2. Acid Base Disorders and blood gas analysis Flashcards Preview

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Flashcards in 2. Acid Base Disorders and blood gas analysis Deck (55)
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1
Q

What is pH?

A

The pH is equal to -log10 [H+].

2
Q

Why is isohydria important?

A

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.

3
Q

What is a buffer?

A

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.
4
Q

Most important buffer systems in

  1. Blood plasma
  2. RBC
  3. Tissue cells
A
  1. Carbonic acid-bicarbonate / primary – secondary phosphate / protein-proteinate (albumin)
  2. Carbonic acid-bicarbonate / primary – secondary phosphate buffer / protein-proteinate (haemoglobin)
  3. Carbonic acid-bicarbonate / primary – secondary phosphate buffer / protein-proteinate (cytoplasmic proteins)
5
Q

The most important physicochemical buffer system in all fluid compartments of the body

A

Carbonic acid – bicarbonate system

6
Q

The vital buffer system

A

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)
7
Q

Indication of acid/base evaluation

A
  • Routine test in emergency patients.

- Gives info about acid-base status, and about function of vital buffer systems

8
Q

Sample and sampling of acid/base evaluation

A
  • 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
9
Q

Method of acid/base evaluation

A
  • Analyzers utilize ionselective electrodes (ISE) to measure pH and CO2.
  • Based on the measured parameters the HCO3, ABE and other parameters are calculated
10
Q

pH of blood

A

7.35-7.45

11
Q

pCO2

A

Partial CO2 pressure, resp. parameter - 40 mmHg

12
Q

Metabolic acidosis

A

pH < 7,4
HCO3 < 20mml/l
BE < -3,5mmol/l

13
Q

Metabolic acidosis - causes

A
  • 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)
14
Q

Metabolic acidosis - effects

A
  • Hyperventilation
  • Hypercalcaemia
  • Vomiting, depression
  • Hyperkalaemia
  • In urine: titratable acidity incr
15
Q

Metabolic acidosis - treatment

A
  • Providing adequate ventilation

- If pH <7.2 infusion therapy involving alkaline fluid

16
Q

HCO3

A

Bicarbonate - metabolig parameter - 21-24 mmol/l

17
Q

Anion gap

A
  • 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
18
Q

Normal anion gap

A

Hyperchloraemic - Cl- replaces HCO3-

  1. Diarrhoea: HCO3-loss
  2. Early kidney failure: H+ retention, decr NH3 excretion
  3. Renal tubular acidosis: Prox/dist tubular defect
  4. Acidifying substances: NH4Cl
19
Q

Increased anion gap

A

Normochloraemic - Unmeasured anions replaces HCO3-

  1. Azotaemia/uraemia: Kidney failure – organic acid accumulation
  2. Lactacidosis: Shock, hypovolaemia, poor tissue perfusion, tissue necrosis
  3. Ketoacidosis: Diabetic – incr hepatic prod of KB´s
  4. Toxicosis: Ethylene glycol toxicosis
20
Q

Metabolic alkalosis - causes

A
  • Incr alkaline intake
  • Incr ruminal alkaline prod
  • Decr hepatic NH3 catabolism (liver failure)
  • Incr acid loss
  • Ion exchange: hypokalaemia
21
Q

Metabolic alkalosis - effects

A
  • Decr. HR
  • Hypoventilation
  • Muscle weakness – hypokalaemia
  • Hypocalcaemia
  • Ammonia toxicosis
  • Arrhythmia, biphasic P, QT incr, flat T, U wave,
  • Paradoxical aciduria
22
Q

Metabolic alkalosis - treatment

A

Generally enough to treat the underlying electrolyte imbalance

23
Q

Respiratory acidosis

A

pH < 7.4
pCO2 > 40mmHg
pO2 < 40mmHg

24
Q

Respiratory acidosis - causes

A
  • Upper airway obstruction
  • Pleural cavity disease
  • Pulmonary disease
  • Depression of central control of respiration
  • Neuromuscular depression of respiratory muscles
  • Muscle weakness
  • Cardiopulmonary arrest
25
Q

Respiratory acidosis - effects

A

Dyspnoea, cyanosis, suffocation, muscle weakness, tiredness.

