Acid/Base Disorders

Robin Connell MS RN
Fall 2008
 Objectives
Define Acid/ Base influence in the body
Know the normal values of the components of Blood
Gas
Relate abnormal Blood Gases to Electrolyte
Disturbances
Discuss Treatment options for those with complex
metabolic disorders
Correlate patient diagnosis to potential acid/base
disturbances
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 Acid / Base Balance

Homeostasis – the ability of the body to keep all

bodily systems within normal range
pH- measure of hydrogen ion concentration denoting
acidity or alkalinity of a solution
pH- expressed in the form of a logarithm
pH- demonstrated on a scale from 0-14

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pH Scale
Human pH Scale
 Acid / Base
Acid = a substance that can donate hydrogen ions
H2CO3 (carbonic acid) →( H+) + (HCO3-)

Base is a substance that can accept hydrogen ions

HCO3- + (H+)→ H2CO3

PaCO2- is controlled by the lungs and refers to the

pressure exerted by dissolved CO2 gas in blood.

PaO2-refers to the pressure exerted by dissolved oxygen in

the blood
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 pH in the Human Body

Normal Range pH 7.35↔ 7.45

How does the body maintain this narrow normal
range?
Chemical buffering mechanisms: Kidneys & Lungs
The more (H+) the more acidic the solution.
Compatibility with life ═ pH 6.8→ 7.8. This range
equals a ten fold difference in (H+) concentration

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 pH Laboratory Test

pH is most optimally determined by arterial blood gas

analysis
Blood Gases can be done by one certified in this
procedure
RNs, RPT, Physicians
Normal Arterial Blood Gas Values
PH 7.35-7.45 pH< 7.35 acidosis

PaCO2 35-45 < 35 (respiratory alkalosis)

>45 (respiratory acidosis)

Pao2 80-100mmHg

HCO3 22-26 mEq/L

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 Respiratory System

Lungs are the initial and primary organ in the control

of pH
Changes in the rate and the depth of respiration can
have significant and immediate affects on the pH of
the individual
Kidneys have a secondary affect and are called into
action if the respiratory system can not affect a change
in the pH.
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Chemical Buffering Mechanisms

Buffering results in a change in the amount of H+ ions

through release or removal of H+ ions
Body’s Major Buffer is bicarbonate (HCO3-) and
carbonic acid (H2CO3)
Normally there are 20 to1 Ratio HCO3- to H2CO3 if
this ratio is upset the pH will change
Buffers prevent major changes in the pH of body
fluids
by removing or replacing H+
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 Buffers
Body’s major extracellular buffer is the bicarbonate-
carbonic acid buffer system
CO2 is a potential acid; when dissolved in H2O
(CO2+H2O)=H2CO3 so when CO2↑ carbonic acid is
also↑ and vice versa
Kidneys regulate the bicarbonate level in the ECF
( In the presence of respiratory acidosis and most
metabolic acidosis kidneys excrete H+ and conserve
bicarbonate ions)
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 Buffers

Lungs under influence of respiratory center (Medulla)

control CO2 (and thus carbonic acid)
It adjusts ventilation in response to the amount of
CO2, and to a lesser extent O2
↑ CO2 has an immediate effect on respiratory efforts;
but declines over time for the next 1-2 days. So after 2
days elevation of blood CO2 has only a weak effect as
a respiratory stimulant.
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 Lungs
Partial pressure of O2 in arterial blood (PaO2)
influences respiration, but does not do so unless PaO2
falls below 60mmHg
Lungs compensate for metabolic disturbances by either
conserving or retaining CO2
Metabolic acidosis – respirations is ↑ = elimination of
CO2 (lighten the acid load)
Metabolic alkalosis – respiration is ↓= retention of
CO2 (increasing the acid load)
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 Effects of pH on Potassium

Generally acidic states cause potassium to shift from

the cells →ECF ↑ plasma potassium concentration
The opposite happens in alkalemia; potassium shifts →
the cells ↓the plasma potassium concentration.
(metabolic and respiratory)
Hypokalemia is commonly present in patients in
patients with metabolic alkalosis
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 Acidemia
 A shift in potassium out of the cells can occur in acidemia
(metabolic or respiratory) respiratory being a weaker stimulus

 H+ ions shift →the cells to correct the low plasma pH to

preserve cellular electroneutrality cellular potassium shift from
the cells → the ECF

 Hyperkalemia is less marked when do to lactic acidosis or

ketoacidosis then when due to renal failure or diarrhea

 Hyperkalemia does occur in untreated diabectic ketoacidosis,

due more to insulin lack
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 Metabolic Acidosis

Clinical disturbance characterized by ↓pH and ↓

bicarbonate concentration
Lungs hyperventilate to ↓ CO2 concentration
 Anion Gap
 Metabolic Acidosis can be divided into two forms depending on
the values of the serum anion gap

Anion Gap (AG) = Na+ - (CL- + HCO3-)= 8-12mEq/L

or
Anion Gap (AG) = Na+ + K+ - (CL- + HCO3-) = 12-16mEq/L

Anion Gap reflects normally unmeasured anions (phosphates,

sulfates, and protein in plasma)
An Anion Gap ≥16 suggests excessive accumulation of
unmeasured anions

