Basics
Description
- Mechanical ventilation is machine generated flow of gas into and out of the lungs that acts as a substitute for normal respiratory function
Basic Concepts: Physiology and Pulmonary Mechanics
- Mechanical ventilation is positive pressure ventilation indicating that forced gas delivery generates positive pressure during inspiration
- Negative pressure ventilation:
- Natural respiratory pattern
- At rest (functional residual capacity) surface tension of alveoli is balanced by elastic recoil of chest wall; alveoli pressure equals atmospheric pressure at this point
- In inspiration, lungs expand causing alveolar pressure to become negative compared with atmospheric pressure and air travels down pressure gradient into lungs
- Exhalation is normally passive, but can be made active with the use of accessory muscles in the setting of airway obstruction/increased airway resistance
- Minute ventilation (MV):
- Total volume of breaths in 1 min
- Breaths in 1 min is respiratory rate (RR)
- Standard breath is called tidal volume (TV)
- MV = TV RR: Each component can be adjusted to control ventilation
- Oxygenation is controlled with adjusting fraction of inspired oxygen (FiO2) and positive end-expiratory pressure (PEEP)
- Compliance:
- Describes lung distensibility
- Defined as change in volume with given change in pressure
- Decreased lung compliance can be caused by problems with the lung parenchyma (i.e., pneumonia, ARDS) or problems with the chest wall/pleura (i.e., abdominal distension)
- Lung compliance determines plateau pressure:
- Plateau pressure is the steady state pressure; represents the attenuated pressure that is distributed to the small airways and alveoli during positive pressure ventilation
- Goal ≤30 mm Hg
- Resistance:
- Defined as change in pressure with given flow
- Main determinant is airway radius
- Increased resistance can be caused by problems with the airways (i.e., bronchospasm), problems with the endotracheal tube (i.e., secretions), or problems with ventilator tubing
- Resistance determines peak pressure:
- Peak pressure is the pressure seen in the larger airways before delivered volume is distributed to smaller airways and alveoli
- Also determined by TV delivered
- Goal ≤40 mm Hg
Diagnosis
Signs and Symptoms
- Indications for mechanical ventilation:
- Failure to oxygenate:
- Diffusion defect (i.e., pulmonary edema, pneumonitis, pneumonia)
- Severe ventilation/perfusion mismatch (i.e., PE, severe hypoventilation)
- Severe shock:
- Shock = oxygen supply does not meet oxygen demand by tissues
- Mechanical ventilation can help improve shock states in 2 ways:
- Increased oxygen delivery
- Reducing overall oxygen demand by replacing organ system with high oxygen requirement
- Failure to ventilate:
- Obtundation/sedation
- Loss of ability to control diaphragm or intercostals (i.e., high spinal cord injury)
- Severe myopathy
- Dysfunctional chest wall (i.e., flail chest, increased abdominal pressures leading to decreased chest wall excursion, obesity)
- Increased dead space (large PE, airway obstruction)
- Metabolic acidosis (creates need for higher MV to compensate)
- Other:
- Patient safety/need for evaluation
- Predicted deterioration in clinical course
- Ventilation strategy should specifically address the indication for mechanical
ventilation!- Example: In the setting of severe acidosis a preferred mode would be one where you could control MV closely
- Example: In severe pulmonary edema controlling the MV is not as important as ensuring oxygen delivery
History & Physical Exam
- Focus on underlying etiology for respiratory failure
- Exam on mechanical ventilation should include assessing oxygen saturation, evaluating end-tidal CO2 (ETCO2) with capnometry and capnography (see below), auscultating lung sounds/air movement, observing chest wall rise, palpating for abdominal distension
- ETCO2:
- Capnometry is the quantitative partial pressure of ETCO2.
- Capnography is the graphic representation of the changes in ETCO2 with respiratory cycle
- Normal lungs have a small degree of ventilation/perfusion mismatch as well as anatomic dead space. As a result, ETCO2 is usually around 2 " 5 mm Hg lower than PaCO2
- Capnometry will be affected by: Amount of dead space or ventilation/perfusion mismatch; changes in metabolic CO2 production (although ratio between PaCO2 and ETCO2 will not change); venous return (also will not affect ratio)
- Evaluation of the ETCO2 waveform can be very useful:
- Can help assess response to bronchodilator therapy as waveform in airway obstruction has a steeper upslope instead of a plateau given the prolonged expiratory phase
- Can help assess adequacy of CPR (will see return of waveform with good compressions)
- Can help assess cause of tachypnea or dyssynchrony
- Monitor hemodynamic status closely with mechanical ventilation
Diagnosis Tests & Interpretation
Lab
- Arterial blood gas (ABG):
- Should be checked within 15 " 30 min of initiation of mechanical ventilation and repeated with any change in clinical status
- pH and PaCO2 will help assess ventilation
- PaO2 will assess oxygenation
- With ability to assess continuous oxygen saturation and ETCO2 need for frequent ABGs, even after change in ventilator settings, may be eliminated or reduced
- Serum chemistries including basic electrolytes with bicarbonate, liver function, renal function may help assess acid/base status which will affect ventilation strategy
- Hemoglobin/hematocrit will help describe state of oxygen delivery
Imaging
Imaging may include beside US, chest x-ray, and chest CT to assess for endotracheal tube placement and pathophysiology of the lung and chest wall
Differential Diagnosis
See indications for mechanical ventilation above
Treatment
Pre-Hospital
Respiratory support per local EMS protocol
Initial Stabilization/Therapy
- Cardiac monitor
- BP monitoring
- Pulse oximetry
- End-tidal CO2 monitoring when available
Ed Treatment/Procedures
Critical actions include: Choosing appropriate ventilatory mode; assessing and adjusting ventilator settings; standard postintubation care; treatment of the underlying process.
