Medsurg Midterm Reviewer PDF

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St. Mary's School

2024

Ramos, Monette A.

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body fluid electrolytes homeostasis medical terminology

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This document is a midterm reviewer for a medical surgical course (NCMB312). It covers body fluid and electrolytes, including components, distribution, and regulation. This document also discusses the systemic routes of gains and losses for water and electrolytes.

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[NCMB312] MEDSURG 1 MIDTERM REVIEWER NAME: RAMOS, MONETTE A. MIDTERM | BSN 3-YA-2B 3rd YEAR | A.Y. 2023 - 2024 WEEK 7: LESSON 1: BODY FLUID AND ELECTROLYTES ECF is further subdivided into compartments. The two In good health, a delicate balance of fluids, elect...

[NCMB312] MEDSURG 1 MIDTERM REVIEWER NAME: RAMOS, MONETTE A. MIDTERM | BSN 3-YA-2B 3rd YEAR | A.Y. 2023 - 2024 WEEK 7: LESSON 1: BODY FLUID AND ELECTROLYTES ECF is further subdivided into compartments. The two In good health, a delicate balance of fluids, electrolytes, acids, main compartments of ECF are: and bases maintains the body. a) Intravascular fluid/Plasma This balance, or homeostasis, depends on multiple accounts for approximately 1/3 of ECF and is physiological processes that regulate fluid intake and output, found within the vascular system. as well as the movement of water and the substances b) Interstitial fluid dissolved in it between body compartments. accounting for approximately 2/3 of ECF, Almost every illness has the potential to threaten this balance. surrounds the cells. Even in daily living, factors such as excessive temperatures or vigorous activity can disturb homeostasis if adequate water The other compartments of ECF include and salt intake are not maintained. 1. Lymph Therapeutic measures, such as the use of diuretics or 2. Transcellular fluids. nasogastric suction, can also disturb the body's homeostasis Examples unless water and electrolytes are replaced. ○ Cerebrospinal 50-60% of body weight is water. ○ Pericardial Two factors that influence body water distribution: ○ Pancreatic ○ Age ○ Pleural ○ Gender ○ Intraocular Infants — 70-80% ○ Biliary Most of their body fluid are found in ECF. ○ Peritoneal Fluids in the ECF can easily be lost. ○ Synovial fluids The fluid-electrolyte balance of an infant can easily be upset Male — 60% There are great amount of water in the male body than female body Because male are more muscular than female Muscle can store water Female — 50% Female have more adipose tissue than males. Fats do not store water. SYSTEMIC ROUTES OF GAINS AND LOSSES Water is vital to health and normal cellular function, serving Systemic Routes of Gains and Losses Water and electrolytes as: are gained in various ways. 1. A medium for metabolic reactions within cells. Healthy people gain fluids by drinking and eating, and their 2. A lubricant. daily average intake and output (1 & 0) of water are 3. A transporter for nutrients, waste products, and other approximately equal (Table 10-2). substances. 4. An insulator and shock absorber. 5. A means of regulating and maintaining body temperature 6. Eliminate waste Products DISTRIBUTION OF BODY FLUIDS The body's fluid is divided into two major compartments: 1. Intracellular fluid (ICF) Found within the cells of the body. Constitutes approximately two thirds of the total body fluid in adults. (2/3) Vital to normal cell functioning. It contains solutes such Insensible Water Loss as oxygen, electrolytes, and glucose, and it provides a Is invisible vaporization from the lungs and skin. Normally, medium in which metabolic processes of the cell take 600 to 900 ml/day is lost. place. Only water is lost by insensible perspiration. 2. Extracellular fluid (ECF) ○ Excessive sweating (sensible perspiration) due to fever, Found outside the cells and or high environmental temperature causes large losses Accounts for about one third of total body fluid. (1/3) of water and electrolytes. Although ECF is smaller of the two compartments, it is the transport system that carries oxygen and nutrients Body Fluid Regulation to, and waste products from. body cells. Under normal conditions, the following mechanisms regulates normal fluid volume and electrolyte concentrations: 1 1. Osmoreceptors Hydrostatic pressure is the pressure exerted by 2. ADH fluid on the walls of the blood vessel. 3. RAAS Hydrostatic pressure pushes fluid out of the 4. ANP capillary toward the ICF. Specialized neurons in the hypothalamus 2. Osmotic pressure Highly sensitive to serum osmolality is the pressure exerted by the solutes within the Increased osmolality osmoreceptors stimulates hypothalarnus plasma. to synthesize ADH (vasopressin) Osmotic pressure pulls fluid into the capillary from Decreased osmolality - ADH (vasopressin) is inhibited (ADH: the ICF. Retains water in the renal tubules) Triggers thirst promoting increased fluid intake Thirsty when ECF volume decreases by approx 700ml (2% of body weight) Also sensitive to changes in BV & BP through the info relayed by baroreceptors (stretch) Fluids & electrolytes move among cells, compartments, tissue spaces, and plasma by the processes of: These forces oppose each other at every capillary membrane and balance each other out in healthy (homeostatic) conditions. 