Do We Need Mechanical (Artificial) Ventilation During Anaesthesia?
World Small Animal Veterinary Association World Congress Proceedings, 2004
Yves Moens, PhD, PD, DECVA
University of Veterinary Medicine Vienna
Vienna, Austria

Mechanical ventilation in veterinary medicine is needed in the field of emergency treatment and cardiopulmonary reanimation, in the field of anaesthesia and finally in the field of intensive care. According to the field the type of apparatus and the degree of sophistication of devices will differ. Whereas an ambu bag may suffice during emergency CPR, during anaesthesia a relatively simple ventilator is needed if continuous manual ventilation is not an option. Intensive care for patients in respiratory failure benefits from the use of dedicated and more perforant ventilators.

Patients requiring mechanical (manual) ventilation can generally be divided in those who have problems with oxygenation and those who have a problem with ventilating. These are the patients with a partial pressure of oxygen (PaO2) below 50 mmHg on supplemental inspired 02 and those with a PaCO2 above 50-60 mmHg. A combination is possible and is often encountered.

Hypercapnic respiratory failure occurs when the lung is normal but ventilatory function insufficient. This causes respiratory acidosis due to insufficient CO2 removal. This happens regularly during anaesthesia because of interference of the anaesthetics and analgesics at central level causing hypoventilation. Muscle relaxants act at the level of the neuro-muscular interface and can cause complete paralysis of the respiratory muscles. Interference with the function of the efferent neurons to the respiratory muscles can also be caused by trauma and diseases (e.g., cervical neck injury, myasthenia gravis). In practice respiratory acidosis is common during anaesthesia with supplemental O2 and unless a means of estimating PaCO2 is present (blood gas analysis or capnography) this may remain unnoticed. O2 saturation measured by pulsoximetry will remain in acceptable limits. Hypercapnia is much better tolerated than hypoxemia in healthy individuals. An increase in heart rate and reddish mucous membranes are clinical indicators of hypercapnia. Respiratory acidosis during anaesthesia can however be detrimental when the animal has already a metabolic acidosis. This will worsen the degree of acidosis to a possibly life-threatening degree. Hypoxemic respiratory failure occurs when the gas exchange is insufficient at the level of the alveolo-capillary interface, in presence of pronounced ventilation/perfusion mismatch, shunt, or simply by a low inspired fraction of O2 (FIO2). Examples are different pathologies with intrapulmonary changes (pneumonia, oedema, contusion...). Such patients are less likely to be anaesthetised as such or at least represent an increased risk/challenge. In severe cases they will have to be ventilated for a longer period as an important therapeutic measure. Increased survival rate of such veterinary patients compared to no ventilatory support has been demonstrated.

A particular reason to adopt mechanical ventilation during anaesthesia with inhalation agents is the fact that it promotes the quick establishment and maintenance of a stable plane of anaesthesia.

When using mechanical (manual) ventilation it is important to be familiar with the physiologic and pathophysiologic effects. During normal breathing pressures decrease in the airways and the pleura during inspiration. Mean intrathoracic pressure remains about zero. With classic mechanical ventilation it is the inverse and intrathoracic pressure becomes positive (intermittent positive pressure ventilation, IPPV). Because of this unphysiologic aspect of IPPV this technique was only lately accepted in the 20th century as a means of ventilating patients (opposed to negative pressure ventilation). This increase in intrathoracic pressure leads to a decrease in cardiac output (CO) by compressing pulmonary vessels and by impeding venous return. The level of mean intrathoracic pressure is a function of respiratory rate, peak inspiratory pressure (PIP), inspiratory time and the presence of positive end-expiratory pressure (PEEP). These values must be kept as low as possible to limit the decrease in cardiac output. The negative effects of increased intrathoracic pressure will be most pronounced in hypovolemic patients and patients with compromised cardiac function. It can be necessary to postpone the institution of mechanical ventilation until the patient is cardiovascularly stable and well perfused, possibly inotropic support is necessary. Recent developments in endoscopic diagnostic and surgical procedures necessitate special anaesthetic considerations and very often carefully managed mechanical ventilation. Both thorascopy and celioscopy induce marked cardiopulmonary changes and these must be added to the cardiopulmonary changes induced by mechanical ventilation itself. As an example the increased intraabdominal pressure needed for celioscopy (capnoperitoneum) diminishes venous return and causes hypoventilation by pressure on the diaphragm. In human one lung ventilation is a common procedure to facilitate certain intrathoracic procedures. In clinical veterinary medicine it is sporadically used.

