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Cardio Pulmonary > Cardiovascular Meds > Flashcards

Cardiovascular Meds Flashcards

1
Q

List drug strategies to improve cardiac function

A
  1. Directly increase cardiac contractility
  2. Reduce workload of the heart by:
    • reducing contractility → direct effect
    • reducing afterload → indirect effect
    • reducing preload → indiriect
  3. Increase myocardial blood flow
  4. Manage hemostasis
  5. Other
    • antiarrhythmic drugs
    • statins
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2
Q

what are ionotropic agents?

A

used to increase force of contraction

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3
Q

T/F: intravenous positive iontrophic agents can be used anywhere

A

FALSE

should only be used in inpatient settings

and then only in pts manifesting S/S of low CO-syndrome

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4
Q

T/F: pt services are probably on hold with pts recieving IV ionotropic therapy

A

TRUE

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5
Q

List several ionotrophic agents

A
  1. Dopamine
  2. Dobutamine
  3. Milrinone
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6
Q

what is the effect of low-dose dopamine?

A

associated with dilation within renal and splanchnic vasculature resulting in enhanced diuresis

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7
Q

what is the effect of moderate-dose dopamine?

A

enhances cardiac contractility and HR

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8
Q

what is the effect of high-dose dopamine?

A

increased afterload through peripheral vasoconstriction

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9
Q

describe dobutamine

A
  1. +ionotrophic and chronotrophic agent
    • (increased contracility and HR)
  2. decreases afterlod
  3. beta-receptor agonist
  4. improved end organ perfusion
    • improves MAP
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10
Q

describe Milrinone

A
  1. type 3 phosphodiesterase inhibitor
  2. increases iontrophy, chronotrophy, and lusitrophy
    • contractility, HR, rate of myocardial relaxation
  3. increases intramyocardial ATP
  4. potent vasodilator
  5. used in management of pulmonary HTN
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11
Q

what is Digitalis used to treat and how does it work?

A
  1. Used to treat impaired cardiac contractility typically caused by HF
  2. works by directly increasing cardiac contracility
    • direct ionotrophic effects
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12
Q

what else is digitalis referred to as?

A
  1. Foxglove
  2. cardiac glycoside
  3. digoxin
  4. digitoxin
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13
Q

how does Digitalis increase cardiac contracility?

A
  1. increases Ca2+ influx into myocytes
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14
Q

what are the electrophysiological effects of digitalis?

A
  1. increases the AV node’s refractory period, decreasing the ventricular response (anti-arrhythmic)
    • used to treat A-Fib, Atrial tachycardia and HF
    • can cause reflex stimulation of the vagus nerve
    • decrease HR and contractility
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15
Q

List drug classes that work to directly reduce contractility and thus reduce workload of the heart

A
  1. Beta-blockers
  2. Ca2+ channel blockers
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16
Q

what is the effect on the heart when a beta-1 agonist is given?

A

increased HR

increased contractility

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17
Q

what is the clinical use of beta-1 agonists? What is the impact on cardiac work?

A
  1. Clinical use
    • treat conditions of severe cardiac decompensation
      • cardiovascular shock
      • in conjunction with cardiac surgery
      • HF
  2. Impact on cardiac work
    • increases work load of the heart
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18
Q

what is the effect on the heart when a beta-1 antagonist is given?

A

decreased HR

decreased contractility

limit impact on sympathetic NS on the heart

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19
Q

what is the clinical use of a beta-1 antagonist and what is the effect on cardiac work?

A
  1. Clinical use
    • used to treat compromised or diseased hearts
  2. Impact on cardiac work
    • reduces workload of the heart
    • reduces functional capacity
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20
Q

T/F: Beta-1 antagonists affect primarily the heart

A

TRUE

(called beta-blockers)

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21
Q

what is the effect of beta-blockers on the heart?

