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Cardiopulm > CV meds > Flashcards

CV meds Flashcards

1
Q

drug strategies to improve cardiac function

A
  • directly increase cardiac contractility
  • reduce work load of the heart
  • increase myocardial blood flow
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2
Q

How do drugs reduce workload of the heart

A
  1. reduce contractility (direct)
  2. reduce afterload (indirect)
  3. reduce preload (indirect)
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3
Q

Cholinergic receptors

A
  • muscarinic
  • nicotinic

activated by ACH

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4
Q

Andrenergic Receptors

A
  • alpha (1 and 2)
  • beta (1 and 2)

activated by NE

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5
Q

Beta-1 agonists:

response when stimulated

A

increased HR and contractility

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6
Q

Beta-1 agonists:

clinical use

A

treat conditions of cardiac decompensation

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7
Q

Beta-1 agonists:

impact

A

increases work load of the heart

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8
Q

Beta-1 antagonists:

response when stimulated

A
  1. decreased HR and contractility

2. limit impact of sympathetic NS on heart

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9
Q

Beta-1 antagonists:

clinical use

A

treat compromised or diseased hearts

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10
Q

Beta-1 antagonists:

impact

A
  1. reduce work load of the heart

2. reduces functional capacity

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11
Q

What are some conditions of cardiac decomposition (low CO)

A
  • CV shock

- HF

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12
Q

Ionotropic agents used to:

A
  • increase force of contraction
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13
Q

When should IV + ionotropic agents be used

A
  • inpatient settings

- volume overload with evidence of organ hypofusion

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14
Q

T/F: PT probably on hold with patients receiving IV ionotropic therapy

A

True

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15
Q

Ionotropic Agents:

Dopamine

A

naturally occurring catecholamine

precursor to NE

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16
Q

Ionotropic Agents:

Dopamine low dose

A

renal and splanchnic vasculature dilation = enhanced diuresis

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17
Q

Ionotropic Agents:

Dopamine mod dose

A

enhance cardiac contractility and HR

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18
Q

Ionotropic Agents:

Dopamine high dose

A

increased afterload through peripheral vasoconstriction

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19
Q

When is dopamine used for cardiac trx?

A
  1. severe HF

2. moderate HTN

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20
Q

Ionotropic Agents:

Dobutamine

A
  • beta receptor agonist.
  • increases inotropy and chronotropy
  • decreases afterload
  • improves end organ perfusion (improves MAP)
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21
Q

Ionotropic Agents:

Milrinone

A
  • 3 phosphodiesterase inhibitor
  • increases inotropy, chronotropy, and lusitropy = increased rate of myocardial relaxation
  • increases intramyocardial ATP
  • potent vasodilator
  • management of pulm HTN
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22
Q

Digitalis is used to treat

A
  1. impaired cardiac contractility (HF)
  2. A-Fib
  3. tachycardia
  4. HF
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23
Q

T/F: Digitalis increases CO at rest and during exercise but does not prolong life

A

True

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24
Q

How does digitalis work

A
  1. increases CA2 influx into myocytes

2. Increases AV node’s refractory period, decreasing ventricular response

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25
Q

Digitalis can cause reflex stimulation of the vagus nerve, resulting in:

A

decreased HR and contractility

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26
Q

Drug strategies to improve cardiac function

A
  1. Directly increase cardiac contractility
  2. Reduce work load of the heart (reduce contractility and O2 demand)
  3. Increase myocardial blood flow
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27
Q

drug strategies to reduce work load of the heart

A
  • directly reduce contractility
  • reduce afterload
  • reduce preload
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28
Q

drug strategies to increase myocardial blood flow

A
  • increase blood flow

- manage hemostasis (manage clots)

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29
Q

How do beta blockers work

A
  • antagonists to B-1 receptor

- have negative chronotropic and ionotropic effects (reduces workload)

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30
Q

Non-specific beta blockers

A
  • positive effect on heart.

