Blood Gases What are they and why do we use them? Follow up in tutorial in week 12 CResp Week_10_Lecture 2_10_11 1

Blood Gases

What are they and why do we use them?

Follow up in tutorial in week 12

CResp Week_10_Lecture 2_10_11 1

Session Plan Different types of blood gas

analysis Arterial Venous Capillary

Clinical uses of arterial blood gases

Oxygenation of the blood Efficiency of ventilation (mainly CO2 removal)

Introduction to hyperventilation and it’s effects Acid/base status – simple pictures

Follow up in tutorial 2 in week 12CResp Week_10_Lecture 2_10_11 2

Type I and Type II respiratory failure

Methods of obtaining blood for gas analysis

Arterial Arterial stab

puncture of radial (or other) artery Indwelling arterial line

Capillary Primarily neonatal and paediatric use Becoming more common for adult patients with chronic

disease as less invasive than an arterial stab pH and PaCO2 more accurate but PaO2 has 0.4 kPa variance

Venous Indwelling venous line Brief cannulation of a vein (easier than an arterial stab) Less invasive but limitations to usefulness


Information on an arterial blood gas (ABG)

pH PaCO2

PaO2

HCO3-

BE SaO2


pH revisited Reflection of the hydrogen ion

concentration (-log [H+]), i.e. how acidic the blood is

Linked to CO2 by the equation: CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3

-

Normal pH for the body is 7.4 Normal range in the body is 7.35 - 7.45 i.e. how ‘acidotic’ (<7.4) or ‘alkalotic’

(>7.4) the blood is


PaCO2

Partial pressure of CO2 in blood (‘a’ means arterial) CO2 will affect acid-base balance and therefore pH, from

the equation: CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3

-

Normal values 4.7-6.0 kPa (35-45 mm Hg)

The HCO3- generated by CO2 is only small in comparison

to the overall HCO3- concentration

The body has a large reserve of HCO3- the form of

sodium bicarbonate (NaHCO3)


PaO2

Partial pressure of oxygen in arterial blood

Normal values 11-14 kPa (80-100 mm Hg)

Atmospheric PaO2 ~ 20 kPa (1 kPa ~ 7.6 mmHg)

Remember the Hb dissociation curve


SaO2 Saturation of haemoglobin with oxygen in arterial blood

Extent to which haemoglobin in arterial blood is saturated with oxygen measured on an arterial blood sample

Normal values 95-98%

SpO2 can be measured via pulse oximeters

saturation of arterial blood in the peripheries


HCO3-

HCO3- = Bicarbonate ion concentration

Normal value 22-26 mmol/L

St HCO3- = Standard Bicarbonate – the

plasma bicarbonate concentration that would be present if the PaCO2 was normal Accounts for the respiratory influence on HCO3

- and so enables metabolic component to be determined


BE – Base Excess Reflects the NON respiratory side of acid-base balance as it

takes the buffering capabilities of the RBC into account and hence the amount of

Quantity of strong acid or base required to restore pH to normal at normal paCO2◦ Negative value indicates acid has been added or base removed -

there is a base deficit – therefore shows metabolic acidosis◦ Positive value indicates acid has been removed or base added - base

is present in excess therefore shows metabolic alkalosis More complete analysis of buffering than HCO3

- alone (equivalent to standard deviation of the Standard HCO3

-) Acute changes in HCO3- from an increase/decrease in CO2 are not

reflected in the BE – it is a pure reflection of the metabolic contribution to HCO3

- rise or fall Normal value: – 2 to + 2 mmol/L


Normal ranges of Arterial Blood Gases

pH 7.35-7.45 paCO2 4.7-6 kPa paO2 11-14 kPa HCO3

- 22-26 mmol/L BE +2 to -2 SaO2 95-98%


Normal Values of Venous Blood Gases (for reference only)

For reference, sometimes taken when arterial sample is difficult to get (or accidentally!)

pH 7.34 – 7.37 PvCO2 5.8 - 6.1 kPa (44 – 46 mmHg) PvO2 5.0 – 5.5 kPa (38 – 42 mmHg) HCO3

- 19 - 24 mmol/L SvO2 ~ 75%

i.e. more acidotic, richer in CO2, and less O2 content when compared to arterial sample

Is a reflection of cardiac output and tissue metabolism not only lung function.


Capillary Blood

Gives a reasonably accurate indication of arterial pH and PaCO2 BUT the PaO2 has a variance of approximately 0.4 kPa.

Use is increasing outside the neonatal field

More acceptable for showing trends in blood gas analysis over time – not reliable for a ‘snapshot’ analysis


Clinical assessment of ABGs

Oxygenation must know FiO2 = fraction of inspired

oxygen Efficiency of ventilation

(mainly reflected in the PaCO2) hence type of Respiratory failure

Acid-base status/balance and whether the derangement is respiratory or metabolic in origin


Oxygenation

FiO2 = fraction of inspired oxygen Room air =0.21 i.e. 21%

PaO2 and SaO2

Either normal or low Unless FiO2 is greater than air when they

maybe raised (but SaO2 never greater than 100%!)


