Antihypertensive Flashcards

(192 cards)

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
α1-Blockers doxazosin mesylate (Cardura®) prazosin hydrochloride (Minipress®) tamsulosin hydrochloride (Flomax®)* terazosin hydrochloride (Hytrin®)
*Tamsulosin is not used to control BP but is indicated solely for symptomatic control of BPH.
26
α1-Blockers doxazosin mesylate (Cardura®) How does it reduces PVR and BP?
Commonly used α1-blocker Reduces peripheral vascular resistance and BP by dilating both arterial and venous blood vessels
27
Β-Receptor Blocker medication
nebivolol hydrochloride (Bystolic®)
28
Β-Receptor Blocker nebivolol hydrochloride (Bystolic®) Mechanism of action
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.
29
Angiotensin-Converting Enzyme (ACE) Inhibitors Large group of? Often use? May be combined with a? or 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.
30
TO KNOW medications: ACE Inhibitors Ends in suffix?
"Pril" captopril (Capoten®) enalapril (Vasotec®) perindopril (Coversyl®) ramipril (Altace®)
31
Other ACE Inhibitors
benazepril (Lotensin®) fosinopril sodium lisinopril (Prinivil®) cilazapril (Inhibace®) quinapril (Accupril®) trandolapril (Mavik®)
32
ACE Inhibitors: Explain mechanism of Action 2 functions of angiotensin II
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]
33
ACE Inhibitors: Indications
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
34
ACE Inhibitors: Captopril and Lisinopril
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.
35
Prodrugs
inactive in their administered form and must be metabolized in the liver to an active form so as to be effective.
36
ACE Inhibitors: Mechanism of Action
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.
37
ACE Inhibitors: Primary Effects on BP
Cardiovascular and renal BP: reduce BP by decreasing SVR
38
ACE Inhibitors: Primary Effects on HF How does it help with HF? Diuresis? Decreases? (2)
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
39
ACE Inhibitors: Cardioprotective Effects
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
40
ACE Inhibitors: Renal Protective Effects
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
41
ACE Inhibitors: Adverse Effects
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
42
captopril (Capoten) 1. Uses. 2. Half-life 3. Adminstered
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
43
enalapril (Vasotec) 1. Routes 2. what does not require cardiac monitoring? 3. What is considered a Prodrug? 4. Improves? 5. Reduces?
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
44
Angiotensin II Receptor Blockers 1. Also referred to as? 2. Effects?
Also referred to as angiotensin II blockers Well tolerated Do not cause a dry cough
45
Angiotensin II Receptor Blockers Medications
losartan (Cozaar®) telmisartan (Micardis®) Other: eprosartan mesylate (Teveten®) valsartan (Diovan®) candesartan cilexetil (Atacand®) olmesartan (Benicar®) azilsartan medoxomil potassium (Edarbi®)
46
Angiotensin II Receptor Blockers: Mechanism of Action
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
47
Comparison of ACE Inhibitors and Angiotensin II Receptor Blockers
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).
48
Angiotensin II Receptor Blockers: Indications
Hypertension Adjunctive drugs for the treatment of HF May be used alone or with other drugs such as diuretics
49
Angiotensin II Receptor Blockers: Adverse Effects
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.
50
losartan (Cozaar) Beneficial for pts with? Used in caution in pts? Not taken by?
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
51
Calcium Channel Blockers 1. Indication 2. Mechanism of action
Primary use: treatment of hypertension and angina Hypertension: cause smooth muscle relaxation by blocking the binding of calcium to its receptors, thereby preventing contraction
52
Calcium Channel Blockers: Mechanism of Action results in?
