Medical Surgical Nursing Fluid and Electrolytes

1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM GENERAL CONCEPTS Aged client - 40% Intake = Output = Fluid FLUID AND ELECTROLYTE Balance TRANSPORT Sensible losses...

1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM GENERAL CONCEPTS Aged client - 40% Intake = Output = Fluid FLUID AND ELECTROLYTE Balance TRANSPORT Sensible losses PASSIVE TRANSPORT ✓ Urination SYSTEMS ✓ Defecation ✓ Wound drainage ✓ Diffusion Insensible losses ✓ Evaporation from ✓ Filtration skin ✓ Osmosis ✓ Respiratory loss from lungs ACTIVE TRANSPORT SYSTEM FLUID COMPARTMENTS ✓ Pumping Intracellular ✓ 40% of body weight ✓ Requires energy Extracellular expenditure ✓ 20% of body weight DIFFUSION ✓ Two types o INTERSTITIAL Molecules move across a (between) biological membrane o INTRAVASCULAR from an area of higher to (inside) an area of lower concentration AGE-RELATED FLUID CHANGES Membrane types Full-term baby - 80% ✓ Permeable Lean Adult Male - 60% ✓ Semi-permeable  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM ✓ Impermeable ACTIVE TRANSPORT SYSTEM FILTRATION Solutes can be moved against a concentration Movement of solute and gradient solvent across a membrane caused by Also called “pumping” hydrostatic (water Dependent on the pushing) pressure presence of ATP Occurs at the capillary FLUID TYPES level If normal pressure Isotonic gradient changes (as Hypotonic occurs with right-sided heart failure) edema Hypertonic results from “third ISOTONIC SOLUTION spacing” No fluid shift because OSMOSIS solutions are equally Movement of solvent concentrated from an area of lower Normal saline solution solute concentration to (0.9% NaCl) one of higher concentration HYPOTONIC SOLUTION Occurs through a Lower solute semipermeable concentration membrane using osmotic Fluid shifts from hypotonic (water pulling) pressure solution into the more  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM concentrated solution to BARORECEPTOR REFLEX create a balance (cells Respond to a fall in swell) arterial blood pressure Half-normal saline Located in the atrial walls, solution (0.45% NaCl) vena cava, aortic arch HYPERTONIC SOLUTION and carotid sinus Higher solute Constricts afferent concentration arterioles of the kidney resulting in retention of Fluid is drawn into the fluid hypertonic solution to create a balance (cells VOLUME RECEPTORS shrink) Respond to fluid excess in 5% dextrose in normal the atria and great saline (D5/0.9% NaCl) vessels REGULATORY MECHANISMS Stimulation of these receptors creates a Baroreceptor reflex strong renal response that Volume receptors increases urine output Renin-angiotensin- aldosterone mechanism Antidiuretic hormone  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM RENIN-ANGIOTENSIN- RENIN-ANGIOTENSIN- ALDOSTERONE ALDOSTERONE Renin Aldosterone ✓ Enzyme secreted by ✓ Mineralocorticoid that kidneys when arterial controls Na+ and K+ pressure or volume blood levels drops ✓ Increases Cl- and ✓ Interacts with HCO3- concentrations angiotensinogen to and fluid volume form angiotensin I ALDOSTERONE NEGATIVE (vasoconstrictor) FEEDBACK MECHANISM RENIN-ANGIOTENSIN- ECF & Na+ levels drop → ALDOSTERONE secretion of ACTH by the Angiotensin anterior pituitary → release of aldosterone by ✓ Angiotensin I is the adrenal cortex → fluid converted in lungs to and Na+ retention angiotensin II using ACE (angiotensin ANTIDIURETIC HORMONE converting enzyme) Also called vasopressin ✓ Produces Released by posterior vasoconstriction to pituitary when there is a elevate blood pressure need to restore ✓ Stimulates adrenal intravascular fluid volume cortex to secrete aldosterone  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM Release is triggered by Cells shrink from fluid loss osmoreceptors in the and can no longer thirst center of the function properly hypothalamus CLIENTS AT RISK Fluid volume excess  Confused decreased ADH Comatose Fluid volume deficit  Bedridden increased ADH Infants FLUID IMBALANCES Elderly Enterally fed Dehydration WHAT DO YOU