PHYSIOLOGY REVIEW
Ø Fluid Compartments
o Extracellular Fluid
§ 1/3 of body water located here
o Interstitium, lymph, blood, body cavities
§ Divided into: IV, IT, Transcellular spaces
o Intracellular Fluid
§ 40% of body weight of an adult
Ø Electrolytes
o Most Prevalent in ECF – Na (Cation), Chloride (Anion)
o Most Prevalent in ICF – Potassium (Cation), Phosphate (Anion)
Ø Fluid Regulation
o Gastrointestinal
o Renal
§ Renin-Angiotensin-Aldosterone System
o Adrenocortical
§ Glucocorticoids – anti-inflammatory, inc glucose (Cortisol)
§ Mineralocorticoids – Inc Sodium retention and potassium excretion (Aldosterone)
§ Where Na goes, H2O follows
o Pituitary
§ Posterior – ADH (reabsorbs water)
§ Factors stimulating ADH:
· Stress
· Nausea
· Nicotine
· Morphine
o Hypothalamic
§ Thirst mechanism
o Insensible Water Loss
§ Vaporization from skin and lungs
§ Increased by accelerated body metabolism
o Cardiac
§ ANP & BNP – antagonist to RAAS à Natriuresis & Diuresis à Dec BP
§ In response to inc atrial pressure and hypernatrermia
Ø Mechanisms Controlling Fluid Movement
o Hydrostatic Pressure - push
o Oncotic Pressure – pull by proteins
o Osmotic Pressure – determined by solute concentration
Ø Causes of fluid shifting
o Elevation of venous hydrostatic pressure
§ Fluid overload, heart and liver failure, venous insufficiency
o Decrease in plasma oncotic pressure
§ Renal/liver disease, malnutrition
o Elevation interstitial oncotic pressure
§ Trauma, burns, inflammation
o Shift of interstitial fluid to plasma
§ Hypertonic solutions
FLUID VOLUME DEFICIT
Ø Types
o Isotonic – water loss = electrolytes loss
o Hypertonic – water loss > electrolytes loss
o Hypotonic – water loss < electrolytes loss
Ø Common Manifestations:
o Thirst
o Dry mucus membrane
o Decreased skin turgor and capillary refill
o Postural hypoBP, Increased PR, Dec CVP
o Dec UO, concentrated urine
o Weight loss
Ø Management:
o Correct underlying cause
o Rehydration
o Prevent further losses and inc fluid compartment volumes
FLUID VOLUME EXCESS
Ø Types:
o Isotonic
§ Inadequately controlled IVT
§ Kidney disease
§ Long-term steroid therapy
o Hypertonic
§ Excessive sodium intake
o Hypotonic
§ Heart failure
§ SIADH
§ Wound irrigation with hypotonic fluids
§ Early kidney disease
§ Uncontrolled IVT
Ø Common Manifestations:
o Edema
o Jugular vein distention
o Bounding pulse, inc BP and CVP
o Polyuria
o Weight gain
o Dyspnea, crackles, pulmonary edema
Ø Management:
o Treat underlying cause
§ Diuretics
§ Sodium restrictions
§ Paracentesis
§ Thoracentesis
SODIUM (135-145 mEq/L)
Ø Primary cation in ECF
Ø Eliminated through sweat, urine, and feces
Ø Controlled by kidneys through aldosterone
Ø Essential for nerve conduction and muscle contraction
HYPERNATREMIA
Ø Causes:
o Excessive sodium intake
o Inadequate water intake
o Excessive water loss
o Disease states
o DI
o Primary hyperaldosteronism
o Cushing syndrome
o Uncontrolled DM
Ø Significant Manifestations:
o Rare except for those with altered thirst mechanism
o Restlessness, agitation, coma
o Intense thirst
o Dry swollen tongue, sticky mucous membrane
o Lethargy
Ø Management:
o Tx underlying cause
o Diuretics
o Gradually reduce
o Sodium dietary restriction
HYPONATREMIA
Ø Causes:
o Excessive sodium loss
o Inadequate sodium intake
o Excessive water gain
o Disease states:
§ SIADH
§ Heart Failure
§ Primary hypoaldosteronism
Ø Significant Manifestations:
o Irritability, apprehension, confusion, dizziness, coma
