Hypercapnia & Hypoxia Flashcards

1
Q

Define hypoxia

A

reduced O2 in tissues

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2
Q

Define hypoxaemia

A

reduced O2 in the blood

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3
Q

List the mechanisms behind hypoxia and hypoxaemia

A

reduced oxygen inspiration

cannot get 02 to lungs

cannot get 02 inot blood

reduced systemic O2

cannot bind to Hb

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4
Q

Provide a list of causes relating to reduced oxygen inspiration

A

Equipment related

Anatomy

Altitude

Hypoventilation

URT Obstruction

Pneumothorax

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5
Q

Provide a list of causes relating to inability to get oxygen into the lungs

A

Equipment

URT Obstruction

Pneumothorax

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6
Q

Provide a list of causes relating to reduced systemic O2

A

Anaemia (see pulse oximetry slide later)

Heart disease (e.g. resulting in output failure)

Hypovolaemia
-Periphery shuts down as preferential shunting to vital organs occur

Extreme vasoconstriction
-In cold environment the periphery is shut down for preferential shunts to vital organs

Sepsis (discussed more in later lectures)

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7
Q

Provide a list of causes relating to oxygen being unable to bind to Hb and/or cannot get off of Hb

A

Haemoglobinopathy

Methemoglobinemia

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8
Q

Provide a list of causes relating not being able to get oxygen into the blood

A

VQ mismatch

Intrapulmonary Shunts

Diffuse alveolar/interstitial disease

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9
Q

Explain how equipment reduces oxygen inspiration and reduces the amount of O2 getting into the lungs

A

Kinked/obstructed ET (endotracheal) tube.
If you have the luxury of a Capnograph, this will be spotted quickly (the wave form will look a bit like a sharks fin).

Obstructed due to a build up of mucous or it could be something physiological such as bronchoconstriction.

Rarely, it could be a kinked or damaged tube on the breathing system. These tubes are normally pretty robust so it wouldn’t be a common problem.

Breathing system may not be working properly due to leak (leak tests down prior to anaethesia)

Issue with oxygen supply

Resolution:
Unkink tube or re-intubate with a new tube.

If it is physiological, treat the root cause.

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10
Q

Explain how anatomy reduces oxygen inspiration

A

BOAS (brachycephalic obstructive airway syndrome)
-narrowed airways mean inspiration of reduced amounts of O2
-doesnt always lead to hypoxia but means higher risk
-airways can become easily obstructed

Resolution:
Short term intubate
Some may require surgery in the long term

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11
Q

Explain how altitude reduces oxygen inspiration

A

Lower atmospheric pressure which means decreased partial pressure of oxygen

Hyperventilation due to low atmospheric pressure

Leads to hypocapnia

An example of the link between CO2 and O2 is how the body compensates for lower atmospheric pressures by hyperventilating.

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12
Q

Explain how hypoventilation reduces oxygen inspiration

A

Results in hypercapnia

Very common cause

Partial pressure of oxygen in the alveoli (PAO2) decreases
Partial pressure of carbon dioxide in the alveoli (PACO2) rises

Resulting in hypercapnia
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13
Q

Explain how URT obstruction reduces oxygen inspiration and reduced the amount of oxygen getting into the lungs

A

Loss of pharyngeal muscle tone
Regurgitation
Vomiting
Laryngospasm
Stick injury
Laryngeal oedema
Tracheal collapse
Foreign body

Depending on the severity of the obstruction there may either be reduced O2 inspired or complete inability to get O2 to the lungs

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14
Q

Explain how pneumothorax reduces oxygen inspiration and reduced the amount of oxygen getting into the lungs

A

Air has reached the lungs but it escapes into the space between lung and chest wall and cannot take part in efficient gas exchange

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15
Q

Explain how Haemoglobinopathy lead to the inability of oxygen binding to Hb

A

Carbon monoxide binds to haemoglobin with much greater affinity and prevents the carriage of oxygen.
Shifts the haemoglobin-oxygen dissociation curve to the left

Exposure to even small concentrations of CO (carbon monoxide) hinder the ability of Hb to deliver oxygen to the body, because carboxyhaemoglobin forms more readily than oxyhaemoglobin (HbO2) does.
Carbon monoxide is produced in normal metabolism and is a common chemical, but excessive exposure can lead to big problems.

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16
Q

Explain how Methemoglobinemia leads to the inability of Hb to remove oxygen

A

Elevated methaemoglobin in the blood, haemoglobin iron is in the oxidized or ferric state and cannot reversibly bind oxygen – paracetamol toxicity
Methaemoglobin is a type of haemoglobin which carries oxygen through the blood but doesn’t release it to the cells
When there is too much methaemoglobin produced, it starts to replace normal haemoglobin, and therefore oxygen is not released and doesn’t reach tissues

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17
Q

Briefly outline some causes of VQ mismatch

A

All lung dysfunction lowers PaO2 via V-Q imbalance, e.g., asthma, pneumonia, atelectasis, pulmonary oedema, horse on its back (common problem in Equine anaesthesia!)

