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Med surg > Cardio Pharm > Flashcards

Cardio Pharm Flashcards

1
Q

What are the 4 categories of drugs used to treat htn

A

RAAS inhibitors, calcium channel blockers, sympatholytic agents, vasodilators

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2
Q

What are the 4 categories of RAAS drugs

A

Ace inhibitors
ARB inhibitors
Aldosterone antagonists
Renin antagonist

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3
Q

Indications for ace inhibitors

A

Heart failure
Htn
Diabetic nephopathy
Left ventricular dysfunction after MI

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4
Q

Effect of ace inhibitors

A

Block the production of angiotensin 2 causing

  1. vasodilation
  2. excretion of water and Na+
  3. reabsorption of K+
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5
Q

Side effects of ace inhibitors

A
  1. severe hypotension on the first dose
  2. angioedema
  3. rash, and report of metallic taste
  4. cough due to build up of bradykinin
  5. hyperkalemia
  6. neutropenia
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6
Q

Interventions ace inhibitors

A
  1. CBC to monitor WBC
  2. electrolyte panel to monitor for hyperkalemia
  3. epi if they develop angioedema
  4. tell them to report metallic taste
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7
Q

Ace inhibitors admin

A
  1. Give captopril one hour before meal
  2. avaiable only in oral form
  3. Take 2-3 times daily for htn 3 times daily for Hf
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8
Q

Ace inhibitors teaching

A

1.signs of hyperkalemia
-weakness,parasthesia,palpitations
Muscle twitching
2.signs of infection
-sore throat
3.report metallic taste or cough

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9
Q

Ace inhibitors contraindications

A
  1. pregnancy
  2. hypotension
  3. liver failure with elevated AST and ALT
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10
Q

Ace inhibitors interactions

A
  1. captopril absorption is decreased by food
  2. increases lithium toxicity
  3. NSAIDs decrease effectiveness of ace inhibs
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11
Q

Name the ARBs

A
  1. Losartan
  2. irbesartan
  3. candesartan
  4. valsartan
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12
Q

Action ARBs

A

Block angiotensin 2 receptors

Producing the same effects as ace inhibitors

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13
Q

Arbs side effects

A
  1. headache
  2. hypotension
  3. angioedema(less chance then ace inhibitors)
  4. insomnia
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14
Q

Arbs interventions

A
  1. epi for angioedema

2. monitor and report CNS symptoms

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15
Q

Arbs teaching

A
  1. report swelling of mouth and throat
  2. report headaches or insomnia
  3. can not take if you’re pregnant
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16
Q

Arbs interactions

A

Phenobarbital lowers losartan blood levels

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17
Q

Aldosterone antag action

A

Treats hypertension and heart failure that occurs right after an MI

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18
Q

Prototype aldosterone antagonist

A
  1. spironolactone

2. eplerenone

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19
Q

Aldosterone antag action

A

Blocks aldosterone receptors causing

  1. sodium and water retention
  2. retention of potassium
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20
Q

Aldosterone antag side effects

A

Hyperkalemia

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21
Q

Aldosterone antag interventions

A
  1. Monitor for hyperkalemia

2. monitor BUN and creatinine for patients at high risk for hyperkalemia

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22
Q

Aldosterone antag administer

A
  1. will take 4 weeks to reach max effect

2. reduce dose for patients taking CYP3A4 inhibitors.

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23
Q

Aldosterone antag contraindications

A
  1. type 2 diabetics with microalbuminuria
  2. lactation
  3. hyperkalemia
  4. high serum creatinine and decreased creatinine clearance
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24
Q

aldosterone contraindications

A
  1. DM 2 with microalbuminemia
  2. elevated creatinine levels(0.6-1.2) or decreased creatinine clearance (88-137)
  3. lactation
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25
Q

aldosterone interactions

A
  1. drugs that inhibit CYP3A4 such as ketoconazole, erythromycin, verapamil may increase risk for toxicity and hyperkalemia
  2. may cause lithium toxicity
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26
Q

direct renin inhibitors action

A

binds to renin and prevents the activation of angiotensin 1 causing NaCl + water secretion and causes potassium retention and causes vasodilation

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27
Q

direct renin inhibitor side effects

A
  1. diarrhea and stomach pain
  2. angioedema (less chance then ACE inhibitors)
  3. hyperkalemia
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28
Q

direct renin inhibitors prototypes

A

1.Aliskiren

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29
Q

direct renin inhibitors interventions

A
  1. monitor kidney function
  2. monitor and report cough
  3. monitor for hyperkalemia
  4. monitor for GI symptoms
  5. watch for angioedema treat with epi
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30
Q

direct renin inhibitors admin

A
  1. may take 2 weeks to see full effect
  2. take at the same time everyday relative to meals.
  3. High fat meals decrease absorption
  4. comes only in oral
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31
Q

direct renin inhibitors teaching

A
  1. report s/s of hyperkalemia
    - parasthesia, palpitations, muscle twitching, weakness
  2. report cough or swelling in face
  3. stop taking if pregnant will cause damage after the first trimester
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32
Q

