MARK BILLY L.

PERPETUA, MAN RN

FLUIDS, ELECTROLYTES
and
ACID-BASE BALANCE
 BODY FLUID COMPARTMENTS
 Intracellular: 70%
 Extracellular: 30%
 Interstitial (11-12L: including lymph)
 Intravascular (6L: 3L plasma, 3L formed elements)
 Transcellular (1L: CSF, pericardial, synovial,
intraocular, pleural, sweat glands, digestive
secretions)
 ELECTROLYTES

Active chemicals
 Cation (+) : Na, K, Ca, Mg, H+
 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
 Osmotic Pressure and Oncotic Pressure (pressure exerted by protein alone)
 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
OSMOSIS
DIFFUSSION VS OSMOSIS
 REGULATION OF BODY FLUIDS

 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
 GAINS AND LOSSES

 KIDNEYS – Urine: 0.5-1ml/kg/hr (NORMAL URINE OUTPUT) 60kg – 30-60ml/hr

 SKIN – 0-1000mL per hour (insensible fluid loss)

 LUNGS – 300 mL every day (insensible fluid loss)

 GI Tract – 100-200 mL daily ((insensible fluid loss)

 LAB VALUES AND FLUID STATUS

 Urine specific gravity – measures kidney’s ability to conserve or excrete water

 NORMAL: ( DILUTED - less than )1.010 – 1.025 ( more than – CONCENTRATED)
 BUN – by-product of protein metabolism by the liver (muscle and diet)
 NORMAL: 10-20 mg/dL
 CREATININE – end product of muscle metabolism (better indicator of renal function)
 NORMAL: 0.7-1.4 mg/dL (AZOTEMIA – increase in waste product in the blood)
 Hematocrit – measures the volume of RBC in whole blood
 NORMAL: (hemoDILUTED- Plasma>RBC - less than)M: 42-52% F:35-47& (more than – RBC>Plasma - hemoCONCENTRATED
 FLUID AND ELECTROLYTE BALANCE
 KIDNEYS (urine formation)
 Heart and Blood vessels  Baroreceptors (pressure receptor)
 Lungs  Located in LEFT atrium, carotid, and aortic
arch
 Pituitary glands
 RAAS
 ADH (vasopressin – released by the posterior
pituitary gland)  Natriuretic peptides
 Adrenal Glands  ANP (atrial natriuretic peptide) and BNP (brain
natriuretic peptide)
 Aldosterone
 OSMRECEPTORS
 Parathyroid Glands (parathormone)
 Located on the surface of hypothalamus
 Pushes Ca from the bone into the blood
 Sense changes in sodium concentration
 Released in response to hypocalcemia
FLUID VOLUME
IMBALANCES

MARK BILLY L. PERPETUA, MAN RN

 FLUID VOLUME IMBALANCES
HYPOVOLEMIA  Manifestations:
 Thirst
 Causes:
 Weight loss
 Abnormal fluid losses
 Muscle weakness
 Vomiting,
 Concentrated urine
 Diarrhea
 Cool clammy skin
 GI suctioning
 Sweating  Shock (late sign)
 FLUID VOLUME IMBALANCES
 Medical/Nursing Mngt:
HYPOVOLEMIA
 If mild: Increase OFI
 Dx:
 If severe: Parenteral fluid
Elevated BUN and Crea resuscitation (PLR or
Elevated hematocrit PNSS

Elevated urine specific  I/O and weight monitoring

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

MARK BILLY L. PERPETUA, MAN RN

 ELECTROLYTE IMBALANCE

 EARLIEST manifestation of electrolyte imbalance

 Numbness, tingling, paresthesia

 UNIVERSAL manifestation of electrolyte imbalance

 Muscle weakness
 SODIUM

 SODIUM
Major EXTRACELLUAR cation
Normal: 135-145 mEq/L
Function: Aids in muscular contraction and
nerve impulse transmission
 SODIUM IMBALANCES
 HYPONATREMIA  Manifestations:

 Causes:  Headache

 Sodium loss  Irritability

 Low sodium intake  Disorientation

 Water gain (SIADH – Syndrome of  Muscle twitching

Inappropriate Anti Diuretic Hormone  Tremors
Release)
 Weakness
 Decreased aldosterone secretion
 Ataxia
 Diuretics use
 Seizure
 SODIUM IMBALANCES
 HYPONATREMIA
 Med Mngt:  Nsg Mngt:
 Parenteral sodium  Identify patient at risk
replacement  WOF initial S/Sx, N&V
 Water restriction  Encourage increase Na in diet
 Increased Sodium in DIET  Monitor VS and Neuro status
 SODIUM IMBALANCES
 HYPERNATREMIA  Med/Nsg Mngt:
 Manifestations:  Hypotonic solution
infusion (gradual lowering
 NEUROLOGIC: of Sodium)
restlessness
 Diuretics
 Other (same with
Hyponatremia)  Low SODIUM diet
 Avoid OTC drug with
high Na content
 POTASSIUM
 POTASSIUM
 Major INTRACELLUAR cation
 Normal: 3.5 – 5.5 mEq/L
 Function:
 Aids in neuromuscular contraction and nerve impulse
transmission
 Has high affinity with hydrogen ion (H+)
 Located in the muscle and GI tract
 POTASSIUM IMBALANCES
 HYPOKALEMIA  Manifestations:
 Causes:  Skeletal muscle weakness
 GI loss (vomiting, suctioning,  Cramps and paresthesia
diarrhea)  Fatigue
 Decreased K-intake  ECG: extra “U” wave
 Diuretics (potassium-wasting)  Decreased bowel sound
 Paralytic ileus
 Weak pulse/hypotension
 POTASSIUM IMBALANCES
HYPOKALEMIA  IV replacement
(INCORPORATION)
 Med Mngt:  K-sparing diuretics
 If not severe: K-rich foods
 If severe:  Nsg Mngt:
 Oral potassium drugs
 WOF early S/Sx
 Kalium durule: taken with
meals
 Liquid KCL: taken with
juice
 POTASSIUM IMBALANCES
 K-sparing  K-wasting
 Spirinolactone  Loop (furosemide, bumetanide,
torsemide)
 Amiloride
 Thiazide (diuril, hydrochlorodiuril,
 Triamterene metolazone)
 Osmotic (mannitol)
 POTASSIUM IMBALANCES
HYPOKALEMIA
 K-rich foods Carrot
Potato Raisin
Beans Avocado
Apricot Tomato
Prunes Orange
Banana
 POTASSIUM IMBALANCES
HYPERKALEMIA
 Causes:  Manifestations:
 Decreased renal excretion  Paresthesia/Irritability
of potassium  Abdominal cramping
 Increased K intake  Diarrhea
 Injury (Burns)  ECG: tall-peaked/tented T-
wave
 POTASSIUM IMBALANCES
 HYPERKALEMIA
 Med/Nsg Mngt:
 ECG and VS monitoring
 Potassium RESTRICTION
 Dextrose 10% in water with regular insulin (IV)
 “whenever glucose enters the cell, it brings potassium with it”
 Sodium bicarbonate (alkaline – combats acidosis thereby decreasing K+ level)
 Mild: Diuretics
 Mod-Severe: Kayexalate (Sodium Polyesterene sulfonate)
 cation-exchange resin (oral/enema) – (+) effective: Diarrhea
 WOF: hypoactive bowel movement
 CALCIUM
 CALCIUM
 Positively-charged ion
 Normal: 8.5-10.5 mg/dL or 4.5-5.5 meq/L
 Function:
 99% in bones and teeth, 1% in ECF
 Neural transmission
 Muscular contraction
 Blood clotting
 CALCIUM IMBALANCES
HYPOCALCEMIA  Manifestations:
 Causes:  Classic sign: TETANY
 Trosseau’s sign
 Low calcium intake
 Chvostek’s sign
 Ca malabsorption
 Arrhythmias
 Excessive Ca loss
 Fractures, tremors
 Parathyroid and thyroid
surgeries  Muscle cramps
 Laryngospasm
 CALCIUM IMBALANCES
HYPOCALCEMIA
 Med/Nsg Mngt:
High-Ca diet
IV Ca gluconate (Severe)
Vit. D and Parathormone
Seizure precaution
Prevent trauma: SAFETY!
 CALCIUM IMBALANCES
HYPERCALCEMIA  Manifestations:
 Causes: Change in LOC
Immobility Altered mental status
Excess intake of Ca Muscle weakness
Hyperparathyroidism Check for kidney
stones
Hypervitaminosis
ECG: short ST-segment
 CALCIUM IMBALANCES
 HYPERCALCEMIA
 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
 MAGNESIUM
 Normal: 1.3-2.3 mg/dL
 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
 HYPOMAGNESEMIA  Manifestations:
 Causes:  Classic sign: TETANY
 Trosseau’s sign
 GI losses
 Chvostek’s sign
 Ileum problems
 d/t accompanying hypoCa
 Alcohol withdrawal
 Alteration in psychological status
 Medications
 Cardiac arrhythmias
 Increased susceptibility to
digitalis toxicity
 MAGNESIUM IMBALANCES
 HYPOMAGNESEMIA
 Meds:
 Med/Nsg Mngt:
 Oral magnesium salts
 Mild: increase Mg in the diet
 IV magnesium SO4
 Green leafy veg
 Administered slowly
 Nuts
 Check DTR
 Seeds
 WOF: oliguria (<100mLx4hrs)
 Legumes
 Antidote: Calcium gluconate
 Grains
 Seafood
 Cocoa
 MAGNESIUM IMBALANCES
HYPERMAGNESEMIA
 Causes:  Manifestations:
 Kidney injury  Depression of CNS and
peripheral neuromuscular
 Diabetic ketoacidosis junction
 Excess Magnesium infusion  Ventricular block
 Addison’s disease  Cardiac arrest
 MAGNESIUM IMBALANCES
HYPERMAGNESEMIA
 Med/Nsg Mngt:
 Restrict Mg in diet
 Diuretics
 Calcium gluconate or calcium
chloride
 Reverse the effect of Mg on
cardiac muscle
 ACID-BASE
IMBALANCES

