Module 1. Acid Base Balance Flashcards
Identify and interpret acid base disorders
An acid or base disorder is a deviation from the normal pH of the blood.
Normal physiological pH is within the range 7.35-7.45
a. A pH < 7.35 is an acidaemia
b. A pH > 7.45 is an alkalaemia
(pH = -log10[H+])
HCO3 =bi carbonate which is a base.
CO2 is considered an acid (because when it is dissolved in water, it increases the concentration of H+.)
Carbonic anhydrase equation;
H+ plus HCO3- <=> H2C03 <=> H20 + CO2. So if CO2 increases the pH of the blood is becoming more acidic.
To identify and interpret acid/base disorders:
1. first see if pH is decreased or elevated.
2.Then look at pCO2 to determine if there is respiratory acidosis (increased pCO2) or respiratory alkalosis.
3.Then look at bicarb to see if there is a metabolic alkalosis (increased bicarb) or metabolic acidosis.
4. Check the calculated base excess (a negative base excess=metabolic acidosis, whereas a positive base excess= metabolic alkalosis)
5. Work out what is changing most in the same direction as the pH (or rather a change also of acidosis or alkalosis.ie if more acidic, CO2 up, pH down or HCO3- down)., to determine what is the primary problem (ddx respiratory acidosis/alkalosis or metabolic acidosis/alkalosis).ie resp issue involves CO2 and this will go in opposite direction as the pHCO2 increase and pH decrease both =increased acidity) whereas HCO3- is the metabolic component and if this the primary issue, it will change in same direction as pH.
6.Is the secondary process compensatory?
7. Do the measurements seem to correspond to clinical state of the patient?
Identify primary and secondary acid base disorders and compensatory mechanisms
Respiratory Alkalosis = PCO2 <35
Respiratory Acidosis = PCO2 >38
Metabolic Acidosis = HCO3 < 15
Metabolic Alkalosis = HCO3 >23.
Primary disorder has a problem in same direction as the problem with the pH.
Secondary compensatory change has a change in the opposite direction to the primary problem. Compensatory changes are usually insufficient to return pH to normal. Compensatory changes require time (respiratory compensation occurs within 8-12 hours, and metabolic compensation occurs within 1-3 days). Note that it is best to consider a compensatory change as “possibly” compensatory but be mindful of other ddx of the change.
List causes of acidosis and alkalosis
Causes of RESPIRATORY ALKALOSIS; (occurs due to hyperventilation, therefore decreased PCO2 as pushing more out);
a) Hypoxaemia
b)Pulmonary dz
c)Pain/stress/excitement/exercise
d)Hyperthermia
e)Fever/sepsis/cytokine release (eg SIRS)(Systemic Inflammatory Response Syndrome)
f)Excessive positive pressure ventilation
g)Pulmonary thromboembolism
h)Compensation for metabolic alkalosis
ddx for RESPIRATORY ACIDOSIS;(increased CO2 by hypoventilation)
a) CNS dz eg drugs or brainstem issue
b)Neuromuscular dz (eg tick paralysis, botulism, polyradiculoneuritis, Myasthaenia gravis etc)
c)Airway obstruction (fb, laryngeal dz et
d) Diaphragm dz/impairment (eg abdominal enlargement)
e) Pleural space dz
f)Rebreathing circuit (ie high dead space)
g) Severe pulmonary dz
h) Compensation for metabolic alkalosis
g) Malignant hyperthermia
ddx for METABOLIC ACIDOSIS
1. Hyperchloraemic metabolic acidosis (normal anion gap because loss of HCO3 balanced by increase in Cl);
a) GI loss of bicarb (d+/v+ with reflux from duodenum)
b) Renal loss of bicarb (proximal tubule acidosis, carbonic anhydrase inhibitor)
c) Renal hydrogen retention (distal tubular acidosis, hypomineralocorticism)
d) i/v nutrition
e) Dilutional acidosis (eg large volume of saline)
f)Compensation for respiratory alkalosis
g) ammonium chloride
2. With normochloraemia (ie elevated anion gap because decreased HCO3 not matched by and increase in Cl);
a)Paraldehyde toxicity
b)Lactic acidosis**
c) uraemia (kidney failure, phosphate/sulphate acidosis)
d) methanol toxicity
e)Salicyclate poisoning
f)ethanol toxicity (ketoacidosis)
g) ethylene glycol intoxication
h) diabetic ketoacidosis
i)starvation (ketoacidosis)
ddx of METABOLIC ALKALOSIS (almost always no anion gap as hypochloraemia due to Cl being lost along with H+. HCO3 is resorbed);
a) Gastric losses (v+ due to high git obstruction**)
b) furosemide
c) excessive alkalinization therapy
d) severe hypokalaemia
e)hypermineralocorticism
f)compensation for respiratory acidosis
Discuss the anion gap and its diagnostic use
Anion Gap(AG)= difference between measured concentrations of major cations and anions.
