1.acid Base Balance

:prepared by
Abdalhady alghwary
CCRN- PHH
16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 1

Outlines
 Acid base terminology
 Regulation system
 Definition of the arterial blood gases.
 Indications of the arterial blood gases .
 Contraindications and cautions of the arterial blood gases.
 The deferent between the artery and vein .
 Procedure of the arterial blood gases.
 Complications .
 Patient teaching .
 Step for interpretation.
 Acid base disorder
 examples

Acid Base terminology
Acid-base balance refers to the mechanisms the
body uses to keep its fluids close to neutral pH (that is,
neither basic nor acidic) so that the body can function
normally.
control of acid base balance and oxygenation is
essential for optimal function of chemical reactions,
enzymes , and tissue oxygenation
Arterial blood pH is normally closely regulated
to between 7.35 and 7.45.

.Acid Base terminology cont
acids Any ionic or molecular substance
that donate hydrogen ion H+
Strong acid ： HCl, H2SO4, H3PO4.

Weak acid ： H2CO3, CH3COOH.
bases
Any ionic or molecular substance
that accept a hydrogen ion H+.
Strong alkali ： NaOH, KOH.
Weak alkali ： NaHCO3, NH3,
CH3COONa.
COONa
 Strong acid Hcl H+ +cl-
 Weak acid H2co3 H2O +Co2
 Strong base OH OH + H+
 Weak base Hco3 Hco3 + H+
 pH is H+ (inverse relationship)


Acidemia has depressant affect on CNS
Alkalemia has a stimulant effect on the CNS by
binding calcium to circulating protein.

Mixed venous blood gas
Sample obtained from the distal port of a pulmonary
artery catheter ,used to augment assessment of the
oxygenation status of tissue .

Acid Base Regulation
Systems that act to protect the body against

fluctuation in pH by combing with excess hydrogen
ions or bicarbonate.
The buffer system usually consist of strong acid and
weak base

H＋
load
ECF lung ICF Renal Bone
Buffers RBC Respiratory ＋

H ＋－ K H+ excretion Release
control exchange bicarbonate bone salt
Hb others reabsorption
buffers
Buffers Ca2 ＋＋
H2CO3 CO2
H2PO4
Acid
excretion In chronic
Expiration metabolic
acidosis
Immediately minutes hours days Very slow

Acid base regulation
1. Carbonic acid system (extracellular fluid)
H+ + Hco3 - H2co3 H2o + CO2
2. Protein buffers (intracellulary)
Hb is the most well known protein buffer, hemoglobin
acts as abase and has a high affinity for hydrogen
ions and Co2
Hb- + H+ HHb
Hb + Co2 Hb . Co2

3. Phosphate buffer
HPO4 -2 + H+ H2PO4-
H2Po4 cannot be reabsorbed and is eliminated in the
urin,extra sodium is reabsorbed in to the ECF
4. Ammonia
 the deamination of glutamin by glutaminase,occures in renal
tubules leading to ammonia NH3 production.
 Acidosis stimulate glutaminase activity
NaCl +NH3+ H+ NH4CL + Na+

 NH4 + cannot be reabsorbed and is excreated in the urin,
 HCO3 and extra sodium are reabsorbed into the ECF

Respiratory system
Begins working withen 3-12 min of an acid base balance
changes.
Renal system
Compensation is slow taking 48 -72 hr to be effective

Correction vs. compensation
Correction (primary system affected is repaired ,all
acid parameters return to normal)
Compensation can be partial or complete

Assessing oxygenation
 requierment for adequate oxygenation include:
 Adequate ventilation.
 Healthy alveolar capillary membrane.
 Adequate cardiac outbut .
 Functional/adequate hemoglobin to carry oxygen .

Oxygenation information obtained
from ABGs
Arterial Po2
Arterial saturation Sao2

Non invasive Spo2(pulse oximetery)
influencing factors
 Hypothermia
 Hypotension
 Hypovolemia

Definition
Arterial blood gases (ABGs) : are
diagnostic tests performed on blood taken from
an artery which contains oxygen and carbon
dioxide and others elements .

Indications
1- Evaluate acute
respiratory
distress and
assist in
determine
therapeutic 2- Evaluate the
interventions. effectiveness of
respiratory
intervention.

Cont’ Indications
3- Document the
existence and
severity of a
problem with
oxygenation or
carbon dioxide
exchange.
4- Analyze acid –
base balance.

