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Lab diagnostics > 2. Acid base disorders and blood gas analysis > Flashcards

2. Acid base disorders and blood gas analysis Flashcards

1
Q

Explain isohydria

A

It is the concentration of hydrogen ions in the body which is tightly controlled within a narrow range.

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2
Q

what happens when the pH changes?

A

The stability is essential for cell membranes and for enzyme activity, if it changes it might lead to electrolyte imbalance and can cause a change in muscle irritability too.

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3
Q

Why is buffers important?

A

In the body there are chemical reactions that produce hydrogen ions rapidly, this can lead to change in pH. When the production of H ions is too rapid for the body to eliminate, intra and extracellular buffers are important and essential for life.

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4
Q

What are the characteristics of a buffer?

A

A buffer solution resist pH changes. A buffer can maintain the pH even when diluted or acid/base is added to it. It is typically a mixture of a weak acid (or base) and one of its salts.

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5
Q

What happens if the H+ in the body starts to increase?

A

The conjugate basis can uptake this excess.

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6
Q

What happens if the H+ in the body starts to decrease?

A

More weak acids can dissociate to raise the H+ back to the normal level.

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7
Q

What is the most important physico-chemical buffer system in all fluid compartments?

A

the Carbonic acid-bicarbonate system.

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8
Q

The most important buffer system: blood plasma:

A

Carbonic acid - bicarbonate buffer system, primary - secondary phosphate buffer, protein-proteinate buffer system ( albumin albumin + H+)

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9
Q

The most important buffer system: RBC

A

Carbonic acid - bicarbonate buffer system, primary - secondary phosphate buffer, protein-proteinate buffer system.( haemoglobin + O2 haemoglobin + H+)

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10
Q

The most important buffer system: Tissue cells

A

Carbonic acid - bicarbonate buffer system, primary - secondary phosphate buffer, protein-proteinate buffer system. (cytoplasmic proteins cytoplasmic + H+)

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11
Q

What forms the vital buffer system?

A

Lungs and kidneys form the vital buffer system, the respiratory and the renal responses are continually closely interacting.

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12
Q

Explain the buffer capacity of the lungs:

A

The lungs are restrain or excrete CO2 to regulate pH. Example: Increase H+ (reduced ph in ECF), the equation will move to the left. Generating extra CO2 leads to hypercapnia (CO2 retention) this stimulate the ventilation and the lungs can eliminate the CO2.
inc.CO2 - H2O excrete via lungs.

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13
Q

What is the kussmaul breating?

A

Normal frequency of breathing but very deep inspiration and expiration. The capacity to retain CO2 is limited, because of the O2.

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14
Q

Explain the buffering capacity of the kidney:

A

The kidneys can retain or excrete H+, and effectively regenerate the HCO3- via complex tubular mechanism, but this takes some time. (hours-days) Example: If the CO2 levels within the body increase, the equation will push to the right and produce excess H+ and HCO3- and then H+ can be eliminated by the kidneys.
inc.CO2 - H2O -> H2CO3 -> inc.H+ + inc.HCO3- -> excrete via kidneys.

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15
Q

What is the goal or indication on acid-base evaluations?

A

It is a routine test in emergency patients. It informs about acid-base status and about function of vital buffer systems. They also measure blood-gas parameters, electrolytes, haemoglobin, haemotocrit, lactate and glucose.

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16
Q

when we do an acid-base evaluation: what do we sample?

A

Anticoagulated blood is necessary (Ca-equilibrated Li-heparinised syringe). Arterial samples are needed for respiratory function. Venous or arterial can be useful for infor about the metabolic status of the animals.

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17
Q

when we do an acid-base evaluation: How do we sample?

A

Astrup-technique, air contamination must be avoided. In air contaminated samples pO2 will increase. (150mmHg pO2 is in air), pO2 may decrease shortly after sampling as CO2 evaporates into air or increase in case of longer storage, produced by the metabolism of blood cells.

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18
Q

when we do an acid-base evaluation: How do we store the samples?

A

Not for more than 5-10 min at room temp and not more than 30min at 0-4C.

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19
Q

What method does the analyzers use?

A

ISE (ionselective electrodes to measure pH and CO2. Based on the results HCO3, ABE and other parameters are calculated. analyzed in 37C. The solubility of gases is dependent on temp, however 37 degrees are the patients temperature.

