Good afternoon, I'm Rhonda Cadena. I'm a neurointensivist at the Carolinas Medical Center for Atrium Health in Charlotte, North Carolina. I have no disclosures. For this talk, I will review high-yield topics as listed on the ABPN outline for the Neurocritical Care Boards, including airway management, pulmonary physiology, mechanical ventilation, and pulmonary diseases of ARDS, COPD, asthma, PE, and pulmonary edema. Let's start with a case. Imagine this patient who is a 36-year-old male with myasthenia gravis, who presents with respiratory distress and fever. On exam, he has weakness of his neck flexors and extensors and is tachypneic, but handling his secretions appropriately. He arrives on six liters of O2 by nasal cannula, and his ABG is shown here with a CO2 of 43 and a PaO2 of 72. Now, the first step in any airway management is to decide how best to oxygenate and ventilate the patient. Knowing when to pull the trigger on a more invasive method is key. This patient who is handling his secretions well and without hypercapnia, non-invasive ventilation with a BiPAP is appropriate. In these patients, the use of BiPAP before hypercapnia has developed has been shown to prevent intubation and prolonged ventilation. However, later on, the patient's work of breathing has increased and you obtain a repeat ABG, which demonstrates a rising CO2 of up to 56 with associated respiratory acidosis and now has a PaO2 of 86 but is on a non-rebreather. This patient now requires intubation. The indication for intubation of all patients includes hypoxia, hypercapnia, the inability to protect the airway, including the inability to handle secretions, and the need to decrease metabolic demands such as those who are in shock. Prior to intubation, a thorough airway assessment should be done to predict a difficult airway so that you can be prepared with adjuncts if needed. A good mnemonic that you can see here is the Lemon Law, which includes looking externally for any signs that might make bagging difficult if the airway is not easily obtained. E is to evaluate for a favorable direct laryngoscopy, and you could use the 3-3-2 rule that you can see here in the picture on the right, which includes an incisor distance of three finger breasts, the hyoid mental distance of three finger breasts, and the thyroid mental distance of two finger breasts. M is to assess the Malampati score. This is to determine the size of the tongue in relation to the mouth opening to assess for the possible difficult visualization with direct laryngoscopy. O is looking for any obstruction that might block the visualization once inside, and N is for neck mobility in that the inability to hyperextend the neck will put you at a disadvantage for a successful intubation. After your airway assessment, the intubation should proceed with a systematic process so that key steps are not forgotten, such as the one you see here, which is the P's involving positioning of the patient, pre-oxygenating, preparing key equipment, paralyzing and sedating, intubating when the team is ready, and then following a post-intubation process. The function of the lungs is gas exchange of oxygen and carbon dioxide, and occurs by diffusion across the alveolar capillary membranes. Gas exchange is dependent on the driving pressure, the volume, and the airflow in order to reach these areas. For inspiration in an unassisted breath, the diaphragm contracts, creating negative interthoracic pressure, so air flows from a higher pressure or atmosphere to a negative pressure in the lungs. In a ventilator-induced breath, the ventilator creates the higher pressure, so air flows from a higher pressure or the vent to a lower pressure, the alveoli. The lungs expand during inspiration, creating a higher pressure in the lungs, and when inflated, airflow ceases. Expiration occurs by the recoil of the filled elastic lungs that lead to exhalation of the inspired air. I will now talk about basics of ventilators. Although there are non-conventional modes, they are not commonly used in the neuro-ICU, and so I will not be discussing them here, which includes high-frequency oscillation, proportional assist ventilation, or PAV, and neutrally adjusted ventilation assist, or NAVA. After intubation, the ventilator mode that best suits the patient and the disease should be chosen in order to provide optimal oxygenation and ventilation. The two most common basic modes are pressure control seen on the left and volume control seen on the right. A knowledge of the waveforms is important to understand, not just for the exam if you're taking it, but also for bedside management. In pressure control, you can see a constant pressure leading to a rise in volume. There is a decline in flow as the volume is reached, and then there is a reversal with the release of pressure leading to exhalation. In volume control, you can see a constant flow leading to a rise in volume and a gradual rise in pressure. A couple of things to point