ACID-BASE

BALANCE

Dr .Walaa Ameen
DISCUSSION HEADINGS
BASICS
NORMAL PHYSIOLOGY
ABNORMALITIES
METABOLIC ACID BASE DISORDERS
RESPIRATORY ACID BASE DISORDERS
 Acid
Any compound which forms H ions in solution
(proton donors)
eg: Carbonic acid releases H ions
Base
Any compound which combines with H ions
in solution (proton acceptors)
eg:Bicarbonate(HCO3) accepts H+ ions
 Normal pH : 7.35-7.45
Acidosis

Physiological state resulting from abnormally low

plasma pH
Alkalosis
Physiological state resulting from abnormally high
plasma pH
Acidemia: plasma pH < 7.35
Alkalemia: plasma pH > 7.45
Henderson-Hasselbach equation
pH = pKa + log([HCO3-]/.03xpCO2)

pH = 6.1 + log([HCO3-]/.03xpCO2)

Shows that pH is a function of the RATIO

between bicarbonate and pCO2
PCO ventilatory parameter (40 +/- 4).
HCO metabolic parameter (22-26 mmol/L).
 ACIDS
1-VOLATILE ACIDS:
Produced by oxidative metabolism of CHO,Fat,Protein
Average 15000-20000 mmol of CO per day
Excreted through LUNGS as CO gas

2-FIXED ACIDS (1mEq/kg/day)

Acids that do not leave solution ,once produced they
remain in body fluids Until eliminated by KIDNEYS
Eg: Sulfuric acid ,phosphoric acid , Organic acids
Are most important fixed acids in the body
Are generated during catabolism of:
amino acids(cystine,methionine)
Phospholipids(hydrolysis)
nucleic acids
Response to ACID BASE challenge

1. Buffering.
Buffers are always present and
can act fast to reduce amount of
free H+ ions.
2. Compensation.
Buffers
First line of
defence.
The fastest (seconds minutes) but the weakest.
Two most common chemical buffer groups

Bicarbonate
Non bicarbonate (Hb,protein,phosphate)
buffer systems act instantaneously.
Regulate pH by binding or releasing H.
Respiratory Acid-Base Control
Mechanisms
When chemical buffers alone cannot prevent
changes in blood pH.
the respiratory system is the second line of
defence against changes.
Eliminate or Retain CO
Change in pH are RAPID
Occuring within minutes
Renal Acid-Base Control
Mechanisms
The kidneys are the third line of defence against
wide changes in body fluid pH.
movement of bicarbonate
Retention/Excretion of acids
Generating additional buffers
Long term regulator of ACID BASE balance.
May take hours to days for correction.
Renal regulation of acid basebalance

Role of kidneys is preservation of bodys

bicarbonate stores.
Accomplished by:
Reabsorption of 99.9% of filtered bicarbonate
Excretion of acids:
Titratable acidity (mainly phosphate)
Ammonium salts
Renal reabsorption of bicarbonate
Proximal tubule:
70-90%
Loop of Henle:
10-20%
Distal tubule and
collecting ducts:
4-7%
NET ACID EXCRETION
Hydrogen Ions
Are secreted into tubular fluid along
Proximal convoluted tubule (PCT)
Distal convoluted tubule (DCT)
Collecting system
CO2 + H2O H2C03 H + HCO3
AcidBase Balance Disturbances

Interactions among the Carbonic AcidBicarbonate Buffer System and

Compensatory Mechanisms in the Regulation of Plasma pH.
AcidBase Balance Disturbances

decreased

Interactions among the Carbonic AcidBicarbonate Buffer System and

Compensatory Mechanisms in the Regulation of Plasma pH.
Four Basic Types of Imbalance
Metabolic Acidosis
Metabolic Alkalosis
Respiratory Acidosis
Respiratory Alkalosis
 Acid Base Disorders
Disorder pH [H+] Primary Secondary
disturbance response
Metabolic acidosis [HCO3-] pCO2
Metabolic alkalosis [HCO3-] pCO2
Respiratory pCO2 [HCO3-]
acidosis
Respiratory pCO2 [HCO3-]
alkalosis
Metabolic Acidosis
Primary AB disorder
HCO pH
Gain of strong acid
Loss of base(HCO)
 ANION GAP CONCEPT
To know if Metabolic Acidosis due to
Loss of bicarbonate
Accumulation of non-volatile acids
Provides an index of the relative conc of plasma
anions other than chloride,bicarbonate
[serum Na - (serum Cl + serum HCO)]
Unmeasured anions unmeasured cations
12-16 mmol/L.
Mostly represent ALBUMIN
Concept of
Anion Gap
CAUSES OF METABOLIC ACIDOSIS
(High anion gap)(Normochloremic)

