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
increase PEEP
re-open alveoli with PEEP
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:
pneumopericardium
acute lung injury
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