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Antihypertensive Flashcards

1
Q

Blood pressure calculation

A

(BP) = CO × SVR

CO = cardiac output
SVR = systemic vascular resistance

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2
Q

High-normal BP

A

Systolic blood pressure (SBP) of 130–139 mm Hg or diastolic blood pressure (DBP) of 85–89 mm Hg

Affects estimated 7.5 million Canadians

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3
Q

CNS

SVR

A

Centrally acting adrenergic

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4
Q

Local

SVR

A

Peripherally acting adrenergic

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5
Q

Hypertension Defined by Its Cause

  1. Essential hypertension
  2. Secondary hypertension
  3. Malignant hypertension, it is a
A

Essential hypertension (idiopathic, primary)
90 to 95% of cases

Secondary hypertension
**5 to 10% of cases
**Most commonly result of pheochromocytoma, pre-eclampsia, renal artery disease, sleep apnea, thyroid disease, or parathyroid disease

Malignant hypertension
BP above 180/120; a medical emergency

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6
Q

Goals of antihypertensive therapy

Achieve pressure less than?

A

Reduction of cardiovascular and renal morbidity

Achieve pressure less than 140/90 mmHg

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7
Q

Hypertension + diabetes: less than _______ mmHg

Hypertension + chronic kidney disease: less than _______ mmHg

GOAL BP

A

Hypertension + diabetes: < 130/80 mmHg

Hypertension + chronic kidney disease: < 140/90 mmHg

Less than 140/90 or 120/ 80 (as per Brenda)

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8
Q

Parasympathetic nervous system

stimulates? 3

function in BVs?

A

Stimulates smooth muscle, cardiac muscle, glands

relax BVs

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9
Q

Sympathetic nervous system

stimulates? 3

function in BVs?

A

Stimulates the heart, blood vessels, skeletal muscle

Contracts BVs

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10
Q

Antihypertensive Drugs

A

Medications used to treat hypertension

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11
Q

Antihypertensive Drugs Categories 7

A

Adrenergic drugs

Angiotensin-converting enzyme (ACE) inhibitors

Angiotensin II receptor blockers (ARBs)

Calcium channel blockers

Diuretics

Vasodilators

Direct renin inhibitors

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12
Q

Parasympathetic NS hormone

A

ACh

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13
Q

Sympathetic NS hormone

A

NE

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14
Q

Adrenergic Drugs: Five Subcategories

A

α2-Receptor agonists (central)- brain

Adrenergic neuron blockers (central and peripheral)

α1-Receptor blockers (peripheral)- heart and BVs

β-Receptor blockers (peripheral)-heart and BVs

Combination α1- and β-receptor blockers (peripheral)- heart and BVs

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15
Q

Centrally Acting Adrenergic DrugS

A

clonidine

OTHER:
methyldopa

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16
Q

Centrally Acting Adrenergic:

clonidine and methyldopa

Mechanism of action:

A

Stimulate α2-adrenergic receptors in the BRAIN (which normally inhibit NE release from adrenergic terminals)

Decrease sympathetic outflow from the CNS (results in DILATION due to decreased sympathetic response)

Decrease norepinephrine (sympathetic) production

Stimulate α2-adrenergic receptors, thus reducing renin activity in the kidneys

BVs dilate, renin decreases and it result in decreased BP

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17
Q

Peripherally Acting α1-Blockers MEDICATION

A

doxazosin

OTHER:
prazosiN
terazosin

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18
Q

Peripherally Acting α1-Blockers:

doxazosin, prazosin, and terazosin

Mechanism of action:

A

Block α1-adrenergic receptors (which normally contricts BVs and viceral organ sphincter)

When α1-adrenergic receptors are blocked, BP is decreased.

Dilate arteries and veins

α1-Blockers also increase urinary flow rates and decrease outflow obstruction by preventing smooth muscle contractions in the bladder neck and urethra.

Use: benign prostatic hyperplasia (BPH)

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19
Q

Beta-blockers 3 medications

A

propranolol, metoprolol, and atenolol

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20
Q

ß-Blockers

propranolol, metoprolol, and atenolol

2 effects
Long term use causes?

A

Reduction of the heart rate through β1-receptor blockade

Cause reduced secretion of renin

Long-term use causes reduced peripheral vascular resistance.

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21
Q

Dual-Action α1- and β-Receptor Blockers

labetalol mechanism of action?

Used for?

A

Dual antihypertensive effects of reduction in heart rate (β1-receptor blockade) and vasodilation (α1-receptor blockade)

used for pregnant women with HTN

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22
Q

Adrenergic Drugs: Indications

A

All used to treat hypertension

Treats glaucoma

BPH: doxazosin, prazosin, and terazosin

Management of severe heart failure (HF) when used with cardiac glycosides and diuretics

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23
Q

Adrenergic Drugs: Adverse Effects

A

High incidence of orthostatic hypotension, syncope

Most common:

Bradycardia with reflex tachycardia
Dry mouth
Drowsiness, sedation
Constipation
Depression
Edema
Sexual dysfunction

Other:
Headaches
Sleep disturbances
Nausea
Rash
Cardiac disturbances (palpitations), others

Slow position changes!!

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24
Q

α2-Adrenergic Receptor Stimulators (Agonists)

clonidine and methyldopa

  1. INDICATION
  2. AE
  3. Used in conjunction with?
A

Not typically prescribed as first-line antihypertensive drugs

Adjunct drugs to treat hypertension after other drugs have failed

High incidence of unwanted adverse effects: orthostatic hypotension, fatigue, and dizziness

Used in conjunction with other antihypertensives such as diuretics

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25
Q

α1-Blockers

doxazosin mesylate (Cardura®)

prazosin hydrochloride (Minipress®)

tamsulosin hydrochloride (Flomax®)*

terazosin hydrochloride (Hytrin®)

A

*Tamsulosin is not used to control BP but is indicated solely for symptomatic control of BPH.

