Mechanical Ventilation (2024)

November 17, 2024November 21, 2024 ~ iEM Education Project Team ~ Leave a comment

by Elham Pishbin, Hamidreza Reihani

You have a new patient!

A 70-year-old male with a history of severe chronic obstructive pulmonary disease (COPD) presents to the emergency department (ED) with complaint of progressive dyspnea and productive cough. Vital signs are as follows: PR=108/min, RR=46/min, BP=130/90 mm Hg, T=37.8°C (axillary), SpO2=76% (with 5 L/min O2with nasal cannula). He is awake but confused. You request a blood gas test and initiate standard medical treatment for COPD exacerbation (Nebulized short-acting beta-agonists, antibiotics, and systemic glucocorticoids). You are concerned about the patient’s respiratory status and prepare for the possibility that he may need additional respiratory support in the emergency department.

Introduction

Mechanical ventilation (MV) is often essential to successfully managing critically ill patients. Patients may require MV because of respiratory failure, airway protection, or as part of the management of their illness to support their respiratory function and to reduce the work of breathing. Emergency physicians should have a solid understanding of mechanical ventilation and its indications, modes, and troubleshooting. Here, we provide a simplified guide to managing MV in the emergency department (ED) setting.

Physics of MV

MV involves pumping air with a positive pressure into the patient’s lungs and allowing the patient to exhale the air spontaneously. The aim is to deliver oxygen to the lungs, keep the distal airways open for oxygen exchange, and allow carbon dioxide release upon exhalation. The ventilator uses pressurized air to overcome the resistance of ventilator tubing, the endotracheal tube (ETT), and airways. When the resistance to airflow increases or lung compliance decreases (lung compliance is inversely related to the elastic recoil of the lungs), higher pressure is required to inflate the lung [1, 2]. Common causes of high resistance are obstruction of the ETT by tube biting or a mucus plug, airway secretions, and bronchospasm. Common causes of poor compliance are pneumothorax, alveolar oedema, right main stem intubation, and air trapping [2].

Exhalation occurs passively due to pressure differences between the alveoli (higher pressure) and the ventilator (lower pressure). Notably, ventilators can administer a positive end-expiratory pressure (PEEP) to decrease this pressure gradient, thereby preventing the lungs from excessive collapse [2].

Control Variables and Ventilator Modes

The control variables on a ventilator determine how to pump the air (the air volume, the time over which the air is delivered, the frequency of delivering the air over a minute, and the speed at which the air travels). The alarms and monitors show whether the controls we set are appropriate and how the lungs respond [3].
After a patient is intubated and connected to a ventilator, the ventilator mode and settings should be established. First, specify volume-controlled ventilation (VC) or pressure-controlled ventilation (PC) [1].

VC ventilation

VC ventilation is the most familiar and the most commonly used of MV modes in the ED [4].

The key parameters which should be set on the ventilator include [2]:

Tidal volume (Vt): the amount of air pumped into the patient in each breath (measured in milliliters)
Respiratory rate (RR)
Fraction of inspired oxygen (FiO2)
Positive end-expiratory pressure (PEEP): the baseline airway pressure at the end of expiratory. PEEP stents open the distal airways for gas exchange.
Flow rate*: the speed at which Vt is pumped through the circuit (measured in liters per minute)
Inspiratory time (Ti) *: the time (in seconds) over which the ventilator pumps the Vt

(*These parameters are often automatically set, but this depends on the ventilator)

In VC ventilation, pressure cannot be set as it depends on airway resistance and lung compliance. Increased airway resistance or worsened lung compliance will increase pressures in the airways, increasing the risk of barotrauma. Barotrauma due to elevated pressures is one disadvantage to VC. The advantage of VC ventilation is that the VT is guaranteed, and minute ventilation is stable.

PC ventilation

PC ventilation applies constant inspiratory pressure throughout inspiration, whether the ventilator or the patient triggers the breath [2]. In PC ventilation, the Vt cannot be set directly, so the operator sets the inspiratory pressure instead of Vt. Flow rate and Vt are dependent variables in PC ventilation. This is a disadvantage of PC ventilation since increased resistance or decreased compliance will lead to smaller Vt delivery, diminished ventilation, and carbon dioxide retention. Other key parameters, like Vt, PEEP, RR, and FiO2, are the same as VC ventilation. The advantage of PC ventilation is that airway and pulmonary pressures are set at the inspiratory pressures, preventing barotrauma. In addition, the patients can regulate their inspiratory flow rate and increase it according to their inspiratory efforts. This improves patient-ventilator synchrony [2].