direct renin inhibitors contraindications

A
  1. hypercalcemia, dehydration, hyperkalemia
  2. under age 18
  3. pregnant or lactated
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33
Q

interactions direct renin inhibitors

A
  1. synergistic effect with other hypotensive drugs
  2. decreases blood levels of furosemide
  3. Atorvastatin and ketoconazole increase blood levels of aliskiren
  4. Irbesartan decreases blood levels of aliskiren
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34
Q

calcium channel blockers therapeutic uses

A
  1. mild to moderate hypertension

2. One type of calcium channel blockers can effect the arterioles and the heart

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35
Q

calcium channel blockers prototypes

A
  1. Nifedipine (ni-fed-ipine)

2. Verapamil (works on both arteries and heart) (a dihydropyridine)

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36
Q

calcium channel blockers action

A

blocks calcium channels leading to

  1. vasodilation
  2. increased coronary perfusion
  3. increased heart rate (low BP stimulates baroreceptor reflex)
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37
Q

calcium channel blockers side effects

A
  1. reflex tachycardia from the rapid drop in BP
  2. lightheadness,dizziness,facial flushing(vasodilation)
  3. peripheral edema
  4. gingival hyperplasia (big gums, bleeding)
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38
Q

calcium channel blockers interventions

A
  1. give with bblockers to prevent tachycardia
  2. monitor HR, report dizziness, edema
  3. check gums periodically
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39
Q

calcium channel blockers teaching

A
  1. facial flushing and a feeling of heat is normal
  2. encourage regular dental care
  3. report rapid heart beat
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40
Q

calcium channel blockers contraindication

A
  1. acute MI
  2. GI obstruction
  3. aortic stenosis
  4. unstable angina
  5. children
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41
Q

calcium channel blockers interactions

A
  1. melatonin increases BP and pulse rate
  2. ginkgo and ginseng and grapefruit juice increase blood levels
  3. St Johns wort decreases blood levels
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42
Q

what are the 5 types of sympatholytics

A
  1. alpha 1 adrenergic blockers
  2. beta adrenergic blockers
  3. adrenergic neuron blockers
  4. centrally acting alpha 2 agonists
  5. alpha/beta blockers
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43
Q

what do alpha 1 receptors do

what do beta 2 receptors do

A
  1. vasoconstriction when stimulated

2. vasodilation, increase rate and force of contraction

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44
Q

alpha 1 adrenergic blockers uses

A
  1. hypertension

2. BPH

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45
Q

alpha 1 adrenergic blockers prototypes

A
  1. doxazosin (dox-a-zosin)

2. prazosin

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46
Q

alpha 1 adrenergic blockers

A

blocks the alpha 1 adrenergic receptors causing vasodilation

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47
Q

alpha 1 adrenergic blockers side effects

A
  1. orthostatic hypotension, especially on first dose and dose increase
  2. reflex tachycardia (a reflex to maintain CO)
  3. headache
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48
Q

alpha 1 adrenergic blockers interventions

A
  1. monitor orthostatic blood pressure (take BP laying down wait one min take it sitting up, wait one min take it standing up) report a deviation of 20
  2. monitor and report headaches
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49
Q

alpha 1 adrenergic blockers admin

A

give at bed time to avoid orthostatic blood pressure effects

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50
Q

alpha 1 adrenergic blockers teaching

A
  1. orthostatic hypotension teaching
    - take at bedtime, rise slowly from lying to sitting or standing
  2. report dizziness, syncope, rapid heartbeat, palpitations
  3. report heads
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51
Q

alpha 1 adrenergic blockers contraindications

A
  1. children

2. hypotension

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52
Q

alpha 1 adrenergic blockers interactions

A

1.sildenafil and other phosphodiesterase inhibitors may increase risk for hypotension

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53
Q

beta blockers uses

A
  1. hypertension(all bblockers expect esmolol, sotalol)
  2. angina pectoris(only atenolol, metoprolol)
  3. decrease mortality following MI (only atenolol and metoprolol)
  4. dysrhthmias (only atenolol, metoprolol)
  5. HF(only metoprolol and atenolol)
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54
Q

beta blocker action

A

blocks beta receptors in the heart reducing heart rate and contractility this decreases CO and prevents reflex tachycardia
They also work on the kidneys by decreasing the release of renin. This lowers the vasoconstrictive effect of angiotensin 1 and the fluid retention from aldosterone

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55
Q

what is the difference between transudate and exudate

A

transudate is fluid that was pushed through the capillaries by high pressure. Exudate was pushed through the capillaries due to inflammation.

