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To optimize

enzyme activity
hemoglobin saturation with oxygen
myocardial contractility
rates of chemical reaction within cells

Regulation of [H+]
Buffer systems
Ventilatory responses
Renal responses

Regulation of [H+]
Buffer systems
Bicarbonate buffering system
Hemoglobin buffering system
Protein buffering system
Phosphate buffering system
Rapid (1 to 3 minutes)
Incomplete

Regulation of [H+]
Bicarbonate buffering system

CO2 + H2O

Carbonic
anhydrase

H2CO3

H+ + HCO3-

most important
readily available
representing over 50% of the total buffering capacity

Regulation of [H+]
Ventilatory responses
within 1 to 5 minutes
or in alveolar ventilation
to produce appropriate changes in CO2 conc.
incomplete

Regulation of [H+]
Renal responses
Regulate H+ by acidification or alkalinization of the urine
Acidosis:
H+ actively secreted into renal tubules
Na reabsorbed and combine with HCO3Slow to act (12 to 48 hours)
But continue, until pH return to almost 7.4

The compensatory changes tend to return the pH toward a normal


value despite the continued presence of the primary acid-base
abnormality
compensatory responses frequently result in mixed acid-based
disturbances
differentiation between primary respiratory and metabolic causes
of acid-based disturbances is necessary to ensure proper treatment

Suffix
-osis
indicates a primary process which, if unopposed, will
produce a corresponding pH changes
-emia
refers to the pH
more than one primary process may be present

Metabolic Alkalosis
Alkalemia (> 7.45)
Hyperbicarbonatemia (>27 mEq/L)

Metabolic Alkalosis
Pathophysiology
Generating factors
Nasogastric suction
Diuretic administration
Maintenance factors
dependent on continued stimulus for the reabsorption of
[HCO3-]from the distal renal tubules
Renal hypoperfusion/hypovolemia
hypokalemia

Metabolic Alkalosis
Physiologic effects
Hypokalemia
Hypocalcemia
Ventricular arrhythmias
Potentiate the toxicity of digoxin
Compensatory hypoventilation
PaCO2 PaO2

Metabolic Alkalosis
Compensatory responses
increased reabsorption of H+ by renal tubule cells
decreased secretion of H+ by renal tubule cells
the efficiency of renal compensation mechanism
is dependent on the presence of cations and chloride
alveolar hypoventilation
initially stimulate the medullary chemoreceptors
offset the compensatory effect of alveolar hypoventilation

with time, CSF pH is normalized by active transport of HCO3


volume of ventilation decreased despite persistance PCO

Metabolic Alkalosis
Treatment
Etiologic therapy
expansion of intravascular volume to increase renal perfusion
0.9 % saline might be preferable to LR
lactate provide additional substrate for generation
of [HCO3-]
administration of potassium to reverse hypokalemia
allows the kidney to excrete excess HCO3 Nonetiologic therapy
provision of hydrogen ions
ammonium chloride, arginine hydrochloride or
0.1 N hydrochloride acid (up to 0.2 mEq/kg/h)
administration of acetazolamide renal HCO3- wasting

Metabolic Acidosis
Occurs when accumulation of any acid in the body other than CO2
Acidemic pH (< 7.35)
Hypobicarbonatemia (< 21 mEq/L)
as a consequence of
buffering by [HCO3-] of endogenous or exogenous
acid loads abnormal external loss of [HCO3-]

Metabolic Acidosis

Causes
Decreased renal tubule elimination of H+
renal failure
cirrhosis of the liver ( conversion of lactate to glucose
Increased metabolic production of H+
anaerobic glycolysis
DKA
metabolism of Amino acids (in hyperalimentation)
idiopathic
excessive loss of gastrointestinal fluids
diarrhea, iliostomy
renal tubular acidosis

Metabolic Acidosis
2 types:
With anion gap
(Na+ - { Cl- + [HCO3-] } )
13 mEq/L
excess production of lactic acids or ketoacids
increased retention of waste product (sulfate/phosphate)
ingestion of toxic quantities of substances (aspirin)
Without anion gap (n: 9 13 mEq/L)
diarrhea, biliary drainage, renal tubular acidosis
[HCO3-] is loss externally Cl Hyperchloremic non gap acidosis