3. Oncotic pressure Osmotic pressure specifically exerted by the albumin within the bloodstream is termed colloid oncotic pressure or colloid osmotic pressure. A colloid is fluid consisting of nonsoluble substances that are evenly distributed within a solvent. Blood is an example of a colloid solution. It is a mixture of blood cells and plasma which contains water, proteins, enzymes, and other solutes. These forces oppose each other at every capillary membrane and balance each other out in healthy 1. Osmosis (homeostatic) conditions. Movement of water/liquid/solvent across a semipermeable membrane from a lesser concentration 2. DIFFUSION to a higher concentration. Movement of particles, solutes, molecules from an area of Osmolality and osmolarity are terms that describe the higher concentration to an area of a lower concentration concentration of solutes or dissolved particles in a through a semipermeable membrane. solution. Factors affecting rate of diffusion: ○ Osmolality a. Size of the molecules: larger size moves slower than ○ Osmolarity smaller size. Osmolality is the number of milliosmoles of solute (the b. Concentration of solution: wide difference in standard unit of osmotic pressure) perkilogram of concentration has a faster rate of diffusion. solvent; it is expressed as milliosmoles per kilogram c. Temperature: 1 in T = 1 rate of diffusion (mOsm/kg). Osmolarity is the number of milliosmoles (the standard unit of osmotic pressure) per liter of solution; it is expressed as milliosmoles per liter (mOsm/L). Facilitated Diffusion Require assistance from a carrier molecule to pass through a semipermeable membrane. E.g., insulin-glucose Regulation of Fluid within the Body Compartments Normal movement of fluids through the capillary wall into the tissues depends on Starling's Laws of Capillary Forces. Capillary forces are the two forces at every capillary membrane: 1. Hydrostatic Pressure (Hydraulic Pressure) 2 Electrolytes Substances present in ICF & ECF that carry electrical charge. These charged particles are called Electrolytes. ○ Cations(+) ○ Anions(-) The major "cations" in body fluid are sodium, potassium, calcium, magnesium, and hydrogen ions. The major "anions" are; ○ Chloride ○ Bicarbonate 3. Filtration ○ Phosphate Movement of both solute and solvent across a ○ Sulfate semipermeable membrane from an area of higher pressure to ○ Negatively charged protein ions. lower pressure Movement of water and solutes occurs from an area of high hydrostatic pressure to an area of low hydrostatic pressure. Example: The kidneys filter approximately 180 L of plasma per day. 4. Active Transport Movement of solute from lower concentration to higher concentration using energy (ATP) e.g., Na-K pump FUNCTION OF ELECTROLYTES IN THE BODY 1. Promote neuromuscular irritability (muscle contraction and relaxation). 2. Maintain body fluid volume and osmolality. 3. Distribute body water between fluid compartments. 4. Regulate acid-base balance. SODIUM (Na+) - 135 - 145 mEq/L (mmol/L) Major cation in ECF; major contributor of plasma osmolality ECF Na+ level determines whether water is retained, excreted or translocated. SODIUM-POTASSIUM PUMP Functions: ○ Skeletal/ heart muscle contraction, nerve impulse transmission, Normal ECF osmolality, Normal ECF volume. SODIUM (Na+) and Water Regulator ○ Thirst: Is the major control of actual fluid intake. The thirst center in the hypothalamus is activated once the body loses at least 2% of fluids. ○ Kidneys: The major organs controlling output. Excrete average of 1,500 ml of fluids/day in form of urine. ○ ADH. Retains water in the renal tubules. ○ RAAS. Aldosterone retains sodium and water. Sodium primarily determines osmolality (concentration). body fluids. COMPOSITION OF BODY FLUID POTASSIUM (ECF: 3.5 - 5.0 mEq/L or mmol/L) Extracellular and intracellular fluids contain oxygen from the Major ICF cation lungs, dissolved nutrients from the gastrointestinal tract, Functions: excretory products of metabolism such as carbon dioxide, and ○ Regulates CHON synthesis, glucose use & storage, charged particles called "ions". maintains action potentials in excitable membranes 3 Any change in blood K+ seriously affects physiologic activities ○ Regulated by the kidney & GIT (exact mechanism are (a decrease of 1 meq/L = 25% difference in total ECF K+ not known) concentration) POTASSIUM.(K+) Regulator CHLORIDE (CI-) 98 - 106 meq/L (mmol/L) ○ Aldosterone and hydrogen ions regulate potassium Major ECF anion; work with Na+ to maintain ECF osmotic level. pressure ○ Aldosterone retain sodium and excretes potassium. Important in the formation of HCL in the stomach (Aldosterone is pro-Na+," and anti - K+.") ○ Participates in chloride shift (exchange between CI & ○ Increase aldosterone secretion: Hypokalemia HCO3) ○ Decrease aldosterone secretion: Hyperkalemia ○ Alkalosis increase potassium excretion that result: Tonicity of Body Fluids Hypokalemia. Refers to the concentration of particles in a solution The ○ Acidosis decrease potassium excretion that result to: normal tonicity or osmolarity of body fluids is 275-290 Hyperkalemia. mOsm/L CALCIUM — 8.8 - 10.5 mg/dl (2.25 - 2.75 mmol/L) 1. Isotonic Fluid 2 forms: Body fluids are ISOTONIC comparable with 0.9% 1. Bound: attached to CHON (albumin) NaCl 2. Unbounce (lonized): 2. Hypotonic Fluid "Free" calcium have a lesser or lower solute conc. than plasma; ex. Active form is 0.45%, 0.33%NaCl soln ECF 3. Hypertonic Fluids have a higher or greater conc. of solutes (usually Functions: sodium) compared with plasma; ex. is D5 NS ○ Bone strength & density, activation of enzymes or reactions, skeletal/ cardiac muscle contraction, nerve impulse transmission, blood clotting CALCIUM (Ca++)Regulation ○ Ca++ and phosphorus: 99% found in bones and teeth, 1% in blood. ○ Ca++ and phosphorus have inverse relationship. ○ If both are elevated: insoluble precipitate will form. ○ Low total CHON (Protein) and albumin: low total serum Ca++ ○ Parathormone (PTH) elevates serum calcium levels through withdrawal of calcium from bones or bone resorption. Increase PTH: Increase serum calcium Decrease PTH: Decrease serum calcium ○ Thyrocalcitonin lowers serum calcium levels by depositing calcium into the bone. Increase Thyrocalcitonin: decrease serum calcium Decrease Thyrocalcitonin: Increase serum calcium Vitamin D promote calcium absorption. PHOSPHORUS (P) 2.5 - 4.5 mg/dl (0.8-1.45 mmol/L) Major anion ICF (80% is in bones) Functions: ○ Activating B-complex vitamins, ATP, assisting in cell division, cooperating in CHO, CHON & FAT metabolism, acid-base buffering, calcium homeostasis; balanced & reciprocal relationship w/ Ca++ PHOSPHORUS (P) Regulator ○ Regulated by PTH: PTH = P PTH = P MAGNESIUM (Mg++) 1.8-3.6 mg/dl (0.75-1.07 mmol/L) 60% stored in bones & cartilages; much more is stored in ICF WEEK 7: LESSON 2: FLUID VOLUME IMBALANCES (heart, liver, skeletal muscles) FLUID VOLUME DISTURBANCES Functions: Hypovolemia ○ ICF - skeletal muscle contractions, CHO metabolism, Fluid volume deficit (FVD), or hypovolemia, occurs when loss ATP formation, Vitamin B-complex activation, DNA of ECF volume exceeds the intake of fluid. synthesis, CHON synthesis It occurs