A

negative chronotropic and ionotrophic effect

(reduces workload of the heart)

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22
Q

differentiate between the 2 subtypes of beta-blockers

A
  1. non-specific beta-blocker
    • positive effect on the heart
    • negative effect (smooth muscle contraction) on bronchial smooth muscle
  2. cardioselective beta-blocker
    • specific for B-1 receptors which are found most frequently on cardiac tissue
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23
Q

Beta-blockers suffic

A

-olol

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24
Q

Adverse effects of beta-blockers

A
  1. receptor overreach
    • can cause bronchoconstriction which is not a problem in most ppl but becomes a problem in those with pulmonary disease (cor pulmonale)
  2. can cause excessive depression of cardiac function
  3. OH
  4. depression, lethargy and sleep disorders (long term use)
  5. reduced peak HR
  6. reduced exercise capacity
    7.
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25
Q

how to calculate HRmax for someone on a beta-blocker

A

HRmax = 164 - 0.7*age

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26
Q

what is the effect of Ca channel blockers on the heart?

A
  1. reduce calcium entrance into myoctyes causing:
    • reduced contractility
    • reduced energy demands on heart
    • reduced CO
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27
Q

AE of Ca channel blockers

A
  1. decreased BP
  2. flushing
  3. bradycardia
  4. HA
  5. dizziness
  6. peripheral edema
  7. May increase risk of MI

*result in peripheral vasodilation which explains many AE

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28
Q

List drugs that reduce afterload

A
  1. Alpha blockers
  2. direct vasodilators
  3. beta-blockers
  4. centrally acting agents
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29
Q

what is the effect of alpha blockers?

A

smooth muscle relaxation, vasodilation and decreased TPR

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30
Q

what is TPR?

A

Total Peripheral Resistance (aka systemic vascular resistance or SVA)

  • the resistance to blood flow offered by all of the systemic vasculature beds to blood flow
  • largely determined by changes in blood vessel diameter
    *
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31
Q

AE of alpha blockers

A
  1. these are systemic drugs with systemic effects
  2. reflex tachycardia secondary to hypotension
  3. OH
  4. edema of LE
  5. syncope
  6. SOB
  7. Weakness
  8. N/V
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32
Q

how do direct vasodilators work?

A

work directly on smooth muscle cells to cause relaxation and thus reduce afterload and the workload on the heart

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33
Q

how can beta-blockers reduce afterload?

A

reduce vascular smooth muscle contraction and SVR

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34
Q

how do centrally acting agents act to reduce afterload?

A
  1. appear to inhibit sympathetic outflow from the brainstem
    • decrease HR
    • decrease contractility
    • decrease TPR
  2. act like alpha 2 antagonists
  3. often given with a diuretic
35
Q

AE of centrally acting agents

A
  1. dry mouth
  2. dizziness
  3. drowsiness
  4. hypotension
36
Q

how does influencing preload reduce the workload of the heart?

A

changes in blood volume affect arterial pressure by changing CO

they influence the Frank-Sterling law to reduce LVEDV and thus reduce cardiac contracility

37
Q

list drug classes that work to reduce preload

(and thus reduce the workload of the heart)

A
  1. Diuretics
    • loop diuretics
    • thiazide diuretics
    • potassium sparing diuretics
  2. ACE inhibitors
  3. ARBs
  4. Aldosterone antagonists
38
Q

how do diuretics reduce preload?

A

they increase the amount of urine formed

  • increases diuresis which decreases blood volume
  • act directly on the kidneys to increase water and sodium excretion
39
Q

how do loop diuretics work?

A
  1. act on the ascending limb of the loop of Henle
  2. inhibit the reabsorption of Na+ and Cl-
  3. loss of K+
40
Q

how do thiazide diuretics work?

A
  1. act on the distal convoluted tubules to inhibit Na+ reabsorption
41
Q

how do K+ sparing diuretics work?

A
  1. interfere with sodium-potassium exchange mechanism in distal convoluted tubules
  2. are less effective at producing diuresis but are K+ sparing
42
Q

rank the diuretic classes based on AEs

A

loop > thiazides > potassium sparing

43
Q

loop diuretics are used more for _______

A

diuresis than HTN control

44
Q

Diuretics AEs

A
  1. geriatric pts → more susceptible to resulting hypotension
  2. dehydration
    • OH
    • increased TPR
    • activate renin-angiotensin system
  3. Electrolyte imbalance
    • hyponatremia → AMS
    • hypernatremia → cardiac dysrhythmias
  4. OH and falls precaution
  5. Can cause urinary incontience secondary to increased urine production
45
Q

why do pts on diuretics call them “water pills?

