Critical Care Management

MonitoringCopy Link!

Whether or not a patient needs ICU level of care is addressed in Disease Severity and Disposition.

Lab, Vitals, and ImagingCopy Link!

Lab Monitoring

Vitals and Monitoring

Chest Imaging

Cardiac Diagnostics

Respiratory Failure in COVIDCopy Link!

Updated Date: December 20, 2020

Acute Respiratory Distress SyndromeCopy Link!

Literature Review (Acute Lung Injury): Gallery View, Grid View
Literature Review (ARDS):
Gallery View, Grid View

One of the most severe complications of COVID-19 is ARDS. ARDS is an acute clinical syndrome associated with inflammation and damage to the lungs. In ARDS, lungs become stiff and their ability to oxygenate the blood is impaired. Worldwide, mortality rates for ARDS are estimated to be 35-46% (Bellani et al). Because ARDS has implications for the management and treatment of respiratory failure, it is important that clinicians are able to recognize and diagnose it.

Most patients with COVID-19 who require ICU care develop ARDS. See the pathophysiology section for more information about why COVID causes ARDS. From onset of symptoms, the median time to:

COVID ARDS mortality is thought to be around 39% (95% CI 23-56%) according to a meta-analysis of studies covering more than 10,815 COVID patients with ARDS internationally (Hasan et al).

The Berlin Definition of ARDSCopy Link!

The Berlin definition of ARDS requires the following four criteria:

  1. Acute onset (within 1 week)
  2. Bilateral opacities on chest xray or CT
  3. PaO2/FiO2 ratio <300mmHg with a minimum of 5 cmH20 PEEP (or CPAP)
  4. Must not be fully explained by cardiac failure or fluid overload

The severity of ARDS is graded using this scale:


PaO2/FiO2 (on PEEP/CPAP >5)

Mortality (all cause, cohort)










Kigali Modification of Berlin Criteria for ARDSCopy Link!

The Berlin definition of ARDS has limited applicability in settings where blood gas analyzers, chest radiographs, and/or positive pressure ventilation are not reliably available. The Kigali Modification to the Berlin criteria has been developed to address this gap (Riviello et al).

The Kigal modification requires the following four criteria to diagnose ARDS:

  1. Acute onset (within 1 week or less)
  2. Bilateral opacities on chest xray or ultrasound not fully explained by pleural effusions or masses
  3. SpO2/FiO2 <315 (no PEEP requirement; SpO2 must be <=97% for accurate estimation by this method).
  4. Must not be fully explained by cardiac failure or fluid overload

Key differences in the Kigali Modification include allowing ultrasound as a method of identifying pulmonary opacities, the use of SpO2 instead of PaO2, and the lack of requirement for PEEP. Several studies have validated the use of SpO2 in place of arterial blood gases (Chen et al; Sanz et al; Brown et al) and ultrasound in place of chest xray for diagnosing ARDS (Lichtenstein). One single center study has validated the modification in ventilated patients (Vercesi et al). However, a large validation study comparing the Kigali Modification to the Berlin Criteria is needed.

When patients are not mechanically ventilated, the FiO2 will need to be estimated.

Tool: Management of Respiratory Failure where access to arterial blood gases is limited

Tool: Respiratory Care Pocket Reference (English) ( Español)

Tool: Imputed PaO2 (from SpO2) Calculator

Supplemental OxygenCopy Link!

Updated Date: December 20, 2020

See relevant sections in Inpatient Management (listed below) for options in patients that do not require intubation and mechanical ventilation. Some of these can be performed in the ICU or outside of the ICU depending on the institution:

IntubationCopy Link!

Updated Date: December 20, 2020
Literature Review:
Gallery View, Grid View

CandidacyCopy Link!

There are several potential indications for intubating a patient with respiratory failure. These include:

  • Persistent or rapidly worsening hypoxemia despite maximal oxygen therapies
  • Ventilatory failure (e.g. hypercapnia, fatigue, apnea or obstructive disease)
  • Severe work of breathing
  • Altered mental status that impairs either ability to protect airway or comply with oxygen therapies
  • Mechanical airway obstruction
  • Presence of a shock state
  • Presence of severe acidosis

Ultimately, the decision to intubate is based on multiple factors including the patient’s complete clinical scenario (including goals of care) as well as the availability of local resources to safely manage the airway and provide mechanical ventilation. Of note, early in the pandemic there were anecdotal reports advocating for earlier intubation of COVID patients as compared to other patients with respiratory failure from other causes. However, there are no data to support this practice. Intubation criteria for COVID patients with respiratory failure are generally the same as for non-COVID patients with respiratory failure.

