Acid base disorders related to the respiratory system.Blood gas analysis and the renal compensation that happens in respiratory acid base disorders.

1. RESPIRATORY
ACIDOSIS AND
ALKALOSIS
Presented by:
Dr Anwar H Siddiqui
Ph.D. Scholar
Department of Physiology, J N Medical College, AMU, Aligarh

2. The body and pH.

3. Buffer System
 Provide or remove H+ and stabilize the pH.
 Include weak acids that can donate H+ and weak
bases that can absorb H+.
 Change in pH, after addition of acid, is less than
it would be in the absence of buffer.

4. Buffer System

5. Acid base disorder
 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.
 Normal acid base values
pH pCO2 HCO3
-
Range 7.35- 7.45 36-44 22-26
Optimal Value 7.4 40 24

6. Acid base disorder
 Clinical disturbances of acid base metabolism
classically are defined in terms of the
HCO3- /CO2 buffer system.
 Acidosis – process that increases [H+] by increasing
PCO2 or by reducing [HCO3-]
decrease in the blood pH below normal range
 Alkalosis – process that reduces [H+] by reducing
PCO2 or by increasing [HCO3-]
Elevation in blood pH above the normal range

7. Respiratory Acid base disorder
 Respiratory acid-base disorders are those abnormalities
in acid-base equilibrium initiated by a change in the
arterial carbon dioxide tension (PaCO2 )--the respiratory
determinant of acidity in the following equation:
 Henderson Hasselbalch equation:
pH = 6.1 + log [HCO3-]/ 0.03 PCO2
 Kassirer-Bleich equation:
[H+] = 24 × PCO2 / [HCO3-]
(Remember this formula !!!!!)

8. Respiratory Acid base disorder
There are two respiratory acid-base
disorders:
respiratory acidosis and
respiratory alkalosis.

9. Respiratory Acidosis
 Respiratory acidosis is the acid-base disturbance initiated by an
increase in PaCO2.
 The level of PaCO2 is determined by the rate of carbon dioxide
production (VCO2) and the rate of alveolar ventilation (VA), as
follows:
PaCO2 = K x VCO2 / VA where K is a constant.
 An increase in arterial pCO2 can occur by one of three possible
mechanisms:
 Presence of excess CO2 in the inspired gas
 Decreased alveolar ventilation
 Increased production of CO2 by the body

10. Respiratory Acidosis
 Overproduction of carbon dioxide is usually matched by
increased excretion (due to increased alveolar
ventilation)
 Most cases of respiratory acidosis reflect a decrease in
alveolar ventilation.
 Alveolar hypoventilation leads to an increased PaCO2 (ie,
hypercapnia).
 The increase in PaCO2, in turn, decreases the
bicarbonate (HCO3
–)/PaCO2 ratio, thereby decreasing
the pH.

11. Respiratory Acidosis

12. Respiratory Acidosis
 In acute respiratory acidosis, the PaCO2 is elevated above the upper
limit of the reference range (over 6.3 kPa or 45 mm Hg) with an
accompanying acidemia (pH <7.36).
 In chronic respiratory acidosis, the PaCO2 is elevated above the
upper limit of the reference range, with a normal or near-normal
blood pH secondary to renal compensation and an elevated serum
bicarbonate (HCO3
− >30 mm Hg).
 The expected change in pH with respiratory acidosis can be
estimated with the following equations:
Acute respiratory acidosis – Change in pH = 0.008 × (40 – PaCO 2)
Chronic respiratory acidosis – Change in pH = 0.003 × (40 – PaCO 2)

13. Aetiology Acute Respiratory Acidosis
NORMAL AIRWAY AND LUNGS ABNORMAL AIRWAY AND LUNGS
Central nervous system depression
GA/ Sedative overdose
Head trauma/Cerebrovascular accident
Cerebral edema
Brain tumor/Encephalitis
Upper airway obstruction
Coma induced hypopharyngeal obstruction
Aspiration of foreign body or vomitus
Laryngospasm or angioedema
Obstructive sleep apnea
Neuromuscular impairment
High spinal cord injury, Guillain-Barre syndrome
Status epilepticus, Botulism, tetanus
Crisis in myathenia gravis
Hypokalemic myopathy
Drugs or toxic agents (curare, succinylcholine,
aminoglycosides, organophosphates)
Lower airway obstruction
Generalized bronchospasm
Severe asthma
Bronchiolitis of infants and adults
Ventilatory restriction
Rib fractures with flail chest
Pneumothorax, Hemothorax
Impaired diaphragmatic function
Disorders involving pulmonary alveoli
Severe bilateral pneumonia
Acute respiratory distress syndrome
Severe pulmonary edema
Iatrogenic events
Misplacement of airway cannula during mechanical
ventilation
Bronchoscopy associated respiratory arrest
Increased CO2 production with constant mechanical
Ventilation
Pulmonary perfusion defect
Cardiac arrest, Severe circulatory failure
Massive pulmonary thromboembolism, Fat or air
embolus