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 Types of Anion Gaps
High Anion Gap Acidosis: Results from excessive
accumulation of fixed acids ≥ 30 mEq/L = High Anion Gap
Acidosis

High Anion Gap Acidosis: Ketoacidosis, Lactic Acidosis,

Late phase Salicylate poisoning, Ethylene Glycol Toxicity

H+ is buffered by Bicarbonate causing Bicarbonate to ↓an

the anion gap ↑ normal limits.
 Clinical Manifestations
Headache, confusion, drowsiness, ↑ RR and depth of
respirations, N/V, peripheral vasodilation, ↓ Cardiac
Output occurs when pH ≤ 7.0, ↓BP, cold clammy skin,
dysrhythmias and shock

Lactic Acidosis-most commonly seen in patients with

significant cardiopulmonary problems and sepsis.
 Normal Anion Gap Acidosis

Diarrhea-direct loss of Bicarbonate in the stool, ECF

volume depletion, and concentration of the remaining
chloride, also referred to as hyperchloremic acidosis
Excessive chloride due to IV infusion
Use of diuretics

A reduced or negative anion gap is primarily caused

by hypoproteinemia usually a rare occurance.
 Metabolic Acidosis
ABG’s look like: ↓ Bicarbonate ≤ 22 mEq/L ↓pH ≤
7.35
↓ serum Bicarb level
Hyperkalemia may accompany shift K+ out of the cell
into the ECF
Hyperventilation to decrease CO2 as compensatory
mechanism
Management: correct metabolic defect
if ↑ Cl- eliminate source
Give Bicarb for pH≤ 7.1 or HCO3≤ 10
 Metabolic Acidosis
Example: Patient with diabetic ketoacidosis

pH = 7.05
HCO3 = 5 mEq/L( primary disturbance)
PaCO2 = 12mmHg (compensatory
hyperventilation)
Base excess (BE) = -30
Acidosis depresses myocardial contractility, lowers the
fibrillation threshold.
 Metabolic Alkalosis
 Excess HCO3
 High pH (decreased H+ concentration)
 High plasma bicarbonate concentration
 Causes= by a gain in bicarbonate or loss of hydrogen
 Compensation=lungs hypoventilate to increase PaCO2

 Common causes = vomiting or gastric suction ( loss of H+

and CL- ions
 Overuse of diuretics, Excessive alkali ingestion
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 Hypokalemia & Alkalosis

Kidneys conserve K+ → H+ excretion increases

Cellular K+ moves out of the cell → ECF to help
maintain serum level. (as K+ leaves the cell H+ enters
to maintain electroneutrality.
 Metabolic Alkalosis
Example : patient with vomiting

pH 7.62
HCO3 45
PaCO2 48
BE 16
Serum Potassium is often below 3.5mEq/L

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 Respiratory Acidosis
H2 CO3 Excess can be acute or chronic
Acute is more dangerous
Renal compensation is very slow
High PaCO2 can quickly produce a sharp decrease in
plasma pH
Causes: always due to inadequate excretion of CO2
(inadequate ventilation)
Pulmonary Edema, pneumothorax, atelectasis, overdose
of sedatives etc…
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 Signs and Symptoms
↑ PaCo2 ↑pulse and Respiratory rate,↑BP, mental
cloudiness, and a feeling of fullness in the head↑
cerebrovascular vasodilation

Example: Acute Respiratory Acidosis

pH 7.26
PaCO2 56
HCO3 24
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 Chronic Respiratory Acidosis
 Patient may complain of weakness, dull headache
 pH may be low normal like 7.35 (if complete
compensation has occurred)
 PaCO3 ≥ 45 mmHg

 Example: Chronic Respiratory Acidosis

pH 7.38
PaCO2 76
HCO3 42
BE +14
Remember when PaCO2 is chronically elevated??????? 29
 Respiratory Alkalosis

H2CO3 deficit due to hyperventilation causing excess

“blowing off” of CO2 decrease in Plasma H2CO3
Signs and Symptoms:
Fever, extreme anxiety, hypoxemia, gram negative
Bacteremia, Pulmonary Emboli, Excessive ventilation
by ventilators

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 RespiratoryAlkalosis
Acute: pH 7.52
PaCO2 30mmHg
HCO3 24
BE +2.5mEq/L

Chronic: pH 7.40
PaCO2 30
HCO3 18mEq/L
BE -5 31
 Mixed Acid Base Imbalances
Respiratory Alkalosis Plus Metabolic Acidosis
Example:
pH 7.4
PaCO2 18mmHg
HCO3 16mEq/L
BE -10
Examples of Disorders that cause mixed acid/base
imbalances: Cardiopulmonary Arrest, Salicylate
Intoxication, Renal failure and vomiting etc…
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Systemic Assessment of Blood Gas

First look at the pH:

Determine the primary cause of the disturbance this is
done by evaluating the PaCo2 and HCO3 in relation to
the pH
Determine if compensation has occurred

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 Questions??????

Practice on Blood Gas Problems

Look on-line