AG= ([Na+]+[K+]) - ([Cl-]+[HCO3-])
Normal AG dogs 12-24 mEq/L
Normal AG cats 13-27 mEq/L
Calculation of the AG can help differentiate causes of metabolic acidosis.
There are some other unmeasured ions which along with the measured ones, ensure electroneutrality is maintained.
In a metabolic acidosis (=decrease in [HCO3-] then in order to maintain electroneutrality, there is either an increase in chloride (and a normal anion gap) OR there is no increase in chloride, but an increase in unmeasured anions (and an increased anion gap).
The body strives to maintain electroneutrality.
Technically the AG = ([Na+]+[K+]+[unmeasured cations]) - ([Cl-]+[HCO3-]+[unmeasured anions]).
Unmeasured cations include some proteins, Calcium, and Magnesium.
Unmeasured anions include albumin, phosphate, lactate, ketones.
Patients with marked hypoproteinaemia may have falsely low AG, making interpretation in these circumstances unreliable.
Describe the management of acidaemia and alkalaemia
For METABOLIC ACIDAEMIA, fluid choice will be something with bicarbonate (HCO3-) in it eg Hartmann’s, Plasmalyte, Lactated Ringers etc.
For METABOLIC ALKALOSIS (eg classic high fb) choose 0.9% NACl.
Correct for hypovolaemia/perfusion issues.
Additional bicarb spiking beyond what is in selected fluid therapy is usually not required when treating acidosis and can cause worsening hypokalaemia and driving oxygen dissociation curve to left, causing worsening hypoxaemia.
For RESPIRATORY ACIDOSIS manage airways, (remove fb, manual ventilation, treat underlying dz as appropriate)
For RESPIRATORY ALKALOSIS correct issues of hyperventilation as appropriate.
Discuss the physiology of lactate production and its use as a perfusion marker
Lactate is produced due to anaerobic metabolism where lactate and H+ are produced. An increase in lactate is not always accompanied by altered ph but when it is accompanied by acidaemia (decreased base excess) = Lactic Acidosis.
Most common cause of hyperlactaemia is hypoxaemia therefore hyperlactaemia often looked at for likely marker of hypoperfusion.
Usually when do have lactate elevations, they are responsible for most of what seeing in negative base excess.
Whilst the degree of hyperlactaemia is concerning, of more concern is if it is persisting after appropriate tx. Such persistence is associated with a very poor px and cell injury, organ failure and death.
Describe the pathophysiology of hyperlactataemia
CAUSES OF HYPERLACTAEMIA;
TYPE A (due to hypoxia);
1. hypoperfusion (shock)
2. increased muscle activity (seizures)
3. severe hypoxaemia (eg severe anaemia)
4. carbon monoxide poisoning
5. local hypoperfusion (eg GDV dogs, Feline Aortic Thromboembolism)
(note hypoxaemia=decreased partial pressure of oxygen in blood, whereas hypoxia=reduced tissue oxygenation)
TYPE B (no tissue hypoxia);
B1 (lactate increased due to underlying disease)
a) diabetes mellitus (reduced intracellular glucose available for metabolism)
b) severe liver dz
c) neoplasia or sepsis (hypermetabolic state)
B2 (increased lactate due to drug or toxin)
a) eg Paracetamol, cyanide, beta agonist etc
B3 congenital mitochondrial or gycolytic pathway dysfunction.
