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Clients with Acid-Base

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

 Assess PaCO2: norm: 35 to 45 mm Hg


 Respiratory acidosis: >45 mm Hg
 Respiratory alkalosis: <35 mm Hg

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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

 Administer exogenous alkali


 Sodium bicarbonate

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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

 Interpret arterial blood gas values

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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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