A ventilator mode is a specific setting on the ventilator that determines how the ventilator assists the patient by giving a breath. It also defines the amount of respiratory support that the ventilator provides for the patient [5].

It is important to note that each ventilator mode has advantages and disadvantages. There is no perfect ventilation mode that fits all patients. The best mode is the mode with which you and your team are most familiar [2].

Two primary ventilator modes that are most commonly used in the ED are Assist/Control Ventilation (ACV) Mode and Synchronous Intermittent Mandatory Ventilation (SIMV) Mode [4].

Assist/Control ventilation (ACV)

This mode is designed to offer full respiratory support for patients with minimal or no spontaneous breathing by delivering a preset number of mandatory breaths. However, if the patient tries to breathe, the ventilator will also assist that breath [5]. The patient will always receive at least the preset number of breaths (regardless of his/her respiratory effort). In this regard, ACV is the most appropriate initial mode in ED patients who are initially paralyzed and sedated [1].

ACV can be set as either volume-control or pressure-control. In VC/ACV, we set these parameters: Vt, flow rate, basal respiratory rate, and sensitivity to the patient’s respiratory effort (trigger). We can adjust the sensitivity control to make it easier or harder for the patient to trigger an assisted breath from the ventilator.
In PC/ACV, instead of Vt, we set the Ti. In this mode, Vt is dependent on the patient’s lung compliance and airway pressure. The advantage is avoiding barotrauma, but the disadvantage is that a specific preset Vt cannot be guaranteed [4].

To ensure ventilator synchronization, a breath initiated by the patient takes precedence over a preset breath. If the ventilator is programmed to deliver 12 breaths per minute, it will provide a breath every five seconds in the absence of spontaneous breathing. However, if the patient makes a spontaneous effort, the ventilator will provide an extra breath and reset the timer for another five seconds. The main challenge is that patient-initiated breaths are not proportional to his effort. When the patient makes an inspiratory effort, the ventilator provides a full Vt, which can lead to hyperventilation and poor patient-ventilator synchronization. Adequate sedation is necessary to prevent spontaneous breathing efforts when a patient is ventilated in the ACV mode. [1].

Synchronous Intermittent Mandatory Ventilation (SIMV)

This mode offers intermittent ventilatory support to patients by delivering mandatory breaths and supporting spontaneous breaths. Mandatory breaths are delivered at a preset rate. The ventilator delivers at least a preset number of mandatory breaths to the patient, similar to ACV. Patients with no respiratory effort, will receive the preset number of breaths. Patients with spontaneous breathing at a lower rate than the ventilator preset rate will receive the preset number of breaths with full Vt. In these two scenarios, SIMV is very similar to ACV. However, if a patient has spontaneous breathing at a rate higher than the preset respiratory rate, additional respiratory effort beyond the preset rate will only be partially supported proportional to the patient’s respiratory effort. This makes SIMV an appropriate mode for less sedated patients with some degree of spontaneous breathing [1].

Pressure Support Ventilation (PSV)

In this mode, the ventilator assists the patient’s spontaneous breaths during the inspiratory phase of breathing. It is often used to help the patient overcome the airway resistance caused by the endotracheal tube and the ventilator circuit. The patient should be alert or on light sedation and able to follow commands. When the patient triggers a breath, the ventilator supports it by adding pressure to facilitate breathing. The operator sets the FiO2, PEEP, and inspiratory pressure on the ventilator based on how much support the patient needs to receive. In PSV, RR, Ti, and flow rate are determined by the patient. The higher the pressure support, the easier it will be for the patient to take a breath. The ventilator supports inspiration until the inspiratory flow falls below a preset measure [2,6].

When choosing PSV, it is also necessary to set an appropriate backup mode (for example, SIMV) and ventilator alarms [6].

Typical initial ventilator settings: Although required settings depend on whether PC or VC ventilation is selected, the principles are similar in both modes [1]. Typical initial ventilator settings include the following: [1,2,4]

