Lab 2 - Acid/base disorders, blood gas analysis

Question 1

How do you treat meatbolic acidosis

Answer 1

Ventilation or ir pH is less that 7.2 infusion therspy with alkaline fluid using ABE to calculate amount. This means that the actual base excess is a theraputic parameter!

Question 2

Metabolic acidosis causes

Answer 2

􏰀 HCO3- loss: diarrhoea, ileus, kidney tubular disturbance
􏰀 increased acid intake: i.e. fruits, too acidic silage, 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

Question 3

Metabolic acidosis effects

Answer 3

􏰀 Kussmaul-type breathing - hyperventilation (not panting!!)
􏰀 Hypercalcaemia: increased mobilisation from bones in case of long term acidosis (TCa - decr protein binding (here in bones), and decreased binding of calcium ions to albumin (anion albumin is bound to ca during alkalosis)
􏰀 Vomiting, depression
􏰀 Hyperkalaemia: decreased cardiac muscle activity; sinoatrial, or atrioventricular block, bradycardia.
􏰀 In urine: titratable acidity increases (except for the processes of renal origin) incr. H+

Question 4

Normal anion gap/hyperchloraemic

Caused by what and how

Answer 4

Diarrhoea: HCO3- loss

Early kidney failure: H+ retention, decreased ammonia excretion

Renal tubular acidosis: Proximal (Fanconi syndrome) or distal tubular defect

Acidifying substances: NH4Cl (NH4+)

Question 5

Increased anion gap/normochloraemic

Caused by what and how

Answer 5

Caused by unmeasured anions!!

Azotaemia or uraemia:
Advanced kidney failure – organic acid accumulation

Lactacidosis:
Shock, hypovolaemia, poor tissue perfusion, tissue necrosis

Ketoacidosis:
Diabetic ketoacidosis – increased hepatic production of ketone bodies

Toxicosis:
Ethylene glycol toxicosis (also alcohol)

Question 6

Metabolic alkalosis Causes

Answer 6

􏰀 Increased alkaline intake: overdose of bicarbonates, or feeding
rotten food
􏰀 Increased ruminal alkaline production: high protein intake, low carbohydrate intake,
anorexia, hypomotility
􏰀 Decreased hepatic ammonia catabolism (liver failure) ammonia is not turned into urea, incr ammonia!
􏰀 E.g. abomasal displacement leads to Paradoxial aciduria causing Incr. Acid loss(sequestration, vomiting) and secretion(H+ instead of K+for Na+)

Question 7

Metabolic alkalosis Effects

Answer 7

􏰀 Breathing-depression (compensatory respiratory acidosis) - low breathing rate, hypoventilation
􏰀 Muscle weakness – hypokalaemia
􏰀 hypocalcaemia due to the increased Ca2+ binding ability of albumin anions during alkalosis
􏰀 Ammonia toxicosis when decr ammonia catabolism!
􏰀 Arrhythmia, biphasic P, QT increases (AV conduction disorder), flat T, U wave bc. Hypokalemia!

Question 8

Metabolic alkalosis treatment

Answer 8

In general it is enough to treat the underlying electrolyte imbalance.

Question 9

Respiratory acidosis

Causes:

Answer 9

􏰀Upper airway obstruction
􏰀 Pleural cavity disease: pleural effusion, pneumothorax
􏰀 Pulmonary disease: severe pneumonia, pulmonary oedema, 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

Question 10

Respiratory acidosis effects

Answer 10

Dyspnoea(shortness of breath), cyanosis, suffocation, muscle weakness, tiredness

Question 11

Respiratory acidosis Treatment

Answer 11

􏰀 assisting the ventilation - providing fresh air or oxygen therapy
􏰀 treatment of the cause: e.g. diuretic treatment: in case of fluid accumulation in the
lungs, pulmonary oedema; specific cardiologic treatment: in case of underlying
cardiac disease; treatment of pneumonia, removal of fluid from pleural space etc.
􏰀 mildly anxiolytic/sedating drugs to decrease the fear and excitement of animals caused by hypoxia

Question 12

Respiratory alkalosis

Causes:

Answer 12

􏰀Increased loss of CO2: hyperventilation due to:

• excitation
• forced ventilation (anaesthesia) 􏰀 epileptiform seizures
• fever, hyperthermia
• interstitial lung disease

Question 13

Respiratory alkalosis effects

Answer 13

􏰀Hyperoxia, decreased pCO2 : pO2 ratio, may lead to apnoea(breathing interruption)
􏰀increased elimination of HCO3- by the kidneys

Question 14

Respiratory alkalosis treatment

Answer 14

Anxiolytic or mild sedative drugs in case of hyperexcitation. It is important to increase the pCO2 level by closing nose or nostrils

Question 15

Hypoventilation causes

Answer 15

Hypoxaemia 􏰂: depends on the degree of hypercapnia, and the FiO

􏰀 upperairwayobstruction
􏰀 pleural effusion: fluid accumulation in pleural cavity
􏰀 drugs or disorder affecting central control of respiration e.g. general anaesthesia
􏰀 neuromuscular disease, which affects on respiratory system, also muscle weakness
e.g. hypokalaemia
􏰀 overcompensation of metabolic alkalosis

Question 16

Hypoventilation effects/signs

Answer 16

How low O2 depends on how effective the alveoli are(CO2): and the degree of hypercapnia - how incr thr co2 is which will influence ox

dyspnoea: shortness of breath
cyanosis: low O2 saturation -> blueish discoloration of skin/mucous membranes

Question 17

Hypoventilation treatment

Answer 17

• assisting the ventilation e.g. assisted breathing, oxygen therapy
• diuretic treatment: in case of fluid accumulation in the lungs, pulmonary oedema; or in the thoracic cavity (treatment that get rid of water and salts through urine)
• mildly anxiolytic/sedating treatment

Question 18

Hyperventilation causes

Answer 18

Hyperoxaemia: usually present together with increased SAT.

􏰀 iatrogen: forced ventilation during anaesthesia (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.

Question 19

Venous samples are not used check gas exchange mechanism and blood oxygenstion capacity, but it can be used for

Answer 19

Oxygen saturation in venous blood on the other hand informs about tissue O2 usage and venous SAT below 60% indicates that the body is in lack of oxygen, and ischemic diseases occur.

Question 20

Method of acid-base evaluation:

Answer 20

• enter the patients body temperature for correction (temp dep) so the machine corrects the values according to this

Question 21

acid-base evaluation: when, why, mechanism

Answer 21

• routine test in emergency patients
• acid-base status, and about the function of vital buffer systems
• ISE - ion selective electrodes convert activity of ions in a solution to a potential which can be measured useing a pH meter

Question 22

Method of gas-exhange, interpretation parameters

Answer 22

• enter the patients body temperature for correction (temp dep) so the machine corrects the values according to this
• normoventilation, hypoventilation or hyperventilation.

For individual changes of oxygen : Hyper/o-oxemia, hyper/o-capnia

Question 23

Gas exchange evaluation: when, why, mechanism

Answer 23

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

The blood gas analyzers directly measure the pCO2 and pO2 with ion specific electrodes