Antihypertensives Flashcards
1
Q
Epidemiology of hypertension (HTN)
A
- ~50% of adults in the US
- Increasing prevalence globally
- ~$131 billion/year & 670,00
- “Silent Killer”
- Leading cause of cardiovascular disease/death globally
- Increased risk for heart disease & stroke: leading causes of death in US
2
Q
Describe normal blood pressure (BP)
A
- Systolic BP <120; Diastolic BP <80
- Must be maintained for organ perfusion
- Affected by age, weight, sex, race
- Depends on cardiac output (CO) and total peripheral resistance (TPR)
3
Q
What variables do antihypertensive medications work on the affect BP
A
- Heart rate (HR)
- Stroke Volume (SV)
- Total peripheral resistance (TPR)
4
Q
Describe short term BP regulation (seconds-minutes)
A
- Barorecptor reflex: stretch receptors in large arteries of thorax/neck
- Humoral factors: catecholamines (adrenal), arginine-vasopressin (pituitary), and angiotensin II (kidneys)
5
Q
Describe long term BP regulation (hours-days)
A
- Kidneys: Renin-angiotensin system (RAAS)
6
Q
Describe how baroreceptors work in BP regulation
A
- Posture change -> venous pooling -> drop in BP -> postural baroreflex activated
7
Q
Describe orthostatic hypotension
A
- AKA postural hypotension
- Abnormal drop in BP when changing positions: ≥20 mmHg systolic and/or ≥10 mmHg diastolic
- Due to delayed/inadequate baroreceptor reflex
- Risk factors: Age >60, Parkinson’s disease, medications
8
Q
Describe hypertension
A
- regulation of BP is the same
- Setpoint of baroreceptors & blood volume is changed
- Diagnosed by 2 or more BP checks at separate visits
9
Q
Describe essential hypertension
A
- ~95%
- AKA primary HTN
- gradual onset
- lifelong
10
Q
Describe secondary HTN
A
- ~5%
- early childhood/later in life
- dramatic onset
- may be related to treatable condition
11
Q
Classes of antihypertensives
A
- Diuretics
- Sympatholytics
- Vasodilators
- Renin-Angiotensin System (RAS) Inhibitors
- Calcium channel blockers (CCB)
12
Q
Describe diuretics
A
- increased renal excretion of water & sodium, decreased plasma volume
- decreased blood volume = decreased stroke volume = decreased cardiac output
- 3 groups based on where they act win nephron: Thiazides (first line therapy), Loop, and Potassium sparing
13
Q
Describe differences between Thiazides, Loop, and Potassium sparing diuretics
A
- Thiazides: act on distal tubule, less potent than loop diuretics
- Loop: act on the loop of Henle, more potential for side effects
- Potassium sparing: act in collecting duct, mild diuretic effect, “spare” potassium
14
Q
Lists diuretic drugs
A
- Chlorthalidone
- Hydrochlorothiazide
- Bumetanide
- Spironolactone
- Metolazone
- Furosemide
15
Q
Adverse effects of diuretics
A
- Hypokalemia: weakness, fatigue, confusion; often requires supplementation to prevent
- Hyperkalemia (potassium sparing): muscle cramps, weakness, paresthesia
- Hyponatremia: confusion, lethargy, seizures
- Electrolyte imbalances may be fatal if not addressed
- Fluid depletion: tachycardia, increased CO & TPR (baroreceptor), may activate RAAS
- Impaired glucose & lipid metabolism
- Orthostatic hypotension: take early in the day
16
Q
Describe sympatholytics
A
- Generally work to descries sympathetic drive
- Classified based on where they work: Beta blockers, Alpha blockers, Presynaptic adrenergic inhibitors, Centrally acting agents, Ganglionic blockers
17
Q
Describe beta blockers
A
- MOA: bind to beta receptors in heart/lungs blocking binding of catecholamines
- decrease renin = decrease blood volume = SV = decrease CO
- decrease contractility = decrease SV = decrease CO
- decrease HR = decrease CO
- Adjunct therapy
18
Q
Considerations in beta blocker drug selection
A
- Cardioselectivity
- Intrinsic sympathomimetic activity (ISA)
- Membrane stabilization activity
- Lipophilicity
- “Newer” generation
19
Q
Describe cardioselectivity and ISA
A
- Cardioselectivity: non-selective (preferred in other conditions) and selective ( less bronchoconstriction; beta 1>beta 2)
- ISA: maintain HR
20
Q
Describe membrane stabilization
A
- Normalize excitability of cardiac cell membrane
- Propranolol, metoprolol
21
Q
Describe lipophilicity and 3rd generation beta blockers
A
- Lipophilicity: alters CNS effects (Propranolol)
- 3rd generation: vasodilation due to alpha1 blockade (Antioxidant effects)
22
Q
Adverse effects of beta blockers
A
- Generally well tolerated
- Bronchoconstriction. (asthma)
- Excessive HR/myocardial depression
- Impaired glucose & lipid metabolism
- Orthostatic hypotension
- Mask hypoglycemia
- Fatigue/depression
- Decreased HR
- Increased rate of perceived exertion (RPE)
- If abruptly stopped: MI, arrhythmia, sudden death
23
Q
