End Tidal CO₂ Monitoring

Methodology: As anaesthetic depth increases, ventilatory function (minute ventilation = respiratory rate x tidal volume) decreases and therefore CO₂ increases in a dose-dependent fashion. End tidal CO₂ (ETCO₂) monitors continuously sample gas at the endotracheal connector and measure the CO₂ partial pressure using proportional absorption of infra-red light. A continuous wave form can be generated which will demonstrate three phases of expiration during each respiratory cycle: A = dead space gas with no CO₂; B = mixed gas with rising CO₂; C = alveolar gas with a CO₂ plateau from which the ETCO₂ peak value is read. This should correspond to the arterial PaCO₂ in animals that don't have lung disease. An alveolar gas "plateau" may not be obtained in animals with small tidal volumes (e.g., cats). D = the next inspiration - inspired gas should not contain CO₂.

Monitors display the peak ETCO₂ value, respiratory rate, and usually inspired CO₂ value.

Table 1. ETCO₂ values (mm Hg) during anaesthesia with spontaneous ventilation

Physical signs of high CO₂ include high HR, RR, BP and injected, pink mm's.

Side-stream sampling sensor systems are continuously drawing gas via a length of small tube from the airway (ET tube adapter) to an infrared spectrometer located in a distant monitor. This technology is mechanically complex, expensive to maintain (requires a vacuum pump, dehumidification, and real time measurement of pressure drops in the system), and causes waste gas pollution.

Mainstream sampling sensor systems are electronically complex with the optical sensor being located at the ET tube adapter. This has been made possible by improved optics and miniaturisation. The main disadvantages were cost, size sensors increasing dead space, and fragility. New technology has overcome these problems.

Most commonly the end-tidal CO₂ reading changes because of:

1.  Failure to detect ETCO₂ due to

•    Failed intubation, airway disconnection, or airway occlusion
•    Lack of pulmonary blood flow (cardiac arrest, air embolis).

2.  High ETCO₂ caused by

•    Deep anaesthesia
•    Inadequate removal of CO₂ by exhausted soda-lime or low fresh gas flows in non-rebreathing circuits
•    Rebreathing expired gas (e.g., defective valves or increased dead space)

3.  Low ETCO₂ caused by

• Light anaesthesia or pain causing gasping respiration
• Excessive ventilation - usually from manual ventilation
• Sampling error - inadequate tidal volume in small dogs, cats, or rabbits
• Sampling error - heartbeats during expiration in deep chested animals can force small puffs of gas up the trachea causing "bumps" in phase "C" of the CO₂ waveform ("cardiac" oscillations). The monitor reads each one as a breath causing ETCO₂ readings to vary and read erroneously high respiration rate.

Picture 1 Waveform with loss of CO2 detection.

Picture 2 Waveform seen with small tidal volume.

Problem Management: Hypoventilation in Anaesthesia

Definition

 ETCO₂ > 55 mm Hg; PaCO₂ > 55 mm Hg

Recognition

 Reduced rate or depth of ventilation

 Difficulty maintaining anaesthesia

 Increased heart rate, increased blood pressure, injected mm's

Best Clinical Assessment

 End expired CO₂ measurement

Causes

 Persistent apnoea post induction of anaesthesia

 Excessive anaesthetic depth/excessive respiratory depression

 Inability to expand the chest: lung or pleural pathology, distended abdomen, pain, position

 Airway obstruction

First response

 Check that the patient is breathing

 Check the patients pulse

 Check the mucous membrane colour

Treatment

1.  Squeeze the rebreathing bag to give a positive pressure breath

a.  Check that there is normal chest expansion and that there is not an airway obstruction

2.  Response to apnoea (especially following induction of anaesthesia)

a.  Give 1 positive pressure breath of oxygen every 30 seconds until breathing commences

3.  Administer oxygen if mucous membranes remain muddy with IPPV

4.  Reduce anaesthetic depth - decrease vaporiser setting by 1/3

5.  Improve positioning

6.  Consider continuous intermittent positive pressure ventilation (IPPV)

Table 2

Pulse Oximetry

Methodology: Pulse oximetry is the continuous non-invasive monitoring of peripheral capillary bed haemoglobin O₂ saturation or SpO₂ by absorption of infrared light. The absorption characteristics of haemoglobin vary with the SaO₂. The infrared light must be transmitted through skin or mucosa, subcutaneous tissue, bone, and the blood volume filling the capillary bed (the total sum of which = "background light absorption"), as well as the arterial pulsatile blood volume (used to determine SpO₂). The pulse oximeter SpO₂ reading will change if either the SaO₂ or the background light absorption change.

