Exam 2 Heart

Question 1

Fast Action Potentials

Answer 1

Have all phases of cycle

Found in atria, ventricles, Purkinje Fiber

Question 2

Slow action potentials (pacemakers)

Answer 2

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

Question 3

Effective refractory period

Answer 3

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

Question 4

Relative refractory period

Answer 4

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

Question 5

Parasympathetic

Answer 5

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

Question 6

Sympathetic

Answer 6

Increase Ca++ currents

Increase HR

Question 7

V-W Type I

Answer 7

Na+ channel blockers, affects transmission

Local anesthetics

Question 8

V-W Type II

Answer 8

Sympatholytic agents (beta blockers)

Question 9

V-W type III

Answer 9

Prolonged depolarization (potassium channels blockers)

Question 10

V-W Type IV

Answer 10

Calcium channel blockers

Question 11

Procainamide, disopyramide

Answer 11

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

Question 12

Quinidine

Answer 12

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

Question 13

Lidocaine

Answer 13

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

Question 14

Propafenone, Flecainide

Answer 14

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

Question 15

V-W Type 1C

Answer 15

ADR - Very arrthythmogenic

Particularly in damaged hearts because of high affinity

Question 16

Beta-Blockers (Type II)

Answer 16

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

Question 17

K+ channel blocker (Type III)

Answer 17

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

Question 18

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

Answer 18

Ibutilide > Dofetilide&raquo_space; Sotalol»Amiodarone

Question 19

Amiodarone

Answer 19

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

‘Weak’ - primary effect on K+ channels

Question 20

K+ channel blockers (Type III)

Answer 20

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

Question 21

Verapamil and Diltiazem

Answer 21

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

Question 22

Adenosine

Answer 22

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

Net effect: decrease automaticity

Question 23

Digoxin

Answer 23

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

Question 24

Angina

Answer 24

Pain brought on by ischemia

-oxygen supply vs demand

Question 25

Functional consequences of angina

Answer 25

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

Question 26

Factors determining myocardial oxygen demand

Answer 26

HR, preload, after-load, contractility

Question 27

Fixed stenosis angina

Answer 27

Stable occlusion of coronary artery

Question 28

Coronary artery spasm angina

Answer 28

Occlusion/damage of coronary artery | Spasm --> occlusion

Question 29

Unstable angina

Answer 29

Dislodging of plaque --> thrombosis/spasm

Question 30

Nitroglycerin, isosorbide

Answer 30

Nitrate for angina -forms NO: increase guanylate cyclase, cGMP leads to vasorelaxation -isosorbide causes coronary steal

Question 31

Nitrates & PD5 inhibitors

Answer 31

Both drugs increase cGMP: increases venous pooling and DECREASES BP

Question 32

Ranolazine

Answer 32

Angina drug | Decrease intracellular sodium/sodium-dependent calcium channels --> Decrease myocardial contractility, and oxygen demand

Question 33

Ivabradine

Answer 33

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

Question 34

Digoxin

Answer 34

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

Question 35

Dopamine | Intermediate dose: <10ug/kg/min

Answer 35

Beta-agonist Increase inotrophy Increase contractility

Question 36

Dopamine | High dose: > 10ug/kg/min

Answer 36

Vasoconstriction | Alpha-stimulation: increase arterial/venous constriction

Question 37

Dobutamine

Answer 37

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

Question 38

Isoproterenol

Answer 38

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

Question 39

Amrinone and milrinone

Answer 39

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