Results in: Decreased peripheral smooth muscle tone Decreased SVR Decreased BP
53
Calcium Channel Blockers: Indications
Angina Hypertension: amlodipine (Norvasc®) Antidysrhythmias Migraine headaches Raynaud’s disease Cerebral artery spasms after subarachnoid hemorrhage (prevention): nimodipine
54
amlodipine (Norvasc®) indication
Hypertension: amlodipine (Norvasc®)
55
Diuretics Indication
First-line antihypertensives in the Canadian Hypertension Education Program guidelines for the treatment of hypertension
56
Diuretics mechanism of action
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
57
What are the most commonly used diuretics for hypertension.
Thiazide diuretics (e.g. hydrochlorthiazide)
58
Vasodilators drugs
sodium nitroprusside (Nipride®) Others: diazoxide (Proglycem®) hydralazine (Apresoline®) minoxidil (Loniten®)
59
Vasodilators: Mechanism of Action
Directly relax arteriolar or venous smooth muscle (or both) Used for their ability to cause peripheral vasodilation Results in decreased SVR
60
Vasodilators: Indications
Treatment of hypertension May be used in combination with other drugs Sodium nitroprusside and IV diazoxide are reserved for the management of hypertensive emergencies.
61
Vasodilators: Adverse Effects [hydralazine]
dizziness, headache, anxiety, tachycardia, edema, dyspnea, nausea, vomiting, diarrhea, hepatitis, systemic lupus erythematosus, vitamin B6 deficiency, and rash
62
Vasodilators: Adverse Effects [minoxidil]
T-wave electrocardiographic changes, pericardial effusion or tamponade, angina, breast tenderness, rash, and thrombocytopenia
63
Vasodilators: Adverse Effects [sodium nitroprusside]
bradycardia, decreased platelet aggregation, rash, hypothyroidism, hypotension, methemoglobinemia, and (rarely) cyanide toxicity
64
Vasodilators: hydralazine (Apresoline®) Routes and usage
Orally: routine cases of essential hypertension Injectable: hypertensive emergencies
65
Vasodilators: sodium nitroprusside (Nitropress®) 1. Indication 2. Contraindication
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)
66
Treatment of Hypertension eplerenone (Inspra) Class Contraindication
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
67
Treatment of Pulmonary Hypertension
bosentan (Tracleer®) Other drugs used to treat pulmonary hypertension: epoprostenol treprostinil ambrisentan sildenafil and tadalafil
68
bosentan (Tracleer®)
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
69
What to assess prior administration? General rule?
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
70
Monitor lab values
(K+, possibly other electrolytes such as Na+ and Cl-, blood glucose, kidney function, liver function)
71
Nursing Implications
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
72
Nursing Implications
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.
73
Nursing Implications
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.
74
Nursing Implications
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
75
Nursing Implications
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
76
ACE Inhibitors can cause? (2) and Laboratory Values to identify and monitor?
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.
77
An adrenergic drug for hypertension, the nurse must assess for? (for every single HTN medication)
Hypotension
78
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?
Captopril and lisinopril
79
HTM medications given for pregnant women
labetalol
80
Has protective effects on the kidneys for pts with diabetes
ACE Inhibitors
81
Ventricular hypertrophy
thickening of wall of ventricular walls-poor pumping
82
ARBs Angiotensin II Receptor Blockers 1. Suffix 2. Do not cause 3. Common adverse effects?
Sartan Cough chest pain
83
Alpha acting HTN medications increases risk for?
Orthostatic hypotension and syncope
84
Drop in BP/ fluid volume stimulates? Renin acts on ACE is released by? ACE acts on angiotensin I to from? Angiotensin II effects (2)
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
Drug that causes less impotence?
nebivolol hydrochloride (Bystolic®)
86
Prodrugs
must be metabolized in the liver to an active form so as to be effective
87
ACE inhibitors suffix examples
PRIL captopril (Capoten®) enalapril (Vasotec®)
88
Nitroprusside is classified as Results
Vasodilator- peripheral vasodilation
89
Doxazocin
α1-Blockers
90
2 drugs that are not prodrugs?
Captopril and lisinopril are not prodrugs.
