Ditt Cardio Arrythmias & Ekg

Front 1

What are the 4 basic classes of antiarrythmic drugs?

Back 1

"No Bad Boy Keeps Clean"
Class I: Na+ channel blockers
Class II: β-blockers
Class III: K+ channel blockers
Class IV: Ca2+ channel blocks

Front 2

List examples of Class 1A antiarrythmic agents

Back 2

Class 1A (Na+ channel)
!A= Alters mycocardial cell membrane

“Double Quarter Pounder ”
Disopyramid, Quinidine, Procainamide

Front 3

List examples of Class 1B antiarrythmic agents

Back 3

IB = Best post-MI, Blocks rapid influx of Na+ ions


“Lettuce, Tomato, Mayo, Pickles”
Lidocaine, Tocainide, Mexiletine, Phenytoin

Front 4

List examples of Class 1C antiarrythmic agents

Back 4

Class 1C = Contraindicated post-MI; slows Conduction

“Fries, Please”
Flecainide, Propafenone

Front 5

List examples of Class 2 antiarrythmic agents

Back 5

Class 2 [β-blockers]


Propanol, Metoprolol, esmolol

Front 6

List examples of Class 3 antiarrythmic agents

Back 6

Class 3 [K+ channel]

Amiodarone, sotalol

Front 7

List examples of Class 4 antiarrythmic agents

Back 7

Class 4 [CCB]

Diltiazem, verapamil

Front 8

List examples of cardiac glycoside agents

Back 8

Digoxin/digitalis

Front 9

What are other antiarrythmic agents, that don't below to a particular class?

Back 9

Adenosine
Mg2+

Front 10

What medications can cause bradycardia?

Back 10

Β-blockers, Ca2+ channel blockers, Digoxin, Amiodarone

Front 11

What are the EKG characteristics of 1st degree AV block?

Back 11

Prolonged PR interval (>200 msec)

Front 12

What are the EKG characteristics of Mobitz type I (2nd degree AV block)

Back 12

PR intervals get progressively longer, until P wave is not conducted

Front 13

What are the EKG characteristics of Mobitz type 2 (2nd degree AV block)

Back 13

No progressive lengthening of PR interval

Front 14

What are the EKG characteristics of 3rd degree AV block?

Back 14

No p waves are conducted; no correlation btw P and QRS complexes

Front 15

What are the EKG characteristics of atrial fibrillation?

Back 15

No p waves
Flat or chaotic baseline
Irregularly irregular narrow QRS complexes

Front 16

What tests should always be performed when looking for underlying causes of new-onset atrial fib?

Back 16

Echocardiogram – looking for structural heart problems
TSH – hyperthyroidism can cause A-fib

Front 17

What classes of drugs are typically used for rate control in atrial fibrillation?

Back 17

β- blocker (metoprolol)
Ca2+ channel blocker (diltiazem or verapamil)

Front 18

What are the two main concerns in the chronic treatment of atrial fibrillation?

Back 18

Rate control vs rhythm control – isn’t clear if pts do better in sinus rhythm vs a-fib

Stroke risk – when atria aren’t contracting normally, blood tends to pool – can development a thrombus that can embolize and cause a stroke

Front 19

What is the risk of stroke associated with atrial fibrillation?

Back 19

3-5% a yr

Front 20

What drug is used to reduce the risk of stroke in patients with atrial fibrillation?

Back 20

Lifelong anticoagulation with Warfarin (Coumadin)

Front 21

What are the EKG characteristics of atrial flutter?

Back 21

Regular, rapid atrial contractions (“saw tooth” baseline)
Atrial rate around 300bpm
Ventricular rate of 300, 150, or 100 bpm

Front 22

What drugs are most commonly used to control the heart rate in acute atrial fibrillation with rapid ventricular response?

Back 22

IV diltiazem
- 0.25mg/kg IV load (usually 15-20mg)
- infusion of 5-10mg/hr
- titrate to keep HR <100

Metoprolol
- 5mg IV q 5 min x 3doses
- 50-100mg PO BID

Front 23

A 66-year-old man with a history of hypertension and diabetes presents to your office with a complaint of palpitations for 1 week. EKG reveals atrial fibrillation with a resting HR of 72. After discussing treatment options, he decides that he would prefer a trial of electrical cardioversion in order to avoid lifelong anticoagulation. What preliminary steps would need to be undertaken before cardioversion?