Sensors and application sites: The most useful sites for application of clip-type sensors in dogs and cats are the tongue, the lip, and the ear in non-pigmented skin. Other useful sites include the paw of cats; across the individual toes of dogs; and the thin skin fold above the hock, caudal to the tibia. When placing the sensor on the desired measurement site, handle the tissue (tongue, ear, etc.) gently to avoid vasoconstriction, which alters the reading. Clipping a small amount of hair from the skin at the application site (e.g., ear, hock, etc.) will improve the sensor's performance. In cats and other small patients, folding a surgical swab over the tongue underneath the probe will improve the performance because this eliminates some light, "damping" the signal.

Patient (probe) movement, such as with shivering, or extraneous light affect pulse oximeter performance. Newer pulse oximeters have processing technology that enhances the signal and reduces motion artifacts.

Most commonly, the pulse oximeter reading changes because of:

1.  Decrease in capillary blood volume (flow), changing background light absorption

• Vasoconstriction from painful stimulation
• Poor perfusion caused by deep anaesthesia
  • Reduce anaesthetic level, administer analgesics
  • Increase IV fluids, consider inotropes

Removing the sensor from the tissue site and repositioning it will cause the monitor to "re-calibrate" itself for this change in blood flow. It should then produce SpO₂ readings similar to what they were prior to the changed blood flow.

2.  Decrease in arterial SaO₂ below 90%

• SpO₂ readings under-read SaO₂ by 2 or 3% so we usually set pulse oximeter alarms at 85 to 87%
• Low SpO₂ may be accompanied by signs of hypoxia (high HR and RR, cyanosis)
• Consider raising the inspired oxygen and improving blood flow
• Inadequate ventilation: at least 1 breath is needed every 30 sec (O₂ 95%)

3.  PCV below 15–20%: consider a transfusion to raise the PCV > 24%

Alarm Settings

When setting the alarms, it is important to remember that the SpO₂ measured by the pulse oximeter will generally be 2–3% lower than SaO₂.We aim to maintain the SaO₂ above 90%; therefore, the recommended alarm settings are:

Table 3

Troubleshooting - What to Do When the SPO₂ Reading Falls

Step 1: Look at the patient. This must always be the first response!

 Is there a palpable pulse?

 Is the animal breathing?

 What is the mucous membrane colour?

 What is happening in surgery?

Step 2: Initiate treatment for any problems recognised.

Step 3: Move the sensor only after it has been established that the patient appears stable. Removing the sensor from the tissue site and replacing it will cause the monitor to "re-set" itself for this change in blood flow and then produce a better SpO₂ reading.

The saturation level obtained should be the same as the reading before the drop occurred.

Problem Management: Hypoxaemia in Anaesthesia

Definition

 SaO₂ < 90%; PaO₂ < 60 mm Hg; PCV < 20%

Recognition - cyanotic or "muddy" mucous membranes

 Tachycardia

 Increased ventilatory efforts

Best clinical assessment

 Pulse oximetry (blood gases if available)

Causes - poor perfusion

 Inadequate haemoglobin concentration

 Inadequate oxygenation of haemoglobin (low FiO₂, lung pathology)

 Inadequate ventilation

First response - assess the mucous membrane colour of the patient

 Check the heart rate or pulse rate

 Check that the patient is breathing

Treatment

1.  Improve pulmonary perfusion

a.  Decrease anaesthetic depth to reduce cardiac depression

b.  Increase vascular volume (increase IV fluid rate) to improve venous return

c.  Administer positive inotropes to increase cardiac contractility

2.  Improve alveolar ventilation

a.  This will raise PaO₂ slightly, but positive pressure ventilation reduces cardiac function, which reduces tissue blood flow and therefore tissue oxygenation. It is probably better to initially concentrate on improving perfusion (above). In addition reducing anaesthetic depth will reduce respiratory depression and therefore improve ventilation.

3.  Improve oxygenation of tissues

a.  Raise the inspired oxygen concentration, commonly to 95% in anaesthesia

b.  Increase the oxygen carrying capacity by raising the haemoglobin concentration

c.  Increase the delivery of oxygen to tissues by raising blood flow (cardiac output) - see Treatment(1) above

d.  Investigate lung pathology