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56
Q

beta blocker side effects

A
  1. rebound hypertension leading to MI if discontinued suddenly
  2. HF
    - cough at night, SOB, edema
  3. bradycardia
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57
Q

beta blocker interventions

A
  1. dont give if HR is lower then 60
  2. must be tapered off
  3. monitor for signs of HF
    - peripheral edema, night cough, SOB
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58
Q

beta blocker admin

A
  1. atenolol should be taken before meals or at bed time

2. metoprolol should be taken with meals

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59
Q

beta blocker contraindications

A
  1. sinus bradycardia or greater then 1st degree heart block
  2. moderate to severe HF
  3. cardiogenic shock
  4. dont use atenolol in PVD or raynaud disease (loss of blood flow to hands or feet in response to cold or stress)
  5. dont use metoprolol in children younger then 6
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60
Q

beta blockers interactions

A
  1. digoxin may cause an additive effect and increase bradycardia
  2. antacids decrease absorption
  3. increase the risk for hypoglycemia when taken with oral hypoglycemic agents
  4. increase the effect of neuromuscular blockers
  5. antimuscarinic and anticholinergic drugs may decrease effect of bblockers
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61
Q

adrenergic neuron blockers use

A

treat hypertension but not first choice b/c they cause severe orthostatic hypotension

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62
Q

adrenergic neuron blocker protoype

A

resirpine (re-sir-peen)

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63
Q

adrenergic neuron blockers action

A

blocks both beta and alpha adrenergic receptors from using norepinephrine. it moves norepinephrine out of the synaptic vesicles into the synaptic cleft where monoamine oxidase breaks down the norepi. It also blocks the reuptake of dopamine into the synaptic vesicles. Dopamine is the precursor for norepi. Stores are depleted within 2 weeks.

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64
Q

side effects of adrenergic neuron blockers

A
  1. severe depression
  2. bradycardia and orthostatic hypotension
  3. GI irritation and diarrhea
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65
Q

adrenergic neuron blockers interventions

A
  1. monitor heart rate and orthostatic vitals
  2. monitor for depression
  3. monitor for GI effects
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66
Q

adrenergic neuron blockers admin

A

administer with food or milk to avoid GI irritation

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67
Q

adrenergic neuron blockers contraindications

A
  1. pregnancy/lactation
  2. peptic ulcer disease
  3. ulcerative colitis(a type of IBD that effects only the colon, it is autoimmune in nature. IBS is not autoimmune rather has to do with muscle contractions)
  4. children
  5. MAOIs
  6. allergy to rauwolfia alkaloids
  7. depression
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68
Q

adrenergic neuron blockers interactions

A
  1. do not use within 14 days of a MAOI or else hypertensive crisis can occur
  2. digoxin can increase risk for bradycardia
  3. St johns wort can increase risk for hypotension
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69
Q

centrally acting alpha 2 agonists uses

A
  1. treat HTN
  2. pain relief if even as epidural
  3. prophylaxis against migraine headaches
  4. withdrawl symptoms of alcohol, opioids, and nicotine
  5. dysmenorrheal and menpausal hot flashes
  6. ADHD
  7. Tourettes syndrome
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70
Q

centrally acting alpha 2 agonist prototype

A
  1. clonidine

2. methyldopa

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71
Q

centrally acting alpha 2 agonist action

A

inhibits innervation of sympathetic neurons in the CNS which decreases stimulation of both alpha and beta receptors in the heart leading to

  1. bradycardia ->decreased CO
  2. vasodilation
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72
Q

centrally acting alpha 2 agonist side effects

A
  1. CNS
    - drowsiness, dizziness
  2. dry mouth
  3. hypertension crisis if not tapered
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73
Q

centrally acting alpha 2 agonists teaching

A
  1. dry mouth will go away after a couple of weeks

2. drug must be tapered

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74
Q

centrally acting alpha 2 agonist admin

A
  1. give at night
  2. comes as a transdermal patch or oral
    - monitor skin for inflammation
    - apply to a dry,hairless spot
    - rotate sites
    - remove old patch before applying new one
    - new patch every week
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75
Q

centrally acting alpha 2 agonist contraindications

A
  1. anticoagulants

2. pts with polyarteritis nodosa or scleroderma cannot use the patch

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76
Q

centrally acting alpha 2 agonist interactions

A

1.TCAs may decrease effectiveness

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77
Q

Alpha/Beta blockers uses

A
  1. treat HTN
  2. HF along with digoxin, ace inhibitors, and diuretics
  3. prolongs chance of survival following MI
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78
Q

Alpha/Beta blockers prototypes

A
  1. Carvedilol (car-vedi-lol)

2. labetalol

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79
Q

alpha/beta blocker action

A
  1. blocks alpha 1 receptors to cause vasodilation
  2. blocks cardiac beta1 receptors to
    - decrease HR and contractility
  3. blocks beta 1 receptors in kidney to
    - decrease release of renin
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80
Q

alpha/beta blockers side effects

A
  1. hypotension
  2. bradycardia
  3. dizziness
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81
Q

alpha/beta blockers admin

A
  1. oral use only

2. give with food to avoid orthostatic hypotension

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82
Q

alpha/beta blocker contraindication

A
  1. severe unstable HF
  2. asthma or other chronic respiratory disorders
  3. heart block or severe bradycardia
  4. cardiogenic shock
  5. lactation
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83
Q

alpha/beta blocker interaction

A
  1. increases risk for hypoglycemia when used with insulin or oral hypoglycemic
  2. increases risk of digoxin toxicity
  3. MAOIs cause bradycardia or hypotension
  4. Cimetidine increases blood levels
84
Q

