Blood Gases Flashcards

(43 cards)

1
Q

Why blood gases are important for physiologists

A

Oxygen service – primarily to monitor hypoxia, however also monitor CO2 retention is patients who utilise the ‘hypoxic drive’

Sleep service

Hypo/normocapnic patients includes some patients with CSA and those with a Cheyne-Stokes breathing (CSB) pattern
Hypercapnic patients have high normal or elevated wake PaCO2which may rise further in sleep. This includes patients with CSA due to drug or substance and primary CSA of infancy. This group also includes patients with obesity hypoventilation syndrome, thoracic cage disorders, neuromuscular disorders and other hypoventilation syndromes

NIV – to monitor CO2 retention and hypoxia and titrate pressures accordingly

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2
Q

Hypoxaemia terminology

A
  • ↓ Blood O2
    • Decreased PO2
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3
Q

Hypoxia terminology

A
  • Decreased SaO2
    • ↓ Tissue O2
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4
Q

Signs and symptoms of hypoxia

A

Restlessness, confusion
Tachypnoea, dyspnoea
Tachycardia, dysrhythmia, hypertensive
Clubbing – Area of Scientific Debate
Right heart failure
General physical appearance

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5
Q

Hypocapnia / Hypercapnia

A

Decreased PCO2 / Increased PCO2

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6
Q

Signs and Symptoms of Hypercapnia

A

Visual : dimmed sight

Respiratory : SOB

Muscular : tremor

Heart : increased heart rate and blood pressure

Skin : sweating

Central : drowsiness, mild narcosis, dizziness. confusion, headache, unconsciousness

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7
Q

pH

A
  • Measure of acidity or alkalinity
    (hydrogen ion activity)
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8
Q

Alkalaemia/ Acidaemia

A

Increased pH / decreased pH

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9
Q

Measured parameters

A

pH
reference range 7.35 - 7.45

Partial pressure of carbon dioxide (pCO2)
reference range 4.7 - 6.0 kPa

Partial pressure of oxygen (pO2)
reference range 11 - 14 kPa

Serum Bicarbonate (HCO3-) [AKA: Standard Bicarb]
reference range 22 - 26 mmol/L

Base Excess (BE)
reference range -3 to 3 mmol/L
The base excess is defined as the amount of H+ ions that would be required to return the pH of the blood to 7.35 if the pCO2 were adjusted to normal.

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10
Q

What is pH?

A

pH is defined as the negative logarithm to base 10 of the hydrogen ion concentration.

pH = -log10 [H+]

Normal reference range 7.35 - 7.45.
Measure of acidemia or alkalemia and is vital to the diagnosis and management of a wide range of conditions.
Outside the acceptable range of pH, proteins are denatured and digested, enzymes lose their ability to function, and death may occur.

H+ reference range is 35–45 nmol/L (nM)
An 0.1 unit fall in pH from 7.4 to 7.3 represents a 25% increase in [H+]

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11
Q

Acid/Base Balance

A

pH is primarily regulated by factors in the Henderson-Hasselbalch equation and “buffering”

pH = pK + log [HCO3-]
α x pCO2

pK = acid dissociation constant
a= the CO2solubility coefficient (derived from Henry’s law – 0.03).
HCO3- from lungs
pCO2 from lungs

Numerator change = metabolic acidosis (reduced HCO3-) or metabolic alkalosis (elevated HCO3-);
Denominator change = either respiratory alkalosis (reduced PaCO2) or respiratory acidosis (elevated PaCO2).

The pK’a value is dependent on the temperature, [H+] and the ionic concentration of the solution. It has a value of 6.099 at a temperature of 37C and a plasma pH of 7.4. At a temperature of 30C and pH of 7.0, it has a value of 6.148. For practical purposes, a value of 6.1 is generally assumed and corrections for temperature, pH of plasma and ionic strength are not used except in precise experimental work.

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12
Q

Which Systems are Involved in Acid/Base Balance?

A

The acid/base status is controlled by a balance between 3 primary functions:
Chemical Buffering (i.e. Carbonic Acid - Bicarbonate System)
Respiratory buffering control of CO2.
Metabolic, Renal control of HCO3-.

These components are used to distinguish between Respiratory and Metabolic disturbances of the acid/base status.

