Diagnostic features of EKG - disorders Flashcards
EKG findings of LV hypertrophy
- Bigger R waves in Left-sided Leads (due to larger muscle mass)
→ I, aVL, V5, V6 - T wave can be inverted
EKG findings of Right Ventricular Hypertrophy
Big R waves in Right-sided Leads
→ V1,V2
EKG findings of Myocardial ischemia
ST depression
T wave inversion - sometimes
EKG findings of ischemia during acute coronary syndrome
T wave inversion
What is transmural injury and what are the
EKG findings of transmural injury
ST elevation
Note: Transmural injury: death of myocardial tissue that extends from the endocardium to the epicardium as a result of a myocardial infarction.
Coronary artery most responsible for MI seen in inferior Leads
inferior Leads are II, III, av1
RCA
Coronary artery most responsible for MI seen in anteroseptal leads
anteroseptal: V1-V2
LAD
Coronary artery most responsible for MI seen in anteroapical leads
V3-V4
LAD (distal)
Coronary artery most responsible for MI seen in anterolateral leads?
V5, V6, I, aVl
CFX
Coronary artery most responsible for MI seen in posterior leads
V1-V2
RCA
(note: V1-V2 is also anteroseptal and responsible for LAD)
EKG findings of myocardial injury/infarction
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.
Can Q waves differentiate between acute MI and one that happened years ago?
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)
What the the giant upright t waves called that are rarely seen in MI?
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
ECG findings in MI in:
Transmural MI
Subendocardial MI
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)
Difference between Stenosis and regurge sounds:
Stenosis: hear the sound before the closing of valves
Regurge: hear the sound after closing of the valves
How can you tell if you have a prolonged QT interval? Why is this important?
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.
Causes of prolonged QT interval
hypocalcemia hypokalemai hypomagnesemia hypothermia Class 1A or 3 anti-arrythmic drugs Congenital Long QT syndrome
How do calcium levels affect the QT intervals?
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)
EKG findings of hypokalemia
- what can this cause?
Prolonged QT
T wave merging with U wave
- Hypokalemia is a common cause of arrhythmias.
Common causes of hypokalemia?
overuse of diuretics and vomiting or diarrhea
EKG findings in: mild hyperkalemia (5.5-7.5)
increased T wave voltages with a distinctive peaked, symmetrical appearance.
EKG findings in: highish hyperkalemia (7.5-9.0)
P waves may flatten and the QRS & T waves widen.
A broad S wave often appears.
EKG findings in: highhh hyperkalemia (>9.0)
sinusoidal pattern appears without P or R waves.
most common cause of hyperkalemia?
renal failure
If unrecognized hyperkalemia often causes fatal arrhythmias (and cardiac arrests)
sinus arrest
Failure of sinus node discharge;
absent atrial depolarization and periods of ventricular asystole
Intermittent episodes of slow and fast rates from SA node or atria
Bradycardia-Tachycardia Syndrome
Inability to mount age-appropriate HR with exercise
Chronotropic Incompetence
First-Degree AV block
how long is the PR interval?
AV conduction is delayed, and the PR interval is prolonged (> 200 ms)
Mobitz I (Wenckebach) - how is the QRS duration?
Progressive prolongation of PR interval until a VENTRICULAR (QRS) beat is dropped;
QRS duration is normal
- AV node is affected
Infranodal diseases
Mobitz II 2nd degree AV block
3rd degree AV block = complete heart block
Mobitz II
2nd degree AV block
intermittently dropped ventricular beats (QRS) preceded by constant PR intervals
Irregular supraventricular tachycardias (SVT)
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)
5 C’s of Atrial Fibrillation
- Cause: Reverse
- Control Rate
- antiCoagulation
- Control Rhythm
- Cure: ablation
medications that control rate
- betablockers
- digoxin
- verapamil
- diltiazem
- Amiodarone
EKG findings of cardiac tamponade
caused by: rapidly accumulating moderate sized or large effusions (can be caused by pericardial effusion)- Heart is unable to fill (sim to restrictive CM)
- Low voltage with sinus tachycardia
- Electrical alternans with sinus tachycardia
Note: Heart is in a Sea of fluid that causes changes with each beat
