1. ACID BASE BALANCE I
D
PAO 5600
Clinical Laboratory Medicine I
C
With Special Thanks To:
Pamela Jaffey MD

2. OBJECTIVES
Identify the sources of H in the body (volatile
H+
1.
and nonvolatile acids)
2. D
Describe the bicarbonat b ff system and it
ib th bi b te
t buffer t d its
clinical utility in terms of acid base balance
3. Id tif i di ti
Identify indications for a arterial blood gas, and
f an t i l bl d d
the normal values of pH HCO3-, pCO2, pO2 and
H,
O2 saturation in an arte erial blood gas
4. Define the relationship b between pH and H+
Dave Kotun, NSU O
Orlando, PA Program 2

3. OBJECTIVES
Describe t e normal physiologic roles p ayed by
esc be the o a phys o og c o es played
5
5.
the lungs (the quot;respiratory componentquot;) and
kidney (the quot;metabolic componentquot;) in acid-base
balance
Define the relationship between pH and the
6.
serum K+ concentration i terms of acid base
i n in f id b
balance
Describe the regulation of th ventilatory rate b
D ib th l ti f the til t t by
7.
the central chemorecep ptors in the medulla and
the peripheral receptors in the carotid bodies and
s
aortic arch Dave Kotun, NSU O
Orlando, PA Program 3

4. Introduction
It is necessary for the body t maintain the blood pH
to
•
within a very narrow range: 77.35-7.45.
A deviation would alter enzy function as well as
yme
create significant cardiovasc
cular disturbance.
Dave Kotun, NSU O
Orlando, PA Program 4

5. Introduction
This is a difficult task for the bod
dy:
Metabolic processes produce 15 - 20mol of H+ in the body daily,
but th body
b t the b d iis capable of f ti ning with plasma llevels
bl f functioni ith l l
between 36- 44 nmol/L; deviations from these levels ultimately
s
can cause death
The body maintains this pH balance with buffer systems as well
as concerted actions of the lungs and kidneys.
The main buffer system utilized by th body is the bicarbonate buffer
he
system.
Dave Kotun, NSU O
Orlando, PA Program 5

6. SOURCES OF H+ IN THE BODY
E
VOLATILE ACIDS
Derived from CO2:
CO2 di l
dissolves iin H2O forms carbonic acid
fo bi id
dissociates into bicarbonate and H+
e
CO2 + H2O H2CO3 H 3- + H+ = THE
HCO
BICARBONATE BUFFER S SYSTEM
Respiration allows H+ to be removed by the Lungs as CO2
e
Dave Kotun, NSU O
Orlando, PA Program 6

7. SOURCES OF H+ IN THE BODY
E
NONVOLATILE ACIDS
Derived from Sources othe than CO2:
er
Metabolic products of su
ulfur and phosphorus containing
compounds
p
Lactic acid
Keto acids (acetoacetate and beta hydroxybutyrate)
e
Excreted by the Kidneys
Dave Kotun, NSU O
Orlando, PA Program 7

8. BICARBONATE BUFFER S
SYSTEM
BUFFER = a weak acid (protonate and “conjugate” base
ed)
(unprotonated ) that minimize chan
nges in H upon addition of
H+
acid or base
BICARBONATE BUFFER:
H2CO3 H+ + HCO3-
-
( acid) ( conjugate base )
Dave Kotun, NSU O
Orlando, PA Program 8

9. UNIQUENESS OF BICARB
BONATE BUFFER
SYSTEM
THE BICARBONATE BUFFER SYSTEM IS UNIQUE:
It has a huge buffering capacity because it communicates with
y
air (it is an open system)
This is in contrast to other buffe of the body which operate in
ers
a c osed syste
closed system
ACID BASE LOCATION
Hb : HHb Hb
Hb- in erythrocytes
Proteins: Hprotein Proteins- intracellular
Phosphate buffer: H2PO4- HPO
H 42- intracellular
Dave Kotun, NSU O
Orlando, PA Program 9

10. INTERRELATIONSHIP OF CO
OMPONENTS OF THE
BICARBONATE BUFFER
THE HENDERSON- HASSELBA
ALCH EQUATION:
In general, the Henderson-Hasselbalch eq ation
gene al Hende son H equation
describes the equilibrium bet
tween pH, a weak acid, and
conjugate weak base (it is useful in the preparation of
buffers)
We will apply the Henderson-
pp y -Hasselbalch equation
q
to the bicarbonate buffer syst
tem after defining some
terms:
Dave Kotun, NSU O
Orlando, PA Program 10

