Modes of Mechanical Ventilation

The Modern Approach to Modes of Mechanical Ventilation

While modes have classically been divided up into pressure or volume controlled modes, a more modern approach describes ventilatory modes based on three characteristics – the trigger (flow versus pressure), the limit (what determines the size of the breath), and the cycle (what actually ends the breath). In both VCV and PCV, time is the cycle, the difference being in how the time to cessation is determined. PSV, by contrast, has a flow cycle.

Note also that the lines between pressure and volume controlled methods are being continually blurred by increasingly complex modes. If alarms and backup modes are properly set, the “disadvantages” of classic modes (e.g. possibility of insufficient minute ventilation in PCV) can be essentially eliminated

For historical reasons, the following modes will be separated into volume controlled, pressure controlled, and other modes

Volume Modes

Assist-Control Ventilation (ACV)

Also known as continuous mandatory ventilation (CMV). Each breath is either an assist or control breath, but they are all of the same volume. The larger the volume, the more expiratory time required. If the I:E ratio is less than 1:2, progressive hyperinflation may result. ACV is particularly undesirable for patients who breathe rapidly – they may induce both hyperinflation and respiratory alkalosis. Note that mechanical ventilation does not eliminate the work of breathing, because the diaphragm may still be very active.

Synchronized Intermittent-Mandatory Ventilation (SIMV)

Guarantees a certain number of breaths, but unlike ACV, patient breaths are partially their own, reducing the risk of hyperinflation or alkalosis. Mandatory breaths are synchronized to coincide with spontaneous respirations. Disadvantages of SIMV are increased work of breathing and a tendency to reduce cardiac output, which may prolong ventilator dependency. The addition of pressure support on top of spontaneous breaths can reduce some of the work of breathing. SIMV has been shown to decrease cardiac output in patients with left-ventricular dysfunction [Crit Care Med 10: 423, 1982]

ACV vs. SIMV

Personal preference prevails, except in the following scenarios: 1. Patients who breathe rapidly on ACV should switch to SIMV 2. Patients who have respiratory muscle weakness and/or left-ventricular dysfunction should be switched to ACV

Pressure Modes

Pressure-Controlled Ventilation (PCV)

Less risk of barotrauma as compared to ACV and SIMV. Does not allow for patient-initiated breaths. The inspiratory flow pattern decreases exponentially, reducing peak pressures and improving gas exchange [Chest 122: 2096, 2002]. The major disadvantage is that there are no guarantees for volume, especially when lung mechanics are changing. Thus, PCV has traditionally been preferred for patients with neuromuscular disease but otherwise normal lungs

Pressure Support Ventilation (PSV)

Allows the patient to determine inflation volume and respiratory frequency (but not pressure, as this is pressure-controlled), thus can only be used to augment spontaneous breathing. Pressure support can be used to overcome the resistance of ventilator tubing in another cycle (5 – 10 cm H20 are generally used, especially during weaning), or to augment spontaneous breathing. PSV can be delivered through specialized face masks.

Pressure Controlled Inverse Ratio Ventilation (PCIRV)

Pressure controlled ventilatory mode in which the majority of time is spent at the higher (inspiratory) pressure. Early trials were promising, however the risks of auto PEEP and hemodynamic deterioration due to the decreased expiratory time and increased mean airway pressure generally outweight the small potential for improved oxygenation

Airway Pressure Release Ventilation (APRV)

Airway pressure release ventilation is similar to PCIRV – instead of being a variation of PCV in which the I:E ratio is reversed, APRV is a variation of CPAP that releases pressure temporarily on exhalation. This unique mode of ventilation results in higher average airway pressures. Patients are able to spontaneously ventilate at both low and high pressures, although typically most (or all) ventilation occurs at the high pressure. In the absence of attempted breaths, APRV and PCIRV are identical. As in PCIRV, hemodynamic compromise is a concern in APRV. Additionally, APRV typically requires increased sedation

Dual Modes

Pressure Regulated Volume Control (PRVC)

A volume target backup is added to a pressure assist-control mode

Interactive Modes

Proportional Assist Ventilation (PAV)

During PAV, the clinician sets the percentage of work of breathing to be provided by the ventilator. PAV uses a positive feedback loop to accomplish this, which requires knowledge of resistance and elastance to properly attenuate the signal

Compliance and resistance must therefore be periodically calculated – this is accomplished by usingintermittent end-inspiratory and end-expiratory pause maneuvers (which also calculate auto PEEP). In addition to percent support, the clinician sets the trigger and the cycle (what actually ends the breath)

The theoretical advantage of PAV is increased synchrony compared to PSV (which provides the same amount of support regardless of how much effort the patient makes)

Proportional Assist Ventilation: Summary

• Independent Variables: % WOB; trigger; cycle
• How It Works: positive feedback loop (requires calcluation of resistance and elastance)
• Theoretical Advantage(s): better synchrony

Neurally Adjusted Ventilatory Assist (NAVA)