- negative effect on bronchial smooth muscle

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31
Q

Cardioselective beta blockers

A

specific for B-1 receptors

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32
Q

Beta-1 specific antagonists:

Adverse Effects

A
  1. receptor over reach: causes bronchoconstriction
  2. excessive depression of cardiac function
  3. OH
  4. depression, lethargy, sleep disorders
  5. reduced peak HR
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33
Q

How do CCB work?

A
  1. reduce calcium entrance into myocytes

2. reduces contractility, energy demands on heart, and CO

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34
Q

CCB AE:

A
  1. peripheral vasodilation
  2. decreased BP
  3. flushing
  4. bradycardia
  5. headaches
  6. dizziness
  7. peripheral edema
  8. increased risk of MI
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35
Q

examples of CCB

A
  1. dilitiazem (cardizem)
  2. felodipine (plendil)
  3. verapamil
  4. nifedipine (procardia)
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36
Q

reduced afterload has what effect on O2 consumption

A

Reduced double product

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37
Q

Where are alpha 1 receptors located?

A

vascular smooth muscle

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38
Q

stimulation of a1 receptors causes

A

smooth muscle contraction = vasoconstriction = decreased radius

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39
Q

blockade of a1 receptors (using a1 blockers) results in

A

smooth muscle relaxation = vasodilation = increased radius = reduced TPR = reduced afterload

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40
Q

A1 blockers

AE:

A
  1. reflex tachycardia secondary to HTN
  2. OH
  3. Edema of LE
  4. Syncope
  5. SOB
  6. Weakness
  7. N/V
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41
Q

A1 blocker examples

A
  1. doxazosin
  2. prazosin
  3. terazosin
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42
Q

How do vasodilators work

A

act directly on smooth muscle relax and increase vascular radius

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43
Q

vasodilators:

hydralazine

A
  1. increases membrane permeability to K

2. hyperpolarization of smooth muscle cells

44
Q

vasodilators:

minoxidil

A
  1. increases membrane permeability to K

2. hyperpolarization

45
Q

vasodilators:

diazoxide

A

increase membrane permeability to K

46
Q

vasodilators:

Nitroprusside

A

causes the release of nitrous oxide

47
Q

beta blocker: effect on kidney

A
  • decrease renin release from kidney
  • decreases angiotensin II
  • decreased blood volume
48
Q

beta blockers: AE

A
  1. bradycardia
  2. dizziness
  3. vertigo
  4. gastric discomfort
  5. sexual dysfunction
  6. joint pain
  7. bronchospasm
49
Q

estimating HR max on beta blockers

A

164-(0.7 x age)

50
Q

central acting agents

A
  • inhibit sympathetic outflow from brainstem
  • decreased HR, contractility, and TPR
  • often given with a diuretic
  • act like alpha 2 antagonists
51
Q

central acting agents:

AEs

A
  1. dry mouth
  2. dizziness
  3. drowsiness
  4. hypotension
52
Q

central acting agent examples

A
  • clonidine
  • guanabenz
  • guanfacine
  • methyldopa
53
Q

Diuretics

A
  • increase the amount of urine formed
  • increase diuresis
  • decrease blood volume
  • acts directly on kidneys to increase water and Na exertion
  • inexpensive
54
Q

Loop diuretics

A
  • acts on ascending limb of loop of henle
  • inhibits reabsorption of Na and Cl
  • Loss of K
  • used more for diuresis than HTN
55
Q

Thiazide diuretics

A
  • acts on distal convoluted tubules to inhibit Na reabsorption
56
Q

K sparing diuretics

A
  • interfere with Na-K exchange mechanism in distal convoluted tubules
  • less effective at producing diuresis but are K sparing
57
Q

why do geriatrics need to be started on lower doses of diuretics?