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13
Q

Buffers in blood

A

The most important pH buffer is the Carbonic Acid - Bicarbonate System
CO2 + H20 <-> H2CO3 <-> H+ + HCO3-

Excess carbonic acid can be converted into carbon dioxide gas and exhaled through the lungs; this prevents too many free hydrogen ions from building up in the blood and dangerously reducing its pH

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14
Q

Mechanism of carbonic acid - bicarbonate system

A

The major buffer system in the ECF is the CO2-bicarbonate buffer system. This is responsible for about 80% of extracellular buffering. It is the most important ECF buffer for metabolic acids but it cannot buffer respiratory acid-base disorders.
Carbonic acid is an intermediate step on the transport of CO2out of the body viarespiratory gas exchange. The hydration reaction of CO2is generally very slow in the absence of a catalyst, butred blood cellscontaincarbonic anhydrase, which both increases the reaction rate and dissociates a hydrogen ion (H+) from the resulting carbonic acid, leavingbicarbonate(HCO3−) dissolved in theblood plasma. This catalysed reaction is reversed in the lungs, where it converts the bicarbonate back into CO2and allows it to be expelled.

When bicarbonate ions combine with free hydrogen ions and become carbonic acid, hydrogen ions are removed, moderating pH changes. Similarly, excess carbonic acid can be converted into carbon dioxide gas and exhaled through the lungs; this prevents too many free hydrogen ions from building up in the blood and dangerously reducing its pH; likewise, if too much OH–is introduced into the system, carbonic acid will combine with it to create bicarbonate, lowering the pH

Because carbon dioxide is non-polar, it cannot dissolve in the bloodstream to travel to the lungs. As such,carbonic anhydraseconverts carbon dioxide and water into carbonic acid, which is polar and thus can travel through the body. In the lungs, carbonic anhydrase converts carbonic acid back into water and carbon dioxide to expel carbon dioxide through the lungs without losing water.

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15
Q

Bicarbonate Control

A

The concentration of HCO3- is controlled by the Kidneys.
The regulation of HCO3- takes hours to days to affect the acid/base balance.
Bicarbonate can be the key to assessing whether a blood gas result is acute, chronic or acute-on-chronic.
If this form of pH modulation is prolonged it may/will lead to renal failure – Kidneys are working considerably harder than usual.

Acute = I.e. someone having an asthma attack. Chronic = I.e. someone with long standing COPD. Acute on Chronic – i.e. someone with COPD having an exacerbation. Acute on chronic typically presents as respiratory failure with partial compensation and particularly deranged PO2/PCO2

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16
Q

Metabolic and respiratory components of carbonic exchange

A

Resp component:
Intracellular metabolism produces metabolites that form acids in water (Carbonic Acid)

Approximately 98% of this acid load is in the form of CO2
CO2 + H2O  H2CO3

Excess CO2 is exhaled by the lungs

Metabolic component:
Function of the kidneys

Base bicarbonate: Na HCO3

Process of kidneys excreting H+ into the urine and reabsorbing HCO3- into the blood from the renal tubules 1) active exchange Na+ for H+ between the tubular cells and glomerular filtrate 2) carbonic anhydrase is an enzyme that accelerates hydration/dehydration CO2 in renal epithelial cells

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17
Q

How does the kidney participate in homeostasis

A

The kidney participates in whole-body homeostasis, regulating acid base balance, electrolyte concentrations, extracellular fluid volume, and regulation of blood pressure. The kidneys have two very important roles in maintaining the acid-base balance: to reabsorb bicarbonate from urine, and to excrete hydrogen ions into urine. The kidney can correct any imbalances by:
Removing excess acid (hydrogen ion) or bases (bicarbonate) in the urine and restoring the bicarbonate concentration in the blood to normal

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18
Q

The Partial Pressure of a Gas

A

The pressure (Tension) of an individual gas in a mixture is referred to as a partial pressure.
The pressure of a mixture of non-reacting gases is the sum of the partial pressures of its constituents. (Dalton’s law of partial pressures).
e.g. the atmosphere contains 20.9% oxygen and has a pressure of 101 kPa therefore:

pO2 = 20.9 x (101-6.3) kPa = 19.8kPa
100

19
Q

Arterial Blood Gas sampling

A

Radial artery the most common site.
Purpose designed ABG Syringe.
~2mL blood.
Lithium Heparin anticoagulant
Eliminate air bubbles.
Rapid analysis (<5min) or on ice water slurry.

20
Q

ABG Alternative

A

ABGs often used in acute settings in which blood gas status requires urgent assessment – Painful for patient!
Capillary Blood Gas (CBG) samples are an acceptable alternative in non-urgent situations (i.e. O2 assessment, NIV outpatient visit)
Earlobe must be adequately vascularised i.e. warmed with a heat source or use of transvasin cream
Equally accurate for PCO2 but PO2 can be underestimated by 0.5-1.0kPa on CBG

21
Q

Arterial Blood Gas Levels

A

Blood gas levels depend upon gases passing from an area of high partial pressure to an area of low partial pressure.
e.g. A high pressure of O2 in alveolar gas causes O2 to diffuse into the pulmonary capillary blood.
In this “oxygen cascade” diagram below a PaO2 <55mmHg will result in tissue hypoxia that produces organ damage.

