Cardiovascular Drugs Flashcards

1
Q

2 most common diseases of heart

A

Congestive Heart Failure (CHF)
&
Coronary Artery Disease (CAD)

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2
Q

Congestive Heart Failure (CHF)

A

Contractibility of heart decreases

  • heart pumps out less than it receives, blood accumulates, heart enlarges.
  • less blood goes out to organs
  • pooling may lead to formation of clots
  • kidneys (sensitive to decrease flow) retain Na and H2O=edema
  • *causes chronic HTN, MI, valve disease, aging
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3
Q

Coronary Artery Disease (CAD)

A

General term for several things that involve insufficient flow of blood to heart muscle

  • arteriosclerosis - aging/narrowing
  • atherosclerosis - fatty deposits/plaque
  • angina - clinical condition - chest pain
  • myocardial infarction - ischemia or death of some heart muscle
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4
Q

Compensatory reflexes

A
  • cardiac enlargement-remodeling
  • sympathetic reflexes - effort to increase blood flow/BP and decrease congestion (release epi/norepi & vasoconstriction/increase HR/force)
  • kidneys retain Na/H2O to increase BP and volume
  • *may help slightly but will eventually weaken the heart
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5
Q

Generalized symptoms of active heart failure

A
  • tiredness
  • weight gain
  • fatigue
  • SOB
  • peripheral edema
  • rapid HR
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6
Q

4 classes of heart failure symptoms

A

Class 1 - symptoms noted with significant exercise or a symptomatic
Class 2 - symptoms noted with mod activity
Class 3 - Symptoms noted with min. Activity
Class 4 - symptoms noted while at rest

A= at risk, D= advanced disease

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7
Q

Left ventricular failure

A
  • pulmonary congestion: blood backs up from L heart into the lungs
  • dyspnea, orthopnea, tachypnea, pulmonary edema, coughing, nocturnal dyspnea
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8
Q

Right ventricle failure

“Venous congestion”

A
  • Fluid backs up into the body first
  • pitting edema
  • ascites (fluid in abdomen)
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9
Q

Congestive heart failure symptoms

A

-right and left sided failure symptoms;
Fatigue, cardiomegaly, periph edema, arrhythmias
-arrhythmias - dead

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10
Q

Pharmacological goals for CHF

A
  • help heart pump more efficiently
  • make work easier for heart; less resistance to blood flow (decreased peripheral resistance)
  • usually multi drug approach
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11
Q

Cardiac Glycosides

A

Digoxin (Lanoxin)

Digitalis derivative
+inotrope, -chronotrope, -dromotrope

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12
Q

Cardiac Glycosides Uses

A
  1. heart failure

2. Arrhythmias - atrial fibrillation, tachycardia

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13
Q

Pharmacological effects of Cardiac Glycosides

A
  • decrease Hr (-chronotropic)
  • increase force of contraction (+inotropic)
  • slow conduction through AV node (lengthen PR interval)
  • improved CO>improves kidney flow, diuresis
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14
Q

MOA of Cardiac glycosides

A
  • inhibits Na/K pump from resetting - slows AV node conduction
  • accelerates entry of Ca, leads to increase Ca in heart muscle - greater myocardial contraction

**maintaining normal K and Ca levels is very important to avoid toxicity.

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15
Q

Pharmacokinetics of cardiac glycosides

A
  • large volume of distribution - loading dose needed aka digitalizing dose
  • narrow therapeutic index
  • long 1/2 life - about 36 hours
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16
Q

Side/Adverse effects of Cardiac glycosides

A
  • anorexia, NVD
  • visual disturbances (green/yellow vision, halos Van Goh)
  • Dig toxicity (arrhythmias)
  • enhanced by hypokalemia (low K) or hypercalcemia (high Ca)

**be careful w/ puts on diuretics (lasix) - eat bananas and other food w/ K

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17
Q

Do not give digoxin if pulse is less than ______ or greater than ______

A

60;100

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18
Q

The 6 Rights

A
  1. Right Patient
  2. Right Drug
  3. Right Dosage
  4. Right Route
  5. Right Time
  6. Right Documentation (HR)
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19
Q