A

they are more susceptible to resulting hypotension

58
Q

Diuretics: AE

A
  1. dehydration
  2. hyponatremia=AMS
  3. hypokalemia = cardiac dysrhythmias
  4. OH
  5. urinary incontinence
  6. toxicity = anorexia, N/V, confusion, weakness, paresthesia
59
Q

Angiotensin II

A
  • constricts walls of arterioles
  • stimulates Na reabsorption in kidneys
  • stimulates aldosterone release from adrenal cortex (reabsorb Na and water)
  • Stimulates catecholamine release
  • vasoconstriction and fluid retention = increased afterload
60
Q

ACE inhibition net effects

A
  1. decreased smooth vascular tone
  2. inhibition of aldosterone secretion ( reduced Na and H2O resorption )
  3. decreased renin activity/production
61
Q

ACE inhibitors:

AE

A

typically well tolerated

  1. allergic rxn
  2. GI discomfort
  3. dizziness
  4. chest p!
  5. persistent cough
  6. weakness
62
Q

where is aldosterone produced?

A

adrenal cortex

63
Q

where does aldosterone act

A

distal convoluted tubule and collecting ducts

64
Q

what does aldosterone do?

A
  • increases reabsorption of Na and water in the kidney

- conserves Na, secretes L, increases water retention and BP

65
Q

Aldosterone antagonists

A
  • act as blocker of aldosterone binding sites
  • eplerenone
  • spironolactone
66
Q

How do Nitrates work?

A
  • venodilator: dec venous return (preload)
  • arteriodilator: dec afterload
  • acts as relaxant for CA smooth muscle and systemic arterial smooth muscle
67
Q

T/F: Nitroglycerin produces vasodilation specifically for coronary arteries

A

False
general dilation
reduces preload and afterload

68
Q

Organic Nitrates for angina pectoris:

MOA

A
  • dec preload and afterload leads to dec cardiac work and dec O2 use
  • dec in MVO2 ( cardiac O2 use) is more important than the increased O2 availability
69
Q

Delivery of Nitroglycerin

A

Oral: 1st pass effect substantial

Sublingual: Best method acutely to avoid 1st pass effect

Buccal

Transdermal: prophylactic

70
Q

Isosorbide Dinitrate

A
  • treats acute episodes and given to prevent angina onset

- long acting

71
Q

isosorbide-5-mononitrate

A
  • long acting

- used primarily for prevention of angina rather than treating an acute situation

72
Q

Nitroglycerin Patches

A
  • not effective acutely
  • must be changed every 24 hrs
  • change where patch is applied to avoid skin rash
  • always use, even if you feel well
  • don’t suddenly stop
73
Q

T/F: If you forget a patch, don’t double up. Just apply 1 as soon as possible

A

True

74
Q

When should you contact an MD when taking Nitroglycerin patches?

A

blurred vision, dry mouth, skin rash, dizziness, or fainting

75
Q

Hemostasis

A
  • process which causes bleeding to be stopped

- requires the combined activity of vascular, platelet, and plasma factors

76
Q

Hemostasis:

vessel wall injury

A

triggers attachment and activation of platelets and causes vasoconstriction

77
Q

Hemostasis:

Platelets

A

become sticky and attach to area of injury

78
Q

Hemostasis:

Plasma factors

A

interact to convert fibrinogen to fibrin which helps form clot

79
Q

Thrombogenesis

A
  • formation of clot (thrombus)
  • can lead to localized vessel occlusion
  • may dislodge and form embolism
80
Q

Embolism

A

blood clot that has moved from site in bloodstream to another site. obstruct artery and block flow

81
Q

Fibrinolysis

A

process that involves break down or degradation of thrombus

82
Q

Anticoagulants

A
  • act by controlling function/synthesis of clotting factors
    Heparin
    Coumadin
83
Q

Antithrombotics

A

Act by inhibiting platelet function (prevents thrombus formation)

  • aspirin
  • plavix
84
Q

T/F: Oral anticoagulants require several days to achieve therapeutic levels

A

True

may be taken for weeks - months

85
Q

Warfarin

A
  • inhibits vit k action

- antidote: treat with vit k and d/c

86
Q

Pradexa

A
  • acts as direct thrombin (factor IIa) inhibitor

- reduce risk of CVA and thrombosis in patients with nonvalvular afib

87
Q

anticoagulants:

