Lab 2 test= Reference ranges and their expected changes in various conditions! Flashcards
What is the blood pH reference range?
When pH is between 7.35-7.45 the state is compensated
(acidosis: <7.4 and alkalosis: >7.4).
This is the blood pH reference range.
The reference range for anion gap
8-16 mmol/L
Parameters and reference range:
The partial pressure of oxygen (mmHg, kPa)
pO2
- *arterial: 88-118 mmHg
venous: 35-45 mmHg**
Indicates the ability of the lungs to oxygenate blood.
Parameters and reference range:
The partial pressure of carbon dioxide (mmHg, kPa)
- *arterial: 35-45 mmHg
venous: 35-45 mmHg**
Indicates the ability of the alveolar gas exchange to remove
the CO2.
It is directly proportional to the rate of CO2 production,
and inversely proportional to alveolar ventilation.
Parameters and reference range: **SAT (%)** oxygen saturation (%)
- *venous: 70-80%
arterial: 90-100%**
oxygen saturation (%); calculated from Hb and pO2
Indicates the fraction of oxygen-saturated hemoglobin
relative to total hemoglobin in the blood.
Fraction of inspired oxygen
FiO2
Room air: 0.209 (20.9%)
O2 enriched: 0.21-1.0
>0.5 risk of O2 toxicity
It is the assumed % of O2 concentration participating in
gas exchange in the alveoli.
Partial CO2 pressure (mmHg, kPa),
respiratory parameter
pCO2
40 mmHg
(35-45)
**HCO3-** Standard bicarbonate (HCO3-) concentration (mmol/l)
21-24 mmol/l
Bicarbonate concentration of plasma, if the blood is
equilibrated to 40 mmHg pCO2 on 37 °C - it`s value
depends on pCO2 - metabolic parameter
ABE
Actual base excess (or demand) or residue (mmol/l)
±3.5 mmol/l
Titratable acidity or basicity; the amount of acid or base
needed to equilibrate blood to pH: 7.4 (pCO2 is stabilized
at 40 mmHg/l on 37 oC) , metabolic parameter
TCO2
Total CO2 concentration in plasma (mmol/l)
23-30 mmol/l
i.e. CO2 content
of blood liberated by strong acid. TCO2 is 5% higher than
plasma HCO3
-
. TCO2 gives no direct information about
respiratory function. TCO2 may be ignored, when HCO3
-
result is presented
SBE
Standard or in vivo base excess (base demand)
±3 mmol/l
Standard or in vivo base excess (base demand), residue in
the whole extracellular space, metabolic parameter
Normal anion gap
(hyperchloraemic)
Diarrhoea
HCO3- Loss
Normal anion gap
(hyperchloraemic)
Early kidney failure
H+ retention, decreased ammonia excretion
Normal anion gap
(hyperchloraemic)
Renal tubular acidosis
Proximal (Fanconi syndrome) or distal tubular defect
Normal anion gap
(hyperchloraemic)
Acidifying substances
NH4Cl
Increased anion gap
(normochloraemic)
Azotaemia or uraemia
Advanced kidney failure – organic acid accumulation
Increased anion gap
Lactacidosis
Shock, hypovolaemia, poor tissue perfusion, tissue necrosis
Increased anion gap
Ketoacidosis
Diabetic ketoacidosis – increased hepatic production of ketone bodies
Increased anion gap
Toxicosis
Ethylene glycol toxicosis (also alcohol)
Normal anion gap
(hyperchloraemic)
Name cases
Diarrhoea
Early kidney failure
Renal tubular acidosis
Acidifying substances
Increased anion gap
(normochloraemic)
Azotaemia or uraemia
Lactacidosis
Ketoacidosis
Toxicosis
Metabolic alkalaemia/alkalosis
Ranges
pH
HCO3
BE
pH > 7.4
HCO3- > 28 mmol/l
BE > +3.5 mmol/l
Metabolic alkalaemia/alkalosis
effects
Breathing-depression
Muscle weakness – hypokalaemia
hypocalcemia due to the increased Ca2+ binding ability of albumin
Ammonia toxicosis
Arrhythmia,
Paradoxical aciduria
Respiratory acidaemia/acidosis
ranges
pH
pCO2
pO2
pH < 7.4
pCO2 > 40 mmHg
pO2 < 40 mmHg
Respiratory acidaemia/acidosis
effects
Dyspnoea,
cyanosis,
suffocation,
muscle weakness,
tiredness.
