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Last updated 12:49 PM on 7/8/26
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23 Terms

1
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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.

2
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What are the immediate buffer systems for pH changes?

Intracellular - protein, haemoglobin, phosphate

Extracellular - plasma protein, bicarbonate, plasma phosphate

Transcellular - K+/H+ exchange

Respiratory

3
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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

4
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What are the signs of acidaemia?

Tachycardia

Hypotension

Arrythmias

Decreased Cardiac Contractility

Insulin Antagonism

Blunted response to Catecholamines

Compensatory hyperkalaemia

5
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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

6
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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-

7
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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

8
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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

9
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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

10
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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

11
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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.

12
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Differentials for a normal Anion Gap (metabolic acidosis)

Dilutional Acidosis

Diarrhoea

Kidney Disease

13
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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)

14
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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

15
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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

16
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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.

17
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What are the two main mechanisms by which metabolic acidosis occurs?

  1. A fall in bicarbonate concentration with a rise in chloride concentration (hyperchloremic metabolic acidosis)

  2. Gain of acid in the system leading to a fall in bicarbonate concentration.

18
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What causes renal loss of bicarbonate?

Appropriate response to a persistent respiratory acidosis (metabolic compensation)

Or renal tubular acidosis as a primary disease process

19
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Two types of renal tubular acidosis (RTA) and causes?

  1. Proximal tubular dysfunction - congenital abnormalities e.g., Fanconi syndrome, toxins, drugs and various diseases

  2. Distal RTA - inadequate hydrogen ion secretion in the distal tubule that prevents maximum acidification of the urine e.g., pyelonephritis and IMHA

20
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When is bicarbonate therapy indicated?

When the acidosis is severe or when the compensatory respiratory alkalosis is considered detrimental to the patient.

21
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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+

22
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What are alternative alkalanising therapies and what is the major difference with sodium bicarbonate?

Tromethamine - no CO2 production

Carbicarb - less CO2 production

23
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What are the main contraindications and risks of sodium bicarbonate administration to the patient with metabolic acidosis?

  1. 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

  2. Paradoxical intracellular acidosis - CO2 crreated by bicarbonate can freely enter cells → lowers pH

  3. Increases in blood lactate in cases of DKA, lactic acidosis and haemorrhagic shock.