Metabolic Acidosis
Compensatory responses
alveolar ventilation
due to stimulation of the carotid bodies by [H+]
rapid as reflected by a rapid in CSF PCO2
CSF pH
inhibition of the activity of the medullary
chemoreceptors
with time normalizes CSF pH
due to active transport of HCO3- into the CSF
inhibition of ventilation provided by medullary
chemoreceptors is removed

Metabolic Acidosis
Compensatory responses
renal tubule secretion of [H+]
the use of buffers present in the bone

Metabolic Acidosis
Physiologic effects
myocardial contractility
pulmonary vascular resistance
response of cardiovascular system to endogenous/exogenous
catecholamines may be impaired

Metabolic Acidosis
Assessment
focus on:
Hypovolemia
Hypoperfusion
Abnormal renal function
Pulmonary pathology interfering with gas exchange

Metabolic Acidosis
Treatment
correction of primary pathophysiologic process
removal of the cause of the accumulation of nonvolatile
acids in the circulation
if severe: (pH < 7.25)
NaHCO3- (mEq) : Wt (Kg) X 0.3 X (24 actual [HCO3-])
2
1 mEq/kg NaHCO3- 180 ml CO2
necessitates a doubling of alveolar ventilation
then repeat ABG after 5 mins

Metabolic Acidosis
Hyperchloremic acidosis (dilitional acidosis)
when plasma HCO3- decreased by extracellular expansion

utilizing large volumes of crystalloid solutions (NS at 30 ml/kg/h


LRS

Rules of thumb for respiratory compensation for


metabolic alkalosis and metabolic acidosis
Metabolic Alkalosis
PaCO2 increases approximately 0.5 0.6 mmHg for each
1.0 mEq/L increase in [HCO3-]
The last two digits of the pH should equal [HCO3-] + .15
Metabolic Acidosis
PaCO2 = [HCO3-] x 1.5 + 8
The last two digits of the pH should equal [HCO3-] + .15

Rules of thumb for [HCO3-] and pH changes in response


to acute and chronic changes in PaCO 2
Decreased PaCO2
pH increases 0.10 for every decrease in PaCO2 of 10 mmHg
[HCO3-] decreases 2 mEq/L for every decrease in PaCO2
of 10 mmHg
pH will nearly normalize if hypocarbia is sustained
[HCO3-] decreases 5 to 6 mEq/L for every chronic decrease in
PaCO2 of 10 mmHg

Rules of thumb for [HCO3-] and pH changes in response


to acute and chronic changes in PaCO 2
Increased PaCO2
pH decreases 0.05 for every increase in PaCO2 of 10 mmHg
[HCO3-] increases 1.0 mEq/L for every increase in PaCO2
of 10 mmHg
pH will return toward normal if hypercarbia is sustained
[HCO3-] increases 4 mEq/L for every chronic increase in
PaCO2 of 10 mmHg

Respiratory Alkalosis
Alkalemic pH (> 7.45)
Hypocarbia (PaCO2 35 mmHg
when minute ventilation exceeds the level required to
excrete the metabolic production of CO2
pain
anxiety
CNS disease
early sign of sepsis

Respiratory Alkalosis
stimulus to breath
mediated by carotid bodies
medullary chemoreceptors

In CSF
active transport of [HCO3-] out of CSF
restore CSF pH to normal
activity of medullary chemoreceptors become normal
ventilation despite persistence PaCO2
mech. ventilation during anesthesia can result in the

Respiratory Alkalosis
Causes
Hyperventilation
iatrogenic (mechanical or self-induced)
pain
anxiety
decreased barometric pressure
CNS injury
arterial hypoxemia
pulmonary vascular disease
cirrhosis of the liver
sepsis
hyperthermia

Decreased metabolic production of CO2


hypothermia
skeletal muscle paralysis

Respiratory Alkalosis
Compensatory responses
reabsorption HCO3- from the renal tubules
urinary excretion of HCO3- in association with Na+, K+
stimulate the activity of phosphofructokinase
glycolysis generation of lactic acid

Respiratory Alkalosis
Physiologic effects
Hypokalemia
Hypocalcemia
tetany due to greater affinity of plasma protein to Ca in alkaline

Cardiac dysrhythmias
Bronchoconstriction
Hypotension
Potentiate the toxicity of digoxin
Alter CBF (8-24 hours)

Respiratory Alkalosis
Treatment
correcting the underlying disorder responsible for
elimination of CO2 by the lung
RR
TV
dead space rebreathing exhaled gas
metabolic production of CO2