Respiratory alkalemia/alkalosis
ranges
pH
pCO2
pO2
pH > 7.4
pCO2 < 40 mmHg
pO2 > 40 mmHg
Respiratory alkalaemia/alkalosis
Effects:
**Hyperoxia, the decreased pCO2 : pO2 ratio may lead to apnoea
increased elimination of HCO3
- by the kidneys**
Hypoxaemia
(<60 mmHg)
hyperoxaemia;
for CO2
hypocapnia or hypercapnia are used.
When may cyanosis be detectable?
Under 40-50 mmHg
Hypoventilation:
pCO2 > 45 mmHg
(most reliable in arterial blood sample)
- Hypoxemia +-: depends on the degree of hypercapnia, and the FiO2.
- *- low O2 saturation** (depends also on blood Hb concentration, RBC count!)
Hypoventilation:
Effects
dyspnoea,
cyanosis
mildly anxiolytic/sedating treatment
Hyperventilation
**PaCO2 < 35mmHg
Hyperoxaemia: usually present together with increased SAT.**
Hyperventilation
Causes:
Causes:
iatrogenic: forced ventilation during anesthesia
(also high FiO2)
seizures, epilepsy
excitation
(mild frequently visiting the vet, extreme e.g. shock after accident)
compensation of severe metabolic acidosis:
Kussmaul-type breathing.
Causes of hypoventilation
Causes:
upper airway obstruction
pleural effusion
drugs or disorder affecting central control of respiration e.g. general anaesthesia
neuromuscular disease, which affects on the respiratory system, also muscle weakness
e.g. hypokalaemia
overcompensation of metabolic alkalosis
Causes of Respiratory alkalemia/alkalosis
Causes:
Increased loss of CO2: hyperventilation
excitation
forced ventilation (anaesthesia)
epileptiform seizures
fever, hyperthermia
interstitial lung disease
Causes of Respiratory acidaemia/acidosis
Causes:
Upper airway obstruction
Pleural cavity disease: pleural effusion, pneumothorax
Pulmonary disease:
- severe pneumonia,
- pulmonary edema,
- diffuse lung metastasis,
- pulmonary thromboembolism
Depression of central control of respiration:
- drugs,
- toxins,
- brainstem disease
Neuromuscular depression of respiratory muscles
Muscle weakness e.g. muscle weakness in hypokalaemia
Cardiopulmonary arrest
Causes of Metabolic alkalaemia/alkalosis
Causes:
Increased alkaline intake:overdose of bicarbonates, or feedingrotten food
Increased ruminal alkaline production:
- high protein intake,
- low carbohydrate intake,
- anorexia,
- hypomotility
Decreased hepatic ammonia catabolism (liver failure)
Increased acid loss:
- vomiting,
- gastric dilatation volvulus syndrome,
- abomasal displacement
Ion exchange: hypokalaemia: due to Henle loop diuretics remember H+/K+ pump!!
(paradoxical aciduria, see Pathophysiology lecture notes!!)
Causes of Metabolic acidaemia/acidosis
- * HCO3
- loss: diarrhea, ileus, kidney tubular disturbance**
- * increased acid intake:** i.e. fruits, too acidic silage, an overdose of
- *acidifying drugs** (ammonium chloride), even vitamin C if long term high doses!
increased acid production e.g. increased lactic acid production, due to anaerobic glycolysis, frequent in anorectic, weak animals
in cattle grain overdose, leading to volatile acid overproduction
increased ketogenesis, leading to ketosis due to relative or objective starvation or diabetes mellitus
decreased acid excretion: renal failure
ion exchange: hyperkalaemia, remember the H/K pump!!
some xenobiotic: ethylene-glycol toxicosis: metabolites are acidic molecules, leading to metabolic acidosis, and finally renal failure will worsen it
Effects of Metabolic acidaemia/acidosis
Effects:
Kussmaul-type breathing - hyperventilation (not panting!!)
Hypercalcaemia: increased mobilisation from bones in case of long term acidosis
(TCa), and decreased binding of calcium ions to albumin (Ca2+)
Vomiting, depression
Hyperkalaemia: decreased cardiac muscle activity; sinoatrial, or atrioventricular
block, bradycardia.
In urine: titratable acidity increases (except for the processes of renal origin)
Most importaint buffersystem
carbonic acid-bicarbonate buffer system:
What forms the vital buffer system
The kidneys and the lungs