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First Aid > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Standing and the valsalva maneuver causes what kind of cardiovascular change?

A

Decreases preload and left ventricular volume

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2
Q

HOCM and MVP murmurs improve under what conditions?

A

Increased preload because there is more blood in the heart to push the structures back to normal anatomy

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3
Q

Regurgitant murmurs and valvular murmurs get quieter or louder with increased afterload?

A

Louder. There is increased pressure causing more backflow through the regurgitant valves

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4
Q

Myocytes

Class I antiarrhythmics block what channels?

A

Sodium channel blockers in myocytes

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5
Q

SCAP

In myocardiac action potentials, the plateau phase is due to efflux and influx of what ions?

A

Influx of calcium
Efflux of potassium

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6
Q

What is the outcome of sodium channel blockers?

A

Decreases the slope of phase 0 depolarization in myocardial cells.

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7
Q

Queen, Prom King, Disappear

Class IA sodium blockers inclue which drugs?

A

Quinidine
Procainamide
Disopyramide

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8
Q

Is Class IA sodium blockers used for atrial or ventricular arrhythmias?

A

Both

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9
Q

What are the adverse effects of Quinidine?

A

Torsades de point,e Headache, tinnitus

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10
Q

What are the adverse effects of Procainamide?

A

SLE-like symptoms

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11
Q

What is the major side effect of Class IA sodium channel blockers? (Quinidine, procainamide, Disopyramidine)

A

Torsades de pointes due to increased QT interval

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12
Q

Does Class IA sodium channel blockers increase or decrease the myocardial action potential?

A

Increase. It has moderate effects.
C>A>B

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13
Q

I’d By Liddy’s Mexican tacos

Class IB sodium channel blockers include which drugs?

A

Lidocaine
Mexiletine

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14
Q

Is Class IB sodium channel blockers used for atrial or ventricular arrhymias?

A

Ventricular

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15
Q

Does Class IB sodium channel blocks increase or decrease the myocardial action potential?

A

Decrease. No potassium channel activity.

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16
Q

When is it best to use class IB sodium channel blockers? (Lidocaine, Mexiletine)

A

Best after an MI. It preferentially affects ischemic ventricular tissue

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17
Q

What is the adverse side effects of class IB sodium channel blockers?

A

CNS depresion

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18
Q

Can I have fries, please

Class IC sodium channel blockers include which drugs?

A

Flecainide
Propafenone

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19
Q

What is the outcome of IC sodium channel blockers on myocardial action potential?

A

They prolong the refractory period in the AV node but they do not increase the length of the action potential

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20
Q

When are class IC sodium channel blockers used?

A

Atrial fibrillation.
Only as a last result in ventricular tachycardia

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21
Q

For what conditions is class IC contraindicated?

A

Structural and ischemic heart disease. Prolonging the refractory period of ischemic heart tissue is not beneficial.

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22
Q

Beta blockers include which drugs?

A

-olol drugs
Metoprolol, propanolol, carvedilol

23
Q

Which receptors do beta blockers work on?

A

B1 receptors - stimulatory heart receptors
B2 receptors - inhibitory receptors on lungs and other organs

24
Q

What is the outcome of beta blockers on B2 receptors of the lungs?

A

It blocks the sympathetic response on B2 receptors.
The normal response is to bronchodilate. If you block that response the outcome is bronchoconstriction

25
Q

Because of the bronchoconstriction effects of beta blockers, they are contraindicated in which patients?

A

COPD and asthma

26
Q

What is the MOA of beta blockers on pacemaker cells?

A

Increases the slope of phase 4 in pacemaker cells by decreasing Calcium currents. This decreases heart rate

27
Q

In what conditions is beta blockers best used in?

A

SVT, ventricular rate control in A.fib and A.flutter. Prevent ventricular arrhythmia post MI.

28
Q

What are some adverse effects of beta blockers?

A

Bradycardia, AV block, sedation, exacerbation of asthma, impotence

29
Q

AIDS

Class III antiarrhymics (potassium channel blockers) include which drugs?