MARK BILLY L. PERPETUA, MAN RN

 ACID-BASE REGULATION

BUFFER SYSTEM
RESPIRATORY REGULATION
RENAL REGULATION
 ACID-BASE REGULATION
BUFFER SYSTEM
 pH (potential for hydrogen ion (H+)) (0.007 = 3 vs 0.07 = 2)

 REMOVE or RELEASE hydrogen ion

 Excessive hydrogen ion (ACIDOSIS) →
BUFFERS BIND
 Decrease in hydrogen ion (ALKALOSIS) →
BUFFERS RELEASE hydrogen ion
 ACID-BASE REGULATION
RESPIRATORY REGULATION
 RETAINS or ELIMINATES Carbon Dioxide
(potential acid)
Increased Removal of
INCREASED respiration excessive
carbon dioxide (tachypnea) carbon dioxide
(carbonic acid –
acidosis) Stimulates
respiratory
center (medulla)
INCREASED Reduced Retention of
Bicarbonate respiration carbon dioxide
(Alkalosis) (bradypnea)
 ACID-BASE REGULATION
RENAL REGULATION
 ELIMINATES or RETAINS HCO3 (alkaline)
 ELIMINATES or RETAINS hydrogen ion (acidic)
INCREASED Kidneys reabsorb and Decrease in hydrogen
Hydrogen ion regenerate bicarbonate ion (alkalosis) and
and EXCRETE hydrogen
(acidosis) increase in HCO3
ion
Increase in hydronium
INCREASED Bicarbonate is EXCRETED ion (acidosis) and
Bicarbonate and hydronium ion is decrease in
(alkalosis) RETAIN bicarbonate
 METABOLIC ACIDOSIS
 Causes:  Manifestations:
 Loss of bicarbonate (HCO3) INCREASED
 Intestinal loss RESPIRATORY RATE
 Diuretics
(Kussmaul’s respiration)
 Accumulation of acids
 Lactic acid CNS depression
 Ketoacids hyperkalemia
 Uremia/Azotemia
 Salycilate poisoning
 METABOLIC ACIDOSIS
 Dx:  Med/Nsg Mngt:
ABG analysis Correct underlying
cause
Hyperkalemia
Bicarbonate
ECG: Tall Peaked T-wave administration
Hemo/peritoneal
dialysis
 METABOLIC ALKALOSIS
 Causes:  Manifestations:
 Gain of bicarbonate (HCO3)  Respiratory depression
 Alkali intake  Hypokalemia
 Loss of hydrogen ion  Decreased GI motility and paralytic
 Vomiting ileus
 Suction  ECG: extra “U” wave

