Mumurs And Valve Disease and Anti Arrhythmia Drugs Flashcards

1
Q

What are 4 common symptoms of Valve disease and which one is most common?

A

Dyspnea on exertion (most common), angina, syncope and palpitations.

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2
Q

As far as etiology, what are the 3 most common conditions encountered today and what valve problem does it lead to?

A
  1. Degenerative process like calcification. Just happens with age. Aortic calcification.
  2. Myxomatous degeneration in Mitral Valve Prolapse
  3. Congenital issues like bicuspid aortic valve.
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3
Q

What 3 things are we thinking as to the patho behind a valve issue?

A

Pressure overload, volume overload, or a specific disease process like an infection or heart failure.

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4
Q

What is the jones major criteria for RHD?

A
J: joints involved
O: myOcarditis
N: Nodules that are subcutaneous 
E: Erythema marginatum
S: Syndenhams Chorea
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5
Q

What are the minor criteria for RHD? What is the mnemonic?

A
C: CRP increased
A: Arthralgia 
F: Fever
E: Elevated ESR and ASO titer or anti DNAse B
P: Prolonged PR
A: medical history of rhumatism
L: leukocytosis
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6
Q

What is the criteria to diagnose RHD?

A

2 major criteria or

1 major and 2 minor

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7
Q

RF is virtually the only cause of what?

A

Acquired MS

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8
Q

5 common symptoms of a patient with Mitral Stenosis?

A

Exertional Dyspnea, Fatigue with low CO, cough orthopnea, PHT and RHF with edema.

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9
Q

What age does the typical patient with MS present with?

A

4th decade

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10
Q

What is the syndrome associated with MS and explain whats going on?

A

Ortner syndrome. Hoarseness because of compression of the left recurrent laryngeal nerve.

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11
Q

3 physical exam findings for MS?

A

Malar rash or blue face
Increased s1
Opening snap after s2.

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12
Q

How do we describe what we hear when listening to a MS murmur?

A

Low frequency that starts at the opening snap and decreases in volume. During diastole. Starts back up again right before S1 during atrial contraction.

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13
Q

What is the best way to hear the MS murmur?

A

Use bell, have patient lay left lateral decubitus position and listen at the apex.

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14
Q

When do you use anticoagulant for MS?

A

If there is Afib. Don’t want to have an embolism.

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15
Q

What is the most common etiology of chronic MR?

A

MVP, so myxomatous degeneration

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16
Q

3 common causes of Acute MR?

A

Rupture of Chordae tendinae, rupture of pap muscle, or IE.

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17
Q

Big picture, what is the problem going on with acute MR?

A

Got to think forwards and backwards. LA pressure is jacked up and then there isn’t enough blood getting through the heart to pump for the body.

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18
Q

What is going on with the symptoms of MR?

A

Can be asymptomatic for years, but then you can appreciate LA dilation and backing up to the right side of heart.

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19
Q

What kind of murmur is MR?

A

Holosystolic

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20
Q

Where is MR best heart and what part of the stethoscope is used?

A

Apex and diaphragm

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21
Q

Where does MR murmur radiate?

A

Left axilla

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22
Q

What happens to s1 during MR murmur?

A

Decreased or normal

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23
Q

When do cardiac troponin levels increase, when do they hit peak levels after MI, how long are they typically elevated for?

A

They elevate in 4-6 hours and peak at 8-12 hours. 5-7 days.

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24
Q

What are the same levels for CK-MB?

A

Rise in 4-8 hours, peak at 24 hours and return in 48-72 hours.

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25
Q

3 symptoms of MVP?

A

Asymptomatic to arrhythmias, chest pain, and syncope

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26
Q

What type of murmur is MVP?

A

Systolic

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27
Q

What is a state you can find your patient in with MVP?

A

Hyper adrenergic state because of anxiety or palpitations

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28
Q

What is a “click” and why would you have a systolic click with MVP?

A

A click is abnormal closure of a valve, so you would have a systolic click with MVP because the valves, which prolapsed during systole, are closing.

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29
Q

Top 3 causes of AS?

A

Calcification due to age, Rheumatic, and radiation scarring

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30
Q

4 symptoms of AS?

A

Exertional dyspnea, angina, syncope and CHF.

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31
Q

What happens with pulse pressure, SV, and systolic pressure in a patient with AS?

