11. Acid-based Regulation Flashcards
State the normal ranges for the main ABGs (arterial blood gases)
Hb (Men): 13.5-17.5 g/dl
Hb (Women): 12.0-15.5 g/dl
pH: 7.35-7.45
pCO2: 4.5-6.0 kPa (34-45 mmHg)
pO2: 10-14 kPa (75-105 mmHg)
HCO3-: 22 - 26mmol/L
CO: <10%
MetHb: <2%
Base excess: -2 < BE < 2 mmol/L
NB: 1 kPa = 7.5 mmHg
Define base excess
In physiology, base excess and base deficit refer to an excess or deficit, respectively, in the amount of base present in the blood
The value is usually reported as a concentration in units of mEq/L, with positive numbers indicating an excess of base and negative a deficit
A typical reference range for base excess is −2 to +2 mEq/L (or mmol/L)
Calculations are based on the Henderson-Hasselbach equation
What is the acid-base status of the patient determined by?
It is determined by the balance between input/loss of acids and bases from the patient (via the lungs and/or kidneys), as well as the products of metabolism, reflected by changes in arterial blood partial pressure
Outline changes in arterial pCO2
Changes in arterial pCO2 should produce changes in alveolar ventilation such that the pCO2 remains within the normal range, thus a normal pCO2 implies a normal alveolar ventilation and chemical control of CO2
o High pCO2 indicates alveolar hypoventilation
o Low pCO2 indicates alveolar hyperventilation
Outline the effect on blood gases of acute respiratory acidosis (uncompensated)
Insufficient ventilation
pCO2 ↑
pH ↓
pO2 ↓
Base excess remains within the normal range
Outline respiratory acidosis
Respiratory acidosis is a medical emergency in which decreased ventilation (hypoventilation) increases the concentration of carbon dioxide in the blood and decreases the blood’s pH (a condition generally called acidosis)
Carbon dioxide is produced continuously as the body’s cells respire, and this CO2 will accumulate rapidly if the lungs do not adequately expel it through alveolar ventilation
Alveolar hypoventilation thus leads to an increased PaCO2 (a condition called hypercapnia)
The increase in PaCO2 in turn decreases the HCO3−/PaCO2 ratio and decreases pH
Acute respiratory acidosis occurs when an abrupt failure of ventilation occurs
Chronic respiratory acidosis may be secondary to many disorders, including COP
Define acidosis
An excessively acid condition of the body fluids or tissues
Outline the effect on blood gases of acute respiratory alkalosis (uncompensated)
Over-ventilation
pCO2 ↓
pH↑
pO2 remains normal (although high, there is no upper limit on the normal range)
Base excess remains within the normal range
Define alkalosis
An excessively alkaline condition of the body fluids or tissues, which may cause weakness or cramp
Define hypercapnia
Hypercapnia, also known as hypercarbia and CO2 retention, is a condition of abnormally elevated carbon dioxide (CO2) levels in the blood
Outline the mechanism of respiratory alkalosis
The mechanism of respiratory alkalosis generally occurs when some stimulus makes a person hyperventilate
The increased breathing produces increased alveolar respiration, expelling CO2 from the circulation
This alters the dynamic chemical equilibrium of carbon dioxide in the circulatory system
Circulating hydrogen ions and bicarbonate are shifted through the carbonic acid (H2CO3) intermediate to make more CO2 via the enzyme carbonic anhydrase according to the following reaction:
HCO3- + H+ –> H2CO3 –> CO2 + H2O
This causes decreased circulating hydrogen ion concentration, and increased pH (alkalosis)
Outline the mechanism of respiratory acidosis
Metabolism rapidly generates a large quantity of volatile acid (H2CO3) and nonvolatile acid
The metabolism of fats and carbohydrates leads to the formation of a large amount of CO2
The CO2 combines with H2O to form carbonic acid (H2CO3)
The lungs normally excrete the volatile fraction through ventilation, and acid accumulation does not occur
A significant alteration in ventilation that affects elimination of CO2 can cause a respiratory acid-base disorder
The PaCO2 is maintained within a range of 35–45 mm Hg in normal states
Outline the Bohr effect
The Bohr effect is a physiological phenomenon first described by Christian Bohr
Haemoglobin’s oxygen binding affinity is inversely related both to acidity and to the concentration of carbon dioxide
Since carbon dioxide reacts with water to form carbonic acid, an increase in CO2 results in a decrease in blood pH, resulting in haemoglobin proteins releasing their load of oxygen
Conversely, a decrease in carbon dioxide provokes an increase in pH, which results in haemoglobin picking up more oxygen
Why does more CO2 make blood more acidic?
