science saving life intensivecare foundation. Handbook of Mechanical. Ventilation. A User's Guide. The Intensive Care Foundation. Mechanical ventilation is the most used short-term life support technique worldwide the future of mechanical ventilation, addressing avenues for improvement. How does a ventilator work? The ventilator is connected to the person through a tube. (endotracheal or ET tube) that is placed into the mouth or nose and down.
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2/ Initiating (and de-escalating) mechanical ventilation. text (pdf). THINK: Conventionally, we distinguish between lung damage due to high. An important concept to remember: normal breathing is a negative-pressure phenomenon; mechanical ventilation is. POSITIVE pressure ventilation. The end . Mechanical Ventilation. CMV modes include or Assist Control (AC) includes Pressure Controlled (PC), or. Volume Controlled (VC) ventilation. Pressure.
Initial RR should be comfortable for the patient bpm should suffice. A very important caveat on this is for patients with severe metabolic acidosis.
For these patients, the minute ventilation should at least be matched to their pre-intubation ventilation as failure to do so will worsen acidosis and can precipitate complications such as cardiac arrest.
Pay close attention to blood pressure and patient comfort while doing this. An ABG should be obtained 30 minutes after intubation and changes to the ventilator settings should be made in accordance with ABG findings. Attention should be given to the volume curves in the ventilator display as a reading showing that the curve is not coming back to zero at the time of exhalation is indicative of incomplete exhalation and development of auto-PEEP and corrections to the vent should be made immediately.
To correct for hypoxia increasing any of these parameters should raise the oxygenation.
Special attention should be paid to the possible adverse effects of raising PEEP which can cause barotrauma and hypotension. Raising FiO2 does not come without its concerns as high FiO2 can cause oxidative damage in the alveoli. Another important aspect of managing oxygen content is to define a goal for oxygenation. A sudden drop in oxygen saturation should raise suspicion for tube misplacement, pulmonary embolism, pneumothorax, pulmonary edema, atelectasis, or development of mucus plugs. Hypercapnia: To modify CO2 content in blood one needs to modify alveolar ventilation.
Raising the rate or the tidal volume, as well as increasing T low, will increase ventilation and decrease CO2. Consideration has to be made while increasing the rate, as this will also increase the amount of dead space and might not be as effective as tidal volume.
Other important circumstances are those of elevated pressures. As discussed, two pressures are important in the system: peak and plateau. The peak pressure is a measure of airway resistance as well as compliance and includes the tubing and bronchial tree. Plateau pressures are a reflection of alveolar pressure and thus of lung compliance. If there is an increase in peak pressure, the first step to take is to do an inspiratory hold and check the plateau. Elevated peak pressure and normal plateau pressure: high airway resistance and normal compliance.
For diagnosis, you will find a patient with unilateral breath sounds and a dull contralateral lung atelectatic lung. Pneumothorax: Diagnosis will be made by hearing breath sounds unilaterally and finding a hyper-resonant contralateral lung.
In intubates patients, placement of a chest tube is imperative as the positive pressure will only worsen the pneumothorax. Atelectasis: Initial management consists of chest percussions and recruitment maneuvers. The accumulation of trapped air will increase pulmonary pressures and cause barotrauma and hypotension. The patient will be difficult to ventilate.
To prevent and resolve auto-PEEP, enough time should be given for the air to leave the lungs during exhalation. The same effect can be achieved by using a square waveform for inspiratory flow, what this means is that we can set the ventilator to deliver the full flow from beginning to end of inhalation. Other techniques that can be implemented are to assure adequate sedation to prevent patient hyperventilating and the use of bronchodilators and steroids to decrease airway obstruction.
If auto-PEEP is severe causing hypotension, disconnecting the patient from the vent and letting time for all the air to be exhaled may be a life-saving measure. Important causes include hypoxia, auto-PEEP, not satisfying patients oxygenation or ventilation demands, pain and discomfort.
After ruling out important causes as pneumothorax or atelectasis, patient comfort should be considered and proper sedation and analgesia should be assured. Consider changing the ventilator mode as some patients may respond better to different modes of ventilation.
Special Circumstances Special attention to vent settings should be taken in the following circumstances: COPD is a special case, as lungs in pure COPD have high compliance which causes a high tendency for dynamic airflow obstruction due to airway collapse and air trapping, making COPD patients very prove to develop auto-PEEP. Using a preventive ventilation strategy with high flow and low respiratory rate may help prevent auto-PEEP.
Another important aspect to consider in chronic hypercapnic respiratory failure due to COPD or another reason is that there is no need to correct the CO2 back to normal, as these patients usually have a metabolic compensation for their respiratory problems.
To prevent this, CO2 goals should be determined based on pH and previously known or calculated baseline.
Asthma: As with COPD patients with asthma are very prone to air trapping, although the reason is pathophysiologically different. In asthma, air trapping is caused by inflammation, bronchospasm, and mucus plugs, not airway collapse.
Cardiogenic pulmonary edema: High PEEP may decrease venous return and help resolve pulmonary edema as well as aid in cardiac output. The concern should be to make sure the patient is adequately diuresed before extubating, as the removal of the positive pressure may precipitate new pulmonary edema. An open lung strategy with high PEEP and low tidal volume have been shown to improve mortality.
Pulmonary embolism is a difficult situation. Intubating these patients will increase RA pressure and further decrease venous return, which may precipitate shock.
If there is no way to prevent intubation, careful attention to blood pressure and initiation of vasopressors should be done promptly. Severe pure metabolic acidosis is a concern. When intubating these patients, careful attention should be paid to their pre-intubation minute ventilation. If this ventilation is not provided when starting mechanical support, pH will drop further possibly precipitating cardiac arrest.
Other Issues Weaning from Mechanical Ventilation Mechanical ventilation can be a lifesaving intervention and has impacted millions of lives since its invention, but it is not without complications.
Shortening the ventilator time has shown to reduce ventilation-related complications like pneumonia, so actively pursuing liberation from mechanical ventilation the so called ventilation weaning is imperative in every ventilated patient.
After these criteria have been satisfied it is time to perform a spontaneous breathing trial SBT. This is usually protocolized in all intensive care units ICU and should be performed in every patient who is stable and in whom the indication for mechanical ventilation has resolved. The second parameter is the SBT itself.
To perform this, the ventilator support should be reduced to a minimum. This can be done either via T-piece or pressure support.
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.
Normal I:E is 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.
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. Risk of barotrauma is dependent on Ppeak, while cardiac output response depends on Pmean. 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 , ].
It does not reduce lung edema can cause it or prevent mediastinal bleeding. It can be delivered through a mask and is can be used in obstructive sleep apnea esp.
All these alterations were responsive to treatment. High pressure and PEEP improve atelectasis, but may cause pneumothorax.
Used to decrease the work of breathing. Used to wean patient from ventilator and indicated in obstructive sleep apnea. Courey, A. Critical Care Nurse, 31 3 , Modes of mechanical ventilation. Understanding the Alphabet Soup of Mechanical Ventilation.
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Concentration of oxygen in the inspired air. Set number of ventilator breaths per minute. Breaths can be triggered by: Flow of air into the lung can target a predetermined flow rate i.
Signal for a ventilator to end inspiration may be related to volume i. Volume of gas exchanged with each breath. Pressure remaining in the lungs at end expiration. Provides additional pressure during inspiration to ensure a larger V t with minimal patient effort.