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Reyes Hospital
NURSING SERVICE DEPARTMENT
A
Case Presentation
On
HYPERTENSION
May 2017
NURSING SERVICE DEPARTMENT
HYPERTENSION
I. OBJECTIVE
The participant will be able to:
Name:JRA
Age:30 y/o
Birthdate:8/28/1986
Citizenship: Filipino
Sex:Female
Chief Complaint:Headache
Patient experienced seldom headache, she takes pain reliever and take
a complete bed rest to manage and relieve such disturbance. She also
B. RESPIRATORY SYSTEM
effective on her because the soreness was relieved. She also claimed that
she had seasonal rhinitis especially when she inhales dust and strong odor
and seldom, she has runny nose when the weather changes especially
C. ENDOCRINE
She claimed that she has not experienced any signs of abnormalities.
Neither has she experienced goiter nor tumor nor some other alterations
D. GASTROINTESTINAL SYSTEM
The patient experienced thirst and hunger like any other normal
hyperacidity whenever meals are not taken on time. She claimed to have
E. MUSCULOSKELETAL SYSTEM
She experienced fatigue and muscle pains. She also claimed to have
and taking pain reliever. The patient has an aged posture as observed.
F. GENITO-URINARY SYSTEM
She also claimed that her urination is normal as far as she can
Time Assessed:9:00 AM
-Encourage oral
fluids, if
appropriate
Contraindicated Monitor BP
Dizziness
Generic name: This with carefully
medication is
Clonidine hypersensitivity Orthostatic whendiscontinuing
used alone or
hypotension
Brand name: with other to clonidine or clonidine; hyperte
medications
Catapres any adhesive Somnolence ( nsion usually
to treat high
layer dose- returns within 48
Classification: blood
dependent)
pressure (hyp components of hr.
Alpha-agonist ertension)
the transdermal Xerostomia (d
hypotensive ag ry mouth)
ent
system. Take this drug
Headache
Dosage: Use cautiously exactly as
(dose-
75 mcg/tab, with severe dependent) prescribed. Do not
STAT dose
coronary miss doses. Do
Fatigue
insufficiency, not discontinue
recent Hypotension the drug unless so
MI, cerebrovasc instructed.
ular disease; chr
onic renal
Attempt lifestyle
failure;
changes that will
pregnancy,
reduce your blood
lactation.
pressure: Stop
smoking and
using alcohol; lose
weight; restrict
intake of sodium
(salt); exercise
regularly.
Report urinary
retention, changes
in vision,
blanching of
fingers, rash.
Hyperkalemia.
Generic name: Hypokalemia, Hyperkalemia Monitor I&O ratio
Chronic renal
including that , GI and pattern in
Potassium disease. Acute discomfort patients receiving
caused by
chloride and irritation, the parenteral
diuretics. dehydration.
Digitalis diarrhea, rash drug. If oliguria
Heat cramps. (rare). occurs, stop
intoxication
Brand name: without AV Severe tissue Tablets: infusion promptly
block. Esophageal and notify
K-lyte destruction. physician.
and GI
Adrenal ulceration,
bleeding, Monitor for and
insufficiency. report signs of GI
Dosage: obstruction,
perforation. ulceration
600mg/tab, (esophageal or
1tab TID x 6 Familial periodic
epigastric pain or
doses (8am, paralysis. hematemesis).
1pm, 8pm)
Acidosis
Be alert for
(potassium potassium
chloride intoxication
(hyperkalemia,
products). may result from
Alkalosis any therapeutic
dosage, and the
(potassium patient may be
bicarbonate asymptomatic.
products).
Tablets:
Esophageal
compression
due to enlarged
left atrium.
Decreased GI
motility.
Name of Indication Contraindicati Adverse Nursing
Drugs on effect Consideration
HEART
Pulmonary circulation
are blood vessels that carry blood away from the heart. All arteries, with
the exception of the pulmonary and umbilical arteries, carry oxygenated
blood.
Pulmonary arteries
The pulmonary arteries carry deoxygenated blood that has just returned
from the body to the heart towards the lungs, where carbon dioxide is
exchanged for oxygen.