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26
Q

α1-Blockers

doxazosin mesylate (Cardura®)

How does it reduces PVR and BP?

A

Commonly used α1-blocker

Reduces peripheral vascular resistance and BP by dilating both arterial and venous blood vessels

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27
Q

Β-Receptor Blockermedication

A

nebivolol hydrochloride (Bystolic®)

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28
Q

Β-Receptor Blocker

nebivolol hydrochloride (Bystolic®)

Mechanism of action

A

Uses: hypertension and HF

Action: blocks β1-receptors and produces vasodilatation, which results in a decrease in systemic vascular resistance (SVR)

Less sexual dysfunction

Do not stop abruptly; must be tapered over 1 to 2 weeks.

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29
Q

Angiotensin-Converting Enzyme (ACE) Inhibitors

Large group of?

Often use?

May be combined with a? or a?

A

Large group of safe and effective drugs

Often used as first-line drugs for HF and hypertension

May be combined with a thiazide diuretic or a calcium channel blocker.

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30
Q

TO KNOW medications: ACE Inhibitors

Ends in suffix?

A

“Pril”

captopril (Capoten®)

enalapril (Vasotec®)

perindopril (Coversyl®)

ramipril (Altace®)

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31
Q

Other ACE Inhibitors

A

benazepril (Lotensin®)
fosinopril sodium
lisinopril (Prinivil®)
cilazapril (Inhibace®)
quinapril (Accupril®)
trandolapril (Mavik®)

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32
Q

ACE Inhibitors:

Explain mechanism of Action

2 functions of angiotensin II

A

Inhibit ACE, which is responsible for converting angiotensin I (through the action of renin) to angiotensin II

Angiotensin II is a potent vasoconstrictor and causes aldosterone secretion from the adrenal glands.

Block ACE, thus preventing the formation of angiotensin II

Prevent the breakdown of the vasodilating substance bradykinin

Ability to decrease SVR (a measure of afterload) and preload

Can stop the progression of left ventricular hypertrophy

Lower BP

[inhibits ACE enzymes which leads to vasodilation; ACE usually leads to vasoconstriction]

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33
Q

ACE Inhibitors:Indications

A

Hypertension

HF (drug used either alone or in combination with diuretics or other drugs)

Slow progression of left ventricular hypertrophy after myocardial infarction (MI) (cardioprotective)

Renal protective effects in patients with diabetes

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34
Q

ACE Inhibitors: Captopril and Lisinopril

A

Are not prodrugs.

Prodrugs are inactive in their administered form and must be metabolized in the liver to an active form so as to be effective.

Captopril and lisinopril can be used if a patient has liver dysfunction, unlike other ACE inhibitors that are prodrugs.

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35
Q

Prodrugs

A

inactive in their administered form and must be metabolized in the liver to an active form so as to be effective.

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36
Q

ACE Inhibitors: Mechanism of Action

A

Inhibit ACE

ACE: converts angiotensin I (formed through the action of renin) to angiotensin II

Angiotensin II: potent vasoconstrictor that induces aldosterone secretion by the adrenal glands

Aldosterone: stimulates sodium and water resorption, which can raise BP

Renin–angiotensin–aldosterone system

ACE Inhibitors thus lower BP.

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37
Q

ACE Inhibitors: Primary Effects on BP

A

Cardiovascular and renal

BP: reduce BP by decreasing SVR

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38
Q

ACE Inhibitors: Primary Effects on HF
How does it help with HF?
Diuresis?
Decreases? (2)

A

Prevent sodium and water resorption by inhibiting aldosterone secretion

Diuresis: decreases blood volume and return to the heart

Decreases preload, or the left ventricular end-diastolic volume [Preload: amount the ventricles stretch at the end of diastole/ filling of blood phase] [balloon fillng with air; how much it stretches]

Decreases work required of the heart

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39
Q

ACE Inhibitors: Cardioprotective Effects

A

ACE inhibitors decrease SVR (a measure of afterload) and preload.

Used to prevent complications after MI

Ventricular remodeling: left ventricular hypertrophy, which is sometimes seen after MI

Have been shown to decrease morbidity and mortality in patients with HF

Drugs of choice for hypertensive patients with HF

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40
Q

ACE Inhibitors: Renal Protective Effects

A

Reduce glomerular filtration pressure

Cardiovascular drugs of choice for patients with diabetes

Reduce proteinuria

Standard therapy for diabetic patients to prevent the progression of diabetic nephropathy

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41
Q

ACE Inhibitors: Adverse Effects

A

Fatigue, dizziness, headache, impaired taste
Mood changes
First-dose hypotensive effect
Possible hyperkalemia
Dry, nonproductive cough, which reverses when therapy is stopped
Angioedema: rare but potentially fatal
Others

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42
Q

captopril (Capoten)

  1. Uses.
  2. Half-life
  3. Adminstered
A

Uses: prevention of ventricular remodeling after MI; reduces the risk of HF after MI

Shortest half-life

Must be administered 3 or 4 times throughout the day

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43
Q

enalapril (Vasotec)

  1. Routes
  2. what does not require cardiac monitoring?
  3. What is considered a Prodrug?
  4. Improves?
  5. Reduces?
A

Only ACE inhibitor available in both oral and parenteral preparations

enalapril at intravenous (IV) does not require cardiac monitoring

Oral enalapril sodium: prodrug
Improves patient’s chances of survival after an MI

Reduces the incidence of HF

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44
Q

Angiotensin II Receptor Blockers

  1. Also referred to as?
  2. Effects?
A

Also referred to as angiotensin II blockers

Well tolerated

Do not cause a dry cough

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45
Q

Angiotensin II Receptor Blockers
Medications

A

losartan (Cozaar®)

telmisartan (Micardis®)

Other:
eprosartan mesylate (Teveten®)
valsartan (Diovan®)
candesartan cilexetil (Atacand®)
olmesartan (Benicar®)
azilsartan medoxomil potassium (Edarbi®)

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46
Q

Angiotensin II Receptor Blockers: Mechanism of Action

A

Affect primarily vascular smooth muscle and the adrenal gland

Selectively block the binding of angiotensin II to the type 1 angiotensin II receptors in these tissues

Block vasoconstriction and the secretion of aldosterone

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47
Q

Comparison of ACE Inhibitors and Angiotensin II Receptor Blockers

A

ACE inhibitors and angiotensin II receptor blockers (ARBs) appear to be equally effective for the treatment of hypertension.