Directing acting vasodilators uses

A
  1. moderate to severe hypertension
  2. IV form is used to treat hypertensive crisis
  3. used with digoxin to treat HF on a short term basis
85
Q

Direct acting vasodilator prototype

A
  1. Hydralazine
  2. Minoxidil (topically helps with male pattern baldness)
  3. Nitroprusside
86
Q

Hydralazine action

A
  1. dilates arterioles
    - decrease peripheral resistance
    - decreases arterial blood pressure but does not affect venous pressure
  2. increase HR
  3. increase contractility
87
Q

direct acting vasodilator side effect

A
  1. tachycardia
  2. headache
  3. palpitations
  4. systemic lupus erythematosus like syndrome may occur
    - facial rash, joint pain, fever, nephritis, pericarditis
  5. edema
  6. abrupt withdrawl leads to hypertensive crisis and HF
88
Q

direct acting vasodilator interventions

A
  1. advise patients that headache and palpitations may occur especially after the first dose report if they dont go away
  2. monitor and report orthostatic blood pressure and for tachycardia
  3. monitor and report for SLE
    - facial rash, joint pain, fever, nephritis, pericarditis
  4. combine with diuretic to minimize fluid retnetion
  5. taper the drug
89
Q

direct acting vasodilators admin

A
  1. oral, IM, IV
  2. do not mix
  3. give oral with food to enhance effectiveness
90
Q

direct acting vasodilators contraindications

A
  1. rheumatic heart disease caused by mitral valve dysfunction
  2. MI
  3. tachycardia
91
Q

direct acting vasodilator interactions

A

1.MAOIs can cause severe hypotension

92
Q

what is another name for atrial dysrhtmias

A

supraventricular dysrhtmias

93
Q

what are the 4 categories of drugs that are used to treat dysrhythmias

A 
Class 1 (sodium channel blockers)
Class 2 (beta adrenergic blockers)
Class 3 (potassium channel blockers
Class 4 (calcium channel blockers)
94
Q

describe the 3 subtypes of class one dysrhythmic drugss

A 
class 1A: moderate effect on sodium blockage: increases the refractory period
Class1B: small effect on sodium blockage: shortens refractory peroid
Class 1C: largest effect on sodium blockade: slight increase refractory peroid
95
Q

class 1A uses

A

broad spectrum antidysrhtmics used for a fib and futter and supraventricular and ventricular tachycardias

96
Q

Class 1A prototypes

A
  1. Quinidine(long term treatment)
  2. Procainamide (short term treatment due to severe adverse effects)
  3. Disopyramide
97
Q

Class 1A action

A

blocks moderate amount of sodium into cells of the mycardium, bundle of His, bundle branches, and purkinje fibers.

  1. slows impulse conduction
  2. decrease automaticity of ventricles
  3. lengthen refractory period (the amount of rest needed before another contraction can occur)
98
Q

why is a fib dangerous

A

the atria does not empty completly therefore clots from on the walls. When afib is fixed the clots are disloged.

99
Q

Class 1A side effects

A
  1. GI symptoms(common with sodium channel blockers)
    - n/v, diarrhea
  2. hypotension
  3. widen QRS and prolong QT interval. If the QRS gets to wide or the QT gets to long the drug must be discontinued
  4. Procainamide causes SLE in 50% of patients and Agranulocytosis (decrease in wbcs(granulocytes)
  5. may cause speed shock if given to fast
    - flushing, headache, irregular HR, hypotension, coma
100
Q

class 1A interventions

A
  1. monitor and report GI symptoms, blood pressure and heart rate
  2. keep patients supine during admin when hypotension is a problem
  3. monitor ECG withhold if cardiac changes occur
  4. give patients warfarin several weeks before and after therapy to prevent emoblism
  5. monitor for SLE and agranulocytosis if on procainamide long term
101
Q

class 1A admin

A
  1. give one hour before or two hours after a meal

2. avoid infusing with other drugs

102
Q

class 1A interactions

A
  1. anticholinergic drugs cause increased anticholinergic symptoms (tachycardia)
  2. cholinergic drugs can decrease theraputic effect
  3. amiodarone increases risk for heart block
  4. quinidine increases digoxin levels and warfarin levels
  5. grapefruit juice can cause toxicity
103
Q

Class 1B uses

A

IV:controls ventricular dysrhythmias caused by MI, cardiac procedures or digoxin toxicity
Local:provides anesthesia

104
Q

class 1B prototypes

A
  1. Lidocaine

2. mexiletine

105
Q

class 1B action

A

blocks a small amount of sodium from entering the cells of the myocardium, bundle of His, bundle branches, and purkinje fibers

