Acid Base Disorders Flashcards
(23 cards)
Define: acid; base; alkali; pH
Acid: any hydrogen-containing substance that is capable of donating a proton( H+ ion) to another substance.
Base: any substance that accepts protons and releases hydroxide ions.
Alkali: a base that is soluble in water
pH: the concentration of H+ ions
Buffer system
Buffer system: a chemical system that maintains a narrow range of pH in living organisms by resisting changes in pH caused by internal and external influences. Consists of weak acid + conjugate base OR weak base + conjugate acid.
The body has buffer systems in place that normally regulate acid base balance. These include:
1. Chemical buffers (seconds):
Phosphate
Bicarbonate
Protein
2. Brainstem respiratory centres(1-3min)
3. Renal mechanisms(hrs-a dy)
Henderson-Hasselbalch equation
The relationship between pH, HCO3- concentration in mM, and dissolved CO2 concentration is expressed mathematically by the Henderson-Hasselbalch equation.
pH = pK + log ( [HCO3-] / [CO2] )
pK is constant: pK H2CO3 = 6.1
pH depends on the ratio between [HCO3-] and [CO2]
The ratio between [HCO3-] and [CO2] in ECF is 20:1
pH = pK + log ( [HCO3-] / [CO2] )
= 6.1 + log 20/1
= 6.1 + 1.3
= 7.4
Respiratory regulation of acid base balance
The respiratory system eliminates CO2 an acid from the blood while replenishing its supply of O2.
Carbon dioxide generated by cellular respiration enters erythrocytes in the circulation and is converted to bicarbonate ions for transport in the plasma.
Healthy individuals expel CO2 from the lungs at the same rate it is formed in the tissues. During carbon dioxide unloading the reaction shifts to the left, and H+ generated from carbonic acid is reincorporated into water. Because of the protein buffer system H+ produced by CO2 transport is not allowed to accumulate and has little or no effect on blood pH.
If pCO2 rises, it activates medullary chemoreceptors (via cerebral acidosis promoted by excessive accumulation of CO2) that respond by increasing respiratory rate and depth.
As ventilation increases, more CO2 is removed from the blood, pushing the reaction to the left and reducing the H+ concentration.
When blood pH rises the respiratory center is depressed.
As respiratory rate drops and respiration becomes shallower, CO2 accumulates pushing the equilibrium to the right and causing the H+ concentration to increase.
Renal regulation of acid base balance
Reabsorption of HCO3- in the proximal tubule
Exctretion of H+ as a titratable acid (H2PO4-)
Excretion of H+ as NH4+
Renal-Respiratory compensation in acidosis
Respiratory Compensation:
Mechanism:
The primary respiratory response to acidosis is to increase ventilation (hyperventilation) to exhale more carbon dioxide (CO2).
Effect:
By removing CO2, the respiratory system lowers the partial pressure of CO2 (Pco2) in the blood, which helps to counteract the acidosis by shifting the carbonic acid equilibrium and raising the blood pH.
Speed:
This compensation is relatively rapid, often occurring within minutes to hours.
Renal Compensation:
Mechanism:
The kidneys play a longer-term role in acid-base balance by adjusting the excretion and reabsorption of bicarbonate and hydrogen ions.
In Acidosis:
In acidosis, the kidneys increase bicarbonate reabsorption (conservation) and hydrogen ion excretion into the urine.
Effect:
By conserving bicarbonate, the kidneys help to buffer excess acid, while eliminating hydrogen ions helps to remove acid from the blood.
Speed:
This compensation is slower, taking several hours to days to become effective, especially in chronic conditions.
Renal-Respiratory compensation in alkalosis
Approach to acid base disorders
Perform an initial clinical evaluation to help determine the most likely underlying cause.
Order initial laboratory studies: ABG and BMP
Determine the primary acid-base disorder
Calculate the expected compensatory(or secondary) response
Perform further diagnostic workup (to determine mechanism and cause)
In metabolic acidosis: anion gap and delta gap
In metabolic alkalosis: urinary chloride and potassium levels
Reference ranges in acid base disorders
pH: 7.35-7.45
pCO2: 35-45 mmHg
HCO3-: 21-27 mEq/L
pO2> 80mmhg
Anion gap: 6-12 (10-12 if K+ is taken into consideration)
outline the acid base disorders and their mechanisms of compensation
- Metabolic acidosis (↓HCO3- → ↓pH)
Increased ventilation (↓PCO2 → ↑pH) - Metabolic alkalosis (↑HCO3- → ↑pH)
Decreased ventilation (↑PCO2 → ↓pH - Respiratory acidosis (↑PCO2 → ↓pH)
↑ reabsorption of HCO3- and
↑ excretion of H+ by the kidneys
(↑ HCO3- → ↑ pH) - Respiratory alkalosis (↓PCO2 → ↑pH)
↓ reabsorption of HCO3- and
↓ excretion of H+ by the kidneys
(↓HCO3- → ↓pH)
Metabolic acidocis
Metabolic acidosis: a reduction in the concentration of HCO3- ions resulting in a pH< 7.35. It can be due to excess H+ ions or loss of HCO3-
Anion gap
Anion gap: the difference between the concentration of measured cations and measured anions.
Anion gap helps in determining if the cause of metabolic acid is due to accummulation of organic acids or due to loss of HCO3- which is often compensated by Cl-.
Delta gap
Delta gap: value measured in patients with a HAGMA in order to determine if a mixed acid-base disorder is present.
causes of high anion gap in acidosis
MUDPILES
causes of normal anion gap in acidosis
FUSEDCARS
Metabolic alkalosis
Definition: an increase in the concentration of HCO3- ions that results in a pH > 7.45. It can be due to hydrogen ion loss or increase in HCO3- ions.
Causes of metabolic alkalosis
Respiratory acidosis
Definition: a pH below 7.35 due to reduction in alveolar ventilation resulting in retension of CO2.
Respiratory acidosis causes
Respiratory alkalosis
Definition: a pH > 7.45 and low pCO2 due to alveolar hyperventilation (increased RR and/or tidal volume)
Respiratory alkalosis causes
Mixed acid base disorder
The simultaneous presence of ≥ 2 primary acid-base disorders (e.g respiratory alkalosis and metabolic acidosis in salicylate intoxication)
Usually manifests with near normal pH in the presence of substancial changes in both HCO3 and pCO2 and lesser-than-expected or greater-than expected compensatory responses.
Different formulas have been formulated to calculate compensatory responses and this will help in determining the presence of mixed acid base disorders:
If the expected compensatory response differs from the lab findings-mixed acid base disorder is present.
If the expected compensatory response aligns with lab findings there is no mixed acid base disorder.
arterial blood sampling procedure
Radial artery puncture with arterial blood gas (ABG) sampling
(1) The wrist is positioned in mild dorsiflexion and the skin is prepped.
(2) The radial artery is located by palpation and the needle is advanced at a 30–45° angle.
(3a) As the needle enters the artery, (3b) blood flashback is seen in the syringe.
(4) Blood is allowed to fill the syringe without aspirating.
(5) The needle is removed and pressure is applied over the puncture site with gauze.
(6) Pressure is maintained for 3–5 minutes.