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Ventilators: Why and how (Proceedings)

Article

Hypoventilation (decreased rate and/or depth of breathing) is a common consequence of general anesthesia and results in increased arterial carbon dioxide concentrations (PaCO2).

Hypoventilation (decreased rate and/or depth of breathing) is a common consequence of general anesthesia and results in increased arterial carbon dioxide concentrations (PaCO2). Hypercarbia in healthy dogs and cats unpredictably has opposing impact on the cardiovascular system. Sometimes hypercarbia causes catecholamine release and sympathetic stimulation. The resulting tachycardia and increased blood pressure are often outside accepted normal limits and may be mistaken as signs of inadequate depth of anesthesia. Alternatively, hypotension and poor peripheral circulation may be observed because hypercarbia (acidemia) decreases myocardial contractility. Severe hypercarbia induces vasoconstriction in the splanchnic circulation to an extent that hepatic blood flow is decreased and this effect has been incriminated as the cause of hepatic failure in some animals after anesthesia. Hypoventilation should not be permitted in animals at risk from increased intracranial pressure (ICP). PaCO2 regulates cerebral blood vessel diameter and only a small increase PaCO2 causes cerebral vasodilation and increased ICP. Patients with head trauma, intracranial masses, meningitis, and spinal cord lesions may develop long lasting neurological signs after hypoventilation during anesthesia.

On a practical point, moderate to severe hypoventilation complicates inhalation anesthesia by decreasing uptake of isoflurane or sevoflurane such that depth of anesthesia may be inadequate for surgery or medical procedure.

Recognition of Hypoventilation

Blood gas analysis provides an exact measure of ventilation. Normal PaCO2 in dogs and cats is around 38 and 34 mm Hg, respectively. A moderate increase in PaCO2 is tolerated in healthy animals, above 50 mm Hg is significant hypoventilation, and 20 mm Hg above normal is severe hypoventilation.

Hypoventilation may be the result of a decrease in respiratory rate or a decrease in tidal volume, or both. A respiratory rate of 5 breaths/min or less should be considered as high likelihood of hypoventilation. The reverse is not true as hypercarbia can be present in an animal breathing 10-20 breaths/min or 50 breaths/min. An estimate of tidal volume can be attempted by observation of the rebreathing bag; each breath should be approximately 15 ml/kg when the dog is breathing 12 /min.

Capnography provides a reasonable estimate of PaCO2 in most patients. Measurement of exhaled CO2 at the end of each breath (end-tidal CO2 or ETCO2) provides a value that is approximately 4-6 mm Hg less than PaCO2. The ETCO2 measurement may not be representative of PaCO2 when the animal's breathing is very shallow or when major lung collapse is present.

Reasons for Controlled Ventilation

1. Treat or prevent hypercarbia

Prevent severe hypercarbia in healthy patients

Prevent hypercarbia and increased ICP in neurologic patients

Prevent hypercarbia and increased IOP in ocular (globe) surgery

Prevent hypercarbia and decreased portal flow in hepatic disease

Prevent hypercarbia and cardiovascular effects in cardiac disease patients

Prevent hypercarbia in patients with thoracic insufficiency e.g. chest wall trauma, Guillain-Barré

Provide ventilation in patients paralyzed with neuromuscular blocking agents

2. Optimize isoflurane or sevoflurane delivery

Maintain constant delivery of inhalation agent and avoid inadequate agent uptake

3. Improve oxygenation

In patients with major lung collapse, e.g. diaphragmatic rupture, pneumothorax

4. Decrease work of breathing

Lung disease, such as pulmonary edema or bronchospasm, can increase respiratory muscle oxygen requirement from 5% to 25-30% of total oxygen delivery, thus decreasing oxygen available for other organs.

Old or sick patients may benefit from artificial ventilation for this reason.

Reasons For Mechanical Ventilator Use

1. Maintains constant ventilation and avoids uneven or dangerous hand ventilation

2. More labor efficient

Artificial Ventilation

Terms that have the same meaning are controlled ventilation, manual or mechanical ventilation, and intermittent positive pressure ventilation (IPPV). PaCO2 within normal range can be achieved in dogs and cats with a respiratory rate of 12 breaths/min and tidal volume of 15 ml/kg, or with a respiratory rate of 20 breaths/min and tidal volume of 11 ml/kg. Calculation of tidal volume should take into account the body conformation of the patient, for example, the tidal volume should be calculated based on the ideal weight for an overweight patient. The target tidal volume is produced in most patients with a peak inspiratory pressure of 15 to 20 cm H2O as measured by the pressure gauge on the circle circuit. Using inspiratory pressure as a guide to the volume delivered can be quite inaccurate. Small thin dogs may require little pressure to inflate the lungs whereas a heavy dog may require a pressure of 30 cm H2O, especially if positioned on the operating table in a prone, head-down tilt for perineal surgery. Furthermore, the position of the pressure gauge within the anesthetic circuit configuration may influence the pressure relationship between the patient end of the circuit and the gauge. Measurement of end-expired carbon dioxide concentration by capnography can provide a guide to adequacy of ventilation when inspiratory pressure is used as the end point.

