basic hydrogen ion homeostasis, acid base disturbances and management.

2. The power of hydrogen

3. 1. Why not in mmol, mEq, or mg?
2. Does the letter p of pH mean partial pressure
as with pCo2 and pO2?
3. Why in acidosis when H+ increases, the pH
decreases ?

4. H+ is kept at a very low level compared with other ions.
 In a liter of pure water at 25 o C the number of moles of H+ is
about 0.0000001, this is written as 1 x 10-7.
 The superscript -7 is the power, the exponent or the
logarithm.
 The pH (or the power of hydrogen) is the negative logarithm
of H+ concentration .
40 nmol/L = 0.0000004 mol/L = 10-7.4 the pH is 7.4

5. Major body constituent.
Physical properties will affect
homeostasis.
Water ionizes spontaneously
into hydrogen and hydroxyl
ions.
Neutral water
_
• H+
= OH = 10 -7
• pH is 7
Alkaline if pH > 7
Acidic if pH <7

7. A single highly reactive positive charge.

8. Protein structure- function.
 Ionic and hydrogen bonding
will determine the final
morphology.

9. pH influences:
1. Function of all enzymes.
2. Normal electrolyte
distribution.
3. Myocardial performance
(contractility).
4. Hemoglobin function.

10. 1 Metabolic lactate, phosphate, sulphate, acetoacetate or b-hydroxy-butyrate
acids
Non-volatile.
Must be metabolized and excreted in urine.
40-80 mmol/day H+ load.
1 Respiratory Carbonic acid
acids
Volatile, very efficient lung excretion
CO2 + H2O ⇄ H2CO3 ⇄ H+ + HCO−3
15,000 mmol/day H+ load.

11. H + homeostasis is essential for life.
NormalpH 7.35-7.45
Compatible with life 6.8-8
Three systems for hydrogen homeostasis :
 Chemical buffering (immediate).
 Respiratory compensation (hours).
 Renal compensation (2-4 days).

12. Simple chemical neutralization.
The first line of defense.
A weak acid and its associate base.
1. Bicarbonate-carbonic acid system
2. Plasma proteins
3. Hemoglobin

13. CO2 + H2O ⇄ H2CO3 ⇄ H+ + HCO−3

14. CO2 + H2O ⇄ H2CO3 ⇄ H+ + HCO−3

15.  The respiratory system forms the single most important organ
+
system involved in the control of H concentration.
 PaCO2 is inversely proportional to alveolar ventilation.
 Small changes in ventilation can have a profound effect on pH.
 Ventilation is controlled by pH of CSF.

16. PCT Reabsorption of
bicarbonate .
CA- regulated.
DCT Addition of new
bicarbonate
Excretion of H+
Aldosterone- regulated

17. The normal acid-base status
pH 7.35-7.45
Bicarbonate (HCO3-) 22-26 mmol/L
PCO2 35-34 mmHg
 An acid–base disturbance disrupts at least two of
these three variables.

18. The base excess-deficit is the amount or base that
must be added to blood or removed from it to return
pH to 7.4 and to return the paCo2 to 40 mmHg at full
oxygen saturation and 37o C.
Positive values indicate metabolic alkalosis.
Negative values indicate metabolic acidosis.

19.  It is the difference between major measured cations and major
measured anions.
 Anion gap = [Na+] – ([Cl-] + [ HCO3-])
 Normal range 12±3 mEq/L (plasma proteins represent 11mEq/L).
Unmeasured cations include K+, Ca++, & Mg++.
 Unmeasured anions include PP, phosphates, sulphates and
organic acids.
 Increased AG in metabolic acidosis reflects an increase in the
organic acids.

20. Increase in Anion Gap / Decrease in bicarbonate
< 0.4 Hyperchloraemic normal anion gap acidosis
0.4 - Consider combined high AG & normal AG
0.8 acidosis BUT note that the ratio is often <1 in
acidosis associated with renal failure
1 to 2 Usual for uncomplicated high-AG acidosis
Lactic acidosis: average value 1.6
DKA more likely to have a ratio closer to 1 due
to urine ketone loss (esp if patient not
dehydrated)
>2 Suggests a pre-existing elevated HCO3 level so
consider:
a concurrent metabolic alkalosis, or
a pre-existing compensated respiratory acidosis

21. Acids are corrosives
to their containers!

22. The respiratory system is unable to remove sufficient
CO2 from the body →high PCO2 levels (hypercapnia).
The following reaction becomes displaced to the right
by the increased PCO2:
CO2 + H2O ⇄ H2CO3 ⇄ H+ + HCO−3
The consequence of this defect is an increased [H+]
(i.e. acidosis – reduced pH), and an increased [HCO−3].