LACTIC ACIDOSIS TOXINS

KETOACIDOSIS Ethylene glycol

Diabetic Methanol

Alcoholic Salicylates

Starvation
RENAL FAILURE
(acute and chronic)
 Normal anion gap(Hyperchloremic)
MET.ACIDOSIS causes
Gastrointestinal
bicarbonate loss
A. Diarrhea
B. External pancreatic or
small-bowel drainage
C. Ureterosigmoidostomy,
jejunal loop, ileal loop
D. Drugs
Renal acidosis
1. Proximal RTA (type 2)
2. Distal (classic) RTA (type
1)
B. Hyperkalemia
Drug-induced
hyperkalemia (with
renal insufficiency)
A. Potassium-sparing diuretics
(amiloride, triamterene,
spironolactone)
D. ACE-Is and ARBs
E. Nonsteroidal anti-inflammatory
drugs
Other
A. Acid loads (ammonium chloride,
hyperalimentation)
B. Loss of potential bicarbonate: ketosis
with ketone excretion
C. Expansion acidosis (rapid saline
 Cilnical Features
Symptoms are specific and a result of the underlying pathology
Respiratory effects:
Hyperventilation
CVS:
myocardial contractility
Sympathetic over activity
Resistant to catecholamines
CNS:
Lethargy,disorientation,stupor,muscle twitching,COMA,
CN palsies
Others : hyperkalemia
Metabolic Alkalosis
pH due to HCO or acid
Initiation process :
in serum HCO
Excessive secretion of net daily production of fixed acids
Maintenance:
HCO excretion or HCO reclamation
Chloride depletion
Pottasium depletion
ECF volume depletion
Magnesium depletion
 CAUSES OF METABOLIC ALKALOSIS
I. Exogenous HCO3 loads
A. Acute alkali administration
B. Milk-alkali syndrome
II. Gastrointestinal origin
1. Vomiting
2. Gastric aspiration
3. Congenital chloridorrhea
4. Villous adenoma
III. Renal origin
1. Diuretics
2. Posthypercapnic state
3. Hypercalcemia/hypoparathyroidism
4. Recovery from lactic acidosis or ketoacidosis
5. Nonreabsorbable anions including penicillin, carbenicillin
6. Mg2+ deficiency
7. K+ depletion
Chloride responsive alkalosis
Low urinary chloride concentration(<15 meq/L)
Gastric acid loss
Diuretic therapy
Volume depletion
Renal compensation for hypercapnea
Chloride resistant alkalosis
Elevated urinary chloride (>25 meq/L)
1 mineralocorticoid excess
Severe pottasium depletion
 Compensation for Metabolic Alkalosis

Respiratory compensation: HYPOVENTILATION

PCO=0.6 mm pCO 2 per 1.0 mEq/L HCO3 -
Maximal compensation: PCO 55 60 mmHg
Hypoventilation not always found due to
Hyperventilation
due to pain
due to pulmonary congestion
due to hypoxemia(PO < 50mmHg)
AcidBase Balance Disturbances

Metabolic Alkalosis
 Metabolic Alkalosis
Decreased myocardial contractility
Arrythmias
cerebral blood flow
Confusion
Mental obtundation
Neuromuscular excitability
Hypoventilation
pulmonary micro atelectasis
V/Q mismatch(alkalosis inhibits HPV)
Contraction Alkalosis
Loss of HCO poor, chloride rich ECF
Contraction of ECF volume
Original HCO dissolved in smaller volume
HCO concentration
Eg : Loop diuretics/Thiazides in a generalised
edematous pt.
Respiratory Acidosis
PCO pH
Acute(< 24 hours)
Chronic(>24 hours)
 RESPIRATORY ACIDOSIS - CAUSES
CNS DEPRESSION
DRUGS:Opiates,sedatives,anaesthetics
OBESITY HYPOVENTILATION SYNDROME
STROKE
NEUROMUSCULAR DISORDERS
NEUROLOGIC:MS,POLIO,GBS,TETANUS,BOTULISM,HIGH CORD
LESIONS
END PLATE:MG,OP POISONING,AG TOXICITY
MUSCLE:K,PO,MUSCULAR DYSTROPHY
AIRWAY OBSTRUCTION
COPD,ACUTE ASPIRATION,LARYNGOSPASM
 CONT..
CHEST WALL RESTRICTION
PLEURAL: Effusions, empyema,pneumothorax,fibrothorax
CHEST WALL: Kyphoscoliosis, scleroderma,ankylosing
spondylitis,obesity
SEVERE PULMONARY RESTRICTIVE DISORDERS
PULMONARY FIBROSIS
PARENCHYMAL INFILTRATION: Pneumonia, edema
ABNORMAL BLOOD CO TRANSPORT
DECREASED PERFUSION: HF,cardiac arrest,PE
SEVERE ANEMIA
ACETAZOLAMIDE-CA Inhibition
RED CELL ANION EXCHANGE: Loop diuretics, salicylates, NSAID
 Compensation in Respiratory Acidosis
Acute resp.acidosis:
Mainly due to intracellular buffering(Hb,Pr,PO)

