Lab 2 Flashcards
The most important physico-chemical buffer system in all fluid compartments of the body?
the carbonic acid - bicarbonate system
What forms the Vital buffer system?
the kidneys and the lungs.
They are continually closely interacting
explain the Buffering capacity of the lungs:
the lungs can retain the CO2, or excrete it to regulate the pH acutely.
Ex: Increased H+ (reduced ECF pH): the equation will move to the left, generating extra CO2, lead to hypercapnia, which stimulate the ventilation and the lungs can eliminate the CO2.
What is Kussmaul breathing?
is observed because the pulmonary capacity to excrete CO2 is huge. Normal frequency of breathing but very deep inspiration and expiration.
Explain buffering capacity of the kidneys:
The kidneys can excrete or retain H+, and also effectively regenerate the HCO3- via complex tubular mechanisms - takes hours/days.
Ex: If 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.
What kind of sample is necessary for acid/base analysis?
anticoagulated blood (Ca-equilibrated Li-heparinised syringe).
Why is arterial samples essential?
for assessment of respiratory function, but either venous or arterial samples can provide useful information on the metabolic status of the animal.
What is the “Astrup-technique”?
A closed sampling method to avoid air contamination of the sample.
What can happen in air contaminated samples?
- pO2 will be increased (150mmHg pO2 is in atmospheric air)
- pCO2 may be decreased (shortly after samling as CO2 evaporates into the air
- pCO2 may be increased (in case of longer storage, produced by the metabolism of blood cells)
How should the samples be stored?
Not more than 5-10 min at room temp. and not more than 30 min at 0-4*C (refrigerator)
What method is used for Acid/base analysis?
analyzers utilize ionselective electrodes (ISE) to measure pH and CO2. Based on the measured parameters the HCO3-, ABE and other parameters are calculated.
What temperature are the samples analyzed at?
37*C
the solubility of gases is dependent on?
temperature, and the measured values need to be corrected to the temperature of the patient.
Routinely used acid-base parameters:
- pH
7.35-7.45
Routinely used acid-base parameters:
- pCO2
40 mmHg
Routinely used acid-base parameters:
- ABE
+-3.5 mmol/l
Routinely used acid-base parameters:
- TCO2
23-30 mmol/l
Routinely used acid-base parameters:
- SBE
+-3 mmol/l
Evaluation of AB state:
- Step 1
Evaluate wheter acidosis or alkalosis is present according to the pH!
- Blood pH reference range
- pH <7.35 acidosis is decompensated
- pH >7.45 alkalosis is decompensated
Evaluation of AB state:
- Step 2
Search for the cause of the observed pH alteration
- The predominant change of pCO2 refers to primary respiration
- the predominant change of HCO3- and ABE refers to primary metabolic processes
Respiratory background of pH alterations:
pCO2 shows a strong shift in the same direction as the pH.
- When pCO2 is >40mmHg, more of it bounds to water and forms carbonic acid.
Increase of pCO2 in respiration can be called?
A shift in “acidic” direction
What happens in case of impaired gas exchange in the lungs?
the remaining high CO2 forms carbonic acid and shifts the pH to acidosis: respiratory acidosis
What happens during hyperventilation?
too much CO2 is exhaled which will cause elevation of the pH: respiratory alkalosis.
Metabolic background of pH alterations:
Eg: in case of lactic acid production metabolic acidosis occurs, both metabolic parameters are shifted in acidic direction.
- HCO3- being an anion decreases in acidosis and increases in alkalosis.
Calculation of Actual base excess:
is a calculated parameter which was defined to aid correction of acid-base disturbances.
- when metabolic alkalosis is seen this paramter shifts from 0 to the positive range: in metabolic acidosis to negative range.
How is compensatory effect detected:
the given parameter is shifted in opposite direction compared to the pH.
What is “mixed acidosis”
sometimes all parameters are shifted significantly in the same direction as the pH - this is observed mostly in advanced acidosis.
Evaluation of AB state:
- Step 3
Evaluate whether compensation effort is visible in the result or not!
- If either the respiratory or the metabolic parameters is shifted in the opposite directin than the pH - the compensatory effect is visible
Eg: in metabolic acidosis the lungs try ot compensate by highly effective gas exchange; very deep breath and longer gas exchange (Kussmaul breathing)
Kussmaul breathing helps to:
excrete alot of CO2, so pH is acidic and CO2 changes alkaline direction.
Metabolic acidosis
- Causes:
- HCO3- loss: diarrhoea, ileus, kidney tubular disturbance
- Increased acid intake: fruits, too acidic silage, overdose of acidifying drugs, Vitamin C.
- Increased acid production: increased lactic acid production, anaerobic glycolysis, frequent in anorectic, weak animals.
- In cattle grain overdose: 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 (H/K pump!!)
- Some xenobiotic: ethylene-glycol toxicosis: metabolies are acidic molecules, leading to metabolic acidosis, and finally renal failure will worsen it.
Metabolic acidosis
- Effects:
- Kussmaul-type breathing - hyperventilation
- Hypercalcaemia: increased mobilisation from bones in case of long term acidosis (TCa), and decreased binding of calcium ions to albumin (Ca2+)
- Hyperkaaemia: decreased cardiac muscle activity; sinoatrial, or atrioventricular block, bradycardia
Metabolic acidosis
- Treatment:
- providing adequate ventilation
- if pH <7.2 infusion therapy involving alkaline fluid
What is the Anion gap?
a useful parameter when attempting to determine the cause of metabolic acidosis. The anion gap describes the difference between the commonly measured cations in plasma, and the commonly measured anions.
reference range for anion gap:
8-19 mmol/l
Metabolic alkalosis
- Causes:
- 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
- Increased acid loss: vomitting, gastric dilatation volvulus syndrome, abomasal displacement.