- Postintubation care is of utmost importance. Includes: Sedation and/or analgesia; confirmation of tube placement; adjustment of ventilator settings based on clinical condition and ABG; establishing ETCO2 gradient if using capnometry; elevating head of bed; placement of NG or OG tube.
- Settings common to most modes include:
- RR:
- In all modes, but will be set by patient in more spontaneous modes
- Normal starting rates can vary from 12 " 20
- Consider underlying pathophysiology before arbitrarily setting rate (i.e., elevated ICP, severe asthma)
- Fraction of inspired oxygen (FiO2):
- Oxygen concentration in gas mixture
- Usually start out with FiO2 of 1 (100%) but wean down quickly after confirmation of stable oxygenation with prompt ABG
- PEEP:
- Pressure that is applied to end expiration to maintain alveolar recruitment
- Significant increase in work of breathing is required to open up collapsed alveoli
- Collapsed alveoli do not participate in gas exchange, creating ventilation/perfusion (V/Q) mismatch and difficulty oxygenating and ventilating
- By stenting open more alveoli, increased PEEP can improve oxygenation, especially at lower TVs (although be careful of high PEEP and overdistension which can lead to significant alveolar injury)
- With normal chest wall compliance, basic starting PEEP will be 5 " 10 mm Hg
- In setting of low chest wall compliance (obesity, anasarca, abdominal distension) may need to start with higher PEEP, around 10 " 15 mm Hg
- Inspiratory:expiratory ratio (I:E): Will alter flow rates. Allows for optimal mechanics in disease specific situations: E.g., increase E fraction in obstructive airway disease to prevent "breath stacking. " Normal ratio ’ Ό1:2.
Basic modes of ventilation:
- Early, classic modes of ventilation allowed for only simple ventilator/patient interaction and limited control of small number of variables
- Continuous mandatory ventilation (CMV):
- CMV is the classic mode where only 1 variable can be set
- Allows for NO interaction between the patient and the ventilator " all breaths are fully controlled breaths
- Breaths are delivered only at a set rate " time is the trigger for every breath
- Breaths are defined only by the control:
- Volume controlled (also known as volume cycled) CMV: Delivers set volume with each breath and guarantees certain MV
- Pressure controlled (also known as pressure cycled) CMV: Delivers constant flow of gas until set inspiratory pressure reached which guarantees peak pressures will be reasonable
- The variable that is not set cannot be controlled (i.e., may have very high peak inspiratory pressures in order to deliver a certain TV or may dangerously hypoventilate in order to keep safe airway pressures)
- Assist " control (AC):
- Similar to CMV in that all breaths are the same controlled breaths based on machine determined variables
- In AC, patient can trigger a breath, but the same machine controlled breath is delivered
- Spontaneous breath trigger is either the reduction in airway pressure or the increase in air flow as patient initiates breath
- Intermittent mandatory ventilation (IMV):
- Delivers controlled breath at set RR
- Patient may breath spontaneously between these breaths; however:
- Spontaneous breaths are not supported
- Can lead to breath stacking as ventilator does not take patients spontaneous breaths into consideration
- In some IMV modes, spontaneous breaths can be pressure supported, but this is not the rule
- Synchronous intermittent mandatory ventilation (SIMV):
- Same as IMV, but ventilator tries to synchronize patient's spontaneous breaths with those set by RR
- Lowers risk of breath stacking
- Pressure support ventilation (PSV):
- Ventilator augments patient's spontaneous breaths with set amount of pressure
- If support is adequate to meet needed driving pressure and patient is able to initiate breaths, often most comfortable mode
- Most modern ventilators and newer modes allow for much more complex interaction between ventilator and patient as well as increased control of multiple variables:
- Newer modes are quite variable and are dependent on patient specifics.
