Many of the beneficial and adverse effects of mechanical ventilation are associated with the mean airway pressure.
In order to fully understand mean airway pressure, we first need to clarify the normal pressures in the lungs during both inhalation and exhalation and the changes that occur both during normal breathing and during a mechanically ventilated breath.
The fall in intrapleural pressure facilitates movement of gases into and out of the lungs and importantly also improves venous return to the heart.
During positive pressure ventilation, which is what occurs during mechanical ventilation, the mean intrathoracic pressure is usually positive. So the pressure increases during inhalation and decreases during expiration.
The consequence of this, for venous return (blood flowing back to the heart), is that it is greatest during exhalation and may be compromised if the expiratory time is too short or mean alveolar pressures too high.
It is related to the amount of pressure applied and the duration of time that pressure is applied for. This applies to both the inspiratory phase and the expiratory phase of the cycle.
Shunt is perfusion without ventilation and is the other side of the coin to dead space ventilation- see below. This occurs in the lungs when the blood passes through from the right side of the heart to the left side without participating in gas exchange. Hypoxemia is the outcome of such a shunt.
There are two types of shunt- anatomical and capillary shunt.
Anatomical shunt occurs when blood passes from the right side of the heart to the left side without going through the lungs at all. Normal anatomic shunt occurs with the Thesebian veins which are minute valveless veins in the walls of all four heart chambers and which drain the myocardium. The bronchial circulation- i.e. that which supplies blood to the tissues of the lungs also contributes to a normal anatomical shunt.
So you can see from the diagram that this blood supply does not pass by an alveolus supplied with oxygen. Therefore there is no gas exchange. The non-reoxygenated blood then joins the oxygenated blood causing a dilutional effect.
Positive pressure ventilation can, however, increase pulmonary vascular resistance which can increase blood flow through an anatomic shunt thereby decreasing blood flow through the lungs and worsening hypoxemia. So one needs to be cautious when there is an anatomic shunt present.
Capillary shunt occurs when the blood is flowing past an alveoli, but that alveoli is unventilated. Then again there is no gas exchange taking place. So again, as you can see from the diagram, poorly oxygenated blood then mixes with the oxygenated blood 'watering' it down in effect.
A capillary shunt can be as a result of a number of conditions including ARDS, pulmonary oedema, atelectasis and pneumonia.
Positive pressure ventilation can usually manage to overcome two things.
Firstly, during inspiration, it can exceed alveolar opening pressure which helps to recruit otherwise collapsed, and therefore non-functioning, alveoli which in turn will improve oxygenations.
Secondly, positive pressure ventilation will provide an expiratory pressure greater than alveolar closing pressure which then prevents collapse of the same alveoli.
Tidal Volume = amount of gas inhaled or exhaled with a single breath.
Minute Ventilation = volume of gas breathed in one minute = tidal volume multiplied by respiratory rate.
Ventilation is either dead space ventilation or alveolar ventilation
Dead space ventilation can be either mechanical dead space or anatomical dead space.
Mechanical dead space refers to the ventilator circuit and the rebreathed gases that this causes. The conducting part of the lungs i.e. trachea, bronchus, bronchioles, and terminal bronchioles, play no part in gas exchange and amount to about 150mls. This is the anatomic dead space.
This anatomic dead space is a fixed amount. So if the tidal volumes become smaller then the anatomic dead space becomes a bigger proportion of that tidal volume. As a consequence, in order to compensate for this, there will need to be a greater minute volume to maintain alveolar ventilation. So the respiratory rate would need to be increased.
This is collapse or closure of the lung resulting in that area no longer contributing to oxygenation.
Ventilator Induced Lung Injury
Overdistension of the alveolar causes lung injury. The plateau should ideally be as low as possible, preferably below 30cmH2O. Over distension is also limited by using lower tidal volumes or a lung protective strategy.
Ventilator-associated pneumonia most often results from aspiration of secretions around the cuff. Patient positioning and suctioning can help reduce the risk.
High inspired oxygen is considered toxic and it is not recommended to use oxygen concentrations above 60% if possible.
Hyperventilation lowers PaCO2 and increases pH. Respiratory alkalosis causes hypokaleamia, decreases ionised calcium and increased affinity of haemoglobin for oxygen.
For those patients with a chronically compensated respiratory acidosis i.e. COPD a relative hyperventilation can occur when mechanical ventilation is provided. if a normal PaCO2 is established in such patients then there may develop an elevated pH. So hypercapnia may be preferred in these cases.
Positive pressure ventilation can reduce cardiac output which can result in hypotension. The increased intrathoracic pressure decreases venous return and right heart filling which may reduce cardiac output.
There can be reductions in atrial natriuretic peptide and elevations in anti diuretic hormone with mechanical ventilation. Along with the decreased renal perfusion due to lowered cardiac output there can be worsening urine output.
Gastric distension and stress ulcer formation can both occur. Bundles of care should include stress ulcer prophylaxis to help prevent this.
It is crucial to get nutritional support right with the mechanically ventilated patient. Underfeeding can result in respiratory muscle catabolism and overfeeding increases metabolic rate and therefore raises the required minute ventilation.
Delirium is a problem commonly encountered with the mechanically ventilated patient. In order to minimise the possibility, it is important to be aware of which sedative agents are being used; for example propofol versus dexmedetomidine.
Both polyneuropathy and poly myopathy can result from prolonged ventilation. With paralysis ventilator diaphragm dysfunction can occur. Early mobilisation seems to be increasingly important in this type of patient.
The placement of an endotracheal tube or tracheostomy tube puts the patient at risk of laryngeal oedema, trauma, ventilator acquired pneumonia and long-term dysphagia.
Being ventilated may make it difficult for the patient to sleep. Studies have shown that ITU patients will only sleep for very short periods of time, a matter of minutes. This can exacerbate any delirium they may suffer.
For the patient to be comfortable on the ventilator they need to work well together. When this does not happen it is known as asynchrony. This can occur because of auto PEEP, incorrect flow or time settings or poor trigger sensitivity for example.
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