Antihypertensives Flashcards

1
Q

3 main factors affecting blood pressure

A

CO
Blood volume
Resistance
- artery walls flexibility
- artery diameter
- blood viscosity or thickness

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2
Q

Causes of HTN

A

essential HTN is UNKNOWN

psychological and physiological stress
High Na and low K and Ca - facilitates RAAS increasing BP
metabolic syndrome - obesity, dyslipidaemia, diabetes - mainly affects afterload/SVR since larger body mass (excess fat and sugar) the longer the blood vessels, in response, the heart has to pump harder to get the same amount of pressure getting into the tissues putting a strain in the heart overtime increasing chance of having CADs
smoking - excess vasoconstriction
environmental factors - eg. pollution as air pollutants enter the systemic circulation and causes vasoconstriction
genetic factors

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3
Q

long-term consequences of HTN

A

heat performance gets overused leading to several CADs:

Heart failure - when RAAS gets overused causing blood retention in the systemic circulation (pulmonary/ peripheral oedema)
Accelerated atherosclerosis > MI
Renal failure - renal arteries are damaged overtime and narrows causing insufficient bladder perfusion in the kidneys
Stroke - blood vessels in the brain gets damaged
Weakened blood vessel walls > aortic/ cerebral aneurysms

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4
Q

Classes of Antihypertensive meds

A

ACE inhibitors
ARBs - ACE II receptor blockers
Beta-blockers
Calcium channel blockers
Diuretics

Centrally acting antihypertensives (methyldopa)
Peripheral vasodilators (hydralazine)

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5
Q

Pharmacodynamics of ACE inhibitors

A

inhibits conversion of ACE I to ACE II causing:
decreased vasoconstriction > decreased SVR
decreased aldosterone production > increasing Na+ and H2O excretion
decreased BP
increased renal blood pressure

indications: HTN, heart failure and nephropathy

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6
Q

Ace inhibitor meds

A

quinapril
lisinopril
enalapril
captropril
fosinopril

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7
Q

adverse effects of Ace inhibitors

A

Hypotension (monitor for orthostatic hypotension and dizziness)
Hyperkalaemia (since aldosterone is inhibited K+ are retained)
Angioedema (blocks airway, swelling underneath the skin)
Cough (ACE inactivates bradykinin - which mediates inflammation causing vasodilation)

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8
Q

Nursing considerations for Ace inhibitors

A

monitor hypotension
monitor K+ levels - avoid diet rich in K and Na
assess angiodema (swelling of the face and mouth)
educate NOT TO SUDDENLY STOP ACEIs as it causes REBOUND HTN

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9
Q

ACE inhibitors contradictions

A

pregnancy - teratogenic effects on foetus

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10
Q

Pharmacodynamics of ARBs/ Angiotensin II receptor blockers

A

Blocks angiotensin II receptors in the smooth muscles of the arteries inhibiting vasoconstriction
High affinity to AT II receptors causing vasodilation
Lowers BP and increase blood volume to the heart

Indicators:
HTN
alternative to ACE inhibitors to manage HF and diabetic nephropathy

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11
Q

AT II receptor blocker/ ARB meds

A

losartan
candesartan

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12
Q

adverse effects of ARBs

A

Hypotension
Hyperkalaemia

DO NOT CAUSE COUGH as it does not accumulate bradykinin

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13
Q

Pharmacodynamics of beta-blockers

A

Antagonist at sympathetic (noradrenaline) beta receptors
Blocks:
alpha-1 receptors: decreased SVR
beta-1 receptors:
- decreased HR and myocardial contractility > reduced myocardial O2 demand
- inhibits renin release > inhibit Na+ and H2O retention > reduce preload and decrease SVR
- slows development of atherosclerotic plaques

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14
Q

Indicators of beta blockers

A

HTN
Stable angina
Cardiac dysrhythmias after MI
HF
secondary prevention after MI

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15
Q

Beta blocker meds

A

Cardioselective Beta-1 blockers:
metoprolol
celiprolol
bisoprolol

Beta and Alpha-1 blockers:
labetalol
carvedilol
sotalol

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16
Q

Adverse effects of Beta blockers

A

Bradycardia
Bronchospasm
Drowsiness and fatigue
Worsen CHF

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17
Q

Contradictions for beta blockers

A

Pts with asthma/COPD - beta blockers can block beta-2 receptors in the lungs causing bronchospasm
Pts with DM - beta blockers inhibits beta cells in the pancreas preventing glycogenolysis causing hypoglycaemia

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18
Q

Nursing considerations for beta blockers

A

DO NOT STOP ABRUPTLY - risk of rebound HTN, instead decrease dose slowly
monitor hypotension - risk of falling from orthostatic hypotension
educate to change position slowly
monitor S&S of HF - wet lung sounds, weight gain, oedema

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19
Q

Pharmacodynamics of calcium channel blockers/ CCBs

A

blocks Ca channels by inhibiting Ca influx into smooth muscles and myocardial cells
- smooth muscle relaxation> vasodilation including coronary blood vessels
- reduce AV conduction
- decrease heart workload

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20
Q

CCB meds

A

3 classes:
Verapamil - myocardium
Nifedipine - smooth muscle
Diltiazem - myocardium & smooth muscle

