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ACID-BASE IMBALANCE

Prepared by Ms. Jucar

MARIETTA C. JUCAR, RN, MN

Objectives

At the end of the session, the students will


define acid-base imbalance;
describe the 3 major chemical buffer system;
discuss the roles of lungs and kidneys in the
acid base balance;
identify the different types of acid base
imbalances;
discuss etiologic factors that cause acid base
imbalances;
interpret arterial blood gas values.

OVERVIEW OF ACIDS AND BASES


Definition of terms
Acid- any substance releasing a hydrogen ion when
dissolved in water.
Base any substance binding a hydrogen ion when
dissolved in water.
Buffer binds H ion from body fluids (acting as
base) release H ion into body fluids (acting as acid).
Anaerobic metabolism cellular metabolism
occurring without the presence of oxygen.
Chemoreceptors special cells in the respiratory
center of the brain sensitive to changes in the CO2
concentration of ECF.

pH - expresses the acidity or alkalinity of a


solution
7.35 to 7.45 is normal
>7.45 is alkaline
< 7.35 is acidic
6.8 or 7.8 is incompatible w/ life
Acidosis abnormal H+ or in HCO3 ions
Alkalosis abnormal in H+ ions & in
HCO3 ions

SOURCES OF ACIDS
Waste products of CHO,(converted to free H
ions)
Protein, and fat metabolism
CO2 : waste product of glucose breakdown
and other metabolic reactions (removed by
breathing).
Sulfuric acid CHON breakdown
Lactic acid incomplete glucose breakdown
under anaerobic (no O2) conditions
Ketoacids incomplete breakdown of FA
(under anaerobic conditions)

SOURCES OF HCO3 IONS

Comes from breakdown of carbonic acid,


intestinal absorption of ingested HCO3
pancreatic production of HCO3,
movement of cellular HCO3+ into the ECF,
and kidney resorption of filtered HCO3
Foods that can produce acids & bases.
Meats = a dietary source of acids
Fruits = dietary source of bases
Vegetables = dietary source of acids & bases

MAGKARIBAL

Activities that produce acids


Strenuous exercise
Starvation = formation of ketone bodies d/t
fat utilization instead of CHO.
Catabolic processes = release organic
acids into the ECF (breakdown)
ABG Values Show
Amount of O2 in the serum
Amount of CO2 in the serum
pH, or percentage of H+ in solution

ABG Analysis reveals


a. If the patient has enough O2 to maintain
perfusion
b. If enough CO2 is eliminated
c. The ratio of H+ to HCO3
pH (7.35-7.45)
Reflects H+ concentration
< 7.35- Acidosis
> 7.45 Alkalosis

PaCO2 (35-45 mmHg)


Partial pressure of CO2 in arterial blood
< 35 mmHg hypocapnia (R.alkalosis)
> 45 mmHg hypercapnea (R. acidosis)
PaO2 (80-100 mmHg)
Partial pressure of O2 in arterial blood
HCO3 (22-26 mEq/L)
HCO3 concentration in plasma of blood
that has been equilibrated at a PaCO2 of
40 mmHg, and w/ O2 to fully saturate the
hgb.

Buffers chemicals that maintain pH by


ensuring a stable H+ concentration.
BUFFER SYSTEMS
a. H2CO3 HCO3 buffer system
b. PO4 buffer system
c. Protein buffer system.
d. Potassium Hydrogen exchange
e. Respiratory Control of H+ Balance
f. Kidneys

a. H2CO3 HCO3 buffer system


- largest in ECF (plasma & interstitial fluid)
Characterized by a series of chemical reactions between H2CO3
& HCO
Takes place in the fluids and renal tubules.
Involves electrolytes
Buffering
a. LUNGS (rapid)
Alkalotic state - Hypoventilation (retains H2CO3)
Acidotic state - Hyperventilation (expels CO2 and retain H2O)
b. KIDNEYS (slow)
Alkalotic states reabsorb H+ & excrete alkaline urine
Acidotic states conserve or make new HCO3 & excrete
acidic urine

b. Phosphate Buffer System


PO4 are highly concentrated in the ICF.
Acts as weak acids/base to buffer a stronger
acid/base
takes place in the renal tubules where the
greatest concentration of PO4 exists.
Buffering
Brings the pH back to normal by moving the H+
from the plasma to the urine and eliminating the
acid through the urine.

c. Protein Buffer System.