Controlled ventilation is produced by generating a pressure at the endotracheal tube that is higher than the pressure in the lungs so that gas flows into the lung and pressure equalizes. The increase in intrathoracic pressure impedes return of venous blood to the heart and transiently decreases stroke volume. The best technique to avoid excessive cardiovascular depression is to maintain a short inspiratory time and a longer exhalation time (see Fig 1).

Figure 1

Mechanical Ventilators: Value, Power Up, Troubleshooting

Use of a mechanical ventilator provides necessary patient care while leaving a pair of hands free to take care of other business. The ventilator will provide a constant degree of ventilation without pauses to take time to measure blood pressure, or enter data on a record, or to open a pack of suture. Controlled ventilation can ensure an even plane of anesthesia in a patient that is hypoventilating during anesthesia and it will prevent hypercarbia in patients that cannot tolerate ICP or acidosis.

The mechanical ventilator will substitute for hands squeezing the rebreathing bag on a circle circuit. Connection of the ventilator to the circuit is shown in Fig. 2.

Figure. 2

Procedure

1. Connect ventilator to electrical supply

2. Connect ventilator to oxygen source

3. Connect ventilator to scavenger system

4. Insert adapter with pressure feedback tubing between expiratory valve and circle hose (if present)

5. Ventilator control panel: Set respiratory rate (frequency)

Set maximum inspiratory pressure limit (if available)

Insure volume knob is not set too high

Set minute volume 15 ml x kg x 12 (if available)

Adjust inspiratory:expiratory time ratio, usually 1:2 or 1:3 (if available)

6. Remove rebreathing bag from circle and connect tubing from bellows

7. Close circle pop-off valve

8. Turn on ventilator (allow bellows to partially fill with oxygen first)

Adjust tidal volume to achieve target volume or pressure or ETCO2 30-40 mm Hg

9. Observe chest movement

10.There should be no need to alter the oxygen flow into the anesthetic circuit

*If the patient was hypoventilating but at the desired plane of inhalation anesthesia, it may be necessary after a few minutes to decrease the vaporizer to avoid patient becoming more deeply anesthetized.

At the end of anesthesia it will be necessary to hand ventilate the patient at a decreased RR after disconnection from the ventilator to allow PaCO2 to increase and stimulate breathing.

Alarms

1. Pressure feedback: Insert T-adapter on the expiratory limb of the circle next to the one-way valve

2. Alarms if the pressure in the circle is too low

Pop-off valve open

Endotracheal tube cuff not inflated

Endotracheal tube disconnect

3. Alarms if the pressure in the circle exceeds the preset value

Tidal volume too large for patient

Kinked or obstructed endotracheal tube

External pressure on patient's chest

Cautions

Both cardiovascular and respiratory adverse effects are possible consequences of controlled ventilation. Positive pressure inflation increases intrathoracic pressure and right atrial pressure. Cyclical increases in right atrial pressure alter blood volume return to the heart and decrease cardiac output. Ventilator-induced lung injury can result from excessive stretching causing alveolar rupture. Overstretching (35 cm H2O) can cause diffuse alveolar damage, cytokine release and bacterial translocation.

Dogs and cats suffering from acute lung injury due to automobile collision are at risk for further damage from controlled ventilation. Unfortunately, pulmonary contusions are not homogenous and ventilation even to normal volume can result in overdistension of alveoli that were not previously damaged. Further, although airway pressure may be normal this pressure may not reflect high local intrapulmonary pressures. Inspiratory pressures in these patients should be monitored and kept low.

Assessment of Problems

1. Assess the severity of the problem: Is it the patient or the ventilator?

2. Very important to check the patient

Is the thorax moving?

Auscultate for air movement both sides of chest using a stethoscope

Is the patient hypoxic? Membrane color? SpO2 (pulse oximeter) > 90%?

Assess blood pressure and capillary refill time.

3. Consider changing to manual bagging while ventilator is checked out.

Troubleshooting

Mechanical Ventilators In Icu

The previous description of controlled ventilation applies to use during anesthesia. More considerations are important for long-term ventilation. Patients requiring mechanical ventilation in the ICU for ≥ 24 hours will need to breathe 40-60% inspired oxygen to avoid oxygen toxicity pathology in the lungs. Consequently, the ventilator set-up must include a cylinder of air for blending with oxygen. Patients are usually sedated with continuous IV infusions of propofol, 0.2-0.3 mg/kg/min, and continuous infusions of fentanyl, 5 µg/kg/h, or diazepam, 0.5 mg/kg/h.

Airway care includes changing endotracheal tube position every 3-4 hours, changing the endotracheal tube daily, suction of secretions and instillation of saline into the trachea, and inserting a humidifier (Gibeck) between the endotracheal tube and circle.

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