37. Cardiac Glycosides, Antianginals, and Antidysrhythmics Flashcards
1
Q
What increases in heart failure
A
preload and afterload
2
Q
volume of blood in the ventricles at the end of diastole (end diastolic pressure)
A
preload
3
Q
resistance left ventricle must overcome to circulate blood; increased means increased cardiac workload
A
afterload
4
Q
what causes increase in preload
A
- hypervolemia
- regurgitation of cardiac valves
- heart failure
5
Q
what causes increase in afterload
A
- hypertension
- vasoconstriction
6
Q
high risk for HF without symptoms or structural disease
A
stage 1 (A) HF
7
Q
some levels of cardiac changes without symptoms of heart faulre
A
stage 2 (B) HF
8
Q
structural heart disease w/ symptoms of HF
A
stage 3 (C) HF
9
Q
severe structural heart disease and marked symptoms of HF at rest
A
stage 4 (D) HF
10
Q
heart failure nonpharmacologic treatment
A
- limit Na to 2g per day
- possible fluid restriction
- stop smoking
- manage obesity
- aerobic exercise
11
Q
normal atrial natriuretic peptide (ANP)
A
20-77 pg/mL
12
Q
normal brain natriuretic peptide (BNP)
A
less than 100 pg/mL
13
Q
BNP level positive for HF
A
- greater than 100 pg/mL
- acute HF: looking for values greater than 400 pg/mL
14
Q
what class of drugs is digoxin
A
cardiac glycoside
15
Q
MOA of Digoxin
A
- inhibits Na-K ATPase
- promotes increased force of cardiac contraction, cardiac output, and tissue perfusion
- decreases ventricular rate
16
Q
uses of Digoxin
A
heart failure and afib
17
Q
adverse reactions to Digoxin
A
- bradycardia
- cardiac dysrhythmias
- thrombocytopenia
18
Q
side effects of Digoxin
A
- dizziness
- mental disturbances and confusion
- N/V/D
- headache
- weakness
19
Q
how to administer Digoxin by IV
A
slowly by direct IV injection over minimum of 5 minutes
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
21
Q
contraindications for Digoxin
A
- hypersensitivity
- ventricular fibrillation
22
Q
What does it mean that Digoxin has positive inotropic action?
A
increases myocardial contraction and stroke volume
23
Q
What does it mean that Digoxin has negative chronotropic action?
A
decreases HR
24
Q
What does it mean that Digoxin has negative dromotropic action?
A
decreases conduction of heart cells
25
Half life of Digoxin
30-40 hours -> can accumulate and cause toxicity
26
Common signs of Digoxin toxicity
- anorexia
- N/V/D
- bradycardia
- PVCs and heart block
- headache
- malaise
- confusion/delirium
- visual illusions
27
What level of Digoxin is considered toxic
2 ng/mL or greater
28
What is the antidote to Digoxin?
Digoxin-immune fab -> binds w/ Digoxin to form complex molecules that can be excreted in urine
29
Drug interactions that increase risk for Digoxin toxicity
- 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
When would you want to hold giving Digoxin?
if apical pulse is less than 60 bpm
31
nursing interventions for Digoxin use
- monitor pulse
- monitor edema/HF sighs
- monitor serum Digoxin and K levels
- encourage pt to eat foods high in K
32
What class of drugs is Milrinone lactate?
phosphodiesterase inhibitors
33
MOA of Milrinone lactate
- inhibits PDE
| - increases myocardial contraction stroke volume, vasodilation, and cardiac output
34
Nursing precautions for Milrinone lactate
- not to be given IV greater than 48-72 hours
- can cause severe cardiac dysrhythmias
- requires ECG and cardiac status monitoring
35
List some other classes of meds that are used to treat heart failure
- 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
angina that occurs w/ predictable stress or exertion
classic (stable) angina
37
angina that occurs frequently with progressive severity unrelated to activity; unpredictable regarding stress/exertion and intensity
unstable (preinfarction) angina
38
angina that occurs during rest
variant (Prinzmetal or vasospastic) angina
39
6 S's for stable angina
- sudden onset
- substernal
- spreads to the arm
- squeezing in character
- short duration
- sublingual NTG relieves pain
40
4 R's for unstable angina
- recent onset
- resistant (progressive)
- rest angina
- recurrent (in early post infarction period)
41
MOA of NTG
acts directly on smooth muscle of blood vessels to cause relaxation and dilation and increases O2 supply
42
uses for NTG
- control angina
- HTN emergency
- pulmonary edema
- heart failure
43
side effects of NTG
- headache
- N/V
- hypotension
- dizziness
- weakness
- syncope
- edema
44
Adverse reactions to NTG
- orthostatic hypotension
- tachycardia
- paradoxical bradycardia
- circulatory collapse
45
How should IV and topical NTG be administered
- 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
T/F: NTG should be tapered when discontinuing to prevent rebound myocardial ischemia
True
47
contraindications for NTG
- increased intracranial pressure
- anemia
- cardiomyopathy
- shock
48
MOA of beta blockers
- block beta 1 and beta 2 receptor sites
| - cause decrease HR and force of contraction
49
side effects of beta blockers
- hypotension
- bradycardia
- bronchoconstriction (nonselective)
- lethargy
- GI disturbance
- depression
50
What caution should be taken w/ beta blockers?
should be tapered when discontinuing to avoid rebound tachycardia and dysrhythmias
51
side effects of calcium channel blockers
- dizziness
- decreased BP
- bradycardia
- headache
- nausea/constipation
- peripheral edema
52
What is the first step of treatment for both stable and unstable angina?
NTG
53
rapid depolarization caused by influx of Na ions which cause positive charge in cell; affected by class I antidysrhythmics
phase 0 of cardiac action potential
54
initial repolarization (some K out very quickly)
phase 1 of cardiac action potential
55
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
phase 2 of cardiac action potential
56
rapid repolarization caused by large efflux of K ions; affected by class III antidysrhythmics
phase 3 of cardiac action potential
57
resting membrane potential between heartbeats; affected by class II antidysrhythmics
phase 4 of cardiac action potential
58
MOA of Na channel blockers (class I)
- decrease Na influx into cardiac cells
- decrease conduction velocity
- suppression of automaticity (decreasing ectopic foci)
- increased recovery time
- mainly used in emergencies
59
Examples of class I antidysthrymics (Na channel blockers)
- Procainamide
- Lidocaine
- Fecainide
60
MOA of beta-adrenergic blockers (class II)
decrease conduction velocity, automaticity, and recovery time; used more frequently
61
Examples of class II antidysthrymics (B-blockers)
- Propranolol
| - Metoprolol
62
MOA of class III antidysrhythmics
- prolong repolarization
- increases refractory periods and prolongs action potential duration
- emergency treatment of ventricular dysrhythmias when others are ineffective
63
Examples of class III antidysrhythmics
- Amiodarone
| - Sotalol
64
MOA of calcium channel blockers (class IV)
- 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
Examples of class IV antidysrhythmics
- Verapamil
| - Diltiazem
