11. • By altering TV or f in mechanically
ventilated patients.
• ↑Minute Ventilation will ↓ PaCO2.
• Recommended guidelines are to
–Target the TV 5-8 mL/kg of (IBW)
–Pplateau <30 cm H2O.
12. • What are the factors that affect PaCO2
during mechanical ventilation?
13. • VCO2, carbon dioxide
production;
• VA, alveolarventilation;
VE , minute ventilation;
VD , dead space
ventilation;
• VT, tidal volume;
• TI, inspiratory time;
TE, expiratory time;
• f, respiratory rate.
22. • How to correct Respiratory alkalosis in
mechanically ventilated patient?
23. • We have to treat Hyperventilation
• For VCV, ↓ minute ventilation by ↓ f, and
then ↓ VT if necessary .
• for PCV, decrease f first and then decrease
inspiratory pressure, if necessary.
25. • primary ↓ in HCO3 (< 22 mEq/L) and pH
<7.35 .
26. • What are the pathophysiology of
Metabolic acidosis?
27. Pathophysiology
• HCO3 loss: Renal or GIT
• Decreased renal acid excretion
• Increased production of non-volatile acids
a. Ketoacids
b. Lactate
c. Poisons
d. Exogenous acids
28. • What are the causes of high AG
metabolic acidosis?
29. Causes of High AG Metabolic Acidosis
• Starvation
• Ketoacidosis: Diabetic, Alcoholic
• Lactic Acidosis
• Toxicity: Methanol, Ethylene Glycol,
Propylene Glycol, Paraldehyde, Salicylates.
• Renal Failure
30. • What are the causes of Non AG
metabolic acidosis?
32. • What are the menifestation of
metabolic acidosis?
33. Manifestations of Metabolic Acidosis
CARDIOVASCULAR:-
• Impaired cardiac contractility,
• ↑ pulmonary vascular resistance,
• ↓ in CO, BP & hepatic and renal Blood flow,
Sensitization to reentrant arrhythmias & reduced
threshold of VF,
• Attenuation of cardiovascular responsiveness to
catecholamines
34. RESPIRATORY:-
• Hyperventilation
• strength of respiratory muscles & muscle
fatigue
• Dyspnea
CEREBRAL:-
• Inhibition of metabolism
• Mental status changes (somnolence & coma)
35. METABOLIC:
• Increased metabolic demands
• Insulin resistance
• Inhibition of anaerobic glycolysis
• Reduction in ATP synthesis
• Hyperkalemia(secondary to cellular shifts)
• Increased protein degradation
36. • What are the management of Metabolic
acidosis?
37. General measures:-
• Correct Any respiratory component of the
acidemia.
• PaCO2 to be maintained (≈30) to partially
return pH to normal.
• If pH < 7.20*, NaHCO3 (usually a 7.5%
solution), may be necessary.
38. The amount of NaHCO3 given :
• empirically as a fixed dose (1 mEq/kg)
or
• derived from the base excess and the calculated
bicarbonate space
NaHCO3 = Base Deficit × 30% × body weight in
Kg
• Only 50% of the calculated dose is given, after
which another ABG is measured”
39. • Serial ABG are mandatory to avoid
complications(e.g, overshoot alkalosis and
sodium overload) and to guide further
therapy.
• pH>7.25 is sufficient to overcome the adverse
physiological effects of the acidemia.
• Profound or refractory acidemia may require
acute hemodialysis
40. • NaHCO3 in treating cardiac arrest and low
flow states is not recommended - Paradoxical
intracellular acidosis - particularly when CO2
elimination is impaired
• Alternate buffers that do not produce CO2 ,
such as Carbicarb or tromethamine (THAM) .
41. Specific therapy of Metabolic acidosis
• DKA: Replacement of the existing fluid deficit
(as a result of a hyperglycemic osmotic
diuresis) as well as insulin, potassium,
phosphate, and magnesium.
• Lactic Acidosis:- restoring adequate
oxygenation and tissue perfusion.