Outline oxygenation in terms of arterial blood oxygen, ventilation, perfusion and V/Q mismatch
Arterial Blood Oxygenation is defined by PaO2 and is normally expected to be somewhere between 80-100mmHg.
SpO2 is the percentage of haemoglobin saturated with oxygen compared with haemoglobin not carrying oxygen. It is usually 95% or more. It is not the same as PaO2 but is usually similar.
PaO2 can only be determined from arterial sample.
PaO2 less than 80mm HG=hypoxia and supplementation required.
PaO2 60mmHg means if already supplementing O2 and still at this level, needs mechanical ventilation.
V=ventilation and Q=perfusion.
V/Q is used to describe ventilation compared with perfusion of an alveolocapillary unit.
If V/Q high, have normal ventilation but poor perfusion eg thrombus.
If V/Q low, have normal perfusion but low ventilation (oxygenation) eg due to pneumonia, aspiration, pulmonary disease etc.
In real terms, cannot measure V/Q without radioisotopes and nuclear imaging.
Recall the physiological causes of hypoxaemia and associated disease processes
Hypoxaemia = abnormally low concentration of oxygen in arterial blood.
Causes of hypoxaemia;
Anaemia (although arguably might be more of a hypoxia)
Low inspired oxygen (eg under ga and not turned oxygen on)
Hypoventilation
Diffusion impairment (eg pulmonary fibrosis)
V/Q mismatch
Shunt (blood bypasses lungs).
Use the P:F ratio and A-a Gradient in reference to oxygenation
P=PaO2
F=Fractionally inspired oxygen.(ie how much oxygen is there in the air that is being breathed in?) Normal room air is 21%=0.21. If parient has 1 nasal line in, assume F=40%=0.40. If have 2 nasal lines in, F is approx 60% and if intubated and on 100% oxygen only, F=100%=1.
Normal P:F ratio is400 to 500.
A-a Gradient is the gradient between the alveoli and normal blood.
PAO2=partial pressure of oxygen in alveoli.
PaO2 is partial pressure of oxygen in artery.
PAO2 should be 5-10mmHg higher than PaO2. (Normal A-a gradient is 5-10)
When there is >10 as a difference between PAO2 and PaO2 it suggests a pulmonary parenchymal issue is the cause of hypoxaemia (ie higher amount O2 was in the alveoli but unable to pass across to the artery). A normal gradient (with hypoxaemia) suggests that it is due to another cause eg hypoventilation.
The A-a gradient can only be utilised on patient’s breathing room air as the normals for this come from measurements on room air at sea level as per
PAO2 approx = 150 - (PaCO2/0.8).
(Normal PaCO2=32 to 46 mm Hg).
Discuss the parameters involved in assessment of ventilation
Consider ventilation by looking at PCO2 and Oxygenation.
PCO2 can assess either as PaCO2 (normal 34 to 45) or PvCO2 (normal is 4-6mmHg higher than PaCO2) (ie normal 38-51mmHg).Difference between PvCO2 and PaCO2 might be greater if severely hypoperfused.
Low PCO2 rarely of clinical concern.
High PCO2 indicates hypoventilation or inability to “blow off excess CO2)
DDx for high PCO2;neuromuscular dz (eg snakebite, tick paralysis), thoracic wall dz (eg rib fx, pain, deformity) or pleural space dz (eg pleural effusion).
A PCO2 of >60mmHg usually indicates a need for mechanical ventilation.
Need to also assess in light of oxygenation. eg if hypoxic, might develop compensatory hyperventilation and lead to low PCO2.
PaO2 + PaCO2 should be >120, if not, there is either an issue with ventilation, or with oxygenation.
Describe and explain Base Excess
Base Excess is the amount of acid or base required to return the pH to 7.4 with normal PCO2 (40mmHg) at room temperature (37C). Negative base excess=metabolic acidosis. Positive base excess =metabolic alkalosis (too much base).
Base excess is the purest way of measuring what the disturbance is.