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21
Q

CCBs indicators

A

HTN
Angina
Dysrhythmias

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22
Q

CCBs adverse effects

A

Constipation
Nocturia (waking up during the night and urinate)
Headache (cerebral vasodilation)
Hypotension, postural hypotension and fatigue (risk of falls)

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23
Q

Nursing considerations for CCBs

A

Orthostatic hypotension (risk of falls) - encourage to sit in the side of the bed for few minutes then rise up slowly
Change positions slowly when lying

DO NOT STOP MEDS ABRUPTLY! it can cause rebound HTN/ Angina
DO NOT DRINK GRAPEFRUIT JUICE - can cause severe hypotension
ELEVATE leg to reduce oedema
ENCOURAGE fluids, fruits, and fibre rich diet for CONSTIPATION

24
Q

Pharmacodynamics of Diuretics

A

act to reduce Na reabsorption in the kidneys
reduce H20 retention
decrease blood volume and plasma Na

25
4 main classes of Diuretics
Loop diuretics Thiazide diuretics K sparring diuretics Osmotic diuretics
26
Pharmacodynamics of Loop diuretics
Acts on loop of henley Inhibit Na+ & Cl- reabsorption (25%) > Na+ loss > decreased reabsorption of H20 > increase UO and decrease blood volume VERY STRONG DIURESIS
27
Loop diuretic meds
Furosemide
28
Loop diuretics indicators:
HTN HF or CHF renal disease Pulmonary and Peripheral oedema
29
Loop diuretics adverse effects
HYPOKALAEMIA - highest risk (< 3 mmol/L) Dehydration Hypotension Hyponatraemia Hyperglycaemia
30
Nursing considerations for Loop diuretics
obtain and monitor vitals monitor input and ouput Replace K+ if below normal
31
Pharmacodynamics of Thiazide diuretics
acts on DCT/ distal convoluted tubule inhibit reabsorption of Na+ & Cl- (5%) > decreasing reabsorption of water > increase UO and decrease blood volume LESS DIURESIS compared to Loop diuresis
32
Thiazide diuretic meds
bendroflumethiazide chlortalidone indapamide
33
Thiazide diuretics adverse effects
HYPOKALAEMIA - less intense compared to loop diuretics (< 3mmol/L) Hypotension Hyperglycaemia Hyponatraemia Dehydration
34
Thiazide diuretics indicators
HTN HF renal disease Oedema
35
Nursing considerations for thiazide diuretics
obtain and monitor vitals monitor input and output replace K+ if levels below normal daily weights AVOID for pts with GOUT AVOID this meds for pts with SULFA ALLERGY
36
Pharmacodynamics of K+ sparring diuretics
Aldosterone antagonist increase Na+ & H20 excretion > reabsorb K+
37
K+ sparring diuretic meds
Spironolactone
38
K+ sparring diuretics indicators
HTN Oedema Hypokalaemia
39
K+ sparring diuretics adverse effects
HYPERKALAEMIA (> 5 mmol/L) hypotension diarrhoea gastritis drowsiness erectile dysfunction
40
Nursing considerations for K+ sparring diuretics
AVOID FOODS HIGH IN K monitor K+ levels (risk of hyperkalaemia)
41
Pharmacodynamics of osmotic diuretics
increase viscosity of the filtrate H20 can’t be reabsorbed increase excretion of Na+ & Cl-
42
Osmotic diuretics indicators:
Cerebral oedema Decreased intraocular pressure (fluid inside the eyes)
43
osmotic diuretics adverse effects
Oedema blurred vision N&V, diarrhoea urinary retention
44
Nursing considerations for osmotic diuretics
IV ONLY! perform neuro assessment and LOC (lvl of consciousness) for cerebral oedema
45
adverse effects of diuretics to older adults
DEHYDRATION POSTURAL HYPOTENSION ELECTROLYTE IMBALANCES RISK FOR: falls, incontinence, confusion, constipation and fever
46
what is “triple whammy” when taking antihypertensives
a combination of ACE inhibitors, ARBs, diuretics and NSAIDs
47
adverse effects of “triple whammy”
decrease renal function
48
Pharmacodynamics of methyldopa
a prodrug converted into methylnoradrenaline active metabolite that binds to alpha-2 receptors in the brain stem reducing sympathetic stimulation > decrease SVR > slows HR
49
adverse effects of methyldopa
postural hypotension mental clouding (less wakeful or aware) GI upsets
50
nursing considerations for methyldopa
AVOID ALCOHOL (increase sedation effects) TAKE IT WITH FOOD if feeling nauseated
51
Pharmacodynamics of Hydralazine
direct acting vasodilator selective arterioles dilator > decrease SVR > increases HR and myocardial contractility
52
Hydralazine indicators
HTN (especially for pregnant mothers) HF
53
hydralazine adverse effects
Tachycardia hypotension fluid retention GI upset headache dizziness
54
Pharmacodynamics of Glyceryl Trinitrate/ GTN
decreases smooth muscle contractility act mainly on veins and arterioles reduces preload and some afterload > decreases BP
55
GTN indicators
HTN prior to STEMI and stroke clot retrieval