Systemic arteries
Systemic arteries can be subdivided into two types muscular and elastic
according to the relative compositions of elastic and muscle tissue in
their tunica media as well as their size and the makeup of the internal and
external elastic lamina. The larger arteries (>10mm diameter) are
generally elastic and the smaller ones (0.1-10mm) tend to be muscular.
Systemic arteries deliver blood to the arterioles, and then to the
capillaries, where nutrients and gasses are exchanged.
The Aorta
The aorta is the root systemic artery. It receives blood directly from the left
ventricle of the heart via the aortic valve. As the aorta branches, and
these arteries branch in turn, they become successively smaller in
diameter, down to the arteriole. The arterioles supply capillaries which in
turn empty into venules. The very first branches off of the aorta are the
coronary arteries, which supply blood to the heart muscle itself. These are
followed by the branches off the aortic arch, namely the brachiocephalic
artery, the left common carotid and the left subclavian arteries.
Aorta the largest artery in the body, originating from the left ventricle of
the heart and extends down to the abdomen, where it branches off into
two smaller arteries (the common iliacs). The aorta brings oxygenated
blood to all parts of the body in the systemic circulation.
Arterioles
Arterioles, the smallest of the true arteries, help regulate blood pressure
by the variable contraction of the smooth muscle of their walls, and deliver
blood to the capillaries.
Veins are blood vessels that carry blood towards the heart. Most veins
carry deoxygenated blood from the tissues back to the lungs; exceptions
are the pulmonary and umbilical veins, both of which carry oxygenated
blood. Veins differ from arteries in structure and function; for example,
arteries are more muscular than veins and they carry blood away from the
heart.
Veins are classified in a number of ways, including superficial vs. deep,
pulmonary vs. systemic, and large vs. small.
Superficial veins
Superficial veins are those whose course is close to the surface of the
body, and have no corresponding arteries.
Deep veins
Deep veins are deeper in the body and have corresponding arteries.
Pulmonary veins
The pulmonary veins are a set of veins that deliver oxygenated blood from
the lungs to the heart.
Systemic veins
Systemic veins drain the tissues of the body and deliver deoxygenated
blood to the heart.
Atrium sometimes called auricle, refers to a chamber or space. It may be
the atrium of the lateral ventricle in the brain or the blood collection
chamber of a heart. It has a thin-walled structure that allows blood to
return to the heart. There is at least one atrium in animals with a closed
circulatory system.
Right atrium is one of four chambers (two atria and two ventricles) in the
human heart. It receives deoxygenated blood from the superior and
inferior vena cava and the coronary sinus, and pumps it into the right
ventricle through the tricuspid valve. Attached to the right atrium is the
right auricular appendix.
Left atrium is one of the four chambers in the human heart. It receives
oxygenated blood from the pulmonary veins, and pumps it into the left
ventricle, via the atrioventricular valve.
Ventricle is a chamber which collects blood from an atrium (another heart
chamber that is smaller than a ventricle) and pumps it out of the heart.
Right ventricle is one of four chambers (two atria and two ventricles) in
the human heart. It receives deoxygenated blood from the right atrium via
the tricuspid valve, and pumps it into the pulmonary artery via the
pulmonary valve and pulmonary trunk.
Left ventricle is one of four chambers (two atria and two ventricles) in the
human heart. It receives oxygenated blood from the left atrium via the
mitral valve, and pumps it into the aorta via the aortic valve.
XII. PATHOPHYSIOLOGY
Narrative Pathophysiology
Cardiac output and peripheral vascular resistance (PVR)
Cardiac output and PVR are two important factors that maintain normal
blood pressures and it has been suggested that increased cardiac output
resulting from sympathetic dysfunction is the trigger for the development
of HTN and increases in PVR is essentially the physiologic response to
accommodate change in pressure and maintain homeostasis.
