Ap Ii Exam 2 Ekg

Front 1

AP II EXAM 2 EKG

Back 1

AP II EXAM 2 EKG

Front 2

Supraventricular dysrhythmia

Back 2

Dysrhythmia that originates at the SA node.

Normal QRS

Front 3

Ventricular dysrhythmia

Back 3

One that originates from the ventricle.

Wide QRS ( > 0.12s)

Front 4

What lead do you look at for dysrhythmias?

Back 4

Lead II

Front 5

What are the five steps approach for rhythm analysis?

Back 5

1. presence of P wave?
2. QRS width?
3. regularity of rhythm?
4. relationship of P waves to QRS complex?
5. HR

Front 6

How do you tell if a rhythm originates from a supraventricular or ventricular origin?

Back 6

Supraventricular origin: from SA node. Associated with a P wave.

If originates from AV node--> No P wave.

But BOTH will have a narrow QRS.

Originating from ventricle: No P wave and WIDE QRS.

Front 7

What lead do we look at for rhythm analysis?

Back 7

Lead II

Front 8

Examples of supraventricular cases?

Back 8

1. A-Fib
2. Atrial flutter
3. PSVT (aka SVT)

Front 9

Atrial Fibrillation

Back 9

Irregularly Irregular

Absensce of P wave


Most commonly occurring sustained arrhythmias.

Front 10

What are the causes of A-Fib?

Back 10

1. HTN
2. CHF
3. hyperthyroidism
4. valvular heart disease
5. AMI
6. surgery
7. cardiomyopathy
8. ethanol

Front 11

Treatment of A-Fib pharmacologically:

Back 11

1. IV diltiazem
2. IV beta blocker (metoprolol or esmolol)
3. IV amiodarone

NOTE: esmolol is short acting which is the preferred choice.

Front 12

If pt. is hemodynamically stable during A-Fib, then Tx should include?

Back 12

Pharmacolgic therapy as described above.

Front 13

What might happen if fibrillation has been present longer than 48 hrs?

Back 13

Thromboembolism may result in the course of treatment.

High risk of left ventricular embolism formation causing a stroke. Use anticoagulants.

Front 14

What is Atrial Flutter?

Back 14

Abnormal rhythm in the atria

Saw Tooth Pattern

Absolutely Regular



Atrial rate: 300 bpm

Front 15

Treatment for Atrial Flutter?

Back 15

Same as A-Fib

NOTE: for hemodynamic instable pts, rely on synchronized DC cardioversion. This is true for BOTH A-Fib and A-flutter.

Front 16

PSVT (SVT) or Paroxymal supraventricalur tachycardia

Back 16

1. narrow QRS
2. HR ~ 170-250 bpm
3. rhythm may be regular or irregular.
4. no P wave

Front 17

How do you know what's causing the PSVT?

Back 17

1. Perform carotid massage or vagal maneuver to slow down rhythm.

2. Give Adenosine to slow rhythm down.

Front 18

Treatment of PSVT

Back 18

Hemodynamically instable--> perform DC Cardioversion.

Hemodynamically stable--> vagal maneuvers, IV adenosine.

Other agents: IV beta blockers (esmolol).

Front 19

EKG diagnosis of ventricular dysrhythmias

Back 19

QRS will be wide

Usually regular rhythm

Front 20

Examples of ventricular dysrhythmias

Back 20

1. V-tach
2. Torsades de pointes
3. V-fib

Front 21

V-Tach

Back 21

1. nonsustained VT
2. Sustained VT

Front 22

Non-sustained VT

Back 22

< 30 sec

Spontaneously terminates

Front 23

Causes of non-sustained VT

Back 23

1. benign when no structural disease is present.
2. with structural dz present--> marker for sustained VT
3. electrolyte imbalances, heart strain, cardiac ischemia

Front 24

Procainamide

Back 24

Treats NSVT

For symptomatic with preserved left ventricular function.

20 mg/min

Front 25

Other Tx for NSVT

Back 25

With poor LV function, use Amiodarone 150 mg bolus.

For unstable pts--> synchronized cardioversion

Front 26

Sustained Ventricular Tachycardia (SVT)

Back 26

Wide QRS

HR > 100

Mono or Polymorphic--> look further.

Hemodynamically stable or not?

Front 27

Causes of monomorphic VT

Back 27

1. electrolyte imbalances
2. persistent ischemia
3. hypoxia
4. drug effects
5. anemia
6. hypotension

Front 28

Treatment of monomorphic VT

Back 28

Procainamide at dose of 20 mg/min. if LV function is still present.

