Clinical Scenario: A 57 year old male undergoes upper abdominal surgery. He refused an epidural. The intraoperative course was uneventful. He was given 2mg hydromorphone in the OR. He was extubated, breathing 360 ml tidal volumes; arousable. Shortly after arrival to the recovery room, the patient develops acute respiratory distress. His respiratory rate increases to 33 breaths per minute, SpO2 is 92%, heart rate increases to 110 beat/min, blood pressure 98/50 mmHg. On examination, his pupils are pinpoint but reacting, he is moving air into both of his lungs but there is little air entry into his lung bases.
A non-rebreather facemask is placed: his SpO2 remains 92%.
1. Identify the problem
What is the principle diagnosis?
The patient is clearly in acute respiratory distress; however the cause and reversibility of the problem are unclear. It is imperative that the bedside clinician have a systematic approach to diagnosis and management. The cause of the problem may lie at any stage in the process of initiating a breath to exchanging gas. This tutorial focuses on the diagnosis.
Patients in recovery room with acute respiratory distress have one or more of the following three problems: failure to ventilate, as characterized by a high PaCO2, failure to oxygenate, as characterized by low PaO2, or failure to maintain their airway (figure 1). All three may co-exist: for example, a patient that receives excess opioids my hypoventilate, obstruct their airway due to opioids and carbon dioxide narcosis, and become hypoxic due to absorption atelectasis, failure to replenish alveolar oxygen and alveolar CO2 buildup. Nevertheless, the primary problem is failure to ventilate, due to central loss of respiratory drive. Hence, to make a diagnosis, one needs to identify the primary problem.
There are three major components to the respiratory apparatus:
- Central chemoreceptors: in the brainstem that detect carbon dioxide and initiate the respiratory pump. This requires an intact brainstem and cervical nerve roots.
- The respiratory pump: the phrenic nerves (and on occasion the intercostals nerves) initiate diaphragmatic contraction. This requires and intact neuromuscular junction and sufficient diaphragmatic muscular tissue to increase the volume of the thoracic cavity. This leads to increased negative pressure within the pleura, stretching the alveoli. Flow of gas into the alveoli is known as ventilation.
- Alveolar-capillary interface: gas must flow across the alveolar capillary interface to enter and leave the blood. This is known as ventilation perfusion matching and is reliant on alveolar gas volume (particularly in end expiration – the functional residual capacity) and pulmonary blood flow.
The problem is either central – a problem of respiratory drive, peripheral – a problem of the respiratory pump, large airway – a problem of gas transfer, or alveolar – a problem of gas exchange (figure 2).
- Central Ventilation: the neurologic system is not activating respiration in response to an increase in arterial CO2 tension
- Peripheral Ventilation: the thoracic pump (chest and diaphragm) is not effective in guaranteeing adequate minute ventilation.
- Gas Transfer: air does not pass effectively from the upper to the lower airway due for example to increased airway resistance.
- Gas Exchange:
- Gas does not to pass effectively from alveoli to capillaries due to a pathologic process in the interstitial space (diffusion defect).
- Ventilation is being wasted – alveoli are being ventilated but not perfused: dead space ventilation or more air than the blood can utilize (high ventilation/perfusion (V/Q) ratio the extreme version being dead space ventilation).
- Blood flow is inadequately utilized and blood is passing through the lungs without coming into contact with aerated alveoli: perfused but not ventilated – shunt or ventilation falls behind blood flow (low V/Q ratio the extreme version being right to left shunt).
2. Understand the problem
What is the mechanism of injury?
Failure to ventilate is the most common cause of acute respiratory distress in the recovery room. It is characterized by reduced alveolar ventilation which manifests as an increase in the PaCO2 > 50 mmHg (6.5kPa). The best method of classifying this is to follow the respiratory pathways from the brainstem to the alveoli, and then ask whether a pathology exists at each particular site. Often patients have multiple problems: e.g. narcosis, pulmonary edema, pleural effusion, obesity
Central: loss of ventilatory drive due to general anesthetic agents (propofol principally), benzodiazepines, narcosis, stroke or brain injury
Spinal: spinal or epidural anesthesia; spinal cord injury, cervical – loss of diaphragmatic function, thoracic – loss of intercostals.
Peripheral: phrenic nerve injury in neck or thoracic surgery
Persistent neuromuscular blockade; diaphragmatic trauma; myopathic disorders – myasthenia gravis (patient post op thymectomy).
