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NURS 310 Final: final #9

5 pages35 viewsFall 2017

Course Code
NURS 310
Study Guide

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Pharmacotherapy of Hypertension
Blood Pressure & Hypertension
Hypertension = high blood pressure, and is the most common CV disease.
Has two classifications:
Primary - no identifiable cause
Secondary - caused by identifiable factors, such as excessive epinephrine or narrowing
of renal arteries.
*LO1* - Prolonged HTN can lead to damage of small blood vessels resulting in arterial
narrowing. This narrowing can lead to angina, myocardial infarction, peripheral vascular
A serious consequence of HTN is how much harder the heart has to work to pump blood.
Excessive cardiac workload can cause the heart to fail and lungs to fill with fluid (aka
heart failure).
Damaging vessels that supply the brain can lead to TIA’s and strokes.
3 Main Contributing Factors to BP
Cardiac Output - Volume of blood pumped per minute
Increase in CO = increase BP
CO is determined by heart rate and stroke volume (amount of blood pumped by
ventricle in one contraction)
Think: drugs that affect CO, stroke volume or heart rate can affect BP.
Peripheral Resistance - turbulence-induced friction in arteries
Blood flowing at high speeds exerts a force on vascular walls, and the friction
decreases blood velocity.
*More resistance = increased BP
Vasoconstriction = creates more resistance = increases pressure
Blood Volume - average person maintains 5mL of blood volume.
More blood in vascular system exerts more pressure on vascular walls of arteries,
and this increases BP.
Regulating factors of BP:
Vasomotor Centre - a group of neurons in the medulla oblongata
Innervating nerves in arterial smooth muscle are stimulated to either constrict
(increase BP) or dilate/relax (decrease BP). Stimulators include AT2, nitric oxide
The vasomotor centre reacts based on info conveyed by receptors in aorta and
internal carotid artery.
Baroreceptors - sense pressure in large vessels
Chemoreceptors - sense pH and O2/CO2 levels in blood
Emotions can influence BP levels
Endogenous Agents
These include epinephrine and norepinephrine (increases BP); ADH (a
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Renin-Angiotensin-aldosterone system (RAAS)
Homeostatic mechanism to regulate BP
When BP drops/less Na+ in tubules, kidneys secrete renin enzyme which
converts liver protein angiotensinogen to angiotensin I. When passing through
lungs, angiotensin I is converted to angiotensin II (a vasoconstrictor) via the
angiotensin-converting enzyme (ACE).
This increases BP, due to vasoconstriction which increases periph. Resistance.
Angiotensin II also releases two hormones that affect BP
Aldosterone - increases Na+ reabsorption and retainment of water
ADH - increases water conservation, increasing blood volume and BP,
Hypertension Therapy
120/80 = optimal BP measure
Those w/ systolic BP 120-139 and diastolic BP 80-89 considered prehypertensive
Diagnosis of HTN is based on sustained trend of high blood pressure measurements.
Pharmacotherapy of HTN is indicated in clients with:
CV risk factors if BP 140/90 or higher
Target organ damage if BP is 140/90 or higher
Atherosclerotic disease even w/ normal BP
Diabetes or CKD if BP is 130/80 or higher
HTN can be systemic or localized
Systemic HTN = general measure of arterial BP in body
Localized HTN = HTN in vessels surrounding a certain area of the body, such as HTN
in portal vein near liver.
Stage 1 HTN:
Client has systolic 140-159 and diastolic 90-99
Low doses are prescribed once appropriate drug is chosen for client’s HTN.
Two antiHTNs may be prescribed and used concurrently w/ rationale that using two drugs can be
done at lower doses and lead to less side effects and better adherence.
Hypertension Medications/Drugs
PR: Hydrochlorothiazide (HCTZ, Urozide)
MOA: increase volume of urine production (excretion of water and electrolytes), thus
decreasing blood volume in the body and blood pressure.
Changes in urine composition leads to possibility of electrolyte depletion and loss. Major one to
look out for is potassium.
Considered first-liners for HTN because of few side-effects and can control mild-moderate HTN.
Classes of Diuretics:
Potassium-Sparing Type
Don’t use these in clients w/ renal insufficiency or hyperkalemia (K+ levels can
increase to alarming levels)
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