AE

A
  1. excessive bleeding
  2. bruising
  3. bloody stools and urine
  4. bleeding gums
  5. ecchyomosis
  6. thrombocytopenia
  7. back and joint pain due to bleeding into abdomen or joint
  8. GI distress
88
Q

anticoagulants:

special concerns for rehab

A
  1. know why your pt is on an anticoagulant
  2. avoid contact sports and risky activities
  3. don’t use w/aspirin
  4. take care brushing teeth and shaving
89
Q

antithrombotics:

Aspirin

A
  1. suppresses synthesis of prostaglandins and thromboxanes via COX 1 and 2 enzymes
  2. prophylactic trx for preventing MIs
90
Q

antithrombotics:

dipryridamole

A

reduces adenosine metabolism and/or cAMP levels in platelets

91
Q

antithrombotics:

clopidgrogel (plavix)

A

inhibit ADP binding to platelets

92
Q

antithrombotics:

AE

A
  1. hemorrhage
  2. severe HA
  3. joint/back p!
  4. GI distress

no antidote

93
Q

when are thrombolytic drugs used

A
  • facilitate breakdown and dissolution of clots that have already formed
  • facilitate formation of fibrinolysin
  • MIs, CVAs, PEs, acute peripheral arterial occlusion, occlusion of indwelling catheters
94
Q

thrombolytics:

AE

A

1. hemorrhage

  • nose bleeds
  • blood in urine/stools
  • bruising
  • unusually heavy menstrual flow
  • back p! or joint p!
95
Q

arrhythmias can result in

A
  1. impaired pump function
  2. cardiac failure
  3. CVAs
  4. death
96
Q

mechanisms of cardiac arrhythmias

A
  1. abnormal pulse generation
  2. abnormal pulse conduction
  3. combo of these 2
97
Q

Arrythmias:

abnormal pulse generation

A
  • defects in SA or AV nodes

- ectopic foci

98
Q

Arrythmias:

abnormal pulse conduction

A
  • abnormality in conduction pathway

- AV block, bundle branch block

99
Q

Management of Arrhythmias:

Class I Drugs

A
  1. Na channel blockers
    - normalize rate of Na influx into cell
    - stabilize membrane and reduce membrane excitability
  2. Lidocaine- helps manage EKG abnormality / defects during early portion of AP
100
Q

Management of Arrhythmias:

Class II Drugs

A

Beta Blockers

  • primary arrhythmia trx
  • diminish influence of excitatory effects of sympathetic NS
  • dec cardiac automaticity
  • lengthens effective refractory period (slower HR)
101
Q

Management of Arrhythmias:

Class III Drugs

A

Prolong myocyte repolarization:

  • inhibit K efflux
  • slows/stabilizes HR
  • used for ventricular arrythmias
102
Q

Management of Arrhythmias:

Class IV Drugs

A

CCBs
- normalize Ca entry into channel which controls excitability and conduction of tissue

not all CCB are effective in managing arrythmias

103
Q

HMG-CoA Reductase Inhibitors / Statins

A
  • enzyme catalyzes rate of limiting step in cholesterol biosynthesis
  • dec cholesterol synthesis
  • inc removal of LDLs from blood.
  • inc synthesis of HDLs
  • stabilize atherosclerotic plaque
  • reduce risk for MI
104
Q

HMG-CoA Reductase Inhibitors / Statins

AEs

A
  1. rhabdomyolysis
  2. tell pts to promptly report muscle p!, tenderness, or weakness
  3. liver damage
  4. drug intolerance
  5. HA
  6. abdominal p! and constipation
  7. loss of coenzyme Q10
105
Q

Rhabdomyolysis

A

destruction of skeletal muscle

Cardiopulm (20 decks)

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