T4: Acid-Base Homeostasis Flashcards

1
Q

How do you assess whether the primary disorder is respiratory or metabolic?

A

Step 1: If the pH is less than 7.35 the patient = acidotic
If the pH is greater than 7.45 the patient = alkalosis

Step 2: Then you determine whether the primary disorder is respiratory or metabolic using the blood gas. For example if in acidosis and the pCO2 is high, it must be respiratory. If low or normal, it must be metabolic.

In alkalosis, and the carbon dioxide is low, there is respiratory alkalosis. If the PCO2 is high or normal it must be metabolic.

Step 3: compensation. These are secondary changes in bicarbonate and partial pressure of carbon dioxide to correct for the primary disorder.

Changes in bicarbonate concentration (renal regeneration) can occur to compensate for respiratory disorders – this is a slow process. We can get changes in partial pressure of oxygen to correct for bicarbonate disorders – this is fast. Full compensation rarely occurs and over-compensation never occurs.

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2
Q

How can measure bicarbonate?

A

We measure bicarbonate on a blood gas. There is a:
• Bicarbonate (main lab) - this is a classical or actual level. Sometimes called total CO2 because it is calculated in part form CO2.
• Standard bicarbonate – removes respiratory contribution so an abnormal standard bicarbonate tells us that there is a metabolic component to the disorder. It uses Henderson-Hasselbach equation to calculate the bicarbonate form the PH and the corrected pCO2.

A normal standard bicarbonate = purely respiratory disorder.
Abnormal standard bicarinate = shows that there is a metabolic component.

Unless specified assume it is a classical bicarbonate.

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3
Q

What is the anion gap?

A

This is the difference between the sum of measured anions and cations.

Anion gap = ([Na+] + [K+]) – ([Cl-] + [HCO3-])

Increased anion gap means there is a significant amounts of unmeasured anions (e.g. ketones, lactate, salicylate and proteins etc.) Can be useful in determining the cause of metabolic acidosis. There are some anions in healthy patients normally and so the reference range is not zero.

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4
Q

What are the signs and symptoms of respiratory acidosis?

A

Respiratory acidosis presents with a low pH, high carbon dioxide and a compensation is by bicarbonate (normal or elevated).
There is also a low pO2 as this is normally due to a reduced respiratory rate

Metabolic acidosis presents usually
as dyspnea.

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5
Q

What are causes of respiratory acidosis?

A
Defective control of respiration
•CNS depression
•Anesthetics, sedatives etc. 
•Narcotics, opiates etc. 
•CNS disease
•Trauma
•Hemorrhage
•Infarction
•Tumor
•Infection
•Neurological disease
•Spinal cord lesions
•MND
•Guillain-Barre
Defective respiratory function
•Mechanical
•Myopathies
•Pneumothorax
•Pleural effusion
•Inadequate mechanical ventilation
•Pulmonary disease
•E.g. COPD, severe asthma etc 
•Impaired perfusion (e.g. massive pulmonary embolism)
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6
Q

What is the physiological response to respiratory acidosis

A
  • Buffering – limited by hemoglobin
  • Reparatory compensation is not very possible. Increase carbon dioxide stimulates the respiratory Centre but the disease prevents an adequate response

• Renal is by maximal bicarbonate reabsorption – this however takes a while to reach maximal effects
Almost all phosphate is excretes as H2PO4-
Marked increase in urinary ammonium

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7
Q

What is the management for respiratory acidosis?

A
  • Treat underlying cause
  • Maintain adequate arterial partial pressure of oxygen but avoid loss of hypoxic stimulus to respiration
  • Avoid rapid correction of the partial pressure of carbon dioxide as it risks alkalosis due to persistent compensation
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8
Q

What are the signs and symptoms of metabolic alkalosis?

A

Metabolic alkalosis presents with elevated pH, and either a normal or high pCO2 in compensation. We also see a normal pO2 particularly in compensation due to the reduction in reparatory rate in compensation.

  • Usually related to the underlying cause
  • More severe alkalosis can increase protein binding of calcium leading to hypocalcemia which causes headaches, lethargy, neuromuscular excitability, sometimes with delirium, tetany and seizure
  • Lower she threshold for arrythmias
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9
Q

What are causes of metabolic alkalosis?

A
  • Administration of bicarbonate
  • Potassium depletion
    Hypokalemia can lead to alkalosis. The transporter transports sodium in at the expense of potassium or hydrogen ions. In hypokalemia, we can excrete hydrogen ions to spare the sodium ions. In the cells potassium ions are transported out of the RBCs to increase plasma concentration – hydrogen ions move into cells to maintain electroneutrality. This leads to a decrease in plasma hydrogen ion concentration.
  • Loss of hydrogen ions – vomiting. Rich in HCL
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10
Q

What is the physiological response to metabolic alkalosis?

A
  • Hydrogen ions can be released form buffers
  • The respiratory rate is reduced - this is self-limiting as an increase in pCO2 stimulates the respiratory centre.

• Renal compensation is difficult as a decrease in GFR leads to inappropriately high bicarbonate reabsorption. Potassium deficiency contributes to persistence of alkalosis.

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11
Q

What is the management for metabolic alkalosis?

A
  • Treat the underlying cause.

* Treat factors that sustain alkalosis - I.e. replace the potassium.

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12
Q

What are the signs and symptoms of metabolic acidosis?