  1. Slows impulse conduction
  2. decreases automaticity of ventricles, bundle of His, bundle branches, and Purkinje fibers
  3. shortens refractory peroid(the amount of time a cell has to rest before it can respond to another stimuli)
106
Q

class 1B side effects

A
  1. CNS toxicity
    - confusion, drowisness, restlessness, paresthesia, muscle twitching or tremors, seizures, respiratory arrest
  2. hypotension, bradycardia, heart block
  3. small decrease in QR interval
107
Q

class 1B interventions

A

monitor and report CNS toxicity

108
Q

class 1B teaching

A
  1. report numbness of lips and unusual sensations

2. frequent vital sign monitoring occurs during infusion

109
Q

class 1B contraindications

A
  1. allergy to amides
  2. Supraventricular dysrhythmias
  3. untreated bradycardia, heart block
110
Q

interactions class 1B

A
  1. beta blockers, procainamide, and quinidine increase lidocaine effects
  2. phenytoin increases hypotension and bradycardia
111
Q

class 1C use

A

serious supraventricular and ventricular tachydysrhythmias that can not be controlled by other less toxic drugs
-used long term for some supraventricular dysrhythmias

112
Q

class 1c prototypes

A
  1. flecainide

2. propafenone

113
Q

class 1C action

A

provides a large blockade of sodium entry into the cells of the myocardium, bundle of His, bundle branches, and Purkinje fibers

  1. slows impulse conduction
  2. decreases automaticity of ventricles, bundle of his, bundle branches, and purkinje fibers
  3. minimal effect on refractory period (slight increase)
114
Q

class 1C side effects

A
  1. Visual effects
    - blurred vision, difficulty focusing vision
  2. worsening of HF
    - edema
  3. ECG changes
    - widen QRS, prolonged QT and PR intervals
    - 1st degree AV block(long PR)
115
Q

Class 1C interventions

A
  1. monitor and report visual effects
  2. monitor for HF
    - crackles, edema, weight gain
  3. monitor ECG
  4. monitor plasma trough levels
116
Q

class 1C teaching

A
  1. get regular eye check ups

2. report SOB

117
Q

Class 1C interactions

A
  1. increases digoxin levels

2. bblockers and calcium channel blockers potentiate cardiac effects

118
Q

class 2 (beta blockers) prototypes

A
  1. propranolol
  2. acebutolol
  3. esmolol
  4. sotalol
119
Q

class 2 action

A

non selective beta blocker meaning it blocks both beta one and beta 2.

  1. Decrease SNS activity
  2. decreases SA node automaticity
  3. decreases conduction through the AV node
  4. decreases contractility
  5. closes calcium channels similar to calcium channel blockers
  6. prolongs PR interval
120
Q

class 3 uses(potassium channel blockers)

A

manages life threatening ventricular tachycardia or fibrillation that is resistant to other drugs and also treats some atrial dysrhythmias such as afib

121
Q

class 3 prototype

A
  1. amiodarone
  2. bretylium
  3. ibutilide
  4. sotalol(also a class 2)
122
Q

class 3 action

A 
blocks potassium, sodium, and calcium channels and also beta adrenergic receptors
1.decreases automaticity
2.slows conduction through AV node, ventricles and Purkinje fibers
3.decrease contractility
4.dilate coronary and peripheral vessels
Amiodarone
1.widens QRS complex
2.prolongs PR and QT intervals
123
Q

class 3 side effects

A
  1. GI
    - n/v, constipation
  2. pulmonary toxicity with pneumonitis
    - fever, cough and SOB
  3. visual effects
    - optic neuropathy with possible blindness and corneal microdeposits
  4. cardiac effects
    - bradycardia and hypotension
    - worsening HF
  5. Blue-grey discoloration of skin which is harmless
  6. CNS effects
    - dizziness, tremor, hallucination
124
Q

class 3 interventions

A
  1. monitor and report GI symptoms
  2. baseline CXR and pulmonary function test to rule out preexiciting lung disease
    - auscultate breath sounds
  3. monitor vision
  4. monitor heart
    - blood pressure, edema, weight gain
  5. CNS effects
    - dizziness, tremors, hallucination
125
Q

class 3 admin

A
  1. give at consistent times
  2. give IV doses through central line to prevent thrombophlebitis
  3. correct low potassium and magnesium before because they may also cause dysrhymthias
126
Q

class 3 teaching

A
  1. pulmonary function
    - report fever, dry cough, SOB
  2. eyes
    - wear sunglasses and get regular check ups
  3. monitor for bradycardia, weight gain
  4. monitor for CNS effects
    - tremors,dizziness, hallucinations
  5. avoid pregnancy
127
Q

class 3 interactions

A
  1. CYP3A4 inhibitors(grapefruit juice, azole drugs, erythromycin) increase risk for toxicity
  2. CYP34A inducers such as St Johns wort, phenytoin decrease blood levels
  3. Diuretics and drugs that increase QT interval increase risk for dysrhythmias
  4. Beta blockers and calcium channel blockers increase risk for bradycardia
  5. amiodarone increases blood levels of quinidine, procainamide, phenytoin, digoxin, diltiazem, warfarin and some statin drugs
128
Q