A

Amiodarone
Ibutilid
Dofetilide
Sotalol

30
Q

What is the outcome of potassium channel blockers?

A

Increase action potential duration, increase QT interval

31
Q

What conditions is it best to use potassium channel blockers?

A

atrial fibrillation, atrial flutter, VT
All conditions where the action potentials are going too fast

32
Q

What are some side effects of amiodarone? (potassium channel blocker)

A

Thyroid issue (its made of iodine)
Corneal deposits
Neurological effects
Constipation
bradycardia
Need to check PFT, LFT, TFT before using

33
Q

What is the MOA of statins?

A

Inhibit HMG-CoA reductase which decreases cholesterol synthesis

34
Q

Side effects of statins

A

Hepatotoxicity
Myopathy especially when used with fibrates or niacin

35
Q

What is the MOA of bile acid resins?

A

Decreases bile acid circulation
This leads to a compensatory conversion of cholesterol to bile

36
Q

Side effects of bile acid resins?

A

GI upset and decreased absorption of other drugs and fat soluble vitamins

37
Q

Statins preferentially decrease HDL, LDL, or triglycerides?

38
Q

What is the MOA of ezetimibe?

A

Prevents cholesterol absorption at the small intestine brush border

39
Q

What is the MOA of fibrates?

A

Activate PPAR which uipregulates lipoprotein lipase –> break down triglycerides into free fatty acids

40
Q

Fibrates preferentially decrease HDL, LDL, or Triglycerides?

A

Triglycerides

41
Q

What are the 2 main methods of action for Digoxin?

A

Digoxin exerts its effects via:
1. Increased vagal stimulation to the AV node –> decreased HR
2. Inhibits Na/K ATPase leading to increased intracellular calcium –> increased contractility

42
Q

Mineralcorticoid receptor antagonist that improves survival and diuresis in HF patients

A

Spironolactone

43
Q

Loop diuretic used for treatment of pulmonary congestion and fluid retention in HF patients

A

Furosemide

44
Q

MOA of nitrates (nitroglycerin)

A

Increase in cGMP which causes a decrease in intracellular calcium –> myosin dephosphorylation leading to vascular smooth muscle relaxation

This lowers blood pressure, decreases preload and afterload (HF)

45
Q

Where are a1 adrenergic receptors primarily found

A

Peripheral vasculature
Urinary sphincter
Eye

46
Q

Where are b1 adrenergic receptors primarily found

A

heart and kidney

47
Q

where are b2 adrenergic receptors primarily found

A

peripheral vasculature
bronchi (lungs)
uterus

48
Q

Sympathetic stimulation of a1 adrenergic receptors leads to what response

A

A1 receptors are found on the peripheral vasculature.
Sympathetic stimulation leads to vasoconstriction of the peripheral vasculature

Makes sense to constrict blood flow to periphery so that blood can go to skeletal muscle and brain

49
Q

Sympathetic stimulation of B1 adrenergic receptors leads to what response

A

B1 receptors are primarily found on the heart and kidney.
Sympathetic stimulation leads to increased contractility and increased heart rate

50
Q

Sympathetic stimulation of B2 adrenergic receptors leads to what outcome

A

B2 receptors are primarily found on peripheral vascular smooth muscle, bronchi, and
Sympathetic stimulation of B2 causes vasodilation of smooth muscle vasculature, especially in the lungs

B2 is basically inhibitory form of A1 – vasoconstriction vs vasodilation

51
Q

MOA of adenosine

A

Increased potassium efflux in **SA and AV nodal cells **

52
Q

Compare and contrast:
Atropine
Amiodarone
Adenosine

A

Atropine - Muscarinic antagonist
Amiodarone - Potassium channel blocker in myocardial cells
Adenosine - Potassium efflux in SA node

53
Q

Dihydropyridines (amlodipine) act on what sites?

A

Arterial smooth musle = vasodilation.
NO effect on cardiac conduction

54
Q

Diltiazem and Verapamil (Nondihydropyridines) act on what sites

A

Cardiac conduction through the SA and AV node

First Aid (14 decks)

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