Over the last decade the role of SNS in the development and maintenance
of blood pressure has been studied exhaustively and it has been identified
that sympathetic stimulation of the heart, peripheral vasculature, and
kidneys, resulting in increased cardiac output, increased vascular
resistance, plus fluid retention is important in the development and
maintenance of this disease. As evidenced in the Coronary Artery Risk
Development in Young Adults (CARDIA) study, sympathetic overdrive is
often accompanied by low parasympathetic tone, which further
exacerbates the condition. Additionally, several studies have
demonstrated evidence of sympathetic over activity by documenting
increases in norepinephrine spill over in patients with HTN confirming that
sympathetic over activity is a core component in the pathophysiology of
this disease. The renal sympathetic nervous system is a major player in
the development and maintenance of HTN affecting blood pressure via two
pathways, namely, the efferent and afferent pathways. The efferent
pathway carries signals from the SNS to the kidney and increases renin
release thereby activating the RAAS system and increasing sodium and
water retention, all resulting in increased circulating volumes and
therefore increased blood pressures. In addition to the aforementioned
processes the efferent pathway also decreases renal blood flow and to
increase perfusion the kidney triggers the afferent pathway that carries
impulses to the SNS exacerbating sympathetic over activity and thereby
maintaining the high blood pressures.
Endothelial dysfunction
Vasoactive substances
Insulin Resistance:
Damage and dysfunction of endothelial cells results in decreased
production of vasodilators (nitric oxide), resulting in hypertension.
Insulin can increase blood pressure by activating the SNS, increasing
renal sodium reabsorption, hypertrophy of resistance vessels, and/or
alteration of transmembrane ion transport. Conversely,
hypertension can cause altered delivery of insulin and glucose to
the skeletal muscle cells, leading to insulin resistance.
Overactive SNS:
Increased production of catecholamines (epinephrine and
norepinephrine) results in SNS overactivity. This results in an
increased heart rate, increased peripheral vascular resistance due to
systemic vasoconstriction, and hypertension. Additionally, an
overactive SNS effects insulin resistance, vascular remodeling, has
procoagulant effects, which can lead to neospasm and narrowing of
the blood vessels.
Inflammation:
Commonly known as Shift in Pressure-natriuresis relationship.
Caused by increased vascular volume related to a decrease in renal
excretion of salt in the urine, leading to hypertension.
Overactive RAAS:
Contributes to salt and water retention, leading to increased
vascular resistance and hypertension.
Clinical Presentation
Target organ diseases occur in the heart (hypertensive heart disease), brain
(cerebrovascular disease), peripheral vasculature (peripheral vascular
disease), kidney (nephrosclerosis), and eyes (retinal damage).
The retina provides important information about the severity and duration of
hypertension. Damage to retinal vessels provides an indication of concurrent
vessel damage in the heart, brain, and kidney. Manifestations of severe retinal
damage include blurring of vision, retinal hemorrhage, and loss of vision.
Hypertensive 140 90
Diagnostic Studies
Basic laboratory studies are performed to (1) identify or rule out causes of secondary
hypertension, (2) evaluate target organ disease, (3) determine overall cardiovascular
risk, or (4) establish baseline levels before initiating therapy.
Routine urinalysis, BUN, serum creatinine, and creatinine clearance levels are used to
screen for renal involvement and to provide baseline information about kidney
function.
Lipid profile provides information about additional risk factors that predispose to
atherosclerosis and cardiovascular disease.
Treatment goals are to lower BP to less than 140 mm Hg systolic and less than 90 mm
Hg diastolic for most persons with hypertension (less than 130 mm Hg systolic and
less than 80 mm Hg diastolic for those with diabetes mellitus and chronic kidney
disease).
Lifestyle modifications are indicated for all patients with prehypertension and
hypertension and include the following:
Weight reduction. A weight loss of 10 kg (22 lb) may decrease SBP by approximately
5 to 20 mm Hg.
Dietary Approaches to Stop Hypertension (DASH) eating plan. Involves eating several
servings of fish each week, eating plenty of fruits and vegetables, increasing fiber
intake, and drinking a lot of water. The DASH diet significantly lowers BP.
Restriction of dietary sodium to less than 6 g of salt (NaCl) or less than 2.4 g of
sodium per day.
This involves avoiding foods known to be high in sodium (e.g., canned soups) and not
adding salt in the preparation of foods or at meals.
Restriction of alcohol
Regular aerobic physical activity (e.g., brisk walking) at least 30 minutes a day most
days of the week. Moderately intense activity such as brisk walking, jogging, and
swimming can lower BP, promote relaxation, and decrease or control body weight.
It is strongly recommended that tobacco use be avoided.
Stress can raise BP on a short-term basis and has been implicated in the development
of hypertension. Relaxation therapy, guided imagery, and biofeedback may be useful
in helping patients manage stress, thus decreasing BP.