Tidal volume (Vt): a Vt of 6 to 8 mL/kg of estimated ideal body weight (IBW) is appropriate for most patients. The inspiratory pressure should be set in PC ventilation to achieve these Vt targets. Ongoing patient assessment is necessary to avoid excessive Vt. Regardless of VC or PC, initial pressure targets should not exceed 30 cm H2O.
Respiratory rate: a rate of 12 to 18 breaths per minute would be reasonable for most patients and provide adequate ventilation. In special situations, such as patients with severe metabolic acidosis, the respiratory rate should be increased to match pre-intubation minute ventilation.
FiO2: initially should be set at 100%, then lowered to target a SpO2 of 92% – 96% (PaO2 of 60 to 100 mmHg)
PEEP: is routinely set initially at 5 cm H2O, but it can be set at 4 to 20 cm H2O
I/E time ratio: The ratio of inspiratory time to expiratory time. It is commonly set as a ratio of 1:2. In some modes, it is automatically set based on other parameters. In some other modes, it needs to be set by the operator.
Flow rate: is typically set at 60 L/min. (Vt will be delivered at the speed of 60 L/min). Increasing the flow rate will deliver the set Vt faster, reducing the inspiratory time. (It is found in VC modes)
The trigger is a preset change in pressure or flow detected by the ventilator as the patient tries to initiate a breath, and the ventilator supports that breath. It should be set at a level that enables the patient to trigger the ventilator without great effort. For most patients, pressure sensitivity trigger from -0.5 to -2 cm H2O is effective and safe. The 1–3 L/min threshold is appropriate for the flow trigger setting.

When choosing a ventilator mode and parameters, it is essential to ensure adequate ventilation, but it is also important to ensure that the pressure in the ventilator circuit (including the lung) is appropriate [1]. Some important pressures are:

Peak inspiratory pressure (PIP) is the maximum pressure during inspiration. It is a dynamic pressure measured during the inspiration, so it incorporates airﬂow and reﬂects the resistance to airﬂow. It is also reﬂective of dynamic compliance of the entire respiratory system. Decreasing compliance or increasing resistance to airﬂow will increase PIP. It can never be lower than P. plat [4].
Plateau pressure (P. plat) is a static pressure that can be measured at the end of inspiration with a short breath-hold (Figure 1). The goal is to be less than 30 cm H2O. Decreasing the compliance will increase P. plat. Decreasing the Vt will decrease P. plat [4]

Positive End-Expiratory Pressure (PEEP) is the airway pressure at the end of expiration. It helps to keep the smaller airways and the alveoli open, prevents atelectasis, and improves oxygenation. Increased levels of PEEP may lead to lung injury. Additionally, high PEEP can depress cardiac output and lead to hemodynamic compromise [1,4]. When talking about PEEP, most authors mean extrinsic PEEP (PEEPe). In this chapter, when we use PEEP, we refer to PEEPe.
Intrinsic PEEP or auto-PEEP (PEEPi) results from air trapping in the airways. It occurs due to increased expiratory resistance (e.g., bronchospasm, kinked ETT), impaired elastic recoil (e.g., emphysema), and increased minute ventilation (inadequate expiratory time). PEEPi can lead to hemodynamic instability similar to high levels of PEEP [2,4].

Noninvasive ventilation (NIV)

NIV provides continuous positive pressure throughout the breathing cycle via a tight-fitting mask (nasal, oro-nasal, or full-face mask, as shown in Figure 2) rather than an endotracheal tube [7].

No mandatory breath is given by the ventilator so the patient must have spontaneous breathing. The ventilator provides a preset level of pressure when the patient initiates a breath, but inspiratory flow and Ti are completely patient-dependent [4,7]NIPPV can be delivered as continuous positive airway pressure (CPAP) or bi-level positive airway pressure (BiPAP).

CPAP provides constant positive pressure throughout the entire respiratory cycle. Its main effect is applying positive pressure at the end of expiration and exerts a minimal effect on inspiration [4,7].

BiPAP supplies a positive airway pressure during inspiration (IPAP) and a lower positive airway pressure during expiration (EPAP) [4].

IPAP provides pressure support and decreases the patient’s work of breathing. Increasing the IPAP will improve tidal volume and minute ventilation, thereby helping to eliminate CO2 from the alveoli.

EPAP acts similar to PEEP and improves alveolar recruitment and oxygenation by maintaining positive pressure at the end of expiration. EPAP prevents the lung from being fully deflated at the end of expiration, aiding in oxygen exchange across the alveolar-capillary membrane. Therefore, when you need to improve oxygenation, you should increase the EPAP.

The difference between the IPAP and EPAP is called delta pressure. The delta pressure is the same as pressure support in invasive ventilation. When the difference between the IPAP and EPAP is larger, the patient is able to have a larger tidal volume. Therefore, when you need to increase the clearance of CO2, you need to increase the delta pressure. [1,7].

Contraindications to NIV are patients who are uncooperative, hemodynamically unstable, lack protective airway reflexes, lack good respiratory effort, or have maxillofacial trauma. [7,8]

Initial NIV Settings

Initial settings depend on the amount of support that the patient requires, patient comfort, and patient cooperation.