- May be dynamic combination of more traditional types of breaths as described below
- Can often tailor breath delivery to optimize mechanics in specific disease process
- Risks of mechanical ventilation:
- Ventilator-induced lung injury (VILI): Overdistension caused by high pulmonary pressures leads to inflammation and alveolar injury
- Derecruitment injury: Inflammation and injury caused by repetitive opening and collapse of alveoli; can be reduced with appropriate use of PEEP
- Barotrauma outside lungs due to cyclical reinflation (i.e., pneumothorax, pneumoperitoneum, subcutaneous emphysema)
- Oxygen toxicity
- Decreased venous return and subsequent drop in cardiac output/BP due to elevated intrathoracic pressures
- Increased V/Q mismatch due to altered pattern of gas delivery (alveoli that usually do not get significant gas delivery in natural breathing will be responsible for more gas exchange without any augmented blood supply AND overdistension of alveoli may cause compression of alveolar blood supply)
- Loss of upper airway defenses against infection
- Associated risks of sedation (delirium, increased immobility, prolonged illness, etc.)
- Associated risks of immobility (severe myopathy, thrombosis, prolonged illness, etc.)
- Stress ulcer formation
- Problems related to endotracheal tube or tracheostomy such as tracheomalacia or vocal cord paralysis
Medication
- Sedation and analgesia strategies should prioritize pain control, target the lowest level of sedation possible, and utilize intermittent bolus therapy before resorting to infusion
- Oversedation and benzodiazepines are both associated with risk of critical illness delirium
- Propofol: 0.3 " 1 mg/kg IV loading dose, maintenance initiated at
5 " 50 Όg/kg/min IV infusion. Causes vasodilation and associated hypotension. Especially with bolus loading dose. Risk of propofol infusion syndrome with prolonged infusions. - Dexmedetomidine: 0.2 " 1.4 Όg/kg/h. Can be used with loading bolus of 1 Όg/kg. Does not cause respiratory depression. Can be associated with significant bradycardia.
- Ketamine: Load 1 " 3 mg/kg with maintenance 1 " 2
mg/kg/h. Potential benefit is avoiding hemodynamic instability seen with many other agents. Benzodiazepine dosing prior to emergence can help prevent emergence nightmares. There is controversy about using ketamine in patients
with elevated intracranial pressures, but it may actually help maintain cerebral perfusion pressure in mechanically ventilated
patients. - Fentanyl: Bolus 0.5 " 1.5 Όg/kg IM or slow IV. Infusion rates start at 1 Όg/kg/h. Consider prior opiate exposure when dosing.
- Albuterol: 2.5 " 5 mg/5 mL saline q4h via in-line endotracheal delivery
- Ipratropium bromide: 0.5 mg/2.5 saline q4h vial in-line endotracheal delivery
Follow-Up
Disposition
Admission Criteria
ICU admission required for all intubated patients
Pearls and Pitfalls
- Physiology can help you troubleshoot the vent. Remember that you control ventilation by adjusting the TV and RR and that you control oxygenation by adjusting PEEP and FiO2. Peak pressure is determined by airway resistance. Elevated peak pressures can be caused by problems such as bronchospasm, secretions, or kinked tubes. Plateau pressure is determined by lung and chest wall compliance. Elevated plateau pressures can be caused by problems such as ARDS, pulmonary fibrosis, obesity, or edema.
- Knowing the indication for mechanical ventilation is key to choosing the most appropriate and least harmful mode of ventilation and ventilator settings
- It is important to understand whether a breath is controlled or assisted, what triggers a breath, and how the breath is given in order to understand modes of ventilation. Most modern modes of ventilation are a complex combination of different types of breaths based upon goals set by the clinician or interactions with the patient.
- ARDS requires low TV ventilation and open lung ventilatory strategies can be used for severe cases
- Remember to allow time for full expiration for patients with obstructive airway disease
Additional Reading
- Gabrielli A, Layon AJ, Yu M, eds. Critical Care. 4th ed. Philadelphia, PA: Wolters Kluwer, Lippincott Wiliams and Wilkins; 2009.
- Gattinoni L, Protti A, Caironi P, et al. Ventilator-induced lung injury: The anatomical and physiological framework. Crit Care Med. 2010;30:S539 " S548.
- Nagler J, Krauss B. Capnography: A valuable tool for airway management. Emerg Med Clin North Am. 2008;26:881 " 897.
- Serpa Neto A, Cardoso SO, Manetta JA, et al. Association between use of lung-protective ventilation with lower tidal volumes and clinical outcomes in patients without acute respiratory distress syndrome: A meta-analysis. JAMA. 2012;16:1651 " 1659.
- Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Network. N Engl J Med. 2000;18:1301 " 1308.
See Also (Topic, Algorithm, Electronic Media Element)
- Dyspnea
- Respiratory Distress
Codes
ICD9
V46.11 Dependence on respirator, status
ICD10
Z99.11 Dependence on respirator [ventilator] status
SNOMED
444932008 dependence on ventilator (finding)