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    IM Core Excerpt: Invasive Mechanical Ventilation

    This blog is meant to be a resource for physicians who need more information on Invasive Mechanical Ventilation during the COVID-19 pandemic. This information has been pulled from our 18th Edition Internal Medicine Core. 

    Overview | Modes of Mechanical Ventilation | Weaning and Failure to Wean | Noninvasive Ventilation | Nutritional Support

    Overview of Invasive Mechanical Ventilation

    Inflate the cuff of the endotracheal (ET) tube to the lowest possible effective pressure, ~ 15 mmHg. When the pressure exceeds ~ 25 mmHg, serious damage can occur to the tracheal mucosa. 

    The timing of a tracheostomy is controversial and takes into account specific patient variables and the likelihood of requiring prolonged ventilatory support. Typically, a tracheotomy is not performed during the 1st week of intubation (barring other indications). Tracheostomy is not indicated solely to decrease airway resistance during weaning.

    VAP (see more under Ventilator-Associated Pneumonia on page 6-61) is a frequent complication of mechanical ventilation. Quick review: Almost all patients are colonized with gram-negative bacteria in the upper and lower airways within 74–96 hours of endotracheal intubation. It can be very difficult to sort out true pneumonia vs. colonization. Ventilator-associated tracheobronchitis (VAT) has also been described for those without infiltrates. The 2016 IDSA/ATS guidelines recommend against antibiotic treatment for VAT. For a diagnosis of pneumonia, you should see:

    • New or worsening infiltrate
    • Leukocytosis
    • Purulent sputum or endotracheal secretions
    • Fever or hypothermia 

    Noninvasive sampling is preferred to diagnose VAP. Cover both Pseudomonas and MRSA with empiric antibiotic treatment for VAP. In 2016 the CDC proposed new definitions for ventilator-associated events (VAE) and infectious ventilator-associated complications (IVAC), which also include the presence of possible and probable VAP. 

    Modes of Mechanical Ventilation 

    Continuous Ventilation Controlled mechanical ventilation (CMV) has a set rate and a set tidal volume (TV) that does not allow spontaneous breathing. Patient-ventilator asynchrony is a big problem. Therefore, this mode is best used in patients who are heavily sedated, under anesthesia, paralyzed with muscle relaxants, or in a deep coma. Assist/control (AC) is CMV with a set rate and TV, but this mode allows the patient to initiate additional breaths “above the ventilator.” When the machine senses that the patient is attempting to take a breath (the pressure sensor detects a negative pressureinspiratory effort that exceeds a set threshold), it kicks in with a full machine-supported breath at the ordered TV. This is a commonly used mode of ventilation. One caveat: If patients are anxious, hyperventilating, or have obstructive lung disease, they continue to trigger additional full machine breaths, get even more hyperventilated, and are at risk for developing auto-PEEP. This usually occurs when the rate is ≥ the high teens to twenties. 

    Intermittent Ventilation 

    Synchronized intermittent mandatory ventilation (SIMV) is similar to AC in that you dial in a set rate and TV, but spontaneous breaths at a patient-determined rate and TV can be taken between the set breaths. 

    Because this spontaneous breath requires a lot of work from the patient to suck in a breath through the ET tube and the ventilator circuit, we often add pressure support ventilation to the SIMV mode. Therefore, when the patient takes a spontaneous breath, there is a boost of pressure (you set the amount) to help overcome the resistance of the ET tube and the ventilator circuit. 

    Typically, you use a pressure support of 5–20 cm H2O, but you need to titrate this pressure for an individual patient after you see what kind of spontaneous TVs the patient can generate. 

    Note: The above volume-cycled ventilators have a popoff valve set at a certain inflation pressure to prevent over-pressurization of the lungs. 

