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Acid base
Daily filtered load of bicarbonate is 4500 mEq
Proximal tubular absorption of bicarbonate is increased by
ECF volume contraction
increase in Pco2
hypokalemia
Acid anion is filtered in glomerulus as sodium salt
Bicarbonate equivalent to H+ secretion is generated and absorbed in distal nephron
Normal pH is 7.38-7.42
pH values compatible with life 6.8-7.8
Acid production
Endogenous production of acid
combustion of glucose and fatty acids
carbon dioxide (volatile acid) and water
Handled by ventilation
Cellular metabolism
non volatile acids
Blood brain barrier
Freely permeable to co2
responses occur instantaneously
lag in equilibrating with bicarbonate
early stages of metabolic acidosis 2-3 hour lag in respiratory response
hyperventilation may persist even after correction of metabolic acidosis
Single acid base disturbance: the change in concentration of one anion is balanced by a reciprocal change in one other anion.
Mixed acid base disturbance: the anion patterns are more complex
Normal Values
pH = 7.38 - 7.42
[H+] = 40 nM/L for a pH of 7.4
PaCO2 = 40 mm Hg
[HCO3] = 24 meq/L
Acid base definitions
Acid base disorder is considered present when there is abnormality in HCO3 or PaCO2 or pH.
Acidosis and alkalosis refer to in-vivo derangement's and not to any change in pH.
Acidemia (pH < 7.38) and Alkalemia (pH >7.42) refer to derangement's of blood pH.
Kidney and Respiratory system play a key roles in maintaining the acid base status.
Metabolic acidosis | loss of [HCO3] 0r addition of [H+] |
Metabolic alkalosis | loss of [H+] or addition of [HCO3] |
Respiratory acidosis | increase in pCO2 |
Respiratory alkalosis | decrease in pCO2 |
Anion and Cations
Anions |
Cations |
Chloride | Sodium |
Bicarbonate(Total CO2) | Potassium |
Proteins | Calcium |
Organic acids | Magnesium |
Phosphates | |
Sulfates | |
Electrochemical balance means that the total anions are the same as total Cations. For practical purposes anion gap is calculated using only Sodium, Chlorides and Total CO2.((140-(104+24)) = 12.
Compensatory measures
Buffering---occurs immediately
Respiratory regulation of pCO2 is intermediate (12-24 hours)
Renal regulation of [H] and [HCO3] occurs more slowly (several days)
Buffering-
Bicarbonate is in both ICF and ECF and participates in buffering capacity
Extracellular
- almost entirely through bicarbonate whose concentration highest of all buffers
- small contribution from phosphate
Intracellular
Buffer systems
- Hemoglobin can directly buffer protons
- H+ entry into RBC matched by exit of Na and K+
- Hemoglobin can directly buffer dissolved
- intracellular conversion of
Bicarbonate buffer system
Calculated bicarbonate:
calculated using the H-H equation
From arterial blood
Total CO2:
measured from venous blood
includes bicarbonate and dissolved carbon dioxide
runs slightly higher than calculated value from nomogram
Primary changes in bicarbonate leads to metabolic acid base disorder.
Renal (metabolic) compensatory effort: Renal regulation of [H+] and [HCO3]
Major functions
Excretion of Acid
Excretion of free [H]
Excretion of acid stimulated by
Excretion of acid inhibited by
Bicarbonate change for PaCO2 changes
Hypoventilation:
- Expected bicarbonate elevation for chronic CO2 retention (Renal compensation) is
- 0.35 x (current PaCO2-normal PaCO2)
- 0.35 x( 60-40)=0.35x20=7 meq/l
- Expected bicarbonate decrease for acute CO2 retention (Buffering) is
Hyperventilation:
- The expected fall in bicarb for acute decrease in PaCO2 (Buffering) is 0.2 x (normal PaCO2-observed PaCO2)
- The expected fall in bicarb for chronic decrease in PaCO2 (Renal compensation) is : 0.5 x (normal PaCO2-observed (PaCO2)
Compensation is almost complete
Respiratory compensation for Metabolic acid base disturbance
Ventilation and pCO2 relationship
Interrelationship between pH and pCO2
pH | pCO2 | |
7.10 | 79 | 70 |
7.20 | 63 | 60 |
7.3 | 50 | 50 |
7.5 | 32 | 30 |
This formula is usable because in the range of pH values we usually deal with, there is nearly linear relationship between pH and pCO2.