Describe alpha blockers
A
- MOA: bind to alpha1 receptors on vascular smooth muscle, blocking binding of catecholamines
- decrease vasoconstriction = decreased TPR
- Adjunct therapy
- Commonly used in: benign prostatic hyperplasia, post-traumatic stress disorder (PTSD)
24
Q
Adverse effects of alpha blockers
A
- Reflex tachycardia: caused by neg. feedback mechanism; caution in pts with cardiac disease
- Orthostatic hypotension: take at night to lower risk
25
Q
Describe presynaptic adrenergic inhibitors
A
- MOA: inhibit presynaptic norepinephrine release in peripheral adrenergic neurons
- decrease sympathetic mediated excitation of heart & peripheral vasculature (decrease CO/TPR)
- not first line for anything
26
Q
Adverse effects of presynaptic adrenergic inhibitors
A
- orthostatic hypotension
- bradycardia
- tardive dyskinesia
27
Q
Adverse effects on centrally acting agents
A
- Dry mouth
- Dizziness
- Sedation
- Rebound hypertension/tachycardia: due to rebound sympathetic activity
28
Q
Describe ganglionic blockers
A
- MOA: affect pre/post synaptic neurons in sympathetic & parasympathetic pathways
- decrease HR/SV = decrease CO
- not first line for anything
29
Q
Adverse effects of ganglionic blockers
A
- Profound hypotension
- Constipation, urinary retention
- Dry mouth, blurred vision
30
Q
Describe vasodilators
A
- MOA: vasodilator the peripheral vasculature directly at cell
- decrease cGMP = decrease contractility of smooth muscle cells = decrease TPR
- Adjunct therapy: nitric oxide being studied is used in COVID patients
31
Q
Adverse effects of vasodilators
A
- Headache
- Reflex tachycardia: baroreceptor reflex compensation
- Orthostatic hypotension
- Unwanted hair growth: face, ears, forehead
32
Q
Describe RAS inhibitors
A
- Inappropriate activation of renin-angiotensin system -> Angiotensin II
- Stimulates vascular tissue growth, thickening, & hypertrophy of vascular walls
- Vasoconstriction
- Sympathetic nervous system activation
- Aldosterone release -> Sodium/water retention
- Self perpetuating cycle
33
Q
MOA of RAS inhibitors
A
- ACE inhibitors: inhibit enzyme converts angiotensin I to angiotensin II
- ARBs: block angiotensin II receptors in tissues
- Renin inhibitors: inhibit renin conversion of angiotensin to angiotensin I
- decrease fluid/sodium retention = decrease SV = decrease CO
- decrease angiotensin II = decrease vasoconstriction = decrease TPR
- First line therapy (ACE inhibitorsARBs)
34
Q
Adverse effects of RAS inhibitors
A
- Generally well tolerated
- Hyperkalemia (ARBs/ACE inhibitors)
- Dry cough (ACE/Renin inhibitors)
- Angioedema (ACE inhibitors)
- Kidney injury
35
Q
Describe calcium channel blockers (CCB)
A
- MOA: blocks calcium entry into vascular smooth muscle
- decrease HR/SV = decrease CO
- vasodilation = decrease TPR
- First line therapy
36
Q
Adverse effects of calcium channel blockers (CCB)
A
- Peripheral edema
- Orthostatic hypotension
37
Q
Treatment principles of antihypertensives
A
- Dietary modifications: dietary approaches to stop HTN (DASH) diet; moderate alcohol & tobacco use
- Decrease body weight
- Increase physical activity
- Behavior modification & stress management
38
Q
Antihypertensives implications for physical therapy
A
- Underrated patients: increased risk for CV events/stroke
- Reinforce: lifestyle modifications, dietary modifications, & importance of medication compliance
39
Q
Antihypertensives impact on physical therapy
A
- Orthostatic hypotension can lead to fainting/falls: changing positions, exiting warm pools
- With beta blockers: delayed hypoglycemia symptoms, dyspnea, fatigue, unable to use HR to monitor exertion
- Depressed HR & contractility can decrease exercise tolerance
- Electrolyte abnormalities can cause paresthesia, muscle cramps, weakness, increase risk of cardiac dysfunction
40
Q
Physical therapy modifications with antihyptensives
A
- Check BP before & after activities
- Assist patients when changing positions or exiting heated pool
- Use caution with activities that cause widespread vasodilation: widespread application of heat (Hubbard tank, whirlpool)
- Ask patients to check blood glucose prior to activities if on glucose lowering therapies
- Use RPE to gauge activity level in pts especially with beta blockers
- Allow for cool down periods after exercise
- Monitor for signs of electrolyte abnormalities: check for high risk medications
41
Q
Take home points for antihypertensives
A
- HTN is common & increases risk of heart disease & stroke
- Variety of treatments exis
- PT’s play a role in: reinforcing appropriate treatment; helping patients increase physical activity; making modifications to therapy to reduce risk adverse effects