    Pressure Support Ventilation 

    Pressure support ventilation (PSV), when used in a spontaneously breathing patient, supplies only pressure support, and there is no need for mandatory breaths. This is a very comfortable mode for the patient because he or she determines the rate, inspiratory time, and TV. However, you must have a patient with a stable respiratory drive (i.e., not heavily sedated and not paralyzed). More importantly, remember that there is no guarantee as to what tidal volume will be generated at a specific level of pressure support (this will be influenced by airway resistance and compliance of the respiratory circuit and system). If your patient is prone to—and develops—acute HF, the lungs may acutely become stiffer, or less compliant, and for a given level of pressure support a smaller TV will be delivered, potentially causing tachypnea and respiratory distress. The inspiratory pressure can be increased while the underlying cause is addressed. Pressure Control Ventilation Pressure control ventilation (PCV) is a form of ventilation that is actually a throwback to the first ventilators. In this mode, machine breaths are pressure cycled, not volume cycled. You determine the pressure you want the patient to receive on each breath, inspiratory/expiratory ratio, and the rate at which the breaths are delivered. If the patient attempts a spontaneous breath, they get a machine breath at the pressure you have designated.

    This may be helpful in limiting airway pressures in patients with high end-inspiratory plateau pressures in other volume-cycled modes that leave them susceptible to barotrauma. Use of this mode lets you use a low TV and a high PEEP strategy for ARDS since the peak inspiratory pressure is lower on PCV then on AC for any given achieved TV. As with PSV, the TV varies with airway resistance and respiratory compliance. Hence, this mode must be titrated carefully and monitored at the bedside to determine the proper pressure settings and achieved TV.

    Weaning and Failure to Wean 

    Weaning is best accomplished by using protocols. Generally, weaning is performed as the patient stabilizes (Fi O2 ≥ 40%, minimal vasopressor requirements, adequate mentation) and combines a spontaneous awakening trial (sedation/analgesia is reduced to allow the patient to awaken) with a subsequent spontaneous breathing trial (SBT).

    1. SBT protocols have the patient breathe through a T-piece or with low levels of pressure support or tube compensation mode for 30–120 minutes to see how the patient tolerates spontaneous breathing with no or minimal assistance from the ventilator. The respiratory frequency and minute ventilation are monitored along with the patient’s vital signs, respiratory effort, and pattern. If the respiratory rate is < 105 breaths/minute/L (RR/TV), the patient is subsequently extubated as long as they have a suitable cough to protect their airway and do not require the ET tube to remain to facilitate frequent suctioning requirements. The SBT can also be performed on patients who have a tracheostomy in place, and they can be disconnected from the ventilator and placed on a T-piece or trach mask.
    2. Patients who are difficult to wean may be subsequently weaned by using pressure support trials with progressive reduction in the amount of pressure support until they are able to tolerate an SBT as above. 

    Failure to wean—possible causes (DESAT):

    • Drugs (e.g., sedatives). Sedation or altered mental status is one of the most common reasons for failure to wean.
    • Endotracheal tube and electrolyte imbalances. Sometimes the intraluminal diameter of the tube is too small. Over time, it is common for ET tubes to decrease in diameter due to secretions and biofilms adhering to the internal lumen. Automatic tube compensation is a ventilatory mode that dynamically compensates for the increased resistance of the ET tube, thereby making the final stages of weaning more predictable. Hypocalcemia, hypophosphatemia, and hypomagnesemia all impair weaning.
    • Secretions
    • Alkalemia (which decreases the respiratory drive)
    • Too high a PaO2 and too low a pCO2 just before extubation (Keep these parameters near the patient’s baseline.)

    There is potential danger in suddenly switching from positive pressure ventilation in patients with limited cardiac function or occult cardiac ischemia to full spontaneous breathing: stopping positive pressure ventilation → increased venous return → increased cardiac filling pressures → need for increased cardiac output → HF or cardiac ischemia in susceptible patients. Such patients are often treated with diuresis and even IV nitroglycerin in order to temporarily lower the preload. 

    COPD patients with chronic respiratory failure are less able to get rid of CO2, so intubation with a larger-bore endotracheal tube helps decrease airway resistance, and extubation to NiPPV improves outcomes. Also avoid overventilating a COPD patient who is at baseline a CO2 retainer. That is, adjust the minute ventilation (TV × RR) to match the baseline pCO2 (estimated or known from a blood gas). 

    Adjusting a Ventilator 

    Remember: When we are adjusting a ventilator to improve a patient’s ABGs, we have to separate our actions into 2 categories:

    1. Those that change alveolar or minute ventilation (TV × RR) change the patient’s pCO2 and pH. Remember alveolar ventilation is inversely proportional to PaCO2. Alveolar ventilation = (TV – RV) × RR (where RV= residual volume).
    2. Those that alter a patient’s oxygenation are Fi O2, PEEP, and inspiratory/expiratory ratio.

