1. Fluid Volume Balance
1.1. Regulated by three hormones: ADH, Aldosterone and atrial natiuretic peptide.
1.1.1. Aldosterone is secreted by the adrenal cortex and act on the distal tubule of the nephron. It regulates sodium balance by assisting to control blood volume and blood pressure.
1.1.1.1. ADH synthesize hypothalamus and secretes from the posterior pituitary gland. Osmoreceptors in the hypothalamus can sense osmality of the blood and give signal for ADH secretion. ADH causes vasoconstriction.
1.1.2. Atrial natiuretic peptide acts to: Inhibit aldosterone secretion by the adrenal cortex; Reduce renin released by the kidney; Reduce ADH release from posterior pituitary; as a vasodilator; Natriuresis and diuresis.
1.1.2.1. Causing excretion of sodium and water through the kidney by reduction of extracellular fluid volume to normal.
1.1.3. Nursing Diagnosis: Excess fluid volume related to compromised regulatory mechanism.
1.1.3.1. Outcome: Remain free from edema, maintain clear lung sounds, no evidence of dyspnea and remain free of jugular vein distention
1.1.3.2. Interventions: Daily weight preferably same time of day. Rational: Changes in weight indicates changes in body fluid volume.
1.1.3.3. Intervention: Monitor intake and output. Rational: Indicates trends in decreasing urine output related to fluid intake
1.1.3.4. Intervention: Administer diuretics as prescribed. Rational: To promote excretion of excess fluid.
1.1.3.5. Education: Monitor signs and symptoms of excess fluid volume. Educate on the importance of sodium and fluid restrictions. Ensure patient have an emergency plan and is able to execute action. Teach and reinforce knowledge of diuretics.
2. Electrolyte Balance
2.1. Electrolyte: Positively charged cations and negatively charged anions and are produced when salts, acids and bases dissolve in water.
2.1.1. Anion: Chloride, bicarbonate and phosphate
2.1.2. Electrolyte Processes: Simple diffusion, facilitated diffusion and active transport.
2.2. Some normal values: Potassium3.5-5.0 mmol/L, sodium 135-145 mmol/L and protein 64-83g/L
2.2.1. Hypokalemia Causes: Diuretics, magnesium depletion, hyperaldosteronism, dialysis, vomiting and diarrhea.
2.2.1.1. Hyperkallemia Causes: Potassium containing drugs, burns and crush injury
2.2.1.1.1. Symptoms: Irregular pulse, weakness of lower extremity, cardiac standstill and parestesias.
2.2.1.1.2. Treatment: Increase elimination of potassium eg use of diuretics, Kayexlate and salbutamol.
2.2.1.1.3. Education: Signs and symptoms of hyperkalemia. Teach the importance of taking medication as prescribed. Decrease dietary intake of potassium.
2.2.1.1.4. ECG Changes: Ventricular fibrillation, peaked T wave, ST depression, widening QRS and prolonged P-R intervals.
2.2.1.2. Symptoms: Leg cramp, muscle weakness, polyuria, weak irregular pulse and fatigue.
2.2.1.3. Treatment: Increase dietary intake of potassium and giving potassium chloride supplements.
2.2.1.4. Health Education: Signs and symptoms of hypokalemia. Report significant changes to health care provider. Increase dietary intake of potassium. Educate on potassium-sparing diuretics and avoid eating food high in potassium.
2.2.1.5. ECG Changes: Flattened T wave, ventricular dysrhythmias, bradycardia, ST segment depression and presence of U wave.
2.2.2. Hypernatremia Causes: Increase sweating, diabetes insipidus and osmotic diuresis
2.2.2.1. Symptoms: Increase thirst, aggitation, twitching, weakness postural hypotension and swollen tongue..
2.2.2.1.1. Diagnosis: Risk for deficient Fluid volume:
2.2.2.1.2. Outcome: Maintain normal blood pressure, pulse and temperature. Maintain adequate skin turgor, mucous membranes and moist tongue. Maintain orientation to person, place and time.
2.2.2.1.3. Nursing Intervention: Monitor for signs of hypovolemia, cyanosis, cold clammy skin, weak thready pulse, confusion and ogliuria.
2.2.3. Hyperproteinemia Causes: Dehydration, hemoconcentration
2.2.3.1. Symtpms: Numbness, tingling, weight loss, frequent infections.
2.2.4. Hypoproteinemia Causes: Starvation, massive burns, loss of albumin and major infection.
2.2.4.1. Symptoms: Infections, loss of muscle mass, swollen legs and face and fatigue.
2.3. Hyponatremia Causes: Diuretics, adrenal insufficiency, burns, wounds, vomiting and diarrhea.
2.3.1. Symptoms: Confusion, postural hypotension, tachicardia, rapid thready pulse, dry mucous membranes and weight loss.
3. Blood Pressure
3.1. Decrease in sodium concentration or increase in potassium cause a decrease in blood pressure which stimulate the adrenal cortex to release aldosterone.
