NSG INCO 2
Medical-Surgical Nursing
ACID BASE IMBALANCES
PH AND H RELATIONSHIP
o pH – measures H ion concentration
o pH levels are inversely proportional to H concentration
o Acidosis: increase H ions because it releases H ions (the
more acidic, more H ions)
o Basic/Alkaline: increase in pH, decrease in H ions (kidneys
will retain H ions and bicarbonate)
o Acids: release H ions in solution
o Bases: Retain/accept H ions in solution
REGULATION OF ACID-BASE BALANCE
TWO CATEGORIES OF ACIDS
VOLATILE ACID
o Can be eliminated in the body as gas (has the ability to
escape)
o Carbonic Acid (H2CO3)
 only volatile acid produced in the body
 it dissociates into carbon dioxide and water the
CO2 is then eliminated from the body through
the lungs
 Respiratory Acidosis – mababa ang acid, mataas
ang carbon dioxide (potential acid)
NONVOLATILE ACID
o All other acids produced in the body must be metabolized
or excreted from body in fluid
o Ex: Lactic Acid, Hydrochloric Acid, Phosphoric Acid,
Sulfuric Acid
3 SYSTEMS THAT MAINTAIN pH DESPITE CONTINUOUS ACID
PRODUCTION
BUFFERS
o Substances that prevent major change in pH by removing
or releasing H ions
o Maintain acidity and alkalinity
o When excess acid is present in body fluid, they bind with
H ions to minimize change in pH
o If body fluids become too basic or alkaline, they release H
ions, restoring pH
o Major buffer systems
a. Carbonic Acid-Bicarbonate buffer system (CO2 +
Water = H2CO3)
b. Phosphate Buffer System – active in kidneys
c. Protein buffer system – ex. Hemoglobin
BICARBONATE-CARBONIC ACID
Bicarbonate
o A weak base
o When an acid is added to the system, the H ion in the acid
combines with Bicarbonate and the pH changes only
slightly
Kolayn
Carbonic Acid
o A weak acid
o Produced when CO2 dissolves in water
o If a base is added to the system, it combines with Carbonic
Acid and pH remains within the normal range
NORMAL RATIO
o 20 Parts bicarbonate (HCO3) is to 1 part carbonic acid
(H2CO3)
o It is this ratio that maintains the pH within the normal range
o Adding a strong acid to ECF depletes bicarbonate,
changing the 20:1 ratio and causing the pH to drop below
7.35. this is known as ACIDOSIS
o Addition of a strong base depletes carbonic acid as it
combines with the base. The 20:1 ratio again is disrupted
and the pH rises above 7.35, a condition known as
ALKALOSIS
o Intracellular and plasma proteins (serum albumin) -
Contribute to buffering for organic acids produced by
cellular metabolism
o In RBCs, hemoglobin acts as a buffer for H ion
o Inorganic phosphates also serve as extracellular buffers,
helping to maintain a stable pH (found in extracellular
compartment)
RESPIRATORY SYSTEM
o Carbon dioxide is a potential acid
o Acute increases in either CO2 or H ions in the blood
stimulate the respiratory center in the brain
 COPD – increase retention of carbon dioxide in
lungs kaya wag mo taasan ang oxygen (1-2L
only)
 Normal stimulus for breathing is increased in
carbon dioxide because it would stimulate your
respiratory center (medulla oblongata) as a
result both the depth and rate of respiration
increases (hypercapnia)
o As a result, both the rate and depth of respiration
increased. The increased rate and depth of lung ventilation
eliminates carbon dioxide from the body
o Morphine sulfate - Depresses the respiratory center
o Both the rate and depth of respiration decrease and retain
is retained
 RESPIRATORY ALKALOSIS – breathe into brown
paper bag (kulang ka sa carbon dioxide)
RENAL SYSTEM
o Excess nonvolatile acids produced during metabolism
normally are eliminated by the kidneys
Joanna Coline D. Montoya
 NSG INCO 2
Medical-Surgical Nursing
o The kidneys also regulate bicarbonate levels in ECF by
regenerating bicarbonate ions as well as reabsorbing them
in the renal tubules
o In acidosis, when excess H ion is present and the pH falls,
the kidneys excrete H ions and retain bicarbonate
o In alkalosis, the kidneys retain H ions and excrete
bicarbonate to restore acid-base balance