We can expect an almost leniar relationship between pH and acute CO2 changes
Acidosis increases respiratory drive, alveolar ventilation and gets rid of Carbonic acid.
Respiratory system can never completely compensate for a metabolic defect.
Respiratory compensation attempts to maintain pH in a reasonable range.
Compensation is never complete. If the pH is normal there is probably a superimposed second acid base disturbance. Estimation of expected PaCO2 for a given acidic pH also enables us to determine whether respiratory compensation is appropriate.
Anion gap (AG)
- Sum of Cations minus anions
- (Na+K)-(CL+HCO3)
- It is ususually calculated as : anion gap = Na- (CL+HCO3)
- Use the measured total CO2 from venous blood as HCO3
- anion gap is an artifact because some anions are not measured
- gap is mainly due to unmeasured proteins, phosphates and sulfates
- Normal anion gap is 10-12 meq/L (Varies from Lab to Lab)
- increase in anion gap indicates metabolic acidosis
Etiology for acid base disorders
Metabolic acidosis
Normal anion gap
abnormally high bicarbonate loss
Kidney fails to reabsorb
renal tubular acidosis
Kidney fails to regenerate
Diuretics
extra renal loss of bicarbonate
Diarrhea
ileal drainage
acidifying salts have been added
hyperalimentation
ammonium chloride
Increased anion gap
Usually from addition of acid
reduced excretion of inorganic acids
renal failure
retention of sulphates and phosphates
impaired net acid excretion (ATN)
impaired ammonia excretion (Chronic renal failure)
accumulation of organic acids
ketoacidosis
diabetic
starvation
alcoholic
lactic acidosis (impaired cellular respiration with anaerobic glycolysis)
shock
septicemia
profound hypoxemia
ingestion
salicilates
methanol
Treatment
Renal failure: Bicarbonate is not required unless plasma bicarb falls below 16 mEq/L
Distal tubular acidosis: 30-60 mEq of bicarbonate daily
GI losses: Bicarb when the pH falls below 7.1
Lactic acidosis: improve tissue perfusion
Diabetic ketoacidosis: Insulin, bicarb only when the pH falls to 7.0-7.1
Metabolic alkalosis
Metabolic alkalosis
loss of hydrogen ions from the body
vomiting
gastric suction
net rate of renal bicarbonate generation is greater than normal
volume contraction
potassium depletion
increased delivery of sodium to distal tubule (Loop diuretics)
minerelocorticoid excess
Rapid correction of ventilation in a patient with chronic CO2 retention (posthypercapnic alkalosis)
In severe alkalosis
Cardiac arrhythmia
Hypoventilation
Respiratory Acidosis
impaired alveolar ventilation
acute respiratory acidosis (normal bicarbonate)
narcotic overdose
respiratory muscle paralysis
acute airway obstruction
Chronic respiratory acidosis (increased bicarbonate)
COPD
kyphoscoliosis
Obesity hypoventilation syndromes
End stage restrictive pulmonary disease
Respiratory Alkalosis
Respiratory alkalosis
Acute hyperventilation (Light headedness, paresthesias, circumvoral numbness, tingling of extremities and tetany.)
pain
acute salicylism
fever
sepsis
CHF
PE
Mechanical ventilation
anxiety (breath with a paper bag)
Chronic hyperventilation
high altitude
hepatic insufficiency
pregnancy
Diffuse interstitial fibrosis
Recquired lab values/information
Suspect Mixed acid base disorders
Approach to interpreting Acid-base disturbance
What is the [HCO3]
What is the PaCO2