91
AE of antihypertensives to an adult pt
hypotension
92
type of antihypertensive the nirse fill consider when giving 1st dose at bedtime
alpha blockers (prasozin)
93
ACE Inhibitor AE ACE Inhibitor caution
dry, non-productive cough renal insufficiency
94
Interaction of ACE I
potassium NSAIDS
95
alpha 1 blockers
drugs that primarily cause arterial and venous dilation on peripheral sympathetic neurons
96
Cardiac output SVR (systemic vascular resistance) or afterload
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
centrally acting adrenergic drugs function of alpha 2 receptors
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
HTN values
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
malignant HTN
extremely high BP, above 180/120 medical emergency- develops rapidly and results in organ damage
100
orthostatic hypotension
AE of adrenergic blocking drugs involving a sudden drop in BP when pts change position
101
prodrug
a drug that is inactive in its given form must be metabolized by the liver to its active form to be effective
102
essential HTN secondary HTN
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
BP mean arterial pressure
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
Cardiac factors: HR Contractility
B-blockers Calcium channel blockers Centrally acting adrenergics
105
Circulating volume: Salt Aldosterone
ACE I Diuretics
106
Hormones Vasodilators Vasoconstrictors
Vasodilators Prostaglandin ACE I Calcium channel blockers ANGIOTENSIN II blockers
107
Peripheral sympathetic receptors constrictors dilators
a1 blockers and b blockers
108
CNS Local
centrally acting adrenergic peripherally acting adrenergic
109
Nurses key roles
primary prevention detection treatment of HTN 130-139 over 85 to 89 mm Hg = high risk of developing HTN
110
Antihypertensive goals
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
Vasodilators
act directly on vascular SM cells, not through a or b receptors
112
ACh
somatic NS- acts on skeletal muscles parasympathetic- acts on the heart, intestines
113
NE
sympathetic- acts on the heart, adrenal gland
114
Receptors of sympathetic NS
adrenergic and noradrenergic R (alpha or beta receptors)
115
Receptors of parasympathetic NS
located between the postganglionic fibre and the effector cells are called MUSCARINIC and CHOLLINERGIC receptors
116
physiological activity in the muscarinic receptors are stimulated by? inhibited by?
ACh and cholinergic agonist drugs cholinergic antagonists (antichollinergic drugs)
117
physiological activity at the adrenergic R is stimulated by?
Epi, NE, and adrenergic agonists drugs (adrenergic/ beta blockers)
118
Nicotinic R are found on
postganglionic cell bodies in all autonomic ganglia and cause depolarization by opening both sodium and potassium channels
119
Diuretics
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
1st line treatment of adults
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
adrenergic drugs
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
centrally acting alpha 2 receptor agonists function of SNS and result
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
centrally acting adrenergic drugs alpha 2 adrenergic receptors renin
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
alpha 1 blockers location of action
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
beta blockers
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
Dual action of alpha and beta receptor blocker
labetalol periphery dual antihypertensive effects- reduces HR (beta 1 receptor blockade) and vasodilation (alpha 1 receptor blockade)
127
Indications of adrenergic drugs
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
Contraindications of adrenergic drugs
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
AEs of adrenergic drugs
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
abrupt discontinuation of centrally acting alpha 2 receptor agonists can result in
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.
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Adrenergic drugs interactions
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)
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Alpha 2 adrenergic receptor stimulators (agonists)
clonidine- commonly used methyldopa- used in pregnancy mostly high incidence of orthostatic hypotension, fatigue, and dizziness (not 1st line)
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clonidine
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
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Alpha 1 blocker
doxazosin, prazosin, tamsulosin (for BPH) not for pregnancy
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doxazosin
alpha 1 blocker peripherally acting reduces peripheral vascular resistance and BP bu dilating arteries and veins HTN and BPH
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Dual action alpha 1 and beta receptor blockers drug
beta receptor blocker- nebivolol
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nebivolol
beta 1 selective blocker HTN decreases SVR reduces sexual dysfunction do not stop abruptly, tapered over 1-2 weeks
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ACE I
safe and efficacious- one of the 1st line for HTN and HF, diabetes for kidney protection catopril
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captopril
short half-life- dosed more frequently than other ACE I
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ACE I that are not prodrug?
