C6- Cardiovascular And Renal Medications PT 1 Flashcards

1
Q

Inotropic definition (positive and negative medication effects)

A

The strength of contraction
- Positive drugs= stronger force
-Negative drugs = decreased force of contraction

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2
Q

Chronotropic definition definition (positive and negative medication effects)

A

Heart rate

Positive drugs- increased HR
Negative drugs- decreased HR

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3
Q

Dromotropic

A

The speed of electrical impulse

Positive drugs- faster conduction
Negative drugs - slower conduction

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4
Q

What is Preload?

A

Volume of blood in ventricles at end of diastole
-end diastolic pressure

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5
Q

Risk of preload increased in:

A

Hypervolemia

Regurgitation of cardiac valves

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6
Q

What is afterload?

A

The load against which a muscle exerts its force
- resistance left ventricle must overcome to circulate blood

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7
Q

Afterload increased in

A

Hypertension
Vasoconstriction

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8
Q

Increased afterload = increased cardiac __________

A

Cardiac workload

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9
Q

ABCD’s of Hypertension

A

A- Ace inhibitors & ARB’s
B- Beta blockers
C- calcium channel blockers
D- Diuretics

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10
Q

What percentage of the population is affected by hypertension?

A

45% of population

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11
Q

Hypertension prevalence in race:

A

Non-Hispanic black people

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12
Q

Hypertension Normal stage

A

<120/80mmHg

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13
Q

Ace Inhibitors Examles:

A

Lisinopril

** Common ending of “PRIL” **

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14
Q

Ace inhibitors Action and what it results in (what happens to the blood flow? What gets excreted? What is retained? Does it hinder progression in a disease?)

A

Blocking the production of Angiotensin II by blocking the conversion of angiotensin I to angiotensin II

Resulting in:
-Vasodilation
-Excretion of sodium and water (drops blood volume)
-Retention of K+
-Slows progression of diabetic neuropathy

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15
Q

Ace inhibitors not reccommended in people:

A

-Elderly
-African American populations

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16
Q

Advantages of Ace inhibitors:

A

Increase renal blood flow
Lack of aggravation with DM
Infrequent orthostatic hypotension
Lack of aggravation of pulmonary dx

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17
Q

Disadvantages of Ace Inhibitors

A

Cough (must D/C medication)
Angioedema (containdicated)
Hyerkalemia
Headache/dizziness
Orthostatic hypotension - infrequent
GI distress
Kidney function (caution w/ renal issues)
Salty/metallic taste
** Preg. Cat. D **

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18
Q

Ace Inhibitors Drug interactions

A

K+ sparing diuretics lead to hyperkalemia
Diuretics can impact kidneys and lead to hypotension
Alcohol
Beta blockers -enhance the hypotensive effects
NSAID’s- decrease effect of Ace Inhibitors risk

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19
Q

Angiotensin Receptor blockers are also referred to as:

A

ARBs

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20
Q

ARBs Action:

A

Blocks the action of Angiotensin II in the body

Results in:
-vasodilation
-Excretion of sodium and water
-retention of K=
-Resulting in lower blood pressure

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21
Q

ARBs Examples

A

Losartan

** Common ending “SARTAN” **

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22
Q

ARBs Side effects:

A

Angioedema (contrindicated)
Hyperkalemia
Headache
Orthostatic hypotension
GI distress
Kidney function -caution with renal issues
Salty/metallic taste
** PREG. CAT. D **

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23
Q

ARBs relax _____ ______ and lower _____ _____

A

Relax
-blood vessels

Lower
- blood pressure

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24
Q

Who should not use ACEs and ARBs? Specific diseases? conditions?

A

Pregnancy/breastfeeding CAT D.
DO NOT USE IF patient has renal artery stenosis

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25
Q

Nursing teaching ACEs an ARBs

A

Do not use salt substitutes
-contain k+ and ACE & ARB cause body to retain K+
Sit or lie down 2-4 hours after initial dose
-risk of first-dose hypotension
Rise slowly
Avoid NSAIDs
Don’t stop meds w/o consulting physician

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26
Q

ACE & ARB administration what time of day? Take with meals?

A

Taken one hour before meals on an empty stomach

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27
Q

Normal range for Potassium

A

3.5-5.5 mEq/L

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28
Q

Normal range for BUN (indicate renal function)

A

7-22 mg/dL

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29
Q

Normal labs for Creatinine

A

0.7-1.3 for men

0.6-1.1 for women

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30
Q

Beta 1- adrenergic receptors location

A

Located in heart and kidneys

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31
Q

Beta 1 adrenergic receptor stimulation causes: what happens to the heart productivity?