3.1.1. Aldosterone target the kidneys affecting the distal tubule and collecting ducts, promoting sodium reabsorbtion and potassium secretion.
3.1.1.1. Water follows sodium therefore sodium and water is reabsorbed resulting increase plasma volume hence increase blood pressure.
3.1.1.1.1. Diagnosis: 160/95 or greater on three separate readings within reasonable intervals. Diagnostic: Routine urinalysis and serum creatinine, blood chemistry (sodium and potassium) and fasting blood sugar.
3.1.1.1.2. Causes: Renal artery stenosis, coartation or congenital narrowing of the aorta, Cushing's syndrome, hyperaldosteronism, sympathetic stimulant such as cocaine, estrogen replacement therapy, NSAID's and pregnancy induced
3.1.1.1.3. Manifestations: Fatigue, reduced activity tolerance, dizziness, palpitations, angina and dyspnea.
3.1.1.1.4. Risk Factors: Age, family history, gender, heavy alcohol consumption, high sodium intake, obesity, psychosocial stress, cigatette smoking ect.
3.2. Nursing Diagnosis: Risk for ineffective Renal Perfusion
3.2.1. Outcome: Patient will maintain normal blood urea nitrogen and serum creatinine levels, normal serum electrolytes, glomerular filtration rate of 60-89ml/min and normal urine output 0.5mL/kg/hr
3.2.2. Intervention: Monitor for edema. Rational: Edema is indicative of increased fluid retention related as a result of impaired renal function relating to decreased renal perfusion.
3.2.2.1. Intervention: Monitor intake and output. Rational: Calculate intake against output relating to increase fluid retention. Auscultate for crackles or rales. Rational: Indicative of fluid overload.
3.2.3. Intervention: Monitor vital sign. Rational: Hypotention can cause poor renal perfusion and acute renal failure.
3.3. Education: Medication teaching to include purpose and side effects. Cessation of smoking and alcohol, low sodium intake and regular exercise.
3.3.1. Medication Ace Inhibitors such as Benazepril and Enalapril. Loop diuretics as Furosemide and Bumetanide
3.3.1.1. If bp remains high it can lead damage in blood vessels in the body
4. Excretion of Waste Products
4.1. Metabolic waste: Creatinine generated from muscle, urea generated from protein and uric acid generated by the byproduct of prunes.
4.2. Ions: ammonium, bicarbonate, calcium, chloride, magnesium, phosphate and potassium
4.3. Bilirubin generated from hemoglobin
4.4. Metabolites generated from hormones such as human chorionic gonadotrophin. hCG is a hormone that when tested in the blood or urine is present to detect early pregnancy. hCG level starts at 20-50
5. Acid Base Balance
5.1. Keeping the pH of the body at an appropriate level
5.1.1. pH is determined by hydrogen ion concentration. Hydrogen ion come from cellular metabolism. Normal pH 7.35-7.45
5.1.2. Metabolic Acidosis: ph is below 7 meaning the hydrogen ion concentration of fluid is high.
5.1.2.1. Causes: Reduce renal excretion of acids and reduce renal reabsorbtion of bicarbonate
5.1.2.2. Symptoms: Drowsiness, headache, confusion, hyperkalemia, decreased BP and vomiting.
5.1.2.3. Interventions: Monitor vital signs, monitor lab work including ABGs, LOC and monitor intake and output.
5.1.2.4. Treatment: Evaluate and correct electrolyte imbalance, administration of IV sodium bicarbonate
5.1.3. Metabolic Alkalosis: ph is above 8 meaning the hydrogen ion concentration of body fluid is low.
5.1.3.1. Causes: Too many alkali-producing bicarbonate ions and too few acid-producing hydrogen ions. To correct this the kidney would reduce the amount of hydrogen ion secretion in the urine
5.1.3.2. Symptoms: Tachycardia, dysrhythmia, hypoventilation, irritability, vomiting and muscle cramps.
5.1.3.3. Interventions: Monitor lab work including ABG's. Monitor respiratory and heart rate, assess LOC, strength, tone, movement and Trousseau's sign. Encourage intake of fluids.
5.1.3.4. Treatment: Replace water and electrolytes.
5.1.4. C0₂+H₂O↔H₂CO₃↔H⁺+HCO₃⁻. Carbon dioxide is from the cell and is an end-product of metabolism and is distributed into plasma. Carbon dioxide combines with water to make carbonic acid which dissociates into hydrogen and bicarbonate which makes this is equilibrium.
5.1.4.1. An increase in concentration of any of component on one side will cause a shift the equation of the other side leading to increase concentrations of all components on that side.
5.2. Diagnosis: Impaired Gas exchange
5.2.1. Nursing Outcome: Adequate oxygenation, improved ventilation and normal parameters of blood gas.
5.2.1.1. Interventions: Monitor respiration rate, monitor O2 saturation and administer oxygen as needed, monitor for cyanosis,
5.2.2. Education: Demonstrate purse-lip breathing to patient. Cessation of smoking and educate patient on use of oxygen