Pharm - Therapies for hypertension

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Arterioles: - most important for controlling BP
- if you can't control arterioles, you can't control BP
- carries blood to capillaries
Veins: - have one way valves
- more distensible (related to the amount of muscle)
What is cardiac output (CO)?: HR x SV
- average adult: 5L/min
What is stroke volume?: Vol x FOC
Determined by:
- preload & afterload (PVR)
- myocardial contractility/force of contraction (FOC) - starling's law
What is cardiac preload?: pressure in the right side of the heart as blood returns to the heart
What is cardiac afterload?: the pressure the heart must pump against to eject blood (PVR)
What are the determinants of cardiac output (CO)?: - heart rate
- blood volume
- FOC
- venous return
What are the determinants of peripheral vascular resistance (PVR)?: 1. viscosity
2. vessel diameter
3. vessel length
What is the formula for BP?: BP = HR x VOL x FOC x PVR
or
BP = HR x SV x PVR
or
BP = CO x PVR
How is arterial pressure regulated?: 1. ANS (Autonomic Nervous System)
2. RAAS (renin-angiotensin-aldosterone system)
3. Kidneys
How does ANS (autonomic nervous system) affect BP?: - rapid or steady state control
- sympathetic activation --> increases BP
How does RAAS help regulate BP?: - vasoconstriction
- H20 retention
What are the causes of hypertension?: - Obesity
- Diabetes
- Stres
- Genetics
- Diet, alcohol, Na+, low K+, low Ca++
- atherosclerosis (stiffening)
- renal artery stenosis (narrowing)
What is Stage 1 hypertension?: 140/90
to 159/99
What is stage 2 hypertension?: greater than 160/100
What is pre-hypertension?: 120/80
to 139/89
What is normal BP?: 120/80
How is hypertensions diagnosed?: - when 2 or more measurements taken on subsequent visits 1 week apart are greater than 140/90
- take 2 measurements each visit and get the average
* goal is less than 140/90 & less than 130/80 for people with diabetes or renal failure
What drugs can be taken for stage 1 hypertension for people WITHOUT compelling indications?: - Thiazide diuretic + optional
What drugs can be taken for stage 2 hypertension for people WITHOUT compelling indications?: - 2 diuretics drugs + other
What drugs are recommended for uncomplicated hypertension?: - diuretics
- beta blockers
What are lifestyle modifications to manage hypertension?: 1. Reduce sympathetic nervous system stimulation:
- decrease smoking
- decrease caffeine
- decrease stress
- increase exercise
- decrease weight
2. Reduce atherosclerosis by:
- decreasing saturate fat intake
- decreasing smoking
- limit alcohol
- increase exercise --> increase HDL
- control diabetes
3. Reduce circulating volume
- decrease dietary Na+ (800-2000mg/day)
4. DASH diet
- increase fruits/vegetables
- low fat foods
How to increase compliance of managing hypertension?: - educate
- self-monitoring
- collaborative relationship
- simple regimen
- lowest cost
What are some examples of antihypertensive drugs?: 1. Diuretics
2. Beta Blockers
3. Ca++ Channel blockers

4. Direct acting vasodilators
5. ACE inhibitors
6. Angiotensin II receptor blockers
What are the actions Thiazide diuretics?: - reduce blood volume (passive H20 loss secondary to Na+ excretion)
- reduction of arterial resistance
What are the adverse effects of Thiazide diuretics?: - hypokalemia (low K+)
- dehydration
- hyperglycemia (high blood sugar)
- hyperuricemia (high uric acid levels) - azotemia (increased BUN)
Explain the role of catecholamines and beta receptors in relation to SNS (sympathetics nervous system) activation.: SNS activation stimulates the release of catecholamines which then bind to beta receptors to increase HR, BP, FOC of the heart and increase RR & dilation of bronchioles in the lungs
What are beta 1 receptors and where are they found?: when activated, they increase:
- HR
- BP
- FOC (force of contraction)

*they are located in the heart
What are beta 2 receptors and where are they found?: when activated, they increase:
- RR
- bronchodilation

*they are located in the lungs
What are beta blockers and what is their MOA?: - block activation of beta receptors by catecholamines (producing opposite effects)

