?

A

renal failure

If unrecognized hyperkalemia often causes fatal arrhythmias (and cardiac arrests)

25
Q

sinus arrest

A

Failure of sinus node discharge;

absent atrial depolarization and periods of ventricular asystole

26
Q

Intermittent episodes of slow and fast rates from SA node or atria

A

Bradycardia-Tachycardia Syndrome

27
Q

Inability to mount age-appropriate HR with exercise

A

Chronotropic Incompetence

28
Q

First-Degree AV block

how long is the PR interval?

A

AV conduction is delayed, and the PR interval is prolonged (> 200 ms)

29
Q 
Mobitz I (Wenckebach)
- how is the QRS duration?
A

Progressive prolongation of PR interval until a VENTRICULAR (QRS) beat is dropped;
QRS duration is normal

  • AV node is affected
30
Q

Infranodal diseases

A

Mobitz II 2nd degree AV block

3rd degree AV block = complete heart block

31
Q

Mobitz II

A

2nd degree AV block

intermittently dropped ventricular beats (QRS) preceded by constant PR intervals

32
Q

Irregular supraventricular tachycardias (SVT)

A

i. Atrial fibrillation (no discrete Ps, and irregularly irregular)
ii. Multifocal atrial tachycardia (3 or more P waves)
iii. Atrial flutter with variable conduction (flutter waves, sawtooth)
* note: supraventricular (above the ventricles)

33
Q

5 C’s of Atrial Fibrillation

A
  1. Cause: Reverse
  2. Control Rate
  3. antiCoagulation
  4. Control Rhythm
  5. Cure: ablation
34
Q

medications that control rate

A
  1. betablockers
  2. digoxin
  3. verapamil
  4. diltiazem
  5. Amiodarone
35
Q

EKG findings of cardiac tamponade

A

caused by: rapidly accumulating moderate sized or large effusions (can be caused by pericardial effusion)- Heart is unable to fill (sim to restrictive CM)

  1. Low voltage with sinus tachycardia
  2. Electrical alternans with sinus tachycardia

Note: Heart is in a Sea of fluid that causes changes with each beat

CV wk1 and wk2 (31 decks)

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