A

Pulse pressure becomes more narrow, SV and systolic pressure decrease.

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32
Q

What’s going on with pulses and AS?

A

Either have parvis pulses which are weka and decreased due to CO drop or tarsus pulses which are delayed and decreased as you go up the carotid.

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33
Q

What kind of murmur is AS and where do you best hear it and where can it radiate to?

A

Harsh systolic murmur. Right 2nd intercostal space. Radiates into carotid.

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34
Q

What is the gallavardin phenomenon?

A

Murmur radiates to the apex like MR

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35
Q

2 causes of acute AR?

A

IE and dissection

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36
Q

5 causes of chronic AR?

A

Syphilis, calcification, aortic dilation, ankylosing spondylitis, RF

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37
Q

What is the main pathophysiology of AR?

A

Volume overload starting in left side of heart and working backwards.

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38
Q

What type of murmur is AR and where is it best heard?

A

Diastolic murmur at left 3rd ICS

39
Q

What syndrome can TS be associated with?

A

Carcinoid

40
Q

What is identification of TS in jugular venous pressure?

A

Prominent A wave.

41
Q

What type of murmur is TS and what is the sign associated with it?

A

Diastolic murmur. Corvallos sign. Murmur increases with inspiration and decreases with expiration.

42
Q

TR is associated with what marker in the JVP waveform?

A

Prominent V wave.

43
Q

What type of murmur is TR?

A

Holosystolic

44
Q

Where can we best hear Pulmonary Stenosis and where does it radiate to?

A

2-3 Left ICS and radiates to left shoulder and clavicle

45
Q

Most cases of PR are due to what, what type of murmur is PR and where do we best hear the murmur?

A

Pulmonary HTN. Diastolic. 2nd LSB.

46
Q

What are the 4 continuous murmurs?

A

PDA that is machine like, AV fistula, ASD with super high LA pressure, and coarctation

47
Q

What are the 4 families of drugs to treat arrhythmias?

A

Sodium channel blockers, beta blockers, potassium channel blockers, cardioactive calcium blockers.

48
Q

What 3 cardiac cells/tissues have fast action potentials?

A

Ventricles, atrial muscle cells, purkinje fibers

49
Q

What two tissues/cells have slow action potentials?

A

SA node and AV node.

50
Q

What two channels are establishing resting membrane potential or restores the membrane potential?

A

Sodium potassium pump and sodium/calcium exchanger.

51
Q

What are the two channels responsible for pacemaker action potential depolarization initially and what activates the channels?

A

Funny or leaky sodium and potassium channels. Both coming in. Hyper polarization activates them.

52
Q

What channel continues the depolarization after the leaky/funny channels?

A

Transient calcium channels

53
Q

What ion and channel is responsible for phase 0 of the pacemaker action potential?

A

Calcium. Slow L type (long acting)

54
Q

What are the 3 main factors determining the firing rate or automaticity of the pacemaker cells?

A

Slope of phase 4 which will increase or decrease rate, threshold potential level, resting potential

55
Q

What are the specific type of activation and inactivation gates?

A

M and h

56
Q

What is meant by class 1 drugs being state dependent blockers?

A

They don’t mess around with channels at rest, just activated or inactivated. This means they aren’t messing with normal firing tissue, just high frequency.

57
Q

MOA of Class 1A drugs?

A

Selective for blocking open or activated sodium channels which leads to a slower upstroke of sodium influx phase 0 or slower spontaneous of phase 4.

58
Q

What are the 3 effects of class 1a drugs?

A

Slows conduction velocity, prolongs action potential duration, and prolongs QRS and Qt.

59
Q

What type of cells will be targeted by class 1a drugs?

A

Ectopic pacemaker cells with faster rhythms.

60
Q

What else do class 1a drugs block?

A

Potassium channels

61
Q

Class 1A drugs dissociate with what type of kinetics?

A

Intermediate

62
Q

Procainamide is used to treat what arrhythmia by directly working where in the heart?

A

V tach by directly depressing the SA and AV node

63
Q

3 adverse effects of procainamide?

A

Qt prolongation, tornadoes de pointes, and too much inhibition

64
Q

2 uses for quinidine?

A

Sustained ventricular arrhythmia and sometimes to restore atrial rhythm in Afib or flutter.