 Loss of potassium  S/Sx of hypocalcemia

 Diuretics  Tingling and spasms
 METABOLIC ALKALOSIS
 Dx:  Med/Nsg Mngt:
ABG analysis Avoid antacids
Hypokalemia Anti-emetics
ECG: Extra “U” wave Correct underlying
cause
NaCl and KCL infusion
 RESPIRATORY ACIDOSIS
 Causes:
 DISORDERS that
restrict/limit the RELEASE of
Carbon dioxide in the  Manifestations:
LUNGS
 TACHYcardia
 Asthma
 TACHYpnea
 Emphysema  Mental cloudiness
 Chronic bronchitis  Cerebrovascular dilation
 Pneumonia  Hyperkalemia
 pneumothorax  Increased ICP (severe)
 RESPIRATORY ACIDOSIS
 Dx:  Med/Nsg Mngt:
ABG analysis Correct underlying
cause
Hyperkalemia
BRONCHODILATOR
ECG: Tall-peaked T
wave Semi-fowler’s position
Purse-lip breathing
 RESPIRATORY ALKALOSIS
 Causes:  Manifestations:
EXCESSIVE release Lightheadedness
of Carbon dioxide in (vasoconstriction)
the LUNGS Numbness and tingling
(Hyperventilation) (hypocalcemia)
 RESPIRATORY ALKALOSIS
 Dx:
ABG analysis Med/Nsg Mngt:
Correct underlying
cause
BROWN BAG
Slow breathing
ARTERIAL BLOOD GAS
INTERPRETATION

MARK BILLY L. PERPETUA, MAN RN

NORMAL VALUES

 pH (ACID - less than - 7.35 – 7.45 – more than – ALKA)

 PaCO2 (ALKA less than- 35 – 45 – more than – ACID)
 HCO3 (ACID - less than - 22 – 26 – more than – ALKA)
ALLEN’S TEST

DONE BEFORE
A RADIAL
PUNCTURE
 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?
 PRACTICE

 pH 7.29 (acid)
 pH 7.52 (alka)
 PaC02 50 (acid) - respiratory
 PaC02 37 (normal) - RESPI
 HCO3 30 (alka) - metabolic
 HCO3 28 (alka) - METABOLIC
 PARTIALLY
 UNCOMPENSATED
COMPENSATED
METABOLIC ALKALOSIS
RESPIRATORY ACIDOSIS
 PRACTICE

 pH 7.43 (NORMAL –ALKA)

 pH 7.31 (acid)
ACID<7.4>ALKA) -
 PaC02 48 (acid) - respiratory
 PaC02 50 (ACID)
 HCO3 30 (alka) - metabolic
 HCO3 35 (ALKA)
 PARTIALLY COMPENSATED
 FULLY COMPENSATED
Respiratory acidosis
METABOLIC ALKALOSIS
 PRACTICE

 pH 7.31 (ABNORMAL - ACID)

 pH 7.49 (ABNORMAL – ALKA)
 PaC02 33 (ALKA)
 PaC02 32 (ALKA)
 HCO3 19 (ACID)
 HCO3 26 (NORMAL)
 PARTIALLY
 UNCOMPENSATED
COMPENSATED
RESPIRATORY ALKALOSIS
METABOLIC ACIDOSIS
 PRACTICE

 pH 7.38 (normal – acid)  pH 7.27 (abnormal – acid)

