2. Acid Base Disorders and blood gas analysis Flashcards
What is pH?
The pH is equal to -log10 [H+].
Why is isohydria important?
Essential for cell membranes and enzyme activities. Any change in pH may lead to electrolyte imbalance, and can cause a change in muscle irritability, too.
What is a buffer?
A solution that can maintain a nearly constant pH if it is diluted, or if relatively small amounts of strong acids or bases are added.
- They resist pH changes.
- A buffer solution is typically a mixture of a weak acid (or base) and one of its salts.
Most important buffer systems in
- Blood plasma
- RBC
- Tissue cells
- Carbonic acid-bicarbonate / primary – secondary phosphate / protein-proteinate (albumin)
- Carbonic acid-bicarbonate / primary – secondary phosphate buffer / protein-proteinate (haemoglobin)
- Carbonic acid-bicarbonate / primary – secondary phosphate buffer / protein-proteinate (cytoplasmic proteins)
The most important physicochemical buffer system in all fluid compartments of the body
Carbonic acid – bicarbonate system
The vital buffer system
Formed by the kidneys and the lungs:
- Buffering capacity of lungs: can retain CO2, or excrete it to regulate pH acutely
- Buffering capacity of kidneys: can excrete or retain H+, and regenerate HCO3 - via complex tubular mechanisms (hours to days)
Indication of acid/base evaluation
- Routine test in emergency patients.
- Gives info about acid-base status, and about function of vital buffer systems
Sample and sampling of acid/base evaluation
- Anticoagulated blood
- Arterial samples for resp. function, but either venous or arteria l for metabolic status
- Closed sampling
- Stored max 5-10 min at room temp, 30 min. at 0-4 °C
Method of acid/base evaluation
- Analyzers utilize ionselective electrodes (ISE) to measure pH and CO2.
- Based on the measured parameters the HCO3, ABE and other parameters are calculated
pH of blood
7.35-7.45
pCO2
Partial CO2 pressure, resp. parameter - 40 mmHg
Metabolic acidosis
pH < 7,4
HCO3 < 20mml/l
BE < -3,5mmol/l
Metabolic acidosis - causes
- HCO3-loss
- incr acid intake
- incr acid prod (frequent in anorectic, weak animals)
- in cattle grain overdose (leading to volatile acid overprod)
- incr ketogenesis
- decr acid excretion: renal failure
- ion exchange: hyperkalaemia
- some xenobiotic: ethylene-glycol toxicosis: metabolites (leading to metabolic acidosis)
Metabolic acidosis - effects
- Hyperventilation
- Hypercalcaemia
- Vomiting, depression
- Hyperkalaemia
- In urine: titratable acidity incr
Metabolic acidosis - treatment
- Providing adequate ventilation
- If pH <7.2 infusion therapy involving alkaline fluid
HCO3
Bicarbonate - metabolig parameter - 21-24 mmol/l
Anion gap
- A useful parameter to determine the cause of metabolic acidosis
- The difference bw the commonly measured cations in plasma, and the commonly measured anions.
- Reference range: 8-16 mmol/l.
- To determine whether metabolic acidosis is due to primary HCO3-loss or accumulation of organic acids
Normal anion gap
Hyperchloraemic - Cl- replaces HCO3-
- Diarrhoea: HCO3-loss
- Early kidney failure: H+ retention, decr NH3 excretion
- Renal tubular acidosis: Prox/dist tubular defect
- Acidifying substances: NH4Cl
Increased anion gap
Normochloraemic - Unmeasured anions replaces HCO3-
- Azotaemia/uraemia: Kidney failure – organic acid accumulation
- Lactacidosis: Shock, hypovolaemia, poor tissue perfusion, tissue necrosis
- Ketoacidosis: Diabetic – incr hepatic prod of KB´s
- Toxicosis: Ethylene glycol toxicosis
Metabolic alkalosis - causes
- Incr alkaline intake
- Incr ruminal alkaline prod
- Decr hepatic NH3 catabolism (liver failure)
- Incr acid loss
- Ion exchange: hypokalaemia
Metabolic alkalosis - effects
- Decr. HR
- Hypoventilation
- Muscle weakness – hypokalaemia
- Hypocalcaemia
- Ammonia toxicosis
- Arrhythmia, biphasic P, QT incr, flat T, U wave,
- Paradoxical aciduria
Metabolic alkalosis - treatment
Generally enough to treat the underlying electrolyte imbalance
Respiratory acidosis
pH < 7.4
pCO2 > 40mmHg
pO2 < 40mmHg
Respiratory acidosis - causes
- Upper airway obstruction
- Pleural cavity disease
- Pulmonary disease
- Depression of central control of respiration
- Neuromuscular depression of respiratory muscles
- Muscle weakness
- Cardiopulmonary arrest
Respiratory acidosis - effects
Dyspnoea, cyanosis, suffocation, muscle weakness, tiredness.