26
Q

Respiratory acidosis - treatment

A
  • Assisting the ventilation
  • Treatment of the cause
  • Cardiac disease; treatment of pneumonia
  • Mildly anxiolytic/sedating drugs
27
Q

Respiratory alkalosis

A

pH > 7.4
pCO2 < 40 mmHg
pO2 > 40 mmHg

28
Q

Respiratory alkalosis - causes

A
  • Increased loss of CO2: hyperventilation
  • excitation
  • forced ventilation (anaesthesia)
  • epileptiform seizures
  • fever, hyperthermia
  • interstitial lung disease
29
Q

Respiratory alkalosis - effects

A
  • Hyperoxia, incr. pCO2 : pO2 ratio, may lead to apnoea

- increased elimination of HCO3 by the kidneys

30
Q

Respiratory alkalosis - treatment

A
  • Anxiolytic or mild sedative drugs

- Incr pCO2 level by closing nose

31
Q

ABE

A

Actual base excess (or demand) or residue, metabolic parameter - ±3.5 mmol/l

32
Q

TCO2

A

Total CO2 conc. in plasma (liberated by strong acid) - 23-30 mmol/l

33
Q

SBE

A

Standard or in vivo Base Excess - metabolic parameter - ±3 mmol/l

34
Q

Primary / secondary resp. change

A

Primary: predominant change of pCO2
Secondary: predominant change of HCO3-

35
Q

Resp. background of pH alteration

A

pCO2

36
Q

Metabolic background of pH alteration

A

HCO3- and ABE

37
Q

Metabolic alkalosis

A

pH>7,4, HCO3->28mmol/l, BE>3,5mmol/l

38
Q

Blood/gas analysis sampling

A
  • Arterial blood for resp., venous blood for gross changes only
  • Anticoagulated
  • Closed sample
  • Within 15 min / on ice
39
Q

Blood/gas analysis method

A

Directly measure pCO2 and pO2 w. ion specific electrodes

40
Q

paCO2

A

Partial arterial CO2 pressure = 35-45 mmHg

41
Q

pqO2

A

Partial arterial O2 pressure = 88-110 mmHg

42
Q

SAT / SatO2

A

Oxygen saturation calculated from Hb and pO2
= Venous: 75-80%
= Arterial: 90-100%

43
Q

FiO2

A

Fraction of inspired oxygen
= Room air: 0,209
= O2 enriched: 0,21-1,0
= > 0,5: risk of O2 toxicity

44
Q

Blood/gas interpretation

A

paO2 and PaCO2

45
Q

Hypo/hyperoxaemia

A

<60mmHg / >60mmHg

46
Q

Hypo/hypercapnia

A

Decr. CO2 / Incr.CO2

47
Q

Normal paO2 in room air

A

80-110mmHg and 97-100% saturation

48
Q

Cyanosis

A

<45-50 mmHg of paO2

49
Q

Hypoventilation

A
  • PaCO2 > 45mmHg

- Hypoxaemia: depends on hypocapnia and FiO2

50
Q

Hypoventilation - causes

A
  • upper airway obstruction
  • pleural effusion
  • drugs or disorder affecting central control of respiration
  • neuromuscular disease
  • overcompensation of metabolic alkalosis
51
Q

Hypoventilation - effects

A

dyspnoea, cyanosis

52
Q

Hypoventilation - treatment

A
  • assisting the ventilation
  • diuretic treatment
  • mildly anxiolytic/sedating treatment
53
Q

V/Q - Ventilation perfusion mismatch

A
  • normal ventilation with inadequate perfusion

- inadequate ventilation with normal perfusion

54
Q

Hyperventilation

A
  • PaCO2 < 35mmHg

- Hyperoxaemia: usually present together with incr SAT

55
Q

Hyperventilation - causes

A
  • iatrogen: forced ventilation during anaesthesia
  • seizures, epilepsy
  • excitation
  • compensation of severe metabolic acidosis