FLUIDS, ELECTROLYTES and ACID-BASE BALANCE

Body fluid compartments

 Intracellular: 70%
 Extracellular: 30%
o Interstitial (11-12L: including lymph)
o Intravascular (6L: 3L plasma, 3L formed elements)
o Transcellular (1L: CSF, pericardial, synovial, intraocular, pleural, sweat glands,
digestive secretions)

Electrolytes
 Active chemicals
o Cation (+) : Na, K, Ca, Mg, H+
o Anion (-) : Cl, HCO3, PO4, SO4, protein ions

Regulation of body fluids

 OSMOSIS – mov’t of SOLVENT from area of LOWER to HIGHER concentration of SOLUTE
o Osmotic Pressure and Oncotic Pressure
 DIFFUSION – mov’t of SOLUTE from area of HIGHER to LOWER concentration of SOLUTE
 HYDROSTATIC PRESSURE – pressure exerted by the fluids on the walls of the blood
vessels
 FILTRATION –Mov’t of H2O from HIGHER to LOWER hydrostatic pressure – capillary level
 OSMOLALITY – number of dissolved particles contained in a unit of fluid
 TONICITY – ability of all solutes to cause an osmotic driving force that promotes water
mov’t between compartments
 HYDROSTATIC PRESSURE – pressure exerted by the fluids on the walls of the blood
vessels
 FILTRATION –Mov’t of H2O from HIGHER to LOWER hydrostatic pressure – capillary level

Gains and losses

 KIDNEYS – Urine: 0.5-1ml/kg/hr
 SKIN – 0-1000mL per hour
 LUNGS – 300 mL every day
 GI Tract – 100-200 mL daily

Lab values and fluid status

 Urine specific gravity – measures kidney’s ability to conserve or excrete water
o NORMAL: 1.010 – 1.025
 BUN – by-product of protein metabolism by the liver (muscle and diet)
o NORMAL: 10-20 mg/dL
 CREATININE – end product of muscle metabolism (better indicator of renal function)
o NORMAL: 0.7-1.4 mg/dL
 Hematocrit – measures the volume of RBC in whole blood
 o NORMAL: M: 42-52% F:35-47&

Fluid and electrolyte balance

 KIDNEYS
 Heart and Blood vessels
 Lungs
 Pituitary glands
o ADH
 Adrenal Glands
o Aldosterone
 Parathyroid Glands
 Baroreceptors
o Located in LEFT atrium, carotid, and aortic arch
 RAAS
 Natriuretic peptides
o ANP and BNP
 OSMORECEPTORS
o Located on the surface of hypothalamus
o Sense changes in sodium concentration

FLUID VOLUME IMBALANCES

HYPOVOLEMIA
 Causes:
o Abnormal fluid losses
 Vomiting,
 Diarrhea
 GI suctioning
 Sweating
 Manifestations:
o Thirst
o Weight loss
o Muscle weakness
o Concentrated urine
o Cool clammy skin
o Shock (late sign)
 Dx:
o Elevated BUN and Crea
o Elevated hematocrit
o Elevated urine specific gravity
 Medical/Nursing Mngt:
o If mild: Increase OFI
o If severe: Parenteral fluid resuscitation (PLR or PNSS
 o I/O and weight monitoring
o VS monitoring

HYPERVOLEMIA
 Causes:
o CHF
o Renal failure
o Liver Cirrhosis
o Excessive intake of Salt (Na)
 Manifestations:
o Distended Neck Veins (JVD)
o Edema
o Crackles/SOB/Wheezing
o Weight gain
o Elevated BP
o Increased UO
 Dx:
o Decreased BUN and Crea
o Elevated NA in urine
o CXR (Pulmonary Edema)
 Medical/Nursing Mngt:
o Correct the cause
o Diuretics (Furosemide/Thiazide)
o Hemodialysis
o I/O and Weight and VS monitoring
o Assessment of breath sounds and degree of edema
o Na and fluid restriction

ELECTROLYTE IMBALANCES

 EARLIEST manifestation of electrolyte imbalance

o Numbness, tingling, paresthesia
 UNIVERSAL manifestation of electrolyte imbalance
o Muscle weakness