Respiratory acidosis - treatment
- Assisting the ventilation
- Treatment of the cause
- Cardiac disease; treatment of pneumonia
- Mildly anxiolytic/sedating drugs
Respiratory alkalosis
pH > 7.4
pCO2 < 40 mmHg
pO2 > 40 mmHg
Respiratory alkalosis - causes
- Increased loss of CO2: hyperventilation
- excitation
- forced ventilation (anaesthesia)
- epileptiform seizures
- fever, hyperthermia
- interstitial lung disease
Respiratory alkalosis - effects
- Hyperoxia, incr. pCO2 : pO2 ratio, may lead to apnoea
- increased elimination of HCO3 by the kidneys
Respiratory alkalosis - treatment
- Anxiolytic or mild sedative drugs
- Incr pCO2 level by closing nose
ABE
Actual base excess (or demand) or residue, metabolic parameter - ±3.5 mmol/l
TCO2
Total CO2 conc. in plasma (liberated by strong acid) - 23-30 mmol/l
SBE
Standard or in vivo Base Excess - metabolic parameter - ±3 mmol/l
Primary / secondary resp. change
Primary: predominant change of pCO2
Secondary: predominant change of HCO3-
Resp. background of pH alteration
pCO2
Metabolic background of pH alteration
HCO3- and ABE
Metabolic alkalosis
pH>7,4, HCO3->28mmol/l, BE>3,5mmol/l
Blood/gas analysis sampling
- Arterial blood for resp., venous blood for gross changes only
- Anticoagulated
- Closed sample
- Within 15 min / on ice
Blood/gas analysis method
Directly measure pCO2 and pO2 w. ion specific electrodes
paCO2
Partial arterial CO2 pressure = 35-45 mmHg
pqO2
Partial arterial O2 pressure = 88-110 mmHg
SAT / SatO2
Oxygen saturation calculated from Hb and pO2
= Venous: 75-80%
= Arterial: 90-100%
FiO2
Fraction of inspired oxygen
= Room air: 0,209
= O2 enriched: 0,21-1,0
= > 0,5: risk of O2 toxicity
Blood/gas interpretation
paO2 and PaCO2
Hypo/hyperoxaemia
<60mmHg / >60mmHg
Hypo/hypercapnia
Decr. CO2 / Incr.CO2
Normal paO2 in room air
80-110mmHg and 97-100% saturation
Cyanosis
<45-50 mmHg of paO2
Hypoventilation
- PaCO2 > 45mmHg
- Hypoxaemia: depends on hypocapnia and FiO2
Hypoventilation - causes
- upper airway obstruction
- pleural effusion
- drugs or disorder affecting central control of respiration
- neuromuscular disease
- overcompensation of metabolic alkalosis
Hypoventilation - effects
dyspnoea, cyanosis
Hypoventilation - treatment
- assisting the ventilation
- diuretic treatment
- mildly anxiolytic/sedating treatment
V/Q - Ventilation perfusion mismatch
- normal ventilation with inadequate perfusion
- inadequate ventilation with normal perfusion
Hyperventilation
- PaCO2 < 35mmHg
- Hyperoxaemia: usually present together with incr SAT
Hyperventilation - causes
- iatrogen: forced ventilation during anaesthesia
- seizures, epilepsy
- excitation
- compensation of severe metabolic acidosis