11. H&H
Henderson-Hasselbalch equation
Consider the ionization of a weak acid HA which has some pKa. It is often convenient to be able to relate the pH of a solution of a
n
weak acid to the pKa of the acid and the extent of ionization. The reaction would be
n
HA (reversible arrows) H+ + A-
The acid dissociation constant (Ka) for this reaction would be given by the equation
e
This equation can be rearranged to isolate the hydrogen ion concentration on the left, because, remember, we want an equation
relating the pH of the solution to the pKa and the extent of ionization of t weak acid. The rearranged form of the equation is
the
By definition, log 1/ [H+] = pH , and log 1/Ka = pKa , so that by taking t log of the equation above, we get the equation
the
This is the well-known Henderson-Hasselbalch equation that is often used to perform the calculations required in preparation of buffers
d
for use in the laboratory, or other applications. Notice several interesting facts about this equation.
First, if the pH = pKa, the log of the ratio of dissociate acid and associated acid will be zero, so the concentrations of the two species
will be the same. In other words, when the pH equals the pKa, the acid w be half dissociated.
will
Second, notice that as the pH increases or decreases by one unit relative to the pKa, the ratio of the dissociate form to the associated
form of the acid changes by factors of 10 That is if the pH of a solution is 6 and the pKa is 7, the ratio of [ A ]/[ HA] will be 0.1, will if
10. is, 7 A-]/[ 01
the pH were 5, the ratio would be 0.01 and if the pH were 7, the ratio wo ould be 1.
Also, note that if the pH is below the pKa, the ratio will be < 1, while if th pH is above the pKa, the ratio will be >1. In short, there is
he
a lot of information in the Henderson-Hasselbalch equation. You would be wise to study this equation to understand its various
e
ramifications. Dave Kotun, NSU O Orlando, PA Program 11

12. DEFINITIONS RELATED TO H
HENDERSON
HASSELBALCH EQUATION
Q
DEFINITIONS
-log H+ = pH and H+ a inversely proportional
are
As H+ increases, pH decreases
As H + decreases, pH increases
-log Ka = pKa
Ka = the dissociation constant of a weak acid
n
BICARBONATE BUFFER SSYSTEM EQUILIBRIUM AS
DEFINED BY HENDERSON-HASSELBALCH
EQUATION:
EQUATION
pKa + log HCO3- conjugate base/
pH = g
H2CO3conjugate acid
Dave Kotun, NSU O
Orlando, PA Program 12

13. Henderson Hasselbach
Two equivalent forms o the equation are
of
and
Here, pKa is − log10(K where Ka is the
Ka)
acid dissociation consta
ant, that is:
for the reaction:
Dave Kotun, NSU O
Orlando, PA Program 13

14. CALCULATION OF NML pH W
WITH THE
HENDERSON-HASSELBALCH EQUATION
Q
Definitions:
pKa of bicarbonate buffer = 6.1
Solubility coefficient of CO2 in water = 0. 03
pCO2 = the partial pressure of CO2 in an arterial blood gas
e
Normal = 40 mm Hg
Carbonic acid (H2CO3) = (0 ) (pCO2) = (0.03) (40)
( (0.03) (p ( )( )
Normal value of HCO3- in an arterial blood gas = 24 mEq/L
pH = 6.1 + log 24 meq/ L
(0.03)
(0 03) (40 mm Hg)
pH = 6.1 + log 20 = 6.1 + 1.3 = 7.4 ( normal pH)
Dave Kotun, NSU O
Orlando, PA Program 14

15. CONCLUSION
Henderson-Hasselbalch equa ation allows abnormalities in the
pH to be understood on the ba of changes in the ratio of
asis
bicarbonate to the pCO2
pH = HCO3- ::pCO2
The lungs and kidney continuuously work to adjust pCO2 and
bicarbonate to maintain a norm pH
mal
Dave Kotun, NSU O
Orlando, PA Program 15

16. OF
ACID- BASE BALANCE
pCO2 = the RESPIRATORY COMPONENT
Y
because:
It depends upon the Rate of Respiration
p p p
HCO3- = the METABOLIC C
COMPONENT because:
It’s plasma concentration is m
maintained by the kidney,
and is affected by amount of nonvolatile acids made
Dave Kotun, NSU O
Orlando, PA Program 16

