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Pharm - Therapies for hypertension


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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)?
- 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
- 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 SV 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?
to 159/99
What is stage 2 hypertension?
greater than 160/100
What is pre-hypertension?
to 139/89
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
- 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?
- 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
- 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?
- 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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