• Salicylate toxicity:- Alkalinization of the urine
with NaHCO3 to a pH >7.0 increases its
elimination
48. Miscellaneous
• Massive blood transfusion
• Acetate-containing colloid solutions
• Alkaline administration with renal insufficiency
• Alkali therapy
• Combined antacid and cation-exchange resin
therapy
• Hypercalcemia
Milk-alkali syndrome
Bone metastases
• Sodium penicillins
• Glucose feeding after starvation
49. • What are the menifestation of
metabolic alkalosis?
50. Manifestations of Metabolic Alkalosis
•Cardiovascular
Arteriolar constriction
Reduction in Coronary BF/ Anginal threshold
Predisposition to refractory SV & V arrhythmias
(especially if pH > 7.6)
•Respiratory - Hypoventilation (Compensatory)
Hypercapnia / Hypoxemia
51. • Metabolic
Stimulation of anaerobic glycolysis & organic
acid production
Reduction plasma ionized Calcium conc
Hypokalemia (secondary to cellular shifts)
Hypomagnesemia & Hypophosphatemia
• Cerebral
Reduction in Cerebral BF mental status
changes (stupor, lethargy & delirium)
N-M irritability (related to low ionized plasma Ca)
Tetany , Hyperreflexia , Seizures
52. • What are the management of
metabolic alkalosis?
53. • Correction of metabolic alkalosis is never
complete until the underlying disorder is treated.
• On controlled ventilation, any respiratory
component causing alkalemia should be
corrected by ↓ MV to normalize PaCO2 .
• TOC for Cl-sensitive metabolic alkalosis -
administration of iv saline (NaCl) and potassium
(KCl).
• H2 -blocker therapy is useful when excessive loss
of gastric fluid is a factor.
54. • Acetazolamide may also be useful in edematous
patients.
• Alkalosis associated with primary ↑ in
mineralocorticoid activity readily responds to
aldosterone antagonists (spironolactone).
• When pH > 7.60, treatment with:
iv HCl(0.1 mol/L) , NH4Cl(0.1 mol/L) , arginine
hydrochloride,
Or
hemodialysis.
56. First: Initial clinical assessment based on clinical
details
• From history, examination and investigations make a clinical
decision as to what is the most likely acid-base disorder
• Be aware that in some situations the history may be
inadequate, misleading or the range of possible diagnosis is
large
• Mixed disorders are always very difficult
Structured approach to diagnosis
57. Second: Acid – Base Diagnosis
Perform a systematic evaluation of the blood gas and
other results and make an acid-base diagnosis
Finally: Clinical Diagnosis
Synthesize the information to make an overall clinical
diagnosis
59. When you read an ABG which
parameter you read first?
• Oxygenation
60. • Look at the PaO2, SaO2 and FiO2 of patient
• Predicted minimum
–PaO2 = FiO2 x 5,
–COPD = FiO2 X 3
• Normal PaO2/FiO2 ratio:105mmHg/0.21=500,
• < 300 = ARDS(ALI included in it;Berlin criteria)
Adequacy of Oxygen
61. • First look at the pH – any deviation from normal
• ed pH < 7.35, Acidemia, then Uncompensated disorder
• ed pH > 7.45, Alkalemia, then Uncompensated disorder
• pH (7.35 – 7.45) – Normal, then there must be either no
disorder or a compensated disorder
Classify pH as normal, acidemia and alkalemia
62. Grading ACIDAEMIA ALKALAEMIA
Mild 7.30-7.34 7.46-7.50
Moderate 7.20-7.29 7.51-7.54
Severe <7.2 >7.55
Incompatible with
life
<6.8 >7.8
63. • Respiratory – if pH and PaCO2 move in Opposite
direction in relation to normal values. (OR)
• Metabolic – if pH and PaCO2 move in Same
direction. (SM)
• Primary Respiratory acidosis – ↓ pH & ↑ PaCO2
• Primary Respiratory alkalosis - ↑ pH & ↓ PaCO2
• Primary Metabolic acidosis – ↓ pH and ↓ PaCO2
• Primary Metabolic alkalosis –↑ pH and ↑ PaCO2
Analyze: disorder is Respiratory or
Metabolic
64. • With time body tries to bring pH towards normal.