 SODIUM
o Major EXTRACELLUAR cation
o Normal: 135-145 mEq/L
o Function: Aids in muscular contraction and nerve impulse transmission
 SODIUM IMBALANCES
o HYPONATREMIA
 Causes:
  Sodium loss
 Low sodium intake
 Water gain
 Decreased aldosterone secretion
 Diuretics use
 Manifestations:
 Headache
 Irritability
 Disorientation
 Muscle twitching
 Tremors
 Weakness
 Ataxia
 Seizure
 Med Mngt:
 Parenteral sodium replacement
 Water restriction
 Increased Sodium in DIET
 Nsg Mngt:
 Identify patient at risk
 Watch out for initial S/Sx, N&V
 Encourage increase Na in diet
 Monitor VS and Neuro status
o HYPERNATREMIA
 Manifestations:
 NEUROLOGIC: restlessness
 Other (same with Hyponatremia)
 Med/Nsg Mngt:
 Hypotonic solution infusion (gradual lowering of Sodium)
 Diuretics
 Low SODIUM diet
 Avoid OTC drug with high Na content

 POTASSIUM
o Major INTRACELLUAR cation
o Normal: 3.5 – 5.5 mEq/L
o Function:
 Aids in neuromuscular contraction and nerve impulse transmission
 Has high affinity with hydrogen ion
 Located in the muscle and GI tract
 POTASSIUM IMBALANCES
o HYPOKALEMIA
 Causes:
  GI loss (vomiting, suctioning, diarrhea)
 Decreased K-intake
 Diuretics (potassium-wasting
 Manifestations:
 Skeletal muscle weakness
 Cramps and paresthesia
 Fatigue
 ECG: extra “U” wave
 Decreased bowel sound
 Paralytic ileus
 Weak pulse/hypotension
 Med Mngt:
 If not severe
K-rich foods
 If severe:
Oral potassium drugs
 Kalium durule: taken with meals
 Liquid KCL: taken with juice
IV replacement (INCORPORATION)
K-sparing diuretics
 Nsg Mngt:
 Watch out for early S/Sx
 K-sparing
 Spirinolactone
 Amiloride
 Triamterene
 K-wasting
 Loop (furosemide, bumetanide, torsemide)
 Thiazide (diuril, hydrochlorodiuril, metolazone)
 Osmotic (mannitol)
 K-rich foods
 Potato
 Beans
 Apricot
 Prunes
 Carrot
 Raisin
 Avocado
 Tomato
 Orange
 Banana
o HYPERKALEMIA
 Causes:
 Decreased renal excretion of potassium
  Increased K intake
 Injury (Burns)
 Manifestations:
 Paresthesia/Irritability
 Abdominal cramping
 Diarrhea
 ECG: tall-peaked/tented T-wave
 Med/Nsg Mngt:
 ECG and VS monitoring
 Potassium RESTRICTION
 Dextrose 10% in water with regular insulin (IV)
 Sodium bicarbonate
 Mild: Diuretics
 Mod-Severe: Kayexalate (Sodium Polyesterene)
cation-exchange resin (oral/enema) – (+) effective: Diarrhea
WOF: hypoactive bowel movement

 CALCIUM
o Positively-charged ion
o Normal: 8.5-10.5 mg/dL or 4.5-5.5 meq/L
o Function:
 99% in bones and teeth, 1% in ECF
 Neural transmission
 Muscular contraction
 Blood clotting
 CALCIUM IMBALANCES
o HYPOCALCEMIA
 Causes:
 Low calcium intake
 Ca malabsorption
 Excessive Ca loss
 Parathyroid and thyroid surgeries
 Manifestations:
 Classic sign: TETANY
Trosseau’s sign
Chvostek’s sign
Arrhythmias
Fractures, tremors
Muscle cramps
Laryngospasm
 Med/Nsg Mngt:
 High-Ca diet
 IV Ca gluconate (Severe)
 Vit. D and Parathormone
  Seizure precaution
 Prevent trauma: SAFETY!
o HYPERCALCEMIA
 Causes:
 Immobility
 Excess intake of Ca
 Hyperparathyroidism
 Hypervitaminosis
 Manifestations:
 Change in LOC
 Altered mental status
 Muscle weakness
 Check for kidney stones
 ECG: short ST-segment
 Med/Nsg Mngt:
 Increase fluid administration
 Ca restriction in diet
 Calcitonin (Calcimar – route: SC)
 IV phosphate
 Mithramycin – prevents release of Ca from the bone
 Increase fiber
 Strain urine/WOF kidney stones (Flank pain!)