Both are well tolerated.

ARBs do not cause cough.

There is evidence that ARBs are better tolerated and are associated with lower mortality after MI than are ACE inhibitors.

It is not yet clear whether ARBs are as effective as ACE inhibitors in treating HF (cardioprotective effects) or in protecting the kidneys (as in diabetes).

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48
Q

Angiotensin II Receptor Blockers: Indications

A

Hypertension

Adjunctive drugs for
the treatment of HF

May be used alone or with other drugs such as diuretics

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49
Q

Angiotensin II Receptor Blockers: Adverse Effects

A

Upper respiratory infections and headaches most common
Dizziness, inability to sleep
Diarrhea
Dyspnea, heartburn
Nasal congestion
Back pain
Fatigue
Hyperkalemia is less likely to occur than with the ACE inhibitors.

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50
Q

losartan (Cozaar)

Beneficial for pts with?
Used in caution in pts?
Not taken by?

A

Beneficial in patients with hypertension and HF

Used with caution in patients with renal or hepatic dysfunction and in patients with renal artery stenosis

Not to be taken by breastfeeding women

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51
Q

Calcium Channel Blockers

  1. Indication
  2. Mechanism of action
A

Primary use: treatment of hypertension and angina

Hypertension: cause smooth muscle relaxation by blocking the binding of calcium to its receptors, thereby preventing contraction

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52
Q

Calcium Channel Blockers:Mechanism of Action results in?

A

Results in:

Decreased peripheral smooth muscle tone

Decreased SVR

Decreased BP

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53
Q

Calcium Channel Blockers: Indications

A

Angina
Hypertension: amlodipine (Norvasc®)
Antidysrhythmias
Migraine headaches
Raynaud’s disease
Cerebral artery spasms after subarachnoid hemorrhage (prevention): nimodipine

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54
Q

amlodipine (Norvasc®) indication

A

Hypertension: amlodipine (Norvasc®)

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55
Q

Diuretics Indication

A

First-line antihypertensives in the Canadian Hypertension Education Program guidelines for the treatment of hypertension

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56
Q

Diuretics mechanism of action

A

Decrease plasma and extracellular fluid volumes

Results
1. Decreased preload
2. Decreased cardiac output
3. Decreased total peripheral resistance

Overall effect
Decreased workload of the heart and decreased BP

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57
Q

What are the most commonly used diuretics for hypertension.

A

Thiazide diuretics (e.g. hydrochlorthiazide)

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58
Q

Vasodilators drugs

A

sodium nitroprusside (Nipride®)

Others:
diazoxide (Proglycem®)
hydralazine (Apresoline®)
minoxidil (Loniten®)

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59
Q

Vasodilators:Mechanism of Action

A

Directly relax arteriolar or venous smooth muscle (or both)

Used for their ability to cause peripheral vasodilation

Results in decreased SVR

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60
Q

Vasodilators: Indications

A

Treatment of hypertension

May be used in combination with other drugs

Sodium nitroprusside and IV diazoxide are reserved for the management of hypertensive emergencies.

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61
Q

Vasodilators: Adverse Effects [hydralazine]

A

dizziness, headache, anxiety, tachycardia, edema, dyspnea, nausea, vomiting, diarrhea, hepatitis, systemic lupus erythematosus, vitamin B6 deficiency, and rash

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62
Q

Vasodilators: Adverse Effects [minoxidil]

A

T-wave electrocardiographic changes, pericardial effusion or tamponade, angina, breast tenderness, rash, and thrombocytopenia

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63
Q

Vasodilators: Adverse Effects [sodium nitroprusside]

A

bradycardia, decreased platelet aggregation, rash, hypothyroidism, hypotension, methemoglobinemia, and (rarely) cyanide toxicity

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64
Q

Vasodilators: hydralazine (Apresoline®)

Routes and usage

A

Orally: routine cases of essential hypertension

Injectable: hypertensive emergencies

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65
Q

Vasodilators: sodium nitroprusside (Nitropress®)

  1. Indication
  2. Contraindication
A

Used in the critical care setting for severe hypertensive emergencies; titrated to effect by IV infusion

Contraindications: known hypersensitivity to the drug, severe HF, and known inadequate cerebral perfusion (especially during neurosurgical procedures)

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66
Q

Treatment of Hypertension
eplerenone (Inspra)
Class
Contraindication

A

New class: selective aldosterone blockers

Blocks action of aldosterone in kidney, heart, blood vessels, and brain

Contraindicated in patients with known drug allergy, elevated potassium (>5.5 mmol/L), or severe kidney impairment

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67
Q

Treatment of Pulmonary Hypertension

A

bosentan (Tracleer®)

Other drugs used to treat pulmonary hypertension:

epoprostenol
treprostinil
ambrisentan
sildenafil and tadalafil

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68
Q

bosentan (Tracleer®)

A

Treatment of Pulmonary Hypertension

Specifically indicated only for the treatment of pulmonary artery hypertension in patients with moderate to severe HF

Action: blocks receptors of the hormone endothelin

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69
Q

What to assess prior administration?

General rule?

