Anesthesia

Mechanical Ventilation

Outline

Theory of mechanical ventilation

Physiology of ventilation’s impact on the body

Talk about set up and troubleshooting

• Huge shoutout to Erik for creating those documents, we will go through them so there is some understanding when they go out to everyone

PPV

PPV - Positive-pressure ventilation

• manual compression of the rebreathing bag
• mechanical ventilator
• Indications
• Support ventilation in patients suffering from hypoventilation
• Manipulate alveolar ventilation in hypoxemic patients
• Limit the development of atelectasis over the duration of an anesthetic episode

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• Ventilator - Essentially an extra pair of hands
• eliminates the need for the anesthetist to continually provide manual IPPV

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Types of Ventilators

• Ventilators used for anesthesia purposes
• Simpler, shorter term use
• Ascending vs descending

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• Ventilators used in critical care settings
• Much more complex, longer term use

How it works

• Electrically powered and pneumatically driven
• Ascending (much more common) vs descending bellows
• For ascending → bellows ascend during expiration
• superior to descending bellows (which descend during expiration) → a leak is more easily noticed with the ascending bellows
• The ventilator bellows is depressed by compressed gas
• typically air or oxygen,
• enters the bellows housing under pressure
• Benefit of gas driving ventilator
• prevents electrical parts from coming into contact with the high-oxygen gas within the bellows → which may be a fire hazard

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How it works

How it works

• Anesthesia ventilators may be time-, volume-, or pressure-cycled
• Most common is volume - what we have
• I.e. the user sets the tidal volume or minute volume and the respiratory rate in breaths per minute.
• The ventilator will then set the amount of time each breath takes based on this information
• The inspiratory-to-expiratory (I:E) ratio
• may also be set in some ventilators - ours is standard
• default setting of 1 : 2

Setting Respirations

Volume you set is based on tidal volume

• Can be calculated at 10 to 15 mL/kg for each breath unless otherwise discussed with attending clinician
• appropriate tidal volume should be titrated individually on the basis of
• the partial pressure of end-tidal CO2
• avoidance of an excessive peak inspiratory pressure
• Volume-cycled ventilators
• may result in excessive peak inspiratory pressures
• always start at zero and work your way up!!!
• initial inspiratory pressures depend on the size of the animal and disease → a reasonable starting peak inspiratory pressure is 12 mm Hg.

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Setting Respirations

Target PaCO2 for animals on a ventilator:

• 35 to 45 mmHg
• Adjust your ventilator settings when you are outside of this range
• If below 35 mmHg -> need to decrease the amount you are respiring
• If above 45 mmHg -> need to increase the amount you are respiring

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If this is persistent despite adjusting respirations, other things may need troubleshooting -> talk to your doctor throughout this process, but especially if not improving after you adjust

Diseases

There may be some pathologies that we will have to take into account when setting up the ventilator volume for our patients

• lung compliance changes
• Pulmonary fibrosis
• bronchospasm
• Pneumothorax
• Pleural effusion
• Diaphragmatic hernia
• Lung lobe torsion
• Etc.

Ventilator Failures

• Disconnection of the power
• Disconnection of driving gas source
• Leak in the bellows housing
• Incorrect internal setup after cleaning
• Incorrect setup on the anesthetic circuit
• Check all of the spots!
• Leak around the ET tube

If you can’t figure it out quickly - Switch them back!!!

Effects of PPV

The use of mechanical ventilation in an anesthetized patient directly alters the patient’s respiratory system including:

• inspired gas content
• gas exchange
• work of breathing

In addition, other systems, most importantly the cardiovascular system, are significantly impacted by ventilatory support

Effects of PPV - Cardiovascular

Both spontaneous and mechanical ventilation alter cardiovascular function by changing the intrathoracic pressure and lung volume, which in turn impact the cardiovascular system directly by altering preload, afterload, and/or heart rate

Ventilation can also alter cardiovascular performance indirectly, by altering PaCO2 or PaO2 levels

Effects of PPV - Cardiovascular

Reminders of Cardiovascular Physiology:

Preload - The initial stretching of cardiac myocytes (muscle cells) before contraction, determined by the volume of blood in the ventricles at the end of diastole

Afterload - The pressure or "load" the heart must work against to eject blood during systole which is determined by systemic vascular resistance (blood pressure), aortic valve stenosis, and aortic pressure.

CO = SV * HR

SV = Preload * Contractility / Afterload

Effects of PPV - Cardiovascular

Respiration affects the cardiovascular performance normally

• The effect on right ventricular preload is likely the predominant factor
• With spontaneous ventilation air moves into the lungs due to a decrease in the intrapleural pressure and the creation of a negative pressure gradient between the mouth/nostril and alveoli
• Due to the pressure gradient between the peripheral and intrathoracic venous system, blood flow into the thorax and right atrium increases
• With the increase in flow, right atrial blood volume or preload is increased
• As the latter is the major determinant of cardiac output in patients with normal myocardial contractility, stroke volume and cardiac output increase.

Effects of PPV - Cardiovascular

With positive‐pressure ventilation:

• Intrapleural pressure increases during inspiration, leading to a decrease in venous return and right ventricular output
• The magnitude of the decrease in right ventricular preload is dependent on the degree and duration of intrapleural pressure change
• Specifically, strategies such as ventilatory strategies that use large tidal volumes, PEEP, or short expiratory times, have a greater negative impact on venous return and right ventricular preload

Effects of PPV - Cardiovascular

With positive‐pressure ventilation:

• As lung volume increases, total pulmonary vascular resistance increases secondary to compression of intra‐alveolar capillaries.
• Since pulmonary vascular resistance is the major determinant of right ventricular afterload, this will increase
• With normal tidal volume breathing, this effect is minimal
• the impact can be clinically significant when lung volumes are well above FRC for a large proportion of the respiratory cycle

References

Grimm, K. A., Lamont, L. A., Tranquilli, W. J., Greene, S. A., & Robertson, S. A. (2015). Veterinary Anesthesia and Analgesia: The Fifth Edition of Lumb and Jones. Wiley-Blackwell.

Johnston, Spencer A., and Karen M. Tobias, eds. Veterinary Surgery : Small Animal. Second edition. St. Louis, Missouri: Elsevier, 2018. Print.

Image references from above or link included in slide description

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