Addtional Modes, Strategies, Parameters

Inverse Ratio Ventilation

Inverse Ratio Ventilation (IRV) is a subset of PCV in which inflation time is prolonged (In IRV, 1:1, 2:1, or 3:1 may be use. Normal I:E is 1:3). This lowers peak airway pressures but increases mean airway pressures. The result may be improved oxygenation but at the expense of compromised venous return and cardiac output, thus it is not clear that this mode of ventilation leads to improved survival. IRV’s major indication is in patients with ARDS with refractory hypoxemia or hypercapnia in other modes of ventilation [Am J Surg 183: 151, 2002]

Adaptive Support Ventilation

Calculates the expiratory time constant in order to guarantee sufficient expiratory time and thus minimize air trapping

Tube Compensation

Positive End Expiratory Pressure (PEEP)

Note: PEEP is not a ventilatory mode in and of itself

Does not allow alveolar pressure to equilibrate with the atmosphere. PEEP displaces the entire pressure waveform, thus mean intrathoracic pressure increases and the effects on cardiac output are amplified. Low levels of PEEP can be very dangerous, even 5 cm H20, especially in patients with hypovolemia or cardiac dysfunction. When measuring the effectiveness of PEEP, cardiac output must always be calculated because at high saturations, changes in Q will be more important than SaO2 – never use SaO2 as an endpoint for PEEP. The effects of PEEP are not caused by the PEEP itself but by its effects on Ppeak and Pmean, both of which it increases. Risk of barotrauma is dependent on Ppeak, while cardiac output response depends on Pmean. In fact, in a recent study of ARDS patients, it was shown that increasing PEEP from 0 to 5, 10, and 15 cm H2O was met with corresponding decreases in CO [Crit Care Med 31: 2719, 2003]

PEEP is indicated clinically for 1) low-volume ventilation cycles 2) FiO2 requirements > 0.60, especially in stiff, diffusely injured lungs such as ARDS and 3) obstructive lung disease. Do NOT use in pneumonia, which is not diffuse, and where PEEP will adversely affect healthy tissue and worsen oxygenation. One way to gauge the effect of PEEP is to look at peak inspiratory pressure (PIP) – if PIP increases less than the added PEEP, then the PEEP improved the compliance of the lungs.

A recent phenomena in the understanding of PEEP is the principle of recruitable lung volume: while this cannot be calculated, it can be estimated by looking at CT scans: atalectasis containing air is recruitable, that devoid of air is not, the idea being only apply PEEP to recruitable lungs, otherwise you may just be inducing ARDS [NEJM 354: 1775, 2006]. The effects of PEEP can also be monitored by tracking the PaO2/FiO2 ratio (it should increase).

ARDSnet II: 8.3 vs. 13.2 cm H2O: in patients with acute lung injury and ARDS who receive mechanical ventilation with a tidal-volume goal of 6 ml per kilogram of predicted body weight and an end-inspiratory plateau-pressure limit of 30 cm of water, clinical outcomes are similar whether lower or higher PEEP levels are used [NEJM 351: 327, 2004]

PEEP should not be used routinely. It does not reduce lung edema (can cause it) or prevent mediastinal bleeding.

Continuous Positive Airway Pressure (CPAP)

Positive pressure given throughout the cycle. It can be delivered through a mask and is can be used in obstructive sleep apnea (esp. with a nasal mask), to postpone intubation, or to treat acute exacerbations of COPD

Prone Ventilation

May improve oxygenation by redistributing pulmonary blood flow, however a multicenter, randomized trial of 304 patients showed that this improved oxygenation is not accompanied by a change in survival [NEJM 345: 568, 2001] – this was corroborated by two smaller, subsequent randomized controlled trials, which showed an insignificant trend towards improved mortality [J Trauma 59: 333, 2005; Am J Respir Crit Care Med 173: 1233, 2006]. This may not hold for neurosurgery patients – in a study of 16 SAH (H&H 3 or higher) patients in ARDS, PaO2 increased from 97.3 to 126.6 mm Hg in the prone position and brain tissue oxygen partial pressure increased from 26.8 to 31.6 mm Hg (both p <.0001), despite the fact that ICP increased from 9.3 to 14.8 mm Hg and CPP decreased from 73.0 to 67.7 (both p <.0001) [Crit Care Med 31: 1831, 2003]

High Frequency Oscillatory Ventilation

In one study of 5 patients with TBI and ARDS (390 datasets of ICP, CPP, PaCO2 collected), treated HFOV with – ICP increased in 11 of 390 datasets, CPP was reduced (<70 mmHg) in 66 of 390, and P(a)CO2 variations (<4.7 kPa; >6.0 kPa) were observed in 8. All these alterations were responsive to treatment. PaO2/FIO2 improved in four patients [Acta Anaes Scand 49: 209, 2005]

High Frequency Percussive Ventilation

10 severe TBI patients with a Glasgow Coma Score (GCS) < 9, placed on HFPV. There was an increase in PF ratio (91.8 to 269.7, p < 0.01), PEEP (14 to 16 +/- 3.5), and mean airway pressure (20.4 to 23.6) 16 hours after institution of HFPV. There was a decrease in ICP (30.9 to 17.4, p < 0.01), PC02 (37.7 to 32.7, p < 0.05), and PIP (49.4 to 41, p < 0.05) at 16 hours [J Trauma 57: 542, 2004]

Neurotransmitters

Definition

Neurotransmitters are chemicals located and released in the brain to allow an impulse from one nerve cell to pass to another nerve cell.