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20
Q

Acid-base parameters: pH

A

pH of blood 7.35-7.45 (-log H+)

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21
Q

Acid-base parameters: pCO2

A

partial CO2 pressure, respiratory parameter; 40 mmHg

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22
Q

Acid-base parameters: HCO3-

A

Bicarbonate conc: 21-24mmol/L, depends on pCO2, metabolic parameter

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23
Q

Acid-base parameters: ABE

A

Actual base excess (or demand) It is the amount of base and acid needed to equilibrate blood to pH 7.4, metabolic parameter. +- 3.5 mmol/l

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24
Q

Acid-base parameters: TCO2

A

total CO2 conc in plasma, 23-30mmol/l. CO2 content of blood liberated by strong acid. TCO2 is 5% higher than plasma HCO3-, gives no direct info about respiratory function. If we have HCO3- result, this may be ignored.

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25
Q

Acid-base parameters: SBE

A

Standard or in vivo base excess, residue in the whole extracellular space, metabolic parameter +-3mmol/l

26
Q

Evaluation of AB state: step 1

A

Evaluate if acidosis (under 7.4) or alkalosis (over 7.4) is present according to the pH.

27
Q

Evaluation of AB state: step 2

A

Search for the cause of the observed pH alteration. Both acidosis and alkalosis can occur due to metabolic or respiratory changes. Change in pCO2 = primary respiratory, change in HCO3- and ABE= primary metabolic process.

28
Q

Explain the respiratory background:

A

pCO2 shows a strong shift in the same direction as the pH. Equilibrium point of pCO2 is 40mmHg, if it is bigger than this value it binds to water and forms carbonic acid. Increase of pCO2 can be called shift in acidic direction. When we have impaired gas exchange in the lungs CO2 forms carbonic acid and shifts pH to acidosis: respiratory acidosis. When hyperventilation is present, too much CO2 is exhaled which will cause elevation of pH; respiratory alkalosis.

29
Q

Explain the metabolic background:

A

When pH alteration is caused by metabolic processes or kidney malfunction, the cause can be detected bu the changes of the metabolic parameters: HCO3- and ABE. During lactic acid production metabolic acidosis occur, both are shifted in acid direction. HCO3- decrease when acidosis and increase in alkalosis. ABE =0 , + when alkalosis, - when acidosis.

30
Q

Evaluation of AB state: step 3

A

Evaluate whether compensation effort is visible in the result or not. If either the respiratory or the metabolic parameter is shifted in the opposite direction than the pH - the compensatory effect is visible. In the metabolic acidosis the lungs try to compensate by highly effective gas exchange - very deep breath and longer gas exchange - helps to excrete a lot of CO2, so pH is acidic and CO2 changes in alkaline direction.

31
Q

Example of what can cause the established changes: metabolic acidosis:

A
  • HCO3- loss, diarrhea, ileus, kidney tubular disturbance.
  • Increased acid intake: fruits
  • Increased acid production ; lactic acid prod
  • in cattle grain overdose
  • Increased ketogenesis
  • decreased acid excretion
  • ion exchange: hyperkalemia, H/K pump
32
Q

Values of metabolic acidosis::

A

pH under 7,4, HCO3- under 20mml/l, BE under -3.5mmol/l.

33
Q

Effects of metabolic acidosis::

A
  • hyperventilation: kussmaul-type breathing
  • hypercalcaemia:bones
  • vomitting, depression
  • hyperkalaemia: cardiac muscle decrease
  • in urine: acidity increased
34
Q

Treatment of metabolic acidosis::

A 
Providing ventilation (fresh air). If pH is under 7.2 infusion is necessary with alkaline fluid. ABE x BW x K (mmol/l)
K= coefficient for small animals:0.3, large: 0.2. NaHCO3 infusion.
35
Q

What is the anion gap?

A

useful parameter when attempting to determine the cause of metabolic acidosis. difference between anions and cations in plasma. referance range: 8-16 mmol/L, decreased HCO3-, increase Cl-

36
Q

Normal anion gap:

A

Diarrhea- HCO3- loss,
early kidney failure - H+ retention, decreased ammonia excretion,
acidifying substances - NH4Cl

37
Q

Increased anion gap:

A

Azotonia - advanced kidney failure, organic acid accumulation., lactacidosis - shock, hypervolemia, tisuue necrosis., ketoacidosis - diabetic ketoacidosis, ketone body production increase., toxicosis- ethylene glycol toxicosis

38
Q

Causes of metabolic alkalosis:

A
  • increased alkaline intake: feeding rotten food.
  • increased ruminal alkaline production: high prot intake.
  • decreased hepatic ammonia catabolism (liver failue)
  • increased acid loss- vomitting.
  • ion exchange: hypokalemia.
39
Q

Effects of metabolic alkalosis:

A
  • Breathing depression.
  • muscle weakness.
  • hypocalcaemia.
  • ammonia toxicosis.
  • Arrhytmia.
40
Q

Treatment of metabolic alkalosis:

A

treat underlying electrolyte imbalance.