17. REGULATION OF VENTIL
LATORY RATE IN
THE LUNGS
CENTRAL CHEMORECEPTORS IN THE MEDULLA:
Are sensitive to pCO2 a pH
and
∴ Increase in pCO2 ( and decrease in pH )
Increase in Venntilatory Rate
RECEPTORS IN CAROT BODIES AND IN
TID
AORTIC ARCH: Are Sen nsitive to arterial pO2 (the
partial pressure of oxyggen)
When pO2 < 60 m mmHg, Ventilatory Rate
Increases - the “ hy ypoxic drive” takes over
control of ventilatio
on
Dave Kotun, NSU O
Orlando, PA Program 17

18. Significance of Hypoxic Drive in COPD
These patients have em mphysema or chronic
bronchitis
and chronically havve:
Increased pCO2 and decreased pO2
d
When they have exacer rbation of their illness
with further decrea in pO2, their hypoxic
ase
drive takes over
Excessive O2 administraation (e g pure O2) during
(e.g.
exacerbation of COPD c could inhibit the hypoxic
drive of respiration and cause significant pCO2
p d g p
retention and death
Dave Kotun, NSU O
Orlando, PA Program 18

19. Regulation of Acid-Base Balance by the Kidney
BICARBONATE REABSORP PTION
Occurs in the proximal a distal renal tubule
and
H+ EXCRETION
Occurs in the distal rena tubule
al
Removes nonvolatile ac (waste products of
cids ( p
metabolism)
Sulfuric and phosphoric acids generated from protein
c
metabolism
t b li
Ketoacids generated fro fatty acid metabolism
om
(acetoacetate; beta hyd
beta-hyd droxybutyrate; acetone)
Accumulation of these ketoacids leads to a serious disorder
in diabetics: diabetic ketoacid dosis (further discussion in a
(
future lecture) Dave Kotun, NSU O
Orlando, PA Program 19

20. EFFECT OF pH ON PLASM K+
MA
CONCENTRATION
As pH increases ( serum H+ decreases) (ALKALOSIS)
H+ shifts from the intraccellular extracellular
compartments, and
K + shifts from the extraacellular intracellular
compartments HYPO OKALEMIA
As H decreases ( serum H+ iincreases) (ACIDOSIS)
A pH d )
H + shifts from the extraacellular intracellular
compartments,
compartments and
K + shifts from the intrac
cellular extracellular
compartments HYPE
p ERKALEMIA
Dave Kotun, NSU O
Orlando, PA Program 20

21. ARTERIAL BLOOD GAS: NORMAL VALUES
AND INDICA
ATIONS
NORMAL VALUES
pH = 7.35- 7.45
pCO2 = 35 – 45 mm Hg (the partial pressure exerted
by
b CO2)
HCO3-= 22- 26mEq/L (c calculated by a machine from the
Henderson-Hasselbalch E ti )
Hd H lb l h Equation)
pO2 = 80- 100 mmHg (the partial pressure exerted by
O2 )
O2 Saturation = 95- 100 (the percentage of
0%
hemoglobin saturated w O2)
with
Dave Kotun, NSU O
Orlando, PA Program 21

22. ARTERIAL BLOOD GAS: N
NORMAL VALUES
AND INDICATIONS
Measurements of abo are MORE
ove
ACCURATE from
ARTERIAL BLOOD t than VENOUS BLOOD
Because pH and pC 2 vary depending on site
CO
that venous blood w obtained from
was
(bicarbonate will als vary because it is
so
related to the pH an pCO2).
nd
Values of pH and pC 2 from arterial blood
CO
drawn from differen parts of body are same.
nt
Dave Kotun, NSU O
Orlando, PA Program 22

23. ARTERIAL BLOOD GAS: N
NORMAL VALUES
AND INDICATIONS
The value of bicarbon
nate from peripheral
venous blood
Is approximated fro the total CO2 or CO2
om
content
And is a a few mEq lower than the total CO2
The total CO2 is a a bit higher because it also
has dissolved pCO2
CO2 content = dissolv p CO2 + HCO3-
ved
Dave Kotun, NSU O
Orlando, PA Program 23

24. ARTERIAL BLOOD GAS: C
CRITICAL VALUES
Tell me, what is a cr
me ritical value?
pH < 7.25; > 77.55
pCO2 < 20; > 660
HCO3- < 15; > 40
pO2 < 40
O2 saturation < 75%
Dave Kotun, NSU O
Orlando, PA Program 24