when water and electrolytes are lost in the same ○ ECF - regulates blood coagulation & skeletal muscle proportion as they exist in normal body fluids, so that the ratio contractility of serum electrolytes to water remains the same. 4 Different from dehydration Not as valid in older adults because the skin has ○ FVD (hypovolemia) should not be confused with lost elasticity. DEHYDRATION, which refers to loss of water alone, Slowness in filling of veins of the hands and feet with increased serum sodium levels. FUNCTIONAL ASSESSMENT ○ FVD may occur alone or in combination with other ○ Nurse provides if the patient is unable to carry out imbalances. self-care activities ○ Serum electrolyte concentrations can remain normal, ○ ↓ OFI due to avoid Urinary Incontinence increase, or increase in FVD. Wear diapers CAUSES Urinal ○ Loss of body fluids + fluid intake Pace fluid intake ○ Abnormal fluid losses ○ Remind to drink adequate fluids (very warm or humid ○ Vomiting weather) ○ Diarrhea ○ Correction of Fluid Loss ○ GI suctioning Oral route (If not severe) ○ Sweating IV (If acute or severe) ○ Decreased intake Isotonic electrolyte solutions (For hypotensive ○ Nausea patient with FVD to expand plasma volume) ○ Lack of access to fluids Lactated Ringer's ○ Third space fluid shifts 0.9% NaCl Edema (In burn) Hypotonic (Normotensive, to provide electrolytes Ascites (liver dysfunction) and water for renal excretion of metabolic wastes ○ Diabetes insipidus -0.45% NaCl Decreased ability to concentrate urine (deficit of MEDICAL MANAGEMENT ADH or nephron resistance to ADH) ○ Strict Monitoring (to avoid volume overload) Interferes with water reabsorption I&O ○ Adrenal insufficiency Weight Impaired production of aldosterone Vital signs Osmotic diuresis DCVP ○ Increase in urine output CLOC Hemorrhage Breath sounds Coma Skin color CLINICAL MANIFESTATION Treatment is based on the severity of fluid loss and ○ Acute weight loss pt. response ○ ↓ skin turgor ○ Depressed Renal Function (Oliguria) ○ Oliguria Determine the cause of depressed renal function ○ Concentrated urine Prerenal azotemia (FVD) ○ Capillary filling time prolonged Intrarenal azotemia (Acute tubular necrosis ○ ↓ CVP from prolonged FVD) ○ ↓ BP ○ Fluid challenge test (While hemodynamic response to ○ Flattened neck veins this treatment is t is monitored) ○ Dizziness Administer 100 to 200 mL of normal saline solution ○ Weakness over 15 minutes ○ Thirst and confusion Vital signs ○ ↑ pulse Breath sounds ○ Muscle cramps Sensorium ○ Sunken eyes CVP ○ Nausea UO ○ ↑ temperature Provide fluids rapidly enough to attain adequate ○ Cool, clammy, pale skin tissue perfusion without compromising the DIAGNOSTICS cardiovascular system. ○ ↑ Hgb and Hct ↑ UO,↑ BP,↑ CVP (Normal renal function) ○ ↑ Serum osmolality 25% intravascular volume loss or rapid fluid ○ ↑ Urine osmolality volume loss. ○ ↑ Urine specific gravity ○ ↓ Urine Na ○ ↑ BUN and Creatinine GERONTOLOGIC CONSIDERATIONS ○ 1 & O from all sources ○ Daily weight ○ SE & interaction of medications ○ Documentation and prompt reporting of disturbances ○ In most adult patients, it is useful to monitor skin turgor to detect subtle changes. 5 NURSING MANAGEMENT ↑ in total body water (Due to sodium) ○ Intake and Output CAUSES ○ q8 or q1 (Accurate) ○ Fluid overload or function of the homeostatic ○ May impact the mortality of patients mechanisms responsible for regulating fluid balance. ○ Expect a concentrated urine Heart failure ○ Daily body weight Renal failure ○ 0.5 kg weight loss is approximately 500 ml fluid loss Cirrhosis of the liver ○ Closely monitored ○ Another contributing factor Tachycardia (weak) Consumption of excessive amounts of table/other Severe hypotension sodium salts Tachypnea Excessive administration of sodium-containing Peripheral pulses fluids CVP CLINICAL MANIFESTATION Temperature ○ Expansion of the ECF ○ Skin and tongue turgor Edema Pinch skin Ambulatory (ankles) Dependent on interstitial fluid volume Supine (sacrum) Skin flattens more slowly Distended jugular veins Remain elevated for many seconds (Severe) Crackles Over the sternum ○ Tachycardia Dorsal surface of the hand ○ Bounding pulse Inner aspects of the thighs ○ ↑BP Forehead ○ ↑CVP Tongue turgor is not affected by age ○ Respiration system Smaller tongue Tachypnea Longitudinal furrows Shortness of breath Crackles Cough Orthopnea Signs and Symptoms ○ GI system Acute weight gain Ascites ○ Other s/sx Peripheral edema ○ Dry mouth Jugular veins distention ○ Urine Specific Gravity UO > 1.020 DIAGNOSTICS Healthy renal conservation of fluid ○ ↓Hgb and Hct Mental Function (Severe FVD) ○ ↓Serum & urine osmolality ↓ cerebral perfusion ○ ↓Urine Na & specific gravity Mild anxiety ○ Chest x-ray may reveal pulmonary congestion Confusion and agitation MEDICAL MANAGEMENT Lack of cognition, and delirium ○ Pharmacologic Therapy Comatose Diuretics ○ Acute cardiopulmonary decompensation Inhibits the reabsorption of Na and H20 Extensive hemodynamic monitoring The choice of diuretic is based on: ○ Preventing Hypovolemia ○ Severity of the hypervolemic state Identify patients at risk and take measures to ○ Degree of impairment of renal function minimize fluid losses ○ Potency of the diuretic ○ Correcting Hypovolemia Thiazide diuretics Coral fluids Block Na reabsorption in the distal Coral rehydration solutions convoluted tubule (dct) Antiemetics Mild to moderate hypervolemia If oral is not effective Hydrochlorothiazide Parenteral Loop diuretics Enteral Block Na reabsorption in the ascending limb of the loop of henle Hypervolemia Severe hypervolemia Fluid volume excess (FVE), or hypervolemia, refers to an Furosemide (lasix) expansion of the ECF caused by the abnormal retention of water and sodium in approximately the same proportions in which they normally exist in the ECF. Isotonic expansion of the ECF 6 ○ Drinking water (1 mg or more than 1500 mg of sodium per quart) Distilled water (very high in Na) Bottled water (0 to 1200 mg/L) Water softener (+ Na) ○ Check label before drinking ○ ↑ Protein intake NURSING MANAGEMENT ○ Rest Bed rest favors diuresis of fluid ↑ In EFFECTIVE circulating blood volume and renal perfusion Diminished venous pooling ○ Vital Signs MEDICAL MANAGEMENT Note for BP ○ Dialysis Bounding pulse Hemodialysis Tachycardia Peritoneal dialysis ○ Intake & Output Done daily or at regular intervals to identify excessive fluid retention ○ Weight Measured daily 2.2 lb 1 L of fluid ○ Breath Sounds Assessed at regular intervals Crackles Wheezing Diminished breath sounds ○ Edema Monitor the degree of edema Feet and ankles Sacral region ○ Continuous renal replacement therapy Pitting edema A special type of dialysis that we do for unstable Pressing a finger into the affected part patients in the ICU whose bodies cannot tolerate Peripheral edema regular dialysis. Instead of doing it over four hours, Measuring the circumference of the extremity CRRT is done 24 hours a day to slowly and continuously clean out the waste products and fluid from the patient." ○ Nutritional Therapy ○ Support arms and legs to ↓ dependent edema Dietary restriction of Na ○ Other nursing mgt. 6 to 15 g of salt/day Check for loc 250 mg of Na/day Maintain safety Mild sodium - restricted diet Positioning Avoid foods high in Na Na and fluid restriction bacon, sausage, sardines, caviar Avoid OTC medications pizza, burritos Avoid water softeners spam Avoid Parenteral fluids (with Na) salted nuts Prevent skin breakdown beans Slow healing process Sodium salt contributes to edema Turn and reposition at regular intervals lemon juice, onions, and garlic (substitute Pulmonary edema flavoring) Diuretics as ordered Salt substitutes ○ Educating patients about edema Contains K (WOF Hyperkalemia) Recognize and understand edema ○ K sparring diuretics Expansion of the interstitial fluid compartment ○ Advanced kidney disease ↑ Capillary fluid pressure Ammonium chloride Dependent edema ○ harmful in pt. with liver disease Heart failure 7 Hypoproteinemia ↓Capillary oncotic pressure Step 2: Compute for the intracellular fluid volume (63% of the ↑Interstitial oncotic pressure total body water is intracellular fluid) Localized edema Ankle, rheumatoid arthritis ICF = (36 liters) (0.63) Generalized edema = 22.7 Ilters Cardiac failure Anasarca Extracellular Fluid Compartment (ECF) Fluid found outside the cells. It comprises 1/3 (37%) of the total body water. One-third (1/3) of the ECF is in plasma BODY FLUID COMPUTATION Example: How much water is in the circulatory system of a ○ Medications that could cause edema 32-year old female patient who weighs 52 kg? NSAIDS — Inhibits natriuretic effect Estrogens — decreased blood flow in the legs Step 1: Compute for the total body water based on age and Corticosteroids — has an anti-inflammatory sex. property Antihypertensives TBW = (52 kg) (0.5) Vasodilatory edema = 26 kg — weight of water Ascites = 26 liters — volume of water Fluid accumulates in the peritoneal cavity Shortness of breath Step 2: Compute for the extracellular fluid volume (usually Sense of pressure 37% of the total body water). ECF = (26 liters) (0.37) = 9.6 liters Step 3: Compute for the plasma volume. Plasma = (9.6 liters)/3 = 3.2 liters ○ Preserve or restore the circulating intravascular fluid volume Diuretic therapy Restriction of fluids and Na Elevation of the extremities Application of anti-embolism stockings Paracentesis Dialysis Continuous renal replacement therapy WEEK 8: FLUID, ELECTROLYTE IMBALANCES Serum Osmolality FLUID BALANCE Reflects the amount of solute particles in a solution and is a Intracellular Fluid Compartment (ICF) measure of the concentration of a given solution. Fluid found inside the cells. Can be calculated using the formula: It comprises 2/3 (63%) of the total body water. BODY FLUID COMPUTATION (mg/dL) Glucose (mg/dL) BUN = Approximate Value of Serum Normal value = 275-290 mOsm/kg Sodium is the most active determinant of serum osmolality and is therefore actively moved across membranes to ensure osmolality. EXAMPLE: How much water is in the intracellular fluid ELECTROLYTE IMBALANCES AND MANAGEMENT compartment (ICF) of a 25-year old male patient who weighs SODIUM IMBALANCES 60 kg? Sodium (Na+) (135-145 meq/L) The primary extracellular cation. Step 1: Compute the total body water based on age and sex. Always accompanies water in the extracellular fluid compartment. TBW = (60 kg) (0.6) = 36 kg — weight of water Hyponatremia = 36 liters — volume of water Defined as serum sodium less than 135 meq/L. 8 Most common electrolyte abnormality observed in a general ○ Decreased water intake (elderly, debilitated, hospitalized population. unconscious clients) Initial approach is the determination of serum Initial osmolality ○ Excessive administration of solutions containing It is caused by sodium loss or water excess. SODIUM Causes: ○ Excessive water loss without accompanying low sodium ○ Diuretics Clinical manifestation: (↑ECF and ↓ICF volume: ICF ○ Low sodium diet Dehydration) ○ Excessive ingestion estion of plain water ○ Extreme thirst ○ Profuse diaphoresis & diuresis ○ Dry, sticky mucous membranes ○ Administration of electrolyte - free solution ○ Oliguria ○ Prolonged vomiting, GI suctioning, draining fistulas ○ Firm, rubbery tissue turgor ○ Edema, ascites, burns ○ Fever ○ Addison's disease (Low aldosterone secre ○ Rough, red, dry swollen tongue ○ Lethargy ○ Restlessness, tachycardia, fatigue Disorientation, hallucination ○ Coma if severe Clinical Findings: ○ Intact thirst mechanisms usually prevent hypernatremia. ○ Its presence is commonly associated with encephalopathy of any cause, or cerebrovascular disease. ○ Orthostatic hypotension and oliguria are typical. Hyperthermia, delirium and coma may be seen with severe hyperosmolality. Treatment ○ Low sodium diet. ○ ↑OFI or administer D5W per IV. ○ Diuretics ○ Dialysis ○ Directed toward correcting the cause of the fluid loss and replacing water and, as needed, electrolytes. Clinical manifestations: (JECF and ICF volume) ○ IV administration of hypotonic solutions ○ Headache Calculation of water deficit: ○ Muscle weakness, fatigue and apathy ○ When calculating fluid replacement, both the deficit and ○ Anorexia, nausea and vomiting the maintenance requirement should be adc each ○ Abdominal cramps 24-hour replacement regimen. ○ Weight loss ○ Calculation of water deficit (cont'd) ○ Postural hypotension Volume to be replaced ○ Seizure, Coma = current TBW x ([Na] -140) 140) Treatment where [Na] is the measured serum sodium. ○ Administration of NaCl 0.9% per IV, plasma expanders (hetastarch). To prevent shock. EXAMPLE: ○ Sodium rich