18
Q

Explain the effect of gravity on VQ ratio

A

Since the pressure of blood being pumped into the lungs is so low, where the blood ends up is usually determined by gravity.

Similarly ventilation is affected by gravity however not as significantly .

Positioning makes a difference; in a standing animal with normal lungs, there will be a small degree of V/Q mismatching with minimal perfusion in the dorsal lung fields and higher in the ventral areas.

19
Q

Explain the effect of diffusion abnormalities on VQ ratio

A

Oxygen enters alveolus, then diffuses across the one-cell layer thick epithelium of the lung, then across the one-cell layer thick endothelium, into the pulmonary artery then into the pulmonary capillary bed where gas exchange takes place and then into the pulmonary vein

When there is a diffusion abnormality, it is often caused by a blockage/interstitial deposition between these two areas within the unit. This is often seen in patients with infiltrative disease of the lungs such as pulmonary fibrosis and it hinders the oxygen from diffusing through the unit sufficiently, which can ultimately lead to hypoxaemia.

20
Q

Explain mismatch as a result of a pulmonary embolism

A

Pulmonary artery splits off into various areas of the lungs

If there is a clot formed, it will be pumped in to a specific area and can then get lodged.

As a result, perfusion to a certain segment of the lung is blocked.

That area is then classified as an area of high V/Q because there is very low perfusion.

The blood that would normally go to this area has to go somewhere else, therefore you end up with a low V/Q in multiple areas.

21
Q

Describe how pulmonary shunts affect VQ

A

In the normal lung, oxygen enters the alveoli and raises the saturation from the venous level of 70% to 100% by the time it reaches the arterial side.

In shunt, no oxygen can get into the alveoli, so the venous saturation is never increased.

In low SvO2 situations, the alveoli are not able to raise the low venous saturation to the normal arterial level. When these two problems are both present, the arterial desaturation becomes even worse.

Blood enters the systemic arterial system without going through ventilated areas of lung.

Most caused by cardiac disorders with right to left shunting such as reverse PDA (Patent Ductus Arteriosus)

May also occur when large areas of the lung are not ventilated e.g., atelectasis

22
Q

List some of the consequences of hypoxia/hypoxaemia

A
  • Decreased brain function (including ventilation)
  • Decreased cardiac function (including output)
  • Made worse where there is concurrent hypercapnia
  • Cardiac dysrhythmia
  • Cardiac arrest
23
Q

Outline the importance of tissue perfusion

A

Perfusion of O2 to tissues is one of the basic needs to sustain life.

Brain tissues will die within minutes if their supply of O2 is interrupted.

Tissues of major organs last only 15-20 minutes without O2.

We cannot afford to wait to see if the animal gets better with cage rest, we need to be proactive and aggressive with our treatments to re-perfuse tissue.

24
Q

Discuss some of the presenting signs of hypoxia/hypoxaemia

A

Tachypnoea, increased respiratory effort, tachycardia (common in patients with adequate compensatory ability).

Patients unable to compensate for hypoxaemia (exhaustion, neurologic or neuromuscular disease) may not show outward evidence of respiratory distress due to respiratory muscle weakness

Cyanosis may be detected by the human eye if the hypoxia is particularly bad

Obtundation or coma may occur in patients with prolonged uncompensated hypoxemia

Death

25
Q

Define cyanosis and explain its causes and physiological response

A

Bluish/purplish discolouration of the skin or mucous membranes due to the tissues near the skin surface having low O2 saturation

Cyanosis can be a poor indicator of hypoxia/hypoxaemia as there are many things that may mask the colour change, e.g. pigmented skin. Lighting in the room, anaemia etc.

Remember: if there is cyanosis it is an emergency situation, and the animal is severely hypoxic
- Overrides all other emergencies except arterial bleed
- Give oxygen by some means
- May be normocapnic or hypercapnic or hypocapnic
- The more anaemic the animal, the more hypoxic it must be before cyanosis is detected
- Mouth breathing, air hunger and cyanosis

26
Q

Outline the Respirtory system regulation of pH when acidosis occurs

A

Lower pH stimulates brain and arteriole receptors

respiration rate increase

decreased blood CO2 levels

Decreasing hydrogen carbonate levels which increases pH restoring homeostasis

27
Q

Outline the Respirtory system regulation of pH when alkalosis occurs

A

increase in pH simulates brain and arterial receptors

respiration rate decreases

leading to increased blood CO2 and hydrogen carbonate levels

lowering the pH and restoring the system to homeostasis

28
Q

Outline the meaning of hypercapnia and list a few of the caused

A

An elevation in the CO2 in arterial blood (PaCO2) above the normal range (35-45mmHg= 4.6-6.0 kpa)

Commonly caused by hypoventilation

(not exhaustive) Also:
Hyperthermia

        Respiritory depression
        
        Lung pathology
        
        Increase in metabolic CO2 production (rare)
29
Q

Outline the consequences of hypercapnia

A

Hypoventilation = reduced O2 exchange

Cerebral vasodilation = increased intracranial pressure

Lowers pH (see acid base lectures)

Stimulates CNS, causing tachycardia and vasoconstriction

CNS depression at high PaCO2

Peripheral vasodilation by direct effect on vessels

Promotes dysrhythmias

One of the causes of Hypoxia/hypoxaemia (reduces the amount of O2 carried in the blood)

Ultimately fatal!

