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Pharm Exam 2 > Cardiac > Flashcards

Cardiac Flashcards

1
Q

Loop Diuretic Drug

A

Furosemide

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2
Q

Furosemide MOA

A

Rapid acting loop diuretic inhibits Na and Cl reabsorption in ascending loop of henle
Decreasing edema and BP

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3
Q

Furosemide Use

A

Powerful diuretic given for massive movement of fluids (trying to unload cardiac system)
Both acute and chronic heart failure
-early or small amounts of fluid retention thiazide diuretics are normally given

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4
Q

Furosemide A/E

A 
Postural hypotension 
Hypo K, Mg, Na, Cl
N/V
Dehydration-- leads to circulatory collapse 
Tinnitus *
Aplastic anemia *
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5
Q

Furosemide Route/Dose

A

IVP starts acting in 5 minutes, duration about 2 hr

give 20mg/min, too fast can cause cardiac arrest

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6
Q

Furosemide Drug interactions

A 
Digoxin: ↓ K = ↑ risk for dig toxicity
↳Dysrhythmias
Ototoxic drugs (aminoglycosides) 
↳Hearing loss
Lithium: ↑Na level
Other antihypertensives: hypotension
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7
Q

Furosemide Monitoring

A

BP (>110/60): hypotension due to high volume diuresis can cause circulatory collapse (before giving)
Weight (Daily)
K level ( 3.5-5) (before giving)

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8
Q

urine output needs to be greater than

A

30mL/hr

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9
Q

Thiazide diuretic Drug

A

Hydrochlorothiazide

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10
Q

Hydrochlorothiazide MOA

A

Blocks reabsorption of Na and Cl in early segment of the distal convoluted tubule
-not effective if GFR <15-20 mL

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11
Q

Hydrochlorothiazide Use

A

Hypertension: 1st choice especially in AA (most effective)
Mild-Moderate heart failure
Mobilize edema associated with hepatic and renal disease (GFR cant be too low though)

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12
Q

Hydrochlorothiazide Contraindications

A

Pregnancy and breast feeding

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13
Q

Hydrochlorothiazide A/E

A

Hypo K, Na, Cl
Dehydration
Increased BG in diabetes
May precipitate gouty arthritis

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14
Q

Hydrochlorothiazide Drug interactions

A

Digoxin toxicity due to loss of K

Other antihypertensives: causes hypotension

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15
Q

Osmotic Diuretic Drug

A

Mannitol

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16
Q

Mannitol MOA

A

In the proximal convoluted tubules, mannitol creates osmotic action that inhibits passive reabsorption of water
– no significant effect on excretion of K

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17
Q

Mannitol Use

A

Can prevent/ slow onset of renal failure in severe hypotension → not excreted like other drugs so it raises BP
Hypovolemic shock
Reduction of intraocular pressure in cases not responding to usual therapy (Glaucoma)

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18
Q

Mannitol Solution

A

normally icy/ crystallized → need to warm in water

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19
Q

Mannitol dose

A

given at a rate for 30-50mL/hr of urine output

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20
Q

Mannitol A/E

A 
HA
N/V
Electrolyte imbalance 
Pulmonary edema
Congestive heart failure edema
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21
Q

K Sparing (Aldosterone) Diuretic Drug

A

Spironolactone

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22
Q

Spironolactone MOA

A

Blocks action of aldosterone in the distal nephron
Since aldosterone promotes Na uptake in exchange for K secretion
Inhibition of aldosterone causes retention of K and excretion of Na

Works slowly over days

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23
Q

Spironolactone Use

A

Hypertension
Edema
Usually given in combo w/loop/ thiazide diuretic due to low diuresis

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24
Q

Spironolactone A/E

A

Hyperkalemia resulting in cardiac dysrhythmias such as V. fib
Gynecomastia
Menstrual irregularities

