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Pathopharmacology of
Acid Base Imbalances
Wanda Lovitz, APRN
After this lecture (& for the exam) you
should be able to:
 Understand the underlying pathophysiology of
acid-base imbalances
 Identify who is at risk for acid-base disorders and
why
 Analyze ABG’s given to you *or* select a set of
ABG’s that would be consistent with a patient
scenario
 Explain what someone looks like who is
experiencing an acid-base disorder
 Discuss what you the nurse can do to treat acidbase disorders
Overview:
Definition of Acid-Base
Regulators of Acid-Base
• Blood buffer system
• Lungs
• Kidneys
Types of Imbalances
• Respiratory acidosis
• Respiratory alkalosis
• Metabolic acidosis
• Metabolic alkalosis
Uncompensated, Partially Compensated
Or Fully compensated
Definitions:
 Acids - Contain H+
 Alkali(Base) -Contain NO H+, but accept them from
acids
 pH
= Measure of concentration of H+ in body fluid
Acid Base
 pH Scale
1-14
7 Neutral (water)
< 7 Acid
> 7 Alkali
 Normal body fluid pH 7.35 - 7.45
PH of various liquids
PH = measurement of acidity or alkalinity of the blood
Three Major Homeostatic Regulators of
Acid-Base
BLOOD BUFFER SYSTEMS
 Lungs
 Kidneys
Blood Buffer System as a regulator of PH
“Buffer” - acts as a chemical
sponge, by either soaking up or
releasing H+ so pH remains stable
BUFFERS JOB  to combine with acid/base
added to the system to prevent marked CHANGE in pH
acts within 1 second!!
Blood buffer system with exercise
Blood Buffer System
Acidic Blood
 Alkalotic Blood
 Decrease in force of cardiac
 Interferes with tissue
contractions
 Decrease in vascular
response to catecholamines
 Decrease in the effect of
some medications
oxygenation
 Intereferes with normal
NEUROLOLGICAL and
MUSCULAR function
Three Main Buffer Systems
Body’s Self Regulator System
 CARBONIC ACID - BICARBONATE SYSTEM
(H²CO³)
( HCO³)
 Phosphate System (need not know for now)
 Protein System (need not know for now)
H2CO3 - HCO3 System
(carbonic acid/bicarbonate system= most important buffer system in the ECF)
If strong acid is introduced into body:
HCl + NaHCO³
(hydrochloric acid) + (sodium bicarb)
H²CO³ + NaCl
(carbonic acid) +“Weak
(sodiumacid
chloride)
”
Dissociates into H²O and CO²
& is excreted by lungs
H+ =  PH (blood is more acidic)
H2CO3 (Carbonic acid) really is all about the LUNGS
CO2 and H2O released with EXHALATION
H2CO3 - HCO3 System
If strong base is introduced into body:
NaOH + H²CO³

NaHCO
3 + H²O
“buffer”
“weak base”
(hydroxide/soda)
(carbonic acid)
(sodium bicarbonate)
(water)
excreted by kidneys
H+ = PH (blood is more alkalotic)
HCO3 (Bicarbonate) is really all about the KIDNEYS
Hydrogen
EXCRETED by the kidney
The ability to maintain a stable pH relies on a
STEADY RATIO:
(base)
HCO³
20
(acid)
H²CO³
1
• Exact quantities not important as long as
ratio remains 20 : 1
Simple Scale Explanation Of HCO³/CO² Ratio
So... Too much acid, need to ADD BASE or (take away acid) to balance the scale
AND ....Too much base, need to ADD ACID (H+) or (take away base)
to BALANCE the scale
Respiratory Control of pH
 Responds in MINUTES to hours
 Remember the ‘blood buffer system responds in SECONDS!
 Lungs are the primary controller of H²CO³ ( H+/acid) supply
CO2 is carried in the blood to the LUNGS. In the
lungs, excess CO2 combines with H2O to form
carbonic acid (H2CO3)
This triggers the lungs to increase or
decrease the rate and depth of ventilation
H²CO³ 
CO² + H²O excreted in exhalation
Rate
Depth
>
of respirations
released
control amount of CO²
<
retained
Respiratory Control of pH
 When pH is ___ then there is an __ in the respiratory
rate/depth
Result: greater excretion of CO² via lungs
“CO2 is blown off”
 When pH is ___ then there is a ___ in the respiratory
rate/depth
Result: “CO² retained”
Renal Control of pH
 Responds in HOURS TO DAYS
 Remember the blood buffer responds in
SECONDS and the lungs respond in MINUTES TO
HOURS
Kidneys are the primary controller of
HCO³ (base/alkalosis) supply
Renal Control of pH
 When pH is __ , kidneys excrete H+
( H+) and HCO³ (bicarb) is formed
and retained.
 When pH is ___ , kidneys retain
H+
(acid or H+)
and HCO³ is excreted.
Acid Base imbalances can be assessed
in the clinical setting by using
serum lab plasma findings….
Find out the”story” behind WHY the ABGs
were ordered
Arterial Blood Gases
“ABG’s”
Purpose: To ASSESS acid-base status and
to determine adequacy of oxygenation and
ventilation
Arterial Blood Gases Consist of:
 pH
 indicates balance or impeding acidosis/alkalosis
 7.35-7.45
 pCO2 (chemoreceptors in the brain)
 respiratory parameter (Lungs can only remove carbonic acid)
 35-45 mm Hg
 HCO3
 metabolic (kidney) parameter (kidneys can remove other acids,
ie. Lactic acid (but NOT carbonic acid)
 22-26 mEq/L
Arterial Blood Gases vs Pulse Oximetry reading
 PaO2 Saturation =
partial pressure of oxygen in the plasma of ARTERIAL blood