A

Metabolic acidosis presents with a low pH, a low bicarbonate and a normal (or low in compensated) pCO2.

  • Nausea, vomiting and anorexia frequently present
  • Subjective sense of dyspnea caused by stimulation of the respiratory Centre
  • Deep labored breathing pattern, known as Kussmaul breathing, in severe acidosis particular in patients with DKA
  • Other symptoms caused by underlying disorder
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13
Q

What are causes of metabolic acidosis?

A

Increased acid formation

Ketoacidosis: 
•Diabetic (DKA)
•Alcoholic (AKA)
•Starvation
•Lactic acidosis: 
•Type A (tissue hypoxia) 
•Type B (metabolic and toxic causes)
Poisoning: 
•Salicylate
•Toxic alcohols (e.g. ethylene glycol, methanol, ethanol)
•Inherited organic acidosis - tend to present in pediatrics

Increased acid formation tends to lead to an increased ion gap.

Decreased acid excretion

  • Uraemia (renal failure) due to reduced glomerular filtrate rate – tend to lead to an increased ion gap
  • RTA type 1 (distal) - hydrogen ions in the distal tubule cannot be transported into the filtrate appropriately (Renal tubular acidosis – this is rare)

Loss of bicarbonate
•GI: diarrhea / fistula - the intestinal fluid is very rich in bicarbonate
Renal:
•RTA type 2 (proximal) - we cannot reabsorb bicarbonate properly
•Carbonic anhydrase inhibitors (e.g. acetazolamide)

Also patients can ingest acid

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14
Q

What is the physiological response to metabolic acidosis?

A

• Hyperventilation - this is self-limiting as it generates CO2
• Carbonate and protein buffering
• Urine hydrogen ion excretion maximized
Increased rate of regeneration of bicarbonate

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15
Q

What is the management for metabolic acidosis?

A
  • Identify and treat the cause
  • Treat with sodium bicarbonate – this needs to be done in very severe cases in pH less than 7.00 in IV – this needs to be very careful
  • Oral bicarbonate also (CKD, RTA type 1 and 2)

Rapid correction impairs oxygen delivery however rebound alkalosis is possible.

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16
Q

What are the signs and symptoms of respiratory alkalosis?

A

Respiratory alkalosis is characterised by a low pH, high carbon dioxide and compensation is by bicarbonate (normal or elevated).
There is also a low pO2 as this is normally due to a reduced respiratory rate.

The signs and symptoms are usually related to the underlying cause. Dyspnea is also commonly seen.

17
Q

What is the physiological response to respiratory alkalosis?

A
  • Release of hydrogen ions from non-bicarbonate buffers
  • Respiratory compensation – inhibitory effect of decreases carbon dioxide overwhelmed by primary cause
  • Decreased renal regeneration of bicarbonate – carbon dioxide is a substrate and so it is preserved
18
Q

What is the management for respiratory alkalosis?

A
  • Treat underlying cause
  • Rapid symptomatic cause by re-breathing
  • Sedation or prevention of hyperventilation by mechanical ventilation
19
Q

What are mixed disorders? Give an example.

A

These are two or more primary acid-base disorders presenting in the same patient. Can either by additive or counterbalance.

Additive
Respiratory failure – an increased pCO2 causing acidosis and a metabolic acidosis due to an increase in lactic acid.

Vomiting and CCF (congestive cardiac failure)– metabolic alkalosis (loss of hydrogen ion form vomiting) and respiratory alkalosis (reparatory rate form CCF)

Counterbalance
Salicylate poisoning – Metabolic acidosis and respiratory alkaloses (from increased respiratory rate stimulated by the salicylate).

Vomiting and renal failure – loss of hydrogen ion causes metabolic alkalosis and metabolic acidosis (due to decrease renal hydrogen ion excretion).

20
Q

What is the diagnosis for the following case:

Na+	127 mmol/L (133-146)
K+	2.2 mmol/L (3.5-5.3)
pH	7.59 (7.35-7.45)
pO2	9.7 kPa (10-13.3)
pCO2	6.2 kPa (4.7-6.0)
A

Metabolic alkalosis

Likely cause is vomiting due to loss of HCl.

21
Q

What is the diagnosis for the following case:

H+ 83 nmol/L (35-45) HCO3- 22.5mmol/L (22-28)
pO2 7.24 kPa (10-13.3) O2 saturation 86%
pCO2 7.75 kPa (4.7-6.0)

A

Respiratory acidosis - high carbon dioxide. There is no compensation as the bicarbonate is not elevated.

22
Q

Why does vomiting cause hypokalaemia?

A

In vomiting, hydrogen ions are lost through the stomach acid. Calcium is also bound to albumin. In acidosis, so that more hydrogen ions can be bound by albumin, some calcium ions are released to make space. These can therefore cause hypercalcemia. In alkalosis, hydrogen ions are released from albumin, calcium ions must bind to album to maintain charge balance.

23
Q

What is Base Excess?

A

Base excess (-2.3 to 3.3 mmol/L) also seen on a blood gas machine. It equates to the amount of acid or alkali needed to titrate the blood pH to 7.40. It takes into all buffers. Like standard bicarbonate, it tells us if there is a metabolic component to the disorder.

Normal base excess = purely respiratory disorder
Negative BE (2.3 mmol/L) in metabolic alkalosis (i.e. a base excess)