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25
Q

Hyperkalemia treatment

A

Injection of insulin

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26
Q

Spironolactone Patient educations

A

Never use salt substitutes or K replacements

Don’t increase intake of K or take another K sparing drug

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27
Q

K Sparing (Non Aldosterone Sparing) Diuretic Drug

A

Triamterene

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28
Q

Triamterene MOA

A

Disrupts Na-K exchange directly in the distal nephron

Works quickly over a few hr

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29
Q

Triamterene Use

A

Hypertension
Edema
Mainly to counteract the K wasting effects of other diuretics *

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30
Q

Triamterene A/E

A

N/V
Leg cramps: increase K
Dizziness
Hyperkalemia

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31
Q

Triamterene Drug interactions

A

ACE, ARB, Direct renin inhibitors ↑ K and can be deadly

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32
Q

K replacement Drug

A

KCl (potassium chloride)

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33
Q

KCl Use

A

When theres a loss of K from vomiting, diarrhea, wound drainage, prolonged diuresis, DKA

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34
Q

KCl A/E

A

Irritate GI tract: abdominal discomfort
N/V/D
Large pills can cause intestinal ulcers and result in bleeding/ perforation
Hyperkalemia
-mild: 5-7: prolonged PR, and tented T waves
-Severe: >7: cardiac arrest due to V-tac/ V-fib.
IVP will cause instant death

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35
Q

KCl Nursing considerations

A

ONLY given through IV pump
10meq/hr or slower
Never add KCl to an existing IV
Dilute 10 meq in 100ml, 40 meq in 500-1000ml (x3 doses)
Check K level before giving each dose
Mix KCl well in the IV solution
PO pill: patient needs to be sitting up right
Liquid KCl: dilute in orange juice according to directions

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36
Q

Removal of Excess K

A
  1. hold K containing food and meds
  2. infuse calcium gluconate (counteract cardiotox)
  3. infuse insulin and glucose to push k into cells
  4. infuse sodium bicarbonate to increase pH and cellular intake of k
  5. give either PO or enema Kayexalate to remove K through the intestines
  6. peritoneal or hemodialysis to remove (Last resort)
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37
Q

Hyperkalemia S/S

A 
Cardiac
Confusion
Anxiety
Dyspnea 
Heaviness and tingling of legs
Numbness and tingling of hands, lips and feet
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38
Q

Atropine MOA

A

Muscarinic antagonists, selectively blocks the effects of acetylcholine at the muscarinic receptors
Increases heart rate

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39
Q

Atropine Use

A 
Significant Bradycardia (symptomatic or doesnt respond to waking the patient up)
Surgical pretreatment to prevent bradycardia during surgery
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40
Q

Atropine A/E

A 
*Tachycardia*
Dry mouth
Blurred vision
Photophobia
Increased intraocular pressure
Urinary retention 
Anhidrosis (decreased in sweating)
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41
Q

Atropine Drug interactions

A

Antihistamine
Phenothiazine
Antipsychotics
TCA

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42
Q

Alpha 1

A

Arterioles and vein constriction

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43
Q

Alpha 2

A

Nerves

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44
Q

Beta 1

A

Heart: increase rate, force, AV conduction speed
Kidney: release of renin

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45
Q

Beta 2

A

Bronchi: dilation, arterioles, heart, lung, skeletal muscles

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46
Q

Dopamine stimulates

A

Alpha 1, Beta 1 and dopamine

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47
Q

Epinephrine stimulates

A

Alpha 1,2 and Beta 1,2

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48
Q

Norepinephrine stimulates

A

Alpha 1,2 and Beta 1

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49
Q

Alpha Adrenergic antagonist Drug

A

Prazosin

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50
Q

Prazosin MOA

A

Inhibits alpha 1 receptors (arterioles and veins) causing vasodilation, resulting in decreased BP and CO

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51
Q

Prazosin Use

A

Essential hypertension
BPH
Raynaud’s (due to vasodilation)

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52
Q

Prazosin A/E

A 
Dizziness
HA
Drowsiness
Impotence 
Reflex tachycardia (decreased CO)
Nasal congestion
Edema
Postural hypotension
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53
Q