Functions as an acid or base (amphoteric).
Takes place inside the cell
albumin and plasma globulins act as the primary
protein buffers in the ECF
Buffering:
When H+ in the blood, protein cross
membrane of RBCs & binds to hgb
molecules

d. Potassium Hydrogen Exchange


Normal: ICF K & H +is > ECF K; H+
Acidosis: ECF H+ exchanges w/ ICF K
Alkalosis: ECF K ICF ; H+ ECF K & H
NORMAL

ACIDOSIS

H K
K H
K H K
K
K K
K
H K K
K

H K

ALKALOSIS

K H K
K H
K H K H K
K K
K
H K K

K
K H
K
K
H

K
K

H K
K
H K K
H
H

H
K

K
H

e. Respiratory Control of H+ Balance

Quick response to A/B imbalance


Hyperventilation and hypoventilation.
CO2 : potent stimulus for ventilation.
Carried by the RBCs, the CO2 readily diffuses
across the blood- brain barrier. Reacting w/ H2O to
form H2CO3 which in turn splits into HCO3 and
H+.

Compensation
a. Excess H+ & CO2
RR CO2 pH
b. Deficient H+ & CO2
RR CO2 pH

b. Kidneys
permanently remove H+ from the body,
reabsorb acids or bases and produce HCO3
ions in the proximal tubule.
Regulates acid or base in the ECF by
excreting either acidic or alkaline urine.
Most powerful regulator of acid/base balance
Slowest response, taking hours or days to
effectively regulate the pH.
Regulation
pH increase renal absorption of HCO3
pH increase renal excretion of HCO3

A. Single Acid Imbalance


1. Metabolic Acidosis (Acute / chronic)
2. Metabolic Alkalosis
3. Respiratory Acidosis
4. Respiratory Alkalosis (Acute / chronic)
B. Mixed Acid-Base Disorders (2 or more
acid/base imbalances are present)

TYPES OF ACID-BASE
IMBALANCES

Metabolic Acidosis
(Base HCO3 deficit < 23mEq/L)
accumulation of metabolic acids (e.g.
lactic acid & ketoacids) that rise in
proportion to HCO3 resulting in ph.
Secondary to an existing disease.

FOUR PROCESSES IN METBOLIC ACIDOSIS


1. Overproduction of H+
a. Excessive breakdown of FA: DKA, Starvation
When glucose is not available for fuel , FA are
broken for energy w/c release large amounts of H+.
b. Anaerobic Glucose breakdown
(Lactic Acidosis)
CAUSES
- Trauma, burns, Heavy exercise
- Intestinal disorders
- Leukemias, lymphomas
- Seizure activity, fever, tissue hypoxia, ischemia
- Shock, poor liver perfusion, cardiac arrest

c. Excessive intake of acidic substances floods the body directly w/ H+


Causes
1. Alcohol: vomiting, inhibits glucose synthesis by
the liver
2. ASA: cross blood-brain barrier & interfere w/
CHO metabolism w/c production of metabolic
acids
3. Methanol ingestion:
= absorbed thru skin, lungs or GIT
= produces optic nerve & CNS toxicity
= organ damage after 24 hrs.
= converted to formaldehyde & formic acid

4. Underelimination of H+
Kidney and Acute/Chronic lung disease
*Kidneys: inability of the tubules to excrete
H+ into the urine
*Lungs: inability to excrete CO2
5. Underproduction of HCO3+
HCO3 is made in the kidneys, liver,
pancreas; failure cause a base-deficit
acidosis
E.g. RF, LF, Pancreatitis, Dehydration

4. Overelimination of HCO3+
loss of excessive intestinal secretions w/c has
high HCO3 concentration
Causes
diarrhea
pancreatic or biliary fistula drainage
ileostomy, intestinal suction
ileal bladder
HCO3 is lost in the urine

Metabolic Acidosis

Loss of base or production of excess acids


Blood pH
Hyperventilation
PaCO2
Blood ph
returns to
normal

Renal Buffering
H+ ion
excretion

HCO3
retention

NH3 NH4
production

Neurological Manifestations
Headache
manifestations
Clinical
Malaise
Weakness
Fatigue
Stupor/coma

CLINICAL MANIFESTATIONS
SNS Manifestations
Vasodilation
Warm, flushed skin, dry
Decreased skin turgor

Respiratory Manifestations
Kussmauls respirations
Fruity breath (DKA)
Gastrointestinal Manifestations
Nausea
Vomiting
Anorexia

What would the nurse


expect for laboratory
levels of a client with
METABOLIC
ACIDOSIS?