class 4 (calcium channel blockers) use

A
  1. converts supraventricular tachycardia to regular
  2. slow rate of a fib and flutter
  3. treats angina and hypertension
129
Q

class 4 prototypes

A
  1. verapamil

2. diltiazem

130
Q

class 4 action

A

blocks calcium channels in the myocardium

  1. slows automaticity of the SA node
  2. slows conduction through the AV node
  3. decreases myocardial contractility
  4. prolonges PR interval
131
Q

class 4 side effects

A
  1. hypotension, bradycardia
    - lightheadedness, dizziness
  2. HF
    - peripheral edema, SOB
132
Q

class 4 interventions

A
  1. keep patient suprine 1 hour post admin to minimize effects of hypotension
  2. look for HF
    - peripheral edema, SOB, bradycardia
  3. I and O
  4. monitor for crackles
133
Q

class 4 admin

A

1.give with food to prevent GI upset

134
Q

class 4 contraindications

A
  1. cardiogenic shock
  2. second or third degree AV block
  3. wolff parkinson white syndrome (an extra electrical pathway between the atria and ventricles exists)
  4. sick sinus syndrome
135
Q

class 4 interaction

A
  1. risk for AV block increases with digoxin
  2. beta blockers increase risk for bradycardia and HF (they are similar drugs)
  3. IV calcium decreases effects
  4. Lithium and cyclosporine levels can be increased
  5. grapefruit juice and increase blood levels
136
Q

what are the 4 categories of drugs for HF

A
  1. diuretics
  2. cardiac glycosides
  3. sympathomimetics
  4. phosphodiesterase inhibitors
137
Q

what is HF

A

the heart isnt able to produce enough CO to meet the demands of the body. The inability of the heart to pump blood out of the heart increases preload. HTN along with fluid buildup increase afterload. this increase in preload and afterload lead to backup into the lungs and tissues. leading to peripheral edema and pulmonary edema. The heart tries to compensate and grows becoming fibrotic.

138
Q

what are the 3 types of diuretics

A
  1. thiazide
  2. loop
  3. potassium sparing
139
Q

thiazide diuretic uses

A
  1. HF and HTN
  2. cirrhosis
  3. renal failure
140
Q

thiazide prototypes

A
  1. hydrocholorothiazide

2. chlorothiazide

141
Q

thiazide action

A

act on the proximal portion of distal convoluted tubule
1.blocks NaCl reabsorption
2.increase excretion of water and K+
Adequate kidney perfusion and GFR are needed for this drug to work

142
Q

thiazide SE

A
  1. hyponatremia,hypochloremia,dehydration,hypokalemia
  2. hyperglycemia, especially in diabetics
  3. hyperuricemia ->gout
143
Q

thiazide interventions

A

watch for those side effects

  1. give with food to minimize GI effects
  2. give last dose by 3p.m to prevent nocturia
  3. eat potassium (citrus fruits, potatoes, bananas)
144
Q

thiazide contraindications

A
  1. allergy to sulfonamides

2. anuria

145
Q

thiazide interactions

A
  1. lithium toxicity
  2. digoxin toxicity with a potassium or magnesium defiency
  3. corticosteroids and amphotericin B increase risk for hypokalemia
  4. decrease absorption with cholestyramine or colestipol
  5. increase blood glucose with insulin and oral sulfonylureas
146
Q

loop diuretics uses

A
  1. pulmonary edema in HF
  2. edema caused by renal, hepatic, or cardiac failure
  3. HTN
147
Q

loops prototypes

A
  1. furosemide
  2. ethacrynic acid
  3. bumetanide
148
Q

loop actions

A

act on ascending loop of henle doing the same thing as the thiazide diuretics

149
Q

loop SE

A
  1. ototoxicity
  2. hyperglycemia
  3. increased uric acid->gout
  4. orthostatic hypotension (b/c it also relaxes veins causing venous pooling)
150
Q

loop interventions and admin

A
  1. monitor for hearing loss
    - tinnitius, veritgo
  2. give oral with food
  3. give undiluted and administer slowly to prevent ototoxicity
  4. protect from light and store oral solutions in refrig
151
Q

loop contraindications

A
  1. pre-eclampsia or eclampsia
  2. hepatic coma
  3. increase in oliguria
152
Q

loop interactions

A
  1. digoxin toxicity with decrease potassium and mag levels
  2. NSAIDs decrease diuretic effects
  3. neuromuscular blocking agents may have prolonged effect
  4. lithium toxicity may occur
  5. amphotericin B and corticosteroids increase risk for hypokalemia
153
Q

potassium sparing uses

A
  1. HTN
  2. edema caused by HF
  3. cirrhosis
  4. nephrotic syndrome
  5. hypokalemia
154
Q

potassium sparing prototypes

A
  1. spironolactone (also an aldosterone antagonist)
  2. triamterene
  3. amiloride
155
Q

potassium sparing actions

A

works on distal portion of distal convoluted tubule

  1. increases excretion of Na
  2. small increase in water excretions
  3. decreased excretion of K+
156
Q

potassium sparing SE

A
  1. hyperkalemia

2. menstrual irregularities, abnormal hair growth, deepening of the voice, gynecomastia (it acts as a steroid)