 MAGNESIUM
o Normal: 1.3-2.3 mg/dL
o Function:
 Increased Mg levels diminishes muscular excitability
 Decreased Mg levels increases muscular contractility
 Vasodilation and decreased peripheral resistance
 30% is protein bound, 70% remains free and ionized
 MAGNESIUM IMBALANCES
o HYPOMAGNESEMIA
 Causes:
 GI losses
 Ileum problems
 Alcohol withdrawal
 Medications
 Manifestations:
 Classic sign: TETANY
Trosseau’s sign
Chvostek’s sign
d/t accompanying hypoCa
Alteration in psychological status
Cardiac arrhythmias
 Increased susceptibility to digitalis toxicity
 Med/Nsg Mngt:
 Mild: increase Mg in the diet
Green leafy veg
Nuts
Seeds
Legumes
Grains
Seafood
Cocoa
 Meds:
Oral magnesium salts
IV magnesium SO4
Administered slowly
Check DTR
WOF: oliguria (<100mLx4hrs)
Antidote: Calcium gluconate
o HYPERMAGNESEMIA
 Causes:
 Kidney injury
 Diabetic ketoacidosis
 Excess Magnesium infusion
 Addison’s disease
 Manifestations:
 Depression of CNS and peripheral neuromuscular junction
 Ventricular block
 Cardiac arrest
 Med/Nsg Mngt:
 Restrict Mg in diet
 Diuretics
 Calcium gluconate or calcium chloride
 Reverse the effect of Mg on cardiac muscle

ACID-BASE IMBALANCES

ACID-BASE REGULATION
 BUFFER SYSTEM
o REMOVE or RELEASE hydrogen ion
o Excessive hydrogen ion (ACIDOSIS) → BUFFERS BIND
o Decrease in hydrogen ion (ALKALOSIS) → BUFFERS RELEASE hydrogen ion
  RESPIRATORY REGULATION
o RETAINS or ELIMINATES Carbon Dioxide (potential acid)

 RENAL REGULATION
o ELIMINATES or RETAINS HCO3
o ELIMINATES or RETAINS hydrogen ion

METABOLIC ACIDOSIS
 Causes:
o Loss of bicarbonate (HCO3)
 Intestinal loss
 Diuretics
o Accumulation of acids
 Lactic acid
 Ketoacids
 Uremia/Azotemia
 Salycilate poisoning
 Manifestations:
o INCREASED RESPIRATORY RATE
o (Kussmaul’s respiration)
o CNS depression
o Hyperkalemia
 Dx:
o ABG analysis
 o Hyperkalemia
o ECG: Tall Peaked T-wave

 Med/Nsg Mngt:
o Correct underlying cause
o Bicarbonate administration
o Hemo/peritoneal dialysis

METABOLIC ALKALOSIS
 Causes:
o Gain of bicarbonate (HCO3)
 Alkali intake
o Loss of hydrogen ion
 Vomiting
 Suction
o Loss of potassium
 Diuretics
 Manifestations:
o Respiratory depression
o Hypokalemia
 Decreased GI motility and paralytic ileus
 ECG: extra “U” wave
o S/Sx of hypocalcemia
 Tingling and spasms
 Dx:
o ABG analysis
o Hypokalemia
o ECG: Extra “U” wave
 Med/Nsg Mngt:
o Avoid antacids
o Anti-emetics
o Correct underlying cause
o NaCl and KCL infusion

RESPIRATORY ACIDOSIS
 Causes:
o DISORDERS that restrict/limit the RELEASE of Carbon dioxide in the LUNGS
 Manifestations:
o TACHYcardia
o TACHYpnea
o Mental cloudiness
o Cerebrovascular dilation
o Hyperkalemia
 o Increased ICP (severe)
 Dx:
o ABG analysis
o Hyperkalemia
o ECG: Tall-peaked T wave
 Med/Nsg Mngt:
o Correct underlying cause
o BRONCHODILATOR
o Semi-fowler’s position

RESPIRATORY ALKALOSIS
 Causes:
o EXCESSIVE release of Carbon dioxide in the LUNGS
o (Hyperventilation)
 Manifestations:
o Lightheadedness (vasoconstriction)
o Numbness and tingling (hypocalcemia)
 Dx:
o ABG analysis
 Med/Nsg Mngt:
o Correct underlying cause
o BROWN BAG
o Slow breathing
o Purse-lip breathing

ABG INTERPRETATION

 3 EASY STEPS:
1. Interpret all
2. What is the problem of the pH?
3. Who has the same problem as the pH?
 Level of compensation:
o Fully compensated: pH (NORMALIZED)
o Partially compensated: CO2 and HCO3 adjusts but pH remains ABNORMAL
o Uncompensated: Either the CO2 or HCO3 does not adjust (NORMAL), pH still
ABNORMAL