LABORATORY RESULTS
ABG:

pH<7.35,

PaCO2 normal,

HCO3 <22mEq/L

K>5.3mEq/L

CL>106mEq/L
Lung Compensation:
increasing RR and depth of respirations
through hyperventilation moving pH to
normal
ABG: Normal pH, PaCO2, HCO3<22mEq/L

What could be the possible


Nursing Diagnoses for a
Client with
METABOLIC ACIDOSIS?

NURSING DIAGNOSES
Deficient fluid volume r/t dehydration
Risk for injury r/t skeletal muscle
weakness
Decreased cardiac output r/t poor
cardiac contractility and decreased
vascular volume.
Impaired memory r/t fluid and
electrolyte imbalances.

What is the BEST


treatment or the goal
of therapy for clients
with
METABOLIC
ACIDOSIS?

COLLABORATIVE MANAGEMENT
Goal
Correct the underlying problem, and
restoring fluid and electrolyte loss
increasing aerobic metabolism,
monitoring for change.

MEDICAL INTERVENTIONS

Hydration
Calcium supplement
Alkalinizing agents (HCO3 <12 mEq/L.)
Hemodialysis or peritoneal dialysis.
DKA- Insulin
Antidiarrials

What would be the


Nursing Interventions
for clients with
METABOLIC
ACIDOSIS?

NURSING MANAGEMENT
Monitor ABG levels
Maintain patent IV access
Administer drugs as ordered.
Monitor I&O
Monitor determinants of tissue O2 delivery
(e.g. PaO2, SaO2,Hgb, cardiac output)
Monitor loss of HCO3 through GIT
OFI, administer fluids
Prepare for dialysis
Institute seizure precautions.

EVALUATION

ABG returns to normal


HR, RR, BP returns to normal
Free from injury

Acute/Chronic
Respiratory
Acidosis
(H2CO3 Excess)

Acute/Chronic Respiratory
Acidosis (H2CO3 Excess)
state of relative excess of acid in
body fluids resulting from retention
or excessive production of CO2.
Hypoventilation CO2 & H+
concentration in the lungs and
blood

WHERE and HOW


does
COMPENSATION occur in
a client
with
RESPIRATORY
ACIDOSIS?

Compensation occurs in the


kidneys
By:
Reducing amount of HCO3+
excreted in the kidneys.
Increased renal absorption
of HCO3.
renal excretion of H+

What are the ETIOLOGIES


contributing to the
development of
RESPIRATORY
ACIDOSIS?

ETIOLOGY
ACUTE CAUSES
Cardiopulmoary arrest
Pneumothorax or hydrothorax
Chest wall trauma
Acute abdominal distention
Drug overdose (sedatives, anesthesia)
Airway obstruction
Pulmonary edema/ARDS
Atelectasis

Cont. ETIOLOGY
ACUTE CAUSES
Pneumonia
Acute neurologic dysfunction from any cause
(cerebral trauma, GBS)
Sleep apnea syndrome = reduced diameter
of upper airway during sleep
Excessive O2 adm to pt with chronic
hypercapnia (excessive CO2 in the blood)
Electrolyte imbalance
Pulmonary emboli

CHRONIC CAUSES
Chronic emphysema and bronchitis
Myasthenia gravis = weakness of voluntary
muscles
Cystic fibrosis
COPD
CHF
Pulmonary fibrosis
Muscular dystrophy= progressive wasting of
the skeletal or voluntary muscles.

Respiratory Acidosis

Hypoventilation
Hypercapnia ( PaCO2)
Blood pH
Renal buffering 48-72 hrs
H+ excretion & HCO3 ret
NH3 - NH4 production

Clinical Manifestations

a. Neurological Manifestations
Headache
Blurred vision
Tremors
Muscle Twitching
Vertigo
Irritability
Disorientation
Lethargy
Coma

Cardiac Manifestations
Tachycardia
BP
Cardiac dysrhythmias
Ventricular fibrillation = first sign of
respiratory acidosis for anesthetized
patients.