RESPIRATORY ACIDOSIS
RISK FACTORS
a. COPD – primary
 Chronic Bronchitis
 Emphysema – barrel chest (hindi maeliminate
CAUSES
and carbon dioxide)
 Asthma
b. Pulmonary edema
c. Acute respiratory distress syndrome

PATHOPHYSIOLOGY
COPD/ARDS/Pulmonary edema
↓
↓ pulmonary surface area for gas exchange (↑dead space in lungs)
↓
Hypoventilation
↓
↑ CO2 retention
↓
CO2 could readily cross blood brain barrier
↓
Cerebral blood vessels dilate (cerebral vasodilation) → headache,
blurring of vision, altered mental changes/status → lungs have
tendency to eliminate CO2 (hypercapnia – attempt to blow off CLINICAL MANIFESTATIONS
CO2) a. Headache – CO2 dilates cerebral blood vessels
↓ b. Hypercapnea – rapid rise in PaCO2 levels
Peripheral vasoconstriction (warm flushed skin, tachycardia) c. Warm flushed skin (due to peripheral vasoconstriction)
↓ d. Tachycardia
↓pH, ↑H ions e. Blurring of Vision
↓ f. Irritability, Decreased level of consciousness
H ions move into ICF, K moves into ECF g. Late signs: Disorientation, coma, confusion
↓ h. Electrolyte disturbance: hyperkalemia (increased
Hyperkalemia neuromuscular irritability – HIGH AND FAST)

MANAGEMENT
**Pag binigyan mo ng antihypertensive meds, magcocomplain ng a. Maintain patent airway
headache (effective ang meds because of vasodilation) – same b. Give medications as prescribed
rationale sa Cerebral vasodilation c. Administer antibiotic as ordered
d. Administer O2 (1-2L)
e. Perform tracheal suctioning, postural drainage, coughing
and deep breathing
f. Oral and IV fluids

Kolayn
Joanna Coline D. Montoya
 NSG INCO 2
Medical-Surgical Nursing
COMPENSATION COLLABORATIVE MANAGEMENT
a. Uncompensated a. Treat underlying cause, removing causative agent
 Normal bicarbonate b. Anxiety – anxiolytics and sedatives
b. Partially compensated c. Patients breath into brown paper bag with cupped hands
 Increased bicarbonate d. Allay anxiety. Recommend activities that promote
c. Fully compensated relaxation (Deep breathing)
 Normal pH e. Provide undisturbed rest periods
f. Stay with patient during periods of extreme stress and
RESPIRATORY ALKALOSIS anxiety
a. Anxiety/ Panic attack – most common cause
g. Offer reassurance and maintain calm, quiet environment
PATHOPHYSIOLOGY h. Institute safety measures and seizure precautions (pad
Anxiety/Panic Attack side rails) (seizure = side lying to promote drainage of
↓ secretions)
Hyperventilate
METABOLIC ACIDOSIS
↓
Causes: Acute Renal Failure
↓CO2, ↑pH, ↓H ions → move to ECF
↓ ↓ PATHOPHYSIOLOGY
↑ binding of Ca and Protein K move into ICF Acute Renal Failure
↓ ↓ ↓
Hypocalcemia Hypokalemia Kidneys don’t excrete excess acids
↓ ↓
↓ cell wall integrity, ↑ cell wall permeability, ↑ cell excitability ↓pH, ↑H ions
↓ ↓
Hypercalcemia H ions into ICF
↓ ↓
↓Cell excitability K pushed to ECF
↓ ↓
↓Neuromuscular Irritability Hyperkalemia

MANIFESTATIONS
a. Tachycardia
b. Anxiety, restlessness
c. Light headedness, paresthesia
d. Increased Deep Tendon Reflex (hyperreflexia), positive
Trousseaus and Chvostek’s sign
e. Tetany → laryngospasm → laryngochonstriction →
respiratory arrest
f. Decreased LOC
g. Convulsions, Seizures

