ACID-BASE BALANCE

I. Concepts of Acid-Base Balance

Acid, Bases, and Salts

• Acid. An acid is one type of compound that contains the hydrogen ion.
• Base. A base or alkali is a compound that contains the hydroxyl ion.
• Salt. A salt is a combination of a base and an acid and is created when the positive ions of a
base replace the positive hydrogen ions of an acid.
• Important salts. The body contains several important salts like sodium chloride, potassium
chloride, calcium chloride, calcium carbonate, calcium phosphate, and sodium phosphate.

Potential of Hydrogen

• pH. The symbol of pH refers to the potential or power of hydrogen ion concentration within
the solution.
• Low pH. If the pH number is lower than 7, the solution is an acid.
• High pH. If the pH is greater than 7, a solution is basic or alkaline.
• Neutral pH. If the pH is 7, then the solution is neutral.
• Changes. A change in the pH of a solution by one pH unit means a tenfold change in
hydrogen concentration.

Acid-base balance - equilibrium between the acid and base elements of the blood and body fluids.

Body's 3 mechanism to maintain acid-base balance:

1. Buferring mechanism
o Acid-base buffer - a solution containing two or more chemical compounds that prevent marked change in
hydrogen ions
o Buffer acts immediately to trap (H+) temporarily until renal and respiratory mechanisms act.
2. Respiratory compensation mechanism
o Lungs
o Lungs
• Under the control of medulla, controls CO2 and the carbonic acid content in the ECF by adjusting the
ventilation (by increasing PaCO2 which is a powerful stimulant for respiration) in response to the amount of
CO2 in the blood.
• Breathing faster or deeper (hyperventilation) - eliminates more CO2 resulting in increase pH.
• Slow, shallow breathing (hypoventilation) - accumulates CO2 and decreases pH.
1. Renal regulation of acid-base balance
o Kidneys - regulates bicarbonate level in the ECF and makes long term adjustment to pH.
• Regenerate and reabsorb bicarb from the renal tubular cells
 • In acidosis, excretes excess hydrogen ions and conserves bicarb ions and vice versa in alkalosis.
• Kidneys cannot compensate for the metabolic acidosis created by kidneys itself.

Acid base imbalance/disturbance:

• Common in the clinical practice, especially in critical units.
• Identification of specific imbalance is important to ascertain the underlying cause of the disorder and determininng
the appropriate treatment.
• It is important to take note of the acidity or alkalinity of the blood (pH) which is maintained by homeostatic
mechanism.
• Blood gas analysis is often used to identify the specific acid-base disturbance and degree of compensation.
• Diagnosing acid-base imbalance:
o Arterial Blood Gas (ABG)
o Anion gap estimation

Anion Gap estimation

• The difference between measure major positive and negative charges.
• Normal value is 8-14 mEq/L
• The sum of measured cations is greater than of measured anions due to the presence of unmeasured anions
(proteins, phosphates, sulfates, and organic acids as lactic acid and ketones)
• Increased anion gap may be the only clue that metabolic acidosis is present in a mixed acid-base disorder.

Arterial Blood Gas analysis

• Results from this provides information about alveolar ventilation, oxygenation, and acid-base balance.
• Still it necessary to evaluate the concentration of serum electrolytes (sodium, potassium and chloride) and CO2 as
they are the first sign of an acid-based disorder.
• Health history, PE should always be part of the assessment.

ABG parameters

Parameters Normal Values

• PH (H+) 7.35 - 7.45

• PCO2 partial pressure CO2 35 - 45 mmHg
• PO2 >80 mmHg
• HCO3 bicarbonate 22 - 26 mEq/L
• BE base excess +- 2mEq/L
• Oxygen saturation (SaO2%) >94%

ABG interpretation
1. Clasify the pH
• >7.45 alkalosis
• <7.35 acidosis

2. Determine the cause of disturbance

• Evaluate the PaCO2 and HCO3 in relation to pH
• ROME
o Respiratory
o Opposite - value of PaCO2 in relation to pH goes at opposite direction.
• E.G Respiratory acidosis - pH low, PaCO2 high
o Metabolic
o Equal - HCO3 and pH goes in the same direction
• E.G. Metabolic alkalosis - pH high, HCO3 high
3. Determine the compensation