out, volume control has a variable pressure, and pressure control has a variable volume. An inspiratory pause seen on the bottom right can tell you a great deal of information regarding the patient's lung mechanics. Seen here, the peak inspiratory pressure, PIP, and the plateau pressure, or PIP, can be determined. An elevated peak inspiratory pressure may be seen in cases of resistance to the driving pressure, such as might be seen in bronchospasm, and an increase in plateau pressure might be seen in cases of decreased lung compliance. Positive end-expiratory pressure, or PEEP, is positive transpulmonary pressure at the end of expiration. PEEP allows for alveolar recruitment to improve oxygenation by increasing surface area and prevents reduced lung volumes and alveolar collapse during expiration. It is important to note that with conventional ventilation, the target pressure setting discussed on the last slide represents pressure above any PEEP, and so the driving pressure for gas flow is the difference between the two. Auto PEEP, seen on the right, is also known as intrinsic PEEP. In this situation, expiration is not complete before the next breath begins. Because not all of the inspired air exits the lung, the next breath occurs from a higher lung volume. This constitutes an additional inspiratory load as the respiratory system must overcome the positive transpulmonary pressure in order to trigger another breath. Due to the increasing pressure with each breath, it can lead not only to patient discomfort, but also hemodynamic instability. In this situation, the treatment would be to disconnect the patient from the ventilator in order to allow for the escape of the retained air. There are a variety of monitoring techniques at our disposal, some related to the ventilator waveforms seen in the previous slides. Others, such as the Entidal Carbon Dioxide Monitor, can tell us things such as underventilation, as seen in acute airway occlusion, or loss of a waveform that can include an apnea or complete occlusion or cardiac arrest, or some of the traditional findings that you can see here. Other hemodynamic monitoring includes the telemetry monitoring, the physical exam, bedside echo, and labs. The physical exam can actually tell you a lot, including assessing for signs of shock using urine output and peripheral extremity temperature, assessing for volume overload with JVD and pinning edema, and the passive leg raise that might give an indication of fluid responsiveness in the hypotensive patient. More invasive monitoring is done with arterial lines, central lines, and pulmonary artery catheters. There are important pulmonary function tests that we can do in the neuro ICU, such as the negative inspiratory force, or NIF, which is the pressure that can be generated at the beginning of a functional residual capacity. So basically, the patient exhales and then inhales forcefully with an occluded airway. This is a test of diaphragm strength. The maximal expiratory pressure, or MEP, is the maximal pressure that can be generated during exhalation. This is a marker of the ability to cough in clear secretions. And the forced vital capacity is the volume of air that can be blown out after a full inspiration, which then demonstrates the full ventilatory ability in pulmonary compliance. Gas exchange occurs across the alveolar capillary membranes from region of high pressure to low pressure. At the top of an upright lung, the perfusion pressure is low, given minimal to low blood flow, and the pressure in the distended alveoli exceeds the pressure in the vasculature. This leads to a higher ventilation to perfusion mismatch. In the lower zone, or zone three, there is a large pulmonary blood flow under a higher pressure. Although the alveoli are minimally distended, this leads to a perfusion ventilation mismatch. And zone two allows optimal ventilation and perfusion. This concept can be considered in prone positioning. In the supine position on the left, in which you see the heart, the alveoli are small in the most perfusion-dependent portion of the lung. In addition, the chest wall increases the resistance. In the prone positioning on the right, perfusion is still high in the posterior aspect, and the alveoli are in maximal expansion, but the chest wall resistance is now removed. All of this leads to less of a ventilation perfusion mismatch. Brain injury can lead to abnormal respiratory patterns, and the pattern depends on the region affected, as you can see here. Let's review a case. This is a 28-year-old male who experienced a shallow dive into a lake. He experienced acute quadriplegia, and he was unable to get out of the water, which led to a drowning. He was pulled out by his friends. He had no pulse, and CPR was initiated for which they received ROSC. He was intubated upon arrival of the EMS. His exam on arrival was consistent with quadriplegia and a high spinal cord injury. His CT findings are shown, which shows a C6 