SEE? Hypovolemia Irritability Hypervolemia Confusion Water intoxication Dizziness Weakness DEHYDRATION Extreme thirst  urine output Loss of body fluids  Fever increased concentration Dry skin/mucous of solutes in the blood membranes and a rise in serum Na+ Sunken eyes levels Poor skin turgor Fluid shifts out of cells into Tachycardia the blood to restore balance  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM WHAT DO WE DO? WHAT DO YOU SEE? Fluid Replacement - oral Mental status or IV over 48 hrs. deterioration Monitor symptoms and Thirst vital signs Maintain I&O Tachycardia Maintain IV access Daily weights Delayed capillary refill Skin and mouth care Orthostatic HYPOVOLEMIA hypotension Isotonic fluid loss from the Urine output < 30 ml/hr extracellular space Cool, pale extremities Can progress to hypovolemic shock Weight loss Caused by: WHAT DO WE DO? ✓ Excessive fluid Fluid replacement loss (hemorrhage) Albumin replacement ✓ Decreased Blood transfusions for fluid intake hemorrhage ✓ Third space Dopamine to fluid shifting maintain BP MAST trousers for severe shock  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM Assess for fluid S3 gallop overload with Increased CVP, treatment pulmonary artery HYPERVOLEMIA pressure and pulmonary artery Excess fluid in the wedge pressure extracellular (Swan-Ganz) compartment as a result of fluid or sodium JVD retention, excessive Acute weight gain intake, or renal failure Occurs when Edema compensatory EDEMA mechanisms fail to restore fluid balance Fluid is forced into tissues by the Leads to CHF and hydrostatic pressure pulmonary edema First seen in WHAT DO YOU SEE? dependent areas Tachypnea Anasarca - severe Dyspnea generalized edema Pitting edema Crackles Pulmonary edema Rapid, bounding pulse Hypertension  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM WHAT DO WE DO? ✓ SIADH Fluid and Na+ ✓ Rapid infusion restriction of hypotonic solution Diuretics ✓ Excessive tap Monitor vital signs water NG Hourly I&O irrigation or enemas Breath sounds ✓ Psychogenic Monitor ABGs and polydipsia labs WHAT DO YOU SEE? Elevate HOB and give O2 as ordered Signs and symptoms of increased Maintain IV access intracranial pressure Skin & mouth care ✓ Early: change Daily weights in LOC, N/V, muscle WATER INTOXICATION weakness, twitching, Hypotonic cramping extracellular fluid shifts into cells to attempt to ✓ Late: restore balance bradycardia, widened pulse Cells swell pressure, Causes: seizures, coma  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM WHAT DO WE DO? Prevention is the best treatment Assess neuro status Monitor I&O and vital signs Fluid restrictions IV access Daily weights Monitor serum Na+ Seizure precautions  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM ELECTROLYTES MAJOR CATIONS Charged particles in EXTRACELLULAR solution ✓ SODIUM (Na+) Cations (+) INTRACELLULAR Anions (-) ✓ POTASSIUM Integral part of (K+) metabolic and ELECTROLYTE IMBALANCES cellular processes Hyponatremia/ POSITIVE OR NEGATIVE? hypernatremia Cations (+) Hypokalemia/ ✓ Sodium Hyperkalemia ✓ Potassium Hypomagnesemia/ Hypermagnesemia ✓ Calcium Hypocalcemia/ ✓ Magnesium Hypercalcemia Anions (-) Hypophosphatemia/ ✓ Chloride Hyperphosphatemia ✓ Bicarbonate Hypochloremia/ Hyperchloremia ✓ Phosphate ✓ Sulfate  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM SODIUM Aldosterone also has a function in water Major extracellular and sodium cation conservation when Attracts fluid and serum Na+ levels are helps preserve fluid low volume SODIUM-POTASSIUM PUMP Combines with Sodium (abundant chloride and outside cells) tries to bicarbonate to help get into cells regulate acid-base balance Potassium (abundant inside cells) tries to get Normal range of out of cells serum sodium 135 - 145 mEq/L Sodium-potassium pump maintains SODIUM AND WATER normal If sodium intake concentrations suddenly increases, Pump uses ATP, extracellular fluid magnesium and an concentration also enzyme to maintain rises sodium-potassium Increased serum Na+ concentrations increases thirst and Pump