Kolayn
Joanna Coline D. Montoya
 NSG INCO 2
Medical-Surgical Nursing
CLINICAL MANIFESTATIONS
a. Kussmaul’s respiration – breathing is rapid and deep,
SOB
 ↓HCO3, ↑H ions (kidneys will excrete H ions and
retain bicarbonate)
 For body to compensate, body will eliminate
carbon dioxide
b. Headache
 ↑CO2 → cerebral vasodilation → Headache
c. Signs of hyperkalemia
d. ECG:
 Tall T waves
 Prolonged PR interval
 Widened QRS

MANAGEMENT
a. Sodium Bicarbonate per IV (alkalinizing solution) – to
reduce the effect of the acidosis on cardiac function. Flush
it with NSS
b. Dialysis for Renal Failure
c. Institute safety precautions as necessary. Keep the bed in MANIFESTATIONS AND COMPLICATIONS
the lowest position, side rails raised. a. Electrolyte Imbalance: Hypocalcemia, Hypokalemia
d. Keep the clocks, calendars and familiar objects at bedside. b. Dizziness, Confusion, Muscle Twitching, Paresthesia
Reorient to time, place, and circumstances as needed. c. Headache
Allow significant others to remain with the client as much d. Decreased LOC
as possible. e. Nausea/ Vomiting
f. Late sign: Tetany, convulsions
METABOLIC ALKALOSIS
o Caused by vomiting and prolonged gastric suction OVER ALL MANAGEMENT
o Increase of H production a. Administer O2 as ordered
b. Seizures precautions
RISK FACTORS
c. Maintain patent IV
o Commonly associated with use of thiazides, furosemide,
d. Administer diluted potassium solutions with an infusion
other diuretics that deplete potassium stores, hydrogen
pump (hypokalemia)
and chloride ion loss from kidneys
e. Monitor I and O
o Excessive acid loss from GI tract – most common cause
f. Infuse ammonium chloride no faster than 1L over 4 hours.
PATHOPHYSIOLOGY Don’t administer to patients with hepatic or renal disease.
Causes  Rapid administration = hemolysis or RBC
↓ destruction
Loss of H ions/Chloride g. Carbonic Anhydrase Inhibitors (Diamox): increases renal
↓ excretion of HCO3
↑pH, ↑HCO3, ↓H ions
↓ ↓ CRITICAL TO REMEMBER
↑ binding of Ca with proteins H ions to ICF move to ECF RESPIRATORY AND METABOLIC ACIDOSIS
Result to the following:
↓ ↓
Hypocalcemia K moves to ICF a. Hyperkalemia
↓ b. CNS depression and may lead to coma
Hypokalemia c. Cerebral vasodilation
d. Increased ICP
Compensation: Kidneys retains H ions, remove HCO3
e. Peripheral vasoconstriction
f. Increased BP (hypertension)

Kolayn
Joanna Coline D. Montoya
 NSG INCO 2
Medical-Surgical Nursing
RESPIRATORY AND METABOLIC ALKALOSIS ALKALOSIS
Result to the following: CNS stimulant → SEIZURE
↓
a. Hypokalemia
CNS vasoconstriction
b. CNS stimulation and may lead to seizures
↓
c. Cerebral vasoconstriction
↓ Cerebral tissue perfusion
d. Increased ICP
↓
e. Peripheral vasodilation
Cerebral Ischemia
f. Hypotension
↓
g. Destroy ionized calcium that leads to hypocalcemia
Cerebral hypoxia
IN CAPSULE ↓
ACIDOSIS ALKALOSIS Cerebral tissue injury
CNS Depressant CNS Stimulant ↓
CNS Vasodilation CNS Vasoconstriction INFLAMMATION
Increased ICP Increased ICP ↓
Peripheral vasoconstriction Peripheral Vasodilation ↑ ICP
(hypertension) (hypotension) ↓
Hyperkalemia Hypokalemia Peripheral vasodilation
Hypocalcemia ↓
↓BP

ACIDOSIS
CNS depressant → COMA
↓
Cerebral vasodilation
↓
↑ Capillary Permeability
↓
IVC → ISC
↓
Cerebral Edema
↓
↑ ICP
↓
Peripheral Vasoconstriction
↓
↑BP

Kolayn
Joanna Coline D. Montoya