Modes of IPPV-mechanical ventilation

Four factors determine IPPV: volume, pressure, flow and time. Two basic options for ventilators are commonly offered. Volume-cycled ventilators deliver a preset tidal volume (Vt) with each breath. The danger is barotrauma following alveolar over-distension when the pressure to deliver Vt becomes to high (e.g., hernia diaphragmatica). Pressure-cycling delivers a variable volume until a preset airway pressure is reached. In case of a low lung compliance Vt might be to low and hypoventilation induced. Newer ventilators offer both options. No distinct difference in cardiopulmonary side-effects of volume versus pressure-cycling have been shown.

Intermittent mandatory ventilation (IMV) provides IPPV at preset time intervals independent of the presence of spontaneous breathing. The patient might "fight" with I MV. Danger is occasional hyperinflation and barotrauma. When anaesthesia plane is adequate the spontaneous respiration is then best abolished by administration of an opioid and temporary manual hyperventilation. Another option is curarisation. Assist-control (A/C) either delivers a preset ventilator driven breath or allows the patient to trigger a breath that is then assisted by the ventilator. This is an interesting respiratory mode when respiratory drive is normal but Vt to low, each breath having a full Vt support. When respiratory rate is high this may result in hypocapnia. Mostly a preset rate of "rescue" breaths will be delivered if respiratory rate is insufficient. A ventilator with IMV (volume-or pressure-cycled) will suffice to manage ventilation during anaesthesia. Very often volume-cycled ventilators are not suitable to ventilate small cats and dogs and special modifications are needed. Pressure-cycled ventilators can in principle be used for both. A/C is an interesting but not essential option. Other options like synchronised IMV (SIMV), continuous positive pressure (CPAP) and bi-level positive airway pressure (BIPAP) are more useful for intensive care ventilators and not needed during anaesthesia. Intensive care ventilators are not designed to be used during inhalation anaesthesia. Some modifications (vaporisers) are necessary and the principle will be mostly that of a semi-open system (non-rebreathing) which uses high flows. However they can be used easily to ventilate patients under total intravenous anaesthesia, mostly with an O2/air mixture. The feature of PEEP can be interesting for both the anaesthesia and intensive care setting. PEEP keeps alveoli from collapsing at the end of expiration. PEEP is used in patients with decreased functional residual capacity and with intrapulmonary shunt due to atelectasis. PEEP has a negative influence on cardiac output. Ventilator settings are determined by the type of ventilator available and the underlying pulmonary pathophysiology. During general anaesthesia and the likely presence of hypoventilation a normal patient with healthy lungs would have a Vt of about 15 ml/kg, a respiratory rate of 12/min and no PEEP The gas mixture can be solely 02 or a mixture of O2/N2O.O2 toxicity is not a problem during clinical anaesthesia but must be considered during prolonged intensive care ventilatory support with a high inspired O2. There is increasing evidence that high O2 fractions also increase the atelectasis formation. Therefore during normal anaesthesia a mixture of 02/air might be a good option (e.g., F102 40-50%). An animal with pulmonary parenchymal disease would receive a kg (low)Vt of 6-8 ml/Kg, rr of 15/min and to start a PEEP of 5 cmH2O and F1O2 of 100%. Guided by the PaO2, fine tuning of FIO2, PEEP and PIP can be done.

Complete and adequate management of anaesthesia is only possible with well understood and correctly applied mechanical ventilation. This is a good learning school to prepare for managing longer ventilatory support in critical patients.

References

1.  Evassilev, M McMichael An overview of positive pressure ventilation J Vet Emergency and Critical care 14 (1), 2004,15-21

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Yves Moens, PhD, PD, DECVA
University of Veterinary Medicine Vienna
Vienna, Austria


MAIN : Anaesthesiology : Artificial Ventilation
Powered By VIN

Friendly Reminder to Our Colleagues: Use of VIN content is limited to personal reference by VIN members. No portion of any VIN content may be copied or distributed without the expressed written permission of VIN.

Clinicians are reminded that you are ultimately responsible for the care of your patients. Any content that concerns treatment of your cases should be deemed recommendations by colleagues for you to consider in your case management decisions. Dosages should be confirmed prior to dispensing medications unfamiliar to you. To better understand the origins and logic behind these policies, and to discuss them with your colleagues, click here.

Images posted by VIN community members and displayed via VIN should not be considered of diagnostic quality and the ultimate interpretation of the images lies with the attending clinician. Suggestions, discussions and interpretation related to posted images are only that -- suggestions and recommendations which may be based upon less than diagnostic quality information.

CONTACT US

777 W. Covell Blvd., Davis, CA 95616

vingram@vin.com

PHONE

  • Toll Free: 800-700-4636
  • From UK: 01-45-222-6154
  • From anywhere: (1)-530-756-4881
  • From Australia: 02-6145-2357
SAID=27