prevents cell the release of ADH, swelling and creates which triggers kidneys an electrical charge to retain water  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM allowing water loss; can be neuromuscular renal (diuretic use) or impulse transmission non-renal (vomiting) HYPONATREMIA Hypervolemic - water gain is greater than Serum Na+ level < 135 Na+ gain; edema mEq/L occurs Deficiency in Na+ Isovolumic - normal related to amount of Na+ level, too much body fluid fluid Several types WHAT DO YOU SEE? ✓ Dilutional Primarily neurologic ✓ Depletional symptoms ✓ Hypovolemic ✓ Headache, N/V, muscle ✓ Hypervolemic twitching, ✓ Isovolemic altered mental status, stupor, TYPES OF HYPONATREMIA seizures, coma Dilutional - results from Hypovolemia - poor Na+ loss, water gain skin turgor, tachycardia, Depletional - decreased BP, insufficient Na+ intake orthostatic Hypovolemic - Na+ hypotension loss is greater than  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM Hypervolemia - ✓ Monitor client edema, hypertension, in ICU weight gain, HYPERNATREMIA bounding tachycardia Excess Na+ relative to body water WHAT DO WE DO? Occurs less often than hyponatremia MILD CASE Thirst is the body’s ✓ Restrict fluid main defense intake for When hypernatremia hyper/isovolem occurs, fluid shifts outside the cells ic May be caused by hyponatremia water deficit or over- ✓ IV fluids and/or ingestion of Na+ increased po Also may result from diabetes insipidus Na+ intake for WHAT DO YOU SEE? hypovolemic hyponatremia Think S-A-L-T SEVERE CASE ✓ Skin flushed ✓ Infuse ✓ Agitation hypertonic ✓ Low grade NaCl solution fever (3% or 5% ✓ Thirst Neurological NaCl) symptoms ✓ Furosemide to Signs of hypovolemia remove excess WHAT DO WE DO? fluid  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM Correct underlying ✓ Na+/K+ pump disorder ✓ Renal Gradual fluid regulation replacement ✓ pH level Monitor for s/s of SODIUM/POTASSIUM PUMP cerebral edema Monitor serum Na+ Uses ATP to pump level potassium into cells Pumps sodium out of Seizure precautions POTASSIUM cells Creates a balance Major intracellular RENAL REGULATION cation Increased K+ levels  Untreated changes in increased K+ loss in K+ levels can lead to urine serious neuromuscular Aldosterone secretion and cardiac causes Na+ reabsorption and K+ problems excretion Normal K+ levels = 3.5 - 5 mEq/L BALANCING POTASSIUM PH Most K+ ingested is Potassium ions and excreted by the hydrogen ions kidneys exchange freely Three other influential across cell factors in K+ balance membranes :  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM Acidosis  ✓ Irregular, weak hyperkalemia (K+ pulse moves out of cells) ✓ Orthostatic Alkalosis  hypotension hypokalemia (K+ ✓ Numbness (paresthesias) moves into cells) WHAT DO WE DO? HYPOKALEMIA Increase dietary K+ Serum K+ < 3.5 mEq/L Oral KCl supplements Can be caused by GI IV K+ replacement losses, diarrhea, Change to K+-sparing insufficient intake, diuretic non-K+ sparing Monitor EKG changes diuretics (thiazide, IV K+ REPLACEMENT furosemide) WHAT DO YOU SEE? Mix well when adding to an IV Think S-U-C-T-I-O-N solution bag ✓ Skeletal muscle Concentrations weakness ✓ U wave (EKG should not exceed changes) 40-60 mEq/L ✓ Constipation, Rates usually 10-20 ileus mEq/hr ✓ Toxicity of digitalis HYPERKALEMIA glycosides Serum K+ > 5 mEq/L  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM Less common than ✓ Dietary hypokalemia restriction Caused by altered Moderate kidney function, ✓ Kayexalate increased intake (salt Emergency ✓ 10% calcium substitutes), blood gluconate for transfusions, meds cardiac effects (K+-sparing diuretics), ✓ Sodium cell death (trauma) bicarbonate WHAT DO YOU SEE? for acidosis Irritability MAGNESIUM Paresthesia Helps produce ATP Muscle weakness Role in protein (especially legs) synthesis & EKG changes (tented carbohydrate T wave) metabolism Irregular pulse Helps cardiovascular Hypotension system function Nausea, abdominal (vasodilation) cramps, diarrhea Regulates muscle WHAT DO WE DO? contractions Mild HYPOMAGNESEMIA ✓ Loop diuretics (Lasix)  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM Serum Mg++ level < ✓ Muscle 1.5 mEq/L weakness Caused by poor ✓ Leg/foot dietary intake, poor GI absorption, cramps excessive GI/urinary ✓ Hyper DTRs losses ✓ Tetany High risk clients ✓ Chvostek’s & ✓ Chronic Trousseau’s alcoholism ✓ Malabsorption signs ✓ GI/urinary WHAT DO YOU SEE? system Cardiovascular disorders ✓ Sepsis ✓ Tachycardia ✓ Burns ✓ Hypertension ✓ Wounds ✓ EKG changes needing debridement WHAT DO YOU SEE? WHAT DO YOU SEE? Gastrointestinal CNS ✓ Dysphagia ✓ Altered LOC ✓ Anorexia ✓ Confusion ✓ Nausea/vomiti ✓ Hallucinations ng WHAT DO YOU SEE? WHAT DO WE DO? Neuromuscular Mild  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM ✓ Dietary Renal dysfunction is replacement most common cause Severe ✓ Renal failure ✓ IV or IM ✓ Addison’s magnesium disease sulfate ✓ Adrenocortical Monitor insufficiency ✓ Neuro status ✓ Untreated DKA ✓ Cardiac status WHAT DO YOU SEE? ✓ Safety MAG SULFATE INFUSION Decreased neuromuscular Use infusion pump - no faster than 150 activity mg/min Hypoactive DTRs Monitor vital signs for Generalized hypotension and weakness respiratory distress Monitor serum Mg++ Occasionally level q6h nausea/vomiting Cardiac monitoring WHAT DO WE DO? Calcium gluconate as an antidote for Increased fluids if overdosage renal function normal HYPERMAGNESEMIA Loop diuretic if no response to fluids Serum Mg++ level > Calcium gluconate 2.5 mEq/L for toxicity Not common  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM Mechanical serum levels ventilation for (Parathyroid pulls) respiratory depression With high Ca++ levels, Hemodialysis (Mg++- calcitonin is released free dialysate) by the thyroid to CALCIUM inhibit calcium loss from bone (Calcitonin 99% in bones, 1% in keeps) serum and soft tissue HYPOCALCEMIA (measured by serum Ca++) Serum calcium < 8.9 Works with mg/dl phosphorus to form Ionized calcium level bones and teeth < 4.5 mg/Dl Role in cell Caused by membrane inadequate intake, permeability malabsorption, Affects cardiac pancreatitis, thyroid muscle contraction or parathyroid Participates in blood surgery, loop clotting diuretics, low CALCIUM REGULATION magnesium levels WHAT DO YOU SEE? Affected by body stores of Ca++ and by Neuromuscular dietary intake & ✓ Anxiety, Vitamin D intake confusion, Parathyroid hormone irritability, draws Ca++ from muscle bones increasing low twitching,  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM paresthesias ✓ Hyperparathyr (mouth, oidism fingers, toes), WHAT DO YOU SEE? tetany Fractures Fatigue, confusion, Diarrhea lethargy, coma Diminished response Muscle weakness, to digoxin hyporeflexia EKG changes Bradycardia  cardiac arrest WHAT DO WE DO? Anorexia, nausea/vomiting, Calcium gluconate decreased bowel for postop thyroid or sounds, constipation parathyroid client Polyuria, renal calculi, renal failure Cardiac monitoring WHAT DO WE DO? Oral or IV calcium If asymptomatic, treat replacement underlying cause HYPERCALCEMIA Hydrate the patient Serum calcium > 10.1 to encourage diuresis mg/dl Loop diuretics Ionized calcium > 5.1 Corticosteroids mg/dl PHOSPHORUS Two major causes The primary anion in ✓ Cancer the intracellular fluid  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM Crucial to cell WHAT DO YOU SEE? membrane integrity, muscle function, Musculoskeletal neurologic function ✓ muscle and metabolism of weakness carbs, fats and ✓ respiratory protein muscle failure Functions in ATP ✓ osteomalacia formation, ✓ pathological phagocytosis, fractures CNS platelet function and formation of bones ✓ confusion, and teeth anxiety, HYPOPHOSPHATEMIA seizures, coma Cardiac Serum phosphorus < ✓ hypotension 2.5 mg/dl ✓ decreased Can lead to organ cardiac output system failure Hematologic Caused by respiratory ✓ hemolytic anemia alkalosis ✓ easy bruising (hyperventilation), ✓ infection risk insulin release, WHAT DO WE DO? malabsorption, diuretics, DKA, MILD/MODERATE elevated parathyroid ✓ Dietary hormone levels, interventions extensive burns  