BiPAP usually is initiated at 10 cm H2O for IPAP and 5 cm H2O for EPAP. Based on the patient’s clinical response, these parameters can be titrated later by 1 to 2 cm H2O at a time. However, the maximum pressure for IPAP should not exceed 20 cm H2O because this may lead to barotrauma [8,9].

Typical initiated settings for CPAP are 5 to 15 cm H2O [4,7].

Ventilator Troubleshooting

Patient-ventilator dys-synchrony refers to patients who develop respiratory distress after undergoing mechanical ventilation [10]. Emergency physicians must be familiar with patient-ventilator interactions so that life-threatening complications of mechanical ventilation can be promptly identified and managed [11]. In Figure 3, we present a systematic approach to detect life-threatening conditions in patients who suddenly deteriorate and become hemodynamically unstable (profound hypotension or cardiac arrest) under mechanical ventilation [1, 10].

Revisiting Your Patient

After 30 minutes, you reevaluate your patient. The patient remains in respiratory distress with SpO2 of 79%, despite nebulized beta-agonists, steroids, antibiotics, and the use of 7 L/min O2 via face mask. The patient’s blood gas reveals a pH of 7.22, PCO2 of 80 mm Hg, and PaO2 of 55 mmHg. You decide to put him on NIV using an oro-nasal mask. You choose BiPAP mode and set IPAP=12 cm H2O, EPAP=7 cm H20, and FIO2= 90%. After 5 minutes, the patient becomes agitated on the NIV mask, even with verbal direction and support. The pulse oximeter remains low at a SpO2 of 85%.

What would be the next appropriate step in the management of this patient?

You recognize your patient has not sufficiently improved despite maximal medical therapies. You decide to prepare for intubation and mechanical ventilation. The patient is fully sedated, paralyzed, and intubated using RSI (rapid sequence intubation). You prepare to choose a ventilation mode and set the parameters on your ventilator.

Which mode of ventilation and control parameters are most ideal for your patient?

The patient is sedated and paralyzed during RSI, so the VC/ACV mode is the best choice. Your senior says, “The best mode is the mode most familiar to you.” No data suggest the advantage of PC over VC (or vice versa) in patients with COPD. You review your goals in MV of your COPD patient: improve oxygenation and ventilation, minimize PEEPi, and prevent barotrauma.

You set the ventilator as:

Mode: ACV (VC/ACV)
FiO2= 100%
Vt= 500 cc
Respiratory rate= 14
PEEP= 5cm H2O
I/E: 1/4

You base your tidal volume on the patient’s 170 cm height and weight of 90 kg. You set the I/E ratio at 1:4 to optimize a longer expiratory time and titrate the FiO2 until the SpO2 falls between 88% to 92% [12]. A chest X-ray confirms the tip of the endotracheal tube is located above the carina. The patient is admitted to the medical ICU for further management and treatment.

Authors

Elham Pishbin

Elham Pishbin is a full-time associate professor of emergency medicine (EM) with 16 years of experience as a faculty member of the department of EM at Imam Reza Hospital, affiliated with Mashhad University of Medical Sciences, Mashhad, Iran. She is a member of the Iranian national board of EM and contributed to establishing the first EM residency program at Mashhad University of Medical Sciences in 2008, the fifth EM residency program in Iran, and a significant milestone in the development of EM in the country.

Hamidreza Reihani

Dr. Hamidreza Reihani, a professor of emergency medicine at Mashhad University of Medical Sciences in Iran, is also a member of the national board of emergency medicine. He holds fellowships in medical education, research, and clinical informatics. With 15 years of experience in emergency medicine, he has made significant contributions, including founding an academic Emergency Department (ED) at his university and educating over 100 specialists in the field. Dr. Reihani has also been actively involved in interdisciplinary and undergraduate education, research (with more than 60 published articles), peer review, and editorial roles for two academic journals. His expertise and dedication are reflected in his contributions to both the previous and current editions of this book.

