case study about hypertension with electrolyte imbalance part 1

INTRODUCTION HYPERTENSION

Hypert Hypertens ension ion is one of the most most commo common n worldw worldwid ide e dis diseas eases es 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 arbitr arbitrary ary.. Furth Furtherm ermor ore, e, the relat relation ionshi ship p betwee between n system systemic ic arter arterial ial pres pressu sure re and and morb morbid idit ity y app appears ears to be quan quanti tita tati tive ve rath rather er than than qualit qualitati ative. ve. A level level for high high blood blood press pressur ure e must must be agree agreed d upon upon in clin clinic ical al prac practi tice ce for for scre screen enin ing g pati patien ents ts with with hype hypert rten ensi sion on and and for for instituting diagnostic evaluation and initiating therapy. Because the risk to an individual patient may correlate with the severity of hypertension, a clas classi sifi fica cati tion on syst system em is esse essent ntia iall for for maki makin ng deci decisi sion ons s abou aboutt aggressiveness of treatment or therapeutic interventions. Base Based d on reco recomm mmen enda dati tion ons s of the the Seve Sevent nth h Repo Report rt of the the Join Jointt National Committee of Prevention, Detection, Evaluation, and Treatment of High High Blood Blood Press Pressur ure e (JNC (JNC VII), VII), the class classifi ificat cation ion of blood blood press pressur ure e (expressed in mm Hg) for adults aged 18 years or older is as follows:    

Normal - Systolic lower than 120, diastolic lower than 80 Prehypertension 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 3050 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 other hand, hand, modif modifiab iable le factor factors s includ includes es diabet diabetes, es, stres stress, s, 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. Prehyperte Prehypertensio nsion, n, a new category category designat designated ed in the JNC VII report, 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 caus cause. e. Appro pproxi xim mately tely 95 95% % of Amer Americ ica an adults ults have have ess essenti ential al 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 Americ Americans ans.. In Mexica Mexican n Ameri American cans, s, the preval prevalenc ence e and incide incidenc nce e of  hypertension is similar to or lower than in whites. The National Health and Nutrition 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 grows sig signif nifica icantl ntly y with with increa increasin sing g age in all sex and race race groups groups.. Nati Nation onal al heal health th su surv rvey eys s in vari variou ous s coun countr trie ies s have have sh show own n a high high prevalence of poor control of hypertension. These studies have reported that that preval prevalenc ence e of hypert hypertens ension ion is 22 22% % in Canada Canada,, of which which 16 16% % is contr controll olled; ed; 26.3% 26.3% in Egypt, Egypt, of which which 8% is contr controll olled; ed; and 13.6% 13.6% in China, of which 3% is controlled. Hypertension is a worldwide epidemic; in many many coun countr trie ies, s, 50 50% % of the the popu popula lati tion on olde olderr than than 60 year years s has has hypert hypertens ension ion.. Overa Overall, ll, appro approxim ximate ately ly 20 20% % of the world' world's s adults 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. Pota Potass ssiu ium m home homeos osta tasi sis s is main mainta tain ined ed pred predom omin inan antl tly y thro throug ugh h the 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.

2. 3. 4. 5.

Gain knowledge about the pathophysiology of Hypertension and electrolyte imbalances, what are the risk factors and how it is treated. Gain insights about its manifestations and etiology. Be familiar with its possible complications Be well versed with its management 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 community 2. 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

NURSING PROCESS

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.  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:

F

+

+

Legend:

M

+

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

Normal Findings

Hair And Scalp

Vital Signs: BP:160/100 Face and Skull T: 35.9 P: 87 R: 15 Skin

Eyes Ears

Nose Lips Tooth and gums Tongue Neck 

Thorax and Lungs

Heart Abdomen

Extremities

Abnormal Findings

Evenly distributed thick, silky, resilient hair. No infection or infestation. Rounded, smooth skull contour, absence of  nodules or masses, symmetric or slightly asymmetric facial features, symmetric facial movements From light to deep brown Uniform in color No edema lesions noted, no pigmentation Brings back to previous state after pinching Normal temperature @ 37C Symmetrically aligned with equal movements Slightly yellowish sclera Symmetrical in shape and aligned in the outer canthus of the eye No tenderness, recoils after it is foiled No discharge No discharge, no lesion and tenderness, no obstruction No blister/cracks, moist Pink gums, not swollen Dark gums Smooth and white shiny enamel  Yellowish teeth Centered, no lesions, smooth movement Equal in size, head centered with muscles ( trapezius and sternocleidomastoid) equal in size No unusual mass noted upon palpation No enlargement of lymph nodes  Trachea is in midline position No distention of veins, No enlargement of thyroid gland Spine is vertically aligned, no tenderness, pain, or unsual mass upon palpation  Tactile fremitus present Clear breath sounds Has a regular rate and rhythm Unblemished skin Uniform in color, no swelling or lump noted  Tympanic sound heard upon auscultation Symmetric contour Symmetric movements caused by respirations No tenderness No edema, deformities, tenderness noted Dirty fingernails Have symmetrical lower and upper extremities Clean fin ernails and toenails

NEUROVITAL SIGNS MONITORING Glasgow coma Scale:

Guidelines: 09/01/09 4 Eye opening 6 Motor response 4 Verbal response Total DIAGNOSTIC EXAMS 14 Laboratory procedures BLOOD CHEMISTRY