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM ✓ Oral ✓ Cardiac supplements irregularities SEVERE ✓ Hyperreflexia ✓ IV ✓ Eating poorly replacement ✓ Muscle weakness using ✓ Oliguria potassium WHAT DO WE DO? phosphate or sodium Low-phosphorus diet Decrease absorption phosphate with antacids that HYPERPHOSPHATEMIA bind phosphorus Treat underlying Serum phosphorus > cause of respiratory 4.5 mg/dl acidosis or DKA Caused by impaired IV saline for severe hyperphosphatemia kidney function, cell in patients with good damage, kidney function hypoparathyroidism, CHLORIDE respiratory acidosis, Major extracellular DKA, increased anion dietary intake Sodium and chloride maintain water WHAT DO YOU SEE? balance Think C-H-E-M-O  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM Secreted in the Arrhythmias stomach as WHAT DO WE DO? hydrochloric acid Aids carbon dioxide Treat underlying transport in blood cause HYPOCHLOREMIA Oral or IV Serum chloride < 96 replacement in a mEq/L sodium chloride or Caused by potassium chloride decreased intake or solution decreased HYPERCHLOREMIA absorption, metabolic Serum chloride > 106 alkalosis, and loop, mEq/L osmotic or thiazide Rarely occurs alone diuretics Caused by WHAT DO YOU SEE? dehydration, renal failure, respiratory Agitation, irritability alkalosis, salicylate Hyperactive DTRs, toxicity, hyperpara- tetany thyroidism, Muscle cramps, hyperaldosteronism, hypertonicity hypernatremia Shallow, slow WHAT DO YOU SEE? respirations Metabolic Acidosis Seizures, coma  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM ✓ Decreased ACID-BASE BASICS LOC Balance depends on ✓ Kussmaul’s regulation of free respirations hydrogen ions Concentration of ✓ Weakness hydrogen ions is Hypernatremia measured in pH ✓ Agitation Arterial blood gases are the major ✓ Tachycardia, diagnostic tool for dyspnea, evaluating acid-base tachypnea, balance HTN ARTERIAL BLOOD GASES ✓ Edema pH WHAT DO WE DO? 7.35 - 7.45 PaCO2 Correct underlying 35 - 45 mmHg cause HCO3 22-26 mEq/L Restore fluid, ACIDOSIS electrolyte and acid- pH < 7.35 base balance Caused by IV Lactated Ringer’s accumulation of solution to correct acids or by a loss of acidosis bases ALKALOSIS ACID-BASE BALANCE  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM pH > 7.45 Phosphate buffer - Occurs when bases effective in renal accumulate or acids tubules are lost Protein buffers - most REGULATORY SYSTEMS plentiful - hemoglobin RESPIRATORY SYSTEM Three systems come into play when pH Lungs regulate blood rises or falls levels of CO2 ✓ Chemical CO2 + H2O = buffers Carbonic acid ✓ Respiratory High CO2 = slower system breathing (hold on to ✓ Kidneys carbonic acid and CHEMICAL BUFFERS lower pH) Low CO2 = faster Immediate acting breathing (blow off Combine with carbonic acid and offending acid or raise pH) Twice as effective as base to neutralize chemical buffers, but harmful effects until effects are temporary another system takes KIDNEYS over Reabsorb or excrete Bicarb buffer - mainly excess acids or bases responsible for into urine buffering blood and interstitial fluid Produce bicarbonate  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM Adjustments by the Step 5 - What is the kidneys take hours to PaO2 and SaO2? days to accomplish STEP 1 - CHECK THE PH Bicarbonate levels pH < 7.35 = acidosis and pH levels pH > 7.45 = alkalosis increase or decrease Move on to Step 2 together STEP 2 - WHAT IS THE CO2? ARTERIAL BLOOD GASES PaCO2 gives info (ABG) about the respiratory component of acid- Uses blood from an base balance arterial puncture If abnormal, does the Three test results change correspond relate to acid-base with change in pH? balance ✓ High pH ✓ pH ✓ PaCO2 expects low PaCO2 ✓ HCO3 (hypocapnia) INTERPRETING ABGS ✓ Low pH Step 1 - check the pH expects high Step 2 - What is the PaCO2 (hypercapnia) CO2? STEP 3 – WATCH THE BICARB Step 3 - Watch the bicarb Provides info Step 4 - Look for regarding metabolic compensation  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM aspect of acid-base PaO2 reflects