Prazosin Drug interactions

A

Diuretics and other hypotensive agents potentiate effects

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54
Q

Prazosin Nursing considerations

A

Monitor for 1st dose effect

Impotence is a major reason for nonadherence in men

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55
Q

Beta Adrenergic Antagonist Drug

A

Propranolol

Metoprolol

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56
Q

Propranolol MOA

A

NON-SELECTIVE Beta 1 and 2 adrenergic blocker (lung, heart, kidney)
Blocks adrenergic receptors in the cardiac (beta 1) and the lungs (beta 2); renal (beta 1) suppresses renin secretion

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57
Q

Propranolol Use

A

MI
CAD
HTN - better at lowering HR but still used as a 1st line treatment for HTN
Cardiac dysrhythmias

58
Q

Propranolol Therapeutic effect

A

Antihypertensive

Reduced HR, CO

59
Q

Propranolol A/E

A 
Hypotension
Bradycardia
Bronchoconstriction 
Depression 
Rapid withdrawal can cause angina or dysrhythmias that will lead to another MI
60
Q

Propranolol Drug interactions

A

Ca Channel Blockers: cause cardiac suppression, very low HR/BP

61
Q

Propranolol Contraindications

A

Bronchitis
COPD
T1DM
T2DM

62
Q

Propranolol Nursing implementations

A

・Take apical pulse and BP before giving
↳ Do not give if pulse is <60 or BP is <90-110 and call MD
・May mask tachycardia symptoms of hypoglycemia

63
Q

Beta blocker Indications

A 
Angina 
HTN
Cardiac dysrhythmias
MI
Heart failure
64
Q

Metoprolol MOA

A

Selective beta blocker (better for those who have lung problems)
Blocks Beta 1 cardiac receptors (Heart and Kidneys)
Reduces HR, force contraction, AV duration through the nodes, reduces secretion of renin

65
Q

Metoprolol Use

A

1st choice antihypertensive
Angina
MI
Heart failure

66
Q

Metoprolol A/E

A 
Bradycardia
Decreased CO
AV heart block 1st, 2nd degree 
Heart failure
Cardiac excitation (when suddenly stopped can cause another MI if previously had one)
67
Q

Centrally acting Alpha 2 agonist Drug

A

Clonidine

68
Q

Clonidine MOA

A

Activates the central Alpha 2 receptors (nerves) in the brainstem and this reduces sympathetic outflow to blood vessels and the heart

69
Q

Clonidine Use

A

Hypertension

Sometimes pain

70
Q

Clonidine A/E

A 
Drowsiness
Sedation 
Xerostomia (dry mouth)
Constipation 
Impotence 
Rebound hypertension (when stopped abruptly)
Fetal harm 
Euphoria
Hallucinations 
Abuse
71
Q

ACE Inhibitor Drug

A

Captopril, Lisinopril, Enalapril

72
Q

Captopril MOA

A

Lowers BP by inhibition of Angiotensin Converting Enzyme

  • This disrupts the conversion of angiotensin 1 to 2 in the kidneys
  • Since angiotensin 2 is a powerful vasoconstrictor, vasodilation occurs and BP is lowered
73
Q

Captopril Use

A

Hypertension
Heart failure
MI
BP med of choice for DM since it slows progression of ESRD

74
Q

Captopril A/E

A

1st dose hypotension
Arthralgia
Cough (increased bradykinin in lungs) - may need to change to a different class
Angioedema
Bradycardia
Neutropenia (will occur within the 1st week)
Agranulocytosis (will occur within the 1st week)
Fetal injury
Hyperkalemia

75
Q

Captopril Drug interactions

A

other antihypertensives: hypotension

76
Q

Captopril Nursing implementation

A

・Take BP and apical pulse before giving
・Report unexpected fever
・May cause hypoglycemia in Dm → check BG

77
Q

Angiotensin 2 Receptor Blocker (ARB) Drug

A

Losartan

78
Q

Losartan MOA

A

Blocks access of angiotensin 2 to its receptors in blood vessels, the adrenals and other tissues
-causing dilation of arteries and veins

79
Q

Losartan Use

A

Hypertension
Diabetic retinopathy (type 1) - slows development
Those who cannot tolerate ACE inhibitors