Intubation ProcedureCopy Link!

PreparationCopy Link!

  1. Provider protections. Intubation is potentially a high risk aerosol generating procedures.
  1. Treat all intubations as a presumed COVID positive patient unless they have been fully ruled-out for COVID.
  2. Intubation should be done in a negative pressure room whenever possible (SCCM). Negative pressure rooms remove viral aerosolized particles at different rates based on the air changes/hour(ACH). OR’s are mandated to achieve at least 15 ACH’s yielding 99% airborne viral removal in 18 minutes. This is different for ICU’s and you may want to contact your facilities engineers to clarify ACH for your ICU beds. Calculate time necessary for your facility following CDC guidelines(Negative Pressure Airborne Clearance Times) and facility recommendations
  3. PPE:
  1. Intubating with the necessary PPE is often unfamiliar/difficult to many providers - consider practicing via simulation (APSF) and/or have it performed by the most experienced provider available
  2. Intubation should be done under airborne precautions. recommendations include disposable hair bouffant or cap, eye protection (face shield only vs face shield AND protective eyewear), either N95 or PAPR (N95 + hood for neck protection), fluid resistant gowns, double gloves, leg protection (boot covers) to below the knee These recommendations exceed the standards of the American Society of Anesthesiologists on 3/20/2020, the Society of Critical Care Medicine on 3/20/2020, and the Anesthesia Patient Safety Foundation on 2/12/2020
  1. Collect Materials: With the exception of the laryngoscope, DO NOT bring the following equipment into the room - only remove what you may need and discard or sterilize materials taken into the room after intubation even if not used. However, it is important that this equipment is easily and quickly accessible during intubation in case a difficult airway is encountered.
  1. Airway boxes (e.g. nasopharyngeal airways, oral airway, syringes, needles, laryngeal masks, “bougie” stylet, extra endotracheal tubes (ETTs) 6.0-8.0 for adults)
  2. Medication boxes (e.g. paralytics, vasopressors (e.g. phenylephrine, ephedrine, epinephrine, norepinephrine), lidocaine, labetalol, esmolol, propofol/etomidate, midazolam)
  3. Laryngoscope We recommend dedicated video laryngoscope if available, or the laryngoscope that is most familiar to the provider.
  1. Set up the ventilator (or bag valve mask in select circumstances):
  1. Correct placement of HEPA (bacterial/viral) filters depend on the circuit type and humidification system (See OpenCriticalCare Filter Placement FAQ). Always refer to manufacturers’ recommendations. In most circumstances a two filter setup should be used
  1. If available, place one HEPA (bacterial/viral) filter on inspiratory limb closest to the machine to protect against inadvertent backflow and device contamination
  2. Place one HEPA (bacterial/viral) filter between the endotracheal tube and the expiratory valve to avoid risk of contamination to the room
  1. If EtCO2 monitor utilizes mainstream infrared measurement (i.e. does not sample gas into the analyzer and then exhaust into the room) then may utilize a single HEPA (bacterial/viral) filter either between ETT and patient Wye or at the expiratory limb closest to the ventilator. If EtCO2 monitor utilizes sidestream sampling of gas, then a HEPA (bacterial/viral) filter must be placed between the endotracheal tube and the EtCO2 sampling port (See OpenCriticalCare Filter and ETCO2 Placement FAQ).
  2. If no ventilator is immediately available and a bag valve mask will be used until the ventilator is available, make sure it has a HEPA (bacterial/viral) filter.
  1. Decide who will be in the room:
  1. Rapid Sequence Induction (RSI) should be performed by the most experienced airway provider, preferably with a video laryngoscope, if available (SCCM)(APSF). Always perform a difficult airway assessment to determine if RSI is appropriate, and/or what back up preparations should be taken in the case of anticipated difficulty.
  2. Limit the providers in the room to only those who are necessary. Generally this means:
  1. One person who will be intubating
  2. One assistant (often a nurse)
  3. One ventilator manager (often a respiratory therapist)
  1. Assign roles and airway plan (who will “hold/do” what)
  2. Someone should also be available immediately outside the room to access additional airway equipment as needed.
  1. Checklist prior to starting/ induction:
  1. Difficult airway assessment performed and intubation plan determined
  2. Suction available
  3. Pulse oximetry (ideally audible)
  4. Blood pressure cuff (ideally cycling q1 minute)
  5. Ventilator set up with predetermined settings entered. If using EtCO2 monitor in-line, it should be connected and ready (or color change (colorimetric) device if sidestream or mainstream capnography not available)
  6. Free-flowing IV access
  7. Post-intubation sedation and vasopressors ready
  8. Viral filter in-line
  9. Induction medications ready
  10. Non-rebreather face mask with reservoir, connected to oxygen source with the flow turned off until ready to preoxygenate

ProcedureCopy Link!