09/02/09 4 6 5 15

Date Indications/ ordered purposes Results in  To determine any DO: abnormalities in 09/01/09 the chemical @ 3pm composition, structure, and

Normal values

BUN: 2.9-9.3 mmol/L Creatinine: 4-150 umol/L S odium:

Results

Interpretation

5.03 mmol/L

This is a normal finding

114.92

This is a normal

properties of the blood

135-145 mmol/L Potassium: 3.5-5.3 mmol/L

umol/L

finding

101.2 mmol/L

This indicates hyponatremia This indicates hypokalemia

1.75 mmol/L HGT

DO: 09/01/09 @ 3pm

SGPT

DO: 09/01/09

ASSURE TEST (Helicobacter pylori Test) HGT

DO: 09/01/09

Hematology

 To determine presence H. pylori in the blood

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

DO: 09/01/09

 To determine any abnormalities in blood composition such as WBS,

HGT in mg/dl: 60-130 mg/dL HGT in mmol/dl: 3.3-7.2 mmol/dL 0.38 IU/L

23.2 IU/L

Negative

Negative

This is a normal finding

127 mg/dL

This is a normal finding

HGT in mg/dl: 60-130 mg/dL HGT in mmol/dl: 3.3-7.2 mmol/dL WBC: 5-10 x 10 g/l Hct: 0.40

165 9.07

7.0 mmol/dL

8.7x10 g/l 0.53

This is a normal finding This is a normal finding

RBC, etc.

Hgb: 120-170 Bleeding time: 1-5 mins Clotting time: 3-7 mins Reticulocyte: 0.5-1.5% Differential Count Segmenters: 0.50-0.70 Lymphocytes: 0.20-0.40 Bands/stabs: 0-0.05 Eosinophils: 0.01-0.05 Monocytes: 0.01-0.08 Basophils: 0-0.01 Platelet Count: 150-450 x 10 g/l Erythrocyte

175 n/a n/a n/a

0.84 0.12 n/a 0.0-0.12 0.04 0-0.12

This is a normal finding

248x10g/l This is a normal finding

BLOOD CHEMISTRY

09/02/09

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

FBS in mg/dl: 70-105 FBS in mmol/L: 3.9-5.8 Cholesterol: 3.1-7.3 Triglycerides: 0.45-1.81 HDL 0.78-195 LDL: 1.72-4.63 Na: 135-145 K: 3.5-5.5 Calcium: 2.1-2.8 Magnesium: 1.58-2.55

129 7.1 3.4 mmol

This is a normal finding

0.45 mmol 0.78 mmol 2.54 mmol

This is a normal finding This is a normal finding

n/a n/a

This is a normal finding

1.75 mmol 2.38 mmol This indicates hypocalcemia

ANATOMY AND PHYSIOLOGY

Myocardi ummiddle layer Endocardi um- inner layer Heart Chambers CARDIOVASCULAR SYSTEM – responsible for the transport of O 2 and CO2, nutrients and waste products. I. Anatomy Heart

of

Atriareceiving chambers

upper

Ventricles- lower pumping chambers

the

Location:

Heart Valves AV Valves- between atria and ventricles



Apex- left at 5th intercostals space

Bicuspid - left AV valve



Base-towards the shoulder at 2 nd rib

Tricuspid- right AV valve Semilunar Valves

Coverings and walls Pericardium- a double layer sac that encloses the heart

Pulmonic- at the pulmonary trunk

Three layers Epicardiumouter layer

Aortic- at the aorta Cardiac Circulation Coronary arteriessupplies blood to the heart

II. Physiology of the Heart Conduction System of  the Heart Two types of   controlling system 1. Autonomic Nervous System Symphatetic stimulationincreases heart rate

2.

Parasymphateti c stimulation– decreases heart rate 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 heart Veins-brings blood back to the heart Tunics

Interna Media Externa

Physiology of   Circulation Arterial 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 pressure in arteries at peak ventricular contraction

the the the of  

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 Pressure Hypotensionlow BP; systolic

BP of below 100 mmHg Hypertension 140/90 or higher

FLUID AND ELECTROLYTE BALANCE Fluid Compartmentsmain 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

Sodiumthe 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

PATHOPHYSIOLOGY OF HYPERTENSION (client-centered)

Modifiable Age (30-50) Gender (Male) consumption

Non-modifiable Smoking Heavy alcohol

Vasoconstrictio n

Narrowed lumen

Increased peripheral resistance

Increased intravascular pressure

BP of more than 120/90

Decreased blood flow

Decreased O2 supply in muscle cells

Decreased blood flow in the brain

Muscle weakness

Disorientati on

SYNTHESIS OF THE DISEASE

Irritabili ty

Dizziness

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 HYPOKALEMIA AND HYPONATREMIA (client-centered) Modifiable Factors Poor intake GI losses (vomiting) Excessive perspiration Chronic alcoholism

Decreased potassium in extracellular fluid

Decreased Sodium in extracellular fluid

Decreased depolarization

Osmotic shift of  water

Decreased action potential

Muscle weakness

Slowed smooth muscle contraction

Intracellular edema

Decreased neuronal excitability

Increased brain cell volume

Increased ICP Nausea and vomiting

Irritability Dizziness Disorientation

Headache

Seizures

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.

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