80
Q

Losartan A/E

A

Angioedema

Renal failure

81
Q

Losartan Drug interactions

A

Other antihypertensives

82
Q

Ca Channel Blockers Drugs

A

Verapamil
Diltiazem
Nifedipine

83
Q

Verapamil MOA

A

Inhibits Ca influx through slow channels into myocardial muscle cells
Increases myocardial O2 delivery
Blocks influx of Ca in both blood vessels and the heart

84
Q

Nifedipine MOA

A

Dilates coronary artery and inhibits coronary spasm

-Prevents Ca influx into the slow Ca channel, only works on the arteries not the heart its self

85
Q

Verapamil Use

A 
Hypertension
Reduces HR
Antiarrhythmic for SVT (supraventricular tachycardia) 
Antianginal 
Decreases force of contraction
86
Q

Nifedipine Use

A

Hypertension

Angina

87
Q

Verapamil A/E

A 
Dizziness 
HA
Fatigue
Sleep Disturbances
Hypotension
Bradycardia
Constipation (not with Nifedipine)
Nausea
Edema in legs (more common and serious)
Elevated LFTs 
Severe: Hypotension, Cardiogenic shock, CHF
88
Q

Nifedipine A/E

A

Flushing
Reflex tachycardia
Along with the all from Verapamil

89
Q

Verapamil Drug interactions

A

Grapefruit juice ↑ drug level (no large amounts)
↑ level of digoxin
Potentiates other antihypertensives

90
Q

Verapamil patient education

A

Monitor grapefruit intake - avoid large amounts

Report wt gain

91
Q

Verapamil Nursing implementations

A

Take BP and HR before giving

92
Q

Verapamil Monitoring

A

LFTs
BUN
Cr

93
Q

Hydralazine

A

Vasodilator
Selective dilation of arteriole, no effect on veins
HR increases

94
Q

Hydralazine Use

A

Essential hypertension
Hypertensive Crisis
Heart failure

95
Q

Hydralazine A/E

A

Reflex tachycardia
↑ Blood volume
lupus like syndrome

96
Q

Hydralazine Drug interactions

A

Combo w/ beta blockers to avoid reflex tachycardia

-excessive hypotension

97
Q

Hydralazine IV

A

Most commonly given to HTN crisis BP >220/180

98
Q

Nitroglycerine MOA

A

Vasodilator (Anti-anginal)
Relaxes smooth muscle vasculature by unknown mech.
Reduces preload, afterload, and myocardial O2 consumption

99
Q

Nitroglycerine Use

A

Reduces BP, Chest pain,

Angina

100
Q

Nitroglycerine A/E

A

HA (give Aspirin or Tylenol)
Postural hypotension
Facial flushing

101
Q

Nitroglycerine Sublingual dosing

A

Give 1 tab every 5 minutes 3x if chest pain did not subside with the previous dose
-If not better after 3rd dose call 911 or use MI protocal

102
Q

Nitroglycerine IV

A

Titrate IV drip according to BP

-Used when chest pain isn’t being subdued by Morphine

103
Q

Nitroglycerine Cream

A

Measured in increments
Will not stop sudden chest pain and can take Sublingual tabs for it
Applied to hairless area (chest, upper back, arm, legs)

104
Q

Nitroglycerine Patch

A

Applied same as cream
Clean area before application and after removal
Can be worn in shower or while swimming
Local buring can happen and is not significant
Remove at night to prevent tolerance

105
Q

Nitroglycerine Capsule

A

Prevent chest pain

106
Q

Nitroglycerine Drug interactions

A

Alcohol: worsen hypotension

IV nitro may antagonize heparin ( don’t give in same IV line)

107
Q

Nitroglycerine Nursing implementations

A

Take before known chest pain causing activity
Take BP before giving and 1 hr after for transdermal
Unrelieved chest pain after 15 minutes is usually indicative of MI

108
Q

Digoxin MOA

A 
Increases force of myocardial contraction (slow hard pumps) 
Increases contractility (positive inotropic action) -- antiarrhythmic (changes heart rhythm)
109
Q