Respiratory Manifestations

Initial hyperventilation
Eventual hypoventilation result to Acute hypercapnia
Acute Hypercapnia
- PR & RR BP (acute)
- more serious threat to life than acidemia or hypercapnia
- retained CO2 displaces O2 in the alveoli
- PR & RR BP (acute)
Rapid PaCO2 eg. 60 mmHg

Cerebral vasodilation

cerebral blood flow causing headache

DX Findings (Resp. Acidosis)


ABG= pH, PaCO2, Normal HCO3
pH < 7.35 (acidemia)
PaCO2 > 45mmHg (hypercapnia)
HCO3 (normal)
Cl > 106mEq/L
K+ > 5.3Meq/L
ECG = cardiac dysrhythmias, K+
CXR to determine respiratory dse
Renal Compensation
Reabsorbing HCO3 and excreting H+ to
bring pH to normal
ABG= Normal pH, PaCO2,HCO3

POTENTIAL NURSING DIAGNOSES

Activity Intolerance r/t muscle weakness


Ineffective Breathing Pattern r/t reduced
gas exchange
Fatigue r/t altered tissue perfusion
Impaired memory r/t fluid & electrolyte
imbalance
Risk for injury r/t skeletal muscle
weakness
Altered thought process

COLLABORATIVE MANAGEMENT
Medical
GOAL: Maintain patent airway and enhance gas
exchange
a. Pharmacologic agents
Bronchodilators
Mucolytics
Antibiotics
Thrombolytics or anticoagulants for pulmonary
emboli
b. O2 Rx
Ventilation support : SaO290, respiratory muscle
fatigue
c. Pulmonary hygiene: positioning, tapping, OFI

NURSING MANAGEMENT
Semi-Fowlers position
Administer low flow O2
Monitor ABG levels for changes in pH and CO2
Monitor for symptoms of respiratory failure
(PaO2, PaCO2, respiratory muscle fatigue )
Provide low CHO, high fat diet to reduce CO2
production
Monitor neurologic status (LOC, confusion)
Pulmonary hygiene Monitor V/S
Protect pt from injury
Provide emotional support and reassurance to allay
anxiety
Prevent complications : Monitor RR, and depth,
cyanosis, color of nail beds and mucous membranes for
cyanosis (late finding)

COMBINED
METABOLIC
&
RESPIRATORY
ACIDOSIS
(MIXED ACIDOSIS)

COMBINED METABOLIC & RESPIRATORY


ACIDOSIS (MIXED ACIDOSIS)
Uncorrected acute respiratory acidosis always
leads to anaerobic metabolism and lactic
acidosis.
more severe than single A/B imbalance
COPD w/ DM
Elderly w/ PNA & Diarrhea
RF w/ PE
ABG:
ph (Acidosis)
PaCO2 (Respiratory)
HCO3 (Metabolic)

METABOLIC
ALKALOSIS
(Base HCO3 excess)

METABOLIC ALKALOSIS
Occurs when the HCO3 level rises
above the 27mEq/L and the pH
above 7.45
increased loss of acid (stomach &
kidneys)
Loss of fixed acid decreases H+
concentration

What are the


CAUSES
of
METABOLIC
ALKALOSIS

Etiology: Metabolic Alkalosis


1. Increase of base components (Base Excess)
Oral ingestion of bases
a. Antacids
b. Milk-alkali syndrome
Parenteral base administration
a. Blood transfusion
b. NaHCO3
c. TPN

2. ACID DEFICIT
Prolonged vomiting
Nasogastric suctioning
Cushings syndrome or disease
Hyperaldosterolism
Thiazide diuretics
Pyloric stenosis

Metabolic alkalosis

Excess base or loss of acids


Blood pH
Hypoventilation
PaCO2

Renal buffering
H retention

HCO3
excretion

Blood pH returns
to normal

What are the clinical


manifestations of a client
with
METABOLIC ALKALOSIS

Clinical Manifestations of
Met Alkalosis

Tingling sensation, carpopedal spasms, tetany


ionization of Ca++
- more Ca++ combines with S. proteins
RR: lung compensation
Apathy, stupor & confusion seizures = CNS
involvement
Cardiac dysrhythmias = Na & Mg; appearance
of U wave (K)
motility and paralytic ileus
Postural hypotension

What could be the


Diagnostic Findings of
a client with

METABOLIC ALKALOSIS

DIAGNOSTIC FINDINGS

ABG
ph > 7.45
PaCO2 - normal
HCO3 > 26 mEq/L/
K accompanies metabolic alkalosis
Ca Ca binding increases and the blood
level of Ca decreases
Chloride levels
Compensation: Lungs compensation RR
CO2
= pH or N; PaCO2; HCO3 (no change)

Potential Nursing Diagnoses

Ineffective breathing pattern


High risk for injury
Impaired thought process
Anxiety
MEDICAL MANAGEMENT
Goal: Acid-base balance and prevention of
complications resulting from serum HCO3 levels
higher than desired.
Antiemetics, KCL
F/E replacement
Carbonic Anhydrase inhibitors (Diamox)= for patients
who cannot tolerate rapid volume expansion (HF,CRF)