23. Alveolar CNS depression Head trauma- drugs
hypoventilation NMT Residual NMB
Muscles Myopathy- MG
Chest wall Flail chest- Kyphoscoliosis
Pleura Effusion – pneumothorax
Airway Upper Laryngeal spasm
obstruction Lower Severe
bronchospasm
Parenchymal Pneumonia- ARDS- aspiration
lung disease pneumonitis- interstitial lung
disease ……
CO2 MH- thyroid storm- prolonged seizure- CHO
overproduction overload in TPN

24. 1 CNS depression up to coma
2 Direct myocardial depression
3 Possible hyperkalemia (transcellular)
4 Vasculature Systemic VD Hypotension-
Respiratory bounding pulse
High CO2 Cerebral VD ↑ICP
Pulmonary VC PHT
CNS Depression Narcosis
Autonomic Sympasthetic Apprehension
stimulation Sweating
Tachycardia

25. 1 Measures to ↑ ETT & Mechanical ventilation
alveolar Bronchodilators.
ventilation Brain stem stimulants (dopram).
Reversal of narcotics (naloxone).
Reversal of NDMB.
2 Measures to ↓CO2 Dantrolene- NMB- antithyroid drugs- ↓ CHO intake.
production when↑
N.B. Sodium Is rarely needed unless severe acidosis and
bicarbonate associated with CVS collapse.
Transient ↑in PCO2 (carbicarb, tromethamine:
THAM).
Patients with base When they develop acute respiratory failure the
line chronic aim of therapy is to return PCO2 to their base line
respiratory as normalizing PCO2 to 40 → metabolic alkalosis
acidosis require Oxygen therapy must be carefully titrated (hypoxic
attention. respiratory drive, normalizing PO2 can→ severe
hypoventilation).

26.  Inappropriate alveolar ventilation relative to CO2 production
 The following reaction becomes displaced to the left by the
decreased PCO2:
CO2 + H2O ⇄ H2CO3 ⇄ H+ + HCO−3
 The consequence of this defect is a decreased [H+] (i.e.
alkalosis – high pH), and a decreased [HCO−3].
 Kidneys will excrete increased amounts of HCO3
 The renal response has a slow onset and the maximal response
takes 2 to 3 days .

27. 1 Hypoxia Pulmonary Embolism ↑altitude
Pneumonia
Asthma
Pulmonary edema (all types)
↓ Pulmonary compliance.
2 Neurologic Stroke encephalitis IC tumors
3 Psychiatric Hysterical pain anxiety
4 Sepsis and fever Gram negative septicemia
5 Pregnancy 50%↑MV- PCO2 around 30mmHg-
bicarbonate↓-pH 7.44
6 Liver disease A respiratory alkalosis is the commonest acid-
base disorder found in patients with chronic
liver disease
7 Intoxication Salicylates toxicity
8 Iatrogenic Ventilator induced (common)

28. 1 Hb
ODC →Lt
2 Electrolytes K↓ ECG changes-arrhythmias
Ileus
weakness
Ca↓ (ionized) NM irritability
CVS depression
3 Myocardium Contractile ↓ Contractility
element
4 Respiratory Vasculature Cerebral Ischemia
↓ CO2 Systemic SVR↑
Coronary Spasm
Placenta Perfusion ↓
Pulmonary PVR↓

29. 1 Correction of the cause
The number one priority is correction of any co-existing
hypoxemia
Administration of oxygen in sufficient concentrations and
sufficient amounts is essential.
2
Anxiolytics (lorazepam-midazolam)
3
CO2-enriched air (bag and mask rebreathing of CO2) is not
recommended

30. Low pH + Decrease in plasma bicarbonate.
Compensation:
Respiratory The low pH will stimulate the
chemoreceptors→ hyperventilation
(Kaussmaul’s respiration)
CO2 + H2O ⇄ H2CO3 ⇄ H+ + HCO−3
The respiratory compensation for MA
→Lowering PCO2→ moving the equation
to the left and thus further ↓ HCO−3
Renal -↑ H+ excretion
-↑ reabsorption of all filtered HCO−3
- Generation of new HCO−3

31. 1 Ketoacidosis DM
Strong acid Starvation
gain Alcoholism
High fat diet
→consumption of Lactic acidosis Shock
Hypoxia
HCO−3 Liver failure
(N liver: lactate→ G)
Renal failure Kidney failure to excrete H+
(High anion gap MA) Intoxication Salicylates
Methanol
Propylene glycol (organic solvent)
Cyanide
Paraldehyde
2 GIT Severe diarrhea/fistulae: (pancreatic, biliary,
HCO −
3 loss intestinal, ileostomy, uretro-segmoidostomy)
/ingestion of large amount of anion exchange
Normal anion gap resins
MA Renal PCT RTA-CA inhibitors
(hyperchloraemic) DCT Hypoaldosteronism- spironolactone
Iatrogenic Rapid ECF expansion with bicarbonate free
fluid e.g. Nacl
TPN (Cl)
Mineral acid administration