A

Monitor BP and HR prior to administration of antihypertensives (client and patient).

Need specific parameters. General rule: If apical HR <60 or SBP < 90 contact their HCP; medication will be held if BP and/or HR parameters are lower than above

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70
Q

Monitor lab values

A

(K+, possibly other electrolytes such as Na+ and Cl-, blood glucose, kidney function, liver function)

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71
Q

Nursing Implications

A

Before beginning therapy, obtain a thorough health history and perform a head-to-toe physical examination.

Assess for contraindications to specific antihypertensive drugs.

Assess for conditions that require cautious use of these drugs.

Educate patients about the importance of not missing a dose and taking the medications exactly as prescribed.

Instruct patients to check with their health care provider for instructions on what to do if a dose is missed; patients should never double up on doses if a dose is missed.

Monitor BP during therapy; instruct patients to keep a journal of regular BP checks

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72
Q

Nursing Implications

A

Instruct patients that these drugs should not be stopped abruptly, because this may cause a rebound hypertensive crisis and perhaps lead to stroke.

Oral forms should be given with meals so that absorption is more gradual and effective.

Administer IV forms with extreme caution

Must use an IV pump.

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73
Q

Nursing Implications

A

Remind patients that medication is only part of therapy.

Encourage patients to watch their diet, stress level, weight, and alcohol intake.

Instruct patients to avoid smoking and to avoid eating foods high in sodium.
Encourage supervised exercise.

Teach patients to change positions slowly to avoid syncope from postural hypotension.

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74
Q

Nursing Implications

A

Male patients who take these drugs may not be aware that impotence is an expected effect, and this may influence compliance with drug therapy.

If patients are experiencing serious adverse effects or if they believe the dose or medication needs to be changed, they should contact their health care provider immediately.

Monitor for adverse effects (dizziness, orthostatic hypotension, fatigue) and for toxic effects.

Monitor for therapeutic effects

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75
Q

Nursing Implications

A

Hot tubs, showers, or baths; hot weather; prolonged sitting or standing; physical exercise; and alcohol ingestion may aggravate low BP, leading to fainting and injury. Patients should sit or lie down until symptoms subside.

Patients should not take any other medications, including over-the-counter drugs, without first getting the approval of their health care provider

Educate patients about lifestyle changes that may be needed.
-Weight loss
-Stress management
-Supervised exercise
-Dietary measures

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76
Q

ACE Inhibitors can cause? (2) and Laboratory Values to identify and monitor?

A

ACE inhibitors can cause renal impairment, which can be identified by serum creatinine.

ACE inhibitors can also cause hyperkalemia, so potassium levels need to be monitored.

Monitor serum sodium during therapy.

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77
Q

An adrenergic drug for hypertension, the nurse must assess for?

(for every single HTN medication)

A

Hypotension

78
Q

Are not prodrugs don’t need to be activated in the liver so we can give them to those with live disease

or

drug to give to those with pancreatitis/ cirrhosis?

A

Captopril and lisinopril

79
Q

HTM medications given for pregnant women

A

labetalol

80
Q

Has protective effects on the kidneys for pts with diabetes

A

ACE Inhibitors

81
Q

Ventricular hypertrophy

A

thickening of wall of ventricular walls-poor pumping

82
Q

ARBs

Angiotensin II Receptor Blockers
1. Suffix
2. Do not cause
3. Common adverse effects?

A

Sartan

Cough

chest pain

83
Q

Alpha acting HTN medications increases risk for?

A

Orthostatic hypotension and syncope

84
Q

Drop in BP/ fluid volume stimulates?

Renin acts on

ACE is released by?

ACE acts on angiotensin I to from?

Angiotensin II effects (2)

A

release of renin from kidneys

Renin acts on angiotensinogen to form angiotensin I

Lungs

angiotensin II

acts directly on BVs stimulating vasoconstriction

acts on adrenal glands to stimulate the release of aldosterone> aldosterone acts on kidneys to stimulate the reabsorption of salt (NACL) and water.

85
Q

Drug that causes less impotence?

A

nebivolol hydrochloride (Bystolic®)

86
Q

Prodrugs

A

must be metabolized in the liver to an active form so as to be effective

87
Q

ACE inhibitors suffix

examples

A

PRIL

captopril (Capoten®)
enalapril (Vasotec®)

88
Q

Nitroprusside is classified as

Results

A

Vasodilator- peripheral vasodilation

89
Q

Doxazocin

A

α1-Blockers

90
Q

2 drugs that are not prodrugs?

A

Captopril and lisinopril are not prodrugs.

91
Q

AE of antihypertensives to an adult pt

A

hypotension

92
Q

type of antihypertensive the nirse fill consider when giving 1st dose at bedtime

A

alpha blockers (prasozin)

93
Q

ACE Inhibitor AE

ACE Inhibitor caution

A

dry, non-productive cough

renal insufficiency

94
Q

Interaction of ACE I

A

potassium

NSAIDS

95
Q

alpha 1 blockers

A

drugs that primarily cause arterial and venous dilation on peripheral sympathetic neurons

96
Q

Cardiac output

SVR (systemic vascular resistance) or afterload

A

amount of blood ejected from the L ventricle, L per min

is the resistance to blood flow that is determined by the diameter of the BVs and the vascular musculature, calculated by dividing BP to CO

97
Q

centrally acting adrenergic drugs

function of alpha 2 receptors

A

drugs that modify function of sympathetic NS in the BRAIN by stimulating alpha 2 receptors

alpha 2 receptors are inhibitory and revrses sympathetic effect and decreases BP

98
Q

HTN values

A

exceeds 140/90

prevalence of HTN is highest in Africa and in low and middle-income nations

Canadians who are Black, Indigenous, South Asian, and those with low socioeconomic status are at greater risk

