Lab 2 test= Reference ranges and their expected changes in various conditions! Flashcards

1
Q

What is the blood pH reference range?

A

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.

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2
Q

The reference range for anion gap

A

8-16 mmol/L

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3
Q

Parameters and reference range:
The partial pressure of oxygen (mmHg, kPa)

A

pO2

  • *arterial: 88-118 mmHg
    venous: 35-45 mmHg**

Indicates the ability of the lungs to oxygenate blood.

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4
Q

Parameters and reference range:
The partial pressure of carbon dioxide (mmHg, kPa)

A
  • *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.

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5
Q
Parameters and reference range:
**SAT (%)**
oxygen saturation (%)
A
  • *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.

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6
Q

Fraction of inspired oxygen
FiO2

A

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.

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7
Q

Partial CO2 pressure (mmHg, kPa),

respiratory parameter

A

pCO2
40 mmHg
(35-45)

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8
Q
**HCO3-**
Standard bicarbonate (HCO3-) concentration (mmol/l)
A

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

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9
Q

ABE
Actual base excess (or demand) or residue (mmol/l)

A

±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

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10
Q

TCO2
Total CO2 concentration in plasma (mmol/l)

A

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

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11
Q

SBE
Standard or in vivo base excess (base demand)

A

±3 mmol/l

Standard or in vivo base excess (base demand), residue in
the whole extracellular space, metabolic parameter

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12
Q

Normal anion gap
(hyperchloraemic)
Diarrhoea

A

HCO3- Loss

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13
Q

Normal anion gap
(hyperchloraemic)

Early kidney failure

A

H+ retention, decreased ammonia excretion

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14
Q

Normal anion gap
(hyperchloraemic)
Renal tubular acidosis

A

Proximal (Fanconi syndrome) or distal tubular defect

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15
Q

Normal anion gap
(hyperchloraemic)
Acidifying substances

A

NH4Cl

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16
Q

Increased anion gap

(normochloraemic)

Azotaemia or uraemia

A

Advanced kidney failure – organic acid accumulation

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17
Q

Increased anion gap
Lactacidosis

A

Shock, hypovolaemia, poor tissue perfusion, tissue necrosis

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18
Q

Increased anion gap
Ketoacidosis

A

Diabetic ketoacidosis – increased hepatic production of ketone bodies

19
Q

Increased anion gap
Toxicosis

A

Ethylene glycol toxicosis (also alcohol)

20
Q

Normal anion gap
(hyperchloraemic)
Name cases

A

Diarrhoea
Early kidney failure
Renal tubular acidosis
Acidifying substances

21
Q

Increased anion gap
(normochloraemic)

A

Azotaemia or uraemia
Lactacidosis
Ketoacidosis
Toxicosis

22
Q

Metabolic alkalaemia/alkalosis
Ranges

pH
HCO3
BE

A

pH > 7.4
HCO3- > 28 mmol/l
BE > +3.5 mmol/l

23
Q

Metabolic alkalaemia/alkalosis
effects

A

 Breathing-depression
 Muscle weakness – hypokalaemia
 hypocalcemia due to the increased Ca2+ binding ability of albumin
 Ammonia toxicosis
 Arrhythmia,
 Paradoxical aciduria

24
Q

Respiratory acidaemia/acidosis
ranges
pH
pCO2
pO2

A

pH < 7.4
pCO2 > 40 mmHg
pO2 < 40 mmHg

25
Q

Respiratory acidaemia/acidosis
effects

A

Dyspnoea,
cyanosis,
suffocation,
muscle weakness,
tiredness.

26
Q

Respiratory alkalemia/alkalosis
ranges
pH
pCO2
pO2

A

pH > 7.4
pCO2 < 40 mmHg
pO2 > 40 mmHg

27
Q

Respiratory alkalaemia/alkalosis
Effects:

A

**Hyperoxia, the decreased pCO2 : pO2 ratio may lead to apnoea

increased elimination of HCO3
- by the kidneys**

28
Q

Hypoxaemia

A

(<60 mmHg)

29
Q

hyperoxaemia;

A

for CO2
hypocapnia or hypercapnia are used.

30
Q

When may cyanosis be detectable?

A

Under 40-50 mmHg

31
Q

Hypoventilation:

A

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!)
32
Q

Hypoventilation:
Effects

A

dyspnoea,
cyanosis
 mildly anxiolytic/sedating treatment

33
Q

Hyperventilation

A

**PaCO2 < 35mmHg

Hyperoxaemia: usually present together with increased SAT.**

34
Q

Hyperventilation
Causes:

A

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.

35
Q

Causes of hypoventilation

A

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

36
Q

Causes of Respiratory alkalemia/alkalosis

A

Causes:
Increased loss of CO2: hyperventilation
excitation
forced ventilation (anaesthesia)
epileptiform seizures
 fever, hyperthermia

 interstitial lung disease

37
Q

Causes of Respiratory acidaemia/acidosis

A

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

38
Q

Causes of Metabolic alkalaemia/alkalosis

A

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!!)

39
Q

Causes of Metabolic acidaemia/acidosis

A
  • * 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

40
Q

Effects of Metabolic acidaemia/acidosis

A

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)

41
Q

Most importaint buffersystem

A

carbonic acid-bicarbonate buffer system:

42
Q

What forms the vital buffer system

A

The kidneys and the lungs

43
Q
A