    PEEP 

    Positive end-expiratory pressure (PEEP) is a positive pressure left in the chest at the end of exhalation. This can be done purposely to a patient on a ventilator by closing a valve during exhalation and not allowing the pressure in the airways to return to zero. 

    You dial in a PEEP pressure—the desired end-expiratory pressure—typically 5–15 cm H2O (one can go higher in ARDS). The purpose of utilizing PEEP in mechanically ventilated patients is to help prevent the alveoli from completely collapsing at the end of expiration. This prevents atelectasis and, more importantly, leads to better matching of V/Q while having less of a shunt fraction. PEEP also prevents atelectrauma, which is damage caused by shearing forces that arise during repeated reexpansion of collapsed lung units. 

    Use higher levels of PEEP only with diffuse lung disease! It can actually decrease the PaO2 if used in focal lung disease. Use PEEP in cases of diffuse lung disease if required to maintain the Fi O2 < 60%, while keeping the PaO2 > 60 mmHg. 

    An elevated PEEP can cause:

    • Pneumothorax, ventricular failure, and alveolar damage, which can precipitate or worsen pulmonary edema. The PEEP level recommended in ARDS is based on a nomogram, as discussed previously. Some advocate using the lowest level of PEEP required to oxygenate the patient with a safe Fi O2 (60%).
    • Decreased venous return, causing decreased cardiac output and hypotension. 

    Auto-PEEP

    Auto-PEEP usually happens when the patients are not fully emptying their lungs during expiration prior to the initiation of the next breath. This is known as stacking breaths or generating auto-PEEP. The problem is the respiratory rate is too fast to allow complete emptying. 

    A patient on a ventilator gets auto-PEEP if the ventilator is set up in a way that does not allow the patient to fully exhale before initiating the next breath. This is particularly worrisome in patients who have exacerbations of COPD or who are in status asthmaticus. The auto-PEEP may become severe enough that the patient can suffer barotrauma, hypotension, or hemodynamic collapse secondary to the inability of blood to return to the chest. 

    Auto-PEEP can also occur in spontaneously breathing patients with obstructive lung disease and is responsible for creating dynamic hyperinflation, with all of the consequences of auto-PEEP combined with the increased work of breathing. On physical examination you hear the next breath come in before the exhalation is complete. You can see the potential for auto-PEEP by observing the flow waveform and noting an expiratory flow that does not return to the zero baseline before the initiation of the next breath. 

    Auto-PEEP can be measured in mechanically ventilated patients using either of the following 2 methods:

    1. Insert an end-expiratory pause in the ventilator circuit and observe the airway pressure monitor during the pause.
    2. Use ventilators that automatically measure this. The pressure curve on the flat panel display does not return to the set PEEP level. 

    The treatment of auto-PEEP requires treatment of the underlying obstructive lung disease. More immediately, reduce the RR. The principle is to take action to shorten inspiration and lengthen the expiration. This can include the following interventions:

    1. Decrease the RR, which is the primary effective intervention when there is significant auto-PEEP. This may require sedation if the patient is breathing over the ventilator.
    2. Decrease the TV, which has minimal effect.
    3. Increase the peak inspiratory flow rate (PIFR), which has a slight effect.
    4. Treat bronchospasm and reduce airway secretions (if they are leading to increased airway resistance).

    What do you do if your patient with severe airway obstruction has hypotension related to auto-PEEP after being placed on mechanical ventilation?

    1. Disconnect the patient from the ventilator and slowly bag the patient through the ET tube. Check for tension pneumothorax and mucous plugs and otherwise ensure that the ventilator is functioning properly.
    2. Return the patient to the ventilator with new settings that allow for a longer expiratory phase, generally a lower RR. Specific changes include lowering the RR, increasing the inspiratory flow rate (shortening the time the patient gets for inspiration and, hence, allowing a longer time for expiration), and reducing the TV. 

    Note that the patient must be sedated or sedated and paralyzed to accurately measure the auto-PEEP. 

    As a historical reference, inverse ratio ventilation is a technique that was employed in patients with ARDS, whereby auto-PEEP was purposely generated as a mechanism for “recruiting” alveoli. It has fallen out of favor because of the significant potential for harm and rare utility. 