22
Q

Chemo-receptors and control of ventilation

A

Central chemo-receptors in blood-brain barrier are [H+] sensitive -> drives respiratory accelerator centre.
Hypoxic receptors in carotid bodies drive apneustic centre. [H+] receptors drive “pneumotaxic” centre.
With voluntary, emotional, limbic and humeral control over-riding these.
Hypercapnia causes a significant swing in ventilation when compared with hypoxia.

23
Q

Oxygen Homeostasis

A

Normal range 11 - 14kPa.
Oxygen homeostasis is dependent upon a number of factors:
Inspired oxygen concentration (FiO2).
Inspired oxygen partial pressure.
Tidal volume (VT) Alveolar ventilation (VA).

Homeostasis The property of a system that regulates its internal environment and tends to maintain a stable, constant condition of properties like temperature or pH.

In thenormallung, the V and the Q arenot equal, the normal ratio is about 0.8.This is due to two main reasons:gravityandair. The diagram to the right can be simplified as follows. There is more air in the top of the lung, and there is more blood in the bottom of the lung (because of gravity). This means that some of the blood in the bottom of the lung is not oxygenatedandsome of the air in the top ofthe lung does not have its oxygen extracted.This concept is critical to understand. Disruptions of V and Q are how pulmonary embolisms, pneumonia, and other lung pathologies kill patients.

24
Q

What’s the atmosphere in the alveolus?

A

The amount of CO2 is a function of;
-CO2 production (metabolism)
- CO2 Unloading
- And minute alveolar ventilation

CO2 production is constrained by metabolism

Alveolar ventilation is a function Vd/Vt

If alveolar CO2 increases -> causing CO2 retention then in the tissues, PAO2 must also decrease. Displacement of oxygen molecules by CO2 molecules.