foods in diet 1. A 32y/o 60kg male patient with hypernatremia with Nursing management serum sodium of Na+160 meq/L ○ Identify and monitor patients at risk for hyponatremia. ○ Monitors I&O (identify excess water input or lack of Step 1: Compute for the total body water based on age sufficient water output) and sex. ○ Daily body weight ○ Safety precautions (side rails, supervision of ambulation) TBW = (60 kg) (0.6) = 36 kg — weight of water Hypernatremia = 36 liters — volume of water Serum sodium greater than 145 meq/L Develops from excess water loss, frequently accompanied by an impaired thirst Step 2: Compute for the Volume to be replaced mechanism. Sodium and water excess resulting to edema. Causes: = 36 x 160 - 140 140 = 36 ○ Sodium tablets ○ Hypokalemia, hypercalcemia or sickle cell anemia can = 36 x.14285 ○ cause nephrogenic diabetes insipidus. = 5.14 liters ○ Hyperventilation Nursing management ○ Profuse watery diarrhea ○ Fluid losses and gains are carefully monitored in ○ Excessive salt intake without sufficient water intake patients who are at risk for hypernatremia. 9 ○ Obtains a medication history (1 sodium content) Check for OTC medications (1 sodium content) ○ Monitor I and O ○ Restrict sodium diet ○ Administer diuretics as prescribed ○ Promote safety. ○ Monitored closely for changes in behavior, such as restlessness, disorientation, and lethargy. HIGH IMPACT CONCEPT: ○ Hyponatremia — increase ICF Volume = "Cell swell" ○ Hypernatremia — decrease ICF Volume = "Cell shrink” Respiratory arrest ○ Cardiovascular system: Hypotension Dysrhythmias Myocardial damage POTASSIUM IMBALANCES Cardiac arrest Potassium (Na+) 3.5 - 5.0 meq/L ○ Kidney: Major ICF cation Regulates CHON synthesis, glucose use & Water loss storage, maintains action potentials in excitable membranes. Thirst Renal damage Hypokalemia Note: Hypokalemia also increases the likelihood of A total body deficit of about 350 mEq occurs for each 1 meq/L digitalis toxicity decrement in serum potassium concentration. Changes in ECG changes blood pH and hormones (insulin, aldosterone, and ○ ST-segment depression ẞ-adrenergic agonists) independently affect serum potassium ○ Flat or inverted T wave levels. ○ Increased U wave Causes: ○ K+ wasting diuretics (furosemide [Lasix], ethacrynic acid [Edecrin], hydrochlorothiazide [HydroDIURIL] ○ Severe vomiting & diarrhea, draining intestinal fistula, prolonged suctioning ○ Large doses of corticosteroids ○ IV administration of insulin & glucose Treatment: ○ Prolonged administration of non electrolyte parenteral ○ Elimination of the cause fluids ○ Substitute K-wasting with K-sparing diuretics Clinical Manifestations: Note: Due to ↓ neuromuscular (Spirinolactone [Aldactone] irritability ○ Increase oral intake of K-rich foods/K supplements ○ GI Tract: (Safest way) (mild cases) Anorexia ○ Intravenous replacement is indicated for patients with Nausea & Vomiting Abdominal distention severe hypokalemia. Paralytic ileus. ○ Occasionally, hypokalemia may be refractory to ○ CNS: potassium replacement. Magnesium deficiency may Lethargy make potassium correction more difficult. Concomitant Diminished deep tendon reflexes (hyporeflexia) magnesium repletion avoids this problem. Confusion Mental depression ○ Muscle: Weakness Fatigue Leg cramps Flaccid paralysis Weakness of respiratory muscles Tetany and rhabdomyolysis Nursing management: ○ Monitor for its early presence in patients at risk. Fatigue, anorexia, muscle weakness, decreased bowel motility, paresthesia's, and arrhythmias are signals that warrant assessing the serum potassium concentration. Monitored closely for signs of digitalis toxicity. NURSING ALERT!!! NEVER administer Potassium Chloride (KCI) per IV push or direct IV. 10 ○ This may cause dysrhythmias and cardiac arrest. "No pee No potassium" (UO >30ml/Hr.) to prevent renal damage. KCL to IV should nor exceed 60mEq/L (preferred level: 30mEq/L) Rate should not exceed 10-20mEq/ Hr. to prevent hyperkalemia and cardiac arrest. Use Infusion Pump HIGH IMPACT CONCEPT: Treatment: ○ Decreased neuromuscular irritability "Everything is low ○ Confirm that the elevated level of serum potassium is and slow" genuine. ○ Measure plasma potassium. Withholding of potassium. Hyperkalemia ○ Giving cation exchange resins by mouth or enema: Many are spurious or associated with acidosis. Common Polystyrene sulfate, 40-80 g/day in divided doses. practice of repeatedly clenching and unclenching the fist ○ Emergent treatment is indicated if cardiac toxicity or during venipuncture may raise the potassium concentration muscular paralysis is present, or if hyperkalemia is by 1-2 meq/L by causing local release of muscles from severe (>6.5-7 meq/L) even in the absence of ECG forearm muscles. changes. ○ Insulin plus 10-50% glucose may be employed to deposit potassium with glycogen in the liver. ○ Calcium gluconate per IV may be given intravenously as an antagonist ion. (Antidote for hyperkalemia) ○ Stimulate transcellular shifts by giving beta-adrenergic agonist drugs. ○ Sodium bicarbonate as an emergency measure. Hemodialysis or peritoneal dialysis Nursing management: ○ Encouraging the patient to adhere to the prescribed potassium restriction. ○ Potassium-rich foods to be avoided include many fruits and vegetables, legumes, whole-grain breads, lean meat, milk, eggs, coffee, tea, and cocoa. ○ Check labels of cola beverages (1 K+) Clinical Manifestations: Note: Due to neuromuscular ○ Monitors I&O and observes for signs of muscle irritability weakness and arrhythmias. ○ Gl Tract: ○ When measuring vital signs, an apical pulse should be Nausea & Vomiting taken. Diarrhea HIGH IMPACT CONCEPT: Colic ○ Increased neuromuscular irritability "everything is high ○ CNS: and fast" Numbness ○ The main route for potassium excretion are the kidneys Tingling Muscle CALCIUM IMBALANCES Irritability (Early) Weakness (Late) Calcium (Ca2+) 8.5-10.5 mg/dL Flaccid paralysis Bone strength & density, activation of enzymes or reactions, Hyperkalemia skeletal/ cardiac muscle contraction, nerve impulse ○ Cardiovascular transmission, blood clotting Constitute 2% of body weight, but Ventricular fibrillation only 1% of the total body calcium is in solution in body fluid. Cardiac arrest In plasma, calcium is present as a non-diffusible complex with ○ Kidney: protein (33%); as a diffusible but undissociated complex with Coliguria anions like citrate, bicarbonate, and phosphate (12%); and as Anuria ionized calcium (55%). Hyperkalemia It is the ionized calcium that is necessary for muscle Clinical Findings contraction and nerve function (normal: 4.7 to 5.3 mg/ dL). ○ Peak T waves ○ Prolonged PR intervals Hypocalcemia ○ Flat or absent P wave Seen commonly in critically ill patients due to acquired defects ○ Wide QRS complex in parathyroid-vitamin D axis. Results occasionally in hypotension which responds to calcium replacement therapy Causes: 11 ○ Decrease dietary intake ○ Excess loss of calcium (Renal disease, draining fistula) Calcium absorption (Vit D deficiency, Hypoparathyroidism, hyperthyroidism, hypermagnesemia) ○ Acute pancreatitis ○ Corticosteroids ○ Rapid administration of multiple units of blood that contain an anti-calcium additive Hypercalcemia ○ Intestinal malabsorption Causes: ○ Accidental removal of parathyroid glands ○ Excessive intake of calcium Clinical manifestation: Note: cell membrane permeability = ○ Excessive doses of vitamin D neuromuscular irritability ○ Calcium loss from bone (Immobilization, carcinoma with ○ Central nervous system: bone metastases) Tingling ○ Parathyroid gland tumors Convulsions ○ Multiple fractures ○ Gastrointestinal tract: ○ Hyperparathyroidism Increased peristalsis ○ Certain malignant diseases (multiple myeloma, acute Nausea and vomiting leukemia, lymphomas) Diarrhea Clinical manifestations: Note: cell membrane permeability Abdominal Pain neuromuscular irritability ○ Muscles: ○ Central nervous system: Muscle spasm Diminished deep-tendon reflexes Laryngospasm with stridor Lethargy Tetany (Chvostek's sign and Trousseau's sign) Mental changes (decreased memory & attention ○ Cardiovascular system: span) Dysrhythmias, Coma Cardiac arrest. ○ Gastrointestinal tract: Decreased peristalsis (constipation, paralytic Other signs and symptoms: ileus). ○ Bones: Anorexia Osteoporosis Fracture (these are due to Nausea & vomiting decreased calcium deposited into the bones) ○ Muscles: Laboratory Findings: Muscle fatigue ○ Low serum calcium Hypotonia ○ Elevated serum phosphorus Hypercalcemia ○ Low serum magnesium ○ Cardiovascular system: ○ Prolonged QT interval on the ECG Depressed electrical activity (dysrhythmias) Treatment: Cardiac arrest ○ Asymptomatic hypocalcemia: Other signs and symptoms: High Calcium diet ○ Bones: Oral calcium and vitamin D preparations. Deep bone pain Calcium carbonate is well tolerated and Osteoporosis inexpensive. Pathologic fractures ○ Severe symptomatic hypocalcemia ○ Kidneys: In the presence of tetany, arrhythmias or seizures, Thirst calcium gluconate 10% is administered Polyuria intravenously for 10-15 minutes or via calcium Dehydration infusion. Stones 10-15 mg of calcium per kilogram body weight, or Renal damage 6-8 10-ml vials of 10% calcium gluconate (558-744 Treatment: mg of calcium) is added to 1 liter of D5W and ○ Determining & correcting the cause infused over 4 to 6 hours. ○ Increase fluid intake(3-4L/day) Limit Ca++ consumption Nursing Management: (mild cases ○ Closely monitor for neurologic manifestations (tetany, ○ Provide acid-ash fruit juice (Cranberry & prune juice) seizures, spasms) and vitamin C. ○ Seizure precautions ○ 0.45% or 0.9%NaCL (acute cases) and diuretics: ○ Provide bed rest for comfort, avoid falls (Prevent fracture furosemide (Lasix); oral phosphates; calcitonin ○ Cardiac dysrhythmias & airway obstruction Monitor (Cibacalcin) Corticosteroids or plicamycin (Mithracin) breathing (laryngospasm) used for malignant diseases that do not respond to other ○ Check for signs of bruising or bleeding forms of therapy HIGH IMPACT CONCEPT: To remember clinical Nursing Management: manifestations ○ Encourage increased fluid intake ○ Encourage high fiver diet 12 ○ Collaborates with dietitian to limit food sources of Ca++ ○ Cardiovascular system: ○ Ambulation as tolerated. (prevent hypercalcemia or Tachycardia minimize severity) Hypertension ○ Provide assistance; avoid falls Dysrhythmias ○ Increased calcium increases the effects of digitalis ○ Positive Babinski response (WOF Toxicity) Laboratory Findings: ○ Monitor cardiac rate and rhythm for any abnormalities ○ Decreased serum magnesium levels HIGH IMPACT CONCEPT: To remember clinical ○ Hypocalcemia and hypokalemia manifestations ○ Prolonged QT interval on the ECG ○ Lengthening of the ST segment on the ECG Treatment: ○ Magnesium rich diet Use of IVF containing magnesium as chloride or sulfate, 240-1200 mg/day (10-50 mmol/day) during the period of severe deficit, followed by 120 mg/day (5mmol/day) for maintenance. MgSO4 may also be given intramuscularly in a dosage of 200-800 mg/day (8-33mmol/day) in four divided doses. ○ Serum levels must be monitored. MAGNESIUM IMBALANCES Nursing management: Magnesium (Mg2+) 1.8-3.6 mg/dl ○ Encourage and provide food rich in magnesium About 50% of total body magnesium exists in the insoluble ○ Promote safety, protect client from injury. state in bone. ○ Monitor for laryngeal stridor. (Airway obstruction) Only 5% is present as extracellular cation; the remaining 45% ○ Administer magnesium oral supplement or IV as is contained in cells as intracellular cation. prescribed. Normal plasma concentration is 1.5-2.5 meq/L, with about ○ If giving MgSO4, always check the BP!!! (vasodilation) one-third bound to protein and two-thirds existing as free HIGH IMPACT CONCEPT: To remember clinical cation. manifestations Excretion is via the kidney. Hypomagnesemia Nearly half of hospitalized patients have unrecognized hypomagnesemia. In critically ill patients, arrhythmias and sudden death may be complications. Causes: ○ Chronic alcoholism Hypermagnesemia ○ Severe renal disease Almost always the result of renal insufficiency and the inability ○ Severe malnutrition or starvation to excrete what has been taken in from food or drugs, ○ Intestinal malabsorption syndromes Excessive diuresis especially antacids and laxatives. (drug induced) Potentially life-threatening as it impairs both central nervous ○ Prolonged gastric suction system and muscular function. ○ Draining fistula Causes: Clinical manifestations: ○ Excessive intake of magnesium containing antacids Note: Magnesium inhibits acetylcholine release. ○ Renal failure ○ Therefore, in hypomagnesemia, there is increased ○ DKA acetylcholine release. Clinical Manifestations: ○ Central nervous system: Note: Magnesium inhibits acetylcholine release. Therefore, in Convulsions hypermagnesemia, there is decreased acetylcholine release Paresthesia ○ Decreased BP Tremor ○ Thirst Ataxia ○ Nausea and vomiting Athetoid movements ○ Drowsiness Jerking ○ Diminished or loss of deep tendon reflexes. Nystagmus ○ Muscle weakness ○ Mental changes: ○ Mental obtundation and confusion Agitation ○ Respiratory muscle paralysis or cardiac arrest Depression Laboratory Findings: Confusion and disorientation ○ Elevated serum magnesium, BUN, creatinine, K ○ Muscles. ○ Decreased serum calcium Weakness ○ Increased PR interval on the ECG Cramps ○ Broadened QRS complex with elevated T waves Spasticity Treatment: Tetany ○ Correct underlying cause. ○ Alleviating renal insufficiency 13 ○ Administration of fluids and diuretics ○ Oral phosphate supplements (mild hypophosphatemia, ○ Administration of calcium gluconate per IV as prescribe. renal-wasting disorders, malabsorption, or oncogenic (antagonize magnesium) osteomalacia) ○ Hemodialysis or peritoneal dialysis ○ Vitamin D may (enhance absorption of phosphorus and Nursing Management: calcium). ○ Closely observe for dysrhythmias & early signs of ○ IV phosphorus correction is usually limited to the patient neuromuscular irritability Antidote: Calcium gluconate whose serum phosphorus levels decrease to less than 1 (kept available) mg/dL (0.3 mmol/L). ○ Monitoring of 1&0 Monitor vital signs (hypotension and ○ Monoclonal antibody-type drug, burosumab, (renal shallow respirations) phosphate wasting disorders and hypophosphatemic. ○ Provide health teaching rickets) Nursing management: PHOSPHORUS IMBALANCES ○ TPN: gradually introducing the solution to avoid rapid Phosphorus (P) 2.5-4.5 mg/dl shifts of phosphorus into the cells. Activating B-complex vitamins, ATP, assisting in cell division, ○ Frequently monitors serum phosphorus levels and cooperating in CHO, CHON & FAT metabolism, acid-base documents and reports early signs of buffering, calcium homeostasis; balanced & reciprocal hypophosphatemia (apprehension, confusion, change in relationship w/ Ca++ level of consciousness). ○ Encouraged intake of milk and milk products, organ Hypophosphatemia meats, beans, nuts, fish, poultry, and whole grains. Causes: ○ IV preparations of phosphorus: the rate of phosphorus ○ Inadequate intake administration should not exceed 3 mmol/h, monitor the ○ GI malabsorption disorders (chronic, diarrhea, Crohn's ○ IV site regularly to prevent tissue sloughing and necrosis disease, or celiac disease). due to infiltration. ○ Anorexia & bulimia ○ Alcoholism. ○ Vitamin D deficit (cause low phosphate levels in the Hyperphosphatemia bloodstream). Causes: ○ High intake of antacids. ○ Kidney injury (diminishes urinary phosphate excretion) ○ Heatstroke high phosphate intake ○ Prolonged intense hyperventilation ○ Shift of phosphate from the ICF to ECF. Excessive ○ Alcohol withdrawal vitamin D intake ○ DKA ○ Hypoparathyroidism ○ Respiratory alkalosis ○ Metabolic or respiratory acidosis ○ Hepatic encephalopathy ○ DKA ○ Major thermal burns Clinical Manifestation: ○ Hyperparathyroidism Note: Most symptoms result from decreased calcium levels ○ Hypophosphatemia and soft tissue calcifications. Clinical Manifestation: ○ Tetany Note: Most of the signs and symptoms of phosphorus ○ Tachycardia deficiency result from a deficiency of ATP, 2,3- ○ Anorexia diphosphoglycerate, or both. ○ Nausea and vomiting ○ Paresthesia's ○ Muscle weakness ○ Muscle weakness ○ Signs and symptoms of hypocalcemia ○ Bone pain and tenderness ○ Hyperactive reflexes ○ Chest pain ○ Soft tissue calcifications in lungs, heart, kidneys, and ○ Confusion cornea ○ Cardiomyopathy Treatment: ○ Respiratory failure ○ Phosphate intake should be reduced and phosphate ○ Seizures binders can be given with meals to reduce ○ Hypophosphatemia hyperphosphatemia. ○ Tissue hypoxia ○ Treatment of underlying disorder. ○ Increased susceptibility to infection Nystagmus ○ Calcium carbonate or calcium citrate are (to lower blood Treatment: phosphate levels). WOF: hypercalcemia ○ Prevention of hypophosphatemia is the goal. Oral ○ Sevelamer and lanthanum (Not calcium containing) phosphate supplements (mild hypophosphatemia, Sucroferric oxyhydroxide (iron supplementation) Forced renal-wasting disorders, malabsorption, or oncogenic diuresis with a loop diuretic or saline diuresis can be osteomalacia) used in patients with normal renal function. ○ Vitamin D may (enhance absorption of phosphorus and ○ Hemodialysis calcium). ○ Hyperphosphatemia ○ IV phosphorus correction is usually limited to the patient Nursing management: whose serum phosphorus levels decrease to less than 1 ○ Instructed to avoid phosphorus rich foods, such as hard mg/dL (0.3 mmol/L). cheeses, cream, nuts, meats, whole-grain cereals, dried ○ Prevention of hypophosphatemia is the goal. 14 fruits, dried vegetables, kidneys, sardines, and dairy ○ ABG analysis foods. ○ Hyperkalemia ○ Monitors urine output during diuresis ○ ECG: Tall-peaked T wave ○ Educates the patient about recognizing the signs of MEDICAL/NURSING MANAGEMENT: hypocalcemia, such as muscle cramping, ○ Correct underlying cause ○ Bronchodilator WEEK 8: LESSON 2: ACID-BASE IMBALANCES ○ Postural drainage ACID-BASE IMBALANCES ○ Semi-fowler's position Body fluids contains acids & bases aside from electrolytes ○ Chest clapping H2CO3 acid & base content influence the pH ○ Na Bicarbonate for ventricular fibrillation or potassium HCO3 of the body (amount of H+ in a solution) excess Regulation of pH is accomplished by: ○ Buffer systems Respiratory Alkalosis ○ Kidneys Carbonic Acid Deficit ○ Lungs Loss of CO2 from the lungs at a faster rate than it is produced in the tissue Buffer System CAUSES: Remove or release hydrogen ion ○ Hyperventilation Excessive hydrogen ion (ACIDOSIS) → buffers bind ○ EXCESSIVE release of Carbon dioxide in the LUNGS Decrease in hydrogen ion (ALKALOSIS) → buffers release ○ Anxiety, Fever, Meningitis hydrogen ion ○ ASA Poisoning ○ Pneumonia Renal Regulation ○ Pulmonary Embolism Eliminates or retains HC03 CLINICAL MANIFESTATIONS: Eliminates or retains hydrogen ion ○ Lightheadedness ○ Numbness