RESPIRATORY ACIDOSIS
• Characterized by:
o pH<7.35
o PaCO2 >45mmHg
• Inadequate excretion of CO2 with inadequate ventilation, resulting to elevated plasma CO2 concentrations
• Caused by depression of respiratory center
o Narcotics/over sedation
o Ansthesia
o Respiratory arrest
o Paralysis of respiratory muscles
o Impaired ventilation
o Airway obstruction
• May also be associated in non-emergent situation like sleep apnea.
• Clinical manifestation:
o Increased pulse and respiratory rate
o Restlessness
o Headache
o Drowsiness
o Disorientation
o Coma
o Dysrhythmias
o Hypotension
o Hyperkalemia as a result of H+ shifts into the cells causing shift of potassium out of the cell.
• Assessment and Diagnosis:
o ABG
o Monitoring serum electrolytes
o Chest x-ray
o Drug screen if overdose is suspected
o ECG to identify cardiac involvement
• Management
• The goal of treatment is to improve ventilation
• Pharmacologic agents may be indicated:
o Bronchodilators to reduce bronchial spasm
o Antibiotics for respiratory infections
o Thrombolytics or anticoagulants for pulmonary emboli
• Pulmonary hygiene when necessary to clear respi tract of mucus and purulent drainage
• Adequate hydration if not contraindicated (2-3L/day) to keep mucous membranes moist facilitating removal of
secretions.
• Supplemental O2 as necessary
• If in mech vent, use appropriately to (avoid increase dead space, insufficient rate or volume settings, high FiO2)
so as not to cause rapid CO2 excretion.
RESPIRATORY ALKALOSIS
• Characterized by:
o pH >7.45
o PaCO2 <35 mmHg
• Is always caused by hyperventilation that results to excessive "blowing off" CO2
• Chronic respi alkalosis results from chronic hypocapnia
• Predisposing factors:
o Chronic hepatic insufficiency and cerebral tumors
 • Causes:
o Hypoxemia
o Anemia
o Fever
o Early in the exercise
o Angry
o Psychological dyspnea
• Clinical Manifestation:
o Light headedness - due to vasoconstriction and decreased cerebral blood flow
o Numbness and tingling from decreased calcium
o Tinnitus
o Sometime loss of consciousness
o Tachycardia
o Ventricular and atrial dysrhythmias
o Confusion
o Hypertension
o Blurred vision
• Assessment and Diagnosis
o ABG
o Seum electrolyte evaluation
o Toxicology screen to rule out salicylate intoxication
• Management:
o Depends of the underlying cause
o If caused by anxiety, instruct to breathe more slowly. Antianxiety agents if indicated
o Treatment of other causes is directed towards correcting the underlying cause.

METABOLIC ACIDOSIS
• Characterized by:
o pH <7.35
o Hco3 < 22 mEq/L
• Defined as a primary decreased in plasma HCO3 concentrations
• Chronic metabolic acidosis usually seen with chronic kidney disease.
• Causes:
o Prolonged severe diarrhea
o Renal failure
o Starvation
o Cardiac arrest
o Tissue hypoxia
o DKA
o Sepsis
o Shock
o Alcoholic keto acidosis
• Clinical Manifestation: may vary with severity
o Headache
o Confusion
o Drowsiness
o Increased respi rate, depth
o Nausea
o Vomiting
o Decreased BP
o Cold and clammy skin
 o dysrhythmias
• Assessment and Diagnosis
o ABG
o Hyperkalemia - due to shift of potassium out of the cells.
• Management:
o Directed towards correcting the imbalance
o Sodium bicarb is given when necessary. Caution when giving it during cardiac arrest as it can result to paradoxical
intracellular acidosis.
o In chronic metabolic acidosis, low calcium are treated first to avoid tetany
o Alkalizing agent may be given
o Hemodialysis or peritoneal dialysis

METABOLIC ALKALOSIS
• Characterized by:
o pH >7.45
o HCO3 > 26 mEq/L
• Results from increased bicarb in the ECF
• Predisposing factors:
o Those who are on diuretic therapy that promotes potassium excretion
o Cystic fibrosis
o Chronic ingestion of milk
o External drainage of gastric fluids
• Causes:
o Vomiting
o Gastric suction
o Diuretics such as furosemide
o IV NaHCO3 administration
• Clinical Manifestation:
o Tingling of fingers
o Dizziness
o Hypertonic muscles
o Depressed respiration
o Atrial tachycardia
o Decreased motility
o Paralytic ileus
o Frequent PVCs in ECG
o U waves on ECG
• Assessment and Diagnosis
o ABG
o Urine chloride - will help differentiate the cause of metabolic alkalosis if its vomiting, diuretic therapy or
excessing adrenocorticosteroid secretion.
• Management:
o Treatment is aimed at correcting the underlying cause.
o Includes restoring normal fluid volume by giving sodium chloring fluids.
o In those with hypokalemia, potassium is given as KCL
o H2 receptor antagonist such as cimetidine to reduce production of gastric hydrogen chloride
o Carbonic anhydrase inhibitors is given to patients who cannot tolerate rapid volume expansion.
BURNS
Burn injuries
• are painful, costly, disfiguring and often associated with long term disability
• Most common signs:
o Blisters
o Pain
o Swelling
o White or charred (black) skin
o Peeling of skin
• Burn care includes:
o Optimal fluid resuscitation
o Infection control
o Early excision and grafting
o Enhanced team approach
o Emergence of specialized burn centers