Contraindications and Cautions
2- Patient
with
Previous -1
anticoagulant
surgery in the
or with
artery
known
coagulopathy.
3- Skin
4- Decrease
infection or
collateral
damage of the
circulation.
skin .
Cont’ Contraindications and
Cautions
Sever -5 Serious -6
atherosclerosi injury to the
s .extremity
Patient -8
7- Fibrinolytic with femoral
therapy. graft or
cellulites
Cont’ Contraindications and
Cautions
9- Patients who have had a

cardiac catheterization via
the brachial rout or who
have sclerotic vessels.

The different between the artery and the
vein
Vein Artery
Veins carry blood Arteries receive the blood
. toward the heart . from the heart
In veins the blood is not Blood is under great
under great pressure, pressure in arteries; hence
hence it flows more .it lows fast
slowly .and smoothly
Veins have relatively Arteries have thick and
thin and slightly .elastic muscular walls
.muscular walls
Cont’ The different between the
artery and the vein
Vein Artery
In the vein there is .Arteries have no valves

.internal valve
Dark red in color . . Fresh red in color

Arterial Puncture sites
Redial artery ,
Brachial artery
Femoral artery

Arterial Puncture sites

Equipment
Syringe (1-3 ml size ).
20- 25 G needle with a clear hub.
Syringe cap.
Antiseptic pledgets.
Heparin 1:1000
Gauze dressing .
Ice container .
Local anesthetic .

The procedure
• Preparation phase :
• 1- Patient explication .
• 2- prepare equipment .
• 3- Hand washing .
• 4- select the puncture site on the base of the clinical
situation , how rapidly sample must be obtained , and
the circulatory status of the patient .

Cont’ preparation phase
5- if redial artery is chosen , performing modified
Allen’s test is optional :
 Step 1: tight fist x 20 sec
 Step 2: Occlude radial and ulnar arteries
 Step 3: open hand and look for blanching
 Step 4: release ulnar artery and look for capillary refill (5-7 sec)

Cont’ Allen’s test

Cont’ preparation phase
6- position the extremity
Radial : stabilize the wrist over a small towel .
Brachial : place a rolled towel under the patient elbow
while hyperextending the elbow .
Femoral : rotate the leg slightly outward .

Cont’ the procedure
• Performance phase :
1- prepare the syringe ( if not preheparinized ) .
2- Palpate the pulse and determine the point of maximal
impulse.
3- Local anesthesia may be useful in anxious patient .

Cont’ performance phase
4- clean the over lying skin with antiseptic solution .
5- Use the index finger of your free hand to palpate
the arterial pulse just proximal to the puncture
site
6- grasp the needle as if holding a pencil, direct the
needle with bevel up , and puncture the skin
slowly .
 Radial Artery - 45 insertion angle
 Brachial Artery - 60 - 90 insertion angle
 Femoral Artery - 90 insertion angle

7- When the blood appears stop advance the needle
and allow the blood to flow freely into the syringe .
8- Obtain a sample of 1 to 2 ml , remove the needle
from the artery , immediately apply the direct
pressure to the puncture site with dry gauze for 2 to
3 minute .
a) Prepare the blood sample for the laboratory by
immediately expelling the air bubbles.
 Air bubble =Po2 150 mmhg .
 Air bubble +blood =increasePo2, decrease Pco2

b) Activate the needle stick safety device and
remove the needle .
c) Label the syringe .
 Sample should be analyzed as soon as possible
 If
iced sample can be stored
 Glass syringe – 1 hour
 Plastic syringe – 15 minutes
Remember: Blood is living tissue that

continues to consume O2 and produce CO2

Complications
Bleeding
 hematoma
 thrombosis formation.
Nerve injury .

Steps for interpretation
Step.1 look at the PaO2 level (Does the level of PaO2
?show hypoxemia)
Step.2 look at the pH level , (Is the pH level on the
?acid or alkaline side of 7,40)
Step.3look at the PaCO2 level (Does the PaCO2 level
?show respiratory acidosis, alkalosis, or normalcy)
Step.4 look at the HCO3 level (Does the HCO3 show
?metabolic acidosis, alkalosis, or normalcy)
Step.5 look back at the pH level (Does the pH show a
?compensated condition)

ABG Interpretation
 Look at PaO2
 Reflects 3% of total oxygen in blood
 Normal range 80-100 mmHg at sea level; lower at
higher elevations
 Abnormally low PaO2 = hypoxemia
 At any age, PaO2 lower than 40 mmHg represents a
life-threatening situation

ABG Interpretation
 Look at pH
 Normal 7.35-7.45
 Below 7.35 = Acidosis
 Higher than 7.45 = Alkalosis
 pH less than 6.8 is incompatable with life