fracture and a CT scan of his chest shows bilateral opacities. On day three, he was on vent settings with a PRVC, PEEP of 12. FiO2 was 80%. His ABG is shown here with a CO2 of 44 and a PaO2 of 62. His peak pressures were in the upper 40s. A bronchoscopy was done, which was negative for significant secretions. This slide shows the patient's chest X-ray on day three, which demonstrates bilateral opacities. Based on the Berlin definition, he has ARDS. Acute respiratory distress syndrome is defined by symptoms within one week of clinical insult with imaging showing bilateral opacities, which cannot be explained by cardiac failure or volume overload. In addition, there is hypoxia, which is defined by the ratio of PaO2 to FiO2, also known as the P to F ratio. The severity of ARDS is defined by this ratio in which it is less than 100 in severe ARDS, 101 to 200 in moderate, and 201 to 300 for mild. We do see many conditions in the neuro-ICU that predispose patients to ARDS, which include trauma of the brain and spine, subarachnoid hemorrhage, and stroke. Standard treatment of ARDS is done in the medical ICU, but there are some considerations in the neuro-ICU. A recommendation for the management of ARDS includes optimizing sedation and the use of paralytics to improve vent synchrony and decrease oxygen consumption. However, this can lead to the inability to follow our critically ill neurological patients, and therefore, additional monitoring may be needed, especially if too unstable for frequent imaging. Glucocorticoids have not been shown to be beneficial in mild ARDS, but may have a mortality benefit in moderate to severe ARDS if started within 14 days of symptom onset. However, steroids have been shown to be harmful in some conditions, including traumatic brain injury, so they should be used with caution. ARDS requires conservative fluid management, but in our subarachnoid hemorrhage patients, this could exacerbate basal spasm, and result in ischemic strokes. Other considerations, low tidal volume and permissive hypercapnia are necessary for lung protection strategies in ARDS. However, acutely increased CO2 may lead to elevated ICP, and therefore, incremental increases may be necessary in order to assess ICP stability in our patients. For hypoxia and high PEEP, recommendations for ARDS, the goal for PO2 is greater than 55, and a SAT goal is greater than 88%, but those may not be well tolerated in our brain injury patients. So in the neuro ICU, the goal PO2 should be greater than 60 in patients with brain injury. And when you have a patient that you are increasing PEEP, say high PEEP greater than 50, it may not be well tolerated, especially if they have poor ventricular compliance. So additional monitors may be necessary in order to monitor the ICP. Prone positioning improves oxygenation and mortality in severe ARDS, and it can be attempted in our neuro patients, but you may need some additional neuro monitoring in those patients, given the inability to perform any type of surgery. And you may need some additional neuro monitoring in those patients, given the inability to have the patient with a head up position to help with ICPs. Vent modes in ARDS, APRV can reduce mortality, but this mode can increase ICP in our patients. Inhaled nitric oxide can improve oxygenation, but it really has not been shown to be a good quality. ECMO can be considered in our neuro patients, but we do have to have caution with the heparin that is used in ECMO with our patients with a risk for intracerebral hemorrhage. All neurological patients should have a spontaneous breathing trial unless contraindicated. Some contraindications might include the inability to hold sedation, hypoxia, or intracranial hypertension from hypercapnia or respiratory distress. If unable to extubate, considerations for tracheostomy include severely altered mental status, leading to an inability to protect the airway, inability to clear secretions due to a neurological insult, poor cough reflex, or tracheal trauma. The timing of the extubation is difficult to standardize, and some will not extubate patients with a GCS of less than eight. However, some of these patients with a low GCS can be safely extubated if they have an intact cough and gag and a spontaneous respiratory drive. Other conditions that must be met in patients with neuromuscular weakness include improving muscle strength and the ability to handle secretions, forced vital capacity greater than 15 to 20 ml per kilo, and an F greater than negative 20 without signs of hypoxia. I will now discuss current recommendations on a few of the most common conditions we see in the neuro ICU, starting with COPD and asthma. Asthma is an inflammatory disease of the lungs, usually allergen-mediated, characterized by variable and recurring symptoms, reversible airflow obstruction, and easily triggered bronchospasms. COPD is a chronic and progressive inflammatory disease characterized by alveolar destruction and small