Description

There are approximately 50 neurotransmitters identified. There are billions of nerve cells located in the brain, which do not directly touch each other. Nerve cells communicate messages by secreting neurotransmitters. Neurotransmitters can excite or inhibit neurons (nerve cells). Some common neurotransmitters are acetylcholine, norepinephrine, dopamine, serotonin and gamma aminobutyric acid (GABA). Acetylcholine and norepinephrine are excitatory neurotransmitters while dopamine, serotonin, and GABA are inhibitory. Each neurotransmitter can directly or indirectly influence neurons in a specific portion of the brain, thereby affecting behavior.

Mechanism of impulse transmission

A nerve impulse travels through a nerve in a long, slender cellular structure called an axon, and it eventually reaches a structure called the presynaptic membrane, which contains neurotransmitters to be released in a free space called the synaptic cleft. Freely flowing neurotransmitter molecules are picked up by receptors (structures that appear on cellular surfaces that pick up molecules that fit into them like a "lock and key") located

in a structure called the postsynaptic membrane of another nearby neuron. Once the neurotransmitter is picked up by receptors in the postsynaptic membrane, the molecule is internalized in the neuron and the impulse continues. This process of nerve cell communication is extremely rapid

Once the neurotransmitter is released from the neurotransmitter vesicles of the presynaptic membrane, the normal movement of molecules should be directed to receptor sites located on the postsynaptic membrane. However, in certain disease states, the flow of the neurotransmitter is defective. For example, in depression, the flow of the inhibitory neurotransmitter serotonin is defective, and molecules flow back to their originating site (the presynaptic membrane) instead of to receptors on the postsynaptic membrane that will transmit the impulse to a nearby neuron.
The mechanism of action and localization of neurotransmitters in the brain has provided valuable information concerning the cause of many mental disorders, including clinical depression and chemical dependency, and in researching medications that allow normal flow and movement of neurotransmitter molecules.

Neurotransmitters are chemicals that transmit messages from one nerve cell (neuron) to another. The nerve impulse travels from the first nerve cell through the axon—a single smooth body arising from the nerve cell— to the axon terminal and the synaptic knobs. Each synaptic knob communicates with a dendrite or cell body of another neuron, and the synaptic knobs contain neurovesicles that store and release neurotransmitters. The synapse lies between the synaptic knob and the next cell. For the impulse to continue traveling across the synapse to reach the next cell, the synaptic knobs release the neurotransmitter into that space, and the next nerve cell is stimulated to pick up the impulse and continue it.

Neurotransmitters, mental disorders, and medications

Schizophrenia

Impairment of dopamine-containing neurons in the brain is implicated in schizophrenia , a mental disease marked by disturbances in thinking and emotional reactions. Medications that block dopamine receptors in the brain, such as chlorpromazine and clozapine , have been used to alleviate the symptoms and help patients return to a normal social setting.

Depression

In depression, which afflicts about 3.5% of the population, there appears to be abnormal excess or inhibition of signals that control mood, thoughts, pain, and other sensations. Depression is treated with antidepressants that affect norepinephrine and serotonin in the brain. The antidepressants help correct the abnormal neurotransmitter activity. A newer drug, fluoxetine (Prozac), is a selective serotonin reuptake inhibitor (SSRI) that appears to establish the level of serotonin required to function at a normal level. As the name implies, the drug inhibits the re-uptake of serotonin neurotransmitter from synaptic gaps, thus increasing neurotransmitter action. In the brain, then, the increased serotonin activity alleviates depressive symptoms.

Alzheimer's disease

Alzheimer's disease , which affects an estimated four million Americans, is characterized by memory loss and the eventual inability for self-care. The disease seems to be caused by a loss of cells that secrete acetylcholine in the basal forebrain (region of brain that is the control center for sensory and associative information processing and motor activities). Some medications to alleviate the symptoms have been developed, but presently there is no known treatment for the disease.

Generalized anxiety disorder

People with generalized anxiety disorder (GAD) experience excessive worry that causes problems at work and in the maintenance of daily responsibilities. Evidence suggests that GAD involves several neurotransmitter systems in the brain, including norepinephrine and serotonin.

Attention-deficit/hyperactivity disorder

People affected by attention-deficit/hyperactivity disorder (ADHD) experience difficulties in the areas of attention, overactivity, impulse control, and distractibility. Research shows that dopamine and norepinephrine imbalances are strongly implicated in causing ADHD.

Others

Substantial research evidence also suggests a correlation of neurotransmitter imbalance with disorders such as borderline personality disorders , schizotypal personality disorder , avoidant personality disorder , social phobia , histrionic personality disorder , and somatisation disorder .