25. INDICATIONS FOR ARTE
ERIAL BLOOD GAS
Monitor patients on ve entilators
1.
Monitor critically ill non
nventilator patients
2.
2
Establish preoperative baseline
e
3.
parameters
Regulate electrolyte th herapy
4.
Monitor O2 flow rates
5.
5
Diagnosis and treatme of significant
ent
6.
metabolic disorders
Dave Kotun, NSU O
Orlando, PA Program 25

26. ACID BASE BALANCE II
D-
PATHO
OLOGIC PROCESSES

27. BJECTIVES
Define and contrast the terms acidosis and
t
1.
alkalosis
Describe clinical sce
enarios giving rise to the
2.
following acid base disorders:
Metabolic acidosis; mettabolic alkalosis;
respiratory acidosis; respiratory alkalosis
Describe the pattern of laboratory values
ns
3.
3
for the acid base dis
sorders above
Dave Kotun, NSU O
Orlando, PA Program 27

28. BJECTIVES
4. Describe how the an nion gap calculation
(g
(high vs. normal anion gap) helps to
g p) p
characterize the etioology of metabolic
acidosis
5. Identify mechanisms of respiratory and
metabolic compensa ation for acid base
disorders
6.
6 Utilizing electrolyte and arterial blood gas
data as well as clinic history diagnose the
cal
acid base
acid-base disorders above
Dave Kotun, NSU O
Orlando, PA Program 28

29. EFINITIONS
Acidosis:
A process associate with a DECREASE in pH
ed
and an INCREASE in H+ concentration
pH < 7.35
Alkalosis:
A process associate with an INCREASE in pH
ed
and a DECREASE in H+ concentration
n
pH > 7.45
7 45
Dave Kotun, NSU O
Orlando, PA Program 29

30. DEFINI
ITIONS
Metabolic id i
M t b li acidosis:
Decrease in plasma HCO3-
a
Metabolic alkalosis:
Increase in plasma HCO3-
Respiratory acidosis:
:
Increase in pCO2
Respiratory alkalosis
s:
Decrease in pCO2
Dave Kotun, NSU O
Orlando, PA Program 30

31. Metabolic Acid-Ba Disorders
ase
They Are Called Metabolic Because the Primary
Problem
Involves Nonvolatile Acid
ds
Not CO2, HCO3-, and Renal Function
Dave Kotun, NSU O
Orlando, PA Program 31

32. etabolic Acidosis
There is decreased b b
h d d bicarbonate due to:
d
Increased accumulalation of nonvolatile acids of
loss of HCO3- f m kidney or f
f from from GI tract
Classified as HIGH A ANION GAP or NORMAL
ANION GAP metabol acidosis
olic
ANION GAP = unme easured anions in the
extracellular fluid co
ompartment
Lactate, citrate, pyr
, , py
y
yruvate, phosphate, sulfate
,p p ,
Dave Kotun, NSU O
Orlando, PA Program 32

33. ETABOLIC ACIDOSIS
S
CALCULATION OF ANIO GAP =
ON
Na+ - ( HCO3- + Cl- )
Normal Anion Gap =
8 – 14
High Anion Gap Metaboliic Acidosis has anion gap
> 14
Dave Kotun, NSU O
Orlando, PA Program 33

34. METABOLIC ACID
DOSIS
H+ from nonvolatile acids (ex ketoacids; lactic acid)
x.
x
combines with bicarbonate (H 3- )and pulls bicarbonate
HCO
buffer equilibrium toward carb
bonic acid (H2CO3) and away
from bicarbonate:
CO2 + H2O H2CO3 HCO3-+ H+
A decrease in bicarbonate (wwithout an increase in chloride)
results in increased anion gap
p
Dave Kotun, NSU O
Orlando, PA Program 34

35. ETABOLIC ACIDOSIS
S
HIGH ANION GAP ME
ETABOLIC ACIDOSIS
Caused by:
y
Increased nonvolatile acids
Increased Endogeno Acid Production
ous
Lactic acid, Beta- h
hydroxybutyrate, Acetoacetate
and other organic aacids
Toxins
Salicylate; methano ethylene glycol; ethanol
nol;
Decreased Renal Ex
xcretion of Acids
Renal failure ( ino
organic acids )
Dave Kotun, NSU O
Orlando, PA Program 35