HCO = 1mmol for every 10 mmHg PCO

Minimal increase in HCO

pH change = 0.008 x (40 - PaCO)

Chronic resp.acidosis
Renal compensation (acidification of urine & bicarbonate retention)
comes into action
HCO = 3.5 mmol for every 10 mm Hg PCO
pH change = 0.003 x (40 - PaCO)
Maximal response : 3 - 4 days
 RS:
Stimulation of ventilation ( tachypnea)
dyspnea
CNS:
cerebral blood flow ICT
CO NARCOSIS (Disorientation,confusion,headache,lethargy)
COMA(arterial hypoxemia,ICT,anaesthetic effect of PCO >
100mmHg)
CVS:
tachycardia,bounding pulse
Others:
peripheral vasodilatation(warm,flushed,sweaty)
Post hypercapnic alkalosis
In chronic resp.acidosis
Renal compensation HCO
If the pt intubated and mechanical ventilated
PCO rapidly corrected
Plasma HCO doesnt return to normal
rapidly
HCO remains high
Respiratory Alkalosis
Most common AB abnormality in critically ill
PCO pH
1 process : hyperventilation
Acute: PaCO ,pH-alkalemic
Chronic: PaCO,pH normal / near normal
 CAUSES OF RESPIRATORY ALKALOSIS
A. Central nervous system C. Drugs or hormones
stimulation 1. Pregnancy, progesterone
1. Pain 2. Salicylates
2. Anxiety, psychosis 3. Cardiac failure
3. Fever D. Stimulation of chest
receptors
4. Cerebrovascular accident
1. Hemothorax
5. Meningitis, encephalitis 2. Flail chest
6. Tumor 3. Cardiac failure
7. Trauma 4. Pulmonary embolism
B. Hypoxemia or tissue hypoxia E. Miscellaneous
1. High altitude 1. Septicemia
2. Hepatic failure
2. Septicemia
3. Mechanical ventilation
3. Hypotension
4. Heat exposure
4. Severe anemia 5. Recovery from metabolic
acidosis
 Respiratory alkalosis
CNS:
neuromuscular irritability(tingling,circumoral numbness)
Tetany
ICT(cerebral VC)
CBF(4% CBF per mmHg PCO)
Light headedness,confusion
CVS:
CO& SBP ( SVR,HR)
Arrythmias
myocardial contractility
Others:
Hypokalemia,hypophosphatemia
Free serum calcium
Hyponatremia,hypochloremia
 Acid Base Disorders

Primary disorder Compensatory response

Metabolic acidosis PCO=1.5 X (HCO) + 8 +/ 2[Winters

formula]
Metabolic alkalosis 0.6 mm pCO2 per 1.0 mEq/L HCO3-

Acute respiratory acidosis 1 mEq/L HCO3- per 10 mm pCO2

Chronic respiratory acidosis 3.5 mEq/L HCO3- per 10 mm pCO2

Acute respiratory alkalosis 2 mEq/L HCO3- per 10 mm pCO2

Chronic respiratory alkalosis 5 mEq/L HCO3- per 10 mm pCO2

 MIXED ACID BASE DISORDER
Diagnosed by combination of clinical assessment,
application of expected compensatory responses ,
assessment of the anion gap, and application of
principles of physiology.
Respiratory acidosis and alkalosis never coexist
Metabolic disorders can coexist
Eg: lactic acidosis/DKA with vomiting
Metabolic and respiratory AB disorders can coexist
Eg: salicylate poisoning (met.acidosis + resp.alkalosis)