ABG Interpretation
 Look at PaCO2
 Indicates whether the client can ventilate well enough to
rid the body of waste products from metabolism
 Co2 is the stimulus for respiratory center in medulla which
act to increas or decrease respiration to maintain acid bace
balance.
 Normal 35-45 mmHg
 Less than 35, alkalosis
 Greater than 45, acidosis

ABG Interpretation
 Look at Hco3
 Normal 22-26 mmHg
 Less than 22 acidosis
 Greater than 26 alkalosis
 The kidney regulate the bicarbonate value by excreting or
retaining hydrogen or bicarbonate ions to maintain acid
base balance

Acid base
disturbance

Definition of acid-base disorders
An acid base disorder is a change in the

normal value of extracellular pH that may result
when renal or respiratory function is abnormal
or when an acid or base load overwhelms
.excretory capacity
Respiratory Alkalosis
 Causes of Respiratory Alkalosis
 any condition which cause alveolar hyperventilation
 Psychogenic (fear, anxiety ,pain)
 CNS stimulation (brain injuries , alcohol
intoxication,)
 Hypermetabolic states (fever , thyrotoxcosis )
 hypoxia

 Clinical Presentation
 Cardiovascular
 Increased myocardial irritability, palpitations
 Increased HR
 Respiratory
 Rapid, shallow breathing
 Chest tightness and palpitations

 Clinical presentation
 CNS
 Dizziness, anxiety, panic, tetany,
convulsions,headache,vertigo, difficulty concentrating,
blurred vision, numbness and tingling in extremities,
hyperactive reflexes
 Diagnostic findings
 High pH, low PaCO2
 Hypokalemia, hypocalcemia

 Compensation
 Kidneys conserve H and excrete HCO3
 Low HCO3 indicates body’s attempt to compensate
 With partial compensation, pH is elevated
 With full compensation, pH returns to normal

 Management
 Treat underlying cause
 Rebreathe CO2 using a rebreather mask or paper bag
 Give oxygen if hypoxic
 Medicate as needed with antianxiety or antipyretic
drugs

 Planning and Implementation
 Provide support and reassurance
 Monitor VS and ABGs
 Assist client to breathe slowly
 Provide paper bag or rebreather mask
 Protect from injury
 Administer antianxiety medications and monitor
response

Respiratory Acidosis
 Respiratory Acidosis causes
 Any clinical that causes alveolar hypoventilation such
anesthesia administration.
 Depression of respiratory center (sedative ,narcotic)
 Respiratory muscle paralysis (GBS , muscle relaxant)
 Chest wall disorder(flail chest, pneumothorax)
 CHF, COPD ,pneumonia

 Cardiovascular
 Hypotension
 Delayed cardiac conduction that can lead to heart block,
peaked T waves, prolonged PR intervals, and widened QRS

complexes
 Peripheral vasodilation with thready, weak pulse
 Tachycardia
 Warm, flushed skin

 Respiratory
 Dyspnea, may have hypoventilation with hypoxia
 CNS
 Headache, seizures, altered mental status, papilledema,
muscle twitching, drowsiness , coma
 Diagnostics
 Decreased pH, elevated PaCO2
 Hyperkalemia.

 Compensation
 Increased rate and depth of respirations to blow off
CO2
 Kidneys eliminate H ions and retain HCO3
 HCO3 levels rise when body attempts to compensate
 With partial compensation, pH remains decreased
 With full compensation, pH returns to normal

 Management
 Treatment directed at underlying cause and
improving ventilation
 Implement pulmonary hygiene measures
 Provide adequate fluid intake
 Administer supplemental oxygen cautiously in client
with chronic respiratory acidosis
 Mechanical ventilation if necessary

 Assess respiratory rate and depth
 Monitor for complications and response
 Assess for tachycardia and irregularities
 Monitor ECG for dysrhythmias
 Monitor serum electrolytes and ABGs
 Administer oxygen as indicated and ordered

 Administer medications as ordered and indicated
 Bronchodilators to decrease bronchospasm
 Antibiotics to treat infections
 Respiratory agents to decrease viscosity of secretions
 Anticoagulants and thrombolytics
 Provide good oral hygiene frequently

 Maintain safe positioning

 Keep a calm, quiet environment
 Assess for cyanosis
 Orient confused client frequently
 Position to facilitate maximum lung expansion
 Provide adequate fluid intake

 Look at PaCO2
 Acute ventilatory failure results when PaCO2 exceeds
50 mmHg & pH < 7.30
 Chronic ventilatory failure when PaCO2 >50 and pH >
7.30

Metabolic disorders
 Look at HCO3 level
 Reflects kidney function
 Normal 22-26 mEq/L
 < 22, Metabolic Acidosis
 > 26, Metabolic Alkalosis