36. ETABOLIC ACIDOS
SIS
HIGH ANION GAP META
TABOLIC ACIDOSIS
Lactic acidosis as a cau of high anion gap metabolic
use
acidosis
Serum Lactic Acid Increeases In Conditions With
Impaired Ti
I i d Tissue P f sion
Perfusi
Shock and Hypotensioon
Severe Septicemia
p
Hypoxia
Severe congestive heart failure
Severe anemia
Anaerobic conditions fav glycolysis for energy
vor
increased lactate produc
ction from pyruvate
Dave Kotun, NSU O
Orlando, PA Program 36

37. ETABOLIC ACIDOS
SIS
High anion gap metabolic a acidosis
Keto acidosis as a cause of high anion gap metabolic
fg gp
acidosis
States of insulin deficie
ency cause an increase in
ketoacids
Decreased Insulin increased break down of fat
i
increased acetyl CoA increased ketones (also
called ketoacids – acet
ll d k t id etoacetate; b t
t t t beta
hydroxybutyrate) ketones in blood and urine
ke
Diabetes: patients have a la of insulin
ack
Starvation: inadequate carbbohydrate ingestion
decreased insulin
Alcoholism: same mechanis as starvation ketosis
sm
Dave Kotun, NSU O
Orlando, PA Program 37

38. ETABOLIC ACIDOS
SIS
High anion gap meta
abolic acidosis
Exogenous toxins a a cause of high anion
as
gap metabolic acido i
t b li idosis
Substances Ingested By Alcoholics With
d
Poor Cash Flow:
Methanol (wood alc cohol)
Ethylene glycol (ant tifreeze)
Salicylates (aspirin)
Dave Kotun, NSU O
Orlando, PA Program 38

39. ETABOLIC ACIDOSIS
S
Normal anion gap metabolic acidosis
Causes
Loss of bicarbonate from GI tract or Kidney -
e
anion gap is not inc
creased, because there is
increased reabsorpt tion of chloride anion to
maintain electroneuutrality
Dave Kotun, NSU O
Orlando, PA Program 39

40. METABOLIC ACID
DOSIS
GastroIntestinal Loss of Bicarbonate Rich Fluids
Diarrhea is the most comm cause of normal
mon
anion gap metabolic acidosis
i t b li id i
Pancreatic, Biliary, or Intest
tinal Drainage
Renal Loss of bicarbonate- loss of bicarbonate in
bicarbonate
urine due to renal tubular dis
sease
Renal Tubular Acidosis (RTA)
e.g. caused by chronic renal in
nfection ( pyelonephritis );
chronic obstruction from kidney stones
y
Dave Kotun, NSU O
Orlando, PA Program 40

41. METABOLIC ACIDOSI
IS
NORMAL ANION GAP METAABOLIC ACIDOSIS
LABS ASSOCIATED WITH M
METABOLIC ACIDOSIS
DECREASED plasma HCO3- leads to DECREASED plasma pH
HYPERCHLOREMIA occur with NORMAL ANION GAP
rs
METABOLIC ACIDOSIS:
The kidney reabsorbs increased Cl- to balance the loss of anion
(bicarbonate)
(bi b t )
ACIDOSIS CAUSES HYPER
RKALEMIA
Acidosis increased serum H+ concentration H+ shifts into
m
the cells K+ moves out of the cells into the serum
f
hyperkalemia
This is a compensatory mech
hanism for dealing with acidosis
Dave Kotun, NSU O
Orlando, PA Program 41

42. METABOLIC ALKALO
OSIS
Caused by loss of H+
It is called Metabolic becau primary disorder involves a loss of
use
nonvolatile acid (HCL) or seecretion of H+ by kidney
There is increased bicarbon nate: loss of H+ drives bicarbonate
buffer equilibrium toward in
ncreased production of bicarbonate:
CO2 + H20 H2CO3 HCO3- +H+ (reaction pulled toward direction
of bicarbo
onate))
Dave Kotun, NSU O
Orlando, PA Program 42

43. METABOLIC ALKALOSIS
CAUSES
LOSS OF H+
GASTRIC LOSS of HC
CL
Vomiting
Nasogastric Suction
RENAL LOSS of H+
H
Some diuretics
Increased Aldosterone (Conn’s Syndrome);
e
Increased Cortisol (Cu
ushing’s Syndrome)
There is increased Na+ reabsorption coupled with
+
increased H+ and K+ secretion
Dave Kotun, NSU O
Orlando, PA Program 43

44. METABOLIC ALKALOSIS
Labs
L b associated with metabolic alkalosis
i t d ithh t b li lk l i
Increased bicarbonate leads to increased pH
Hypokalemia occurs as part of a
s
compensatory mech hanism
Decreased plasma H+ H+ shift from the
cells into the serum K+ shifts from the
serum into the cells h
h ll hypokalemia
kl
Dave Kotun, NSU O
Orlando, PA Program 44