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References

Seigel T.A, Johnson N.J. Mechanical ventilation and noninvasive ventilatory support. In: Walls R.M, ed. Rosen’s emergency medicine: concepts and clinical practice. 10th ed. Philadelphia PA: Elsevier; 2023:24-33
Ward J, Noel C. Basic Modes of Mechanical Ventilation. Emerg. Med. Clin. N. Am. 2022;40(3):473-88
Gomersall C, Joynt G, Cheng C, et al. Basic Assessment and Support in Intensive Care. Hong Kong: Chinese University of Hong Kong; 2013:37-54.
Santanilla J.I. Mechanical Ventilation. In Roberts J.R, Hedges J.R, eds. Roberts and Hedges’ clinical procedures in emergency medicine and Acute Care. 7th ed. Philadelphia PA: Elsevier; 2018:152-172.
Hickey S, Giwa A. Mechanical ventilation. StatPearls. 2023 Jan 26.
Abramovitz A, Sung S. Pressure Support Ventilation. StatPearls. 2022. Sep 18.
Gill HS, Marcolini EG. Noninvasive mechanical ventilation. Emerg. Med. Clin. N. Am. 2022;40(3):603-13.
Carlson J.N, Wang H.E. Noninvasive Airway Management. In: Tintinalli J.E, ed. Tintinalli’s emergency medicine: a comprehensive study guide, 9th ed. McGraw Hill Education; 2020: 178-183.
Baker DJ, Baker DJ. Basic Principles of Mechanical Ventilation. Artificial Ventilation: A Basic Clinical Guide. 2020:113-37.
Keith RL, Pierson DJ. Complications of mechanical ventilation: a bedside approach. Clinics in chest medicine. 1996 Sep 1;17(3):439-51.
Gilstrap D, MacIntyre N. Patient–ventilator interactions. Implications for clinical management. American journal of respiratory and critical care medicine. 2013 Nov 1;188(9):1058-68.
Atchinson P.R, Roginski M.A. Chronic obstructive pulmonary disease. In: Walls R.M, ed. Rosen’s emergency medicine: concepts and clinical practice. 10th ed. Philadelphia PA: Elsevier; 2023:806-815

Free open access resources for study

Reviewed and Edited By

Joseph Ciano, DO, MPH, MS

Dr. Ciano is a board-certified attending emergency medicine physician from New York, USA. He works in the Department of Emergency Medicine and Global Health at the Hospital of the University of Pennsylvania. Dr. Ciano’s global work focuses on capacity building and medical education and training in low-middle income countries. He is thrilled to collaborate with the iEM Education Project in creating free educational content for medical trainees and physicians.

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

19 Questions and Answers on the COVID-19 Pandemic from a Emergency Medicine-based Perspective

covid 19 - from a Emergency Medicine-based Perspective

March 27, 2020June 12, 2020 ~ Francesco Adami, Italy ~ Leave a comment

1) What is COVID-19?

Corona Virus Disease 2019 (COVID-19) is the disease caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).

2) What is SARS-CoV-2?

SARS-CoV-2 is a virus belonging to the Coronaviridae family. Spike proteins (S proteins) on the outer surface of SARS-CoV-2 are arranged in a way that resembles the appearance of a crown when viewed under an electron microscope (see Figure 1). S proteins facilitate viral entry into host cells by binding to the angiotensin-converting enzyme 2 (ACE2) host receptor. Several cell types express the ACE2 receptor, including lung alveoli cells. [1].

3) How is SARS-CoV-2 transmitted?

Viral particles can spread from person-to-person through airborne transmission (e.g., large droplets) or direct contact(e.g., touching, shaking hands). We have to remember that large droplets are particles with a diameter > 5 microns and that they can be spread by coughing, sneezing, talking, etc., so do not forget to wear full PPE in the Emergency Department (ED). Other potential routes of transmission are still being investigated.

4) What is the incubation time?

In humans, the incubation period of the SARS-CoV-2 varies from 4 days to 14 days, with a median of about 4 days [2].

5) Can we say the COVID-19 is like the seasonal flu?

No, we can’t say that. COVID-19 differs from the flu in several ways:

First of all, SARS-CoV-2 replicates in the lower respiratory tract at the level of the pulmonary alveoli (terminal alveoli). In contrast, Influenza viruses, the causative agents of the flu, replicate in the mucosa of the upper respiratory tract.
Secondly, SARS-CoV-2 is a new virus that has never met our adaptive immune system.
Thirdly, we do not currently have an approved vaccine to prevent infection by SARS-CoV-2.
Lastly, we do not currently have drugs of proven efficacy for the treatment of disease caused by SARS-CoV-2.

6) Who is at risk of contracting the COVID-19?

We are all susceptible to contracting the COVID-19, so it is essential that everyone respects the biohazard prevention rules developed by national and international health committees. Elderly persons, patients with comorbidities (e.g., diabetics, cancer, COPD, and CVD), and smokers appear to exhibit poor clinical outcome and greater mortality from COVID-19 [3]

7) What are the symptoms of the COVID-19?

