Use of Controlled Ventilation in a Clinical Setting

Introduction

Controlled ventilation has many uses in small animals, such as treating hypercapnia resulting from hypoventilation and hypoxemia. Hypoventilation in animals has many etiologies. Hypoventilation is defined as arterial partial pressure of carbon dioxide (PaCO₂) >60 mm Hg (reference range 35 to 45 mm Hg) in the dog or cat.¹ During anesthesia, most anesthetized animals hypoventilate. Hypoventilation under general anesthesia is commonly induced with clinical doses of premedicants, such as the mu-opioid agonists (i.e., hydromorphone, morphine) and inhalant anesthetics (i.e., sevoflurane, isoflurane). Such hypoventilation warrants the use of intermittent positive-pressure ventilation (IPPV).

An absolute indication for mechanical ventilation is apnea. Common causes of apnea in anesthetized animals include the use of high concentrations of inhalant anesthetics, epidural analgesia with local agents (e.g., lidocaine, bupivacaine) that may block motor transmission to the respiratory muscles (i.e., intercostal muscles or the diaphragm), large intravenous doses of pure mu-opioid agonists, and/or neuromuscular blocking agents (e.g., atracurium).²

The use of IPPV in the nonanesthetized animal is most often associated with alterations in central nervous system (CNS) function and failure to properly maintain PaCO₂ levels. Comatose animals or animals with acute respiratory failure are two common examples in which temporary IPPV is used in nonanesthetized animals. Acute respiratory failure may result from ingestion of certain toxicants, certain pulmonary diseases, and other disorders.² Animals may become comatose as a result of neuromuscular disorders (e.g., excessive depths of anesthesia, intracranial diseases, cervical diseases, neuromuscular junction disorders) that render the CNS incapable of maintaining normal respiratory function. Other causes of hypoventilation that benefit from IPPV include airway obstruction, thoracic restrictive diseases, pulmonary parenchymal diseases, and pleural cavity disorders.³

Hypoxemia arises when there is low oxygen (O₂) content in the blood, whereas hypoxia is a broader term that refers to impaired O₂ delivery and takes into account cardiac output, peripheral perfusion, and O₂ extraction by tissues. The five causes of hypoxemia are diffusion impairment, ventilation/perfusion inequality (V/Q mismatch), shunting (i.e., blood entering the arterial system without going through the ventilated areas of the lung), hypoventilation, and low inspired levels of O₂ (less common).²

The purpose of this article is to review the management of IPPV, as well as the possible harmful effects of controlled ventilation.⁴

Guidelines for Ventilation

The basic parameters that are controlled with IPPV include ventilatory (respiratory) rate, the ratio of inspiration time to expiration time (I:E), inspiratory pressure, and tidal volume. Other factors that may be controlled, depending on the ventilator type, include: positive end-expiratory pressure, continuous positive airway pressure, intermittent mandatory ventilation, and pressure flow.⁵ Respiratory rates are usually 8 to 14 breaths per minute for mechanically ventilated dogs and 10 to 15 breaths per minute for cats. The I:E ratio should be between 1:1.5 and 1:3 to maintain normal hemodynamics during positive-pressure ventilation. The tidal volume is calculated at 10 to 20 mL/kg of body weight. Inspiratory pressure should not exceed 30 cm of H₂O and is commonly set at 13 to 20 cm of H₂O.

When using positive end-expiratory pressure, positive pressure is maintained between the breaths delivered by the ventilator so that end-expiratory pressure is above ambient air pressure, thereby keeping the alveoli open and reducing atelectasis. Continuous positive airway pressure can be used during spontaneous respiration in conjunction with a ventilator to maintain a constant airway pressure above ambient pressure. Intermittent mandatory ventilation is utilized most commonly when weaning an animal from the ventilator, because it allows the animal to breathe spontaneously while delivering mechanical breaths at preset tidal volumes and frequencies in order to ensure PaCO₂ remains normal.

Measuring Carbon Dioxide

Hypercapnia is defined as PaCO₂ levels >50 mm Hg, and it results in respiratory acidosis.³ Clinical indicators of hypercapnia include shallow breaths (panting), breathing against IPPV, cardiac arrhythmias, and loss of consciousness or stupor in the absence of injectable or gaseous anesthetics. The act of panting during hypercapnia is an attempt by the respiratory system to lower carbon dioxide (CO₂) by increasing its loss through expiration. Hypocapnia is defined as PaCO₂ levels <35 mm Hg, and it results in respiratory alkalosis.³ Animals with hypocapnia can experience changes in mental status, such as loss of consciousness (in the absence of injectable or gaseous anesthetics).