* SNS is activated in response to low CO
* catecholamines bind to beta receptors in the heart & lungs (bronchial, cardiac, & skeletal muscle)
What are the effects of beta blockers?: Heart:
- decreased HR (caused by decreased impulse at AV node)
- decreased CO (HR x Vol x FOC) causes decreased BP
- reduced speed of impulse conduction

Lungs:
- decreased RR
- bronchoCONSTRICTION

- block beta receptors in kidney that decreases RENIN
- treats angina (reduces O2 demand)
- treats mycardial infarction - decreased myocardial tissue enlargement & cell death
What is infarction?: the obstruction of blood supply to an organ or region of tissue
What are non-selective beta blockers?: - blocks both beta 1 & beta 2 receptors
What is an example of a non-selective beta blocker?: Propanolol (Inderal)
What are cardioselective beta blockers?: blocks ONLY beta 1 receptors
What is an example of a cardioselective beta blocker?: Metoprolol (Lopressor)
Who should take beta blockers?: People with:
- angina pectoris
- hypertension
- cardiac dysrhythmias
- myocardial infarction
- heart failure
- migraine
- hyperthyroidism
- stage fright
- glaucoma (optic nerve damage caused by intraocular pressure that causes permanent damage to vision)
What are the adverse effects of beta blockers?: - Bronchoconstriction
- bradycardia, AV block
- reduced cardiac output
- precipitation of heart failure
- AV heart block
- inhibition of glycogenolysis
- rebound cardiac excitation with abrupt withdrawal
What are the effects of Metoprolol (Lopressor)?: - slows depolarization, decreases HR & FOC --> decreased CO --> lower BP & decreased O2 consumption
- decreases plasma renin --> lowers BP
- decreased gluconeogenesis
- lipid soluble so it can cross the BBB (stimulate CNS)
- rebound Na+ retention
What is the pharmacokinetics of Metoprolol (Lopressor)?: - 50% of dose is lost via hepatic first pass effect
- half life: 3-7 hrs (BUT antihypertensive effect is not correlated with plasma concentration, it's lasts longer)
- little difference in half life in patients with renal disease
Nursing considerations when giving Metoprolol:: - hypotension and bradycardia are main side effects (observe for these signs)
- check pulse
- watch for signs of CHF (congestive heart failure)
- avoid cold (vasoconstriction)
- no abrupt withdrawal
- wear medic alert bracelet
What are 2 examples of direct acting vasodilators?: 1. Hydalazine
2. Minoxidil
What are the effects of Ca++ entering a cell?: - stimulates SA --> increases HR
- stimulates AV node --> increases conduction velocity
- increases FOC in myocardium
What are the effects of Ca++ Channel blockers?: 1. Arterioles (decrease VSM tone):
- vasodilation
- decreased PVR
- decreased BP (decreased afterload)
2. Heart:
- decreased FOC & SV --> lower BP
- SA node/AV node --> decreased rate of depolarization --> HR
What is the MOA of Ca++ channel blockers?: - less Ca++ influx in cell
- reduced action of CALMODULIN KINASE
- decreased actin-myosin crossbridging in smooth muscle leads to:
- decreased HR, SV, FOC, BP
- vasodilation --> decreased BP
What are Ca++ Channel blockers that have effects on the heart only?: Diltiazem (Cardiazem):
- decreased HR, FOC, SV
- decreased BP
What are Ca++ channel blockers that have effects on the arterioles only?: Nifedipine:
- vasodilation
- decreased BP
What are the adverse effects of Ca++ channel blockers?: - flushing
- vasodilation --> headache
- bradycardia in patients with AV block
- constipation
What are the pharmacokinetics of Ca++ channel blockers?: - half life: 3-6 hours (short)
- requires TID dosing
*****DILTIAZEM - excreted via BILE
- other Ca++ channel blockers are excreted by kidney
What are patient teachings relating to Ca++ channel blockers?: - observe for signs of heart failure
- peripheral edema (vasodilation - start to seep out)
- assess pulse rate (bradycardia)
- constipation
- orthostatic hypotension
What is the MOA of Nifedipine (Adalat)?: - vasodilation of VSM (vascular smooth muscle) only
NET effect: peripheral arterioles --> vasodilation --> lowers BP

**increased HR with reflex tachycardia (ONLY if fast acting type)
What are the adverse effects of Nifedipine (Adalat)?: - flushing
- dizziness
- headache
- peripheral edema
- gingival hyperplasia (gums)
- reflex tachycardia

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Number of cards 52

Created By daisy497