There are four primary symptoms of COVID-19: fever; dry cough; fatigue; and shortness of breath (SOB).

Other symptoms are loss of appetite, muscle and joint pain, sore throat, nasal congestion and runny nose, headache, nausea and vomiting, diarrhea, anosmia, and dysgeusia.

8) What is the severity of symptoms from COVID-19?

In most cases, COVID-19 mild or moderate symptoms, so much so it can resolve after two weeks of rest at home. However, onset of severe viral pneumonia requires hospital admission.

9) Which COVID-19 patients we should admit to the hospital?

The onset of severe viral pneumonia requires hospital admission. COVID-19-associated pneumonia can quickly evolve into respiratory failure, resulting in decreased gas exchange and the onset of hypoxia (we can already detect this deterioration in gas exchange with a pulse oximeter at the patient’s home). This clinical picture can rapidly further evolve into ARDS and severe multi-organ failure.

The use of the PSI/PORT score (or even the MuLBSTA score, although this score needs to be validated) can help us in the hospital admission decision-making process.

10) Do patients with COVID-19 exhibit laboratory abnormalities?

Most patients exhibit lymphocytopenia [11], an increase in prothrombin time, procalcitonin (> 0.5 ng/mL), and/or LDH (> 250 U/L).

11) Are there specific tests that allow us to diagnose COVID-19?

RT-PCR is a specific test that currently appears to have high specificity but not very high sensitivity [12]. We can obtain material for this test from nasopharyngeal swabs, tracheal aspirates of intubated patients, sputum, and bronchoalveolar lavages (BAL). However, the latter two procedures increase the risk of contagion.

However, since rapid tests are not yet available, RT-PCR results may take days to obtain, since laboratory activity can quickly saturate during epidemics. Furthermore, poor pharyngeal swabbing technique or sampling that occurs during the early stage of COVID-19 can lead to further decreased testing sensitivity.

Consequently, for the best patient care, we must rely on clinical symptoms, labs, and diagnostic imaging (US, CXR, CT). The use of a diagnostic flowchart can be useful (see Figure 2).

12) Can lung ultrasound help diagnose COVID-19?

Yes, it can help! The use of POCUS lung ultrasound is a useful method both in diagnosis and in real-time monitoring of the COVID-19 patient.

In addition, we could monitor the patient not only in the emergency department (ED) or intensive care unit (ICU), but also in a pre-hospital setting, such as in the home of a patient who is in quarantine.

In fact, POCUS lung ultrasounds not only allows one to anticipate further complications such as lung consolidation from bacterial superinfection or pneumothorax, but it also allows detection of viral pneumonia at the early stages. Furthermore, the use of a high-frequency ultrasound probe, which is an adoption of the 12-lung areas method [4] and the portable ultrasound (they are easily decontaminated), allow this method to be repeatable, inexpensive, easy to transport, and radiation-free.

There are no known pathognomonic patterns of COVID-19.

The early stages COVID-19 pneumonia results in peripheral alveolar damage including alveolar edema and a proteinaceous exudate [5]. This interstitial syndrome can be observed via ultrasound by the presence of scattered B lines in a single intercostal space (see videos below).

Subsequently, COVID-19 pneumonia progression leads to what’s called “white lung”, which ultrasound represents as converging B lines that cover the entire area of the intercostal space; they start from the pleura to end at the bottom of the screen.

Finally, the later stages of this viral pneumonia lead to “dry lung”, which consists of a pattern of small consolidations (< 1 cm) and subpleural nodules. Unlike bacterial foci of infection, these consolidations do not create a Doppler signal within the lesions. We should consider the development from “white lung” to “dry lung” as an unfavorable evolution of the disease.[6]

(the 5 videos above come from the COVID-19 gallery on the Butterflynetwork website)

13) Can CXR/CT help us in the diagnosis of COVID-19?

Yes, it can help! There are essentially three patterns we observed in COVID-19.

In the early stages, the main pattern is ground-glass opacity (GGO)[7]. Ground glass opacity is represented at the lung bases with a peripheral distribution (see videos below) .

The second pattern is constituted by consolidations, which unlike ground-glass opacity, determine a complete “opacification” of the lung parenchyma. The greater the extent of consolidations, the greater the severity and the possibility of admission in ICU.

The third pattern is called crazy paving[8]. It is caused by the thickening of the pulmonary lobular interstitium.