25
Carbon Dioxide Homeostasis
Normal range 4.7 - 6.0 kPa.. The PaCO2 reflects the balance between the metabolic rate and alveolar ventilation. Carbon dioxide is produced during aerobic metabolism of glucose. Carbon dioxide is highly soluble in body tissues. Carbon dioxide is excreted by the lungs. PaCO2 is inversely related to alveolar ventilation. Any increase in PaCO2 is will most likely be due to a failure of ventilation rather than diffusion
26
Respiratory Failure
Type I Reduced PO2 (< 8.0 kPa) and Normal PCO2 Type II Reduced PO2 (< 8.0 kPa) and Increased PCO2 (> 6.7 kPa) Acute hypercapnic respiratory failure develops over minutes to hours. The pH is usually therefore less than 7.3. Chronic respiratory failure develops over several days or longer. There is sufficient time for renal compensation and an increase in bicarbonate so the pH is usually only slightly decreased.
27
Respiratory Acidosis
Think of CO2 as an acid Failure of the lungs to exhale adequate CO2 pH < 7.35 PCO2 > 6.0 kPa CO2 + H2CO3   pH
28
Causes of Respiratory Acidosis
emphysema drug overdose narcosis respiratory arrest airway obstruction All cause a drastic reduction in ventilation -> CO2 retention -> Acidosis
29
Metabolic Acidosis
Failure of kidney function, due to decreased ability of the kidney to excrete sufficient acid or conserve enough base  blood HCO3 due to kidney dysfunction pH < 7.35 HCO3 < 22 - May see a drop in PCO2 – Respiratory Compensation to ‘blow off’ more CO2 and normalise pH. Limited effect.
30
Causes of Metabolic Acidosis
renal failure diabetic ketoacidosis - ↓ insulin = fat metabolism = ↑ketones (not producing enough insulin so cells metabolise fats instead of glucose). lactic acidosis excessive diarrhea - loss of base reserves cardiac arrest
31
Respiratory Alkalosis
too much CO2 exhaled (hyperventilation)  PCO2, H2CO3 insufficiency =  pH pH > 7.45 PCO2 < 4.7 kPa
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Causes of Respiratory Alkalosis
Hyperventilation / dysfunctional breathing Panic Pain Pregnancy (oxygen consumption and carbon dioxide production increase 20-30% by the third trimester and up to 100% during labor, necessitating increased minute ventilation to maintain normal acid base status. In addition, progesterone directly stimulates the central respiratory center causing a further increase in minute ventilation. ) Acute anemia Salicylate (aspirin) overdose - Direct respiratory centre stimulation All typically cause increased ventilation -> reduced PCO2 -> Alkalosis
33
Metabolic Alkalosis
 plasma bicarbonate pH > 7.45 HCO3 > 26 May see increase in PCO2 – Respiratory Compensation to retain more CO2 and normalise pH. Limited effect.
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Causes of Metabolic Alkalosis
 loss acid from stomach or kidney i.e. vomiting Hypokalemia Low blood potassium levels -> Sodium retention in Kidney Excessive alkali intake i.e. excessive intake of bicarbonate for stomach hyperacidity
35
Example of typical clinical progression in COPD with emphysema
Early disease Worsening airway fn Extensive emphysema PO2 Normal Mild hypoxia Tissue hypoxia PCO2 Low-Normal Rising CO2 worse on ex Increased PCO2 pH Normal Falling pH Normal pH HCO3 Normal Normal Increased HCO3 End stage Profound hypoxia CO2 retention decreased pH slightly raised HCO3
36
Four-step ABG Interpretation
Step 1: Examine PO2 & SaO2 Determine FiO2 – Vital to know if patient is on supplementary O2. Low PO2 (<10.6 kPa) and/or low SaO2 means hypoxia Normal/elevated oxygen means adequate oxygenation Step 2: pH acidosis <7.35 alkalosis >7.45 Step 3: study PCO2 & HCO 3 respiratory irregularity if PCO2 abnormal & HCO3 normal metabolic irregularity if HCO3 abnormal & PCO2 normal Step 4: Determine if there is a compensatory mechanism working to try to correct the pH. Example: Respiratory acidosis Acute (non compensated) respiratory acidosis will have increased PCO2 and decreased pH. In chronic respiratory acidosis (COPD) compensation occurs when the kidneys retain HCO3. pH will return towards normal, HCO3 will increase, PCO2 will remain elevated
37
~ PCO2 – pH Relationship
PaCO2 pH 10.7 7.20 8.0 7.30 5.3 7.40 4.0 7.50 2.7 7.60 Effect of differing PCO2 on pH in absence of compensatory mechanisms
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Normal arterial PO2 10 – 13.3 kPa Normal arterial PCO2 4.6 – 6.0 kPa
39
Arterial blood gases are sampled by brachial or radial artery puncture. Where repeated samples are required arterialised ear-lobe sampling will produce a sample very similar to an arterial sample. Normal values PO2 10.0 – 13.3 kPa pH 7.35 – 7.45 PCO2 4.6 – 6.0 kPa Base Excess (BE) -5 – 5 mmol Standard Bicarbonate (HCO3) 20 – 30 mmol
40
The elimination of CO2 is of great importance in the regulation of acid base balance
CO2 + H2O H2CO3, The lungs are the most important organ in the body for acid excretion. Normally this ratio is maintained by the pulmonary ventilation which keeps arterial PCO2 at 5.3 kPa. Whenever arterial PCO2 tends to rise, the medullary respiratory centre is stimulated, alveolar ventilation is increased and the PCO2 is restored to normal. This delicate mechanism only operates when the sensitivity of the respiratory centre and the respiratory muscles are intact, the respiratory muscles are normal and the lung is not seriously diseased. Whenever hypoventilation occurs, either because of depression of the neuromuscular mechanism or because of mechanical limitations, CO2 must accumulate in the blood
41
Four types of disturbance may be observed
Respiratory acidosis Respiratory alkalosis Non-respiratory acidosis Non-respiratory alkalosis
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OXYGEN THERAPY
An adequate supply of oxygen is essential for the proper function of every tissue in the body. It is normally provided by mechanical operations of the physiological mechanisms of the lungs. The lack of oxygen (hypoxia) is most pronounced in the grey matter of the central nervous system. Complete lack of oxygen for as little as two minutes may lead to cell death. Deficiency of oxygen may be due to a reduction in partial pressure of oxygen in the inspired air or it may arise at any stage in the process of transfer of oxygen from the atmosphere to the mitochondria in the tissue cells. What may cause a deficiency of oxygen supply to the cells? 1 Blocked air way due to physical obstruction or laryngeal spasm 2 Deficiency of oxygen in inspired gas due to reduced barometric pressure or reduced oxygen concentration in a confined space leading to exhaustion of oxygen supply 3 Hypoventilation. This may be caused by a reduced central drive to respiration, weakness on respiratory muscles or increased work of breathing 4 Miss match between ventilation and perfusion. This may be caused by airflow obstruction, reduced lung compliance, abnormal distribution of pulmonary blood flow, right to left shunt 5 Reduced blood flow due to low cardiac output or local disturbance of blood flow 6 Interference with the transport of oxygen due to carbon monoxide poisoning or reduced haemoglobin.
43
Hypoxaemia increases the chemoreceptor drive to respiration. In normal subjects this leads to hyperventilation which should restore the partial pressure of oxygen to a normal level.