Metabolic Acidosis
Metabolic Acidosis causes
Overproduction of organic acide
(ketoacidosis ,starvation)
Renal failure
Diarrhea

Metabolic Acidosis
 Cardiovascular
 Hypotension, dysrhythmias, peripheral vasodilation, cold,
clammy skin
 Respiratory
 Deep, rapid, respirations
 CNS
 Drowsiness, coma, confusion, lethargy, weakness

Metabolic Acidosis
 GI
 N, V, diarrhea, abdominal pain
 Diagnostics
 pH low, HCO3 low, hyperkalemia
 ECG changes related to high potassium levels
 Tall, tented T waves
 Base excess decreases

Metabolic Acidosis
 Compensation
 Lungs eliminate CO2
 Kidneys conserve HCO3
 Urine pH less than 6
 PaCO2 decreases with compensation
 pH returns to normal with full compensation

Metabolic Acidosis
 Management
 Treat underlying problem
 Provide hydration to restore water, nutrients,
electrolytes
 Administer IV alkalotic solution (NaHCO3 or sodium
lactate) may be indicated
 Mechanical ventilation if necessary

Metabolic Acidosis
 Monitor ABGs
 Monitor I&O
 Measure daily weights
 Assess VS, especially respirations
 Assess LOC
 Assess GI function

Metabolic Acidosis
 Monitor ECG for conduction problems
 Monitor serum electrolytes
 Administer medications and fluids as needed

Metabolic Alkalosis
 Metabolic Alkalosis Causes
 Large losses of gastric content (vomiting or nasogastric
suction)
 Prolong use of diuretics
 Ingestion of large amount of bicarbonate as antiacid

Metabolic Alkalosis
 Cardiovascular
 Tachycardia, dysrhythmias, hypertension, atrial
tachycardia
 Respiratory
 Hypoventilation, respiratory failure
 CNS
 Dizziness, irritability, nervousness, confusion, tremors,
muscle cramps, hyperreflexia, tetany, paresthesias,
seizures

Metabolic Alkalosis
 GI
 Anorexia, N, V, paralytic ileus
 Diagnostics
 High pH and HCO3, hypokalemia, hypocalcemia,
hyponatremia, hypochloremia
 Base excess increases

Metabolic Alkalosis
 Compensation
 Lungs retain CO2; and kidneys conserve H and excrete
HCO3
 PaCO2 increases with compensation
 Urine pH greater than 6
 pH returns to normal with full compensation

Metabolic Alkalosis
 Management
 Treat underlying cause
 Acetazolamide (Diamox) used if metabolic alkalosis
occurred due to prolonged diuretic use and inhibits
carbonic anhydrase and promote increase excretion of
Hco3.
 Restore fluid and electrolyte

Metabolic Alkalosis
 Assess LOC
 Assess VS, especially respirations
 Administer medication and IV fluids as indicated
 NS based IV fluid replacement
 Potassium supplementation if hypokalemic
 Histamine-2 receptor antagonists (Tagamet, Zantac) to
reduce production of H ions and loss of H ions from GI

drainage
 Correct other electrolyte imbalances

Metabolic Alkalosis
 Monitor I&O
 Monitor response to therapy
 Monitor ECG for conduction abnormalities
 Monitor ABGs
 Monitor serum electrolytes

AG (anion gap)
Anion gap = Na+ - (Cl¯ + HCO3¯ )
Normal: 122mmol/L (10 - 14 mmol/L)
Increase AG is associated with the accumulation
of anions other than CL- such as ketoacid and
laktec acid .
If the AG is known the cause of acidosis may be
more easily determined.
Is often related to disease process such as diabetic
or starvation ketoacidosis,and lactic acidosis

compensation
 Look back at pH
 If abnormal, the PaCO2 or HCO3 level will be
abnormal = Uncompensated
 Abnormal pH, PaCO2, and HCO3 = Partially
compensated
 Normal pH, abnormal PaCO2 and HCO3 =
Compensated

BE (base excess)
The base excess indicates the amount of excess or

insufficient level of bicarbonate in the system. (A negative
base excess indicates a base deficit in the blood.) A negative
.base excess is equivalent to an acid excess
Normal: -2 to +2 mmol/L
 Increase acid or decrees base will cause decrees Hco3
 Increase base or decrease acid will cause increase
Hco3
 Below -2, base deficit, metabolic acidosis
 Above +2, base excess, metabolic alkalosis

Mixed Acid-Base Disturbances
 Occurs when two or more independent acid-base
disorders occur at the same time
 Example: Client with metabolic acidosis from acute
renal failure may also have a very slow respiratory
rate and retain CO2 -> respiratory acidosis