Major risk factors for CAD, cardiovascular disease, and death. Important RF for Stroke and HF, kidney failure, and peripheral vascular disease (the higher the BP, the higher the chance)

for 40 to 70 YO, the risk of developing cardiovascular diseases doubles with each 20 mmHG increase in systolic BP or 10 mm Hg increase in diastolic BP

99
Q

malignant HTN

A

extremely high BP, above 180/120

medical emergency- develops rapidly and results in organ damage

100
Q

orthostatic hypotension

A

AE of adrenergic blocking drugs involving a sudden drop in BP when pts change position

101
Q

prodrug

A

a drug that is inactive in its given form

must be metabolized by the liver to its active form to be effective

102
Q

essential HTN

secondary HTN

A

unknown cause of HTN (90-95% of cases)

high bp caused by another disease or medication (5 to 10%). If cause of this is eliminated, BP can return to normal

103
Q

BP

mean arterial pressure

A

Bp is determined by the product of CO [4-8 L/min] and systemic vascular resistance (SVR)

MAP is a product of CO and SVR
Calculated as 1/3 (SBP- DBP) + DBP
MAP is a better indicator of tissue perfusion as 2/3 of the cardiac cycle is spent in diastole

greater or equal to 60 is necessary to maintain adequate tissue perfusion

104
Q

Cardiac factors:

HR
Contractility

A

B-blockers

Calcium channel blockers

Centrally acting adrenergics

105
Q

Circulating volume:

Salt
Aldosterone

A

ACE I

Diuretics

106
Q

Hormones

Vasodilators
Vasoconstrictors

A

Vasodilators

Prostaglandin

ACE I

Calcium channel blockers

ANGIOTENSIN II blockers

107
Q

Peripheral sympathetic receptors

constrictors

dilators

A

a1 blockers and b blockers

108
Q

CNS

Local

A

centrally acting adrenergic

peripherally acting adrenergic

109
Q

Nurses key roles

A

primary prevention
detection
treatment of HTN

130-139 over 85 to 89 mm Hg = high risk of developing HTN

110
Q

Antihypertensive goals

A

reduce cardiovascular and renal mortality and morbidity

individualized (sexual dysfunction caused by non-adherence from males), demographic, ethnocultural, cost and ease of medication administration needs to be considered as well.

GOAL:

BP less than 140/90 -non-automated office BP machine
BP less than 135/85 -automatic office BP machine

In PTS with HTN/ diabetes

The goal is BP less than 130/ 80 and 140/90 respectively

111
Q

Vasodilators

A

act directly on vascular SM cells, not through a or b receptors

112
Q

ACh

A

somatic NS- acts on skeletal muscles

parasympathetic- acts on the heart, intestines

113
Q

NE

A

sympathetic- acts on the heart, adrenal gland

114
Q

Receptors of sympathetic NS

A

adrenergic and noradrenergic R (alpha or beta receptors)

115
Q

Receptors of parasympathetic NS

A

located between the postganglionic fibre and the effector cells are called MUSCARINIC and CHOLLINERGIC receptors

116
Q

physiological activity in the muscarinic receptors are stimulated by?

inhibited by?

A

ACh and cholinergic agonist drugs

cholinergic antagonists (antichollinergic drugs)

117
Q

physiological activity at the adrenergic R is stimulated by?

A

Epi, NE, and adrenergic agonists drugs (adrenergic/ beta blockers)

118
Q

Nicotinic R are found on

A

postganglionic cell bodies in all autonomic ganglia and cause depolarization by opening both sodium and potassium channels

119
Q

Diuretics

A

first line, monotherapy/ combination

therapeutic effects: decreased volume of plasma and ECF which results in decreased preload. Leads to decreased CO & total peripheral resistance, which decreases the workload of the heart

thiazide diurects- common in HTN treatment

120
Q

1st line treatment of adults

A

health behaviour management

thiazide, Ace-I, ARB, long-acting CCB, beta-blockers, single-pill combination

B-blockers are not indicated as 1st line for ages 60 and above

long-acting diuretics are preferred over short-acting ones like hydrochlorothiazide

SPC- ACE-I & CCB, ARB & CCB, ACE-1 OR ARB WITH A DIURETIC

RAS- contraindicated in pregnancy and caution in childbearing years

121
Q

adrenergic drugs

A

central action (brain)

Peripheral action (heart/ BVs)

5 types

adrenergic neuron blocker (central & peripheral)

alpha 2 receptor agonists (central)

alpha 1 receptor blockers (peripheral)

beta receptor blockers (peripheral)

combination alpha 1 and beta receptor blockers (peripheral)

122
Q

centrally acting alpha 2 receptor agonists

function of SNS and result

A

clonidine & methyldopa- modify the function of SNS.

the function of SNS: leads to an increased heart rate and force of contraction, the constriction of BVs, and the release of renin from the kidneys- result is HTN

123
Q

centrally acting adrenergic drugs

alpha 2 adrenergic receptors

renin

A

act by stimulating the alpha 2 adrenergic receptors in the brain

receptor stimulation reduces sympathetic outflow from the CNS. this reduction results in a lack of NE production which reduces BP. Also reduces the activity of renin; the hormone and enzyme that converts the protein precursor of angiotensinogen to the protein angiotensin I, the precursor of angiotensin II, a potent vasoconstrictor that raises BP

124
Q

alpha 1 blockers location of action

A

in the periphery

doxazosin, prazosin, and terazosin- also modify the function of SNS

BY:

blocking the alpha 1 adrenergic receptors

when alpha 1 adrenergic receptors are stimulated by NE, they increase BP. When these receptors are blocked, BP is decreased.