45. COMPENSATION FOR ME
ETABOLIC ACID-BASE
DISORDERS
Respiratory compenssation occurs for
metabolic acid-base d
disorders
To assess compensa
ation, remember that pH
= HCO3- pCO2
Henderson-Hasselbal equation shows the
lch
relationship between pH, bicarbonate, and
pCO2 as indicated ab
bove
Dave Kotun, NSU O
Orlando, PA Program 45

46. COMPENSATION FOR META
ABOLIC ACID-BASE
ISORDERS
Respiratory compensa
p y p ation occurs for
metabolic acid-base di
disorders
METABOLIC ACIDOSIS (pH <7.35; H+
S: (p ;
concentration is high)
A primary decrease in bicarbonate results in a
n
decrease in pH; to br
ring the pH up toward
normal, the pCO2 nee to be decreased
eds
This i
Thi is accomplished b increasing
li h d by i i
ventilatory rate to blow off CO2
w
Labs:
L b A decrease in b th HCO3- and pCO2
d i both d CO
Dave Kotun, NSU O
Orlando, PA Program 46

47. COMPENSATION FOR META
ABOLIC ACID-BASE
ISORDERS
METABOLIC ALKAL
LOSIS:
pH > 7.45; H+ conc
centration is low
Remember that pH = bicarbonate pCO2
A primary increase in bicarbonate results in
an i
increased pH; to b i the pH down
d H to bring th H d
toward normal, the pCO2 needs to be raised
This is accomplishe by decreasing
ed
ventilatory rate to r
retain more CO2
Labs: an increase in both HCO3- and pCO2
Dave Kotun, NSU O
Orlando, PA Program 47

48. RESPIRATORY ACID B
BASE DISORDERS
They are called res
spiratory because
the primary problem involves pCO2
m
and pulmonary function
Dave Kotun, NSU O
Orlando, PA Program 48

49. ESPIRATORY ACID
DOSIS
Defect: Retention of CO2 resulting from
O
hypoventilation
Causes
Chronic Obstructive Pulmonary Disease
e
(COPD) emphysem chronic bronchitis (to
ma;
be di
b discussed)d)
Neuromuscular Disorders Causing Weakness
of Respiratory Musc
cles
Spinal cord injury; amyotrophic lateral sclerosis
;
(ALS); multiple sclerosis ( MS)
Guillian- Barre Syn
ndrome
Dave Kotun, NSU O
Orlando, PA Program 49

50. RESPIRATORY AC
CIDOSIS
Defect: Retention of CO2 resulting from
f
hypoventilation
Causes
Respiratory Center Depression
General anesthesia; sedative and narcotic drugs;
CNS brainstem pathology (tumor; trauma;
stroke)
Lung Conditions
Obesity-
Obesity Hypovent tilation Syndrome (Pickwickian
Syndrome)
Flail chest from multiple rib fractures
Kyphoscoliosis
Dave Kotun, NSU O
Orlando, PA Program 50

51. RESPIRATORY AC
CIDOSIS
Defect: Retention of CO2 resulting from
O
hypoventilation
CHRONIC OBSTRUCTIVE LUNG DISEASE AS A CAUSE
OF
RESPIRATORY ACIDOSIS
Smoking Plays An Impo
ortant Role in the Pathogenesis
of these disorders
Dave Kotun, NSU O
Orlando, PA Program 51

52. RESPIRATORY ACID
DOSIS (cont.)
( )
Defect: Retention of CO2 result ting from hypoventilation
EMPHYSEMA:
Destruction of air spaces and loss of elasticity ( due to increased
s
protease activity associated with ssmoking ) results in difficulty
exhaling CO2
CHRONIC O C
C O C BRONCHITIS: S
Criteria for diagnosis- Persistent C
Cough and Sputum Production
for at least 3 Months in 2 Consecu utive Years
Chronic Irritation from Cigarette Smok and Microbiologic Infections
ke
Excessive Mucous Production in S Small and Large Airways
Obstruction
Dave Kotun, NSU O
Orlando, PA Program 52