41
Q

Causes of respiratory acidosis:

A
  • upper airway obstruction
  • pleural cavity disease
  • pulmonary disease
  • depression of central control of respiration
  • neuromuscular depression of respiratory muscles
  • muscle weakness
  • cardiopulmonary arrest
42
Q

Effects of respiratory acidosis:

A

-dyspnoea, cyanosis, suffocation, muscle weakness, tiredness.

43
Q

Treatment of respiratory acidosis:

A
  • assisting the ventilation, fresh air
  • treatment of the cause
  • mildly anoxiolytic/sedating drugs to decrease the fear and excitment of animals caused by hypoxia.
44
Q

Causes of respiratory alkalosis:

A
  • increased loss of CO2 hyperventilation
  • excitation
  • forced ventilation
  • epileptiform seizures
  • fever,hyperthermia
  • intestinal lung disease
45
Q

Effects of respiratory alkalosis:

A
  • Hyperoxia, increased pCO2, ratio may lead to aponea.

- increased elimination of HCO3- by the kidneys

46
Q

Treatment of respiratory alkalosis:

A

Anxiolytic or mild sedative drugs in case of hyperexcitation. It is important to increase CO2 level by closing nose and nostrils.

47
Q

Values of metabolic alkalosis:

A

pH over 7,4, HCO3- over 28mmol/l, BE over 3.5mmol/l.

48
Q

Values of respiratory acidosis:

A

pH under 7,4, pCO2 over 40mmHg, pO2 under40mmHg

49
Q

values of respiratory alkalosis:

A

pH over 7,4, pCO2 under 40mmHg, pO2 over 40mmHg

50
Q

Blood gas analysis: goal:

A

performed to assess effectiveness of gas-exchange i.e. ventilation in the lungs during dyspnoea or anaesthesia.

51
Q

Blood gas analysis: sampling:

A

arterial samles are essential for precise assessment of respiratory fanction. how effective is the gas exchange in the alveoli. Venous blood gas analysis shows gross changes only and informs about the oxygen consumptions. anticoagulated blood is necessary (ca-equilibrated Li heparinised plasma, preheparinised syringe). Astrup teq should be used (tranferring blodd changes the partial pressure). should be measured in 15 minutes or placed into ice.

52
Q

Blood gas analysis: methods:

A

the pCO2 and pO2 is directly measured with ion specific electrodes. The sample are analysed in 37’C.

53
Q

Blood gas analysis: parameters and reference range:

A
  • PaO2 (partial arterial pressure) 88-118 mmHg
  • PaCO2 ability to remove CO2, 35-45mmHg
  • SAT or SatO2 (saturation, calculated from Hb and pO2) Venous 75-80%, arterial 90-100%.
  • FiO2 (fraction of inspired oxygen) room air: 0.209 (20.9%), O2 enriched: 0.21-1.0 > 0.5 risk of O2 toxicity.
54
Q

Hypoventilation: values

A

PaCO2 higher than 45mmHg, hypoxaemia (low level of oxygen in the blood) +- depends on the degree of hypercapnia and the FiO2.

55
Q

Hypoventilation: causes

A
  • upper airway obstruction
  • pleural effusion
  • drugs or disorder affecting central control of respiration
  • neuromuscular disease, which affects the respiratory system, also muscle weakness, hypokalaemia.
  • Overcompensation of metabolic alkalosis
56
Q

Hypoventilation: signs/effects

A

dyspnoea (shortness of breath), cyanosis (blue)

57
Q

Hypoventilation: treatment

A
  • assisting ventilation
  • diuretic treatment: in case of fluid accumulation in the lungs.
  • Mildly sedating treatment
58
Q

Hyperventilation: values

A

PaCO2 lower than 35mmHg, hyperoxaemia: usually present together with increased SAT.

59
Q

Hyperventilation: causes

A

Iatrogen: forced ventilation during anaesthesia

  • Seizures: epilepsy
  • Excitation (mild frequently visiting the vet, extreme shock accident)
  • Compensation of severe metabolic acidosis: kussmaul-type breathing.
60
Q

Hyperventilation: sample

A

Venous samples should not be used! Oxygen saturation in venous blood informs about tissue O2 usage and venous SAT below 60% indicates that the body is in lack of O2 and ischemic diseases occur.

61
Q

What three evaluations has to be analyzed?

A

Acid-base parameters, blood gas analysis and ionogram!

Lab diagnostics (6 decks)

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