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Pharmacology > 37. Cardiac Glycosides, Antianginals, and Antidysrhythmics > Flashcards

37. Cardiac Glycosides, Antianginals, and Antidysrhythmics Flashcards

1
Q

What increases in heart failure

A

preload and afterload

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2
Q

volume of blood in the ventricles at the end of diastole (end diastolic pressure)

A

preload

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3
Q

resistance left ventricle must overcome to circulate blood; increased means increased cardiac workload

A

afterload

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4
Q

what causes increase in preload

A
  • hypervolemia
  • regurgitation of cardiac valves
  • heart failure
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5
Q

what causes increase in afterload

A
  • hypertension

- vasoconstriction

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6
Q

high risk for HF without symptoms or structural disease

A

stage 1 (A) HF

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7
Q

some levels of cardiac changes without symptoms of heart faulre

A

stage 2 (B) HF

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8
Q

structural heart disease w/ symptoms of HF

A

stage 3 (C) HF

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9
Q

severe structural heart disease and marked symptoms of HF at rest

A

stage 4 (D) HF

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10
Q

heart failure nonpharmacologic treatment

A
  • limit Na to 2g per day
  • possible fluid restriction
  • stop smoking
  • manage obesity
  • aerobic exercise
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11
Q

normal atrial natriuretic peptide (ANP)

A

20-77 pg/mL

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12
Q

normal brain natriuretic peptide (BNP)

A

less than 100 pg/mL

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13
Q

BNP level positive for HF

A
  • greater than 100 pg/mL

- acute HF: looking for values greater than 400 pg/mL

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14
Q

what class of drugs is digoxin

A

cardiac glycoside

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15
Q

MOA of Digoxin

A
  • inhibits Na-K ATPase
  • promotes increased force of cardiac contraction, cardiac output, and tissue perfusion
  • decreases ventricular rate
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16
Q

uses of Digoxin

A

heart failure and afib

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17
Q

adverse reactions to Digoxin

A
  • bradycardia
  • cardiac dysrhythmias
  • thrombocytopenia
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18
Q

side effects of Digoxin

A
  • dizziness
  • mental disturbances and confusion
  • N/V/D
  • headache
  • weakness
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19
Q

how to administer Digoxin by IV

A

slowly by direct IV injection over minimum of 5 minutes

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20
Q

nursing safety for Digoxin

A
  • higher doses have no additional benefit in HF but may increase toxicity
  • decreased renal function many lead to toxicity
  • use lean body weight in older adults to calculate dose
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21
Q

contraindications for Digoxin

A
  • hypersensitivity

- ventricular fibrillation

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22
Q

What does it mean that Digoxin has positive inotropic action?

A

increases myocardial contraction and stroke volume

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23
Q

What does it mean that Digoxin has negative chronotropic action?

A

decreases HR

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24
Q

What does it mean that Digoxin has negative dromotropic action?

A

decreases conduction of heart cells

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25
Q

Half life of Digoxin

A

30-40 hours -> can accumulate and cause toxicity

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26
Q

Common signs of Digoxin toxicity

A
  • anorexia
  • N/V/D
  • bradycardia
  • PVCs and heart block
  • headache
  • malaise
  • confusion/delirium
  • visual illusions
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27
Q

What level of Digoxin is considered toxic

A

2 ng/mL or greater

28
Q

What is the antidote to Digoxin?

A

Digoxin-immune fab -> binds w/ Digoxin to form complex molecules that can be excreted in urine

29
Q

Drug interactions that increase risk for Digoxin toxicity

A
  • Diuretics: promote K loss which can increase effect of Digoxin at myocardial cell sites
  • Cortisone: promotes Na retention and K excretion
  • Antacids: decreases absorption of Digoxin if taken together
30
Q

When would you want to hold giving Digoxin?

A

if apical pulse is less than 60 bpm

31
Q

nursing interventions for Digoxin use

A
  • monitor pulse
  • monitor edema/HF sighs
  • monitor serum Digoxin and K levels
  • encourage pt to eat foods high in K
32
Q

What class of drugs is Milrinone lactate?

