HYPERTENSION

Hypertension is one of the most common worldwide diseases afflicting humans. Because of the associated morbidity and mortality and the cost to society, hypertension is an important public health challenge. Over the past several decades, extensive research, widespread patient education, and a concerted effort on the part of health care professionals have led to decreased mortality and morbidity rates from the multiple organ damage arising from years of untreated hypertension.

Defining abnormally high blood pressure is extremely difficult and arbitrary. Furthermore, the relationship between systemic arterial pressure and morbidity appears to be quantitative rather than qualitative. A level for high blood pressure must be agreed upon in clinical practice for screening patients with hypertension and for instituting diagnostic evaluation and initiating therapy. Because the risk to an individual patient may correlate with the severity of hypertension, a classification system is essential for making decisions about aggressiveness of treatment or therapeutic interventions.

Based on recommendations of the Seventh Report of the Joint National Committee of Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VII), the classification of blood pressure (expressed in mm Hg) for adults aged 18 years or older is as follows:

Normal - Systolic lower than 120, diastolic lower than 80 Prehypertension - Systolic 120-139, diastolic 80-99

Stage 1 - Systolic 140-159, diastolic 90-99

Stage 2 - Systolic equal to or more than 160, diastolic equal to or more than 100

Non-modifiable risk factors for hypertension includes family history, age in which primary hypertension typically appears between ages of 30-50 years, gender in which overall incidence is higher in men than in women until about the age 55 years and ethnicity where blacks are at high risks.

On the other hand, modifiable factors includes diabetes, stress, obesity, excessive sodium consumption and substance abuse such as cigarette smoking, heavy alcohol consumption and some illicit drugs are risks for having hypertension.

This is based on the average of 2 or more readings taken at each of 2 or more visits after initial screening. Normal blood pressure with respect to cardiovascular risk is less than 120/80 mm Hg. However, unusually low readings should be evaluated for clinical significance.

Prehypertension, a new category designated in the JNC VII report, emphasizes that patients with prehypertension are at risk for progression to hypertension and that lifestyle modifications are important preventive strategies. Hypertension may be either essential or secondary. Essential hypertension is diagnosed in the absence of an identifiable secondary cause. Approximately 95% of American adults have essential hypertension, while secondary hypertension accounts for fewer than 5% of the cases.

Blacks have a higher prevalence and incidence of hypertension than whites. The prevalence of hypertension was increased by 50% in African Americans. In Mexican Americans, the prevalence and incidence of hypertension is similar to or lower than in whites. The National Health and Nutrition

INTRODUCTION

Examination Survey (NHANES) III reported an age-adjusted prevalence of hypertension at 20.6% in Mexican Americans and 23.3% in non-Hispanic whites.

A progressive rise in blood pressure with increasing age is observed. The third NHANES survey reported that the prevalence of hypertension grows significantly with increasing age in all sex and race groups. National health surveys in various countries have shown a high prevalence of poor control of hypertension. These studies have reported that prevalence of hypertension is 22% in Canada, of which 16% is controlled; 26.3% in Egypt, of which 8% is controlled; and 13.6% in China, of which 3% is controlled. Hypertension is a worldwide epidemic; in many countries, 50% of the population older than 60 years has hypertension. Overall, approximately 20% of the world's adults are estimated to have hypertension. The 20% prevalence is for hypertension defined as blood pressure in excess of 140/90 mm Hg. The prevalence dramatically increases in patients older than 60 years.

HYPOKALEMIA

Potassium, the most abundant intracellular cation, is essential for the life of the organism. Potassium is obtained through the diet, and common potassium-rich foods include meats, beans, fruits, and potatoes. Gastrointestinal absorption is complete, resulting in daily excess intake of approximately 1 mEq/kg/d (60-100 mEq). Ninety percent of this excess is excreted through the kidneys, and 10% is excreted through the gut. Potassium homeostasis is maintained predominantly through the regulation of renal excretion.

Potassium is predominantly an intracellular cation; therefore, serum potassium levels can be a very poor indicator of total body stores. Because potassium moves easily across cell membranes, serum potassium levels reflect movement of potassium between intracellular and extracellular fluid compartments, as well as total body potassium homeostasis.