A

they will frequently require bathroom breaks and

46
Q

S/S of toxicity from diuretics

A
  1. anorexia
  2. N/V
  3. confusion
  4. increased weakness
  5. paresthesia
47
Q

List all the effects angiotension II has

A
  1. constricts walls of arterioles
  2. stimulates Na+ reabsorption in the kidneys
  3. stimulates aldosterone release from adrenal cortex which causes kidneys to reclaim still more sodium and water
  4. stimulates catecholamine release
  5. net effects
    • vasoconstriction
    • fluid retention
    • increased afterload
48
Q

what is the entire goal of the renin-angiotensin system?

A

preserve water and electrolytes

49
Q

what are the net effect of ACE Inhibition?

A
  1. decreased vascular smooth muscle tone
  2. inhibition of aldosterone secretion
  3. decreased renin activity/production
50
Q

AE of ACE inhibitors

A

typically well tolerated

  1. allergic reaction (some may have this and it presents like a cough)
  2. GI discomfort
  3. Dizziness
  4. Chest pain
  5. Persistent cough
  6. Weakness
51
Q

suffix for ARBs

A

(ARBS = angiotensin II receptor antagonists)

suffix = -artan

52
Q

what is aldosterone?

A

a steroid hormone produced by adrenal cortex

  • plays a central role in regulating BP
  • acts at the level of the distal convoluted tubule and collecting ducts
  • increases reabsorption of ions (Na+) and water in the kidney
  • conserves Na+, secretes K+, increases water retention, increases BP
53
Q

list classes of drugs available to treat HTN

A
  1. Direct vasodilators
  2. Beta-adrenergic blockers
  3. Centrally acting agents
  4. Alpha blockers
  5. Ca+ channel blockers
  6. ACE Inhibitors
  7. Angiotensin II receptor antagonists (ARBs)
  8. Diuretics
  9. Aldosterone receptor blockers
54
Q

list drug classes that work to increase blood flow to the myocardium

(thus increasing myocardial blood flow)

A
  1. Nitrates
    • organic nitrates
    • nitroglycerin patches
55
Q

how do nitrates work on the myocardium?

A
  1. venodilator → decrease venous return and decrease preload
  2. arteriodilator → decrease afterload
  3. acts as a relaxant for coronary artery smooth muscle and systemic arterial smooth muscle
56
Q

T/F: organic nitrates like nitroglycerin act specifcally on coronary arteries

A

FALSE
they produce a general vadodilation not specifically a coronary artery dilation

57
Q

how can nitroglycerin be delivered?

A
  1. Oral → first pass effect is substantial
  2. Sublingual → best method to treat acutely/avoids 1st pass effect
  3. Buccal → cheek and gum
  4. Transdermal patches → prophylactic
58
Q

things to remember with nitroglycerin patches

A
  1. not effective acutely/immediately
  2. must be changed every 24 hrs
  3. change where patch is applied to avoid skin rash
  4. always use it even if you are feeling well
  5. don’t suddenly stop using it
  6. don’t double up if patch is forgotten
  7. dispose of used
59
Q

when should a pt contact an MD when they are on a nitroglycerin patch?

A

if they develop blurred vision, dry mouth, skin rash, dizziness, or fainting

60
Q

List drugs that manage hemostasis

A
  1. Thrombolytic agents
  2. Antiplatelet agents
  3. Anticoagulants
61
Q

what is hemostasis?

A
  1. Intrinsic process which causes bleeding to be stopped
  2. requires the combined activity of vascular, platelet and plasma factors
    • vessel wall injury trigger attachment and activation of platelets and causes vasoconstriction
    • platelets become “sticky” and attach to the area of vessel wall injury
    • plasma factors interact to convert fibrinogen to fibrin which helps form clot
62
Q

how do thrombolytics work?

A

act by degrading a formed clot

63
Q

AE of thrombolytics

A
  1. hemorrhage
  2. be alert for signs of heavy bleeding
    • severe HA
    • joint or back pain
  3. no antidote
  4. GI distress
  5. unusal bleeding
64
Q

unusal bleeding sites that may occur when a pt is on thrombolytics

A
  1. nose bleeds
  2. blood in urine or stool
  3. bruising
  4. unusually heavy menstrual flow
  5. back pain or joint pain may indicate abdominal or joint hemorrhage respectively
65
Q

what are anticoagulants?