A

Increased heart rate (pos. chronotropic)
Increase in strength of contraction (inotropic)
Increases cardiac conduction (velocity and automaticity)

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32
Q

Beta 2 adrenergic receptor location

A

Lungs and liver

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33
Q

Beta 2 adrenergic receptor stimulation causes: (What happens with the blood vessels? What happens in the muscles? What happens with the liver (blood glucose)?

A

Vasoconstriction - more blood flow to muscles
Tremor in skeletal muscle
Glycogenolysis - (liver) increase glucose production for energy

34
Q

Beta adrenergic blocking agents (BETA BLOCKERS) action: What do they inhibit? Which results in a decrease of?

A

Inhibit
-cardiac response to sympathetic nerve stimulation by blocking beta receptors

Decrease
-hr and cardiac output
-blood pressure
-renin release

35
Q

Beta 1 and 2 non selective blockers:

A

Propranolol (inderal)

36
Q

Beta 1 cardio selective blocker

A

Metoprolol (lopressor)

37
Q

Alpha 1 AND beta 1. Blocker

A

Carvedilol (Coreg) just for heart failure patients

38
Q

Beta blockers (+/-): Chronotrope, inotrope, dromotrope

A

TRIPLE NEGATIVE

39
Q

Beta adrenergic blocking agents uses:

A

HTN
Heart failure
Angina
Arrhythmia
Glaucoma
Migraine HA
Tremors

40
Q

Beta blockers end in

A

OLOL

41
Q

Beta blockers side effects

A

Bradycardia (60-90 rule)
hypotension (orthostatic)
heart failure (edema, dyspnea, crackles)
Erectile dysfunction
Depression

42
Q

What class of drugs reduce the effect of beta blockers?

A

NSAIDS REDUCE EFFECT OF BETA BLOCKERS

43
Q

Beta Adrenergic Blocking Agents interactions

A

Antihypertensive meds - additive
B-adrenergic agonists
Enzyme inducing agent - enhance metabolism

44
Q

Beta Adrenergic Blocking Agents contraindicated in which conditions?

A

Asthma
Bradycardia
Hyperthyroid

45
Q

Beta Adrenergic Blocking Agents Nursing implications
(Hx of? Who should be weaned off of the med? What can reduce/reverse an overdose?)

A

-Check hx of resp condition- aggravates bronhoconstriction
-Avoid abruptly discontinued in pts with CAD
-Glucagon may reverse overdose
-Check baseline of HR/BP 60/90 rule!
*then call PCP

46
Q

Calcium channel blockers Action? Where does the action take place?

A

Blocking of calcium channels in blood vessels leads to VASODILATION in the arterioles and arteries of the heart

47
Q

Calcium Channel Blockers: blocking of calcium channels in the myocardium the SA node and AV node Decrease…?

A

Force of contraction
HR
Rate of conduction through the AV node

48
Q

Calcium Channel Blockers example

A

Amlodipine

Verapamil

Diltiazem

49
Q

Calcium Channel Blockers uses

A

HTN
Angina
Cardiac dysrhythmias
Alternative to B-blocker
** FIRST CHOICE FOR AFRICAN AMERICANS **

50
Q

Calcium Channel Blockers contraindications

A

Heart block
Hypotension
Bradycardia - 60/90 Rule!
Aortic stenosis
Severe heart failure

51
Q

Calcium Channel Blockers grapefruit juice restriction

A

Delays metabolism
May result in toxicity

52
Q

Calcium Channel Blockers side effects

A

Orthostatic hypotension
Constipation
Reflex tachycardia
Bradycardia/dysrhythmias
Peripheral edema
Gingival hyperplasia/ hypertrophy

** PREG CAT C **

53
Q

Calcium Channel Blockers teaching

A

Change positions slowly
Monitor edema
Monitor blood pressure and hr

54
Q

Calcium Channel Blockers interactions

A

Beta blockers
Digoxin

55
Q

Diuretics used to treat

A

Mild-moderate HTN
Peripheral or pulmonary edema
Heart failure or kidney disease

56
Q

Diuretics action

A

Reduce blood volume through urinary excretion of water and electrolytes
- electrolyte imbalances can occur
-hypo/er-kalemia (K+)
depends on type of diuretic

