Acid-Base Balance Flashcards

1
Q

When does Blood acidity increase?

A

Level of acidic compounds in the body rises (through increased intake or production, or decreased elimination)
Level of basic (alkaline) compounds in the body falls (through decreased intake or production, or increased elimination)
Acidemia is serum pH < 7.35
Acidosis refers to physiologic processes that cause acid accumulation or alkali loss

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2
Q

When does blood alkalinity increase?

A

The level of acid in the body decreases or when the level of base increases.
Alkalemia is serum pH>7.45
Alkalosis refers to physiologic processes that cause alkali accumulation or acid loss

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3
Q

What is the role of the lungs in the control of Acid-Base balance?

A

One mechanism involves the release of carbon dioxide from the lungs.
Carbon dioxide, which is mildly acidic, is a waste product of the processing (metabolism) of oxygen and nutrients (which all cells need) and, as such, is constantly produced by cells. It then passes from the cells into the blood. The blood carries carbon dioxide to the lungs, where it is exhaled. As carbon dioxide accumulates in the blood, the pH of the blood decreases (acidity increases).

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4
Q

How does the brain regulate amount of carbon dioxide?

A

The brain regulates the amount of carbon dioxide that is exhaled by controlling the speed and depth of breathing (ventilation). The amount of carbon dioxide exhaled, and consequently the pH of the blood, increases as breathing becomes faster and deeper. By adjusting the speed and depth of breathing, the brain and lungs are able to regulate the blood pH minute by minute.

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5
Q

What is the role of the kidneys of control of Acid-Base Balance?

A

The kidneys are able to affect blood pH by excreting excess acids or bases. The kidneys have some ability to alter the amount of acid or base that is excreted, but because the kidneys make these adjustments more slowly than the lungs do, this compensation generally takes several days.

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6
Q

What is the Bicarbonate produced and its function?

A

Bicarbonate is produced by the kidneys and acts as a buffer to maintain a normal pH. The normal range for bicarbonate is 22 – 26mmol/l.
If there are additional acids in the blood the level of bicarbonate will fall as ions are used to buffer these acids. If there is a chronic acidosis additional bicarbonate is produced by the kidneys to keep the pH in range.
It is for this reason that a raised bicarbonate may be seen in chronic type 2 respiratory failure where the pH remains normal despite a raised CO2.

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7
Q

What is Base excess?

A

Base excess is the amount of strong acid which would need to be added or subtracted from a substance in order to return the pH to normal (7.40).
A value outside of the normal range (-2 to +2 mEq/L) suggests a metabolic cause for the acidosis or alkalosis.
In terms of basic interpretation
A base excess more than +2 mEq/L indicates a metabolic alkalosis.
A base excess less than -2 mEq/L indicates a metabolic acidosis.

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8
Q

What is the pathophysiology of Respiratory Acidosis?

A

Is Pco2>40 mm Hg (hypercapnia)
Pco2= carbon dioxide partial pressure
Cause is
Decrease in minute ventilation (hypoventilation)

Example:
Decreased ability to breathe due to severe chronic lung disease

Initial Blood pH:
Too Low

Compensatory Mechanism:
Increased excretion of acid in the urine

Compensatory Change in Blood pH:
Increases back toward normal

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9
Q

What is Respiratory Alkalosis?

A

Is Pco2<38 mm Hg (hypocapnia).
Pco2= carbon dioxide partial pressure
Cause is
Increase in minute ventilation (hyperventilation)

Example:
Hyperventilation due to anxiety

Initial Blood pH:
Too High

Compensatory Mechanism:
Increased excretion of alkali in the urine

Compensatory Change in Blood pH:
Decreases back toward normal

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10
Q

What is the pathophysiology Metabolic Acidosis?

A

Is serum HCO3−<24 mEq/L (< 24 mmol/L). HCO3-= bicarbonate.

Causes are:
Increased acid production
Acid ingestion
Decreased renal acid excretion
Gastrointestinal or renal HCO3−loss

Example:
Increased acid production in people with diabetes due to diabetic ketoacidosis

Initial Blood pH:
Too Low

Compensatory Mechanism:
Increased breathing rate to expel carbon dioxide

Compensatory Change in Blood pH:
Increases back toward normal

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11
Q

What is the pathophysiology Metabolic Alkalosis?

A

Is serum HCO3−>28 mEq/L (> 28 mmol/L). HCO3- =bicarbonate.

Causes are:
Acid loss
HCO3−retention
Initial Blood pH: High pH

Example:
Loss of stomach acid due to vomiting

Compensatory Mechanism:
Decreased breathing rate to retain carbon dioxide

Compensatory Change in Blood pH:
Decreases back toward normal

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12
Q

What is an Arterial Blood Gas?

A

Arterial blood gases (ABGs) is a collective term applied to three separate measurements—pH, Pco2, and Po2—generally made together to evaluate acid–base status, ventilation, and arterial oxygenation

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13
Q

What are the common causes of Metabolic Acidosis?

A

Metabolic Acidosis: The body has decreased bicarbonates (less than 22 mEq/L ) in metabolic acidosis and pH less than 7.35.
It can happen due to:
- Increased acid production by the body or the addition of acids from outside.
- Loss of bicarbonate ions due to any reason
When kidneys fail to excrete acids. It can be due to underlying diseases like:
- Diabetic ketoacidosis.
- Severe diarrhoea (loss of HCO3).
- Hypoaldosteronism.
- Acute renal failure (which causes failure to excrete H+).
- Accumulation of acids.
- Lactic acidosis
- Intoxication: Salicylates, methanol, ethylene glycol, formaldehyde, carbon monoxide

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14
Q

What are the common causes of Metabolic Alkalosis?

