1

Acid-base imbalance
SM Copotoiu

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 Buffer sustems of the blood
2

Buffer type The buffering capacity of the

integral blood (mEq/l)

Bicarbonate
Plasmatic 35
Red blood cells 18
Total 53
Non-bicarbonate
Hb and HbO2 35
Proteins 7
Organic phosphate 3
Inorganic phosphate 2
Total
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 Primary ABD and compensatory responses 3

Primary disturbance Compensatory response

pCO2 HCO3-
Respiratory scidosis Metabolic alcalosis

pCO2 HCO3-
Respiratory alcalosis Acidoză metabolică

HCO3-  pCO2
Metabolic acidosis Respiratory alcalosis

HCO3-  pCO2
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Metabolic alcalosis Respiratory acidosis
 Compensatory mechanisms for primary AB 4
disturbances
• Compensation
• Secondary physiologic process
• A response to a primary ABD
• Aims at correcting the pH abnormality

• Correction a therapeutic action aimed to oppose the primary

factor culprit for the alteration
• Primary anomaly: H+, HCO3-, PaCO2

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 Compensations 5

Respiratory:
Immediate
ventilation
PaCO2 ventilatory alcalosis inhibiting ventilation PaCO2 to
balance HCO3-

Pulmonary response to a perfusion with bicarbonate : paCO2 (HCO3-

+ H+ CO2 + H2O)

Pumonary response to chronic alcalosis : inhibition of the respiratory

driving PaCO2 by 0,5 mmHg for eachof 1mEq/l HCO3-pl
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 ABD Renal regulation 6

Noncsrbonic acids produced by the body and eliminated by the kidneysac

sulfuric acid, phosphoric acid, HCl, uric acid, -OH butyric, acetoacetic.

The most abundant weak acid produced: acidic phosphate H2PO4-.

½ of the acids produced by metabolism are neutralized by alimenatry bases

½ neutralized by anionic buffering systems
97-98% of the noncarbonic acids bufferred in the extracellular liquid are
buffered by HCO3.
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 Adverse effects of acidosis 7

•  K+
• Central nervous system depression
• CV depression- direct effects on the vasomotor center,
arteriolar muscles, myocardial contractility
•  cardiac arhythmias
•  precapillary tonus
•  postcapillary tonus

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 Adverse effects of alcalosis 8

•  K+
•  Ca2+ tetanic contractions, myocardial acontractility
• CNS excitation
•  Cerebral blood flow
• Coronary vasoconstriction
•  tissular oxygen availability = the Bohr effect (left shift
of the HbO2 disociation curve)
• incidence of cardiac arrhythmias
• Right-left shunt (only respiratory alcalosis)
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 Differential diagnosis
Disturbance pHa PaCO2 HCO3- 24mEq/l
9

7,36-7,44 36-44mmHg
Resp acidosis   
–acute
–chronic   
Resp alcalosis
–acute
  
–chronic   
Metabolic acidosis
–Acute
,   
–chronic   
Metabolic alcalosis
–Acute
  
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–chronic   
 10

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 ABG interpretation
12

1. pH 7,37-7,42
2. Establish the blood source
• Venous SO2
• Arterial SO2 vs SpO2
3. paCO2
4. paO2
5. HCO3-

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Where are we now? 13

Metabolic acidosis
• pH
• HCO3-
• paO2 Cause?
• Nonventilated assist ventilation
• Ventilated – the operator sets the parameters and controls
ventilation

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 AG 12-18mMol/l 14

• THE LAW OF ELECTRONEUTRALITY

• UNMEASURED ANIONS : proteins,

phosphates,
Lactate, organic anions (toxic?)
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Metabolic acidosis and the AG 17

Normal AG
• Loss of HCO3-
• Substitution by Cl-

AG 
• Endogenous overproduction : lactate, diabetes
• Exogenous : salycilates

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Metabolic acidosis treatment 18

• Correct the cause

• NaHCO3 only if lifetheatening acidosis
• NaHCO2 1,4% izotonic; 8,4% hypertonic

Treatment consequence
• Respiratory acidosis ( CO2production) more obvious to patients
with tissue hypoxia: septic shock, cardiac arrest

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Metabolic alcalosis 19

• pH
• NaHCO3
• paCO2

2 types
• Resitent to Cl-
• Responsive to Cl-

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Metabolic alcalosis resistent to Cl- 20

• Urinary Cl- >> 20mM/l

• Stimulation of NaHCO3 loss: acetazolamide
• Reduction/substitution of acid loss of: H+ pomp
inhibitors
• Frequent cause - hypokaliemia

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Metabolic alcalosis responsive to Cl- 21

• Urinary Cl <<20mM/l

• NaCl 0,9% infusion drives to NaHCO3 loss due to

increased Cl- availability.

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Strong ions 22

• Completely dissociated in solution

• Unmeasurable : Na, K, Ca, Mg
• Strong acids and bases dissociate completely
• SID = strong anion difference = cations (+) – anions(-)
• = AG

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ABG algorithm
When do we have to perform BGA? 23

1. Oxygenation
Acute respiratory decompensation requiring intervention SpO2

2.Ventilation
Acute decompensation or alterations of the minute volume ABG!
If interventional, follow the effects with ABGs!
3. AB Status
New AB imbalance or worsening: ABG. : ABG & following the effects!

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ABG Rules 24

• Not a routine!
• Do not retrieve blood for a spontaneous respiration!
• Monitor SpO2 after altering FiO2 or PEEP
• Do not use venous blood to get informations on the arterial
blood !
• Suppress arterial lines as soon as clinically possible.

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RI (Respiratory index) = D(A-a)pO2/paO2

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Pancreatită ac necroticohemoragică

AVC ischemic trombolizat

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 Cerebral death
Insipidus diabetes
28

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White-coat crime 31

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White-coat crime 32

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