The most accurate means to measure PaCO₂ is by procuring an arterial blood sample and analyzing it mechanically. Numerous veterinary-approved devices to measure arterial blood gases are commercially available.^a,b,c In addition, end-tidal carbon dioxide (_ETCO₂) levels on intubated animals are usually measured continuously via capnography. Although not always as accurate as arterial blood samples, _ETCO₂ levels can be useful when both types of sampling are done simultaneously, especially to compare the differences. Anytime there is doubt about the _ETCO₂ levels, an arterial sample may be checked to verify the results.

Sudden Changes in _ETCO₂

Observations made by the technical staff can be invaluable when managing animals maintained on IPPV. Sudden changes in _ETCO₂ are indicators of serious problems that may be life threatening if not remedied. Sudden decreases in _ETCO₂ may result from a blocked or kinked endotracheal tube, disconnections between ventilator/airway tubing, ventilator failure, airway obstruction, or monitoring device failure.⁵ Changes in the wave pattern on the capnograph are also good indicators that a major change in respiratory status may be occurring.

A typical wave pattern has an end-expiratory plateau that corresponds to the animal’s ventilation. Evaluation of these wave patterns allows a technician to detect leaks and recognize bronchospasms, apnea, and other subtle changes with respiration. Sudden decreases in the height of the plateau on the waveforms may indicate airway leaks. Exponential decreases in the end-expiratory plateau can be indicators of severe cardiovascular disturbances or sudden hyperventilation. A slow decrease in the height of the plateau may also indicate hyperventilation, hypothermia, or vasoconstriction.⁵ Low _ETCO₂ measurements without a good plateau waveform or a slow rate of rise of the waveform are indicative of fresh gas contamination, partial airway obstruction, bronchospasm, rapid breathing rates, or low air flow rates.⁵ Low end-tidal values with an adequate waveform indicate either large physiological dead spaces or the need for calibration of the capnograph. Increased heights to end-tidal plateau waveforms indicate hypoventilation or an increased rate of metabolism.⁵ Increases in the baseline and plateau height indicate the animal is breathing against the ventilator, possibly as a result of breathing inspired CO₂.⁵ All of these changes are indicators that the respiratory status has changed in some way. Close monitoring and intervention are imperative when these alterations are detected. The technician’s role in monitoring ventilatory and respiratory status can make a big difference in the outcome of the case.

Possible Harmful Effects

Although IPPV is extremely beneficial in many cases, it is not without potential harmful effects. For example, animals maintained for long periods of time on IPPV using 100% O₂ run the risk of developing O₂ toxicity. Oxygen toxicity leads to the deterioration of pulmonary function, with pulmonary edema and ultimately death.⁵ In small animals, the recommendation is to use 100% O₂ for ≤ 24 hours. A mixture of 100% O₂ and air (21% O₂) may be used to manage animals that need mechanical ventilation for >24 hours. Close monitoring of arterial blood gases is key to tracking the arterial partial pressure of oxygen (PaO₂). The length of time that the PaO₂ is elevated is more indicative of O₂ toxicity than simply an elevated PaO₂. In dogs, it is reported that toxicity develops within 24 hours of exposure to 100% O₂.⁵

Another side effect of controlled ventilation is the increase in intrathoracic pressure that occurs during inspiration. This increase in pressure causes a decrease in blood entering the thorax, which decreases venous return to the heart and cardiac stroke volume. In most healthy animals, the decrease in venous return is not very concerning, because they can compensate and restore venous return to its normal state. In the compromised animal, however, this compensatory mechanism may not be functioning properly, and cardiovascular failure may occur. Four methods are used to maintain lower (more acceptable) intrathoracic pressures. A shorter application time of IPPV, manifested as I:E ratios between 1:1.5 and 1:3, results in shorter inspiratory periods and lower intrathoracic pressures. The disadvantage to this method is the possibility of decreased distribution of fresh gases within the lungs. Increasing the gas flow rate is a second method to offset shortened inspiratory times, depending on the type of ventilator being used. This method also has its disadvantages. For example, the potential exists for airway damage, with concurrent airway obstruction. Increasing the flow rate of fresh gas in the face of any potential airway obstruction can result in over-inflation of alveoli on the unobstructed side, with secondary rupture. A third method to offset increased intrathoracic pressure is to maintain a low expiratory pressure. Lastly, a fourth method is to apply subatmospheric (negative) pressure during the expiratory phase. By doing so, volume changes in the lungs can be achieved with lower peak pressures.