captopril and lisonopril an advantage for people with liver dysfunction
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Enalapril
ACE I available parenterally
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ACE inhibitors may cause
significant fetal morbidity or mortality during 2nd and 3rd trimester (do not use in pregnancy)
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ACE Inhibitor action and explain hormones involved
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
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Primary effects of ACE I
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
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ACE I- indicator Contraindications AE
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
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ACE I overdose symptoms
hypotension treatment is symptomatic and supportive- give IV fluids to expand BV hemodialysis is effective for the removal of captopril and lisonopril
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ACE I interacttions
NSAIDS- reduces antihypertensive effect, may also predispose pts to acute kidney injury lithium carbonate- lithium toxicity potassium- hyperkalemia
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captopril (ACE I)
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
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enalapril sodium (ACE I)
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
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Angiotensin II receptor blockers (ARBs) Medications Action Indication
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)
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ARBs contraindications Interaction
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)
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ARBs AEs
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
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ARBs toxicity and overdose
hypotension and tachycardia bradycardia occurs less often treatment is symptomatic and supportive -IV fluids to expand BV
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losartan potassium
HTN, HF used in caution in pts with kidney/ liver dysfunction, renal artery stenosis not for breastfeeding women- AE on the infant
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CCBs
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
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Vasodilator medication action indication contraindication AE
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)
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minoxidil, hydralazine, diazoxide (VASODILATOR)
work primarily through arteriolar vasodilation
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sodium nitroprusside (VASODILATOR)
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
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Vasodilator toxicity or overdose
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
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Vasodilator contraindications
other antihypertensive drugs
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hydralazine hcl
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
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Direct renin inhibitors
most recent treat primary HTN sole drug- aliskiren
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aliskiren
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
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eplerenone
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
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bosentan monohydrate hormone related?
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
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trepostinil
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
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prehypertension
systolic- 120 to 129 diastolic- 80 to 89
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lab test
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...
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alpha-adrenergic agonists
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
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alpha adrenergic antagonists
dizziness and syncope
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centrally acting alpha blockers
WBCs serum potassium sodium levels protein in urine
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nonselective b blockers
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)
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beta 1 blockers
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)
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if a pt needs b blocker but has rstrictive airway problems
beta 1 blocker to avoid bronchoconstriction
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if no respiratory illness
non-selective beta-blockers may be effective
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beta blockers have inotropic effect
on the heart (decrease contractility) may worsen HF
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ACE Inhibitors (-pril)
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
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-pine
CCBs cause smooth muscle relaxation by blocking the binding of calcium to its receptors
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ARBs
caution in OAs and kidney dysfunction tolerated with meals reduce dosage if pt has hypovolemia/ liver dysfunction report dyspnea, dizziness, excessive fatigue
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Vasodilator
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
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BP goals
120- 139 mm Hg - systolic 80- 89 mm Hg - diastolic those with diabetes- less than 130/80
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diuretics
dizziness and electrolyte imbalances
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centrally acting alpha blockers
AEs are more pronounced; hypotension, sedation, bradycardia, edema
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CCBs
negative inotropic (decreases cardiac contractility)
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digoxin
increase heart contractility
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decreased chronotropic effects decreased dromotropic effects
decreased HR decreased conduction
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eye exam
HTN impacts vasculature of the eyes-reliable indicator of the long term effectiveness of treatment than BP readings
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alpha adrenergic agonist
first dose syncope- avoid situations that exacerbate this avoid activities that require mental alertness report dizziness, palpitations, and orthostatic hypotension assess sexual functioning
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Beta blocker
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
ACE I -pril
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
ARBs -sartan
work by blocking the binding of angiotensin at the receptors; which decreases BP
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CCBs -dipine (amlodipine)
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