Nursing interventions (Met Alkalosis)


Monitor ABG, electrolyte levels
Maintain patent IV access.
Monitor I & O, ensure adequate hydration.
Monitor determinants of tissue delivery (e.g.
PaO2, SaO2, Hgb levels, cardiac output)
Avoid adm of alkaline substances (e.g.
HCO3, antacids)

Cont. Nursing interventions (Metabolic


alkalosis)
Monitor for electrolyte imbalances
associated with metabolic alkalosis (e.g.
K, Ca, CL)
Monitor for renal loss of acid (e.g. Diuretic
Rx)
Replace ECF w/ Saline , as appropriate.
Monitor PR & rhythm
Administer KCL

RESPIRATORY
ALKALOSIS
(H2CO3 deficit)

RESPIRATORY ALKALOSIS
(H2CO3 deficit)
relative excess of base in body fluids
resulting from respiratory elimination of
CO2.
- may be intentional as with mechanical
ventilation
- Or accidental as in panic attack

ETIOLOGY (R. Alk)

a. Alveolar hyperventilation
Acute hypoxia (early stage): PNA, BA, PE
Hypoxemia: Asphyxiation, high altitudes, shock,
pulmonary fibrosis, cyanotic heart disease
Anxiety
Fever
b. Early stages of Salicylate toxicity = cross the bloodbrain barrier & stimulate the respiratory center
causing hyperventilation
c. CNS: trauma, seizures, catecholamines,
Exercise
Gram-negative sepsis
d. Excessive mechanical ventilation and anesthesia=
intentional
Pregnancy

Respiratory
Alkalosis

Hyperventilation
Hypocapnia ( PaCO2)
Blood ph
Hypoventilation
Retention of CO2

Renal Buffering 48 72
hrs
H+retention

HCO3 exc.

Blood ph returns to
normal

Clinical Manifestation
Light-headedness and dizziness = CO2 crosses the
blood-brain barrier causing vasoconstriction and
cerebral blood flow
Inability to concentrate
Numbness & tingling around the mouth, fingers
and mouth = Ca levels 2 binding of Ca to
protein
Dysrhythmias & muscle weakness = K+ & Ca+
+
Chest pain = 2 coronary spasm
GIT: nausea, vomiting & diarrhea d/t alkalosis
Sweating, palpitation, panic, or air hunger may
also be present.

DIAGNOSTIC FINDINGS (R. Alkalosis)


ABG :pH; PaCO2; HCO3 normal
ph > 7.42 mmHg: - d/t buffering and renal
compensation cannot maintain the H ions at
normal level.
Pa CO2 < 35 mmHg HCO3 = normal
K+ = H+ to ECF; K+ to ICF
Ca++ = severe alkalosis inhibits Ca++ ionization
carpopedal spasm/tetany
PO4 = due to alkalosis causing an increased
uptake of PO4 by the cells
Toxicology serum = to r/o salicylate intoxication

Renal Compensation
Excretion of HCO3 and
absorption of H ions.

NURSING DIAGNOSES
Ineffective breathing pattern
High risk for injury
Anxiety
Impaired memory
Fatigue
Activity intolerance
Altered thought process

COLLABORATIVE MANAGEMENT
GOAL:
a. Promotion of A/B balance
b. Prevention of complications resulting
from PaCO2 levels lower than desired.
Interventions
Encourage slow, deep breathing
Monitor ABG levels for increased pH level.
Monitor for indications of respiratory failure
(PaO2 level, respiratory muscle fatigue,SaO2
level)
Monitor for hyperventilation resulting in
respiratory alkalosis (e.g. hypoxemia, CNS injury,
hypermetabolic states, GI distention, pain, stress).

Nursing
Monitor for CP manifestations of respiratory
alkalosis (e.g. arrhythmias, cardiac output,
and hyperventilation).
Provide O2 Rx., if necessary.
Reduce O2 consumption to minimize
hyperventilation (e.g. promote comfort,
control fever, reduce anxiiety)
Provide ventilatory support, if necessary.
Assess patient for respiratory depression
Provide emotional support and reassurance
to the patient to reduce anxiety

Evaluation
ABG values return to normal
Heart rate, rhythm, and blood
pressure return to normal
The patient remains injury free.

ARTERIAL
BLOOD
ANALYSIS

ABG Interpretation

- provide information about alveolar ventilation,


oxygenation & A/B balance
3 Parameters
pH
PaCO2
HCO3
Pre-test
a. No suctioning prior to blood extraction
b. Allens test
c. Pre-heparinized syringe
d. Container with ice.