Muscle contains the bulk of body potassium, and the notion that muscle could play a prominent role in the regulation of serum potassium concentration through alterations in sodium pump activity has been promoted for a number of years. Insulin stimulated by potassium ingestion increases the activity of the sodium pump in muscle cells, resulting in an increased uptake of potassium. Studies in a model of potassium deprivation demonstrate that acutely, skeletal muscle develops resistance to insulin-stimulated potassium uptake even in the absence of changes in muscle cell sodium pump expression. However, long term potassium deprivation results in a decrease in muscle cell sodium-pump expression, resulting in decreased muscle uptake of potassium.

Thus, there appears to be a well-developed system for sensing potassium by the pancreas and adrenal glands, resulting in rapid adjustments in immediate potassium disposal and for long-term potassium homeostasis. High potassium states stimulate cellular uptake via insulin-mediated stimulation of sodium-pump activity in muscle and stimulate potassium secretion by the kidney via aldosterone-mediated enhancement of distal renal expression of secretory potassium channels (ROMK). Low potassium states result in insulin resistance, impairing potassium uptake into muscle cells, and cause decreased aldosterone release, lessening renal potassium excretion.

In the general population, data are difficult to estimate; however, probably fewer than 1% of people on no medications have a serum potassium level of lower than 3.5 mEq/L. Potassium intake varies according to age, sex, ethnic background, and socioeconomic status. Whether these differences in intake produce different degrees of hypokalemia or different sensitivities to hypokalemic insults is not known. Up to 21% of hospitalized patients have serum potassium levels lower than 3.5 mEq/L, with 5% of patients achieving potassium levels lower than 3 mEq/L. Of elderly patients, 5% demonstrate potassium levels lower than 3 mEq/L.

Hypokalemia generally is associated with higher morbidity and mortality, especially due to cardiac arrhythmias or sudden cardiac death. However, an independent contribution of hypokalemia to increased morbidity/mortality has not been conclusively established.

Patients who develop hypokalemia often have multiple medical problems, making the separation and quantitation of the contribution by hypokalemia, per se, difficult. Some suggestion is observed of increased frequency of diuretic-induced hypokalemia in African Americans. The higher frequency of hypokalemia in this group may be due to the lower intake of potassium among African American men (approximately 25 mEq/d) than in their white counterparts (70-100 mEq/d).

Some suggestion also is observed of increased frequency of diuretic-induced hypokalemia in women. With age, frequency increases, due to increased use of diuretics and poor diet, which often is low in potassium.

HYPONATREMIA

Serum sodium concentration and serum osmolarity normally are maintained under precise control by homeostatic mechanisms involving stimulation of thirst, secretion of antidiuretic hormone (ADH), and renal handling of filtered sodium. Clinically significant hyponatremia is relatively uncommon and is nonspecific in its presentation; therefore, the physician must consider the diagnosis in patients presenting with vague constitutional symptoms or with altered level of consciousness. Irreparable harm can befall the patient when abnormal serum sodium levels are corrected too quickly or too slowly. The physician must have a thorough understanding of the pathophysiology of hyponatremia to initiate safe and effective corrective therapy. The patient's fluid status must be accurately assessed upon presentation, as it guides the approach to correction.

Though clearly not indicative of the overall prevalence internationally, hyponatremia has been observed in as high as 42.6% of patients in a large acute care hospital in Singapore and in 30% of patients hospitalized in an acute care setting in Rotterdam.

Pathophysiologic differences between patients with acute and chronic hyponatremia engender important differences in their morbidity and mortality.

Patients with acute hyponatremia (developing over 48 h or less) are subject to more severe degrees of cerebral edema for a given serum sodium level. The primary cause of morbidity and death is brainstem herniation and mechanical compression of vital midbrain structures. Rapid identification and correction of serum sodium level is necessary in patients with severe acute hyponatremia to avert brainstem herniation and death.

Patients with chronic hyponatremia (developing over more than 48 h) experience milder degrees of cerebral edema for a given serum sodium level. Brainstem herniation has not been observed in patients with chronic hyponatremia. The principal causes of morbidity and death are status epilepticus (when chronic hyponatremia reaches levels of 110 mEq/L or less) and cerebral pontine myelinolysis (an unusual demyelination syndrome that occurs in association with chronic hyponatremia).

The distinction between acute hyponatremia and chronic hyponatremia has critical implications in terms of morbidity and mortality and in terms of proper corrective therapy. Overall incidence of hyponatremia is approximately equal in males and females, though postoperative hyponatremia appears to

be more common in menstruant females. Hyponatremia is most common in the extremes of age; these groups are less able to experience and express thirst and less able to regulate fluid intake autonomously.