If LV function is poor, use AMIODARONE 150 mg bolus.

For unstable pts (i.e. hypotension, PE, etc...)--> Synchronized cardioversion.

Front 29

Treating pulseless ventricular tachycardia

Back 29

1. follow ACLS protocol
2. defibrillate
3. amiodarone
4. lidocaine
5. magnesium

Front 30

Torsades de Pointes

Back 30

Prolonged QT interval

Polymorphic VT which means Ventricular rhythm > 100 bpm

Front 31

Causes of monomorphic VT

Back 31

1. electrolyte imbalances
2. persistent ischemia
3. hypoxia
4. drug effects
5. anemia
6. hypotension

Front 32

Treatment of Torsades

Back 32

Hemodynamically unstable: DC cardioversion

Hemodynamically stable: Magnesium sulfate 2 g IV

NOTE: high incidence of evolving V-Fib quickly.

Front 33

Treatment of monomorphic VT

Back 33

Procainamide at dose of 20 mg/min. if LV function is still present.

If LV function is poor, use AMIODARONE 150 mg bolus.

For unstable pts (i.e. hypotension, PE, etc...)--> Synchronized cardioversion.

Front 34

Treating pulseless ventricular tachycardia

Back 34

1. follow ACLS protocol
2. defibrillate
3. amiodarone
4. lidocaine
5. magnesium

Front 35

Torsades de Pointes

Back 35

Prolonged QT interval

Polymorphic VT which means Ventricular rhythm > 100 bpm

Front 36

marcar

Back 36

to mark, to note, to observe

Hint 36

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Front 37

V-Fib

Back 37

No ability to adequately contract--> NON-perfusing rhythm.

Front 38

Treatment for V-Fib

Back 38

Electrical Defibrillation

Otherwise, pt will die w/in 4-6 mins.

Front 39

Premature Atrial Contractions (PAC)

Back 39

Premature beat arising from atria other than SA node.

Different P wave morphology

QRS complex is narrow

Front 40

PVC

Back 40

Early beat interrupt normal rhythm.

Arise from ventricle

Wide QRS with abnormal appearance from sinus-conducted beats.

Front 41

Heart blocks

Back 41

1st degree AV block

2nd degree AV block

3rd degree AV block

Front 42

First degree block

Back 42

AV impulse delayed--> PR interval longer

It's really not a block, but a prolongation of conduction.

Front 43

Treatment of first degree AV block

Back 43

Usually does not require therapy

Front 44

Second degree AV block

Back 44

1. Mobitz I (Wenckeback)
2. Mobitz II

Front 45

Mobitz I (Wenckeback)

Back 45

1. PR interval lengthens until one P wave is absent. Then a pause occurs.

2. atrial rate is still regular

3. disease is in the AV node.

Front 46

Mobitz I EKG recognition

Back 46

PR interval becomes progressively longer until it's absent.

2. QRS complexes narrow

3. RR intervals shorten if there are more than 2 P waves in a row.

Front 47

Causes of Mobtiz I

Back 47

1. associated with digitalis intoxication, acute inferior MI, RV infarct, acute myocarditis.

2. high vagal tone

Front 48

Treatment for Mobitz I

Back 48

1. reverse the causes
2. avoid medications that impair AV conduction.

Front 49

Mobitz II

Back 49

PR interval remained UNCHANGED.

P wave SUDDENLY disappears (fails to conduct to ventricle).

Front 50

Mobitz II EKG recognition

Back 50

PR interval is same and normal

Some P waves are not conducted

QRS complex broad

Front 51

Causes of Mobtiz II

Back 51

Anterior septal MI

Chronic fibrotic disease

Front 52

Treatment of Mobtiz II

Back 52

Insert temporary pacemaker ASAP followed by a PPM.

Front 53

Third degree AV block

Back 53

Complete heart block

No atrial impulses

Front 54

Physical signs of 3rd degree block?

Back 54

1. bradycardia
2. loss of atrial kick
3. reduced CO

Front 55

Third degree block EKG recognition

Back 55

Its atrial rhythm: sinus or ectopic (can be FIB or Flutter)

Its ventricular rhythm: usually escape beats. Wide QRS.

Front 56

Treatment of third degree block

Back 56

1. transvenous pacer until a PPM (perm. pacemaker) can be placed.
2. atropine
3. isoprel for MI