A

phosphodiesterase inhibitors

33
Q

MOA of Milrinone lactate

A
  • inhibits PDE

- increases myocardial contraction stroke volume, vasodilation, and cardiac output

34
Q

Nursing precautions for Milrinone lactate

A
  • not to be given IV greater than 48-72 hours
  • can cause severe cardiac dysrhythmias
  • requires ECG and cardiac status monitoring
35
Q

List some other classes of meds that are used to treat heart failure

A
  • vasodilators: decrease preload and O2 demand of heart
  • ACE inhibitors or ARBs: vasodilation and decrease blood fluid volume
  • diuretics: decrease fluid volume
  • beta blockers: improves cardiac function
  • nesiritide: inhibits ADH and promotes naturesis
  • BiDil: combo hydralazine (BP) and isosorbide dinitrate (dilator)
36
Q

angina that occurs w/ predictable stress or exertion

A

classic (stable) angina

37
Q

angina that occurs frequently with progressive severity unrelated to activity; unpredictable regarding stress/exertion and intensity

A

unstable (preinfarction) angina

38
Q

angina that occurs during rest

A

variant (Prinzmetal or vasospastic) angina

39
Q

6 S’s for stable angina

A
  • sudden onset
  • substernal
  • spreads to the arm
  • squeezing in character
  • short duration
  • sublingual NTG relieves pain
40
Q

4 R’s for unstable angina

A
  • recent onset
  • resistant (progressive)
  • rest angina
  • recurrent (in early post infarction period)
41
Q

MOA of NTG

A

acts directly on smooth muscle of blood vessels to cause relaxation and dilation and increases O2 supply

42
Q

uses for NTG

A
  • control angina
  • HTN emergency
  • pulmonary edema
  • heart failure
43
Q

side effects of NTG

A
  • headache
  • N/V
  • hypotension
  • dizziness
  • weakness
  • syncope
  • edema
44
Q

Adverse reactions to NTG

A
  • orthostatic hypotension
  • tachycardia
  • paradoxical bradycardia
  • circulatory collapse
45
Q

How should IV and topical NTG be administered

A
  • IV: should be titrated
  • topical ointment: should be removed at night to allow for 12-hour nitrate free period; don’t apply on chest near defibrillates paddle placement
46
Q

T/F: NTG should be tapered when discontinuing to prevent rebound myocardial ischemia

A

True

47
Q

contraindications for NTG

A
  • increased intracranial pressure
  • anemia
  • cardiomyopathy
  • shock
48
Q

MOA of beta blockers

A
  • block beta 1 and beta 2 receptor sites

- cause decrease HR and force of contraction

49
Q

side effects of beta blockers

A
  • hypotension
  • bradycardia
  • bronchoconstriction (nonselective)
  • lethargy
  • GI disturbance
  • depression
50
Q

What caution should be taken w/ beta blockers?

A

should be tapered when discontinuing to avoid rebound tachycardia and dysrhythmias

51
Q

side effects of calcium channel blockers

A
  • dizziness
  • decreased BP
  • bradycardia
  • headache
  • nausea/constipation
  • peripheral edema
52
Q

What is the first step of treatment for both stable and unstable angina?

A

NTG

53
Q

rapid depolarization caused by influx of Na ions which cause positive charge in cell; affected by class I antidysrhythmics

A

phase 0 of cardiac action potential

54
Q

initial repolarization (some K out very quickly)

A

phase 1 of cardiac action potential

55
Q

plateau (due to influx of Ca ions and efflux of K ions) to prolong action potential and promotes atrial and ventricular contraction; affected by class IV antidysrhythmics

A

phase 2 of cardiac action potential

56
Q

rapid repolarization caused by large efflux of K ions; affected by class III antidysrhythmics

A

phase 3 of cardiac action potential

57
Q

resting membrane potential between heartbeats; affected by class II antidysrhythmics

A

phase 4 of cardiac action potential

58
Q

MOA of Na channel blockers (class I)

A
  • decrease Na influx into cardiac cells
  • decrease conduction velocity
  • suppression of automaticity (decreasing ectopic foci)
  • increased recovery time
  • mainly used in emergencies
59
Q

Examples of class I antidysthrymics (Na channel blockers)

A
  • Procainamide
  • Lidocaine
  • Fecainide
60
Q

MOA of beta-adrenergic blockers (class II)

A

decrease conduction velocity, automaticity, and recovery time; used more frequently

61
Q

Examples of class II antidysthrymics (B-blockers)

A
  • Propranolol

- Metoprolol

62
Q

MOA of class III antidysrhythmics

A
  • prolong repolarization
  • increases refractory periods and prolongs action potential duration
  • emergency treatment of ventricular dysrhythmias when others are ineffective
63
Q

Examples of class III antidysrhythmics

A
  • Amiodarone

- Sotalol

64
Q

MOA of calcium channel blockers (class IV)

A
  • blocks Ca access to cells to decrease contractility and conductivity of the heart -> decreases O2 demand and cardiac workload
  • increases refractory period of AV node which decreases ventricular response
65
Q

Examples of class IV antidysrhythmics

A
  • Verapamil

- Diltiazem

Pharmacology (22 decks)

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