Back 23

Anticoagulate with Warfarin for 3-4wks
Transesophageal echo (TEE) to look for atrial thrombus
Cardioversion
Continue warfarin for 4 more weeks

Front 24

Amiodarone is sometimes used to help maintain sinus rhythm in patients with atrial fibrillation. What studies are commonly followed in patients taking amiodarone, to monitor for toxicity?

Back 24

Check the “Ts”
LFTs (liver function tests)
TfTs (thyroid function tests)
PFTs (pulmonary function tests)

Front 25

What are the two most common causes of paroxysmal supraventricular tachycardia (SVT)?

Back 25

SVT occurs when the sinoatrial node rhythm is superseded by a faster rhythm, usually originating in the AV node.


(1) AV nodal re-entry tachycardia (AVNRT)
(2) Wolff-Parkinson White Syndrome

Front 26

What drug can be used to break or slow SVT?

Back 26

IV Adenosine

Front 27

What does a premature ventricular contraction (PVC) look like?

Back 27

Large, wide QRS not associated with a P wave

Front 28

What do we call >3 PVCs in a row?

Back 28

Ventricular tachycardia (VTach)

Front 29

What are the EKG characteristics of ventricular tachycardia (VTach)?

Back 29

Wide-complex tachycardia, arising from the ventricle
Rate is usually 150-250 bpm

Front 30

If untreated, into what rhythm will VTach often degenerate?

Back 30

Ventricular fibrillation – can lead to death

Front 31

How is VTach managed?

Back 31

see above

Front 32

What is the tx of Torsades de Pointes?

Back 32

What it is: Type of VTach with special pattern on EKG
Specially assoc with prolonged QT intervals & can assoc with hypomagnesemia
Tx: Defibrillation
IV Magnesium
Possibly amiodarone

Front 33

Wolff-Parkinson-White (WPW) syndrome is caused by an abnormal connection between atria and ventricles through an accessory bypass tract. What is the most common accessory bypass tract causing WPW syndrome?

Back 33

Bundle of Kent

Front 34

What rhythm is classically described as being “irregularly irregular”?

Back 34

Atrial fibrillation

Front 35

What rhythm is classically described as having a “saw tooth” pattern on the baseline?

Back 35

atrial flutter

Front 36

A 68-year-old man with a history of coronary artery disease (CAD) presents to the ER with a complaint of chest pain and is subsequently admitted to telemetry unit for monitoring. Overnight, the nurse calls you to the bedside because of tachycardia. His heart rate has been 160 beats per minute for the last 3 minutes. You race to the bedside, only to find the patient sitting up comfortably. He denies any pain or dyspnea, and says he feels fine. His BP is 114/72, but the telemetry monitor shows a wide-complex rhythm with a rate of 156, and you diagnose ventricular tachycardia. What are your next steps?

Back 36

First ask, “is the pt hemodynamically stable?” yes

amiodarone, procainamide, or sotalol

check 12-lead EKG and electrolytes

Front 37

While you are waiting for your orders from the previous question to be carried out, the patient begins to complain of feeling “woozy”. You check his blood pressure, and discover that it has fallen to 82/60. The tele monitor still shows ventricular tachycardia with a rate in the 150s-160s. What are your next steps?

Back 37

Now unstable, check for a pulse!

Front 38

Narrow QRS associated with P waves, rate 60

Back 38

Junctional rhythm

Front 39

Chaotic, erratic, wide QRS

Back 39

Ventricular fibrillation

Front 40

Wide QRS, not associated with P waves, rate 20-40

Back 40

Ventricular Rhythm = Ventricular impulses come from the ventricles.

Inherent rate of ventricles is: 15 -40 beats per minute
Idioventricular Rhythm (IVR) or Ventricular Escape Rhythm

May be due to: MI, metabolic imbalances, or severe hypoxia. Treatment includes activation of code, CPR given if patient is pulseless. Lidocaine is contraindicated since it may knock out the last available pacemaker.