However, we should consider four things when we do a CXR/CT exam. First, many patients, especially in the elderly, exhibit multiple, simultaneously occurring pathologies, so it is possible to clinically observe nodular effusions, lymph node enlargements, and pleural effusions that are not typical of COVID-19 pneumonia. Secondly, we have to be aware that other types of viral pneumonia can also cause GGO, so they cannot be excluded during the diagnostic process. Thirdly, imaging can help evaluate the extent of the disease and alternative diagnoses, but we cannot use it exclusively for diagnosis. Lastly, we should carefully assess the risk of contagion from transporting these patients to the CT room.

Quality CT/XR images on proven COVID-19 provided by Prof. Dr. Filippo Cademartiri, Chairman of Radiology , Marche – Italy. pic.twitter.com/MchsLQMf8z
— Martin Schranz (@martinpschranz) March 5, 2020

14) What is the treatment for this type of patient?

COVID-19 patients quickly become hypoxic without many symptoms (apparently due to “silent” atelectasis). Therapy for these clinical manifestations is resuscitation and support therapy. In patients with mild respiratory insufficiency, oxygen therapy is adopted. In severe patients in which respiratory mechanics are compromised, non-invasive ventilation (NIV) or invasive ventilation should be adopted.

15) How can we non-invasively manage the airways of patients with COVID-19?

In the presence of a virus epidemic, we should remember that all the procedures that generate aerosolization (e.g., NIV, HFNC, BMV, intubation, nebulizers) are high-risk procedures.

Among the non-invasive oxygenation methods, the best-recommended solution is to have patients wear both a high-flow nasal cannula (HFNC) and a surgical mask[9]. Still, we should also consider using CPAP with a helmet interface. Furthermore, we should avoid the administration of medications through nebulization or utilize metered-dose inhalers with spacer (Figure 3).

Figure 3 – General schema for Respiratory Support in Patients with COVID-19 (from PulmCrit Blog)

16) How can we invasively manage the airways of patients with COVID-19?

We should intubate as soon as possible, even in non-critical conditions (Figure 3). Intubation is a high contagion risk procedure. As a result, we should adopt the highest levels of precaution[10]. To be more precise:

As healthcare operator, we should wear full PPE. Only the most skilled person at intubation in the staff should intubate. Furthermore we should consider using a video laryngoscope. Last but not least, we should ensure the correct positioning of the endotracheal tube without a stethoscope (link HERE).
The room where intubation occurs should be a negative pressure room. When that is not feasible, the room should have doors closed during the intubation procedure.
The suction device should have a closed-circuit so as not to generate aerosolization outside.
Preoxygenation should be done using means that do not generate aerosols. Let us remember that HFNC and BVM both can generate aerosolization. So, it is important to remember to turn off the flow of the HFNC before removing it from the patient face to minimize the risk and to use a two-handed grip when using BVM, interposing an antiviral filter between the BVM and resuscitation bag and ventilating gently.
Intubation drugs that do not cause coughing should be used. In addition, we should evaluate the use of Rocuronium in the Rapid Sequence Intubation (RSI) since it has a longer half-life compared to succinylcholine and thus prevents the onset of coughing or vomiting.

In conclusion, let us remember that intubation, extubation, bronchoscopy, NIV, CPR prior to intubation, manual ventilation etc. produce aerosolization of the virus, therefore, it is necessary that we wear full PPE.

17) What is the drug therapy for COVID-19?

Currently, there is no validated drug therapy for COVID-19. Some drugs are currently under study. They include Remdesivir (blocks RNA-dependent RNA polymerase), Chloroquine and Hydroxychloroquine (both block the entry of the virus into the endosome), Tocilizumab and Siltuximab (both block IL-6).

18) Is there a vaccine available for COVID-19?

No, there is still no vaccine currently available to the public.

19) What precautions should we take with COVID-19 infected patients?

As healthcare professionals, we should wear full personal protective equipment (PPE) and know how to wear them (“DONning”) and how to remove them properly (“DOFFing”) (see video below). Furthermore, we should wear full PPE for the entire shift and when in contact with patients with respiratory problems.

Resources on COVID-19

[cite]

References

[1] Zheng YY, Ma YT, Zhang JY, Xie X. COVID-19 and the cardiovascular system. NatRev Cardiol. 2020 Mar 5.

[2] del Rio C, Malani PN. COVID-19—New Insights on a Rapidly Changing Epidemic. JAMA. Published online February 28, 2020. doi:10.1001/jama.2020.3072

[3] Yee J et al. Novel coronavirus 2019 (COVID-19): Emergence and Implications for Emergency Care. Infectious Disease 2020. https://doi.org/10.1002/emp2.12034

[4] Belaïd Bouhemad, Silvia Mongodi, Gabriele Via, Isabelle Rouquette; Ultrasound for “Lung Monitoring” of Ventilated Patients. Anesthesiology 2015;122(2):437-447. doi: https://doi.org/10.1097/ALN.0000000000000558.

