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Introduction to mechanical ventilation for junior ICU trainees and nurses.
This page is written with the assumption that the reader has a basic
understanding of respiratory physiology and respiratory failure
The problem
Getting oxygen in
Oxygen uptake via the lungs is dependent on a number of factors. Some can be
manipulated to a large extent by mechanical ventilation:
- PAO2, which in turn can be
manipulated by altering:
- inspired oxygen concentration (FIO2)
- alveolar pressure
- ventilation
- ventilation-perfusion matching - by re-opening collapsed alveoli, thereby
reducing intra-pulmonary shunting
- positive end-expiratory pressure (PEEP) helps re-open alveoli and
splint open alveoli
Getting carbon dioxide out
- Carbon dioxide elimination via the lungs is largely dependent on alveolar
ventilation.
- Alveolar ventilation = Respiratory rate x (tidal volume - dead space)
Main controls
To improve oxygenation:
- increase FIO2
- increase mean alveolar pressure
- increase mean airway pressure
- re-open alveoli with PEEP
To improve CO2 elimination:
- increase respiratory rate
- increase tidal volume
Other controls
- inspiratory time is the time over which the tidal volume is
delivered or the pressure is maintained (depending on the mode)
- in time-cycled modes either inspiratory time or I;E ratio are set
(flow is adjusted to ensure that the set tidal volume is delivered in
that time). These modes include:
- pressure control
- volume control (Siemens and Drager ventilators)
- pressure regulated volume control
- in volume-cycled modes the flow is set and inspiration ends when the
set tidal volume has been delivered. These modes include:
- volume control (Puritan-Bennett and Bear ventilators)
- in pressure support mode the patient determines the duration of
inspiration
- inspiratory pause time is only set in modes where a fixed tidal volume is
set and delivered (volume control and volume preset SIMV modes)
- expiratory time is whatever time is left over before the next breath
- I:E ratio
- =(inspiratory time + inspiratory pause time):expiration
- usually set to 1:2 to mimic usual pattern of breathing
- in general longer inspiratory times:
- improve oxygenation by:
- increasing the mean airway pressure (longer period of high
pressure increases mean airway pressure over the entire respiratory
cycle)
- allowing re-distribution of gas from more compliant alveoli to
less compliant alveoli
- increase risk of gas trapping, intrinsic PEEP and barotrauma by
reducing expiratory time
- are less well tolerated by the patient, necessitating a deeper level
of sedation
- decrease peak pressure by decreasing inspiratory flow
Trigger sensitivity
- this determines how easy it is for the patient to trigger the ventilator
to deliver a breath
- in general increased sensitivity is preferable in order to improve
patient-ventilator synchrony (ie to stop the patient "fighting"
the ventilator) but excessively high sensitivity may result in false or
auto-triggering (ie ventilator detects what it "thinks" is an
attempt by the patient to breath although the patient is apnoeic)
- triggering may be flow-triggered or pressure triggered. Flow triggering is
generally more sensitive.
- the smaller the flow or the smaller the negative pressure the more
sensitive the trigger
Rise time
- determines speed of rise of flow (volume control mode) or pressure
(pressure control and pressure regulated volume control modes)
- very short rise times may be more uncomfortable for the patient
- long rise times may result in a lower tidal volume being delivered
(pressure control mode) or higher pressure being required (volume control
and pressure regulated volume control modes)
Modes of ventilation
In general a ventilator can be set to deliver:
- a certain volume of gas in a set period of time
- the pressure generated in the lung will then be dependent on the
resistance and compliance of the respiratory system
- known as volume control mode
- a certain level of pressure for a set period of time
- the tidal volume delivered will then be dependent on the resistance
and compliance of the respiratory system
- pressure control and pressure regulated volume control modes
- in assist-control modes (volume control, pressure control, pressure regulated volume control) the ventilator guarantees that the
patient will receive the set minimum number of breaths, although he/she is
able to demand (trigger) more
- in pressure support modes the patient only receives breaths when he/she
triggers the ventilator
Respiratory
- nosocomial pneumonia
- barotrauma
- not only due to high pressures also due to high volumes and shear
injury (due to repetitive collapse and re-expansion of alveoli and due
to tension at the interface between open and collapsed alveoli
- causes:
- gas trapping
- occurs if there is insufficient time for alveoli to empty before the
next breath
- more likely to occur:
- in patients with asthma or COPD
- when inspiratory time is long (and therefore expiratory time
short)
- when respiratory rate is high (absolute expiratory time is short)
- results in progressive hyperinflation of alveoli and progressive rise
in end-expiratory pressure (known as intrinsic PEEP)
- may result in:
- barotrauma
- cardiovascular compromise due to high intrathoracic pressure. In
an extreme case can lead to cardiac arrest with pulseless electrical
activity.
- quantitative measurement of intrinsic PEEP can be obtained in an apnoeic
patient by using the expiratory pause hold control on the ventilator. This
allows equilibration of pressures between the alveoli an the ventilator
allowing the total PEEP to be measured. The value for total PEEP can be read
from the airway pressure dial or the PEEP display
- Intrinsic PEEP=Total PEEP-Set PEEP
- Examination of the flow-time curve from the ventilator gives an indication
that there is intrinsic PEEP but does not give an indication of the
magnitude. The patient does not need to be apnoeic.
Cardiovascular effects
Preload
- positive intrathoracic pressure reduces venous return
- exacerbated by
- high inspiratory pressure
- prolonged inspiratory time
- PEEP
Afterload
= ventricular wall tension (T) during contraction
where Ptm=transmural pressure, R=radius and H=wall
thickness
Ptm=intracavity pressure-pleural pressure
By increasing pleural pressure positive pressure ventilation decreases
transmural pressure and hence afterload
Cardiac output
- reduced preload will tend to decrease cardiac output
- reduced afterload will tend to increase cardiac output
- net effect depends on LV contractility. In patients with normal
contractility positive pressure ventilation tends to decrease cardiac output
while in patients with decreased contractility it tends to increase cardiac
output
- effect on cardiac function also important to remember when weaning
patients. Failure to wean may be due to failure to cope with increased
preload and afterload
Myocardial oxygen consumption
- reduced by positive pressure ventilation
Related topics
Weaning
Troubleshooting
More on mechanical ventilation
Tutorial
Click here to download tutorial on basic mechanical ventilation
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