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*Pance Re-Up * > Cardiology #4 Conduction Disorders > Flashcards

Cardiology #4 Conduction Disorders Flashcards

1
Q

In an EKG, what are the following parts related to?
-P wave
-PR segment
-QRS complex
-T wave

A

P wave: atrium contraction
PR segment: AV node
QRS complex: Ventricular contraction
T wave: Ventricular repolarization

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2
Q

How do you calculate the rate of an EKG strip?

A

Count the large boxes in an R - R segment

300 / 1, 2, 3, 4, 5
=300, 150, 100, 75, 60

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3
Q

Explain the process of conduction and relate it to the parts of an EKG

A

-Sinus node sends impulse through RA to AV node (atrial contraction). PR segment (nothing happens) when it goes through AV node. Then, rapid condition through Bundle of His –> contraction of ventricle (QRS complex)

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4
Q

Normal sinus rhythm has a rate of ________

A

60-100 bpm

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5
Q

Sinus bradycardia, which is decreased HR with a rate of __________, has causes such as what?

A

HR < 60 bpm from sinus node

Causes: young athletes, BB, CCB, SA node ischemia, hypothyroid

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6
Q

Treatment for sinus bradycardia

A

-Symptomatic: Atropine (1st line)
–Epinephrine or Transcutaneous pacing

-Asymptomatic
–No treatment needed

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7
Q

Sinus tachycardia is HR > 100 bpm from the sinus node. What are some causes? What is the treatment?

A

-Exercise, stress, kids/infants, fever, pain, hypoxia, shock, cocaine

Treat underlying cause (1st line), BB if needed

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8
Q

What is sinus arrhythmia?

No treatment is needed in most cases.

A

Norma variation of sinus rhythm. Beat to beat variation with respiration. Increase in rhythm with inspiration, decrease in rhythm with expiration.

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9
Q

Sick sinus syndrome is dysfunction of the sinus node leading to what rhythm?

A

Combination of sinus arrest with alternating periods of tachycardia and bradycardia.

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10
Q

What is the MCC of sick sinus syndrome?

A

Sinus node fibrosis

Others: old age

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11
Q

Treatment for sick sinus syndrome

A

-Atropine (first line)

-Long term: Permanent pacemaker (definitive), AICD if alternating

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12
Q

What happens in a junctional rhythm?

What is seen on an EKG with this type of rhythm?

A

AV node becomes the dominant pacemaker

Inverted P waves or not seen at all. Narrow QRS

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13
Q

What segment of an EKG strip is the most useful in determining an AV Block?

A

PRI interval

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14
Q

What does the ECG with a First Degree AV block look like?

Treatment?

A

Prolonged PR interval, but all P waves are followed by a QRS complex

-Asymptomatic: observation
-Atropine (1st line)
-Pacemaker (definitive)

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15
Q

What is the pathophysiology of a 2nd degree AV block? What is the first type of second degree AV Block, what is seen on an ECG, and what is the treatment?

A

Not all atrial impulses are conducted to the ventricles, leading to P waves without QRS complexes

-Mobitz 1: Wenkebach

-ECG: P waves are constant, Progressive PRI lengthening –> dropped QRS

Atropine, Epi, Pacemaker

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16
Q

What is the other type of 2nd degree AV block, what is seen on an ECG, and what is the treatment?

A

Mobitz II

P waves constant, constant/prolonged PRI –> dropped QRS

Atropine or temporary pacing, pacemaker definitive

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17
Q

Both 2nd degree AV blocks occur where in the heart?

A

Bundle of His

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18
Q

Mobitz I causes

Mobitz II causes

A

1 (Wenkebach): inferior wall MI, BB/CCB/Digoxin, Myocarditis

2: Rarely in patients without structured heart disease (myocarditis, endocarditis, myocardial fibrosis)

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19
Q

A third degree AV block is due to AV dissociation. No atrial impulses are reaching the ventricles. Causes of this are similar to 2nd degree AV block because it can progress to a 3rd degree. Name them.