Objectives of the study

1. Gain knowledge about the pathophysiology of Hypertension and electrolyte imbalances, what are the risk factors and how it is treated.

2. Gain insights about its manifestations and etiology.3. Be familiar with its possible complications4. Be well versed with its management5. Apply our learning to our nursing practice in the present and in the future as well

Reasons for choosing the disease

1. To have a full understanding of this disease since it is very common in the community2. To determine the distinctions of this disease from other diseases similar to it in terms of

manifestations.3. To evaluate if we became an effective health care providers to the patient who suffered from this

illness.4. To established a comprehensive knowledge of this disease.5. We find it very interesting

Biographical Data

The name of the patient is Mr. Precious Brando, a 47 year-old, male, born at Bagac, Bataan. He is Roman Catholic and a natural born Filipino citizen, currently residing at Bagac, Bataan, with his wife and his four children.

NURSING PROCESS

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MF

The patient works as a tricycle driver in their town. He works the whole day and perspires a lot. According to his wife, Mr. Precious Brando is a heavy drinker and a chronic smoker for almost 25 years. He consumes almost 21 bottles of gin and 2 packs of cigarette sticks/day. According to his wife, before the patient was diagnosed to have Hypertension in 1990, he stops from eating high-salty foods. The wife also stated that the patient is not fond of consuming fruits.

Pertinent Family History:

A. Genogram:

+

Legend:

MALE

FEMALE

F FATHER

M MOTHER

MR. DIABET

+ POSITIVE FOR HYPERTENSION

B. Narrative: As reflected in the genogram, the patient’s father and his oldest sister also suffered from hypertension which indicates that the said disease runs in their family. No other disease was seen similar to the patient except from hypertension.

History of Past Illness

According to the patient’s wife, the patient has no known serious illness, only occasional cough and colds.

History of Present Illness

The patient was diagnosed as having hypertension in the year 1990. He was able to control his high blood pressure by taking the prescribed anti-hypertensive drug for 8 months which he could not remember the name. However, the patient wasn’t able to comply with his medication regimen and didn’t have follow up consultation because of financial problem.

Few days prior to patient’s admission, the patient experienced headache, nausea and vomiting from unknown reasons, increase in his blood pressure, muscle weakness and drowsiness. He was rushed in a local hospital in Bagac and experienced seizures during his stay. They were advised for transfer to another hospital for further management.

On September 01, 2009 at 3:05 pm, the patient was admitted to the emergency department of Isaac and Catalina Medical Center (ICMC) with chief complaints of increased in blood pressure and decrease sensorium. The attending physician asked the patient’s relative regarding the symptoms experienced by the patient and ordered a series of diagnostic exams which include SGPT, H. pylori test, HCT, BUN, serum creatinine, serum Na, serum K, Complete blood count, FBS, Chest X-ray, cranial CT-scan, and RBS

Body PartsNormal Findings Abnormal Findings

Hair And Scalp Evenly distributed thick, silky, resilient hair. No infection or infestation.

Face and Skull Rounded, smooth skull contour, absence of nodules or masses, symmetric or slightly asymmetric facial features, symmetric facial movements

Skin From light to deep brownUniform in colorNo edema lesions noted, no pigmentationBrings back to previous state after pinchingNormal temperature @ 37C

Eyes Symmetrically aligned with equal movements Slightly yellowish scleraEars Symmetrical in shape and aligned in the outer canthus of the eye

No tenderness, recoils after it is foiledNo discharge

Nose No discharge, no lesion and tenderness, no obstructionLips No blister/cracks, moistTooth and gums Pink gums, not swollen

Smooth and white shiny enamelDark gumsYellowish teeth

Tongue Centered, no lesions, smooth movement

PHYSICAL ASSESSMENT Vital Signs:BP:160/100T: 35.9P: 87R: 15

Neck Equal in size, head centered with muscles ( trapezius and sternocleidomastoid) equal in sizeNo unusual mass noted upon palpationNo enlargement of lymph nodesTrachea is in midline positionNo distention of veins, No enlargement of thyroid gland

Thorax and Lungs Spine is vertically aligned, no tenderness, pain, or unsual mass upon palpationTactile fremitus presentClear breath sounds