Other Inotropes

A

Dopamine, Dobutamine: Used when BP is too low and will not go up with other drugs, will turn finger and toes black, for those who had MI or Open heart surgery

110
Q

Digoxin Therapeutic action

A

Increases diuresis

111
Q

Digoxin Use

A

A. Fib
CHF
Heart failure: 2nd line drug

112
Q

Digoxin A/E

A 
Bradycardia
Heart blocks: slows conduction from SA→AV→Purkinje fibers (1st, 2nd, 3rd degree heart blocks)
Other dysrhythmias
Visual disturbances 
N/V
Confusion
Agitation
113
Q

Digoxin toxicity

A

More common in elderly

114
Q

Digoxin Drug interactions

A 
Many!
Antacids
Antibiotics
Amiodarone
Verapamil
Quinidine
115
Q

Digoxin Nursing implementations

A

❊Absolutely must take apical pulse for 1 full minute before giving (must be above 50-60 in adults and 60-70 in children)

116
Q

Digoxin Monitoring

A

Digoxin level: daily when first started then periodically

K level: hypokalemia can increase risk for Digoxin Toxicity and it’s the most common reason for toxicity

117
Q

Digoxin antidote

A

Digibind

118
Q

Adenosine MOA

A

Decreases automaticity in the SA node and slows conduction through the AV node
Inhibits cyclic AMP-induced Ca influx
-Basically stops the heart and resets the automaticity

119
Q

Adenosine Use

A

Terminating SVT

Wolff parkinson white syndrome

120
Q

Adenosine Route

A

IV bolus closest to the heart

Short half life: 1.5-10 seconds

121
Q

Adenosine A/E

A

Sinus bradycardia

Bronchoconstriction

122
Q

Amiodarone MOA

A

K channel blocker
Slows AV conduction and prolongs AV refractoriness
Blocks repolarization

123
Q

Amiodarone Use

A

Recurrent V. fib
Unstable V. tach
AKA: cardiac arrest

124
Q

Amiodarone A/E

A

Severe hypotension
Bradycardia
Will most likely need pacemaker after

125
Q

Lipid lowering drugs

A

‘Statin’
Atorvastatin
Lovastatin

126
Q

Statins MOA

A

Reduce LDL-C
Elevate HDL
May lower Triglycerides but not prescribed for that
HMG-CoA reductase inhibitor

127
Q

Statin A/E

A 
Dyspepsia
Camps
Flatulence
Constipation 
Abdominal pain 
Myopathy/ Rhabdo (Calf pain)
↳increase CK levels
128
Q

Statin Toxicity

A

Nephrotoxic

Hepatotoxic

129
Q

Statin Patient education

A

Cannot eat or drink grapefruit

Inhibits CYP3A4 enzyme

130
Q

Statin Nursing implementations

A

Most effective for lowering LDLs and total cholesterol
Improve cardiac outcomes: lower risk for HF, MI, sudden death
Rovastatin has the highest risk: dosages need to be reduced in asians

131
Q

LDL goal for Heart disease patients

A

70

132
Q

Statin Monitoring

A

Lipids Q6 mo-annually

133
Q

Ezetimibe MOA

A

Cholesterol blocker
Inhibits dietary absorption of cholesterol secreted in bile
Treatment reduces total cholesterol, LDL-C, TG, slight rise in HDL

134
Q

Ezetimibe A/E

A

Rhabdo

Hepatitis when combo with statin

135
Q

Ezetimibe Toxicity

A

Pancreatitis

136
Q

Fibrates

A

Gemfibrozil

137
Q

Gemfibrozil MOA

A

Decreases VLDL’s there by lowering TG levels
Increase HDL’s
No effect on LDL-C

138
Q

Gemfibrozil Use

A

Treatment usually limited to those in which dietary restriction of saturated fats fails

139
Q

Gemfibrozil A/E

A

Gallstones

Statin induced myopathy

140
Q

Gemfibrozil Toxicity

A

Hepatotoxicity

141
Q

Gemfibrozil Drug interactions

A

Displaces warfarin from albumin
Increasing anticoagulation
Should not be given w/statins

Pharm Exam 2 (4 decks)

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