BURNS
 Causes:
o Thermal
o Chemical
o Electrical
o Radiation
  Depth:
o First Degree (Superficial-partial Thickness)
o Second Degree (Deep-partial Thickness)
o Third Degree (Full Thickness)
 SHOCK PHASE/Fluid Accumulation Phase
o Occurs during the first 48 hours
o S/Sx:
 HYPOVOLEMIA
 Oliguria
 HyperK and HypoNa
 Metabolic acidosis
 PRIORITY: FLUID RESUSCITATION!
 DIURETIC PHASE/Fluid Remobilization Phase
o Occurs after 48 hours
o S/Sx:
 Diuresis
 HypoK and HypoNa
 Metabolic Acidosis (Elimination of HCO3)
 RECOVERY PHASE
o Occurs on the 5th day onwards
o S/Sx:
 HypoCa (granulation repair)
 Negative Nitrogen Balance (Utilization of CHON for repair)
 HypoK

STAGES OF BURN CARE

 Emergent/resuscitative/Shock phase
o Priority: Fluid resuscitation
 Acute/Intermediate/Diuresis
o Priority: Prevention of infection
 Rehabilitative/Recovery
o Priority: Prevention of deformity

FIRST AID!
 STOP the burning process!
 PRIORITY:
o R-emove/rescue patient
o A-ctivate fire alarm
o C-onfine the fire
o E-xtinguish the fire

For FIRE EXTINGUISHER:

 P-ull the pin
  A-im at the BASE
 S-queeze handle
 S-weep from side to side
MANAGEMENT:
 Promote respiratory function (AIRWAY-inhalation injuries)
 Maintain fluid and electrolyte balance
o Parkland Formula: (fluid resuscitation for 24 hours)
 4mL(PLRS)xTBSAxWt(Kg)
 ½ - 1st 8hrs
 ¼ - 2nd 8hrs
 ¼ - 3rd 8hrs
 Relieve PAIN (MORPHINE)
 Prevent INFECTION
 DIET: (High Ca and HIGH CHON)
 GI support: CURLING’s ULCER
 WOUND CARE:
o Wounds dressed (prevent adhesions and contractures)
o Hydrotherapy/Whirlpool
o Debridement (Escharotomy)
o Skin grafting
 TOPICAL ANTIBIOTICS:
o Furacin (Nitrofurazone)
 Apply directly to the burn area
 SE: rash and contact dermatitis
o Mafenide Acetate (Sulfamylon)
 Apply directly to the burn area
 Administer ANALGESIC prior application
o Silver Sulfadiazine (Silvadene)
 Apply to the dressing and not directly on the burn area

SHOCK
 PROFOUND hemodynamic and metabolic disturbances due to inadequate blood flow in
the capillaries and other tissues in the body
 TYPES:
o HYPOVOLEMIC SHOCK
o CARDIOGENIC SHOCK
o DISTRIBUTIVE/VASOGENIC SHOCK

HYPOVOLEMIC SHOCK
 Loss of circulating blood
 Causes:
o Hemorrhage
o Burns
 o Severe dehydration
o Trauma
 Mngt:
o Fluid or Blood replacement

CARDIOGENIC SHOCK
 Decrease in circulating blood volume d/t insufficient CARDIAC pumping
 Causes:
o MI
o HF
o Dysrhytmias/Tamponade
 Mngt:
o Cardiac glycosides
o Dopamine
o Dobutamine

DISTRIBUTIVE/VASOGENIC SHOCK
 MASSIVE vasodilation
 SUBTYPES:
o Neurogenic/Spinal Shock
 Causes: SCI, Head Injury, General Anesthesia
o Septic/Toxic Shock
 Causes: Severe Infection  endotoxin vasodilation
o Anaphylactic Shock
 Causes: Severe allergic reaction  chemical mediators  vasodilation

STAGES of SHOCK
 COMPENSATORY
o Activation of the Sympatho-Adreno-Medullary Response (SAMR)
 ADH release
 Catecholamine (Epi/Norepi) release
 RAAS activation
 DECOMPENSATED/PROGRESSIVE
o Multi-organ Dysfunction Syndrome (MODS) occurs
o HypoBP
o Tachyprnea
o Tachycardia
 IRREVERSIBLE/REFRACTORY STAGE
o Compensatory mechanisms completely fail
o DEATH

 Clinical Manifestations:
o EARLY stage
  Everything is HIGH and FAST except GI and GU
 SNS stimulation
 Diaphoresis
 Cold clammy skin
o LATE stage
 Everything is LOW and SLOW
 Respiratory and cardiac collapse
 Management:
o Promote fluid balance and cardiac output
 CRYSTALLOID (PNSS/PLR)
 COLLOID (ALBUMIN)
o Promote and improve cardiac function
 Positioning (modified Trendelenburg)
 Vasoactive medications (Epinephrine)
 Medical Anti-shock Trousers
 Respiratory, renal, and GI support
 Promote SAFETY!
 Nutritional support