32. Nausea and vomiting
Abdominal pain
Change in sensorium
Tachypnea
Decreased muscle
strength
Decreased myocardial
contractility
Arteriolar dilatation
Venoconstriction
PHT

33. 1
Emergency management of life- E.g. endotracheal intubation, mechanical ventilation,
threatening conditions always has CPR and treatment of hyperkalemia.
the highest priority. Maintain hyperventilation in ventilated patients
Expected PCO2= (1.5 x actual bicarbonate) + 8 mmHg.
2 Specific DKA Insulin, IV fluids, K
LA (shocked) Oxygen, fluids, blood, vasopressors and inotropes
Salicylates Alkalinization of urine by sodium bicarbonate.
3 Correction of any respiratory Reversal of NMB.
component of acidemia Reversal of narcosis
Bronchodilators
4 Losses Fluids Replace deficit
Electrolytes Replace deficit
Sodium Indications if PH < 7.2
bicarbonate Severe hypobicarbonatemia (<4 mEq/L)
NOT be given Severe hyperchloremic acidemia
on a routine Dosage Empirical: Calculated upon base deficit:
basis 1 mEq/kg BDX BW X 30%
In practice half the dose is given.
5 Refractory MA Hemodialysis

34. A metabolic alkalosis is a primary acid-base disorder
which causes the plasma bicarbonate to rise to a level
higher than expected.
Compensatory hypoventilation
Expected pCO2 = 0.7 [HCO3] + 20 mmHg
Hypoventilation may be absent:
•Pain
•Pain with arterial puncture
• Hypoxemia

35. Chloride- Conditions causing Vomiting
90% sensitive
Urine Cl is
low<10
ECF volume
depletion.
CHPS
NG suction
Diarrhea
mmol/L Diuretics
Chloride- Increased H excretion ↑Mineralocorticoid activity,
10% resistant in exchange of Na Hypoaldosteronism, Caushing
Urine Cl is Severe hypokalemia
low>20
mmol/L
Rare causes Others Large doses of NaHCO3(+renal insufficiency)
Massive blood transfusion (citrate in liver→ bicarbonate)
Large doses of sodium penicellin
Addition of Milk alkali syndrome
base to ECF Re-feeding
Recovery from metabolic acidosis

36. 1 Hb
ODC →Lt
2 Electrolytes K↓ ECG changes-arrhythmias
Ileus
weakness
Ca↓ (ionized) NM irritability
CVS depression
3 Myocardium Contractile ↓ Contractility
element
4 Respiratory Vasculature Cerebral Ischemia
↓ CO2 Systemic SVR↑
Coronary Spasm
Placenta Perfusion ↓
Pulmonary PVR↓

37. The cause Cl- Nacl infusion (correction of
sensitive ECF& Na depletion)
Cl- Aldosterone
resistant antagonists(spironolactone)
K infusion (correction of K
depletion)
Temporary ph>7.6 → vit C, Hcl, NH4cl
Acetazolamide to ↑renal
bicarbonate excretion
Refractory Hemodialysis

38. Hypoxemia is areal danger
1. Hypoventilation (respiratory response to metabolic alkalosis)
2. Pulmonary microatelectasis (consequent to hypoventilation)
3. Increased ventilation-perfusion mismatch (as alkalosis inhibits
HPVC)
4. Oxygen unloading may be impaired (shift of the ODC to the left).
 The body’s major compensatory response to impaired tissue
oxygen delivery is to increase COP but this ability is impaired
if hypovolemia and decreased myocardial contractility are
present.
Give oxygen!

39. Step 1. <7.35—acidosis
Look at the pH 7.35-7.45—normal or compensated
acidosis
>7.45—alkalosis
Step 2. PCO2 <35 mm Hg—respiratory alkalosis
Look for respiratory component or compensation for metabolic acidosis
(volatile acid= CO2) (if so, BD* > −5)
PCO2 35-45 mm Hg—normal range
PCO2 >45 mm Hg—respiratory acidosis
(acute if pH <7.35, chronic if pH in
normal range and BE > +5)
Step 3. BD >−5 metabolic acidosis
Look for a metabolic component BE −5 to +5 normal range
(buffer base)
BE >5 alkalosis

40. Put this information together:
1 Acidosis CO2 <35 mm Hg ± BD >−5 acute metabolic acidosis
2 Normal range pH CO2 <35 BD >−5 acute metabolic acidosis
plus compensation
3 Acidosis PCO2 >45 mm Hg normal range BE acute respiratory acidosis
4 Normal range pH PCO2 >45 mm Hg BE >+5 prolonged respiratory
acidosis
5 Alkalosis PCO2 >45 mm Hg BE >+5 metabolic alkalosis
6 Alkalosis PCO2 <35 mm Hg BDE normal range acute respiratory alkalosis
7 If acid-base picture doesn’t conform to any of these, a mixed picture is present.