57
Q

Loop diuretics examples

A

Furosemide (Lasix)

58
Q

Effectiveness of loop diuretics/Furosemide

A

Decreased edema
Increase in fine output
Decrease in blood pressure
Weight loss

59
Q

Loop diuretics efficiency

A

MOST EFFICIENT
Works well on clients with renal impairment
Pulmonary edema caused by heart failure

60
Q

Loop diuretics side effects

A

Electrolyte imbalance
Hypotension (monitor BP, Rise slowly)
Dehydration (monitor I/O, weight same time every day)
Ototoxicity
Hyperglycemia
Hyperuricemia (gout)

61
Q

normal potassium levels

A

3.5-5.5

  • Panic above 6.2 and below 2.8 ***
62
Q

Hypokalemia signs and symptoms

A

Palpitations
Constipation
Neben and tingling
General weakness
Fatigue
Cramping in arm or leg

63
Q

Teach patient about K+ rich foods such as:

A

Bananas
Avocados
Broccoli

64
Q

Loop diuretics Nursing:

A

Avoid taking late in day (avoid nocturia)
Infuse IV doses slowly
ototoxicity
Watch for s&s of low electrolytes (twitching cramping tremors)
Encourage high potassium foods
Urine <30ml/hr stop lasix and notify PCP

65
Q

Loop diuretics interactions

A

Ototoxic (aminoglycosides, Vancomycin)
Hypokalemia (digoxin)
Lithium levels can rise
NSAIDS
Avoid in client with gout or diabetes
Antihypertensives (additive)

66
Q

Use caution administering loop diuretics if patient is allergic to?

A

Sulfa (sulfer)

67
Q

Diuretic (thiazides) name

A

Hydrochlorothiazide (HCTZ)

68
Q

Diuretic (thiazides) Hydrochlorothiazide action blocks what? Promotes?

A

Block reabsorbtion of NA and Chloride (prevent H2O reabsorption)
Promote diauresis

** not as strong as lop diuretics **

69
Q

Diuretic (thiazides) Hydrochlorothiazide helps with what conditions

A

Mild to moderate hypertension * PRIMARY
Edema
Mild to moderate heart failure

70
Q

Diuretic (thiazides) Hydrochlorothiazide side effects:

A

Dehydration
Electrolyte imbalance
Hyperglycemia
Hyperuricemia- gout

71
Q

Diuretic (thiazides) Hydrochlorothiazide administration guidelines (when?) (IF GI UPSET- what do you do?)

A

Take medication first thing in the morning
If GI upset- take with food

72
Q

Diuretic (thiazides) Hydrochlorothiazide Nursing (decrease? Increases what?)

A

Effective decrease in
-BP
-Edema
Increases
-urine output
Not effective with limited renal function

73
Q

Diuretic (thiazides) Hydrochlorothiazide use caution (allergy?)

A

Sulfonamide (sulfa)

74
Q

Diuretic (thiazides) Hydrochlorothiazide interactions

A

Hypokalemia- digoxin
Antihypertensive- added hypotensive
Lithium levels may rise
NSAIDS
** pregnant/breastfeeding **

75
Q

Diuretic Potassium-sparing (spironolactone):

A

Sipironolactone/Aldactone

76
Q

Diuretic Potassium-sparing (spironolactone): action

A

Block action of aldosterone (NA+ and H2O retention) resulting in K+ retention and secretion of (NA+ and H2O)

77
Q

Diuretic Potassium-sparing (spironolactone): used for

A

When Hypokalemia is a risk
-mild HTN
-Heart failure
-combination therapy with K+ wasting drugs
-block actions of aldosterone
-acne

78
Q

Diuretic Potassium-sparing (spironolactone): side effects

A

Hyperkalemia
-cardiac monitoring of increased K+
-treat hyperkalemia with D/C of drug, restrict K+ in diet, inject insulin
Endocrine
-impotence (males)
-irregular menstruation (females)
-gynecomastia

79
Q

Diuretic Potassium-sparing (spironolactone): interactions

A

ACE inhibitors increase risk of hyperkalemia
K+ supplements

80
Q

Diuretic teaching:

A

Reduce Na+ in. The diet
Monitor electrolyte levels
Avoid K+ and Na+ substitutes
Use protection from sunlight
Don’t drink alcohol or take other meds w/o DR approval
Take with food decrease stomach upset
Take med early in day to avoid interrupting sleep to go urinate