    Noninvasive Ventilation

    Noninvasive ventilation (NIV) or NiPPV consists of a mask interface (either full face mask over the nose and mouth or nasal mask) and tubing connected to a device that can provide bilevel positive airway pressure (BiPAP) or continuous positive airway pressure (CPAP). CPAP can be used in pulmonary edema to improve oxygenation when there is no problem with ventilation (CO2 not markedly elevated), while BiPAP is used most commonly, as it will ventilate the patient (blow off CO2) and oxygenate the patient. For BiPAP, both inspiratory pressure (IPAP) and expiratory pressure (EPAP) are ordered. The greater the difference between IPAP and EPAP, the more CO2 will be blown off. Some devices allow measurement of the achieved TV for given IPAP and EPAP settings. However, one can empirically start with IPAP of 10 cm H2O and EPAP of 5 cm H2O and increase these in order to ventilate more (increase IPAP) or oxygenate more (increase EPAP, but also some effect from IPAP). 

    NIV is utilized in spontaneously breathing, awake individuals who do not have a compromised airway but who are in respiratory distress. The indications often are COPD exacerbation, pulmonary edema, or other etiology where the patient is expected to respond to acute therapy for a reversible cause. For some patients, NIV is not sufficient to meet their needs, such as those with severe gas exchange abnormalities, marked distress, developing lethargy, or intolerance for the mask interface. Patients in marked respiratory distress, those for whom NIV is not likely to be sufficient, or those who have contraindications should be intubated. Contraindications include vomiting, massive hemoptysis, intractable respiratory secretions, ongoing aspiration, poor respiratory drive, cardiac or respiratory arrest, inability to tolerate face mask or pressure, facial trauma, surgery or burns, esophageal or gastric surgery, or severe respiratory failure. 

    NIV should be supported and managed with the direct involvement of respiratory therapy. Adjustments may be needed at frequent intervals, and patients should be closely monitored by vital signs, oximetry, and blood gases. Such patients started on NIV for respiratory failure should be managed in a higher level of care, such as initially in the emergency department and then ICU. The patient should be monitored for deterioration that can happen rapidly and may require intubation. 

    Nutritional Support 

    Nutritional support in ICU settings is extremely important and often underemphasized. Use the enteral route whenever possible. After major surgery or the onset of sepsis, metabolic requirements increase dramatically. Requirements peak in 3–5 days. If the patient is unable to eat, start enteral feedings (standard formula for most critically ill patients) as soon as feasible. Even though enteral feeding increases the possibility of aspiration, it is preferred over TPN because it tends to maintain the intestinal epithelium and its natural defenses against bacteria. TPN also has increased risk of bacteremia and fungemia. 

    With enteral feeding, you can decrease the risk of aspiration and pneumonia by keeping the head of the bed elevated ≥ 30°. The position of the head is more important than where the feeding tube is placed (e.g., pre- vs. postpyloric). Per the ASPEN guidelines of 2016: Do not check for gastric residuals in an asymptomatic patient. Routine supplements (e.g., omega-3-fatty acids, arginine, fiber) are not indicated. Prepyloric feeding is satisfactory; usually place postpyloric tubes in those with high risk of aspiration or intolerance to gastric feeding. 

    Refeeding syndrome occurs when severely malnourished patients are fed high-carbohydrate loads (i.e., enteral tube feeds or IVF with glucose). These patients develop low total body levels of electrolytes, specifically phosphorus, Mg2+, and K+. With refeeding syndrome:

    • There is a dramatic increase in circulating insulin levels and a resulting swift uptake of glucose, phosphate, Mg2+, and K+ into the cells—with a precipitous drop of these agents in the serum. The resulting severe hypophosphatemia (lack of ATP and 2-3-diphosphoglycerate) causes heart and respiratory failure, rhabdomyolysis, RBC and WBC dysfunction, seizures, and coma. Hypomagnesemia can result in arrhythmias, including torsades des pointes.
    • Myocardial atrophy from prior starvation increases the propensity for acute heart failure secondary to Na+ and water retention. 

    Prevent refeeding syndrome by starting the feeding of severely malnourished patients slowly and by aggressively replacing phosphate, Mg2+, and K+.

    Check out the next blog in this series: IM Core Excerpt: Hypoexmia

    im core free trial pulmonary medicine

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