Carbon dioxide has the chemical formula CO2
This means that for every one molecule of carbon, there are two molecules of oxygen
When dissolved in water, carbon dioxide forms carbonic acid, H2CO3
Carbon acid can lose two hydrogen atoms, or protons
The loss of protons in a solution is what makes that solution acidic
Outline changes in [HCO3]- concentration and their causes & effects
Changes in the [HCO3]- due to metabolic acids and acid excretion by the kidneys also affects the acid-base status
[HCO3]- is one of two variables that determine [H+] or pH of the blood
The factors which affect the [HCO3]- in the blood are:
o Gaseous - pCO2
o Metabolic - the [HCO3]- falls when metabolic acids (e.g. lactic acid) is buffered
o Renal - the [HCO3]- rises when acid excretion increases, and vice versa
Outline base excess and [HCO3]- concentration
Base excess determines how much of a disturbance to the acid-base status is due to:
o Changes in production/ingestion of metabolic acid
o Changes in excretion of acid by kidneys
The actual [HCO3]- is measured from the patients pH and pCO2, and the difference between this value and the theoretical [HCO3]- (calculated from the patients pCO2, assuming no metabolic or renal disturbances) is the base excess; any change present is solely due to metabolic or renal disturbances
Therefore, if the pCO2 is above or below normal, but the base excess is close to zero (or within the normal range), there is a purely respiratory disturbance
Outline renal compensation with regards to changes in [HCO3]- concentration
Renal compensation; if there is increased metabolic acid levels, [HCO3]- ions buffer this increase
This results in a decrease in [HCO3]- levels in the blood
The kidneys then compensate for this loss, by producing CO2 which forms carbonic acid; this then dissociates into a [HCO3]- ion and a H+ ion (the H+ ion is then transported into the glomerular filtrate, and the bicarbonate ion into the blood)
What are rises/falls in base excess due to?
A rise in base excess is due to:
o An increase in renal excretion of carbonic acid
o Drug administration of a base
o Loss of acid from vomiting
- The result is metabolic alkalosis
A fall in base excess is due to:
o Overproduction of metabolic acids
o Ingestion of an acid
o Reduction/failure of renal acid excretion
- The result is metabolic acidosis
Outline metabolic alkalosis (with respiratory compensation)
Metabolic alkalosis (with respiratory compensation) is seen by an increase in base excess, with a corresponding increase in pH
The pCO2 is also increased as it tries to compensate for the increased pH, which would have been higher if not for this (due to reduced alveolar ventilation)
- pCO2 ↑
- pH↑
- pO2 remains normal
- base excess ↑
Outline metabolic acidosis (with respiratory compensation)
Metabolic acidosis (with respiratory compensation) is seen by a decrease in the base excess with a corresponding fall in pH
The pCO2 is also reduced as it tries to compensate for the reduced pH (increased alveolar ventilation)
- pCO2 ↓
- pH↓
- pO2 remains normal
- base excess ↓
Outline chronic respiratory acidosis (with renal compensation)
Chronic respiratory acidosis (with renal compensation) is seen by a rise in CO2 with only a slight drop in pH accompanied with an increased base excess and reduced pO2
This suggests chronic hypoventilation, which caused the drop in pO2 and rise in pCO2
However, due to this chronic respiratory acidosis, there is an additional acid excretion by the kidney, which accounts for the high base excess and only slightly reduced pH
Often associated with patients with reduced consciousness and reduced ventilation rate
- pCO2 ↑
- pH ↓ (only slight)
- pO2↓
- base excess ↑
Outline chronic respiratory alkalosis (with renal compensation)
Chronic respiratory alkalosis (with renal compensation) is seen by a drop in pCO2 with corresponding increase in pH
However increase in pH only slight due to reduced acid excretion by kidneys in order to try and compensate for the alkalosis
Often associated with hyperventilation and anxiety etc.
- pCO2 ↓
- pH ↑ (only slight)
- pO2 remains normal
- Base excess ↓
What are the 3 main types of respiratory failure?
Type II respiratory failure
Type I respiratory failure
Combined respiratory failure
Outline Type I respiratory failure
Type I respiratory failure:
- pCO2 remains normal (adequate ventilation)
- pH remains normal
- pO2 ↓ (arterial hypoxaemia due to inadequate oxygenation and hence perfusion)
- Base excess remains normal
Define hypoxaemia
An abnormally low concentration of oxygen in the blood
Outline Type II respiratory failure
Type II respiratory failure:
- pCO2 ↑ (indicates inadequate alveolar ventilation)
- pH ↓
- pO2 ↓
- Base excess remains normal
Outline combined respiratory failure
Combined respiratory failure:
- pCO2 ↑ (not as high as in type II)
- pO2 ↓ (greatly reduced; more in than type I and type II)
Outline the treatment options for respiratory failure
Treatment of the underlying cause is required
Endotracheal intubation and mechanical ventilation are required in cases of severe respiratory failure (PaO2 less than 50 mmHg)
Respiratory stimulants such as doxapram are rarely used, and if the respiratory failure resulted from an overdose of sedative drugs such as opioids or benzodiazepines, then the appropriate antidote (naloxone or flumazenil, respectively) will be given
Outline the V/Q ratio and relate it to respiratory failure
In respiratory physiology, the ventilation/perfusion ratio (V/Q ratio) is a ratio used to assess the efficiency and adequacy of the matching of two variables:
V (ventilation) - the air that reaches the alveoli
Q (perfusion) - the blood that reaches the alveoli via the capillaries
The V/Q ratio can therefore be defined as the ratio of the amount of air reaching the alveoli per minute to the amount of blood reaching the alveoli per minute; a ratio of volumetric flow rates
These two variables, V & Q, constitute the main determinants of the blood oxygen (O2) and carbon dioxide (CO2) concentration
The V/Q ratio can be measured with a ventilation/perfusion scan
A V/Q mismatch can cause a type 1 respiratory failure
Outline ‘V/Q mismatch’
Ventilation Perfusion mismatch or ‘V/Q defects’ are defects in total lung ventilation perfusion ratio
It is a condition in which one or more areas of the lung receive oxygen but no blood flow, or they receive blood flow but no oxygen due to some diseases and disorders
The V/Q ratio of a healthy lung is approximately equal to 0.8, as normal lungs are not perfectly matched, which means the rate of alveolar ventilation to the rate of pulmonary blood flow is roughly equal
The ventilation perfusion ratio can be measured by measuring the A-a gradient (i.e. the alveolar-arterial gradient)
Outline pulmonary shunts
A pulmonary shunt is a pathological condition which results when the alveoli of the lungs are perfused with blood as normal, but ventilation (the supply of air) fails to supply the perfused region
In other words, the V/Q ratio (the ratio of air reaching the alveoli to blood perfusing them) is zero
A pulmonary shunt often occurs when the alveoli fill with fluid, causing parts of the lung to be unventilated although they are still perfused
Intrapulmonary shunting is the main cause of hypoxaemia (inadequate blood oxygen) in pulmonary oedema and conditions such as pneumonia in which the lungs become consolidated
The shunt fraction is the percentage of blood put out by the heart that is not completely oxygenated
In pathological conditions such as pulmonary contusion, the shunt fraction is significantly greater and even breathing 100% oxygen does not fully oxygenate the blood
Outline pulmonary contusions
A pulmonary contusion, also known as lung contusion, is a bruise of the lung, caused by chest trauma
As a result of damage to capillaries, blood and other fluids accumulate in the lung tissue
The excess fluid interferes with gas exchange, potentially leading to inadequate oxygen levels (hypoxia)
Unlike pulmonary laceration, another type of lung injury, pulmonary contusion does not involve a cut or tear of the lung tissue
Outline pulmonary lacerations
A pulmonary laceration is a chest injury in which lung tissue is torn or cut
An injury that is potentially more serious than pulmonary contusion, pulmonary laceration involves disruption of the architecture of the lung, while pulmonary contusion does not
Pulmonary laceration is commonly caused by penetrating trauma but may also result from forces involved in blunt trauma such as shear stress
Outline the use of ‘equivalents’ as a unit
An equivalent (Eq) is the amount of a substance that reacts with (or is equivalent to) an arbitrary amount of another substance in a given chemical reaction
It is an archaic unit of measurement that was used in chemistry and the biological sciences in the era before researchers knew how to determine the chemical formula for a compound; the mass of an equivalent is called its equivalent weight
In a more formal definition, the equivalent is the amount of a substance needed to do one of the following:
o To react with or supply one mole of hydrogen ions (H+) in an acid–base reaction
o To react with or supply one mole of electrons in a redox reaction
In practice, the amount of a substance in equivalents often has a very small magnitude, so, especially in medicine, it is routinely described in terms of milliequivalents
Today, mmol/L is much more common than mEq/L
Outline the A-a gradient
The Alveolar-arterial gradient ‘(A-aO2’ or ‘A-a gradient’), is a measure of the difference between the alveolar concentration (A) of oxygen and the arterial (a) concentration of oxygen
It is used in diagnosing the source of hypoxaemia
It helps to assess the integrity of alveolar capillary unit
For example, in high altitude, the arterial oxygen PaO2 is low but only because the alveolar oxygen (PAO2) is also low; however, in states of ventilation perfusion mismatch, such as pulmonary embolism or right-to-left shunt, oxygen is not effectively transferred from the alveoli to the blood which results in elevated A-a gradient
A-a gradient = PAO2 - PaO2
Where:
o PAO2 = pp. of alveolar oxygen
o PaO2 = pp. of arterial oxygen
A normal A-a gradient for a young adult non-smoker breathing air, is between 5–10 mmHg; normally, the A-a gradient increases with age; for every decade a person has lived, their A-a gradient is expected to increase by 1 mmHg; a conservative estimate of a normal A-a gradient is:
normal A-aO2 = < [age in years/4] + 4
Thus, a 40-year-old should have an A-a gradient less than 14
Contrast the causes of both type I and type II respiratory failure respectively
Causes of Type I respiratory failure mainly comprise of diseases which damage lung tissue, including:
o Pulmonary oedema
o Pneumonia
o Acute respiratory distress syndrome
o Chronic pulmonary fibrosing alveolitis
Causes of Type II respiratory failure:
o Chronic obstructive pulmonary disease (COPD); this is the most common cause
o Chest-wall deformities
o Respiratory muscle weakness (e.g. Guillain-Barre syndrome)
o Central depression of the respiratory centre (e.g. heroin overdose)