14. Aetiology Chronic Respiratory Acidosis
NORMAL AIRWAY AND LUNGS ABNORMAL AIRWAY AND LUNGS
Central nervous system depression
Sedative overdose
Methadone/heroin addiction
Primary alveolar hypoventilation
Obesity-hypoventilation syndrome
Brain tumor
Bulbar poliomyelitis
Upper airway obstruction
Tonsillar and peritonsillar hypertrophy
Paralysis of vocal cords
Tumor of the cords or larynx
Airway stenosis post prolonged intubation
Thymoma, aortic aneurysm
Neuromuscular impairment
Poliomyelitis Multiple sclerosis
Muscular dystrophy
Amyotrophic lateral sclerosis
Diaphragmatic paralysis
Myxedema
Myopathic disease
Lower airway obstruction
Chronic obstructive lung disease (bronchitis,
Bronchiolitis, bronchiectasis, emphysema)
Ventilatory restriction
Kyphoscoliosis, spinal arthritis
Obesity
Fibrothorax Hydrothorax
Impaired diaphragmatic Function
Disorders involving pulmonary alveoli
Severe chronic pneumonitis
Diffuse infiltrative disease
Interstitial fibrosis

15. Compensatory mechanism for
Acute respiratory acidosis
 It is completed within 5-10 min from onset of
hypercapnia.
 It originates exclusively from acidic titration of the
body’s non-bicarbonate buffers (hemoglobin,
intracellular proteins and phosphates, plasma proteins):
CO2 + H2O ↔ H2CO3 ↔ HCO3
- + H+
H+ + Buf- ↔ HBuf
 On average, plasma bicarbonate concentration increases
by about 0.1 mEq/L for each 1 mmHg acute increment
in PaCO2

16. Compensatory mechanism for
Chronic respiratory acidosis
 It requires 3-5 days of sustained hypercapnia for completion.
 It originates from up regulation of renal acidification mechanisms
(both in the proximal and distal segments of the nephron) that
result in:
 A transient increase in urinary net H+ excretion; and
 A persistent increase in the rate of renal bicarbonate
reabsorption that maintains the increased plasma bicarbonate
level.
 On average, plasma HCO3
- concentration increases by about 0.3
mEq/L for each mm Hg chronic increment in PaCO2

18. Respiratory Alkalosis
 Respiratory alkalosis is the acid-base disturbance initiated by a
reduction in PaCO2.
 This occurs when there is excessive loss of CO2 by alveolar
hyperventilation.
 Hypocapnia develops when a sufficiently strong ventilatory stimulus
causes CO2 output in the lungs to exceed its metabolic production
by the tissues.
 As a result, partial pressure of CO2 and H+ conc. falls

19. Respiratory Alkalosis
 By far, most cases of respiratory alkalosis reflect an
increase in alveolar ventilation.
 However, in the presence of constant alveolar ventilation
(i.e., mechanical ventilation), decreased carbon dioxide
production (e.g., sedation, skeletal muscle paralysis,
hypothermia, hypothyroidism) can cause respiratory
alkalosis.

20.  Most common acid-base abnormality observed in
patients who are critically ill.
 A common finding in patients on mechanical
ventilation.
 Acute hypocapnia causes a reduction of serum levels of
potassium and phosphate secondary to increased
intracellular shifts of these ions.
 A reduction in free serum calcium also occurs due to
increased binding of calcium to serum albumin.
 Many of the symptoms present in persons with
respiratory alkalosis are related to hypocalcemia.

21. Aetiology Respiratory Alkalosis
Hypoxemia or tissue hypoxia
Decreased inspired O2 tension/High altitude
Bacterial or viral pneumonia
Aspiration of food, foreign body, or vomitus
Larygospasm, Drowning
Cyanotic heart disease, Severe ciurculatory failure
Severe anemia,Hypotension
Left shift deviation of HbO2 curve
Pulmonary embolism
Central nervous system stimulation
Voluntarily
Pain, Anxiety,
Psychosis, Fever
Subarachnoid hemorrhage
Cerebrovascular accident
Meningoencephalitis
Tumor, Trauma
Stimulation of chest receptors
Pneumonia, Asthma
Pneumothorax, Hemothorax, Flail chest
Infant or adult respiratory distress syndrome
Cardiac failure
Noncardiogenic pulmonary edema
Pulmonary embolism, Interstitial lung disease
Drugs or hormones
Doxapram, Xanthines
Salicylates, Catecholamines
Angiotensin II, Vasopressor agents
Progesterone, Medroxyprogesterone
Dinitrophenol, Nicotine
Miscellaneous
Pregnancy, Sepsis, Hepatic failure
Mechanical hyperventilation
Heat exposure, Recovery form metabolic acidosis