Heart Has a regular rate and rhythmAbdomen Unblemished skin

Uniform in color, no swelling or lump notedTympanic sound heard upon auscultationSymmetric contourSymmetric movements caused by respirationsNo tenderness

Extremities No edema, deformities, tenderness notedHave symmetrical lower and upper extremitiesClean fingernails and toenailsBlanch test ( color return < 3 seconds )

Dirty fingernails

NEUROVITAL SIGNS MONITORING Glasgow coma Scale:

Guidelines: 09/01/09 09/02/09Eye opening 4 4Motor response 6 6Verbal response 4 5Total 14 15

Laboratory procedures Date ordered Results in

Indications/ purposes Normal values Results Interpretation

BLOOD CHEMISTRY DO: 09/01/09@ 3pm

To determine any abnormalities in the chemical composition, structure, and properties of the blood

BUN: 2.9-9.3 mmol/LCreatinine: 4-150 umol/LS odium:135-145 mmol/LPotassium: 3.5-5.3 mmol/L

5.03 mmol/L

114.92 umol/L

101.2 mmol/L

1.75 mmol/L

This is a normal finding

This is a normal finding

This indicates hyponatremiaThis indicates hypokalemia

HGT DO: 09/01/09@ 3pm

HGT in mg/dl:60-130 mg/dLHGT in mmol/dl:3.3-7.2 mmol/dL

165

9.07SGPT DO: 09/01/09 0.38 IU/L 23.2 IU/L

ASSURE TEST (Helicobacter pylori Test)

DO: 09/01/09 To determine presence H. pylori in the blood

Negative Negative This is a normal finding

HGT DO: 09/01/09@ 7:15 pm

HGT in mg/dl:60-130 mg/dLHGT in mmol/dl:3.3-7.2 mmol/dL

127 mg/dL

7.0 mmol/dL

This is a normal finding

This is a normal finding

DIAGNOSTIC EXAMS

Hematology DO: 09/01/09 To determine any abnormalities in blood composition such as WBS, RBC, etc.

WBC:5-10 x 10 g/lHct:0.40Hgb:120-170Bleeding time:1-5 minsClotting time:3-7 minsReticulocyte:0.5-1.5%

Differential CountSegmenters:0.50-0.70Lymphocytes:0.20-0.40Bands/stabs:0-0.05Eosinophils:0.01-0.05Monocytes:0.01-0.08Basophils:0-0.01Platelet Count:150-450 x 10 g/lErythrocyte

8.7x10 g/l

0.53

175

n/a

n/a

n/a

0.84

0.12

n/a

0.0-0.12

0.04

0-0.12

248x10g/l

This is a normal finding

This is a normal finding

This is a normal finding

BLOOD CHEMISTRY 09/02/09 To determine any abnormalities in the

FBS in mg/dl:70-105 129

chemical composition, structure, and properties of the blood

FBS in mmol/L:3.9-5.8Cholesterol:3.1-7.3Triglycerides:0.45-1.81HDL0.78-195LDL:1.72-4.63Na:135-145K:3.5-5.5Calcium:2.1-2.8Magnesium:1.58-2.55

7.1

3.4 mmol

0.45 mmol

0.78 mmol

2.54 mmol

n/a

n/a

1.75 mmol

2.38 mmol

This is a normal finding

This is a normal finding

This is a normal finding

This is a normal finding

This indicates hypocalcemia

ANATOMY AND PHYSIOLOGY

CARDIOVASCULAR SYSTEM – responsible for the transport of O2 and CO2, nutrients and waste products.

I. Anatomy of the Heart

Location: Apex- left at 5th intercostals

space Base-towards the shoulder at

2nd rib

Coverings and wallsPericardium- a double layer sac that encloses the heart

Three layers Epicardium- outer layer Myocardium- middle layer Endocardium- inner layer

Heart Chambers Atria- upper receiving chambers Ventricles- lower pumping

chambers

Heart ValvesAV Valves- between atria and ventricles

Bicuspid- left AV valve Tricuspid- right AV valve

Semilunar Valves Pulmonic- at the pulmonary

trunk Aortic- at the aorta

Cardiac Circulation Coronary arteries- supplies

blood to the heart

II. Physiology of the Heart

Conduction System of the Heart

Two types of controlling system1. Autonomic Nervous System Symphatetic stimulation-

increases heart rate

Parasymphatetic stimulation– decreases heart rate

2. Nodal System SA Node – atrial contraction AV Node AV Bundle Bundle Branches Purkinje Fibers

CARDIOVASCULAR SYTEM: THE BLOOD VESSELS

Arteries- carries blood away from the the heartVeins-brings blood back to the heart