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Goals in Mechanical Ventilation: Concepts for the Students

September 2, 2019September 4, 2019 ~ Job Guillen, Mexico ~ Leave a comment

Authors: Dr. Job Heriberto Rodríguez Guillén (@job_rdz), Dr. Sergio Edgar Zamora Gómez (@ezg_galeno)

Introduction

Mechanical ventilation (MV) is one of the cornerstones of life support in the emergency department. It provides time for establishing therapeutic management aimed at the triggering cause of injury until the patient improves physiologic balance (1). Therefore, MV can not be a unique and specific treatment for any disease by itself; but it has two general and fundamental goals: to support the injured lung and protect the healthy lung.

Set your goals: Support and Protect

Support

MV supports the respiratory system; meanwhile, the primary disease becomes under control.

Example: A patient with acute respiratory distress syndrome (ARDS) due to pneumonia, where MV provides support to improve gas exchange and reduce work of breathing (WOB) meanwhile antibiotic treatment induces remission of the infectious disease.

Protect

MV is aimed to avoid complications not related to the primary disease. The patient-ventilator relationship becomes of benefit for the patient as his respiratory function is in the risk of injury because the primary disease does not allow him to breathe properly or because therapeutic interventions can reduce protective airway reflexes and lead to respiratory complications.

Example: Patients presenting neuromuscular diseases (Guillain-Barre syndrome), diseases affecting bulbar muscles (myasthenic crisis), decreased consciousness (stroke, poisoning) or severe traumatic brain injury, all these without lung injury at first but in high risk of pneumonitis and pneumonia due to aspiration of gastric content.

Specific goals of mechanical ventilation

One of the specific objectives of MV is to promote the optimization of arterial blood gases levels and acid-base balance by providing oxygen and eliminating carbon dioxide (ventilation). MV can reduce the work of breathing by taking effort from respiratory muscles and maintaining the long-term respiratory support for patients with chronic diseases.

MV´s circle (2) begins by recognizing the patient´s need for mechanical ventilatory support. Intubation and ventilation decision making is an essential skill for emergency physicians. Consideration of the patient´s needs is the basis of this decision making. The main indications for intubation and mechanical ventilation are (3):

Refractory hypoxemia
Increased respiratory effort
Apnea/hypopnea leading to inadequate ventilation (Hypercapnia)
The inability for airway protection

The goals should be individualized and established according to the clinical situation that led the patient to required ventilatory support. Although standard criteria traditionally have been specified for the onset of MV (3), we must remember that indication for intubation and ventilation is an essential skill for every physician treating critical care patients and the key is just thinking about what the patient needs.

Standard criteria for starting mechanical ventilation
Acute Ventilatory Failure	pCO2 > 50 mmHg + pH < 7.30
Impending Ventilatory Failure	Maintains normal gasometric levels by increasing respiratory effort.
Severe Hypoxemia	pO2 50%

pCO2 and pO2 values at sea level

In general, we can encompass the specific objectives of MV in three fundamental principles that must be fulfilled in every patient by setting the goals according to the primary disease:

Improve oxygenation (O2) and ventilation (CO2)
Reduce respiratory effort
Minimize ventilator-induced lung injury (VILI)

Conclusions

The goals of MV are established based on the primary disease that led the patient to need MV support, under the concept of protecting and supporting the lungs. Primum non nocere; lung-protective ventilation should be initiated in all patients who need it.

References and Further Reading

Frank Lodeserto MD, “Simplifying Mechanical Ventilation – Part I: Types of Breaths”, REBEL EM blog, March 8, 2018. Available at: https://rebelem.com/simplifying-mechanical-ventilation-part/.
Frank Lodeserto MD, “Simplifying Mechanical Ventilation – Part 2: Goals of Mechanical Ventilation & Factors Controlling Oxygenation and Ventilation”, REBEL EM blog, May 18, 2018. Available at: https://rebelem.com/simplifying-mechanical-ventilation-part-2-goals-of-mechanical-ventilation-factors-controlling-oxygenation-and-ventilation/.
Scott Weingart. EMCrit Lecture – Dominating the Vent: Part I. EMCrit Blog. Published on May 24, 2010. Accessed on August 30th 2019. Available at [https://emcrit.org/emcrit/vent-part-1/ ].