A

Inferior Wall MI
AV nodal blocking agents (BB, CCB, Digoxin)
Lyme, Endocarditis, Myocarditis
Hypothyroidism, Hyperkalemia

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20
Q

What does the ECG for a 3rd degree AV block look like?

A

Regular R-R and P-P intervals, but not related to each other

-P’s and Q’s don’t agree, then you have a third degree

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21
Q

Treatment for a 3rd degree AV block

A

-Transcutaneous pacing followed by permanent pacemaker (definitive)

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22
Q

What does an ECG look like in Paroxysmal Supraventricular Tachycardia (PSVT?)

A

Regular, narrow QRS complex
Tachycardia (no discernible P waves)
HR > 100 bpm

If you can’t tell if it’s a P or a T, it must be SVT

23
Q

The treatment for PSVT differs based on the width of the QRS complex. What are the treatments for the following:

Stable (narrow complex)
Stable (wide complex)
Unstable
Definitive

A

Narrow: vagal maneuvers (Valsalva, carotid massage, Adenosine)

Wide: Amiodarone

Unstable: Synchronized (DC) Cardioversion

Definitive: Radiofrequency catheter ablation

24
Q

Wolff-Parkinson White (WPW) is a form of PSVT. Explain the pathophysiology of this condition.

What are the three components of this on an ECG?

A

-Accessory pathway (Bundle of Kent) outside the AV node pre-excites the ventricles, bypassing the AV node, leading to a delta wave.

Wave = Delta Wave
P = PR Interval is short
W = Wide QRS Complexes

25
Q

Management for WPW

A

-Stable: Procainamide (1st line), Amiodarone
-Unstable: DC Cardioversion
-Definitive: Radiofrequency catheter ablation (Destroys the normal pathway)

Treatment is the Same as PSVT

26
Q

What medications should be avoided in PSVT and WPW?

A

AV node blockers (ABCD)
-Adenosine, BB, CCB, Digoxin

27
Q

With atrial flutter, what are you at increased risk for?

A

Arterial thrombus formation that leads to stroke (like A-fib)

28
Q

Symptoms of atrial flutter

A

-Palpitations, fatigue, dyspnea, refractory chest pain, hypotension, AMS

29
Q

What does an ECG show for atrial flutter?

A

Flutter (sawtooth) atrial waves usually around 300 bpm but no clear P waves

30
Q

Treatment for atrial flutter

A

-Stable: Vagal maneuvers, BB or CCB (Diltiazem, Verapamil)

-Unstable: DC Cardioversion

Radiofrequency catheter ablation is definitive

31
Q

Etiologies of Atrial fibrillation

A

-Infection, cardiomyopathies, age, thyroid disorders genetics, drugs, alcohol (use and withdrawal), men, whites

32
Q

What is seen on an ECG for A-fib?

A

-Irregularly irregular rhythm with fibrillatory waves

33
Q

What is Ashman’s Phenomenon in regards to A-fib?

A

Wide QRS after short R-R cycles

34
Q

Treatment for stable A-fib

A

-BB or CCB (Diltiazem or Verapamil)
-Digoxin if heart failure

35
Q

If unstable, what is the treatment for A-fib

A

DC Cardioversion

36
Q

Long term treatment for A-fib

A

-rate control (BB or CCB)
-DC Cardioversion
-RF catheter ablation
-Anticoagulation

37
Q

Describe the timing rule for cardioversion and anticoagulation

How long should anticoagulation be continued afterwards?

A

-AF > 48 hours: anticoagulation for 3 weeks before cardioversion

-AF < 48 hours: anticoagulation prior

Continue anticoagulation for 4 weeks after cardioversion

38
Q

Explain the scoring with the CHA2DS2-VASc Score

What score gives you chronic oral anticoagulation (Warfarin or Novel anticoagulation)?