Drug effects of alpha 1 blockers - dilate arteries and veins which reduces peripheral vascular resistance and decreases BP

reduces systemic and pulmonary venous pressures and increases CO.

they also increase urinary flow rates and decrease outflow obstruction by preventing smooth muscle contractions in the bladder and urethra. Beneficial in BPH

125
Q

beta blockers

A

periphery

propanolol, metoprololand atenolol

for angina and conduction problems

effects: reduction of the HR through beta 1 receptor blockade. Also causes a reduction in the secretion of the hormone renin which reduces both angiotensin II-mediated vasoconstriction and aldosterone-mediated volume expansion

Long term use of beta blockers reduces peripheral vascular resitance

126
Q

Dual action of alpha and beta receptor blocker

A

labetalol

periphery

dual antihypertensive effects- reduces HR (beta 1 receptor blockade) and vasodilation (alpha 1 receptor blockade)

127
Q

Indications of adrenergic drugs

A

HTN

Glaucoma

Clonidine- menopausal flushing

prophylaxis of migraine

symptoms of withdrawal symptoms

alpha 1 blockers- prazosin: helps with symptoms of BPH. Used in severe HF when taken with cardiac glycosides and diuretics

128
Q

Contraindications of adrenergic drugs

A

adrenergic antihypertensive drugs- known allergy

may HF, concurrent MAOIs, severe depression, peptic ulcers severe liver/ kidney disease

Asthma- nonselective beta-blockers

vasodilating drugs- contraindicated in HF

129
Q

AEs of adrenergic drugs

A

bradycardia with reflex tachycardia

orthostatic hypotension

dry mouth, drowsiness, dizziness, depression, edema, constipation, sexual dysfunction

headache, sleep disturbances, nausea, rash, and palpitations

alpha blockers- orthostatic hypotension, syncope (move slowly)

130
Q

abrupt discontinuation of centrally acting alpha 2 receptor agonists can result in

A

rebound HTN

(may be true for other antihypertensive as well)

nonselective blocking drugs: associated with bronchoconstriction and metabolic inhibition of glycogenolysis in the liver which can lead to hypoglycemia. Hyperglycemia can occur as adrenergic drugs can impair insulin release.

change in the dosing regimen should be undertaken gradually and with appropriate patient monitoring and follow-up.

131
Q

Adrenergic drugs interactions

A

alcohol, benzodiazepines, and opioids- additive CNS depression

clonidine- MAOIs, appetite suppressants, amphetamines (decreased hypotensive effects)

diuretics, other hypertensive drugs (increased hypotensive effects)

B-blockers (potentiate bradycardia and increase rebound HTN)

doxazosin-
CNS depressants, alcohol (increase CNS depression
b-blockers, hypotensive drugs (increased hypotension)

132
Q

Alpha 2 adrenergic receptor stimulators (agonists)

A

clonidine- commonly used

methyldopa- used in pregnancy mostly

high incidence of orthostatic hypotension, fatigue, and dizziness (not 1st line)

133
Q

clonidine

A

alpha 2 adrenergic receptor agonists

centrally actinhg

decrease BP and opioid withdrawal

do not D/C abruptly as it can lead to severe rebound HTN

134
Q

Alpha 1 blocker

A

doxazosin, prazosin, tamsulosin (for BPH)

not for pregnancy

135
Q

doxazosin

A

alpha 1 blocker

peripherally acting

reduces peripheral vascular resistance and BP bu dilating arteries and veins

HTN and BPH

136
Q

Dual action alpha 1 and beta receptor blockers drug

A

beta receptor blocker- nebivolol

137
Q

nebivolol

A

beta 1 selective blocker

HTN

decreases SVR

reduces sexual dysfunction

do not stop abruptly, tapered over 1-2 weeks

138
Q

ACE I

A

safe and efficacious- one of the 1st line for HTN and HF, diabetes for kidney protection

catopril

139
Q

captopril

A

short half-life- dosed more frequently than other ACE I

140
Q

ACE I that are not prodrug?

A

captopril and lisonopril

an advantage for people with liver dysfunction

141
Q

Enalapril

A

ACE I available parenterally

142
Q

ACE inhibitors may cause

A

significant fetal morbidity or mortality during 2nd and 3rd trimester (do not use in pregnancy)

143
Q

ACE Inhibitor action and explain hormones involved

A

Kininase- an enzyme that normally breaks down bradykinin, a potent vasodilator

inhibit ACE enzymes which are responsible for converting angiotensin I (formed from the action of renin) to angiotensin II

angitensin II- potent vasocontrictor and induces aldoesterone secretion

Aldosterone stimulates NA and water resorption- which can raise BP

together they are referred to as the renin-angiotensin-aldosterone system > inhibiting this process BP is lowered

144
Q

Primary effects of ACE I

A

cardiovascular and renal

cardio > ability to reduce BP by decreasing SVR. By preventing the breakdown of the vasodilating substance bradykinin and substance P (another potent vasodilator), thus preventing the formation of angiotensin II

this decreases the afterload- the resistance against which the left ventricle must pump to eject its volume of blood during contraction

Effective in the treatment of HF because they prevent sodium and water resorption by inhibiting aldosterone secretion. This causes diuresis, which decreases blood volume and return to the heart, This in turn decreases preload- the left ventricular end-diastolic volume and the work required of the heart

145
Q

ACE I- indicator

Contraindications

AE

A

HTN, HF

decrease preload and afterload

stop the progression of left ventricular hypertrophy- MI (ventricular remodelling). The ability of ACE-I to stop this is called (cardioprotective effects)

protects kidney- decreases GF pressure- a choice for diabetes- reduces proteinuria and diabetic neuropathy

Contraindications

-allergy, angioedema,

-baseline potassium level of 5 mmol/L because this medication can cause HYPERKALEMIA

-kidney decline

-women who are lactating, children, bilateral renal artery stenosis

AEs
fatigue, mood changes, headache, dizziness

DRY NON-PRODUCTIVE COUGH- reversible with discontinuation of therapy (switched to an ARB