Ischemia

A

Inadequate O2 supply to tissues > can lead to necrosis

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20
Q

Coronary Artery Disease is caused by

A
  • ischemia
  • coronary artery obstruction; plaques or clots
  • decreased blood flow to hear muscle due to coronary artery blockage leads to oxygen demand exceeding the oxygen supply
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21
Q

Arteriosclerosis

A
  • due to aging

- vessels are constricted>decrease blood flow

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22
Q

Atherosclerosis

A

Fatty deposits accumulate in the walls of the arteries

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23
Q

Angina (pectoris)

A

Chest pain due to arteriosclerosis and atherosclerosis

**chest pain resulting from imbalance between oxygen demand & oxygen supply

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24
Q

Myocardial Infarction - MI

A
  • complete ischemia to a section of heart
  • if not restored, piece of heart muscle will die
  • depending on size/location, may cause long term impaired function
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25
Q

What are the 3 types of angina

A
  1. Stable classic angina
  2. Unstable angina
  3. Vasospasm of coronary artery
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26
Q

Stable classic Angina

A

Less serious, from fixed obstruction - usually worsened with exercise

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27
Q

Unstable Angina

A

Sudden interruption; partial or complete blockage, may develop at rest (medical emergency)

**plaque fissuring - inflammation, clot formation

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28
Q

What 3 drugs are used to treat anginas

A
  1. Nitrates-nitroglycerin
  2. Beta Blockers - “olol”
  3. Calcium Channel Blockers
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29
Q

Desired result of anti-anginal drugs?

A

Decrease oxygen demand and increase oxygen delivery so the heart always has O2 it needs.

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30
Q

Nitrate MOA

A

Relaxes vascular smooth muscle; (dilates vessels) - makes it easier to push blood out of the heart

31
Q

Nitrate Uses

A

Angina/hypertensive crisis

32
Q

Nitrates Clinical Effect

A
  • reduced O2 demand; reduced work load due to reduced vascular resistance
  • increased O2 delivery by dilating coronary arteries
33
Q

Nitrate Drugs

A
  • nitroglycerin (Nitro-Bid, Transderm Nitro, Nitro Stat)

- isosorbide (Idordil)

34
Q

What is the most common administration of Nitrates?

A

Sublingual - acts w/ in 5 minutes. (Repeat 2more times, seek medical attention of symptoms do not get better)

35
Q

Is nitrate sensitive to air and light?

A

Yes - must be stored properly for best effects of drug

36
Q

What are other ways of administering nitrates

A

As a patch or orally for prophylaxis

37
Q

What is the 1/2 life of nitrates?

A

30-60 min

38
Q

T or F - Nitrates skip the hepatic first pass

A

True

39
Q

Nitrate Side effects

A
  • headaches
  • faintness/lightheadness - hypotension
  • orthostatic hypotension; reflex tachycardia
  • tolerance
40
Q

Beta Blocker Drugs

A
  • propranolol (Inderal)
  • nadolol (Corgard)
  • atenolol (Tenormin)
  • metoprolol (Lopressor)
  • carvedilol (Coreg)
  • nebivolol (Bystolic)
41
Q

T or F: beta blockers can’t be used with nitrates

A

False - they can be used together

42
Q

Why do beta blockers slow the heart down?

A

Bc they work well to..

  • decrease work load
  • decrease HR
  • allow for better refill
  • help with symptoms and longevity
  • fewer arrhythmias
43
Q

What happens when organs receive less O2 or blood from heart?

A
  • fluid buildup
  • brain: dizziness, drowsiness, less alert
  • lungs: SOB, cough
44
Q

How do kidneys compensate when organs receive less blood?

A

Kidneys retain water by retaining Na

**edema occurs everywhere

45
Q

How do we treat water retention from the kidneys?

A

With diuretics

46
Q

Beta Blocker MOA

A

Decrease O2 consumption of heart.