Respiratory Acidosis
Acidemia (pH < 7.35)
Hypercarbia (PaCO2 45 mmHg)
Minute ventilation is insufficient to eliminate CO2 production

Respiratory Acidosis

In CSF
CO2 rapidly crosses BBB
stimulation of ventilation via medullary chemoreceptor
eliminated with time pH restored to normal
by the active transport of [HCO3-] into CSF

Stimulation of ventilation via carotid body


decreased by volatile anesthetics

Respiratory Acidosis
VA = VE VD
Decreases in minute ventilation
Central ventilatory depression
drugs or CNS injury
Airway obstruction
Neuromuscular dysfunction
Increase dead space
COPD
pulmonary embolism
acute form of respiratory failure
Increase CO2 production
sepsis
fever
high glucose parenteral feeding

Respiratory Acidosis
Compensatory responses
renal secretion of [H+]
plasma [HCO3-]

Respiratory Acidosis
Treatment
pH < 7.1
need for tracheal intubation and ventilation support
chronic respiratory acidosis rarely managed with mechanical
ventilation
total body CO2 washout occurs more rapidly than
the kidney can produce a corresponding decrease in
plasma [HCO3-]
metabolic alkalosis with hypokalemia
administration of KCl
avoidance of hyperventilation

Acid-base interpretation
Data :
ABG
Electrolytes
Clinical presentation

Adverse effects of Respiratory or Metabolic acidosis


Hyperkalemia
CNS depression
Cardiovascular depression
(offset by increased secretion of catecholamines)
cardiac dysrhythmias
Hypovolemia ( due to decreased precapillary and increased
postcapillary sphinchter tone)

Adverse effects of Respiratory or Metabolic alkalosis


Hypokalemia
Hypocalcemia myocardial contractility and tetany
CNS excitation
Decreased CBF
Coronary artery vasoconstriction
Leftward shift of oxyhemoglobin dissociation curve (Bohn effect)
cardiac dysrhythmias
Increased airway resistance

Sequential approach to acid-base interpretation


Is the pH life-threatening, requiring immediate intervention ?
Is the pH acidemic or alkalemic ?
Could the entire ABG picture represent only an acute increase or
decrease in PaCO2 ?
If the answer is No, is there evidence of chronic respiratory
disturbance or of an acute metabolic disturbance ?
Are appropriate compensatory changes present ?
Is an anion gap present ?
Do the clinical data fit the acid-base picture ?

Example # 1
65 year-old female has undergone a 12-hour bilateral RND and
flap reconstruction. To replace an estimated blood loss of 2000 ml,
She has received 3 units of PRBC and 9 L of NS. Her BP and HR
Have remained stable on 0.5% to 1% isoflurane in 70 : 30 N2O.
UO is 60 ml/hr. ABG and electrolytes are:
ABG:
pH
7.38
PaCO2
32 mmHg
[HCO3-]
17 mEq/L
Electrolytes:
Na+
140 mEq/L
Cl112 mEq/L
CO2
18 mEq/L
Anion gap 10 mEq/L

Example # 2
A 50 year-old male after 5 days of nasogastric suction,
has the ABG and electrolytes :
ABG:

Electrolytes:

pH
PaCO2
[HCO3-]
Na+
ClCO2

7.50
46 mmHg
35 mEq/L
135 mEq/L
87 mEq/L
36 mEq/L

Example # 3
A 27 year-old male, 1 day after major blunt thoracic and abdominal
Trauma and emergency splenectomy, has been admitted to the ICU
To monitor the effect of a pulmonary contusion. An ABG obtained
Because of deteriorating respiratory status
ABG:
pH
7.21
PaO2 40 mmHg

Electrolytes:

PaCO2
[HCO3-]
Na+
ClCO2
+

49 mmHg
19 mEq/L
144 mEq/L
105 mEq/L
20 mEq/L

Example # 4
A 55 year-old male, alcoholic, disoriented and complaining of
recurrent vomiting and hematemesis, is scheduled for
an emergency laparotomy.
ABG and electrolytes are:
ABG:

Electrolytes:

pH
PaCO2
[HCO3-]
Na+
ClCO2
K+

7.45
34 mmHg
23 mEq/L
135 mEq/L
85 mEq/L
24 mEq/L
4.0 mEq/L