• Role of nurse in the care and management is to provide holistic evident-based care during all phases of burn injury
recovery.

INCIDENCE
• Affects people of all ages and socioeconomic status
• In the Philippines there is a higher incidence of burn injuries between March and April.
• Higher incidence of burn injuries occur in men than women
• Largest proportion of burn injury is flame related.
• Age-related factors that predisposes older adults to burn injury:
o Diminished mobility
o Postural stability
o Strength
o Coordination
o Sensation
o Visual acuity
o Decline memory
• Mortality associated with burn is higher in patients 60 years and older than in younger adults
• Factors that contribute to mortality in older adults:
o The skin of older adults (less elastic and thinner) affects the depth of injury and would healing, resulting in
higher morbidity and mortality amongst aged population.
o Pulmonary function becomes impaired. There is altered airway exchange, lung elasticity, and ventilation
o Decreased cardiac function.
o Malnutrition especially those who are institutionalized
o Decreased kidney and hepatic function which affects medication dosing due to altered medication clearance.

PREVENTION
• Nurse plays an important role in providing education especially in the community and home setting
• The WHO recommends heightened awareness of the burn injury and its risk factors to develop an effective burn
prevention program.
TYPES of BURN INJURY
• Thermal burns: Burns due to external heat sources which raise the temperature of the skin and tissues and cause
tissue cell death or charring. Hot metals, scalding liquids, steam, and flames, when coming in contact with the skin,
can cause thermal burns.
• Radiation burns: Burns due to prolonged exposure to ultraviolet rays of the sun, or to other sources of radiation
such as x-ray
• Chemical burns: Burns due to strong acids, alkalies, detergents, or solvents coming into contact with the skin and/or
eyes
• Electrical burns: Burns from electrical current, either alternating current (AC) or direct current (DC)

BURN DEPTH CLASSIFICATION

• First Degree (partial thickness)
o Affects only the epidermis, or outer layer of skin. The burn site is red, painful, dry, and with no blisters. Mild
sunburn is an example. Long-term tissue damage is rare and usually consists of an increase or decrease in the
skin color.
o Negative Nikolsky's sign (dislodgement of intact superficial epidermis by a shearing force)
o Caused by sunburn, splashes of hot liquid.
o Characteristic: erythema, blanching on pressure, no vesicles
• Second-degree (deep partial thickness)
o Involves the epidermis and part of the dermis layer of skin. The burn site appears
o Caused by flash, scalding or flame burn
o Very painful
o Characteristics: red, blistered, and may be swollen, shiny, wet after blister ruptures.
• Third-degree (full thickness) burns
o Destroys the epidermis and dermis. Third-degree burns may also damage the underlying bones, muscles, and
tendons. The burn site appears white or charred. There is no sensation in the area since the nerve endings are
destroyed.
o Caused by flame, chemicals, scalding, electric current
o Characteristic: wound dry, white, eschar (leathery or hard tissue due to loss of blood supply)

EXTENT OF BURN INJURY

Method used to estimate the Total Body Surface Area (TBSA) affected by burns
1. Rule of Nines
• The most common method used
• Based on the anatomic regions, each representing 9% of the TBSA.
• Guides clinician to quickly obtain an estimate burn size.

2. Lund and Browder Method

• More precise method
• recognizes the percentage of surface area of various anatomic parts in relation to the age of the patient.
• Done by dividing the body into very small areas thus allowing clinicians to obtain a more reliable estimation of TBSA
burned.
• Evaluation should be made upon arrival and reassessed within the first 72 hours because demarcation of the wound
and its depth are more visible and clear at this time.

3. Palmer Method
• Usually used in patients with scattered burns
SOURCE: Brunner and Suddarth's
MANAGEMENT of BURN INJURY
Burn care is typically categorized into three phases.

