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Define the pH equation → and explain how to evaluate them and why
H+ + HCO3- = H2CO3 = H2- + CO2, Assess the respiratory portion first as it can respond to pH shifts within minutes. After that evaluate the metabolic portion.
What are the immediate buffer systems for pH changes?
Intracellular - protein, haemoglobin, phosphate
Extracellular - plasma protein, bicarbonate, plasma phosphate
Transcellular - K+/H+ exchange
Respiratory
What is the delayed buffer system for pH changes, and how long does that take?
The Renal system - excretes H+/HCO3- (and conserves it). Starts within 12-24 hours and can take 2-5 days
What are the signs of acidaemia?
Tachycardia
Hypotension
Arrythmias
Decreased Cardiac Contractility
Insulin Antagonism
Blunted response to Catecholamines
Compensatory hyperkalaemia
What are the signs of Alkalaemia?
Muscle spasms
Stuporous mentation
Arrythmias
Reduces O2 unloading in tissues → hypoxemia
Hypocalcemia
Hypokalaemia
Altered enzyme activity + alterations to cell structures that are dependent on H+ ions
What are the 4 primary acid-base disturbances?
Respiratory Acidosis → Increased PCO2
Respiratory Alkalosis → Decreased PCO2
Metabolic Acidosis → Decreased HCO3/BE-
Metabolic Alkalosis → Increased HCO3/BE-
Why do we use BE (Base excess), and explain what it means
More accurate measure of metabolic changes, is a measure of the amount of acid/base required to bring 1L of blood to pH 7.4.
+ve BE = metabolic alkalosis, -ve BE = metabolic acidosis
Normally will change in same direction as HCO3-, however HCO3- is linked with respiration, therefore BE- is more accurate
What are the causes of Respiratory Acidosis?
Overarching - Hypoventilation
Neuronal, neuromuscular, muscular disease - think ticks, snakes, botulism, myasthenia gravis etc.,
rebreathing/increase in dead space
upper airway obstruction
anterior displacement of diaphragm
restrictive extrapulmonary disease
pleural space disease
severe pulmonary parenchymal disease
bicarbonate therapy in respiratory compromised patients
certain medications - e.g., sedation
malignant hyperthermia
compensation for metabolic alkalosis
What are the causes for Respiratory Alkalosis?
Overarching - Hyperventilation
FAS
hyperthermnia/fever
pulmonary thromboembolism
early pulmonary parenchymal disease
respiratory centre disease - e.g., neoplasia or head trauma
hypoxemia
hyperadrenocorticism (cushings)
excessive mechanical ventilation
compensatory response to metabolic acidosis
Causes of Metabolic Acidosis?
Toxic - ethylene glycol, methanol
Intestinal - loss of HCO3- through diarrhoea
DKA
Dilutional acidosis - dilution of HCO3- (e.g., fluid therapy with non-balanced fluids
Renal - reduced excretion of H+ and reduced update of HCO3-
Lactic Acidosis - marker of shock and poor perfusion
What is the Anion Gap Formula and when is it useful?
[Na+] + [K+] - [Cl-] + [HCO3-]. Can be useful when trying to interpret a metabolic acidosi. Can only interpret it when there are no obvious significant abnormalities to the plasma protein (albumin) levels, as plasma protein makes up a significant portion of the unaccounted for factors in the equation.
Differentials for a normal Anion Gap (metabolic acidosis)
Dilutional Acidosis
Diarrhoea
Kidney Disease
Differentials for a increased anion gap (metabolic acidosis)?
M - methanol, methaldehyde
U - uraemic acid
D - DKA
P - Paracetamol, propylene glycol, paraldehyde
I - Iron, Isoniazid
L - Lactic Acidosis
E - Ethylene Glycol Toxicity
S - Salicylic Acid (Aspirin)
What are the causes of Metabolic Alkalosis?
Gastric or intestinal obstructive processes: lose H+, K+ and Cl- → then reduced resorption of H+ and CL- in the proximal SI
Frusemide administration
Hyperaldosteronism
Hypovolemia/dehydration + hypochloridaemia → Na+ + H20 resorbed by kidneys without CL- to maintain electroneutrality
Compensation for respiratory acidosis
Severe hypokalaemia → Potassium is exchanged with H+ across cell membranes - causes an intracellular acidosis in all the cells including the kidneys → leading to a increase in H+ excretion by the kidneys + an increase in HCO3- resorption
What is Contraction Alkalosis?
When a large amount of Sodium rich fluid is lost from the body → leads to an increase in net concentration of bicarbonate
When should you be concerned about 2 processes occuring at the same time when reading pH?
When you notice that the pH, metabolic markers and respiratory markers all seem to trend in the same direction.
What are the two main mechanisms by which metabolic acidosis occurs?
A fall in bicarbonate concentration with a rise in chloride concentration (hyperchloremic metabolic acidosis)
Gain of acid in the system leading to a fall in bicarbonate concentration.
What causes renal loss of bicarbonate?
Appropriate response to a persistent respiratory acidosis (metabolic compensation)
Or renal tubular acidosis as a primary disease process
Two types of renal tubular acidosis (RTA) and causes?
Proximal tubular dysfunction - congenital abnormalities e.g., Fanconi syndrome, toxins, drugs and various diseases
Distal RTA - inadequate hydrogen ion secretion in the distal tubule that prevents maximum acidification of the urine e.g., pyelonephritis and IMHA
When is bicarbonate therapy indicated?
When the acidosis is severe or when the compensatory respiratory alkalosis is considered detrimental to the patient.
How can hypokalemia play a role in generation and maintenance of s metabolic alkalosis?
Promotes more loss of hydrogen ions from the kidneys
K+ moved from cells to intravascular space in exchange with H+
What are alternative alkalanising therapies and what is the major difference with sodium bicarbonate?
Tromethamine - no CO2 production
Carbicarb - less CO2 production
What are the main contraindications and risks of sodium bicarbonate administration to the patient with metabolic acidosis?
Patients that are hypoventilating - bicarbonate becomes carbonic acid which becomes water and CO2, if the patient isnt ventilating adequately can cause a decrease in pH
Paradoxical intracellular acidosis - CO2 crreated by bicarbonate can freely enter cells → lowers pH
Increases in blood lactate in cases of DKA, lactic acidosis and haemorrhagic shock.