Front 41

Wide QRS, not associated with P waves, rate >100

Back 41

V-Tach

Front 42

Narrow QRS not associated with P waves, rate >60 but <100

Back 42

Accelerated junctional rhythm

Front 43

Wide QRS tachycardia with variable amplitude in a repeating pattern

Back 43

Torsades de Pointes

Front 44

Interpret

Back 44

see above

Front 45

interpret

Back 45

see above

Front 46

interpret

Back 46

see above

Front 47

interpret

Back 47

see above

Front 48

interpret

Back 48

see above

Front 49

interpret

Back 49

see above

Front 50

interpret

Back 50

see above

Front 51

interpret

Back 51

see above

Front 52

interpret

Back 52

see above

Front 53

interpret

Back 53

see above

Front 54

interpret

Back 54

Ventricular Rhythms = Ventricular impulses come from the ventricles.

Inherent rate of ventricles is: 15 -40 bpm
Idioventricular Rhythm (IVR) or Ventricular Escape Rhythm

Front 55

General structure of an EKG tracing:

What does the P wave represent?
PR interval?
QRS complex?
ST segment?
T wave?
U wave?

Back 55

P wave = atrial depolarization

PR interval = conduction thru AV node (less than 0.2 sec, or 3-5 small squares) - measure from start of P to start of QRS complex

QRS complex = ventricular depolarization (< 0.12 sec, or 3 little boxes)

ST segment = isoelectric ventricular contraction

T wave = ventricular repolarization

U wave = hypokalemia

Front 56

Diagnosis?

Back 56

Left Ventricular Hypertrophy:

Marked LVH pattern with prominent precordial lead QRS voltages. ST depression and T wave inversion can be seen with severe LVH in leads with a predominant R wave. Left atrial abnormality is also present.

Front 57

Diagnosis?

Back 57

Left ventricular hypertrophy. Note the striking S wave amplitude in the right precordial leads and R wave amplitude in the left precordial leads. Repolarization abnormalities are present in the left precordial leads, as well as the limb leads. The S wave amplitude in V3 (2.4 mV) plus the R wave amplitude in aVL (1.0 mV) total 3.4 mV, easily satisfying the Cornell voltage criteria in this 76-year-old hypertensive man. Sinus bradycardia (50 beats per minute) is present as well.

Front 58

diagnosis?

Back 58

Evolving inferoposterolateral infarction.

Note the prominent Q waves in II, III, and aVF, along with ST-segment elevation and T wave inversion in these leads, as well as V3 through V6. ST depression in I, aVL, V1, and V2 is consistent with a reciprocal change. Relatively tall R waves are also present in V1 and V2.

Front 59

Diagnosis?

Back 59

Acute right ventricular infarction with acute inferior wall infarction. Note the ST-segment elevation in the right precordial leads, as well as in leads II, III, and aVF, with reciprocal changes in leads I and aVL. ST-segment elevation in lead III greater than in lead II and right precordial ST-segment elevation are consistent with proximal to middle occlusion of the right coronary artery. The combination of ST-segment elevation in conventional lead V1 (V2R here) and ST-segment depression in lead V2 (lead V1R here) has also been reported with acute right ventricular ischemia or infarction.

Front 60

Diagnosis?

Back 60

Complete LBBB with acute inferior myocardial infarction. Note the prominent ST-segment elevation in leads II, III, and aVF, with reciprocal ST-segment depression in leads I and aVL superimposed on secondary ST-T changes. The underlying rhythm is atrial fibrillation.

Front 61

Diagnosis?

Back 61

Left bundle branch block (LBBB). The QRS is widened, with a broad, notched complex in leads I, aVL, and the left precordial leads. Small r waves and broad, deep S waves are present in the right precordial leads. With LBBB, the axis is usually normal or deviated to the left. ST segments and T waves are discordant with the QRS complex throughout the precordium.

Front 62

Diagnosis?

Back 62

Left ventricular hypertrophy. Note the striking S wave amplitude in the right precordial leads and R wave amplitude in the left precordial leads. Repolarization abnormalities are present in the left precordial leads, as well as the limb leads. The S wave amplitude in V3 (2.4 mV) plus the R wave amplitude in aVL (1.0 mV) total 3.4 mV, easily satisfying the Cornell voltage crite- ria in this 76-year-old hypertensive man. Sinus bradycardia (50 beats per minute) is present as well.