Pharmacological management of CV disease

Question 1

parenteral medication?

Answer 1

doesn’t go through GI tract

-IV, sublingual, subcutaneous., intramm, inhaled

Question 2

benefit to parenteral meds?

Answer 2

fast acting!

Question 3

Enteral meds?

Answer 3

by mouth, rectum or transdermal

Question 4

What does Digitalis do?

Answer 4

affects Na-K+ pump and ultimately affects the AV node to dec. conduction speed and increase myocardial contractility

Question 5

side effect of digitalis?

Answer 5

hypokalemia

Question 6

What do nitrates do for chest pain?

Answer 6

relaxes sm. mm to vasodilate–> dec. preload– >dec. afterload–> dec. demand–> relieves angina

Question 7

who get prescribed nitrates?

Answer 7

CHF, acute MI, HTN

Question 8

PT considerations for ppl on nitrates?

Answer 8

nitrates prior to ex. = reduce cardiac workload and improves cardiac fxn, inc. tolerance for activity before angina sets in

Question 9

Beta Blockers

Answer 9

dec. HR, BP and myocardial contractility in order to allow for increased diastole and increase in blood supply to the myocardium

Question 10

mech. of action for beta blockers?

Answer 10

compete with catecholamines for beta receptor sites

Question 11

what do beta blockers treat?

Answer 11

mild HTN, arrhythmias, slows conduction through the AV node

Question 12

side effects of beta blockers

Answer 12

bradycardia, hypotension, bronchospasm, AV block, nausea,fatigue, depression, sleep disturbances

Question 13

Ca Channel Blockers

Answer 13

inhibit flow of Ca to dec. hr and contractility and vasodilate

Question 14

type 1 Ca channel blockers

Answer 14

*verapamil and diltiazem- peripheral vasodilation, decreased HR, decreased contractility
(verapamil= strongest)
can be used with acute MI
verapamil also used as an antiarrthymic

Question 15

type 2 Ca channel blockers

Answer 15

dihydropyridines (all end in “pines”)- strong periph. vasodilators
- no direct effect on HR or arrhymias,

Question 16

which ca channel blockers are used in combination with beta blockers (to allow for lower doses of beta blockers) and in combination with nitrates to treat angina but cannot be used for acute MIs

Answer 16

type 2 ca channel blockers

Question 17

side effects of Ca channel blockers

Answer 17

headache
hypotension
flushing 
edema
SA node dysfunction
tremors
mood swings
fatigue
reflex tachycardia
GI distress

Question 18

examples of Cardiac Glycosides

Answer 18

digitalis

digitoxin

Question 19

what are cardiac glycosides used to treat

Answer 19

CHF

Question 20

how do cardiac glycosides work?

Answer 20

increase Ca influx to myocardial cells
increase SV and contractility
increased renal profusion= diuretic effect
decreases conduction velocity through AV node

Question 21

problem with cardiac glycosides

Answer 21

low margin of safety- toxicity is easily reached

Question 22

s&s of digitoxin/digitalis toxicity

Answer 22

vomitting, nausea, fatigue, drowsiness, anorexia, confusion, visual disturbances, bradycardia, first degree heart block, PVCs, Vtach, a-fib

Question 23

what type of drug is lidocane?

Answer 23

subclass IB antiarrhythmics, blocks Na+ channels

Question 24

biggest problem with antiarrhythmics

Answer 24

they cause arrythmias

Question 25

class 1 antiarrythmics

Answer 25

block Na+ channels, decreases excitability

Question 26

class II antiarrythmics

Answer 26

B-adrenergic blockers

Question 27

class III antiarrhythmics

Answer 27

K+ channel blockers

Question 28

class IV antiarrhythmics

Answer 28

Ca channel blockers

Question 29

how do arrythmias develop?

Answer 29

heart is usually under the control of the SA node, if it slows down too much development of an ectopic pacemaker may develop (random cells begin to take over the job)

Question 30

action of diuretics

Answer 30

reduce circulating fluid to dec. blood volume and dec. blood pressure. Work on varrying places of the renal tube or loop of Henley - Lasix (greatest effects) - thiazides

Question 31

prob with diuretics?

Answer 31

hypotension and arrhythmias or hypokalemia

Question 32

how do ACE inhibitors work?

Answer 32

ACE is the enzyme needed to convert angiotensin I to angiotensin II and angiotensin II is a potent vasodilator that influences aldosterone production and sodium retention, this results in increased BP, well ACE inhibitors stop ACE enzyme from converting angio I to angio II so none of this can happen!

Question 33

what do statins do?

Answer 33

decrease LDL by inhibiting production of cholesterol in the liver and increase HDLs

Question 34

what does Niacin do?

Answer 34

decreases LDLs and triglycerides and increases HDLs

Question 35

what do fish oil and Omega 3 fatty acids do?

Answer 35

decrease triglycerides