Efficiency of ventilation Removal of CO2

Look at PaCO2

Can be up or down


Summary: Control of respiration

Central receptors medullary receptors sensitive to H+ from CO2

which results in an increase in the rate and depth of respiration with rising levels of CO2 and H+

Peripheral receptors Carotid bodies sensitive to

↓ PaO2 < 8-9 kPa ↑ PaCO2 but less so than central receptors ↑ H+ especially if this is metabolic in origin


Efficacy of ventilation/ CO2 removal

Under ventilation of the alveoli leads to ↑paCO2 (and hence acidosis due to increase in H+ )

Hypercapnia/ hypercarbia

Causes Hypoventilation globally

Respiratory centre pathology (e.g. tumour/head injury/stroke)

Drug overdose (e.g. narcotics) Failure of respiratory mechanics

Hypoventilation of alveoli locally resulting in V/Q mismatch

Secondary to consolidation/collapse Mechanisms in week 12CResp Week_10_Lecture

2_10_11 18

Efficacy of ventilation/CO2 removal

Over ventilation of the alveoli relative to tissue metabolism causes ↓PaCO2

Hypocapnia/ hypocarbia

Causes: Increased respiratory drive because of:

Respiratory centre pathology Psychological factors Hyperventilation syndrome (HVS)

CO2 receptors become reset to stimulate an increase in ventilation at a lower level than normal

Hypoxaemia (detected by aortic and carotid bodies)


Hyperventilation

Breathing in excess of metabolic requirements → ↓ PaCO2 → ↑ pH, remember: CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3

-

May be normal physiological acute response to stress

May become chronic, sometimes associated with panic disorders or phobic states Hyperventilation Syndrome (HVS)

ABGs Week_10_Lecture 2_09_10 20

Hyperventilation - Signs and Symptomshttp://www.physiohypervent.org/

Acute Dizziness Paraesthesia – hands, feet, periorally

Chronic - HVS Great imitator Breathlessness on minimal exertion Difficulty taking deep breath Tiredness/ weakness Shoulder/neck pain Chest pain Gastric Oesophageal Reflux (GOR) Nausea Insomnia Anxiety Sighing/ yawning


http://www.physiohypervent.org/

HVS Causes

Often difficult to identify the original factor that sets off the pattern, may be multifactorial

Possible factors: bereavement, chronic pain, withdrawal from

drugs, liver cirrhosis (intracellular acidosis), hypermobility syndrome (mobile thoracovertebral joints), post chest infection


Respiratory Failure

Knowing the levels of oxygen and carbon dioxide in the blood we can determine whether the patient is in what in medicine is defined as Respiratory Failure


Respiratory Failure (RF)

= Failure of oxygenation of the blood (with or without raised carbon dioxide levels)

Caused by inadequate oxygen delivery due to neurological/ mechanical/ chemical dysfunction resulting in a failure of ventilation/gas exchange

Type I respiratory failure - hypoxaemic RF PaO2 < 8KPa PaCO2 = normal or low (why might PaCO2 be LOW if

O2 is low?) Mechanism and clinical examples we will do fully in week 12


Respiratory Failure (RF)

Type II respiratory failure - hypoxaemic & hypercapnic RF◦ PaO2 < 8KPa

◦ AND PaCO2 >6.0KPa (some books 6.5KPa)

Mechanism and clinical examples fully in week 12

Maybe Acute and then may become chronic Precautions of O2 therapy in chronic type II RF

Hypoxic drive theory – wk 12CResp Week_10_Lecture

2_10_11 25

Acid/Base balance

Acidosis - pH < 7.35 (H+ )

Alkalosis pH > 7.45 (H+ )


Clinical Application – remember:

The body needs to keep pH around 7.4 <7.0 and >7.8 for any length of time is

incompatible with life Buffering systems

Chemical Renal Respiratory – the lungs are an integral

part of the removal of H+ ions from the body via ventilation


Causes of Acidosis: ↑ H+ → ↓ pH

Respiratory

Caused by failure of the lungs to remove normal amounts of CO2 generated by the metabolising tissues so ↑ PaCO2 as ↑CO2 causes ↑H+

CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3-

Anything that impairs either gaseous exchange and/or ventilation

Most probably will be in Type II RF as well

Metabolic Caused by either

↑H+ from metabolic acids which overrun the bicarbonate buffer system

↓HCO3- which reduces the

ability of the bicarbonate system to buffer H+

produced from other acids in the body (lactic, ketone bodies etc)