- Ion exchange: hypokalaemia; due to Henle loop diuretics (H/K PUMP!!)
Metabolic alkalosis
- Effects:
- Breathing depression (compensatory respiratory acidosis), low breathing rate, hypoventilateion
- Muscle weakness, hypokalaemia
- Hypocalcaemia due to increased Ca2+ binding of albumin
- Ammonia toxicosis
- Arrythmia, biphasic P, QT increased (AV conduction disorder), flat T, U wave
- Paradoxical aciduria
Respiratory acidosis
- Causes
- 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 eg muscle weakness in hypokalaemia
- cardiopulmonary arrest
Respiratory acidosis
- effects:
- Dyspnoea, cyanosis, suffocation, muscle weakness, tiredness
Respiratory acidosis
- treatment:
- assist the ventilation, providing fresh air r 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 disaease; treatment of pneumonia, removal of luid from pleural space
- mildly anxiolytic/sedating drugs to decrease the fear and excitement of animals caused by hypoxia
Respiratory alkalosis
- Causes:
- Increased loss of CO2: hyperventilation, excitation, forced ventilation (anasthesia), epiletiform seizures, fever, hyperthermia, interstitial lung disease.
Respiratory alkalosis
- effects:
- Hyperoxia, increased pCO2: pO2 ratio, may lead to apnoea
- increased elimination of HCO3- by the kidneys
Respiratory alkalosis
- treatment:
- anxiolytic or mild sedative drugs in case of hyperexcitation. it is important to increase the pCO2 level by closing nose or nostrils, pulling paper sack on the nose until breathing normalizes
Indication/goal of Blood gas analysis?
is performed to assess effectiveness of gas-exchange i.e ventilation in the lungs e.g during dyspnoea or anasthesia
Sample used for Blood gas analysis?
- Arterial samples: precise assessment of respiratory function, i.e how effective the gas exchange in the alveoli is.
- Venous: reflects gross changes only and gives information about how much oxygen is consumed by the body.
Sampling used for Blood gas analysis?
- Anticoagulated blood
- Ca-equilibrated Li-heparinised plasma, preheparinised syringe
Why must the Astrup Technique be used?
because transferring blood to a tube will alter the partial pressure of gases, therefore a closed sampling method should be used.
- the sample must be stored with no air/vacuum space, because the CO2 can evaporate and air contamination causes false increased p=2 pressure.
How to measure Blood gas analysis?
within 15 minutes, or placed on ice, to minimize changes in blood gas partial pressure as a result of continued metabolism.
Method of analyzing Blood gas?
The blood gas anaylzers directly measure the pCO2 and pO2 with ion specific electrodes. The samples are analyzed on standaridized temperature 37*C.
Parameters and reference range:
- paO2
88-118 mmHg
Parameters and reference range:
- paCO2
35-45 mmHg
Parameters and reference range:
- SAT or SatO2
Venous: 75-80&
Arterial: 90-100%
Parameters and reference range:
- FiO2
Room air: 0.209 (20.9%)
O2 enriched: 0.21-1.0
>0.5 risk of O2 toxicity
What are the most important parameters to assess the fas exchange capacity of the animals?
paO2 and paCO2
- Following conclusions can be frawn for the overall effectiveness: normoventilation, hypoventilation or hyperventilation
Normal arterial oxygen pressure (paO2) at room air:
80-110 mmHg
The saturation is around 97-100%
When is cyanosis detectable?
Under 40-50 mmHg
What is higher, pvCO2 or paCO2?
Normal pvCO2 is higher than paCO2
Hypoventilation is when paCO2 is?
> 45 mmHg
Hypoxaemia depends on?
the degree of hypercapnia and the FiO2
Hypoventilation
- Causes:
- upper airway obstruction
- pleural effusion
- drugs or disorder affecting central control of respiration e.g: general anasthesia
- neuromuscular disease, which affects on respiratory system, also muscle weakness e.g: hypokalaemia
- overcompensation of metabolic alkalosis
Hypoventilation
- Effects, signs:
Dyspnoea, cyanosis
Hypoventilation
- Treatment
- assisting the ventilation e.g: oxygen therapy
- diuretic treatment: in case of fluid accumulation in the lungs, pulmonary oedema; or in the thoracic cavity
- mildly anxiolytic/sedating treatment
What is VA/Q?
Additional to hypoventilation arterial blood gas tensions are also influenced by Ventilation-Perfusion Mismatch(VA/Q)
- normal ventilation with inadequate perfusion (insufficient blood passing the alveoli for oxygen)
- inadequate ventilation with normal perfusion (pulmonary capillary blood reaches the alveoli adequate quantities, but ventilation those alveoli has been insufficient to allow enough oxygen
Hyperventilation is when paCO2 is?
< 35mmHg
Hyperoxaemia usually present together with?
increased SAT
Hyperventilation
- Causes:
- iatrogen: forced ventilation during anaesthesia (also high FiO2)
- seizures, epilepsy
- excitation (mild frequently visiting the vet, extreme e.g shock after accident)
Oxygen saturation in venous blood informs about?
tissue O2 usage and venous SAT below 60% indicates that the body is in lack of oxygen, and ischemic disease occur.
The “acid-base” or “blood-gas” analyzers include ion specific electrodes for:
pH, CO2, HCO3- and also ions: Ca2+, Na+, K+, Cl-.
When we interpret the result given by the analyzer we have to interpret all three evaluations: acid-base parameters, blood gas analysis and ionogram!