53. ESPIRATORY ACIDOSIS
Defect: Retention of CO2 resulting from
f
hypoventilation
Neuromuscular disorders as a cause of respiratory
s
acidosis
AMYLIOTROPHIC LAT TERAL SCLEROSIS (ALS)- “Lou
(ALS) Lou
Gherig’s Disease”
Progressive Degenera
g g ation of Motor Neurons in the Brain
and Spinal Cord pr rogressive weakness and wasting of
muscles needed for R
Respiration and Movement
Death typically i
D th t i ll in 3 yeears
Dave Kotun, NSU O
Orlando, PA Program 53

54. RESPIRATORY AC
CIDOSIS
Defect: Retention of CO2 re
esulting from hypoventilation
Neuromuscular disorders as a cause of respiratory acidosis
Multiple sclerosis (MS)
One of the more comm CNS Diseases
mon
Usually characterize by Chronic Remitting and Relapsing
ed
Course
Pathology -Multiple ar
reas of Myelin Loss in the CNS white
matter
Gillian - Barre Syndrom
me
Acute or Subacute illness with motor impairment,
sometimes requiring aassisted ventilation
Causes- preceding up respiratory or gastrointestinal
pper
infection
Immunizations
Dave Kotun, NSU O
Orlando, PA Program 54

55. ESPIRATORY ALKALO
OSIS
Defect: Depletion f
D f t D l ti of CO2 R lti f
Resulting from
hyperventilation
Causes
C
Stimulation of the brains
stem respiratory center
Emotional states: excitement; anxiety
Fever
Pregnancy
Salicylates and Sepsis: Both of these may cause a mixed
respiratory alkalosis and metabolic acidosis
d
Dave Kotun, NSU O
Orlando, PA Program 55

56. RESPIRATORY AL
LKALOSIS
Defect: Depletion of CO2 Resulting from
O
hyperventilation
Causes (cont )
(cont.)
Cardiac disease
Congestive Heart Failure Pulmonary Edema
(rapid breathing)
Severe congestive hea failure results in
g art
hypoperfusion lactic acidosis metabolic
c
acidosis
Mechanical over ventila
ation
Dave Kotun, NSU O
Orlando, PA Program 56

57. ABS IN RESPIRATORY A
ACID BASE
ACID-BASE DISORDERS
Respiratory acidosis
s
pH decreases; pCO2 increases
O
Hyperkalemia (H+ go into cells; K + goes into
oes
the plasma)
Respiratory alkalosis
pH increases; pCO2 decreases
Hypokalemia (H + go into the plasma; K +
oes
goes iinto th cells)
t the ll )
Dave Kotun, NSU O
Orlando, PA Program 57

58. OMPENSATION FOR RESSPIRATORY
CID BASE
CID-BASE DISORDERS
Metabolic compensation occurs for respiratory acid –
base disorders
When assessing compe ensation, remember that pH is
determined by the ratio of bicarbonate to pCO2
Respiratory acidosis (p < 7.35; high H+)
p y (pH g
A primary increase in p 2 (from excessive CO2
pCO
retention) results in a de
ecrease in pH
To bring the pH up towa normal, the kidney
ard
compensates by reabso orbing MORE bicarbonate
Dave Kotun, NSU O
Orlando, PA Program 58

59. OMPENSATION FOR RESSPIRATORY
CID BASE
CID-BASE DISORDERS
Metabolic
M t b li compensation occurs f respiratory acid –
ti for it id
base disorders
When
Wh assessing compe ti remember th t pH iis
i ensation, b that H
determined by the ratio of bicarbonate to pCO2
on
Respiratory alkalosis (pH > 7.45; low H+)
H 7 45;
A primary decrease in pCO2 (from hyperventilation)
results in a increase in pH
To bring the pH down t toward normal, the kidney
compensates by reabso orbing LESS bicarbonate
Dave Kotun, NSU O
Orlando, PA Program 59

60. CALCULATION OF COMPE
ENSATION FACTOR
Purpose:
1. To determine if the c
compensatory change in pCO2 is
appropriate f the prim change iin HCO3- to
i for h imary h
maintain a HCO3-/ pCO2 ratio compatible with normal
O
pH (and if compensato change in bicarbonate is
ory
appropriate for primary change in pCO2)
y
2.
2 To determine if it is a “ simple metabolic OR
simple”
respiratory acid-base disorder, or a mixed acid – base
disorder
Dave Kotun, NSU O
Orlando, PA Program 60