Some causes:◦ Diabetic ketoacidosis◦ Renal disease◦ Sepsis◦ Starvation – protein

metabolism◦ Alcoholic poisoning◦ Cardiac failure◦ Severe diarrhoea – lose

bicarbonate from the gutCResp Week_10_Lecture

2_10_11 28

Causes of Alkalosis - ↑pHRespiratory

Caused by: ventilating at a rate and

depth greater than needed to remove the CO2 produced by tissue metabolism and so causing a decrease in H+

CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3-

Anything that causes hyperventilation

Metabolic Caused by either a

↓H+ or ↑HCO3

- which combine with the H+ in the buffering system and socause a decrease in H+ and so an increase pH

Maybe due to Vomiting Diuretics Constipation Ingestion of HCO3

-


Hence the 4 possible causes of derangement of pH from normal

Respiratory Acidosis- PaCO2 ↑ > 6.0 kPa

Respiratory Alkalosis- PaCO2 ↓<4.7kPa

Metabolic Acidosis- HCO3- <22 mmol/L

Metabolic Alkalosis- HCO3- >26 mmol/L


Clinical Interpretation of ABGs

Stepwise method :-

Look at oxygenation i.e. PaO2 on what FiO2

◦ is the patient in respiratory failure (is the PaO2 below 8KPa)

◦ is it type I or type II?

THEN look at the acid/base balance in relation to PaCO2 and HCO3

-


Interpretation of Acid/base Status

Stepwise :- :-◦ Is the pH acidotic or alkalotic? ◦ Is the PaCO2 up or down?◦ And is this the cause of the derangement in

pH RESPIRATORY OR

◦ Is the HCO3- up or down ?

◦ And is this the cause of the derangement- METABOLIC


Example- Simple PictureRespiratory acidosis

pH 7.27 PaCO2 12.1 kPa PaO2 6.3 kPa HCO3

- 24 mmol/L On 40% oxygen

Clinical diagnosis - # ribs with flail segment Think

Oxygenation? Which type of respiratory failure? Acid/ base derangement Other causes


Example- Simple PictureRespiratory alkalosis


- 22 mmol/L On 2 l/min O2 via nasal cannulae

Patient with lobar pneumonia Think:

Oxygenation → which type of respiratory failure? Why is PaCO2 low? Acid/ base derangement? Other causes of these figures


Example- Simple PictureMetabolic acidosis


- 4.8 mmol/L On 40% oxygen

Patient with known diabetes mellitus and a urinary tract infection

Think Oxygenation ? Is the patient in respiratory failure? Acid/ base derangement? This patient will be tachypnoeic – WHY? Other causes CResp Week_10_Lecture

2_10_11 35

Example- Simple PictureMetabolic alkalosis

pH 7.48 PaCO2 5.6 kPa PaO2 15 kPa HCO3

- 34 mmol/L On room air (FiO2 0.21)

Patient has been vomiting for 24 hours Think

Oxygenation? Is the patient in respiratory failure? Acid/ base derangement? Other causes


Compensation and Mixed Pictures in ABGs

When pH is altered due to respiratory or metabolic disturbance the other system will make a compensatory change to normalise the pH

The body strives to maintain pH around 7.4

Buffering systems Chemical Respiratory Renal

Revisit physiology wk 8 tute and this lecture

To be discussed in more detail in the tutorial 2 in week 12


Conclusion Different types of blood gas analysis Clinical uses of arterial blood gases Type I and Type II respiratory failure

and contributing factors Tutorial in week 12

Discuss the pathophysiological mechanisms that cause RF

Practice analysing clinical examples of ABGs Compensated and mixed cases


Learning Outcomes indicate the normal values for arterial blood gas

analysis recognise the four major deviations from the normal begin to understand the clinical relevance of the

interpretation of blood gases discuss the arterial blood gas changes in types I and

II respiratory failure. recognise the signs and symptoms of

hyperventilation syndrome identify the causes of hyperventilation syndrome


Bibliography Davies, A & Moores, C. (2003). The respiratory

system. Edinburgh. Churchill Livingstone Hough, A. (2001). Physiotherapy in respiratory care.

(3rd ed.). Cheltenham: Nelson Thornes. Pryor, J. A. & Prasad, S. A. (Eds). (2008).

Physiotherapy for respiratory and cardiac problems. (4th ed.). Edinburgh: Churchill Livingstone.

West, J.B. (2005). Respiratory Physiology The Essentials (7th ed). Baltimore: Lippincott

Williams & Wilkins Wilkins, R. L., Sheldon, R. L. & Jones Krider, S. (2005).

Clinical assessment in respiratory care. (5th ed.). St Louis: Mosby.


Documents

Blood Gases What are they and why do we use them? Follow up in tutorial in week 12 CResp Week_10_Lecture 2_10_11 1