1. Emergent/Resuscitative Phase
• On-the-scene-care is the first step. This includes removing the patient from the source of injury and stop the
burning process.
• Duration is from onset of injury to completion of fluid resuscitation
• PRIORITIES:
o Primary survey: ABCDE
• Airway
• Breathing - supplying O2 of needed esp for carbon monoxide poisoning
• Circulation and cardiac status
• Disability - include neurologic deficit
• Expose and examine - while maintaining a warm environment
o Prevent Shock
• Fluid resuscitation is very crucial especially in burns greater that 20% TBSA to maintain adequate organ
perfusion.
• Peripheral IV line (large bore needle) should be established immediately.
o Prevention of respiratory distress
o Detection and treatment of concomitant injuries
o Wound assessment and initial care
• Wrap in dry, clean sheet to prevent wound contamination
• Tetanus prophylaxis

2. Acute/Intermediate Phase
• Follows the emergent phase and begins withing 48 - 72 hours after the burn injury
• PRIORITIES:
o Continued assessment and maintenance of respiratory and circulatory status, fluid and electrolyte balance, and
GI and kidney function.
o Infection prevention
• Burn patients incur the highest risk for health care associated infections (HAI) due to loss of skin barrier.
• Prevention of infection is crucial and can be achieved in various approach
• Use of barrier techniques - proper use of PPEs (gowns, gloves, mask and eye protection)
• Making sure that the environment is clean
• Application of appropriate topical antimicrobial agents
• Excision and closure of the burn wound
• Management of hypermetabolic response.
o Burn wound care - wound cleaning, debridement, topical antibacterial therapy, wound dressing, and wound grafting
if necessary)
o Pain management
o Nutritional support

3. Rehabilitative Phase
• From major wound closure to return to optimal level of physical and psychosocial adjustment.
• It is important to re-evaluate the patient for late complication related to burn injuries
• PRIORITIES:
o Prevention and treatment of scars and contractures
o Physical, occupational, and vocational rehab
o Functional and cosmetic reconstruction
o Psychosocial counselling
o Psychological support.
FLUID and ELECTROLYE ALTERATIONS in BURNS
• Burn injury rapidly forms edema, caused by increased perfusion to the injured area, making the patients prone to
fluid and electrolyte imbalances.
• This fluid shift is caused by the stimulation of local and systemic reactions brought by inflammatory mediators and
results in extensive shift of intravascular fluid, electrolytes and proteins into the surrounding interstitium.
• A superficial burn can form edema within 4 hours. While deeper burn continues to form edema up to 18 hours post
injury.
• Reabsorption of edema begins 4 hours post injury and is complete by 4 days post-burn injury.
• Rate of reabsorption depends on the extent of tissue damage.
• Adequate fluid resuscitation is paramount in burn injury to maintain tissue perfusion. However, extreme caution
should be observe as excessive fluid administration causes edema to both burned and non-burned tissue causing
ischemia and necrosis.
• Hyperkalemia
o Immediately after the injury
o Results from massive cell destruction
• Hypokalemia
o May occur later with fluid shifts and inadequate potassium replacement
• Hyponatremia
o May be present as a result of plasma loss or as a result of water shift from the interstitial space and returns to
the vascular space.

FLUID RESUSCITATION
• Is vital in burn injury esp for burns > 20% TBSA to maintain adequate organ perfusion
• Baseline weight and laboratory result are very important prior to initiation and must be closely monitored to avoid
under or over resuscitation with fluids.
• Shock, ischemic complication and multiple organ dysfunction syndrome occur with under-resuscitation.
• Over-resuscitation can cause heart failure, and pulmonary edema.
• To initiate, it is recommended to establish a peripheral IV line using a large bore needle to facilitate ease of fluid
administration.
• For large volume of fluid, a central venous line is recommended.
• Parkland (Baxter) formula
o Widely used formula for initial fluid resuscitation of burn victims
o 4 ml of Lactated Ringer's solution per Kg of body weight per %TBSA burned. Half of this has to be given during
the first 8 hours after injury and the remaining be delivered in the next 16 hours.
• E.G. patient weight 75 kg with 20% TBSA burned
4x75x20 = 6,000 mL fluid replacement within 24 hours.

• Bedside observation and clinical evaluations are useful to judge the adequacy of resuscitation.
• Closely monitor the following:
o LOC
o Vital signs
o Urine output - should be 30-50 mL/hour