61. CALCULATION OF COMPEN
NSATION FACTOR
Purpose:
A simple acid base disorder is one in which
acid-base
there is only 1prima acid-base disturbance
ary
(e.g. metabolic acid
dosis)
A mixed acid-base d disorder is one in which
there are 2 or more acid-base disturbances
e
occurring at the sam time
me
If the calculated compe ensation is appropriate,
then i
th it is a simple disord
i l di rder
If the compensation is n what is expected, it
not
may b a mixed disorde
be i d di der
Dave Kotun, NSU O
Orlando, PA Program 61

62. CALCULATION OF RESPIRA
ATORY COMPENSATION
FACTOR FOR METABOLIC A
ACID-BASE
ACID BASE DISORDERS
Metabolic id i
M t b li acidosis
pCO2 should decrease by 1.2 mmHg for each fall
in 1.0 mEq/L of HCO3-
Metabolic alkalosis
pCO2 should increase by 0 4 – 0 7 mmHg for
0.4 0.7
each rise of 1.0 mEq of HCO3-
q/L
Dave Kotun, NSU O
Orlando, PA Program 62

63. ALCULATION OF COMPENSSATION FACTOR FOR
ESPIRATORY ACID BASE D
ACID-BASE DISORDERS
Respiratory acidosis
ACUTE
HCO3- rises 1 mEq/L for ea rise of 10 mmHg in p 2
q ach g pCO
CHRONIC
HCO3- rises 3-4 mEq/L for e
each rise of 10 mmHg in Pco2
Respiratory lk l i
R i t alkalosis
ACUTE
HCO3 falls 2-3 mEq/L for each decrease of 10 mmHg in pCO2
23
3-
CHRONIC
HCO3- falls 5 mEq/L for eac decrease of 10 mmHg in pCO2
ch
Dave Kotun, NSU O
Orlando, PA Program 63

64. ONCLUSIONS
Metabolic acid – bas disorders
se
Primary Problem is with Nonvolatile Acids HCO3-
N Acids,
and Kidney
Metabolic acidosis: decrrease in bicarbonate
Metabolic alkalosis: incr
rease in bicarbonate
Compensation is b Adjusti V til t R t and
C ti i by Adj sting Ventilatory Rate d
pCO2 (occurs over minute hours)
es/
Metabolic acidosis: decrrease in pCO2
Metabolic alkalosis: incr
rease in pCO2
Dave Kotun, NSU O
Orlando, PA Program 64

65. ONCLUSIONS
Summary of labs:
Metabolic acidosis
pH decreased;
HCO3- decreased;
;
pCO2 decreased
Normal Anion Gap Meta
abolic Acidosis:
Hyperchloremia
Metabolic alkalosis
pH increased;
HCO3- increased;
pCO2 increased
Dave Kotun, NSU O
Orlando, PA Program 65

66. ONCLUSIONS
Respiratory acid – ba disorders
ase
Primary Problem is with pCO2 and lungs
p
Respiratory acidosis: inc
crease in pCO2
Respiratory alkalosis: de
ecrease in pCO2
Compensation is by Adjussting Reabsorption of HCO3-
by the Kidney (occurs ov days)
ver
Respiratory acidosis: inc
crease in bicarbonate
Respiratory lk l i de
R i t alkalosis: decrease iin bi b t
bicarbonate
Dave Kotun, NSU O
Orlando, PA Program 66

67. ONCLUSIONS
Summary of labs:
Respiratory acidosis
pH decreased
pCO2 increased
HCO3- increased
Respiratory alkalosis
pH increased
pCO2 decreased
HCO3- decreased
Dave Kotun, NSU Orlando, PA Program 67

68. Conclusions
Changes in serum K+ concent
tration resulting from changes
in pH
ACIDOSIS HYPERKALEMIA
A
ALKALOSIS HYPOKALEMIA
A
Note – this concept is ve important in diabetes
ery
Dave Kotun, NSU O
Orlando, PA Program 68

69. ONCLUSIONS
Simple id base di orders
Si l acid – b dis d
One primary problem (re
espiratory or metabolic)
Mixed acid – base diso
orders
TWO ( or more ) PRIMA PROBLEMS
O o oe ARY O S
Examples of Mixed Acid- Base Disorders
COPD with shock and L Lactic Acidosis = Respiratory
p y
Acidosis and Metabolic Acidosis
c
Pregnancy with excess Vomiting = Respiratory Alkalosis
sive
and Metabolic Alk l is
d M t b li Alkalosis
Dave Kotun, NSU O
Orlando, PA Program 69

70. Time for Questions ???????????
Q s
Dave Kotun, NSU O
Orlando, PA Program 70