Hyperkalemia, hypotension

loss of state, rash, anemia, neutropenia, thrombocytosis, agrunocytosis

acute kidney failure

serum potassium levels must be monitored carefully

146
Q

ACE I overdose symptoms

A

hypotension

treatment is symptomatic and supportive- give IV fluids to expand BV

hemodialysis is effective for the removal of captopril and lisonopril

147
Q

ACE I interacttions

A

NSAIDS- reduces antihypertensive effect, may also predispose pts to acute kidney injury

lithium carbonate- lithium toxicity

potassium- hyperkalemia

148
Q

captopril (ACE I)

A

minimize and prevent left ventricular dilation and dysfunction (ventricular remodelling) that can occur in the acute period after an MI

reduce the risk of HF

short half-life - given 3-4 times a day

149
Q

enalapril sodium (ACE I)

A

oral and parenteral (only one)

IV-does not require cardia monitoring unlike beta blockers and CCBs do.

slightly longer half life- given BID

prodrug, pt must have a functioning liver for drug to be converted into an active form

improve chances of survival after MI to reduce HF

150
Q

Angiotensin II receptor blockers (ARBs)

Medications

Action

Indication

A

similar to ACE I

losartan, valsartan, eprosartan, irbesartan, candesartan, telmisartan, azilsartan

block the binding of angiotensin II to type 1 angiotensin II receptors.

type 1 receptor- mediate effects of important effectors in controlling BP and volume in the cardiovascular system,

type 1 R are activated by angiotensin II with resulting effects that include vasoconstriction and aldosterone synthesis and secretion

ACE I such as enalapril- blocks the conversion of angiotensin I to angiotensin II, but angiotensin II may be formed by other enzymes that are not blocked by ACE I

*in contrast to ACE I- ARBs primarily affect vascular smooth muscle and the adrenal gland. By selectively blocking the binding of angiotensin II to the type 1 angiotensin II receptors in these tissues. ARBs block vasoconstriction and the secretion of aldosterone. Angiotensin II receptors have been found in other tissues throughout the body, but the effects of ARB blocking the R are unknown.

Aldosterone stimulates NA and water resorption- which can raise BP

ARBs do not cause cough!

lower mortality after an MI than ACE Is

Indication> potent vasodilating properties

HF, HTN

decrease SVR (a measure of afterload)

151
Q

ARBs contraindications

Interaction

A

allergy, pregnancy, lactation

caution in OAs and pts with kidney dysfunction because of increased sensitivity to their effects and risk of AEs

Assess BP and apical impulse (like other drugs)

interaction- can promote hyperkalemia (esp. when taking with potassium drugs)

152
Q

ARBs AEs

A

upper respiratory infections, and headache

dizziness, inability to sleep, diarrhea, dyspnea, heartburn, nasal congestion, back pain, and fatigue

Rarely, anxiety, muscle pain, sinusitis, cough, and insomnia

Hyperkalemia is less likely to occur with ARBs than with ACE I

153
Q

ARBs toxicity and overdose

A

hypotension and tachycardia

bradycardia occurs less often

treatment is symptomatic and supportive -IV fluids to expand BV

154
Q

losartan potassium

A

HTN, HF

used in caution in pts with kidney/ liver dysfunction, renal artery stenosis

not for breastfeeding women- AE on the infant

155
Q

CCBs

A

HTN, angina (antihypertensive, antidysrhythmic)

treat HTN by their ability to cause smooth muscle relaxation by blocking the binding of calcium to its receptors

first line

amlodipine

nimodipine- prevents cerebral artery spasms that occur after a subarachnoid hemorrhage

used to treat Raynaud’s disease and migraine

156
Q

Vasodilator

medication

action

indication

contraindication

AE

A

act directly on arterial and venous smooth muscle to cause relaxation. DO NOT WORK through adrenergic receptors

minoxidil, hydralazine, diazoxide, sodium nitroprusside

direct-acting vasodilators- ability to cause peripheral vasodilation. This reduces SVR.

Most nitable effets- hypotensive effect

MINOXIDIL- HAIR GROWTH

indication- HTN emergencies in which BP is severely elevated

contra- allergy, hypotension, CAD, HF secondary ti diastolic dysfunction

AE- dizziness, headache, anxiety, N & V, diarrhea, hepatitis, lupus

Minoxidil AE- T wave ECG changes, pericardial effusion, angina, breast tenderness, rash, thrombocytopenia

sodium nitroprusside AE: bradycardia, decreased platelet aggregation, rash, hypothyroidism, hypotension, methemoglobinemia, cyanide toxicity (byproduct of nitroprusside)

157
Q

minoxidil, hydralazine, diazoxide (VASODILATOR)

A

work primarily through arteriolar vasodilation

158
Q

sodium nitroprusside (VASODILATOR)

A

arteriolar and venous effects

given in intensive care, IV (for severe HTN emergencies)- overdose; d/c infusion

contains cyanide- released upon its metabolism- can cause cyanide toxicity

antidote-sodium nitrite and sodium thiosulfate for injection and amyl nitrite for inhalation

contra- allergy, severe HF, inadequate cerebral perfusion

159
Q

Vasodilator toxicity or overdose

A

produces hypotension, tachycardia, skin flushing

treatment-supportive and symptomatic- administer IV fluids, digitalization if needed, and the administration of beta blockers for the control of tachycardia

epinephrine should not be used because of excessive cardia stimulation

160
Q

Vasodilator contraindications

A

other antihypertensive drugs

161
Q

hydralazine hcl

A

essential HTN

less common now

has an injection form

may not require cardiac monitoring

contra- drug allergy, CAD, mitral valve dysfunction

direct acting peripheral vasodilator

162
Q

Direct renin inhibitors

A

most recent

treat primary HTN

sole drug- aliskiren

163
Q

aliskiren

A

mild to moderate HTN

monotherapy/ combination

action- it binds directly to the renin enzyme and blocks the conversion of angiotensinogen to angiotensin I and angiotensin II. This action results in the reduction of plasma renin activity and angiotensin I, angiotensin II, and aldosterone.