157
Q

potassium sparing interventions and admin

A
  1. monitor for endocrine effects
  2. take with food to increase absorption
  3. Hyperkalemia
    - palpitations, irregular pulse
158
Q

contraindications potassium sparing

A
  1. pregnancy
  2. renal failure
  3. hyperkalemia
159
Q

potassium sparing interactions

A

ace inhibitors, ARBs, direct renin blockers, K+ supplements, salt substitues all increase risk for hyperkalemia

160
Q

Cardiac glycosides uses

A
  1. maintenance of HF
  2. dysrhythmias
    - afib
    - aflutter
    - paroxysmal atrial tachycardia
161
Q

cardiac glycoside prototype

A

digoxin

162
Q

cardiac glycoside

A

inhibites sodium, potassium ATPase channels causing

  1. increase in intracellular calcium
  2. supports interaction between actin and myosin
  3. positive inotropic effect
  4. decreases release of angiotensin 2 and renin
  5. decreases vasoconstriction
  6. increases excretion of water and sodium
  7. increases PNS and decreases SNS
    - slows electrical conduction through AV node (negative chronotropic effect)
163
Q

cardiac glycosides SE

A
  1. GI
    - n/v, vomiting, anorexia (may be early toxicity)
  2. CNS symptoms
    - headache, visual disturbanes such as yellow tinged or blurred vision (early toxicity)
  3. dysrhytmias
    - AV block is the most common
164
Q

cardiac glycoside interventions

A
  1. recognize vomiting may cause hypokalemia increasing the risk of toxicity
  2. take apical pulse for a full min (HR must be above 60 to give)
  3. Digoxin immune Fab(digibind) is the antidote
  4. give with or without food
  5. give at the same time everyday
165
Q

cardiac glycoside contraindications

A

1.ventricular fib or tachycardia unless caused by HF

166
Q

cardiac glycoside interactions

A
  1. erythromycin increase digoxin levels
  2. antidysrhtymics (verapamil,quinidine,amiodarone,flecainide) increase digoxin levels; adjust dose
  3. ginseng increases risk for digoxin toxicity
  4. st johns wort decreases digoxin levels
167
Q

sympathomimetics uses

A

increase CO in severe HF but only used short term

168
Q

sympathomimetic prototypes

A
  1. dobutamine

2. dopamine

169
Q

sympathomimetic action

A

activates beta 1 adrenergic receptors

  1. positive inotropic effect
  2. increases kidney perfusion->increased Urine output ->increased sodium excretion ->decreased fluid load ->decreased workload of heart
170
Q

sympathomimetic SE

A
  1. tachycardia
  2. dysrhytmias
  3. anginal pain (report immediately)
171
Q

sympathomimetic Admin

A
  1. peak effect occurs after 10 mins
  2. use dedicated line
  3. correct any fluid volume deficits before administering
172
Q

sympathomimetics contraindications

A
  1. allergy to sulfites
  2. vtach
  3. hypertrophic aortic stenosis
  4. dehydration
  5. children younger then 2
173
Q

sympathomimetics interactions

A
  1. MAOI and TCAs cause toxicitiy with greatly increased risk for tachydysrhthmias (decrease the dose)
  2. general anesthetics can also cause dysrhythmias
  3. Bblockers decrease the effect of dobutamine
174
Q

phosphodiesterase inhibitors uses

A

short term treatment of low CO in HF

175
Q

phosphodiesterase prototypes

A

1.milrinone (mil-re-known)

2inamrinone (in-am-ri-known)

176
Q

phosphodiesterase action

A 
inhibit phosphodiesterase(PDE3) an enzyme that breaks down cAMP. this causes cAMP to accumulate within cardiac cells and leads to
1. positive inotropic effects
177
Q

phosphodiesterase SE

A
  1. hypokalemia
  2. dysrhythmias
  3. hypotension
  4. anginal chest pain
178
Q

phosphodiesterase interventions

A
  1. correct fluid deficits and hypokalemia before beginning infusion
  2. decrease dosage for dysrhythmias or hypotension
  3. monitor for chest pain during infusion
179
Q

phosphodiesterase contraindications

A
  1. aortic or pulmonary valve disorders

2. acute MI

180
Q

phosphodiesterase interactions

A
  1. disopyramide(antidysrhytmic) may cause severe hypotension

2. incompatible in solution with furosemide and procainamide

181
Q

what are the 2 categories for Coronary heart disease

A

1.antilipemics
2.antianginals
CHD is caused by plaques that decrease diameter of coronary arteries. Thrombi can form on these plaques

182
Q

what are the two most common types of antilipemics

A
  1. HMG-CoA reductase inhibitors (statins)

2. Fibrates

183
Q

statin uses

A
  1. reduce LDL and VLDL
  2. increase HDL
  3. reduce mortality in DM 2
  4. reduces risk of MI
184
Q

statins prototypes

A
  1. atorvastatin
  2. simvastatin
  3. Lovastatin
  4. Rosuvastatin
185
Q

how does atherosclerosis work

A

LDL promote atherosclerosis by oxidizing and then attracting monocytes which then turn into macrophages which injest the oxidized LDL.The macrophages then die damaging the blood vessel lining and causing a build up of platelets.
-VLDL are produced in the liver by triglycerides and cholesterol.