airway fibrosis. Recommendations for management of acute exacerbations of asthma and COPD are shown here and are based on the European Respiratory Society and American Thoracic Society recommendations. They include increasing the frequency of inhaled beta-2 agonists, which is best when used with a spacer, as well as inhaled anticholinergics such as ipitropium. Glucocorticoids are recommended in asthma only if refractory to inhaled bronchodilators or the lack of a sustained response due to the concerns for an inflammatory process exacerbating the attack. However, they should be used in all COPD exacerbations as they have been shown to improve lung function and hypoxia and shorten the recovery time. PO steroids are preferred due to the increased risks of IV steroids. Antibiotics, including macrolides such as azithromycin have not been shown to have a benefit in asthma exacerbation unless bacterial infection is suspected. However, they have been shown to reduce treatment failure in patients with moderate to severe COPD or if purulent sputum is present. Magsulfate has been shown benefit in acute severe asthma because it has bronchodilator activity but has not been shown to be beneficial in COPD. With regards to intubation considerations, noninvasive ventilation is better studied in COPD and may reduce intubations and improve survival but could be considered to try an asthma if intubation is eminent. If they cannot tolerate noninvasive ventilation, high flow nasal cannula can be tried. Patients who you should consider intubation include those who have slowing of their respiratory rate, the inability to maintain respiratory effort, those with a depressed mental status, those with worsening hypercapnia with associated respiratory acidosis, or those who have the inability to maintain their oxygen despite high flow supplemental oxygen. Here's a case of neurogenic pulmonary edema. This is a 27-year-old female who presented with an acute subarachnoid hemorrhage. She is otherwise healthy, including no cardiac disease on arrival. She's hypertensive, tachycardic, and she required intubation for hypoxia. Her chest X-ray is shown here on the right, which shows diffuse pulmonary edema, and her CT scan is below that, which shows a diffuse subarachnoid hemorrhage due to aneurysm rupture. Neurogenic pulmonary edema is due to the catecholamine surge and resultant alveolar injury, which is different than ARDS, which is due to inflammation due to the lung injury. During a massive catecholamine surge in this brain injury, there is a transient peripheral vasoconstriction, systemic arterial hypertension, pulmonary hypertension, and altered pulmonary capillary permeability. In some patients, it could also be exacerbated by a negative pressure that's generated from airway obstruction due to their inability to protect their airway. The criteria for neurogenic pulmonary edema is that it is non-cardiogenic pulmonary edema, which would have a normal wedge pressure if you knew. It occurs rapidly, the onset of the neurological injury. It is temporary. It may only involve one lung field, although it can involve both. These patients may require intubation due to the hypoxia, but it's usually PEEP responsive, and they may need diuretics, but it's usually self-limited. The overall incidence of PEs in the U.S. is about one in 1,000 of ICU admissions and carries with it a high mortality. The incidence in the neuro ICU is not well studied and difficult to report based on variabilities in diagnoses and the use of DVT prophylaxis. However, our population is at a higher risk given the hypercoagulable states and immobility, and the recommendations are to start DVT prophylaxis as soon as possible. The hemodynamics associated with the PE are shown on the right. They involve an increase in pulmonary vascular resistance and RV strain. This increased RV pressure leads to compression of the right coronary artery and cardiac ischemia. This then can lead to hypokinesis and subsequent reduced RV cardiac output and subsequent reduced LV cardiac output. This can then lead to hypotension. Gas exchange is affected due to the ventilation of non-perfused regions, which lead to the inability to oxygenate and hypoxia and increased dead space, so unable to ventilate carbon dioxide. However, in the awake patient, the arterial CO2 might be lower due to the compensatory tachypnea. The mainstay in treatment is anticoagulants, including those with submassive PE, meaning that they have right heart strain, but without hemodynamic compromise. In severe cases of hemodynamic compromise, thrombolytics can be considered if there are no contraindications and systemic are preferred over catheter-directed thrombolytics unless there is a significant bleeding risk. I would like to thank you for your time today. Questions will be answered at the end of today's session.

neurocritical care

airway management

mechanical ventilation

pulmonary diseases

intubation process

gas exchange