A

Metabolic Alkalosis:In metabolic alkalosis, the body has decreased acids and pH above 7.45. The primary problem is due to the increase in serum bicarbonate (HCO3-) concentration (more than 26mEq/L), which can be either due to a loss of H+(acid) from the body or a gain in HCO3-(base). It can be due to:
- Severe vomiting resulting in loss of stomach acid
- heavy ingestion of antacids.
- Severe dehydration
- Excess antacids & alkaline drugs.
- Hyperaldosteronism

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15
Q

What is the common causes of Respiratory Acidosis?

A

Respiratory Acidosis:in this condition, there is an increase in the concentration of carbon dioxide ( more than 45 mm/hg) in the body due to the lung’s improper function and hypoventilation. The carbon dioxide that usually leaves the body through exhalation cannot exit the body, and its retention leads to acidosis. The diseases causing respiratory acidosis are:
- CNS depression (anaesthesia).
- Respiratory muscle paralysis
- Diaphragm paralysis,
- Rib fractures
- Obstructive lung diseases e.g. emphysema
- Pulmonary oedema.

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16
Q

What are the common causes of respiratory alkalosis?

A

Respiratory Alkalosis:In this condition, there is a decrease in the concentration of carbon dioxide ( less than 35 mm/hg) in the body due to the lung’s improper function and hyperventilation. Excess carbon dioxide leaves the body due to increased and rapid exhalation. The diseases causing respiratory alkalosis include:
- High altitude (Due to oxygen deficiency)
- Hyperventilation
- Anorexia nervosa
- Early salicylate intoxication

17
Q

What is Anion Gap?

A

Anion Gap = Na+ – (Cl- + HCO3-)
The anion gap is defined as the difference between the plasma sodium concentration (sometimes the sum of the sodium and potassium is used) and the sum of the chloride and bicarbonate

Results from accumulation of organic acids or impaired H+ excretion
- Ketoacidosis, lactic acidosis, chronic kidney disease, or certain toxic ingestion
- Mnemonic CATMUDPILES

18
Q

What is the traditional mneomonic for the causes of a metabolic acidosis with raisd anion gap?

A

‘MUDPILES’
- Methanol
- Uraemia
- Diabetic ketoacidosis (and alcoholic/starvation ketoacidosis)
- Propylene glycol
- Isoniazid
- Lactate
- Ethylene glycol
- Salicylates

19
Q

What is Type 1 respiratory failure?

A

Type 1 Respiratory Failure (Hypoxemic):
Primary Issue: Failure to oxygenate the blood, leading to low oxygen levels.
PaO₂: Less than 60 mmHg (normal: 75-100 mmHg).
PaCO₂: Normal or low (normal: 35-45 mmHg).
Causes:
V/Q mismatch (e.g., pulmonary embolism, pneumonia, asthma).
Shunt (e.g., ARDS, atelectasis).
Diffusion impairment (e.g., interstitial lung disease).
Symptoms: Shortness of breath, cyanosis, confusion.
Treatment: Oxygen therapy, non-invasive ventilation, or invasive mechanical ventilation.

20
Q

What is Type 2 Respiratory failure?

A

Primary Issue: Failure to ventilate properly, leading to both low oxygen and high carbon dioxide levels.
PaO₂: Low (less than 60 mmHg).
PaCO₂: Elevated (above 45 mmHg).
Causes:
Ventilatory failure (e.g., COPD, asthma exacerbations, neuromuscular disorders).
Central respiratory drive impairment (e.g., drug overdose, brain injury).
Obstruction (e.g., severe obesity, chest wall deformities).
Symptoms: Shortness of breath, confusion, drowsiness, headache.
Treatment: Oxygen therapy, ventilation support (e.g., BiPAP, mechanical ventilation).

21
Q

What are the cardiovascular clinical consequences of acidaemia?

A
  • Impaired cardiac contractility
  • Arteriolar dilation
  • Venoconstriction
  • Centralisation of blood volume
  • Increased pulmonary vascular resistance
  • Decreased cardiac output
  • Decreased systemic blood pressure
  • Decreased hepatorenal blood flow
  • Decreased threshold for cardiac arrhythmias
  • Attenuation of responsiveness to catecholamines
22
Q

What are the cardiovascular clinical consequences of Akalaemia?

A
  • Arteriolar constriction
  • Reduced coronary blood flow
  • Reduced anginal threshold
  • Decreased threshold for cardiac arrhythmia
23
Q

What are the Metabolic clinical consequences of Acidaemia?

A
  • Insulinresistance
  • Inhibition of anaerobic glycolysis
  • Reduction in ATP (adenosinetriphosphate) synthesis
  • Hyperkalaemia
  • Protein degradation
  • Bone demineralisation (chronic)
24
Q

What are the Metabolic clinical consequences of Alkalaemia?

A
  • Stimulation of anaerobic glycolysis
  • Formation of organic acids
  • Decreased oxyhaemoglobin dissociation
  • Decreased ionized calcium
  • Hypokalaemia
  • Hypomagnesaemia
  • Hypophosphatemia
25
What are the Neurologic clinical consequences of Acidemia?
* Inhibition of metabolism and cell-volume regulation * Obtundation and coma
26
What are the Neurologic clinical consequences of Alkalemia?
* Tetany * Seizures * Lethargy * Delirium * Stupor
27
What are the Respiratory clinical consequences of Acidemia?
Compensatory hyperventilation with possible respiratory muscle fatigue
28
What are the Respiratory clinical consequences of Alkalaemia?
Compensatory hypoventilation with hypercapnia and hypoxemia