186
Q

statins action

A

they inhibit HMG-CoA reductase, an enzyme which synthesizes cholesterol in the liver. They decrease VLDLs by inhibiting the production of apolipoprotein C-3 which stimulates the production of triglycerides by liver cells.

187
Q

statin SE

A
  1. Myopathy ->rhabdomylosis ->excretion of byproducts causes kidney damage
    - pain in muscles and join
  2. Liver toxicity
188
Q

statin intervention

A
  1. monitor for muscle and joint pain
  2. monitor creatinine phospokinase (CPK) levels if muscle pain occurs
  3. monitor liver function tests
  4. take lovastatin with food for better absorption the rest dont matter just take them in the evening
189
Q

statin contraindications

A
  1. pregnancy
  2. liver disease, jaundice, elevated transaminase
  3. renal failure
  4. MS
  5. children younger then 10
190
Q

statin interactions

A
  1. concurrent use of fibrates or other drugs to lower cholesterol increase risk for myopathy or liver toxicity
  2. drugs that inhibit CYP3A4 (erythromycin, azole antifungal drugs, and protease inhibitors) increase blood levels of lovastatin and atorvastatin
  3. grapefruit juice inhibits CYP3A4
  4. warfarin with a statin can increase risk for bleeding and cause increased PT levels
191
Q

Fibrates uses

A
  1. reduce triglycerides

2. reduce LDL (less effective then statins)

192
Q

fibrates prototypes

A
  1. gemfibrozil
  2. fenofibrate
  3. fenofibric acid
193
Q

fibrates action

A

Activate PPAR alpha (in the liver and adipose tissue) which increases production of the enzyme LPL which
1.decreases production of triglycerides(VLDLs)
2.moderately reduces LDLs
PPAR alpha also increases the production of certain lipoproteins (apolipoproteins A1 and A2) which
1.increase HDL

194
Q

fibrates SE

A
  1. GI
    - n/v diarrhea
  2. Gallstones
    - inability to tolerate fried foods, upper abdominal discomfort, bloating
  3. myopathy
  4. Liver toxicity
195
Q

fibrates interventions

A
  1. monitor for SEs
  2. measure creatine phosphokinase if muscle pain occurs
  3. take 30 mins before breakfast and evening meal
196
Q

fibrates contraindications

A
  1. gall bladder disease
  2. liver dysfunction
  3. severe renal impairment
197
Q

fibrates interactions

A
  1. concurrent statin use greatly increases risk for myopathy
  2. warfarin increases risk for bleeding
  3. when taken with antidiabetic drugs it increases risk for hypoglycemia
198
Q

what are the 3 types of antianginals

A
  1. nitrates
  2. bblockers
  3. calcium channel blockers
199
Q

nitrates uses

A
  1. treament and prophylaxis of angina pectoris

2. IV nitro can control BP and used in HF after MI

200
Q

nitrates prototypes

A
  1. nitroglycerin
  2. isosorbide
  3. amyl nitrate (inhaled)
201
Q

nitro action

A

nitrate turns into nitric oxide (via sulfhydrl)

  1. dilates coronary veins -> fix angina
  2. decrease oxygen demands of stable angina
    - dilate coronary veins
    - decrease preload
  3. increases oxygen supply
    - relaxes spasm of coronary arteries
202
Q

nitrates SE

A
  1. headaches which is severe at first but goes away with continued exposure
  2. orthostatic hypotension (vasodilation of veins
    • > pooling)
  3. tachycardia
  4. tolerance
203
Q

nitrates intervention

A
  1. avoid touching with raw hands as it can be absorbed through skin
  2. monitor orthostatic BP
  3. monitor HR
    - Bblockers to treat tachy
204
Q

nitro admin

A

Sublingual

  • use when chest pain occurs. If not relieved in 5 mins call 911 and take a second tablet. Wait 5 mins and take another if pain doesnt go away
    2. Transmucosal
  • place in buccal area between cheek and gum
    3. transdermal
  • hairless area, rotate sites, remove patches for 10-12 hours daily
205
Q

nitrates interactions

A
  1. increased hypotension when used with alcohol or antihypertensive drugs
  2. PDE5 inhibitors (sildenafil) may cause severe hypotension
  3. Bblockers and calcium channel blockers decrease tachycardia

Med surg (35 decks)

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