Cardiovascular: EKG

Question 0

PR Interval

Answer 0

SA node to AV node

0.12 - 0.2 seconds

Question 1

P Wave

Answer 1

Atrial depolarization

Question 2

QRS Complex

Answer 2

Ventricular depolarization
Atrial repolarization
0.06 - 0.10

Question 3

QT Interval

Answer 3

Ventricular depolarization
Ventricular repolarization
0.20 - 0.40

Question 4

ST Segment

Answer 4

Ventricular depolarization

Question 5

T Wave

Answer 5

Ventricular repolarization

Question 6

Normal Sinus Rhythm

Answer 6

Atrial depolarization in SA node with 60 - 100 bpm

Question 7

Sinus Bradycardia

Answer 7

HR < 60 bpm

Question 8

Sinus Tachycardia

Answer 8

HR > 100 bpm

Question 9

Sinus Arrhythmia

Answer 9

Quickening and slowing of impulse formation in SA node

Beat-to-beat variation of HR

Question 10

Sinus Arrest

Answer 10

Intermittent failure of SA node impulse formation or AV conduction
Occasional absence of P or QRS waves

Question 11

Premature Atrial Contractions (PAC)

Answer 11

Ectopic focus in atrium initiates impulse before SA node
P wave is premature
Common, benign
Can progress to aflutter, tachycardia, or afib
Causes: caffeine, stress, smoking, alcohol, heart disease

Question 12

Atrial Flutter

Answer 12

Ectopic, very rapid atrial tachycardia
Atrial rate: 250-350 bpm (ventricular rate depends upon AV conduction)
Saw-tooth P waves (flutter waves)
Etiology: VHD (mitral), ischemic heart disease, HTN, acute MI, COPD, PE
S/S: Palpitations, lightheadedness, angina
Blood stagnation predisposes atria thrombi

Question 13

Atrial Fibrillation

Answer 13

Atria depolarization 350-600 per min
Irregular undulations without discrete P waves
Etiology: CAD, HTN, VHD
S/S: Palpitations, fatigue, dystonia, lightheadedness, syncope, chest pain
Blood stagnation predisposes atria thrombi

Question 14

1st Degree AV Block

Answer 14

PR interval > 0.2 seconds relatively constantly
Etiology: Various; meds that suppress AV conduction
S/S: No symptoms or significant changes

Question 15

2nd Degree AV Block

Answer 15

AV conduction disturbance, impulses between atria and ventricles fail intermittently
Mobitz I (Weckebach): PR Interval progressively prolonged until one impulse not conducted (benign)
Mobitz II: PR intervals same and normal until one or more not conducted
  Slow HR = decreased CO with block
  Can progress to 3rd degree AV block

Question 16

3rd Degree AV Block

Answer 16

All impulses blocked at AV node, none transmitted to ventricles
Atria and ventricles paced independently
Atrial rate > ventricular rate
Medical emergency, requires pacemaker
Ventricular rate too slow = CO drops, patient may faint
Etiology: Degenerative changes of conduction system, digitalis, heart surgery, acute MI

Question 17

Premature Ventricular Complex (PVC)

Answer 17

Premature ventricular depolarization from ectopic focus
Unifocal: PVCs arise from same ectopic focus with same configuration
Multifocal: PVCs arise from different ectopic foci with different configuration
P wave usually absent, QRS complex has wide, aberrant shape
Bigeminy: Normal sinus impulse then PVC
Trigeminy: 2 Normal sinus impulses then PVC
Etiology: Common in healthy and diseased hearts. Anxiety, caffeine, stress, smoking, heart disease.
S/S: Asymptomatic or palpitations

Question 18

Ventricular Tachycardia (V-Tach)

Answer 18

3+ Consecutive PVCs at ventricular rate > 150 bpm
P waves absent, QRS wide and aberrant
V-tach > 30 sec = life threatening, requires immediate medical intervention
Unable to maintain adequate BP = hypotension
Can degenerate into v-fib = cardiac arrest
Etiology: MI, cardiomyopathy, VHD

Question 19

Ventricular Fibrillation (V-Fib)

Answer 19

Ventricles fibrillate/quiver asynchronously and ineffectively
No CO; patient becomes unconscious
Fibrillatory waves with irregular pattern that is coarse or fine
Requires immediate debfibrillation
Meds to support circulation, IV antiarrhythmics
Etiology: Heart disease, MI, cocaine

Question 20

Ventricular Asystole

Answer 20

Ventricular standstill with no rhythm
Straight-line
Immediate defibrillation and/or meds to stimulate cardiac activity
Etiology: Acute MI, ventricular rupture, cocaine, lightening strike, electrical shock

Question 21

Signs Of MI And Ischemia

Answer 21

ST segment depression
ST segment elevation
Abnormal Q wave
T wave inversion

Question 22

ST Segment Depression

Answer 22

Sign of subendocardial ischemia, digitalis toxicity, or hypokalemia
Evaluated relative to isoelectric baseline at 0.08 sec after J point (junction between QRS end and ST beginning)
Deviations = ST segment depression of 1mm, 2mm, etc.

Question 23

ST Segment Elevation

Answer 23

“Zone of Injury” - MI, Middle
Absolute sign of acute transmural infarction
Can indicate benign early repolarization pattern
Deviations 1mm, 2mm, etc.

Question 24

Abnormal Q Wave

Answer 24

"Central Zone" - MI, Inner Characteristic marker of infarction Loss of positive electrical voltage from necrosis Q wave longer than 0.04msec, larger than 1/3 R wave amplitude

Question 25

T Wave Inversion

Answer 25

"Zone of Ischemia" - MI, Outer Occurs hours or days after MI Delay in repolarization from injury Also in R and L bundle branch blocks, CVA, normal juvenile T wave pattern in children and some adults

Question 26

Hyperkalemia

Answer 26

Widens QRS Flattens P wave Peaks T wave

Question 27

Hypokalemia

Answer 27

Flattens T wave (or inverts) | Produces U wave

Question 28

Hypercalcemia

Answer 28

Widens QRS | Shortens QT interval

Question 29

Hypocalcemia

Answer 29

Prolongs QT interval

Question 30

Digitalis

Answer 30

Depresses ST segment Flattens T wave (or inverts) QT shortens

Question 31

Quinidine

Answer 31

QT lengthens T wave flattens (or inverts) QRS lengthens

Question 32

Beta Blockers

Answer 32

Decrease HR | Blunt HR response to exercise

Question 33

Nitrates (NTG)

Answer 33

Increases HR

Question 34

Antiarrhythmics

Answer 34

May prolong QRS and QT

Question 35

Hypothermia

Answer 35

Elevates ST segment | Slows rhythm