ability balance to pickup O2 from If pH is high, bicarb lungs expected to be high SaO2 less than 95% is (metabolic alkalosis) inadequate If pH is low, bicarb oxygenation expected to be low Low PaO2 indicates (metabolic acidosis) hypoxemia STEP 4 – LOOK FOR COMPENSATION ACID-BASE IMBALANCES If a change is seen in Respiratory Acidosis BOTH PaCO2 and Respiratory Alkalosis bicarbonate, the Metabolic Acidosis body is trying to compensate Metabolic Alkalosis Compensation occurs RESPIRATORY ACIDOSIS as opposites, (Example: for Any compromise in metabolic acidosis, breathing can result compensation shows in respiratory acidosis respiratory alkalosis) Hypoventilation STEP 5 – WHAT IS THE PAO2 carbon dioxide AND SAO2 buildup and drop in pH Can result from neuromuscular trouble, depression of  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM the brain’s respiratory ✓ PaCO2 >45 center, lung disease ✓ HCO3 Normal or airway obstruction CLIENTS AT RISK Compensated ✓ pH Normal Post op abdominal ✓ PaCO2 >45 surgery ✓ HCO3 > 26 Mechanical WHAT DO WE DO? ventilation Correct underlying Analgesics or cause sedation Bronchodilators WHAT DO YOU SEE? Supplemental oxygen Treat hyperkalemia Apprehension, Antibiotics for restlessness infection Confusion, tremors Chest PT to remove Decreased DTRs secretions Remove foreign body Diaphoresis obstruction Dyspnea, RESPIRATORY ALKALOSIS tachycardia N/V, warm flushed Most commonly results from skin hyperventilation ABG RESULTS caused by pain, Uncompensated salicylate poisoning, ✓ pH < 7.35 use of nicotine or  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM aminophylline, WHAT DO WE DO? hypermetabolic Correct underlying states or acute hypoxia disorder (overstimulates the Oxygen therapy for respiratory center) hypoxemia WHAT DO YOU SEE? Sedatives or Anxiety, restlessness antianxiety agents Diaphoresis Paper bag breathing Dyspnea ( rate and for hyperventilation depth) EKG changes Hyperreflexia, paresthesias Tachycardia Tetany METABOLIC ACIDOSIS ABG RESULTS Characterized by Uncompensated gain of acid or loss of bicarb ✓ pH > 7.45 Associated with ✓ PaCO2 < 35 ketone bodies ✓ HCO3 Normal ✓ Diabetes mellitus, Compensated alcoholism, ✓ pH Normal starvation, ✓ PaCO2 < 35 hyperthyroidis ✓ HCO3 < 22 m  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM Other causes ✓ pH < 7.35 ✓ Lactic acidosis ✓ PaCO2 Normal secondary to shock, heart ✓ HCO3 < 22 failure, Compensated pulmonary ✓ pH Normal disease, ✓ PaCO2 < 35 hepatic disease, ✓ HCO3 < 22 seizures, WHAT DO WE DO? strenuous exercise Regular insulin to WHAT DO YOU SEE? reverse DKA Confusion, dull IV bicarb to correct headache acidosis Decreased DTRs Fluid replacement S/S hyperkalemia (abdominal cramps, Dialysis for drug diarrhea, muscle toxicity weakness, EKG Antidiarrheals changes) METABOLIC ALKALOSIS Hypotension, Kussmaul’s Commonly respirations associated with Lethargy, warm & dry hypokalemia from skin diuretic use, ABG Results hypochloremia and Uncompensated hypocalcemia  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM Also caused by ✓ HCO3 >26 excessive vomiting, Compensated NG suction, Cushing’s ✓ pH Normal disease, kidney ✓ PaCO2 > 45 disease or drugs containing baking ✓ HCO3 > 26 soda WHAT DO WE DO? WHAT DO YOU SEE? IV ammonium Anorexia chloride Apathy D/C thiazide diuretics Confusion and NG suctioning Cyanosis Antiemetics Hypotension IV THERAPY Loss of reflexes Muscle twitching Crystalloids – volume expander Nausea ✓ Isotonic (D5W, Paresthesia 0.9% NaCl or Polyuria Lactated Vomiting Ringers) Weakness ✓ Hypotonic (0.45% NaCl) ABG RESULTS ✓ Hypertonic Uncompensated (D5/0.9% NaCl, ✓ pH > 7.45 D5/0.45% NaCl) ✓ PaCO2 Normal  1st semester S.Y 2024 – 2025 MTW 8:00 AM - 10:00 AM Colloids – plasma expander (draw fluid into the bloodstream) ✓ Albumin ✓ Plasma protein ✓ Dextran TOTAL PARENTERAL NUTRITION Highly concentrated Hypertonic solution Used for clients with high caloric and nutritional needs Solution contains electrolytes, vitamins, acetate, micronutrients and amino acids Lipid emulsions given in addition