65
Q

Quinidine adverse effects on heart?

A

Qt prolongation, torsades de pointes, and excessive conduction inhibition

66
Q

What is disopyramide used for and what is the big time adverse effect?

A

Ventricular arrhythmias. Potent antimuscarinic effect

67
Q

MOA for class 1b drugs and what are their kinetics?

A

Selectively block sodium channels of inactivated or depolarize sodium channels. Dissociate with fast kinetics.

68
Q

What do they not do that is different from class 1a drugs?

A

These guys do not block potasssium channels at all so they do not prolong the action potential

69
Q

What is lidocaine used for?

A

Ventricular tachycardia and arrhythmias associated with MI.

70
Q

2 indications for mexiletine?

A

Ventricular arrhythmias and chronic pain due to diabetic neuropathy and nerve injury

71
Q

MOA for class 1c drugs and what are their dissociation kinetics?

A

Selectively block open sodium channels and has slow dissociation kinetics

72
Q

What about class 1c’s effect on potassium channels?

A

Can block some

73
Q

2 indications of flecainide?

A

Supraventricular arrhythmias and sustained V tach or other life threatening ventricular arrhythmias.

74
Q

Who do we not give flecainide to?

A

Patients with pre existing ventricular issues.

75
Q

What is the drug to drug interaction to remember for propafenone?

A

Don’t combine with cyp2d6 or cyp3a4 inhibitors

76
Q

What is the MOA for beta blockers and what is the result?

A

Block funny channels and L type calcium channels resulting in decreased slope and increased threshold. HR down and AV conductance down.

77
Q

4 clinical indications for beta blockers?

A

Tachycardia due to sympathetic activity, Afib and flutter, AV reentrant, and arrhythmias associated with MI.

78
Q

What is the big deal with Esmolol and how is it used?

A

Super short acting so it is used IV and for emergent situations or surgeries.

79
Q

Which potassium channels are open during resting state?

A

Inward rectifying

80
Q

What is the purpose of potassium channels with the action potential, 2 things?

A

Repolarize the cell. Makes possible the refractory period so we limit action potential duration

81
Q

MOA for class 3 drugs and what 3 effects?

A

Block potassium channels. Increase action potential duration, qt interval, and prolong the refractory period.

82
Q

2 indications for amiodarone?

A

Ventricular arrhythmias and atrial fibrillation

83
Q

2 drug to drug interactions for amiodarone?

A

Rifampin, a cyp3a4 inducer, or cimetidine, a cyp3a4 inhibitor.

84
Q

4 adverse effects of amiodarone?

A

Av block, bradycardia, fatal pulmonary fibrosis and hepatitis

85
Q

What is unique about sotalol and what are the 2 clinical indications?

A

It is a class 2 and 3. Life threatening ventricular arrhythmia and a fib.

86
Q

MOA of dofetilide? What unique identifier to remember about it. 2 clinical indications for it?

A

Pure potassium blocker. Blocks the delayed rectifier channel. Cleared by the kidneys so need to make sure person has good renal clearance. Persistent A fib, heart failure and CAD.

87
Q

MOA of Ibutilide? How is it cleared and administered? Use? Adverse effect, 1?

A

Blocks delayed fast potassium rectifier. IV and by liver. Convert a fib and flutter to normal sinus rhythm. Big time QT prolongation.

88
Q

MOA for class 4 drugs and what 3 effects?

A

Blocks activated and inactivated L type calcium channels. Decrease slope, increase l type threshold and prolong refractory period.

89
Q

What 2 effects does verapamil and diltiazem have on the heart rate?

A

Slow SA node depolarization and prolong the action potential and time through AV node.

90
Q

Clinical use of verapamil and diltiazem, 2 things?

A

Prevention of paroxysmal SVT and rate control in a flutter and fib.

91
Q

Adverse effect of verapamil?

A

Constipation

92
Q

MOA for adenosine acting as an anti arrhythmia drug?

A

Increases potassium current and inhibits calcium and funny currents which leads to hyper-polarization and inhibition of action potentials in slow cells.

93
Q

Clinical use of adenosine?

A

Convert paraoxysmal SVT back to sinus rhythm

94
Q

2 adverse effects of using adenosine?

A

Shortness of breath and bronchoconstriction