Mixed
 Mixed acidosis
 pH 7.25, PaCO2 56, PaO2 80, HCO3 15
 Acute pulmonary edema, cardiac arrest
 Mixed alkalosis
 pH 7.55, PaCO2 26, PaO2 80, HCO3 28
 Postoperative clients with severe hemorrhage, massive
transfusions, excessive NG drainage

:Technical Causes of Abnormal Results
1. Room air mixed with sample
a. PaO2 will equilibrate to above 160
2. CO2 will be lower due to equilibration
By Dalton’s Law, the partial pressure of CO2 in room
air is approx. 2 mmHg
 Diffusion is responsible – diffuse from area of
high concentration to low concentration

3- Delay in running sample

a. O2 consumption will continue as will CO2 production
and so the use of ice is very important:
b. Iced, sample will last an hour without a change in the
results
– un-iced, ABG's can be significantly changed after 10
minutes
Iced sample Uniced sample Change in values

c4 c 37 every 10 min
0.001 0.01 ph
mmhg 0.1 mmhg 1 pco2
% 0.01 % 0.1 po2

4. Venous sample drawn

a. Usually this in shocky patient that you expect
low
pressures and dark blood
b. Should doubt when PO2 is significantly lower
than
expected
i. draw venous blood to check comparison or
ii. redraw sample

 5-Capillary samples
a. From infants warmed heel
b. CAUTION – pay attention to puncture site and sample
type
c. ONLY diagnostic values are pH and PaCO2
d. PaO2 value is NOT diagnostic
 6. Heparin
All unnecessary heparin should be ejected from syringe.
excess
heparin dilutional effect Hco3, pco2.

Patient pain
a. Can cause hyperventilation or breath holding
b. An anesthetic may be injected prior to stick for pain,
although this hurts probably as much
• Usually 2% lidocaine
7. Machine errors
a. Improper calibration
b. Air bubbles in electrodes
c. Torn membranes

interpretation Hc03 PaCo2 ph
Res acidosis 24 48 7.31
Met alkalosis 33 45 7.47
Met acidosis 14 36 7.20
Res alkalosis 22 29 7.50

Res acidosis with 31.4 56 7.36
complete met
compensation
Res alkalosis with 21 32 7.43
complete met
compensation
Met alkalosis with partial 33.1 49 7.47
res compensation

Combined res and 15 50 7.09
met acidosis
Combined res and 27.8 33 7.54
met alkalosis

Case study
 A 50 year old insulin dependent diabetic woman was
brought to the ED by ambulance. She was semi-comatose
and had been ill for several days. Current medication was
digoxin and a thiazide diuretic for CHF.
 Lab results
Serum chemistry: Na 132, K 2.7, Cl 79, Glu 815,
Lactate 0.9 urine ketones 3+
ABG: pH 7.41 PCO2 32 HCO3¯ 19 pO2 82
? What is the acid base disorder? Why

Mr. Adams is a 60 y/O with pneumonia. He is
admitted with dyspnea, fever, and ABG
pH 7.28
CO2 56
PO2 70
HCO3 25
SaO2 89%
16:59 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 91-Slide 3

non compensation Resp acidosis

 Ms. Stan is a 24 years old college student. She has
from 4 days history of bloody diarrhea. An ABG
is obtained:
 pH 7.28
 CO2 43
 PO2 88
 HCO3 20
 SaO2 96%

non compensation Metabolic Acidosis

Case 3
 Ph 7.45
 Co2 53
 Hco3 30
 Po2 78

Full compensation Metabolic alkalosis

THANK YOU

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:prepared by

16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 1

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Strong acid ： HCl, H2SO4, H3PO4.

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Systems that act to protect the body against

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Buffers RBC Respiratory ＋

Immediately minutes hours days Very slow

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NaCl +NH3+ H+ NH4CL + Na+

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9- Patients who have had a

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In the vein there is .Arteries have no valves

Dark red in color . . Fresh red in color

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16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 30

16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 31

16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 32

16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 33

16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 34

16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 35

 Plastic syringe – 15 minutes

Remember: Blood is living tissue that

16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 36

16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 37

16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 39

16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 40

16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 41

16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 42

16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 43

16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 44

An acid base disorder is a change in the

16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 46

16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 47

16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 48

16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 49

16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 50

16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 51

16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 52

peaked T waves, prolonged PR intervals, and widened QRS

 Warm, flushed skin

16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 53

16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 54

16:58 ١٤٤٥/٠٧/٢٤ ABG- prepared by abdalhady alghwary 55