Steps
Step 1
Normal Values
pH: 7.35 7.45
paCO2: 35 45 mmHg
HCO3: 22-26/23-27 mEq/dl
paO2: 80-100%
O2 saturation : 95-100%

Step 2: Classify the pH


Normal: 7.35 7.45
Acidemia: < 7.35
Alkalemia : >7.45

Step 3: Look at paCO2


Normal: 35-45 mmHg
Respiratory acidosis: > 45 mmHg
Respiratory alkalosis: <35 mmHg
Step 4: Look at HCO3
Normal: 22-26 mEq/L
Metabolic acidosis: <22 mEq/L
Metabolic alkalosis: > 26 mEq/L

Step 5: Determine whether Respiratory or


Metabolic
ROME
1.Respiratory Opposite: Arrows opposite
directions
ph
PaCO2
HCO3
7.30
50
28
7.45
20
20
2. Metabolic Equal: Arrows in the same
direction
pH
PaCO2
HCO3
7.30
20
18
7.45
50
28

Step 6: Degree of Compensation


A.PARTIALLY COMPENSATED
If CO2 and HCO3 level move towards
the same direction
(both are high & both are low)
ph
PaCO2
HCO3
7.30
50
28
7.45
20
20

B. PARTIAL COMPENSATION
-Acid/base balance is compensated
and pH is still ABNORMAL.
pH
paCO2
HCO3

7.30
50
30

7.30
33
20

C. COMPLETE COMPENSATION
- Acid/base balance is compensated and pH
returns to NORMAL
pH
paCO2
HCO3

N 7.36
50
30

N 7.36
33
20

Compensation absent:
One component (PaCO2 or HCO3) is
abnormal, the other normal
Resp
Met
pH
7.33
7.33
paCO2
50
N 38
HCO3
N 24
20

Exception to the rule: in some


situations, get the median

MARIETTA C. JUCAR, RN, MN

pH ( 7.357.45)

PaCO2
(35-45)

HCO3
Interpretation
(22-26)

Respiratory = pH and PaCO2 moving in opposite direction


(RESP, OPPOSITE, RO)
7.20

60 mmHg 24 mEq/L Resp Acidosis


(N)
Uncompensated

= no change in HCO3

7.20

60 mmHg

37 mEq/l Resp acidosis PC


= opposite direction;

increase in HCO3 pH is
abnormally low

7.42 (N)

60 mmHg

37
mEq/L

Met ALK FC
= opposite direction; 1 is
acidotic; 1 is alkalotic;
LUNGS RETAINED CO2
moving Ph to normal

Metabolic = pH and HCO3 are moving in


the same direction (MET EQUAL, ME)
7.46

34 mmHg

24 mEq/L
(N)

Resp Alkalosis
Uncompensated

7.45

34 mmHg

20 mEq/L

Resp Alkalosis PC
= opposite direction,
1 acidotic,1 alkalotic

7.38
(N)

34 mmHg

20 mEq/L Met Acidosis FC


= Kidneys eliminate HCO3

to balance w/ lowered
acid levels, moving pH
to normal

7.30

40 mm Hg
(N)

20 mEq/L Met. Acidosis


Uncompensated; no

change in PaCO2

7.30

32 mm Hg

20 mEq/L Met Acidosis Partially


Compensated

= decrease in PaCO2

7.42 (N)

32 mm Hg

20 mEq/L

Resp Alk FC

7.46

40 mm Hg
(N)

28 mEq/L

Met Alkalosis
Uncompensated; no
change in PaCO2

7.46

48 mm Hg

28 mEq/L

Met Alkalosis PC;


retention of PaCO2

7.42 (N)

48 mm Hg

28 mEq/L Met Alkalosis Fully


Compensated

7.30

50 mm Hg

20 mEq/L

Mixed Acidosis

7.48

33 mm Hg

29 mEq/L

Mixed Alkalosis

Get half sheet of paper


and interpret the
following for 30 min
by
PAIR

pH

PaCO2 HCO3

pH

PaCO2 HCO3

s
7.48

42

30

6.

7.26

50

21

2 7.34
.

46

24

7.

7.45

30

30

3 7.32
.

38

20

8.

7.32

32

14

4 7.61
.

21

20.6

9.

7.37

28

21

5 7.39
.

49

29.3

10. 7.38

48

29

If you fail to
prepare,
You prepared to
fail!
END