A

Congenital Heart Failure = 1
Hypertension = 1
Age > 75 = 2
Diabetes = 1
Stroke, TIA = 2
Vascular Disease (PAD, MI) = 1
Age 65-74 = 1
Sex (female) = 1

2 or more is the cutoff

39
Q

Explain non-vitamin K antagonistic oral anticoagulants (NOAC)

-Lower risks of ….
-Don’t need to…
-There are two kinds. Name them and explain what they do

A

-Lower risk of bleeding and stroke

-Don’t need to check INR, less drug interactions

-Dabigatran: binds and inhibits thrombin
-Rivaroxaban, Apixaban, Edoxaban: factor Xa inhibitors

40
Q

Regarding Warfarin, when is it preferred and what is the INR goal with this medication?

A

Preferred if HIV+, CKD or anti-epileptic medications (Phenytoin, Carbamezapine)

Bridge with Heparin until therapeutic

INR goal of 2-3

Also monitor PT

41
Q

Is Dual-antiplatelet therapy (Aspirin + Clopidogrel) less or more effective than anticoagulant mono therapy?

A

Less effective

42
Q

Explain what a PVC is, what is seen on ECG, and what the treatment is?

A

Premature Ventricular Complexes (PVC)

Premature beat originating from ventricle

Wide, bizarre QRS complexes occurring earlier. T wave in opposite direction of QRS

No treatment needed

43
Q

What is ventricular tachycardia?

What are some etiologies?

A

3 or more PVC’s at > 100 bpm

Ischemic heart disease (MC) - Post MI
Prolonged QT
Digoxin Toxicity
Hypomagnesemia, Hypokalemia

44
Q

Treatment for V-tach

A

Stable/Sustained (>30 seconds): Amiodarone

Unstable with Pulse: DC Cardioversion

No Pulse = Defibrillation + CPR

45
Q

Explain what Torsades de Pointes looks like on an ECG and name some etiologies

A

-Alterations of QRS amplitude around the isoelectric line (twisting)

Prolonged QT (antipsychotic use!!), hypomagnesemia, hypokalemia, macrolides, Digoxin, Procainamide

46
Q

Treatment for Torsades de Pointes

A

-IV Mag Sulfate

47
Q

What does a patient look like with ventricular fibrillation?

A

Unresponsive, pulselessness, syncope

48
Q

Treatment for ventricular fibrillation?

What is the MCC?

A

Defibrillation + CPR

Ischemic heart disease (Post MI)

49
Q

What are the components of a RBBB on an ECG?

A

-QRS > 120ms
-RsR1 (bunny ears) in V1-V3
-Slurred S waves in I, avL, V5, V6

50
Q

What are the components of a LBBB on an ECG?

A

-QRS > 120ms (wider)
-Broad, notched M-shaped R in V6
-Dominant S wave in V1

51
Q

Adenosine

MOA:
Use:
Adverse Effects:

A

-Slows AV node conduction time and blocks AV nodal reentry pathways
-Used in PSVT and pharmacological stress testing
–vasodilation of coronary arteries mimics increased demand
-Adverse Effects: CP, dyspnea, flushing, bronchospasm, hypertension, MI

52
Q

Atropine

MOA:
Use:
Adverse Effects:

A

-Parasympathetic acetylcholine inhibition –> increased cardiac output
-Used in bradycardia
-Adverse Effects: Xerostomia, blurry vision, flushing

53
Q

Amiodarone

MOA:
Use:
Adverse Effects:

A

-Class III antiarryhthmics (K+ channel blocker) that prolongs the action potential
-Used for stable, wide complex tachycardia
-Adverse Effects: Hypotension, LFT’s increased, thyroid disorders, corneal deposition > 6 months

54
Q

What is Brugada syndrome?

What is seen on the EKG for this condition?

A

Abnormal myocardial depolarization that predisposes young, otherwise healthy people to V-fib and sudden cardiac death.

ST segment elevated and T wave inversion in V1-V3

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