 PaC02 49 (acid) - respiratory  PaC02 33 (alka)
 HCO3 28 (alka) - metabolic  HCO3 20 (acid)
 fully compensated respiratory  Partially compensated
acidosis Metabolic acidosis
 ABG INTERPRETATION

 Level of compensation:
 Fully compensated: pH (NORMALIZED)
 Partially compensated: CO2 and HCO3 adjusts but pH
remains ABNORMAL
 Uncompensated: Either the CO2 or HCO3 does not
adjust (NORMAL), pH still ABNORMAL
 BURNS

MARK BILLY L. PERPETUA, MAN RN

 BURNS
 Causes:  Depth:
 First Degree (Epidermis)
 Thermal
 (+) pain/unblancheable redness
 Chemical  (Superficial-partial Thickness)
 Electrical  Second Degree (Dermis)
 Radiation  (+) pain/weeping/blisters/pearly
white
 (Deep-partial Thickness)
 Third Degree
(Subcutaneous/Muscles/Bones) (Full
Thickness)
DEGREE OF BURNS
 BURNS
 SHOCK PHASE/Fluid Accumulation Phase
 Occurs during the first 48 hours
 S/Sx:
 HYPOVOLEMIA
 Oliguria
 HyperK and HypoNa
 Metabolic acidosis
 PRIORITY: FLUID RESUSCITATION!
 BURNS

 DIURETIC PHASE/Fluid Remobilization Phase

 Occurs after 48 hours
 S/Sx:
 Diuresis
 HypoK and HypoNa
 Metabolic Acidosis (Elimination of HCO3)
 BURNS

 RECOVERY PHASE
 Occurs on the 5th day onwards
 S/Sx:
 HypoCa (granulation repair)
 Negative Nitrogen Balance (Utilization of CHON for repair)
 HypoK
 STAGES OF BURN CARE

 Emergent/resuscitative/Shock phase
 Priority: Fluid resuscitation
 Acute/Intermediate/Diuresis
 Priority: Prevention of infection
 Rehabilitative/Recovery
 Priority: Prevention of deformity
 BURNS
 FIRST AID!
 STOP the burning process!  For FIRE
EXTINGUISHER:
 PRIORITY:
 P-ull the pin
 R-emove/rescue patient
 A-im at the BASE
 A-ctivate fire alarm
 S-queeze handle
 C-onfine the fire
 S-weep from side to side
 E-xtinguish the fire
 E- vacuate
 BURNS
 MANAGEMENT:
 Promote respiratory function (AIRWAY-inhalation injuries)
 Maintain fluid and electrolyte balance
 Parkland Formula: (fluid resuscitation for 24 hours)
 4mL(PLRS)xTBSAxWt(Kg)
 ½ - 1st 8hrs
 ¼ - 2nd 8hrs
 ¼ - 3rd 8hrs
A PATIENT WAS RUSHED  TBSA: (__%) – Total Body Surface Area affected

TO THE ED WHO  FACE – ___%

SUSTAINED BURNS ON  ENTIRE BACK – __%

THE FACE, ENTIRE BACK,  ANTERIOR RIGHT UPPER EXTREMITY – __%

ANTERIOR RIGHT UPPER  ANTERIOR RIGHT LOWER EXTREMITY – __%

EXTREMITY AND THE  GENITALIA – __%

ANTERIOR RIGHT LOWER  110lbs/2.2 = 50kgs

EXTREMITY INCLUDING  PARKLAND FORMULA

THE GENITALIA. THE  =4ML (LRS)XTBSAXWT (KG)
PATIENT WEIGHS 110 LBS.  =4ML X __% X 50KGS
 =____ ml
COMPUTE FOR THE TOTAL  (1/2) - 1st 8 hours (____ ml)
FLUID RESUSCITATION  (1/4) - 2nd 8 hours (____ ml)
FOR 24 HOURS.  (1/4) - 3rd 8 hours (____ ml)
A PATIENT WAS RUSHED  TBSA: (37%) – Total Body Surface Area affected