Ventilating the “Awake” Animal

Although it is easy to control ventilation in anesthetized, surgical patients, there are also multiple uses for IPPV in animals that are not anesthetized or that retain some level of consciousness but are hypoxic and require ventilation. Constant rates of infusion (CRI) of anesthetic induction agents (e.g., propofol) are commonly used to keep animals unconscious and allow for unresisted ventilation. Constant rates of infusion opioids (e.g., morphine, fentanyl) are also used at dosages high enough to depress the respiratory centers in order to allow controlled ventilation.

Another technique commonly used in animals that are comatose but still have a gag reflex or periodically become conscious is to employ neuromuscular blocking agents (e.g., atracurium) to paralyze the respiratory muscles. When neuromuscular blocking agents have been administered, a common method used to evaluate the amount of muscle paralysis present is application of a nerve stimulator. Most commonly, a nerve stimulator is applied to a peripheral nerve, and electrical stimuli are used to assess muscle twitching. With complete paralysis, muscle activity is absent. As the neuromuscular blockade wears off, muscle twitching returns. Using this technique, the technician can record any relevant changes in motor status and readminister the blocking agent as needed before the animal begins to resist the controlled ventilation.

Ventilator Settings

As previously mentioned, most ventilators allow settings of respiratory rate or frequency, tidal volume, I:E ratio, and flow or pressure rate. Adequate ventilation means maintaining a PaCO₂ of 35 to 50 mm Hg or, more commonly, 40 to 45 mm Hg. Adjusting the ventilator settings to achieve this level of CO₂ is one of the primary functions of the anesthetist (while in surgery) or the critical care technician managing the “awake” animal. Initially the primary goal of controlled ventilation is to alleviate hypercapnia. In some animals, CO₂ can be extremely high, even exceeding 60 to 70 mm Hg.

Normal PaCO₂ in an animal breathing room air should be the same as when the animal is inspiring 100% O₂. In contrast, PaO₂ differs greatly when an animal is inspiring room air versus 100% O₂. When the PaO₂ is lower than normal (reference range 80 to 100 mm Hg) in an animal breathing room air, controlled ventilation becomes necessary to maintain essential life functions until the underlying issues can be remedied. While inspiring 100% O₂, PaO₂ should be approximately 400 to 500 mm Hg.² When PaO₂ levels are extremely low (i.e., <70 mm Hg), there is great cause for concern. The initial ventilator settings often have to be adjusted frequently as the animal’s system allows the controlled ventilation to regulate CO₂ and O₂. In order to increase PaO₂, the settings for tidal volume, frequency, and/or flow rates are at the higher end of normal values. Concurrently, this also causes PaCO₂ to decrease. Essential monitoring of changes in PaCO₂ and PaO₂ is achieved via capnography and arterial blood analysis.

Weaning Away From the Ventilator

The process of transferring the work of breathing from the ventilator back to the animal is referred to as “ventilator weaning.” The term “ventilator weaning” may be used to refer to all methods by which this transfer of workload is accomplished.^6,7 It is relatively easy to wean routine surgical cases from controlled ventilation. Generally, by increasing the CO₂ and discontinuing the inhalant anesthetic, the animal will regain the ability to maintain respiratory action at the end of surgery. The CO₂ can be increased by simply shutting the ventilator off and allowing CO₂ to accumulate from apnea. During this time, ventilation is occasionally assisted manually until the animal resumes spontaneous respiration. In addition, CO₂ may be increased by gradually decreasing the respiratory rate, the tidal volume, or the flow rate on the ventilator. Either method is acceptable.

An animal that has been maintained in a drug-induced state to allow for controlled ventilation may require other techniques to be weaned from the ventilator. When long-lasting opioids are used to depress the respiratory centers, they can either be discontinued or reversed with naloxone. When fentanyl is used, simply discontinuing the CRI is enough to reverse its effects within 20 minutes. Neuromuscular blocking agents can either be discontinued or reversed with anticholinergics and anticholinesterase drugs. Reversing neuromuscular agents should be done while maintaining mechanical ventilation, as respiratory muscles do not have the ability to resume ventilation until the blocking agents have worn off.⁴

Conclusion

The use of controlled ventilation in the clinical setting has many appropriate and beneficial uses in small animals. With proper monitoring and ventilation, hypercapnia and hypoxemia can be successfully reversed. By maintaining a staff that is well trained in the use of prolonged IPPV, proper observations and aggressive changes can be made that help achieve a good outcome.