Blood Pressure Agents Flashcards

1
Q

What is angiotensin-converting enzyme responsible for?

A

converting angiotensin I to angiotensin II in the lungs

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2
Q

What is the MOA of ACE inhibitors?

A

blocks ACE, which prevents the vasoconstriction and aldosterone release related to angiotensin II

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3
Q

What are angiotensin II receptors?

A

specific receptors found in blood vessels and in the adrenal gland that react with angiotensin II to cause vasoconstriction and release of aldosterone

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4
Q

What are baroreceptors?

A

Pressure receptors located in the arch of the aorta and in the carotid artery that respond to changes in blood pressure and influence the medulla to stimulate the sympathetic system to increase or decrease blood pressure

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5
Q

What is the cardiovascular center and where is it located?

A

area of the medulla at which stimulation will activate the sympathetic nervous sytem to increase blood pressure and heart rate

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6
Q

What is essential hypertension?

A

sustained blood pressure above normal limits with no discernible underlying cause

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7
Q

What is peripheral resistance?

A

the force that resists the flow of blood through the vessels, mostly determined by the arterioles, which contract to increase resistance; important in determining overall blood pressure

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8
Q

What is the ultimate goal of the Renin-Angiotensin System?

A

The RAAS system causes vasoconstriction and Na2+ and H2O retention which results in an increase in BP.

Increased BP and increased blood volume with increase perfusion to the kidney.

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9
Q

How does HTN affect the RAAS system?

A

In the case of HTN, there is a miscommunication. The increased BP results in vasoconstriction so the kidneys don’t get as much pressure as they want so they release Renin and activate RAAS so they can try to get more blood.

BUT, it has the opposite effect b/c now we have vasoconstriction that decrease reduces blood flow further, which activates the RAAS again.

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10
Q

What is shock?

A

Severe hypotension that can lead to accumulation of waste products and cell death

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11
Q

What is stroke volume?

A

the amount of blood pumped out of the left ventricle with each beat

SV = end diastolic vol - end systolic vol

important in determining BP

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12
Q

What is the formula for BP?

A

HR X SV

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13
Q

Hypertension raises a patient’s risk for CAD. Explain the pathophysiology behind this risk.

A

HTN is due to increased peripheral resistance. This resistance causes thickening of the heart muscle. When it gets too thick, the heart cannot contract completely anymore, which causes hypertrophy, or enlargement of the heart. This causes congestive heart failure (CHF) and CAD.

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14
Q

List 4 conditions related to untreated HTN:

A

CAD and Cardiac Death

Stroke

Renal Failure

Loss of Vision

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15
Q

What is the nurse’s job concerning HTN and the patient?

A

Our job is to educate the patient about the risks of untreated HTN. Often patients see no symptoms of HTN and they don’t enjoy the lifestyle changes needed and adverse effects of the drugs, so they don’t want to continue. We need to teach them and be truthful.

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16
Q

List 5 things that increase BP

A

High levels of psychological stress

Exposure to high-frequency noise

High-salt diet (leads to fluid retention)

Lack of rest (physiological stress)

Genetic predisposition

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17
Q

Which blood pressure agents can we use with children?

A

Mild diuretics - monitor glucose and electrolytes

Calcium Channel Blockers

Beta-Blockers - Adverse effects are possible, so not the first choice

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18
Q

Childhood hypertension is usually ______________.

A

secondary to a primary disease process.

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19
Q

What are the signs of high BP?

A

HA
Vision Changes
Nosebleeds
Ringing in the ear

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20
Q

Why is dehydration a complication of HTN?

A

It can cause hypotension.

It can cause hypertension. The brain releases vasopressin as a result of dehydration, which vasoconstricts vessels, increasing BP.

Also, when dehydrated, the kidneys decrease urine formation which causes the capillaries in the heart and brain to constrict, which increases BP.

The combo of vasopressin and kidney changes causes serious kidney damage and renal disease.

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21
Q

How do blood pressure agents affect pregnancy and lactation? Which ones can we give?

A

Drugs enter breastmilk and can cause serious adverse effects, so we need to find an alternative to breastmilk.

IF benefits outweigh the risk, LABETALOL may be used in pregnancy.

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22
Q

For older adults, we start _____ and go ________. Why?

A

low
slow

Because the elderly are more susceptible to toxic effects. Also, the metabolism has slowed and there may be underlying conditions that effect metabolism and excretion.

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23
Q

We should monitor the elderly for dehydration. Why?

A

Older adults lack a thirst trigger, so they often don’t drink enough.

24
Q

What should we teach our patients about sustained-release or extended-release tablets of Blood Pressure meds?

A

Do not cut, crush, or chew them because it may cause a toxic dose.

25
Q

Should the nurse take BP before or after administering BP meds?

A

immediately before

26
Q

Explain hypOtension.

A

BP BECOMES TOO LOW

When the heart muscle is damaged and unable to pump effectively

With severe blood or fluid loss, the volume drops dramatically

When there is extreme stress and the body’s levels of NE are depleted, it leaves the body unable to respond to stimuli and raise BP.