Drug Therapy
Drug therapy is not recommended for those persons with prehypertension unless it is
required by another condition, such as diabetes mellitus or chronic kidney disease.
The overall goals for the patient with hypertension include (1) achievement and
maintenance of the goal BP; (2) acceptance and implementation of the therapeutic
plan; (3) minimal or no unpleasant side effects of therapy; and (4) ability to manage
and cope with illness.
Drugs currently available for treating hypertension work by (1) decreasing the volume
of circulating blood, and/or (2) reducing SVR.
Diuretics promote sodium and water excretion, reduce plasma volume, decrease
sodium in the arteriolar walls, and reduce the vascular response to catecholamines.
Adrenergic-inhibiting agents act by diminishing the SNS effects that increase BP.
Adrenergic inhibitors include drugs that act centrally on the vasomotor center and
peripherally to inhibit norepinephrine release or to block the adrenergic receptors on
blood vessels.
Direct vasodilators decrease the BP by relaxing vascular smooth muscle and reducing
SVR.
Calcium channel blockers increase sodium excretion and cause arteriolar vasodilation
by preventing the movement of extracellular calcium into cells.
A-II receptor blockers (ARBs) prevent angiotensin II from binding to its receptors in
the walls of the blood vessels.
Thiazide-type diuretics are used as initial therapy for most patients with hypertension,
either alone or in combination with one of the other classes.
When BP is more than 20/10 mm Hg above SBP and DBP goals, a second drug should
be considered. Most patients who are hypertensive will require two or more
antihypertensive medications to achieve their BP goals.
Hyperuricemia, hyperglycemia, and hypokalemia are common side effects with both
thiazide and loop diuretics.
ACE inhibitors lead to high levels of bradykinin, which can cause coughing. An
individual who develops a cough with the use of ACE inhibitors may be switched to an
ARB.
Hyperkalemia can be a serious side effect of the potassium-sparing diuretics and ACE
inhibitors.
Sexual dysfunction may occur with some of the diuretics. Orthostatic hypotension and
sexual dysfunction are two undesirable effects of adrenergic-inhibiting agents.
Patient and family teaching related to drug therapy is needed to identify and
minimize side effects and to cope with therapeutic effects. Side effects may be an
initial response to a drug and may decrease with continued use of the drug.
Hypertensive crisis
Hypertensive crisis is a severe and abrupt elevation in BP, arbitrarily defined as a DBP
more than 140 mm Hg.
Hypertensive crisis occurs most often in patients with a history of hypertension who
have failed to comply with their prescribed medications or who have been
undermedicated.
Nursing Management
Patient and family teaching includes the following: (1) nutritional therapy, (2) drug
therapy, (3) physical activity, (4) home monitoring of BP (if appropriate), and (5)
tobacco cessation (if applicable).
FDAR
Monitor response to
medications to
control blood
pressure
Administer
medications like
diuretics, alpha and
beta antagonists,
1:00 PM calcium channel
blockers, and
vasodilators.
Instruct and
implement to patient
dietary restrictions in
sodium, fat and
cholesterol
The patient will
participate in
activities that reduce
cardiac workload by
R: Demonstrated fluid
balance evidenced by
moist mucous
membranes, good skin
turgor, ans stable vital
signs.
DISCHARGE PLAN
Discharge Diagnosis: Hypertensive Urgency
Medications:
Advised to comply with all of the home medications.
Advised not to miss any doses.
Home medications instructed to patient.
Learn to take your own blood pressure. Keep a record of your results.
Take your blood pressure medicine exactly as directed. Don't skip
doses. Missing doses can cause your blood pressure to get out of
control.
Teachings:
Encouraged to have a good sleeping time and adequate nutrition.
Lifestyle changes
Hygiene:
Observation:
Call your doctor immediately or seek emergency care if you have any of
the following:
Diet:
b. Restrictions:
Follow-up care
We w o u l d l i ke t o t h a n k G o d a s fi n a l l y w e w e r e a b l e t o fi nish
our assignment that have been given to us. This task had been
done with all afford by group members even though a little bit problem
were happened among us while doing this assignment. Luckily, all
the problems can be settle down and we were able to adapt properly
and wisely. Hope that all the afford will give a lot of benefi ts to us and
also to our group project.
END.THANK YOU!