o Dry mucous membranes
o Signs of dehydration
o Cold and clammy skin
Ø Management:
o Tx underlying cause
o IV Hypertonic saline
o Add more sodium in diet
o Safety precautions – side rails and supervise in ambulation
o Administer drugs that block ADH activity as ordered
o Conivaptan (Vaprisol)
o Tolvaptan (Samsca)
POTASSIUM (3.5-5.0 mEq/L)
Ø Primary cation in ICF
Ø Important in neuromuscular and cardiac function
Ø Kidneys – primary route for elimination
Ø Inverse relationship with sodium
HYPERKALEMIA
Ø Causes:
o Excessive potassium intake
o Shift of potassium out of cells
o Acidosis
o Tissue catabolism – fever, sepsis, burns
o Crush injury
o Tumor lysis syndrome
o Renal failure
o Potassium sparing diuretics
o Adrenal insufficiency
o ACE inhibitors
Ø Manifestations:
o Irritability
o Abdominal cramping, diarrhea
o Irregular pulse
o Paresthesias
o Cardiac arrest if sudden or severe
o ECG changes:
§ Widened QRS complex
§ Wide, flat P wave
§ Prolonged PR interval
§ Tall, peaked T wave
Ø Management:
o Restrict K intake
o Sodium Polystyrene Sulfonate (Kayexalate)
o Assess bowel sounds and bowel movements
o Increase fluid intake
o IV insulin with glucose to shift potassium from ECF to ICF
o Sodium bicarbonate to correct acidosis
o Calcium gluconate – for symptom management
HYPOKALEMIA
Ø Causes:
o Potassium loss
o Shift into cells
o Increased insulin
o Alkalosis
o Tissue repair
o Lack of intake
Ø Manifestations:
o Fatigue
o Muscle weakness, leg cramps
o Soft, flabby muscles
o Paralytic ileus
o Paresthesias, decreased reflexes
o Weak, irregular pulse
o Polyuria
o Hyperglycemia
o ECG Changes:
§ Prolonged U wave
§ T wave inversion
Ø Management:
o Potassium supplements and increase dietary intake
§ Ex: Apricot, banana, cantaloupe, prunes, peaches, potatoes, tomatoes
o Potassium Chloride
§ Always dilute, never IV push
§ Invert bag many times to ensure even distribution
§ Should not exceed 10-20 mEq/hr and use infusion pump
CALCIUM (8.5-10.5 mg/dL)
Ø For transmission of nerve impulses
Ø Blood clotting
Ø Tooth and bone formation
Ø Muscle and myocardial contractions
Ø Present in 3 forms:
o Free or ionized – active
o Bound to albumin
o Complexed with phosphate, citrate, carbonate
HYPERCALCEMIA
Ø Causes:
o Increased total calcium levels
o Multiple myeloma
o Bone metastasis
o Prolonged immobilization
o Hyperparathyroidism
o Vitamin D overdose
o Thiazides
o Increased ionized calcium
o Acidosis
Ø Manifestations:
o Lethargy, weakness
o Depressed reflexes
o Bone pain, fractures
o Nephrolithiasis
o ECG Changes:
§ Shortened QT interval
§ Shortened ST segment
Ø Management:
o Loop diuretics – Furosemide (Lasix)
o Hydration with isotonic saline infusion
o Increase OFI to 3-4 L per day
o Diet low in calcium
o Mobilization with weight bearing
o Administer as ordered:
§ Plicamycin (Mithracin)
§ Pamidronate (Aredia) – for metastasis
HYPOCALCEMIA
Ø Causes:
o Decreased total calcium
§ CKD
§ Hyperphosphatemia
§ Primary hyperparathyroidism
§ Vit D deficiency
§ Acute pancreatitis
§ Loop diuretics
§ Chronic alcoholism
§ Diarrhea
§ Decreased serum albumin
o Decreased ionized calcium
§ Alkalosis
§ Citrated blood administration
Ø Manifestations:
o Easy fatigability
o Hyperreflexia
o Laryngeal spasm
o Tetany, seizures
o Chvostek’s Sign - face
o Trousseau’s Sign – arms
o ECG:
§ ST segment elongation
§ Prolonged QT interval
§ Ventricular tachycardia
Ø Management:
o Tx underlying cause
o Do not give via IM – burning, necrosis
