Professional Documents
Culture Documents
Imbalances
Objectives
Describe the interdependence of buffers, excretion of acid by
the lungs, and excretion of acid by the kidneys in the regulation
of acid-base balance.
Describe the impact of electrolytes on acid-base balance.
Describe compensatory actions by the body that maintain acid-
base balance.
Analyze the specific components of arterial blood gases to
determine acid-base balance.
Describe each disorder of acid-base balance.
Identify the specific component, Paco2 or HCO3, that is primary
in each disorder.
Identify the major causes, risk factors, pathophysiology, clinical
manifestations, and outcomes management of each disorder.
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Regulation of Acid-Base
Balance
Normal pH is 7.35 to 7.45
Normal cell function depends on regulating
hydrogen ion (H+)
H+ production increases, pH falls
Modulation of serum pH interdependent
systems
Chemical buffering in blood plasma and cells
Excretion of acids (CO2) by lungs
Excretion of acid or regeneration of base (HCO3) by
kidney
CO2 lowers, pH rises 13 - 3
Regulation of Acid-Base
Balance
Law of mass action
Regulation of volatile acid (can be
converted to gases) by lungs
CO2 produced by cells as by-product of
energy production
CO2 diffuses into blood and mixes with
H2O to produce H2CO3 which then
separates into H+ and HCO3
(bicarbonate)
Lungs help expel or retain CO2
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Regulation of Acid-Base Balance
Regulation of fixed acids (gases not
converted into gases) and
bicarbonate by the kidneys
Kidneys regulate pH by secreting H+
into urine or by regenerating HCO3
for reabsorption into the blood
Kidney regulate works until pH <4.5
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Regulation of Acid-Base
Balance
Urinary buffer systems
Bicarbonate
Ammonia
Phosphate
Principle of electroneutrality effect
Henderson-Hasselbach equation
Relationship among pH, acid, and
bases
20 parts base to 1 part acid
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Acid-Base Regulatory Systems
Acid-base compensation
pH normalized by lungs (within minutes)
and kidneys (within hours)
Acid-base correction
Occurs when problem is resolved
Analysis of arterial blood gases
Determines type of imbalance
Evaluates degree of compensation
Interpreting ABG results (see Critical
Monitoring box)
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Analysis of Arterial Blood
Gases
Classify the pH: norm: 7.35 to 7.45
Acidemia: <7.35
Alkalosis: >7.45
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Analysis of Arterial Blood
Gases
Assess HCO3: norm 22 to 26 mEq/L
Metabolic acidosis: <22 mEq/L
Metabolic alkalosis: >26 mEq/L
Determine if compensated
CO2 and HCO3 are abnormal in opposite
directions (one is acidic and one is
alkalotic)
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Analysis of Arterial Blood
Gases
Identify primary disorder
The acid-base component most
consistent with the pH disturbance
Classify degree of compensation
Simple compensation
Complex compensation
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Disorders of Acid-Base
Balance
Acidosis
Pathologic process causing excess acid
Acidemia
Excess acid in the blood
Decreased serum pH
Alkalosis
Pathologic process causing excess base
Alkalemia
Excess base in blood
Elevated serum pH
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Respiratory Alkalosis
Etiology
Hyperventilatory states
CO2 eliminated
Some causes
Pulmonary disorders (pneumonia, embolism)
Acute anxiety
Stimulant drugs (epinephrine)
Neural disorders (stroke, intracranial lesions)
Pathophysiology
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Respiratory Alkalosis
Clinical manifestations
Hyperventilation
Paresthesias, lightheadedness, confusion
High pH, low PaCO2, HCO3 levels fall with
compensation
Outcome management
Treatment of underlying disorder
Respiratory support
O2therapy
Rebreathing
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Respiratory Acidosis
Etiology: hypoventilatory states
Some causes
COPD, infections, cardiac diseases,
Guillain-Barré syndrome, obesity,
inadequate mechanical ventilation
Pathophysiology
Clinical manifestations
Hypoventilation, hypoxemia
Tremors, seizures, lethargy
Low pH and high PaCO2
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Respiratory Acidosis
Outcome management
Treat underlying cause
Respiratory support
Mechanical ventilation
Cautious O2 administration to CO2 retention
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Metabolic Alkalosis
Etiology
Loss of acid or gain of base
Some causes
Vomiting, long-term gastric suctioning,
administration of NaHCO3, overuse of
diuretics
Pathophysiology
Clinical manifestations
Adaptive hypoventilation
Lethargy, confusion, seizures
High pH and high HCO3
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Metabolic Alkalosis
Outcome management
Treat the underlying disorder
Promote loss of bicarbonate
Acetazolamide sodium (Diamox)
Administer exogenous acid
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Metabolic Acidosis
Etiology
Accumulation of acid or loss of base
Anion gap (Nl 12 ± 4)
Some causes
Lactic acidosis, diabetic ketoacidosis,
azotemic renal failure, diarrhea
Pathophysiology
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Metabolic Acidosis
Clinical manifestations
Compensatory hyperventilation
Low pH and low HCO3
Outcome management
Treatment of underlying disorder
Respiratory support
Mechanical ventilation
Administration of exogenous alkali
Sodium bicarbonate
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Complex Acid-Base
Disorders
Etiology
Suspect when PaCO2 value and
HCO3 levels do not correlate with pH
or when ABG evidence of
compensation exceeds predicted
levels
Some causes
Cardiac arrest, complicated COPD
Pathophysiology
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Complex Acid-Base Disorder
Nursing management
Assessment of clients at risk
Diabetes, renal disease, the older adult
Vomiting, diarrhea, enteric drainage
Burns, fever, sepsis
Total parenteral nutrition (TPN) or enteral
feedings
Mechanical ventilation
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Complex Acid-Base Disorder
Obtain arterial blood gases
Perform Allen’s test before obtaining
Minimize sampling errors
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Diagnosis, Outcomes,
Interventions
Nursing diagnoses
Ineffective Breathing Pattern
Ineffective Tissue Perfusion
Risk for Injury
Outcomes
Collaborative
Interventions
Correct the cause
Provide respiratory support
Administer exogenous acid or alkali
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Thank you!
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