Glossary of Pharm - Therapies for hypertension
Created by daisy497
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- - most important for controlling BP
- if you can't control arterioles, you can't control BP
- carries blood to capillaries
- - 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
- 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
- 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
BP = HR x SV x PVR
BP = CO x PVR
- How is arterial pressure regulated?
- 1. ANS (Autonomic Nervous System)
2. RAAS (renin-angiotensin-aldosterone system)
- 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
- Diet, alcohol, Na+, low K+, low Ca++
- atherosclerosis (stiffening)
- renal artery stenosis (narrowing)
- What is Stage 1 hypertension?
- What is stage 2 hypertension?
- greater than 160/100
- What is pre-hypertension?
- What is normal BP?
- 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
- 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+)
- 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:
- FOC (force of contraction)
*they are located in the heart
- What are beta 2 receptors and where are they found?
- when activated, they increase:
*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?
- decreased HR (caused by decreased impulse at AV node)
- decreased CO (HR x Vol x FOC) causes decreased BP
- reduced speed of impulse conduction
- decreased RR
- 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
- cardiac dysrhythmias
- myocardial infarction
- heart failure
- 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
- 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):
- decreased PVR
- decreased BP (decreased afterload)
- 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?
- decreased BP
- What are the adverse effects of Ca++ channel blockers?
- - flushing
- vasodilation --> headache
- bradycardia in patients with AV block
- 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)
- 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
- peripheral edema
- gingival hyperplasia (gums)
- reflex tachycardia
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