Chest Wall – flail chest; intra-abdominal hypertension (abdominal packs placed).
Pleura – pleural effusions, pneumothorax (patient post op thoracic or retroperitoneal surgery: nephrectomy, abdominal aortic aneurysm, esophagectomy).
Airways – airway obstruction: laryngeal edema, inhalation of a foreign object (tooth or throat pack), bronchospasm.
Oxygenation failure occurs at a microscopic level at pulmonary capillary-alveolar interface. Two different injuries can occur at this level, either individually or in combination:
Diffusion abnormality – thickening of the alveoli (pulmonary fibrosis). There is an obstruction to effective gas exchange due to material in the interstitial space. The patient will have an antecedent history of hypoxemia.
Ventilation/Perfusion Mismatch: Dead Space Ventilation (or high V/Q): alveoli are ventilated but not perfused. This is unusual in the extubated patient, an usually results from significant hypovolemia
Figure 2 Causes of Respiratory Failure
Ventilation Perfusion Mismatch (figure 3): this occurs when lung units well perfused but poorly ventilated. The extreme version is right (as in right side of the heart) to left shunt (blood flows through the lungs without coming into contact with aerated lung tissue. This lung injury is resistant to oxygen therapy. This frequently occurs in patients that have upper abdominal or chest surgery secondary to segmental lung collapse – atelectasis. Atelectasis may actually be worsened by oxygen therapy, due to rapid reabsorption.
Less severe, and usually oxygen sensitive, ventilation-perfusion mismatch is the inevitable consequence of major surgery. The time constants in many lung units are altered due to edema in the lung tissue and secretions in the major and minor airways. This results in an alteration of the dynamics of gas transport: alveolar oxygen tension is slower to be replenished, carbon dioxide is more slowly removed.
Figure 3: Ventilation-Perfusion Mismatch. Alveolar unit A has normal ventilation and perfusion, hence the pulmonary capillary (arterial side) oxygen tension (PcO2) is 100mmHg (13kPa). Unit C is ventilated but not perfused. It does not contribute to gas exchange. Unit B is partially ventilated, but due to it’s long time constant (due to secretions), the alveolar oxygen tension is below normal, and the PcO2 is reduced to 70mmHg (9kPa). When all lung units are accounted for, the result is hypoxemia (PaO2 70mmHg/9kPa)
Figure 4: Oxygen therapy effectively treats ventilation perfusion mismatch by increasing the fraction of gas in the alveolus that is oxygen, thus increasing the PAO2 (alveolar O2). It also reverses pulmonary vasoconstriction and reduces dead space.
Figure 5: Right to left intrapulmonary shunt: in this example, 50% of the pulmonary circulation is flowing thru collapsed lung tissue. Because hemoglobin can only be saturated to 100%, regardless of the quantity of oxygen that is delivered to normal lung tissue, it is not possible to compensate for the intra-pulmonary shunt.
3. Differential diagnosis / Work the problem
How do you make the diagnosis?
Acute respiratory failure is usually a problem of either failure to oxygenate, as characterized by a low PaO2, or failure to ventilate, as characterized by a high PaCO2. Where hypoxemia and hypercarbia co-exist, oxygenation should be considered the primary problem.
Figure 6: Assessing the Patient with Acute Respiratory Failure
The key to making the diagnosis is to look at the patient’s breathing pattern. If the patient is taking slow shallow breaths, with normal synchrony between opening of the mouth to inhale and movement of the chest outwards and downwards, then the problem is most likely ventilatory failure secondary to central respiratory depression. This most commonly results from opioid administration, but may also follow the administration of midazolam/lorazepam or discontinuation of a propofol infusion.
If the patient is taking rapid shallow breaths, the problem is either ventilatory failure secondary to a peripheral problem or oxygenation failure secondary to ventilation-perfusion mismatch. The key to separating the two is the clinical circumstance and the presence or absence of hypoxemia (low SpO2 or requirement for high FiO2). In the absence of hypoxemia, a neuromuscular problem should be considered – such as residual neuromuscular blockade or a dense epidural block that paralyses the intercostal muscles. One also sees this pattern in patients with low physiologic reserve, the malnourished and the critically ill. In patients that have undergone thoracic surgery or retroperitoneal surgery, a high clinical suspicion for pneumothorax should be considered. This is characterized by hypoxemia, unilateral breaths sounds, and, in severe cases, hypotension.