27
Q

Step 1 of Care Management for HTN

A

Lifestyle modifications:

Wt reduction, smoking cessation, moderation of alcohol intake, reduction of dietary salt, increase in aerobic physical activity

28
Q

Step 2 of Care Management for HTN

A

Result of inadequate response to step 1

Add drug therapy to lifestyle changes

29
Q

Step 3 of Care Management for HTN

A

Result of inadequate response to step 2

Consider change in drug dose or class, or addition of another drug for combined effect

30
Q

Step 4 of Care Management for HTN

A

Result of inadequate response to step 3

Second or third agent or diuretic is added if not already prescribed

31
Q

What is the suffix for ACE Inhibitors and what are the 5 we need to know?

A

“-PRIL”

benazePRIL
captoPRIL
enalaPRIL
lisinoPRIL
ramiPRIL

**NOTE: ACE Inhibitors can also end in “at”, ex. ramiPRAT. The “-at” drugs have all the same MOAs and effects, they just work faster and stronger.

32
Q

What are the Labs to assess for before admin of ACE Inhibitors?

A

CBC

Electrolytes

33
Q

What should the nurse assess for before giving ACE Inhibitors?

A

Regular things

Any Salt/Volume Depletion

34
Q

What are the nursing interventions to remember for ACE Inhibitors?

A

Make sure the patient implemented lifestyle changes and encourage the patient to continue

Administer drugs on an empty stomach 1 hour before or 2 hours after meals

Alert the surgeon and mark the patient’s chart prominently if the patient is to undergo surgery

35
Q

What is the suffix for Angiottensin II Receptor Blockers and what are the 6 we need to know?

A
"-SARTAN"
candeSARTAN
irbeSARTAN
loSARTAN
olmeSARTAN
telmiSARTAN
valSARTAN
36
Q

What are the Labs to assess for before admin of Angiotensin II Receptor Blockers?

A

Renal/Liver Fxn

37
Q

What are the nursing interventions to remember for Angiotensin II Receptor Blockers?

A

Alert the surgeon and mark the patient’s chart prominently if the patient is to undergo surgery

Ensure that the female patient is not pg before beginning therapy and suggest the use of barrier contraceptives

38
Q

What is the Renin Inhibitor we need to know?

A

aliskiren

39
Q

What is the suffix for Calcium Channel Blockers and what are the 5 we need to know?

A

“-DIPINE”
amloDIPINE
feloDIPINE
nifeDIPINE

diltiazem
verapamil

40
Q

What does the nurse assess for before admin of Calcium Channel Blockers?

A

Heart block

Sick sinus syndrome

41
Q

What nursing interventions to remember about Calcium Channel Blockers?

A

Monitor the patient’s blood pressure, cardiac rhythm, and cardiac output

42
Q

What are the 3 Vasodilators we need to know?

A

Hydralazine
Minoxidil (also used 4 hair regrowth)
Nitroprusside

43
Q

What labs should the nurse look at before administering Vasodilators?

A

Renal/hepatic fxn

Blood glucose for diabetics (vasodilators decrease blood glucose)

44
Q

Which diuretics are used to lower BP?

A

Thiazides

Potassium-sparing diuretics

45
Q

What is the suffix for Beta-Blockers and what are the 3 we need to know?

A

“-OLOL”
atenOLOL
metoprOLOL
propranOLOL

46
Q

What labs should the nurse assess for before admin of Beta-Blockers?

A

Electrolytes

Renal/Hepatic Fxn

47
Q

What interventions should the nurse perform for patients on Beta-Blockers?

A

Take the apical pulse prior to administering

Do not abruptly withdrawal medication b/c it causes chest pain, MI, and death

Change position slowly

Emphasize the importance of follow-up exams to monitor progress

48
Q

What is the suffix for Alpha-adrenergic Blockers and what are the 2 we need to know?

A

“-amine”
phenoxybenzAMINE
phentolAMINE

49
Q

What is a pheochromocytoma?

A

a benign tumor in the adrenal gland that results in too much hormone production. This leads to increased BP, sweating, HA

50
Q

What is the suffix for Alpha-1 Blockers and what are the 3 we need to know?

A

“-AZOSIN”
doxAZOSIN
prAZOSIN
terAZOSIN

51
Q

What are the Alpha-2 agonists and what are the 3 we need to know?

A

Clonidine
Guanfacine
Methyldopa

52
Q

What are the 2 Alpha- and Beta- blockers we need to know?

A

Carvedilol

Labetalol

53
Q

What are the suffixes for Sympathetic adrenergic agonists, vasopressors, and what are the 6 we need to know?

A

“-AMINE”
dobutAMINE
dopMINE

"-RINE"
ephedRINE
epinephRINE
norepinephRINE
phenylephRINE
54
Q

What are the Blood Pressure-Raising/Orthostatic Hypotension Agents and what are the 2 we need to know?

A

Midodrine

Droxidopa

55
Q

What should a nurse assess for before administering a antihypertensive drug?

A

CV dysfunction:
Vision problems
Urinary Retention
Pheochromocytoma

56
Q

What nursing interventions should the nurse perform when administering antihypertensive drugs?

A

Do not administer Midodrine or Droxidopa to patients who are bedridden

Encourage the patient to void before taking a dose of the drug