  1. Preoxygenate the patient: Preoxygenate the patient for 3-5 minutes, and maintain preoxygenation until neuromuscular blockade (paralytic) has set in. Avoid bag valve mask ventilation if possible.
  1. If the patient is on nasal cannula, simple mask, venturi mask, or non-rebreather: tidal breathing on non-rebreather face mask at 15L/min (in general preoxygenation on nasal cannula, simple facemask or venturi mask are considered suboptimal)
  2. If the patient is on HFNC: increase FiO2 to 1.0 (100%)
  3. If the patient is on BiPAP: maintain BiPAP with tight seal until ready to intubate (turn “OFF” BiPAP flow prior to removing mask). Increase FiO2 to 1.0 (100%)
  4. If bag valve mask ventilation becomes necessary due to impending respiratory arrest or for rescue between intubation attempts:
  1. Use 2-hand technique with oral airway to create tight seal
  2. Ensure viral filter is in line
  3. Provide high frequency/low tidal volume breaths until saturation is optimized
  4. Do not remove mask for 2nd attempt intubation until end exhalation
  5. Consider use of an LMA with bacterial/viral filter to maximize airway patency
  1. Intubate the patient with an RSI technique/video laryngoscopy
  1. Use high dose neuromuscular blockade to promote rapid onset of action (practice may vary, but generally 2 mg/kg succinylcholine or 1.2-1.5 mg/kg rocuronium)
  2. Use awake intubation only when absolutely necessary as deemed by most senior clinician.
  1. After successful intubation:
  1. Inflate cuff
  2. Connect patient directly to ventilator with HEPA (bacterial/viral) filter.
  3. Endotracheal tube placement should be confirmed via quantitative in-line EtCO2 (gold standard > 3 breaths). Other methods for confirming placement include observing bilateral chest rise, hearing bilateral breath sounds, “fogging” of ETT, cuff palpation, or rising SpO2
  4. Secure ETT per hospital policy
  1. Decontaminate equipment:
  1. See Decontamination and Cleaning

Different protocols are used in different circumstances. For some specific examples, please see:

Tool: BWH Operating Room COVID Intubation Protocol

Tool: COVID19 Airway Management Checklist

Tool: South African Society of Anaesthesiologists: Recommendations for airway management for COVID-19 patients

Initial Ventilator SettingsCopy Link!

Tool: Respiratory Care Pocket Reference (Open Critical Care). Detailed pocket reference for ventilator modes and settings, including all the above tables.

  1. Obtain STAT portable chest xray: to confirm endotracheal tube location.
  1. Prioritize CXR and vent settings over procedures (such as central venous catheter placement) if possible.
  2. If portable chest x-ray is not available, confirm endotracheal tube placement with bilateral breath sounds and CO2 detection
  1. Assure adequate sedation
  2. Set mode to volume control (AC/VC)
  1. In some settings airway pressure release ventilation (APRV)is used
  1. Set Initial tidal volume (Vt):
  1. Vt = 6 ml/kgIBW (based on ideal body weight [IBW]), see ARDSNet Table to look up tidal volume by gender and height in cm or inches.)
  1. Set initial respiratory rate
  1. Typical starting rates will be 16-24 titrated to goal minute ventilation of 6-8 L/min
  2. Consider starting rates of 24-28 titrated to goal minute ventilation of 8-12 L/min in setting of acidosis (pH < 7.25) pre-intubation. If blood gas is unavailable, higher initial minute ventilation should be targeted for patients with a pre-intubation respiratory rate above 35.
  1. Set Initial PEEP based on BMI (empirically chosen targets):
  1. BMI < 40: PEEP 5
  2. BMI ≥ 40: PEEP 10
  3. These should be readjusted after half an hour based on FiO2 and ARDSnet grid (see ARDS Oxygenation)
  1. Set Initial FiO2: 100% on intubation then rapidly wean to SpO2 92-96% (Barrot et al) (see ARDS Oxygenation)
  2. Obtain an arterial blood gas (preferred) or a venous blood gas within 30 minutes
  1. Calculate P/F ratio from initial post-intubation ABG. Adjust oxygenation as described in ARDS Oxygenation.
  2. Goal pH 7.20 to 7.45. Adjust ventilation as described in ARDS Ventilation.