o Diet high in calcium
§ Milk
§ Broccoli, kale, mustard greens
§ Small fish with bones – sardines
§ Legumes
§ Tofu
PHOSPHATE
(2.5-4.5 mg/dL)
Ø Primary anion in ICF
Ø Essential for muscle function , RBCs, nervous system
Ø Kidneys – major route of excretion
Ø Inverse with Calcium
HYPERPHOSPHATEMIA
Ø Causes:
o Renal failure
o Chemo agents
o Enemas containing phosphate
o Excessive ingestion
o Large vitamin D intake
o Hypoparathyroidism
Ø Manifestations:
o Similar with hypocalcemia
o Muscle problems, tetany
o Deposition of calcium-phosphate precipitates
Ø Management:
o Tx underlying cause
o Adequate hydration
o Calcium supplements
o Phosphate binding agents
o Dietary phosphate restrictions
HYPOPHOSPHATEMIA
Ø Causes:
o Malabsorption syndrome
o Starvation tx reversal
o Recovery from DKA
o Alcohol withdrawal
o Phosphate binding antacids
o Respiratory alkalosis
Ø Manifestations
o Impaired cellular energy and oxygen delivery
o Muscle weakness
o Cardiac problems
o Osteomalacia
o Rhabdomyolysis
Ø Management
o Food sources
§ Protein rich foods such as dairy, eggs, meat, fish, poultry
§ Cereal grains
§ Processed convenience foods and soft drinks
MAGNESIUM (1.8-3.0 mg/dL)
Ø Involved in metabolism of cellular nucleic acids and CHON
Ø Regulated by GI absorption
Ø Excreted via kidneys
Ø Assessed together with calcium and potassium
Ø Affects neuromuscular excitability
HYPERMAGNESEMIA
Ø Causes:
o Renal failure
o Excessive administration
o Adrenal insufficiency
Ø Manifestations:
o Lethargy, drowsiness
o DTR lost, respiratory and cardiac arrest
Ø Management:
o Calcium chloride, calcium gluconate to oppose effects of Mg on cardiac muscles
o Promote excretion by increasing OFI
o Dialysis
HYPOMAGNESEMIA
Ø Causes:
o Diarrhea and vomiting
o Chronic alcoholism
o Impaired GI absorption
o Prolonged malnutrition
o Polyuria
o Hyperaldosteronism
Ø Manifestations:
o Hyperactive DTR
o Resembles hypocalcemia
§ Inhibition of calcium transport into cell and release inhibited from sarcoplasmic reticulum
o Associated with hypokalemia – intracellular Mg is critical to normal fx of Na-K pump
Ø Management
o Dietary intake
§ Green vegetables, nuts, bananas, oranges, peanut butter
o Magnesium sulfate
§ Too rapid = arrest
CHLORIDE (98-107 mEq/L)
Ø Major extracellular anion
Ø Follows sodium
Ø Maintains acid-base balance by exchanging with bicarbonate
HYPERCHLOREMIA
Ø Causes:
o Excessive NaCl infusion with water loss
o Head injury
o Hypernatremia
o Renal failure
o Medications: Corticosteroids, diuretics
o Alkalosis
Ø Manifestations:
o Tachypnea, dyspnea, tachycardia
o Lethargy, weakness
o Decline in cognitive status
o Deep rapid respiration
Ø Management:
o Tx underlying cause
o Hypotonic IV
o LRS – convert lactate to bicarbonate
o IV Sodium bicarbonate – renal excretion of chloride ions
o Restrict Na, Cl, and fluids
HYPOCHLOREMIA
Ø Causes:
o Addison’s disease
o Reduced intake
o Untreated DKA
o Chronic respiratory acidosis
o Metabolic alkalosis
o Excessive sweating, vomiting, gastric suction, diarrhea
o Diuretics – loop, osmotic, thiazide
o Cystic fibrosis
o Draining fistulas and ileostomies
o Heart failure
Ø Manifestations
o Agitation, irritability, tremors
o Muscle cramps, hyperactive DTR, hypertonicity, tetany
o Slow, shallow respirations
Ø Management
o Tx underlying cause
o PNSS or 0.45% NaCl
ARTERIAL BLOOD GAS ANALYSIS
Ø Normal Values
o pH = 7.35 – 7.45
o PaO2 = 80 to 100 mmHg
o PaCO2 = 35 to 45 mmHg.