A

chemical substances that help prevent or slow the coagulation of blood (formation of clots)

  • these are preventative
  • commonly called blood thinners
  • act by interfering with the proteins in the blood that are involved in the coagulation process
66
Q

list some drugs that are anticoagulants

A
  1. Heparin
  2. Coumadin (Dicoumarol, Warfarin)
  3. Xarelto
  4. Eliquis
  5. Lovenox
67
Q

Anticoagulants are used primarily to treat _____

A
  1. strokes
  2. MIs
  3. DVT
  4. PE
  5. Hx of blood clots, post surgery, inactivity
  6. A-Fib
68
Q

AE of anticoagulants

A
  1. Hemorrhage
  2. bruising, bloody stools, bleeding gums, blood in urine, ecchyomosis
  3. thrombocytopenia
  4. back pain, joint pain
    • bleeding into the abdomen or a joint
  5. GI distress
69
Q

Special Concerns for rehab pts on anticoagulants

A
  1. know why your pt is on an anticoagulant
  2. while using this med, it is very important that one avoids contact sports and other activities that may cause you to be injured
  3. do not use with aspirin concurrently
  4. take special care in brushing teeth and in shaving
    • soft toothbrush and floss gently
    • best to use electric shaver over a blade
70
Q

how do antiplatelet drugs work?

A

prevent platelets from clumping together to form a clot

  • aspirin is a classic drug in this class
  • may also be called blood thinners
71
Q

what is an arrhytmia?

A

any significant deviation from normal cardiac rhythm

can result in:

  1. impaired pump function
  2. cardiac failure
  3. CVAs
  4. death
72
Q

List several mechanisms for a cardiac arrhytmia

A
  1. abnormal pulse generation
    • defects in SA or AV nodes
    • ectopic foci
  2. abnormal pulse conduction
    • abnormality in conduction pathway
    • AV block
    • Bundle branch block
  3. a combo of these
73
Q

Drugs that treat arrhythmias

A
  1. Class I drugs → Na+ channel blockers
  2. Class II drugs → Beta blockers
  3. Class III drugs → prolong myocyte repolarization
  4. Class IV → Ca+ channel blockers
74
Q

describe Class I anti-arrhythmic drugs

A

Na+ channel blockers

  1. normalize the rate of Na+ influx into the cell
  2. stabilize the membrane and reduce membrane excitability
  3. lidocaine is an example
75
Q

describe Class II anti-arrhythmic drugs

A

Beta Blockers

  1. main stay of arrhythmia trx
  2. diminish the influence of the excitatory effects of the sympathetic NS
  3. decreases cardiac automaticity
  4. lengthens the effective refractory period resulting in a slower HR
76
Q

T/F: being on a beta-blocker reduces the liklihood of a second MI

77
Q

describe Class III anti-arrhythmic drugs

A

Prolong myoctye repolarization

  1. inhibit K+ efflux
  2. slows/stabilizes HR
  3. used to treat ventricular arrhythmias
78
Q

describe Class IV anti-arrhytmic drugs

A

Ca+ Channel Blockers

  1. normalize Ca++ entry into the channel thus controlling excitability and the conduction of cardiac tissue
  2. Verapamil, diltiazem
79
Q

T/F: not all Ca++ channel blockers are effective in managing cardiac arrhythmias

80
Q

Statins are _________ lowering drugs

A

cholesterol

81
Q

what drugs are used to treat hyperlipidemia?

A

HMG-CoA Reductase Inhibitors (Statins)

82
Q

how do statins help treat hyperlipedmia?

A
  1. decreased cholesterol synthesis
  2. increased removal of LDLs from blood
  3. some can increase HDLs
  4. stabilize athersclerotic plaques
  5. reduce risk for an MI
83
Q

AE of Statins

A
  1. Rhabdomyolysis
  2. Muscle pain
  3. liver damage → pt should have quarterly liver panels
  4. drug intolerance
  5. HA
  6. abdominal pain
  7. constipation
  8. Loss of Co Enzyme Q10

Cardio Pulmonary (21 decks)

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