Tunics Interna Media Externa

Physiology of CirculationArterial Pulse – alternating expansion and recoil of an artery that occurs with each beat of the ventricles

Blood Pressure – pressure the blood exerts against the inner walls of the blood vessels

Systolic Pressure- the pressure in the arteries at the peak of ventricular contraction

Diastolic Pressure- the pressure when the ventricles are relaxing

Peripheral Resistance- amount of friction encountered by a blood as it flows through the blood vessels

Factors affecting Blood Pressure Neural factors Renal factors Temperature Chemicals Diet

Variations in Blood PressureHypotension- low BP; systolic BP of below 100 mmHg

Hypertension- 140/90 or higher

FLUID AND ELECTROLYTE BALANCEFluid Compartments- main location of water within the body

Intracellular Fluid (ICF)- 2/3 of the body fluids, contained within the living cells

Extracellular Fluid (ECF) – 1/3 of the body fluids;all body fluids outside the cells; includes blood plasma, interstitial, CSF and serous fluids

*Very small changes in electrolyte balance, the solute concentration in various fluid compartments cause water to move from one compartment to another

Sodium- the major extracellular cation, important for water balance, conduction of nerve impulse and muscle contraction

Potassium- the major intracellular cation, necessary for the conduction of nerve impulse and muscle contraction

SYNTHESIS OF THE DISEASE

Factors that predisposed the client to having hypertension includes age in which 30-50 years old are at high risks, being a male is also a risk according to statistics. Smoking which has a vasoconstrictive effect secondary to nicotine content of cigarette played a significant role in the pathogenesis of Hypertension. Likewise, excess alcohol consumption may also increase client’s risks.

Nicotine caused vasoconstriction and consequently narrowing of the lumen of the blood vessels. These both increases the peripheral resistance which increases arterial blood pressure and decreased blood flow which deprived O2 to muscle cells causing muscle weakness and to brain cells which can cause disorientation and irritability.

PATHOPHYSIOLOGY OF HYPERTENSION (client-centered)

Modifiable Non-modifiableAge (30-50) SmokingGender (Male) Heavy alcohol consumption

Vasoconstriction

Narrowed lumen

Increased peripheral resistance

Decreased O2 supply in muscle cells

Decreased blood flow

Increased intravascular pressure

Muscle weakness

Decreased blood flow in the brain

Dizziness Irritability Disorientation

BP of more than 120/90

SYNTHESIS OF THE DISEASE

Factors that predisposed the client to having electrolyte imbalances include poor intake, GI losses (vomiting), excessive perspiration and chronic alcoholism. These factors caused decreased Sodium in extracellular spaces leading to osmotic shift of water. Osmosis can in turn result to increased intracellular edema. The most sensitive cells are the neurologic cells in the brain. Increased in the volume of these cells causes increased ICP which resulted to headache and seizure.

On the other hand, when there is decreased potassium in extracellular spaces due to the above factors, there will be a decreased nerve conduction and muscle contraction. This will lead to symptoms such as disorientation and muscle weakness respectively. Slowed smooth muscle contraction is also the reason for nausea and vomiting.

PATHOPHYSIOLOGY OF HYPOKALEMIA AND HYPONATREMIA (client-centered)

Nausea and vomiting

Slowed smooth muscle contraction

Muscle weakness

IrritabilityDizziness

Disorientation

Decreased neuronal excitability

Decreased action potential

Decreased depolarization

Decreased potassium in extracellular fluid

Seizures

Headache

Increased ICP

Increased brain cell volume

Intracellular edema

Osmotic shift of water

Decreased Sodium in extracellular fluid

Modifiable FactorsPoor intake

GI losses (vomiting)Excessive perspiration

Chronic alcoholism

SIGNS AND SYMPTOMS WITH ETIOLOGY

Headache – because of increased in intracranial pressure caused by fluid shift

Seizures – increased ICP that exceeds seizure threshold

Irritability, dizziness, disorientation – caused by decrease Oxygen supply in the brain or decreased nerve conduction

Nausea and vomiting – resulted from decreased smooth muscle contraction

Muscle weakness – because of decreased muscle contraction secondary to low levels of potassium and sodium; caused also by decreased Oxygen supplies to muscle cells