o HCO3 = 22 to 26 mEq/L
Ø Specimen Collection
o Assess factors that may affect the accuracy of the results such as changes in the oxygen settings, suctioning within the past 20 minutes, and the client’s activities
o Perform the Allen’s test to determine the presence of collateral circulation
§ Explain the procedure the client
§ Apply pressure over the ulnar and radial arteries simultaneously
§ Ask the client to open and close the hand repeatedly
§ Release pressure from the ulnar artery while compressing the radial artery
§ Assess the color of the extremity distal to the pressure point
§ Document the findings
Ø Analyzing ABG Results
o STEP 1:
§ If the pH is elevated, it reflects alkalosis, otherwise, acidosis
o STEP 2:
§ Look at the Pco2
§ Elevated or decreased?
§ Opposite relationship to pH ? If yes, then respiratory imbalance
o STEP 3:
§ Look at the HCO3
§ Elevated or decreased?
§ Corresponding relationship to pH ? If yes, then metabolic imbalance
o STEP 4:
§ Full compensation has occurred if the pH is in a normal range of 7.35 to 7.45
§ If not within normal range, look at the respiratory or metabolic function indicators
§ If the condition is a respiratory imbalance, look at the HCO3 to determine state of compensation
§ If the condition is a metabolic imbalance, look at the PCO2 to determine the state of compensation
RESPIRATORY ACIDOSIS
Ø Cause:
o Carbon dioxide retention from hypoventilation
o Compensation to bicarbonate retention by the kidneys
Ø Manifestations:
o Drowsiness, disorientation, headache
o Hyperkalemia cardiac s/sx
o Seizures
o Hypoventilation with hypoxia
Ø Management:
o Monitor oxygenation status
o Administer oxygen as prescribed
o Place the client in a semi-fowler’s position
o Encourage and assist in DBCTE
o Encourage hydration to thin secretions
o Reduce restlessness by improving ventilation
o AVOID administering tranquilizers, sedatives or opioids à respiratory depression
o Monitor potassium level
RESPIRATORY ALKALOSIS
Ø Cause:
o Increased CO2 excretion from hyperventilation
o Fever, pain
o Overventilation by MV
o Compensation to bicarbonate excretion by kidneys
Ø Manifestations:
o Lethargy, lightheadedness
o Cardiac s/sx rt to hypokalemia
o Tetany, numbness, tingling
o Hyperventilation
Ø Management:
o WOF respiratory distress
o Emotional support to the client
o Provide cautious care with ventilator clients so that they are not forced to take breaths too deeply or rapidly
o Monitor potassium and calcium
o Calcium gluconate as ordered for tetany
o Assist with breathing techniques and breathing aids
o Encourage voluntary holding of breath if appropriate
o Provide use of a rebreathing mask as prescribed
o Provide carbon dioxide breaths as prescribed (Rebreathing into a paper bag)
METABOLIC ACIDOSIS
Ø Causes:
o Inability to excrete acid or loss of base
o Compensation to CO2 excretion by the lungs
o Disease states:
§ DM, DKA
§ Aspirin overdose
§ High fat diet
§ Malnutrition
§ Severe diarrhea
§ Renal insufficiency
Ø Manifestations:
o Drowsiness, confusion, headache, coma
o Deep, rapid respirations
Ø Management:
o WOF respiratory distress
o Assess LOC
o Monitor I&O
o Prepare to administer IV solutions to increase buffer base
o Monitor potassium closely
o As it resolves, K moves back into cells à hypokalemia
METABOLIC ALKALOSIS
Ø Causes:
o Loss of strong acid or gain of base
o Compensatory response of CO2 retention by lungs
o Diuretics
o Excessive vomiting or GI suctioning
o Hyperaldosteronism
o Ingestion or infusion of excessive sodium bicarbonate
o Massive transfusion of whole blood
Ø Manifestations:
o Drowsiness, dizziness
o Hypoventilation (compensation)
o Nausea and vomiting
o Tremors, hypertonic muscles, cramps, tetany, tingling
o Cardiac s/sx rt to hypokalemia
Ø Management:
o WOF respiratory distress
o Monitor potassium and calcium
o Institute safety precautions
o Prepare to administer medications and IV fluids as prescribed to promote kidney excretion of bicarbonate
o Potassium as prescribed
o Treat the underlying cause
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