Rapid shallow breathing with hypoxemia is caused by ventilation perfusion mismatch. This is usually caused by retained secretions and/or atelectasis. This most commonly occurs in patients that have undergone abdominal surgery, are morbidly obese or have been positioned intraoperatively in the Trendelenberg position.
Pulmonary embolism should be suspected in patients that have undergone pelvic or hip surgery with rapid shallow breathing and hypoxemia, associated with tachycardia and hypotension.
An obstructed breathing pattern is suggestive of upper or middle airway pathology. The problem is caused by central loss of pharyngeal tone, and soft tissue obstruction (associated with depressed level of consciousness and anesthesia) or mechanical obstruction to the airway, above, at the level of or below the glottis. Classically the patient has nasal flaring, supraclavicular or intercostal retraction, and a see-saw chest movement: the chest moves inwards as the diaphragm descends. The patient may have inspiratory stridor (supraglottic obstruction), expiratory stridor (glottic or subglottic obstruction) or expiratory wheeze (bronchospasm). Typically hypoxemia is a late complication of airway obstruction. This is important as hypoxia may be rapidly followed by bradycardia and asystole.
4. Solve or resolve the problem
This patient has many risk factors for acute respiratory distress. Does he have ventilatory failure? Quite possibly – he may be narcosed from excessive interoperative opioids. He may be hypoventilating due to splinting (upper abdominal pain due to surgical incision) or persistent partial neuromuscular blockade. He may have upper airway obstruction, due to loss of pharyngeal tone, obstruction with a bite block, laryngeal edema or laryngospasm. He may have severe bronchospasm, and inhaled foreign object (such as a tooth) obstructing a major bronchus, or the presence of blood or gastric contents aspirated from the upper airway. He may have lower airway collapse due to hypoventilation and or absorption atelectasis, diffusion hypoxia (due to oxygen being displaced by nitrous oxide in the alveoli) or alveolar fluid, due to excessive intravenous administration.
Working the problem:
Step 1: Is this failure to oxygenate or failure to ventilate?
The patient has rapid shallow breathing with hypoxemia – this is failure to oxygenate, it may be secondary to peripheral ventilatory failure, or primary to V/Q mismatch.
Step 2: Is this peripheral ventilatory failure or primary V/Q mismatch?
The patient has bilateral air entry into the upper segments of the lungs, with little air entry into the bases. This is primary V/Q mismatch secondary to atelectasis. The patient has an intra-pulmonary shunt, evidenced by the lack of responsiveness to oxygen therapy.
Step 3: How is the diagnosis confirmed?
The diagnosis may be accepted, clinically (there is sufficient clinical suspicion in this case) or confirmed by chest x-ray and arterial blood gas sampling.
Step 4: What is the initial management of this patient?
The patient should nursed in the upright or seated position – the effect of gravity is to recruit lung tissue and increase functional residual capacity. The patient should be encouraged to cough, to mobilize secretions. Consideration should be given to devices that assist in lung recruitment such as incentive spirometry or the use of non-invasive positive pressure ventilation. If the problem worsens or fails to resolve, the patient should be re-intubated and lung recruitment achieved using an ICU grade mechanical ventilator.
- The assessment of the patient with acute respiratory distress involves taking a history, examining the patient and quantifying the degree of respiratory injury.
- This involves determining whether the problem is failure to ventilate, failure to oxygenate or failure to maintain the airway.
- Failure to maintain the airway leads to failure of gas flow and ultimately hypoxemia and hypercarbia. The problem is either central loss of airway patency or mechanical airway obstruction.
- Failure to oxygenate is caused by ventilation perfusion mismatch: the patient typically has a rapid shallow breathing pattern.
- Failure to ventilate is caused by a problem in the central nervous system or a problem with the thoracic pump: the patient typically has a slow shallow breathing pattern.
- Failure to ventilate is an ominous sign.
- Look for an immediately reversible cause of failure to ventilate – such as narcosis, deep sedation or persistent neuromuscular blockade.
- In the absence of a reversible cause, positive pressure ventilation is required.
Figure 7: Failure to Oxygenate vs Failure to Ventilate
This article is entirely the work of Patrick J Neligan MA MB FCAI FJFICM. No part of this article or its illustrations may be reproduced without the author’s permission. Select illustrations were developed in conjunction with Maurizio Cereda MD. © PJN 2012