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PDA II > Exam 2 Heart > Flashcards

Exam 2 Heart Flashcards

1
Q

Fast Action Potentials

A

Have all phases of cycle

Found in atria, ventricles, Purkinje Fiber

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2
Q

Slow action potentials (pacemakers)

A

SA and AV nodes
Responsible for automaticity of these tissues
These have no phase I and no real phase 2

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3
Q

Effective refractory period

A

Time it takes for voltage gated Na+ channels to go from “inactive” to “closed”
Seconds AP cannot be generated

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4
Q

Relative refractory period

A

Some Na+ channels are back to closed
Second AP can be generated takes a much greater depolarization than normal
Arrhythmias happen here

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5
Q

Parasympathetic

A

SA and AV node
Decrease - Ca+, I-F current, APs, HR
Increase - K+ channels

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6
Q

Sympathetic

A

Increase Ca++ currents

Increase HR

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7
Q

V-W Type I

A

Na+ channel blockers, affects transmission

Local anesthetics

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8
Q

V-W Type II

A

Sympatholytic agents (beta blockers)

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9
Q

V-W type III

A

Prolonged depolarization (potassium channels blockers)

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10
Q

V-W Type IV

A

Calcium channel blockers

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11
Q

Procainamide, disopyramide

A

Type IA
Medium affinity for Na+ channels
Intermediate on/off of drug in channel
Decrease conduction velocity/automaticity(through Na+ channels)

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12
Q

Quinidine

A

Type IA
Also blocks K+ channels
QT interval prolongation (can cause Torsades de Pointes)

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13
Q

Lidocaine

A

Type IB
Low affinity for Na+ channels - RAPID on/off of drug on channels
- increased effect of depolarizer tissue
-works best in ventricular arrhythmias

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14
Q

Propafenone, Flecainide

A 
Type 1C
High affinity for Na+ channels
SLOW on/off drug on channels
DECREASE conduction 
Blocks K+ channels too
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15
Q

V-W Type 1C

A

ADR - Very arrthythmogenic

Particularly in damaged hearts because of high affinity

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16
Q

Beta-Blockers (Type II)

A

Decrease sympathetic effects on Ca++ channels

  • SA&raquo_space; AV node; good for some re-entry circuits
  • decrease exercised-induced tachycardia
  • slow vent. response to AFib w.o affect in AV node
17
Q

K+ channel blocker (Type III)

A

Affects repole in pacemaker tissue
Doesn’t completely oblate channels
Lengthens refractory period

18
Q

Delayed Rectifier K+ channel blockers (Type III) - order of purity

A

Ibutilide > Dofetilide&raquo_space; Sotalol»Amiodarone

19
Q

Amiodarone

A

Has properties of all classes (Na, Ca, K, Beta)

‘Weak’ - primary effect on K+ channels

20
Q

K+ channel blockers (Type III)

A

Can be arrhythmogenic
Can lead to early afterdepolarization
Can also lead to prolonged QT
-blocks repole, not used long term

21
Q

Verapamil and Diltiazem

A

Type IV - L-type Ca Channel blockers Act on Ca++ dependent tissues in SA and AV node

Slows conduction
Prolong refractoriness
Slows vent. response to AFIB

22
Q

Adenosine

A

Binds to adenosine receptors and increase K+ channels in atria and SA/AV nodes

Net effect: decrease automaticity

23
Q

Digoxin

A

Vagotonic effects
In SA/AV nodes: decrease Ca++ channels and increase K+ channels
-parasympathetic

24
Q

Angina

A

Pain brought on by ischemia

-oxygen supply vs demand

25
Q

Functional consequences of angina

A

Thickening/thinning of myocardial wall
Systolic hypotension
Contractility decrease
Myocardial damage

26
Q

Factors determining myocardial oxygen demand

A

HR, preload, after-load, contractility

27
Q

Fixed stenosis angina

A

Stable occlusion of coronary artery

28
Q

Coronary artery spasm angina

A

Occlusion/damage of coronary artery

Spasm –> occlusion

29
Q

Unstable angina

A

Dislodging of plaque –> thrombosis/spasm

30
Q

Nitroglycerin, isosorbide

A

Nitrate for angina
-forms NO: increase guanylate cyclase, cGMP leads to vasorelaxation

-isosorbide causes coronary steal

31
Q

Nitrates & PD5 inhibitors

A

Both drugs increase cGMP: increases venous pooling and DECREASES BP

32
Q

Ranolazine

A

Angina drug

Decrease intracellular sodium/sodium-dependent calcium channels –> Decrease myocardial contractility, and oxygen demand

33
Q

Ivabradine

A

Angina drug
Decrease If sodium current in SA node, APs in SA, & HR –> decrease myocardial oxygen demand

-little to no effect on BP, contractility, and conductance

34
Q

Digoxin

A

Cardiac glycoside
Long half life (30-40hr)
Decrease Na+/K+ ATPase
-hypokalemia - increases affinity, leads to toxicity

35
Q

Dopamine

Intermediate dose: <10ug/kg/min

A

Beta-agonist
Increase inotrophy
Increase contractility

36
Q

Dopamine

High dose: > 10ug/kg/min

A

Vasoconstriction

Alpha-stimulation: increase arterial/venous constriction

37
Q

Dobutamine

A

Inotropes-beta-agonists
Racemic mixture that stimulates both beta 1/2 receptors
B1 PREDOMINATE - inotrophic

38
Q

Isoproterenol

A

Inotrope
Non selective beta-agonist
Increases inotrophy/chronotrophy
Decreases PVR

39
Q

Amrinone and milrinone

A

PDE3 inhibitor - increase cAMP
Increase inotropy/CO
Increase relaxation
Increase arteriole>venous dilation –> decrease after-load>preload

PDA II (3 decks)

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