AES: HEADACHE, DIZZINESS, FATIGUE

164
Q

eplerenone

A

selective aldosterone blockers.

reduces BP by blocking actions of aldosterone at its R in kidneys, heart, BVs, and brain.

not for those with elevated serum potassium levels (higher than 5.5) or severe kidney impairment

HTN, postmyocardial infarction

165
Q

bosentan monohydrate

hormone related?

A

works by blocking receptors of the hormone endothelin- which acts to stimulate the narrowing of BVs by binding endothelin Rs in the endothelial (innermost) lining of BVs and in vascular smooth muscle

pulmonary artery HTN

Ambrisentain is similar to bosentan

Pulmonary HTN- epoprostenol and treprostinil

166
Q

trepostinil

A

pulmonary artery HTN

analogue of prostacyclin, a metabolite of arachidonic acid, a naturally occurring prostaglandin that lowers BP; by dilating pulmonary and systemic BVs and by inhibiting platelet aggregation

167
Q

prehypertension

A

systolic- 120 to 129

diastolic- 80 to 89

168
Q

lab test

A

serum sodium, potassium, chloride, magnesium, calcium

serum levels of troponin (elevated after an MI, a reliable indicator of a heart attack)

kidney function studies- including blood urea test, creatinine

liver function studies, ALT, AST

scans and imaging studies- noninvasive ophthalmoscopic exam of the eye structures

assess for conditions- CAD, Addison’s disease, culture, race, ethnicity, obesity, preeclampsia…

169
Q

alpha-adrenergic agonists

A

assess BP, HR, weight

fluid retention and edema- assess heart and breath sounds, intake and output, dependent edema

associated with first dose syncope - encourage pt to lay supine on 1st dose/ give at hs

170
Q

alpha adrenergic antagonists

A

dizziness and syncope

171
Q

centrally acting alpha blockers

A

WBCs

serum potassium

sodium levels

protein in urine

172
Q

nonselective b blockers

A

block both b1 and b2 receptors and will have both heart and respiratory effects

may cause exacerbation of respiratory diseases because of increased bronchoconstriction due to beta 2 blocking) or exacerbation of HF (negative inotropic effects- decreased contractility due to beta 1 blocking)

173
Q

beta 1 blockers

A

cardiac system is affected (pulse and BP will decrease)

assess BP and apical pulse rate before each dose

If systolic BP is less than 90 mm HG or pulse is less than 60 betas/ min (notify DR)

174
Q

if a pt needs b blocker but has rstrictive airway problems

A

beta 1 blocker to avoid bronchoconstriction

175
Q

if no respiratory illness

A

non-selective beta-blockers may be effective

176
Q

beta blockers have inotropic effect

A

on the heart (decrease contractility) may worsen HF

177
Q

ACE Inhibitors (-pril)

A

BP, apical pulse rate, respiratory status (because of the adverse effect of a dry hacking cough)

report angioedema immediately- wean off to avoid rebound HTN

Monitor sodium and potassium levels

potassium increases as an adverse effect

loss of taste

may take weeks to see the full effects

potassium supplements are not needed

178
Q

-pine

A

CCBs

cause smooth muscle relaxation by blocking the binding of calcium to its receptors

179
Q

ARBs

A

caution in OAs and kidney dysfunction

tolerated with meals

reduce dosage if pt has hypovolemia/ liver dysfunction

report dyspnea, dizziness, excessive fatigue

180
Q

Vasodilator

A

baseline neurological assessment, LOC, cognitive ability

hypotension, dizziness, syncope

never give drug without adequate monitoring

always dilute nitroprusside; never infuse at the max dose for more than 10 minutes; may cause cyanide and thiocyanate toxicity; when combined with sodium thiosulfate, toxicity is reduced
-dilute the drug
-avoid use of infusion that has turned blue, green, red
-use volume infusion pump, IV
-monitor BP
-beware of cyanide production

181
Q

BP goals

A

120- 139 mm Hg - systolic

80- 89 mm Hg - diastolic

those with diabetes- less than 130/80

182
Q

diuretics

A

dizziness and electrolyte imbalances

183
Q

centrally acting alpha blockers

A

AEs are more pronounced; hypotension, sedation, bradycardia, edema

184
Q

CCBs

A

negative inotropic (decreases cardiac contractility)

185
Q

digoxin

A

increase heart contractility

186
Q

decreased chronotropic effects

decreased dromotropic effects

A

decreased HR

decreased conduction

187
Q

eye exam

A

HTN impacts vasculature of the eyes-reliable indicator of the long term effectiveness of treatment than BP readings

188
Q

alpha adrenergic agonist

A

first dose syncope- avoid situations that exacerbate this

avoid activities that require mental alertness

report dizziness, palpitations, and orthostatic hypotension

assess sexual functioning

189
Q

Beta blocker

A

change position slowly to avoid syncope, dizziness, and falls

report pulse rate of less than 60/ systolic less than 90 mm Hg

avoid heat, prolonged sitting, standing, exercise

190
Q

ACE I

-pril

A

prevent vasoconstriction caused by angiotensin II

prevent aldosterone which stops sodium and water resorption

prevent breakdown of bradykinin (a potent vasodilator) by angiotensin II

191
Q

ARBs

-sartan

A

work by blocking the binding of angiotensin at the receptors; which decreases BP

192
Q

CCBs

-dipine (amlodipine)

A

may be used to treat angina, dysrhythmias, and HTN

help reduce BP by relaxing smooth muscles and dilating BVs.

if calcium is not present, the smooth muscle cannot contract

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