TO THE ED WHO  FACE – 4.5%

SUSTAINED BURNS ON  ENTIRE BACK – 18%

THE FACE, ENTIRE BACK,  ANTERIOR RIGHT UPPER EXTREMITY – 4.5%

ANTERIOR RIGHT UPPER  ANTERIOR RIGHT LOWER EXTREMITY – 9%

EXTREMITY AND THE  GENITALIA – 1%

ANTERIOR RIGHT LOWER  110lbs/2.2 = 50kgs

EXTREMITY INCLUDING  PARKLAND FORMULA

THE GENITALIA. THE  =4ML (LRS)XTBSAXWT (KG)
PATIENT WEIGHS 110 LBS.  =4ML X 37% X 50KGS
 =7400 ml
COMPUTE FOR THE TOTAL  (1/2) - 1st 8 hours (3700 ml)
FLUID RESUSCITATION  (1/4) - 2nd 8 hours (1850 ml)
FOR 24 HOURS.  (1/4) - 3rd 8 hours (1850 ml)
 TBSA: (__) – Total Body Surface Area affected
 Entire head –
 Entire upper extremities –
 Entire anterior trunk and abdomen –
 Genitalia –
 80lbs/2.2lbs = __ kgs
 PARKLAND FORMULA
 =4ML (LRS)XTBSAXWT (KG)
 =4ML X __% X ___ KGS
 =____ ml
 (1/2) - 1st 8 hours (___ ml)
 (1/4) - 2nd 8 hours (___ ml)
 (1/4) - 3rd 8 hours (___ ml)
 TBSA: (46%) – Total Body Surface Area affected
 Entire head – 9%
 Entire upper extremities – 18%
 Entire anterior trunk and abdomen – 18%
 Genitalia – 1%
 80lbs/2.2lbs = 36.36 kgs
 PARKLAND FORMULA
 =4ML (LRS)XTBSAXWT (KG)
 =4ML X 46% X 36.36 KGS
 =6690 ml
 (1/2) - 1st 8 hours (3345 ml)
 (1/4) - 2nd 8 hours (1672 ml)
 (1/4) - 3rd 8 hours (1672 ml)
 TBSA: (__) – Total Body Surface Area affected
 Entire Right lower extremity – __%
 Anterior Left lower extremity – __%
 Lower back – __%
 55kgs
 PARKLAND FORMULA
 =4ML (LRS)XTBSAXWT (KG)
 =4ML X __% X 55 KGS
 =___ ml
 (1/2) - 1st 8 hours (___ ml)
 (1/4) - 2nd 8 hours (___ ml)
 (1/4) - 3rd 8 hours (___ ml)
 TBSA: (36%) – Total Body Surface Area affected
 Entire Right lower extremity – 18%
 Anterior Left lower extremity – 9%
 Lower back – 9%
 55kgs
 PARKLAND FORMULA
 =4ML (LRS)XTBSAXWT (KG)
 =4ML X 36% X 55 KGS
 =7920 ml
 (1/2) - 1st 8 hours (3960 ml)
 (1/4) - 2nd 8 hours (1980 ml)
 (1/4) - 3rd 8 hours (1980 ml)
 TBSA: (__%) – Total Body Surface Area affected
 Face – ___%
 Entire back – __%
 Half of the left upper extremity – ___%
 Half of the lower extremities – __%
 45 kgs
 PARKLAND FORMULA
 =4ML (LRS)XTBSAXWT (KG)
 =4ML X __% X 45 KGS
 =_____ mL
 (1/2) - 1st 8 hours (_____ ml)
 (1/4) - 2nd 8 hours (_____ ml)
 (1/4) - 3rd 8 hours (_____ ml)
 TBSA: (45%) – Total Body Surface Area affected
 Face – 4.5%
 Entire back – 18%
 Half of the left upper extremity – 4.5%
 Half of the lower extremities – 18%
 45 kgs
 PARKLAND FORMULA
 =4ML (LRS)XTBSAXWT (KG)
 =4ML X 45% X 45 KGS
 =8,100 mL
 (1/2) - 1st 8 hours (4,050 ml)
 (1/4) - 2nd 8 hours (2,025 ml)
 (1/4) - 3rd 8 hours (2,025 ml)
 BURNS
 MANAGEMENT:
 Relieve PAIN (MORPHINE)  WOUND CARE:
 Prevent INFECTION  Wounds dressed (prevent
 DIET: (High Ca and HIGH adhesions and
CHON) contractures)
 GI support: Antacids/PPIs (proton pump  Hydrotherapy/Whirlpool
inhibitors - -prazole
(omeprazole/pantoprazole/esomeprazole/la  Debridement
nsoprazole)
 CURLING’s ULCER
(Escharotomy)
 Skin grafting
 TYPES OF SKIN GRAFT
 Autograft-using the patient's own skin.
 Allograft-using skin obtained from another person.
 Xenograft-free skin grafts obtained from a non-human source (usually a pig)
 BURNS
 TOPICAL ANTIBIOTICS:
 Furacin (Nitrofurazone)
 Apply directly to the burn area
 SE: rash and contact dermatitis