  • negative chronotropic
  • negative inotropic
47
Q

Beta Blocker side effects

A
  • hypotension
  • bradycardia
  • bronchospasm
  • some have black box warning
  • some bleed over to alpha

**discontinue slowly to avoid tachycardia

48
Q

What are the 2 classes of Ca Channerl Blockers?

A

Dihydropyridines and Nondihydropyridines

49
Q

Dihydropyridines

“Dipine”

A
  • Nifedipine (Procardia or Adalat)
  • Amlodipine (Norvasc)
  • Nisoldipine (Sular)
50
Q

Nondihydropyridines

A
  • verapamil (Calan)

- diltiaszem (Cardizem or Tiazac)

51
Q

Ca channel blocker MOA

A

Inhibit movement of CA to reduce heart work load

52
Q

What is the role of Ca?

A
  • responsible for force of contraction
  • HR
  • regulates contraction in vascular arteries/arterioles
53
Q

Dihydropyridines MOA

A

Block entry of Ca into smooth muscle

-allows for the muscles to relax and causes vasodilation > decrease BP

  • lowers arterial pressure > easier work
  • coronary artery vasodilation > more O2
54
Q

Use of Dihydropyridines

A

Angina and hypertension

55
Q

MOA of Nonhydropydridines

A
  • Effect on the pacemaker cells of the heart. > blocks Ca > decreases rate of SA node & decreases the conduction velocity of the AV node.
  • negative chronotropic/dromotropic
  • blocks entry of Ca into the cardiac muscle > decreases FOC
  • neg inotropic
56
Q

Use of Nonhydropyridines

A

Angina
HTN
Arrrhythmias
CHF

57
Q

Side effects of Ca channel blockers

A
  • HA
  • facial flushing
  • dizziness
  • hypotension
  • reflex tachycardia
  • constipation/swelling
  • Xerostomia: dry mouth
58
Q

Drug types used to treat angina

A
  • nitrates
  • beta blockers
  • Ca channel blockers
59
Q

Diseases that can result from an MI

A
  • HF

- cardiac arrhythmias

60
Q

Immediate treatment for an MI

A
Rest
MONA
-morphine
-oxygen
-nitroglycerin
-aspirin
61
Q

Long term MI treatment

A
Rest
Oxygen
Diet change
Stool softener
Treat other complications: HTN/CHF & arrhythmias
62
Q

CHF treatment goal

A

-improve profusion & reduce excess volume

Meds: ACE inhibitors, diuretics, glycosides, BB

63
Q

CAD treatment goal

A

Decrease O2 demand & increase O2 supply

Meds: BB, CCB & nitrates

64
Q

hypertension is the leading cause of…

A

Stroke, heart attack and kidney disease

65
Q

Risk factors for HTN

A
  • over age of 60
  • men & postmenopausal women
  • family history
  • increased cholesterol
  • diabetes
  • smoking
66
Q

Cause of secondary HTN

A

Renal disease, pregnancy, drug induced

67
Q

Cause of primary HTN

A

Cause unknown but associated factors:

  • family history
  • racial disposition
  • obesity
  • stress
  • smoking
  • sedentary life-style
  • high fat diet
68
Q

Non drug therapy for HTN

A

DASH diet - dietary approaches to stop HTN

  • weight reduction
  • moderate alcohol intake
  • increase physical activity
  • rest
  • decrease fat intake
  • avoid tobacco use
69
Q

Pharmacologic approach to HTN

A

-drugs that impact heart, blood vessels, and kidneys

70
Q

Drug types used to treat HTN

A
  • diuretics
  • beta blockers
  • vasodilators
  • CCB
  • ACE inhibitor
  • ARBs
  • Renin inhibitors
71
Q

If BP is down, kidneys will…

A

Retain Na/H2O to increase BP

72
Q

If BP is up, kidneys will…

A

Excrete Na/H2O to decrease BP

73
Q

MOA of diuretics

A

Increase excretion of Na by inhibiting tubular reabsorption of Na

**where Na goes, H2O follows

74
Q

Thiazides type diuretics

A

Hydrochlorothiazide (Hydrodiuril)