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Pharm 2300 > Cardiovascular Drugs > Flashcards

Cardiovascular Drugs Flashcards

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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
What are the 3 types of angina
1. Stable classic angina 2. Unstable angina 3. Vasospasm of coronary artery
26
Stable classic Angina
Less serious, from fixed obstruction - usually worsened with exercise
27
Unstable Angina
Sudden interruption; partial or complete blockage, may develop at rest (medical emergency) **plaque fissuring - inflammation, clot formation
28
What 3 drugs are used to treat anginas
1. Nitrates-nitroglycerin 2. Beta Blockers - “olol” 3. Calcium Channel Blockers
29
Desired result of anti-anginal drugs?
Decrease oxygen demand and increase oxygen delivery so the heart always has O2 it needs.
30
Nitrate MOA
Relaxes vascular smooth muscle; (dilates vessels) - makes it easier to push blood out of the heart
31
Nitrate Uses
Angina/hypertensive crisis
32
Nitrates Clinical Effect
- reduced O2 demand; reduced work load due to reduced vascular resistance - increased O2 delivery by dilating coronary arteries
33
Nitrate Drugs
- nitroglycerin (Nitro-Bid, Transderm Nitro, Nitro Stat) | - isosorbide (Idordil)
34
What is the most common administration of Nitrates?
Sublingual - acts w/ in 5 minutes. (Repeat 2more times, seek medical attention of symptoms do not get better)
35
Is nitrate sensitive to air and light?
Yes - must be stored properly for best effects of drug
36
What are other ways of administering nitrates
As a patch or orally for prophylaxis
37
What is the 1/2 life of nitrates?
30-60 min
38
T or F - Nitrates skip the hepatic first pass
True
39
Nitrate Side effects
- headaches - faintness/lightheadness - hypotension - orthostatic hypotension; reflex tachycardia - tolerance
40
Beta Blocker Drugs
* propranolol (Inderal) * nadolol (Corgard) * atenolol (Tenormin) * metoprolol (Lopressor) * carvedilol (Coreg) * nebivolol (Bystolic)
41
T or F: beta blockers can’t be used with nitrates
False - they can be used together
42
Why do beta blockers slow the heart down?
Bc they work well to.. - decrease work load - decrease HR - allow for better refill - help with symptoms and longevity - fewer arrhythmias
43
What happens when organs receive less O2 or blood from heart?
- fluid buildup - brain: dizziness, drowsiness, less alert - lungs: SOB, cough
44
How do kidneys compensate when organs receive less blood?
Kidneys retain water by retaining Na **edema occurs everywhere
45
How do we treat water retention from the kidneys?
With diuretics
46
Beta Blocker MOA
Decrease O2 consumption of heart. - negative chronotropic - negative inotropic
47
Beta Blocker side effects
- hypotension - bradycardia - bronchospasm - some have black box warning - some bleed over to alpha **discontinue slowly to avoid tachycardia
48
What are the 2 classes of Ca Channerl Blockers?
Dihydropyridines and Nondihydropyridines
49
Dihydropyridines “Dipine”
* Nifedipine (Procardia or Adalat) * Amlodipine (Norvasc) * Nisoldipine (Sular)
50
Nondihydropyridines
- verapamil (Calan) | - diltiaszem (Cardizem or Tiazac)
51
Ca channel blocker MOA
Inhibit movement of CA to reduce heart work load
52
What is the role of Ca?
- responsible for force of contraction - HR - regulates contraction in vascular arteries/arterioles
53
Dihydropyridines MOA
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
Use of Dihydropyridines
Angina and hypertension
55
MOA of Nonhydropydridines
- 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
Use of Nonhydropyridines
Angina HTN Arrrhythmias CHF
57
Side effects of Ca channel blockers
- HA - facial flushing - dizziness - hypotension - reflex tachycardia - constipation/swelling - Xerostomia: dry mouth
58
Drug types used to treat angina
- nitrates - beta blockers - Ca channel blockers
59
Diseases that can result from an MI
- HF | - cardiac arrhythmias
60
Immediate treatment for an MI
``` Rest MONA -morphine -oxygen -nitroglycerin -aspirin ```
61
Long term MI treatment
``` Rest Oxygen Diet change Stool softener Treat other complications: HTN/CHF & arrhythmias ```
62
CHF treatment goal
-improve profusion & reduce excess volume Meds: ACE inhibitors, diuretics, glycosides, BB
63
CAD treatment goal
Decrease O2 demand & increase O2 supply Meds: BB, CCB & nitrates
64
hypertension is the leading cause of...
Stroke, heart attack and kidney disease
65
Risk factors for HTN
- over age of 60 - men & postmenopausal women - family history - increased cholesterol - diabetes - smoking
66
Cause of secondary HTN
Renal disease, pregnancy, drug induced
67
Cause of primary HTN
Cause unknown but associated factors: - family history - racial disposition - obesity - stress - smoking - sedentary life-style - high fat diet
68
Non drug therapy for HTN
DASH diet - dietary approaches to stop HTN - weight reduction - moderate alcohol intake - increase physical activity - rest - decrease fat intake - avoid tobacco use
69
Pharmacologic approach to HTN
-drugs that impact heart, blood vessels, and kidneys
70
Drug types used to treat HTN
- diuretics - beta blockers - vasodilators - CCB - ACE inhibitor - ARBs - Renin inhibitors
71
If BP is down, kidneys will...
Retain Na/H2O to increase BP
72
If BP is up, kidneys will...
Excrete Na/H2O to decrease BP
73
MOA of diuretics
Increase excretion of Na by inhibiting tubular reabsorption of Na **where Na goes, H2O follows
74
Thiazides type diuretics
Hydrochlorothiazide (Hydrodiuril)

Pharm 2300 (6 decks)

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