Measured via ABG (INVASIVE BLOOD TEST)



Free/unbound oxygen molecules
Is an indication of TISSUE PERFUSION
Determined by ALVEOLAR PO2 and NOT related to hgb

Normal 80-100 mm Hg

Start supplemental oxygen if below 60 mm Hg
 SpO2 = measured by PULSE OXIMETRY







NONINVASIVE
Indicates the percent of oxygen bound to hemoglobin.
Measures blood saturation
NOT ABLE TO DETECT TISSUE HYPOXIA
Expressed in percentage
Normal is 95-98 %
Take action if below 90%
Key Definitions
 Primary EVENT
 Is the PROBLEM that initiates the acid-base imbalance
 Hypoventilation, hyperventilation, diarrhea, vomiting, pain
 Primary DISORDER
 Is WHAT RESULTS from the primary event
 Respiratory acidosis/alkalosis, metabolic acidosis/alkalosis
 Compensatory mechanisms
 Physiologic activities that ADJUST THE PH
TOWARD A MORE NORMAL LEVEL without
correcting the underlying cause of the disorder
 If lungs are the source of the problem... Kidneys compensate
 If kidneys are the source of the problem .... Lungs compensate
Primary Acid Base Disorders
Acidosis Occurs:too much carbonic acid OR
not enough bicarb
 H+ in blood (acid)…too much acid
 Examples of PRIMARY EVENTS:
 RESPIRATORY acidosis  problem or cause: HYPOVENTILATION (CO2 retained = EXCESS
CARBONIC ACID)
HCO³in blood (bicarbonate) ….not enough bicarbonate
 Examples of PRIMARY EVENTS:
 → METABOLIC acidosis  problem or cause: EXCESS PRODUCTION OF LACTIC ACID
 Metformin/Glucophage
 ketone production as with DKA
 kidney dysfunction resulting in kidneys unable to secrete acid(phosphorus,uric acid)
 persistent diarrhea = losing base
Diarrhea vs Vomiting:
acid/base
 Secretions BELOW the
stomach (including pancreatic and
biliary secretions) are relatively
ALKALINE
 So prolonged diarrhea could
cause metabolic acidosis
 The body is losing HCO3
(bicarb) – so balance of 20:1
is shifted towards acid.
 Secretions ABOVE the
pyloric sphincter are
relatively ACIDIC
 So…prolonged vomiting
could cause metabolic
alkalosis
 The body is losing acid H+ so the balance of 20:1 is
shifted towards alkaline.
Drawing by nursing student showing effect
of vomiting & diarrhea on ABGs
Alkalosis Occurs:
too much Bicarb OR not enough CARBONIC ACID
 in blood HCO³ (bicarbonate)…too much
BICARBONATE
 Examples of primary events:
 Metabolic ALKALOSIS
 taking excess baking soda, alka-seltzer
problem or cause: hypokalemia causing hydrogen to shift into the intracelllular space,
prolonged vomiting (loss of HCL from vomiting causes hydrogen ions to be lost)
  in blood excretion of hydrogen (H+)…not enough
CARBONIC ACID
 Examples of primary events:

Respiratory ALKALOSIS
  problem or cause: hyperventilation
General Cause of Imbalance is
termed:
¤ “Metabolic”
¤ “Respiratory”
¤ HCO3 (bicarbonate)
¤ H²CO³(carbonic acid)
level changes
secondary to
metabolic
alterations
(kidneys)
level changes
secondary to
respiratory
alterations
(lungs)
Respiratory Acidosis:
Acute & Chronic
 H²CO³ excess in ECF
(too much acid/H+)
 Cause:
 Hypoventilation  “primary event”  CO2 retained (H+)
 Acute vs chronic causes (resp arrest vs COPD)
 ABGs:
 pH < 7.35  A
 pCO2 > 45
A (more H+) retaining CO2 and H2)
 HCO3 22-26 *↔
* HCO3 WNL with acute respiratory acidosis; no time for kidneys to
compensate
Respiratory Acidosis
 Clinical S/S:
 CNS depression causing hypoventilation (head injury, narcotics,
sedatives, anesthesia, pulmonary disorders, pain, abdominal distension,chest
wall deformities, neuruomuscular problems)
 Dyspnea, respiratory distress, shallow respirations
 H/A, restlessness, confusion
 Tachycardia, arrhythmias
  LOC, stupor, coma
 Nursing actions:
 aimed at INCREASING VENTILATION and improving O²CO² exchange
Respiratory Alkalosis
 H²CO³ (CARBONIC ACID) DEFICIT in ECF
 Cause:
 Hyperventilation  primary event CO2 blown off
 Pain, increased metabolic demands such as with fever, sepsis,
some medications (resp stimulants), acute anxiety, any lung
disease that causes SOA, CNS lesions
 ABGs:
 pH > 7.45 ↑ B
 pCO2 < 35 ↓ B (less H+) blowing off CO2 and H2O
 HCO3 22-26 ↔
Respiratory Alkalosis
 Clinical S/S:
 CNS over-excitability




Light headedness, numbness, tingling
Confusion, blurred vison
Numbness of hands and feet
Hyperactive reflexes, seizures
 Nursing Actions:
 Treatment directed toward cause
 Breathing into a paper bag will cause CO2 to be re-breathed
Metabolic Acidosis
 HCO³ (BICARBONATE) DEFICIT in ECF
 excess acids are added OR bicarb is lost
 PH less than 7.35
 HCO3 less than 22
 Causes (primary events):
 Renal disease (kidney impairment affects acid secretion)
 Diabetes (Type I DM) … DKA  ketones (acids)
 Prolonged diarrhea (relative increased acid d/t loss of HCO3)
 Starvation (body using fat for energy resulting in ketosis)
Metabolic Acidosis
 ABGs:
 pH < 7.35  A
 pCO2 - 35-45 ↔
 HCO3 < 22 Acid (less base)
Metabolic Acidosis
 Clinical S/S:
 CNS depression
 Kussmaul respirations (DKA)
 Nursing Actions:
 Treatment directed toward cause
 IV NaHCO3 (sodium bicarbonate)
Metabolic Alkalosis
 HCO³
(BICARBONATE) EXCESS in ECF
 excess H+(acid) are lost or HCO³(base) is
added
 Causes (primary events):
 Increased intake of baking soda, Alka-Seltzer
 Increased loss of HCl such as with prolonged vomiting or
gastric suction
Metabolic Alkalosis
 ABGs:
 pH > 7.45 B
 pCO2 – 35-45 ↔
 HCO3 > 26
B
 Clinical S/S:
 CNS overexcitability
 Nursing actions:
 directed toward cause
In all A/B imbalances the body attempts to
take corrective action in order to maintain
a normal pH
This is referred to as: COMPENSATION
and the compensatory mechanism will be
opposite of the cause…
RESPIRATORY Acidosis/Alkalosis:
Compensation
 Are the results of respiratory
alterations and the KIDNEY
compensates by either:
 conserving HCO3 (bicarbonate) ions (acidosis correction)
 excreting HCO3 (bicarbonate)ions (alkalosis correction)
How fast for the kidneys to compensate? Hours to days
METABOLIC Acidosis/Alkalosis:
Compensation
 Are the results of metabolic alterations
and the LUNGS compensates by either:
 conserving CO2 ions (alkalosis correction)
 excreting CO2 ions (acidosis correction)
(The kidney also attempts to “correct” imbalance by
retaining/excreting HCO³)
How fast for the lungs to compensate? Minutes to hours
Expected Directional Changes in Blood Gases with
Primary Acid-Base Disorders
Primary Disorder
Respiratory acidosis
(acute)
(uncompensated)
Respiratory
alkalosis
(uncompensated)
Metabolic acidosis
(uncompensated)
Metabolic
alkalosis
(uncompensated)
pH
PaCO²
HCO³
Expected Directional Changes in Blood Gases with
Primary Acid-Base Disorders
Primary Disorder
Respiratory acidosis
(acute)
(uncompensated)
Respiratory
alkalosis
(uncompensated)
Metabolic acidosis
pH

(uncompensated)




↔
(uncompensated)
Metabolic
alkalosis
PaCO²

↔
HCO³
↔
↔
↓
↑
Summary Of Compensation Concepts
Respiratory
Compensation
Metabolic
Compensation
(the lungs are attempting to correct
the problem)
(the kidneys are attempting to correct
Rate of compensation
Rapid
Slow
Major organ involved
Lungs
Kidneys
Compensatory activities of Hyper/
organ
hypoventilation
Acid-base problem
triggering activation of
compensation
Metabolic A-B
abnormalities
the problem)
Retention/excretion of H+/HCO³
Respiratory A-B abnormalities
Acid-Base Balance
Before the next lecture, complete the
Acid-Base Prep Work before coming
to class
Will not be collected; however, you will be
called upon to ‘present’
Your patient’ to the group