or tingling of fingers or toes (hypocalcemia) ○ Late: tetany convulsions ○ Hyperpnea (increased RR and depth) ○ Potassium deficit (hypokalemia) DIAGNOSTICS: ○ ABG analysis ○ Hypokalemia Respiratory Regulation ○ hypocalcemia Retains or eliminates Carbon Dioxide (potential acid) MEDICAL/NURSING MANAGEMENT: ○ Correct underlying cause ○ BROWN BAG ○ Slow breathing ○ Purse-lip breathing RESPIRATORY ACID BASE IMABALANCE CYCLE Respiratory Acidosis Carbonic Acid Excess Failure to the respiratory system to remove CO2 from body fluids as fast as it is produces in the tissue. CAUSES: ○ Hyperventilation ○ DISORDERS that restrict/limit the RELEASE of Carbon dioxide in the LUNGS OCOPD ○ Impaired movement of Thoracic Cage ○ Depressed respiratory center ○ Neuromuscular disease CLINICAL MANIFESTATIONS: ○ Tachypnea (increased RR and depth) Metabolic Acidosis ○ Tachycardia Bicarbonate Deficit ○ Visual disturbances Result from abnormal accumulation of fixed acids or loss of ○ Headaches, restlessness base. ○ Drowsiness, confusion CAUSES: ○ Diaphoresis ○ Loss of bicarbonate (HCO3) ○ Ventricular fibrillation ○ Intestinal loss ○ Cyanosis (hypoxia) ○ Diuretics ○ Late: confusion, drowsiness, coma ○ Accumulation of acids ○ Increased ICP (severe) ○ Lactic acid ○ Potassium excess (hyperkalemia) ○ Ketoacids DIAGNOSTICS: ○ Uremia/Azote 15 ○ Salycilate poisoning ○ Identify and treat underlying cause, e.g., excessive intake of sodium bicarbonate or baking soda, vomiting, CLINICAL MANIFESTATIONS: gastric suctioning, intestinal fistulas. ○ Headache ○ Avoid antacids ○ Mental dullness ○ Anti-emetics ○ TRR ○ Kaussmaul's breathing (Deep, rapid breathing which is ACIDOSIS ALKALOSIS an attempt to blow off CO2) ○ Hyperkalemia — CNS Depressant — CNS stimulant ○ CNS depression — CNS vasodilation — CNS vasoconstriction DIAGNOSTICS: — Increased ICP — Increased ICP ○ ABG analysis — Peripheral — Peripheral ○ Hyperkalemia vasoconstriction vasoconstriction ○ ECG: Tall Peaked T-wave (Hypertension) (Hypotension) — Hyperkalemia — Hyperkalemia MEDICAL/NURSING MANAGEMENT: — Hypocalcemia ○ Maintain good respiratory function. ○ Fluid replacement. Water loss may result from hyperventilation. ACID BASE IMBALANCES ○ Protect the client from injury. Risk for injury related to Information obtained from the arterial blood gas measurements: mental dullness. pH ○ Restore electrolyte balance, specifically potassium. Partial pressure of carbon dioxide (PaCO2) ○ Administer Sodium Bicarbonate per IV as prescribed. Partial pressure of oxygen (PaO2) ○ Identify and treat underlying cause, e.g., renal failure, HCO3 level DM, starvation ketoacidosis, shock, chronic diarrhea, Oxygen saturation (O2Sat) ASA. ○ Hemo/peritoneal dialysis ACID-BASE DISTURBANCES Metabolic Alkalosis Normal values: Bicarbonate Excess pH — (Acidosis) < 7.35 - 7.45 > (Alkalosis) Result from loss of hydrogen ion or addition of base to body PaCO2 — (Base) 35 - 45 mmHg (Acid) fluid. HCO3 — (Acid) 22 - 26 meqs/L (Base) CAUSES: PaO2 — (Hypoxia) 80 - 100 mmHg ○ Gain of bicarbonate (HCO3) 02Sat — 95% - 100% Alkali intake ○ Loss of hydrogen ion Vomiting Suction pH PaCO2 HCO3 ○ Loss of potassium Diuretics Alkalosis Acidosis ↓ ↓ ↓ CLINICAL MANIFESTATIONS: ○ Hypoventilation (the body's attempt to conserve CO2) Alkalosis Alkalosis ↑ ↑ ↑ ○ Mental confusion ○ Dizziness Metabolic Acidosis ↓ ↑ ↑ ○ Numbness and tingling of fingers and toes Metabolic Alkalosis ↑ ↓ ↓ ○ Muscle twitching, tetany and seizures (these are due to hypocalcemia because alkalosis damages ionized calcium) 3 STEPS ABG INTERPRETATION ○ Potassium deficit (hypokalemia). 1. Identify if it is acidosis or alkalosis (PH). ○ Decreased Gl motility and paralytic ileus 2. Identify if it is respiratory or metabolic (CO2/HCO3). ○ OECG: extra "U" wave 3. Identify if it is uncompensated or compensated (Partial or Fully). DIAGNOSTICS: ○ ABG analysis 1. Identify if it is acidosis or alkalosis (PH). ○ Hypokalemia ○ ECG: Extra "U" wave PH - 7.25 = Acidosis MEDICAL/NURSING MANAGEMENT: PH - 7.55 = Alkalosis ○ Maintain good respiratory function. ○ Protect the client from injury. Seizures may occur. 2. Identify if it is Respiratory or Metabolic (CO²/HCO3) ○ NaCl or Ammonium Chloride oral or intravenous. ○ KCL infusion PaCO² - ABNORMAL ○ Diamox (Acetazolamide). This is carbonic anhydrase HCO³ - NORMAL inhibitor that increases excretion of bicarbonate by the = RESPIRATORY kidneys. 16 = RESPIRATORY WEEK 9: LESSON 1: BURN INJURY Burns PaCO² - NORMAL Burns is one of the most devastating experiences that a HCO³ - ABNORMAL human individual could ever have, especially in cases of = METABOLIC severe burns. It affects the physiologic, psychologic, social, economic, and spiritual aspects of a person's life. EXAMPLE: Tissue damage caused by exposure to excessive heat. 1. pH - 7.25 = ACIDOSIS Traumatic injury to the skin and underlying tissues caused by PaCO2 - 37 = NORMAL heat, chemical, & electrical injuries (most severe!!!) degree of HCO3 - 21 = ABNORMAL tissue damage is related to: What agent caused the burn = METABOLIC ACIDOSIS UNCOMPENSATED degree of tissue damage is related to: ○ What agent caused the burn ○ Temperature of the burning agent 2. pH - 7.56 = ALKALOSIS ○ Duration of contact with the agent PaCO2 - 40 = NORMAL ○ Thickness of the skin HCO3 - 35 = ABNORMAL = METABOLIC ALKALOSIS UNCOMPENSATED TYPES OF BURNS BY ETIOLOGY 1. Thermal Burns Dry heat flames, hot objects 2. Chemical Burns COMPENSATION: Acids, alkali PaCO2 = ↑ Carbon dioxide = ACID - ACIDOSIS 3. Smoke and Inhalation injury = ↓ Carbon dioxide = BASE - ALKALOSIS Carbon monoxide poisoning, hot air, steam/smoke 4. Radiation Burns HCO3 = ↑ Bicarbonate = BASE - ALKALOSIS Ionizing radiation e.g., nuclear energy, radiation = ↓ Bicarbonate = ACID - ACIDOSIS therapy 5. Cold Thermal Injury (frostbite) Prolong exposure to cold. NORMAL VALUE: 6. Electrical Burns Normal pH: FULL compensation Electric current Abnormal pH: PARTIAL compensation Muscle contractions (Fracture) Risk for cervical spine injury (Fall) Electrical burn: Normal: 7.35 - 7.45 internal damage a. CNS complications, (N) ACIDOSIS SIDE (N) ALKALOSIS b. Cardiac dysrhythmias, SIDE c. Cardiac arrest, 7.35, 7.36, 7.37, 7.38, 7.39, 7.40, 7.41, 7.42, 7.43, 7.44, d. Severe metabolic acidosis, 7.45

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