22. Compensatory mechanism for
respiratory alkalosis
Acute adaptation
 It is completed within 5-10 min from onset of
hypocapnia
 It originates principally from alkaline titration of the
body’s nonbicarbonate buffers (hemoglobin,
intracellular proteins and phosphates, plasma proteins)
 Bicarbonate (HCO 3
-) falls 2 mEq/L for each decrease of
10 mm Hg in the PCO 2;

23. Compensatory mechanism for
respiratory alkalosis
Chronic adaptation
 It requires 2-3 days of sustained hypocapnia for completion.
 It originates from downregulation of renal acidification mechanisms
(both in the proximal and distal segments of the nephron) that
result in
A transient decrease in urinary net acid excretion (mostly a
fall in ammonium excretion and an early component of
increased bicarbonate excretion) that reduces the body’s
bicarbonate stores; and
A persistent decrease in the rate of renal bicarbonate
reabsorption that maintains the decreased plasma
bicarbonate level.

24. Compensatory mechanism for
respiratory alkalosis
 Bicarbonate (HCO 3
-) falls 5 mEq/L for each decrease of 10 mm Hg
in the PCO 2; that is, ΔHCO 3 = 0.5(ΔPCO 2)
The expected change in pH with respiratory alkalosis can be estimated
with the following equations:
 Acute respiratory alkalosis:
Change in pH = 0.008 X (40 – PCO 2)
 Chronic respiratory alkalosis:
Change in pH = 0.017 X (40 – PCO 2)

26. Identify?
Respiratory Acidosis
or
Respiratory alkalosis

27. Arterial Blood Gas Analysis

29. Steps for
Successful
Blood Gas
Analysis

30. STEP 0 • Is this ABG Authentic?
STEP 1 • ACIDEMIA or ALKALEMIA?
STEP 2
• RESPIRATORY or METABOLIC?
STEP 3 • If Respiratory – ACUTE or CHRONIC?
STEP 4 • Is COMPENSATION adequate?
STEP 5 • If METABOLIC – ANION GAP?

31. Is this ABG authentic ?
 Henderson-Hasselbalch equation
pH = 6.1 + log HCO3
-
0.03 x PCO2
pHexpected = pHmeasured = ABG is authentic
 [H+] meq/l = 24 X (PCO2 / HCO3)
H+ ion pH
100 7.00
79 7.10
63 7.20
50 7.30
45 7.35
40 7.40
35 7.45
32 7.50
25 7.60

32. ACIDEMIA or ALKALEMIA?
 pH < 7.35 acidemia
pH > 7.45 alkalemia
 This is usually the primary disorder
 Remember: an acidosis or alkalosis may be present even
if the pH is in the normal range (7.35 – 7.45)

33. RESPIRATORY or METABOLIC?
 IS PRIMARY DISTURBANCE RESPIRATORY OR
METABOLIC?
 pH HCO3 or pH HCO3 METABOLIC
 pH PCO2 or pH PCO2 RESPIRATORY
 In primary respiratory disorders, the pH and PaCO2 change
in opposite directions; in metabolic disorders the pH and HCO3-
change in the same direction.
 RULE- If either the pH or PCO2 is Normal, there might be
mixed metabolic and respiratory acid base disorder.

34. If Respiratory – ACUTE or CHRONIC?
Acute respiratory disorder - ∆pH(e-acute) = 0.008x ∆Pco2
Chronic respiratory disorder - ∆pH(e-chronic)= 0.003x ∆pCO2
.08 change in pH ( Acute )
.03 change in pH ( Chronic )
10 mm
Change
PaCO2
=

35. Is COMPENSATION adequate?
 Usually, compensation does not return the pH to normal (7.35 –
7.45).
If the observed compensation is not the expected compensation, it is likely that
more than one acid-base disorder is present.

36. Case: 6 year old male with progressive respiratory distress
Muscular dystrophy .
Blood Gas Report
Measured 37.0
o
C
pH 7.301
PaCO2 76.2 mm Hg
PaO2 45.5 mm Hg
Calculated Data
HCO3 act 35.1 mmol / L
O2 Sat 78 %
PO2 (A - a) 9.5 mm Hg D
PO2 (a / A) 0.83
Entered Data
FiO2 21 %
pH <7.35 :acidemia
Res. Acidemia : High PaCO2 and low pH
Hypoxemia
Normal A-a gradient
D CO2 =76-40=36
Expected D pH for ( Acute ) = .08 for 10
.08 × 3.6= 0.29
Expected ( Acute ) pH = 7.40 - 0.29=7.11
Chronic resp. acidosis
Hypoventilation
Chronic respiratory acidosis
With hypoxia due to hypoventilation
With renal compensation
HCO3 elevated
D HCO3 (e) = 3.5 (D CO2 /10)
= 3.5 (3.6) = 12.6
HCO3 expected =24+12.6 = 36.6 ± 2