• Lungs and kidneys are primary buffer response systems.
• Primary Respiratory acidosis – ↓ pH & ↑ PaCO2 ↑
HCO3
• Primary Respiratory alkalosis - ↑ pH & ↓ PaCO2 ↓
HCO3
• Primary Metabolic acidosis – ↓ pH and ↓ PaCO2 ↓
HCO3
• Primary Metabolic alkalosis –↑ pH and ↑ PaCO2 ↑
HCO3
• HCO3 & PaCO2 will always move towards same direction
Evaluate compensation and correlate pH,
PCO2, HCO3
65. • If diagnosed Primary respiratory acidosis/alkalosis –
• Is there appropriate renal compensation – Acute or Chronic
• Acute Resp Acidosis: 10 mm Hg ↑ PaCO2 above 40 = ↑HCO3 by 1
mmol/L
• Acute Resp Alkalosis: 10 mm Hg ↓ PaCO2 below 40 = ↓ HCO3 by 2
mmol/L
• Chronic Resp Acidosis: 10 mm Hg ↑ PaCO2 above 40 = ↑HCO3 by 3
mmol/L
• Chronic Resp Alkalosis: 10 mm Hg ↓ PaCO2 below 40 = ↓HCO3 by
4 mmol/L OR
• Rise of PaCO2 by 20 mmHg = fall of pH by 0.1
• Fall of PaCO2 by 10 mmHg = rise of pH by 0.1
Calculate actual compensation seen and match
with expected
66. • If diagnosed Primary Metabolic acidosis/alkalosis
• Look for the expected change in PaCO2 –
• If PaCO2 is Higher, or Lower than that expected –
then
• With a primary metabolic disorder a superimposed
primary respiratory disorder is present
Expected change in PaCO2
• Metabolic acidosis - Expected Compensation in
PaCO2 = 1.5 x HCO3+ 8 (±2)
• Metabolic alkalosis - Expected compensation in
PaCO2 = 0.7 × HCO3+ 21 (±2)
Calculate actual compensation seen and match with expected
67. • If pH is normal – And PaCO2 – is High or Low
• Normal pH with High PaCO2 indicates a Mixed
Respiratory Acidosis & Metabolic Alkalosis
• Normal pH with Low PaCO2 indicates a Mixed
Respiratory Alkalosis & Metabolic Acidosis
• Therefore, if the PaCO2 is 70 mm Hg and the pH is 7.40,
the compensatory change in pH is more than expected
indicating that there is metabolic alkalosis in addition to
the compensation.
Find out if the disorder is mixed
68. • If Metabolic Acidosis is diagnosed – Check Anion Gap
• To assess the associated metabolic disorder and also
explain the cause of metabolic acidosis
• Δ AG/ Δ HCO3 < 0.1 - Combined high AG acidosis + non
AG acidosis
• Δ AG/ Δ HCO3 = 1 - Anion Gap acidosis, DKA due to
urinary ketone loss
• Δ AG/ Δ HCO3 >1.5 Metabolic acidosis and alkalosis
Unmask hidden disorders
69. RESPIRATORY ACIDOSIS:
• Primary change is ↑ in PaCO2 leading to a ↓ in pH
• For each 10 mm Hg ↑ in PaCO2, pH ↓ by 0.05
RESPIRATORY ALKALOSIS:
• Primary change is ↓ in PaCO2 leading to ↑ in pH
• For each 10 mm Hg ↓ in PaCO2 pH ↑ by 0.1
Points to remember
70. METABOLIC ACIDOSIS:
• Primary change is ↓ in HCO3 or ↑ H+ leading to ↓ pH
• For ↓ in HCO3 of 7 – 7.5 mEq/ L, pH ↓ by 0.1
METABOLIC ALKALOSIS:
• Primary change is ↑ HCO3 or ↓ H+ leading to ↑ pH
• For ↑ in HCO3 of 7-7.5 mEq/L - pH ↑ by 0.1
Points to remember