30
Q

OUtline the symptoms of high levels of CO2 are seen within the body

A

Visual - dimmed sight

Auditory - reduced hearing

Respiritory - shortness of breath

Muscular - tremor

Central - drowsiness, mild narcosis, confusion, headache, unconsciousness

Skin - sweating

Heart - Increase HR & BP

31
Q

Outline the relationship between O2 *+& CO2 during hypoventilation

A

Increase in PACO2 (hypercapnia) leaves less space for O2 in the alveoli, subsequently displacing O2 and exasperating hypoxia

32
Q

How can hypercapnia be induced and resolved in the short and long term

A

May be caused by drugs (particularly in anaesthetised patients), you will come across this problem regularly in-practice. You can temporarily fix it with IPPV (intermittent positive pressure ventilation), but more importantly, treat the route cause!

Other causes might include CNS disease, neuromuscular disease, cervical spinal cord disease, large airway obstruction and respiratory muscle fatigue

33
Q

Outline the relationship between O2 & CO2 in areas of low atmospheric pressure

A

An example of the link between CO2 and O2 is how the body compensates for lower atmospheric pressures by hyperventilating.

For example, if you were on Mount Everest, you would hyperventilate, in order to bring your CO2 levels down (hyperventilation= Hypocapnia), allowing more space for O2 in the your lungs, subsequently making up for the reduced inspired O2 (although in reality you are likely to require supplemental O2 as well).

Another nice example of the link between these two gases is free-diving; free divers hyperventilate before a dive to bring their CO2 levels down, this takes away their trigger to breath, leaves more O2 in the lungs and allows them to hold their breath for longer. Do not try this! It takes experience and training and can be dangerous.

34
Q

List the factors that cause a right shift on an oxygen dissociation curve

A

Decreased pH (more acidic)

Increased temp

Increased PC02

35
Q

List the equipment needed in the management of hypoxia and hypercapnia

A

Capnography

Blood gas analyser

Pulse Oximetry

Oxygen supply

Management of underlying disease

36
Q

Explain the use of capnography in the management of hypoxia and hypercapnia

A

Using Capnography in anaesthetised patients we can look at the EtCO2 (which is not the same as, but is close to PACO2) and PACO2 is normally approx. 5mmHg below PaCO2).

37
Q

Explain the use of a blood gas analyser in the management of hypoxia and hypercapnia

A

Blood gases are oxygen and carbon dioxide. Therefore, a blood gas test evaluates the amounts of oxygen and carbon dioxide in the blood and the efficiency of our lungs in moving oxygen into the blood and carbon dioxide from the blood.

Arterial blood gas test measures the levels of arterial oxygen and carbon dioxide while venous blood gas measures the levels of oxygen and carbon dioxide in the vein.

The more useful test would be arterial for lung function.
- Venous is useful for metabolic function.

38
Q

Explain the use of a pulse oximeter in the management of hypoxia and hypercapnia

A

Not accurate in anaemic patients

Tells you the saturation of Hb with O2 (info on the Y axis of O2 dissociation curve.

NB: In a healthy patient with a PCV of 45%, cyanosis would not likely be detectable by the naked eye until the pulse ox drops to around 85%. In an anaemic animal with a PCV of 27%, it may not be detectable until approx. 75% saturation.

Remember that the pulse oximeter measures saturation of O2 on Hb, therefore in anaemia, it might read 100% just because the RBC’s that are there might be fully saturated, yet there are not many RBC’s there.

39
Q

Explain the use of oxygen supplies in the management of hypoxia and hypercapnia

A

Increase the O2 supply whatever the cause…in bad cases it might be too late, but it will never make things worse!

You could use nasal tubes, incubators, masks, O2 tents etc.

Be aware of the pitfalls of oxygen tents – they can become hot and make the patient hyperventilate, they also can make you complacent as you think you’re ‘stabilising’ the patient when in fact you can no longer treat or monitor effectively because they’re inside a tent!

40
Q

Explain the management of underlying diseases in the management of hypoxia and hypercapnia

A

Inotropes for heart failure

Intravenous fluids for hypovolaemia

Ventilate 

Ventilate to reduce collapsing of alveoli, increase partial pressure of O2 in alveoli etc.

41
Q

What shouldn’t be used in the management of hypoxia and hypercapnia?

A

NOT to use respiratory stimulants

General CNS stimulants
Increased CNS metabolic oxygen demand
Increased chance of seizures