 Mafenide Acetate (Sulfamylon)

 Apply directly to the burn area
 Administer ANALGESIC prior application

 Silver Sulfadiazine (Silvadene) - Flammazine

 Apply to the dressing and not directly on the burn area
 SHOCK

MARK BILLY L. PERPETUA, MAN RN

 SHOCK

 PROFOUND hemodynamic and metabolic disturbances

due to inadequate blood flow in the capillaries and other
tissues in the body
 TYPES:
 HYPOVOLEMIC SHOCK
 CARDIOGENIC SHOCK
 DISTRIBUTIVE/VASOGENIC SHOCK
 SHOCK
 Causes:
HYPOVOLEMIC
 Hemorrhage
SHOCK
 Burns
 Loss of circulating blood
 Severe dehydration
 Trauma
 Mngt:
 Fluid or Blood
replacement
 SHOCK
 CARDIOGENIC SHOCK  Causes:
 MI
 Decrease in circulating
blood volume d/t  HF
insufficient CARDIAC  Dysrhytmias/Tamponade
pumping  Mngt:
 Cardiac glycosides
 Dopamine
 Dobutamine
 SHOCK
 DISTRIBUTIVE/VASOGENIC SHOCK
 MASSIVE vasodilation

 SUBTYPES:
 Neurogenic/Spinal Shock
 Causes: SCI, Head Injury, General Anesthesia
 Septic/Toxic Shock
 Causes: Severe Infection → endotoxin →vasodilation
 Anaphylactic Shock
 Causes: Severe allergic reaction → chemical mediators → vasodilation
 SHOCK

 STAGES of SHOCK
 COMPENSATORY
 Activation of the Sympatho-Adreno-Medullary Response (SAMR)
 ADH release
 Catecholamine (Epi/Norepi) release
 RAAS activation
 SHOCK
 STAGES of SHOCK
 DECOMPENSATED/PROGRESSIVE  IRREVERSIBLE/REFRACTORY STAGE

 Multi-organ Dysfunction  Compensatory mechanisms

Syndrome (MODS) occurs completely fail
 HypoBP  DEATH

 Tachyprnea
 Tachycardia
 SHOCK
 Clinical Manifestations:
 EARLY stage  LATE stage

 Everything is HIGH and FAST  Everything is LOW and SLOW

except GI and GU  Respiratory and cardiac collapse
 SNS stimulation
 Diaphoresis
 Cold clammy skin
 SHOCK
 Management:  Vasoactive medications
(Epinephrine)
 Promote fluid balance and
cardiac output  Medical Anti-shock Trousers
 CRYSTALLOID (PNSS/PLR)  Respiratory, renal, and GI
 COLLOID (ALBUMIN)
support

 Promote and improve cardiac  Promote SAFETY!

function  Nutritional support
 Positioning (modified
Trendelenburg)