Mechanical VentilationCopy Link!

Updated Date: December 20, 2020
Literature Review (Ventilator Settings):
Gallery View, Grid View

Tool: Adult Ventilator Protocols and Order Set Templates (OCC). This includes sample ARDS Net lung protective ventilation as well as orders for spontaneous breathing trials (SBTs), difficult to wean patients and cuff leak tests.

This section addresses the management of mechanical ventilation for COVID ARDS specifically, not mechanical ventilation for other indications. It discusses the use of AC/VC as a ventilatory mode. Some settings may prefer APRV, which is not discussed in detail. Pressure support ventilation (PSV) mode is often used as the patient is recovering and preparing for extubation. Content about managing PSV is forthcoming.

This section does not discuss managing COVID ARDS with concurrent obstructive lung disease (asthma, COPD), which ideally should be done by experienced clinicians only.

Improper ventilator management can permanently damage a patient’s lungs. Ventilator management requires significant infrastructure as well as training and expert guidance to call on if needed. This section assumes providers have some background knowledge about mechanical ventilation. See below for links to introductory material on mechanical ventilation.

Tools: Mechanical Ventilation Training Course (English, Spanish)

Tools: Pocket Reference (English, Spanish)

Lung Protective VentilationCopy Link!

Patients with ARDS receiving mechanical ventilation are at risk of lung damage, often referred to as ventilator induced lung injury (VILI). However, steps can be taken to reduce the risk of VILI and decrease mortality for patients with ARDS. This is referred to as lung protective ventilation (LPV).

LPV involves adjusting ventilator settings to achieve the following goals:

  • Tidal volumes (Vt) of 4-6ml/kg ideal body weight (IBW)
  • Plateau pressures (pPlat) less than 30cmH2O
  • Driving pressures less than 15cm H2O
  • Driving pressure is equal to pPlat - PEEP

ARDS Ventilation: Respiratory Rate and Tidal VolumeCopy Link!

Minute ventilation (respiratory rate x tidal volume) helps control pH and PCO2.

  • Titrate minute ventilation to pH and not PCO2 in most circumstances!
  • Low tidal volumes are needed to protect the lungs from ventilator induced lung injury and promote lung healing. To achieve this, we tolerate hypercapnia (functionally no limitation unless clinical limits like seizure or managing increased ICP) and acidemia (pH > 7.2) (Ijland et al).

Adjusting ventilation parameters:

  1. First, set tidal volume
  • Follow ARDSnet ventilation where possible: Starting tidal volume of 6 cc/kgIBW.
  1. Tidal volumes should always be within the 4-8 cc/kg range, ideally 4-6cc/kg based on Ideal Body Weight [IBW]. See ARDSNet table to look up tidal volume by gender and height in cm or inches.
  • Next, adjust rate to meet goal pH 7.20-7.45:
  • The respiratory rate often has to be high to accommodate low tidal volumes; typical RR is 20-35 breaths/minute. In patients with obstructive lung disease these are lower.
  1. If pH > 7.45, decrease respiratory rate
  2. If pH 7.10-7.25, then increase respiratory rate until pH > 7.25, or PaCO2 < 30 (maximum RR= 35 breaths/minute and check for autoPEEP)
  • If pH < 7.10 despite maximum RR:
  • Address reversible causes of metabolic acidosis
  • Increase tidal volume up to 8cc/kg IBW or plateau pressure 30cmH20
  • Deepen Sedation to RASS -3 to -5 or paralyze if needed
  • Initiation of prone ventilation (may improve V/Q matching and ventilate better)
  • Consider extracorporeal membrane oxygenation (ECMO) if available and none of the above is effective

ARDS Oxygenation: PEEP and FiO2Copy Link!

PEEP and Fi02 drive oxygenation. The goal is to deliver a partial pressure of oxygen to perfuse tissues (PaO2 ≥ 65, Sp02 ≥ 92%) while limiting lung injury from high distending pressures (with plateau pressures ≤ 30) and oxygen toxicity (with FiO2 ≤ 60%, SpO2 ≤ 96%). Extensive mammalian animal data demonstrates that hyperoxic injury occurs at an FiO2 ≥ 75% with the rate of injury increasing as FiO2 exceeds that. In multiple mammalian models, an FiO2 of 100% for 48 to 72 hours is associated with nearly 100% mortality rate. In these guidelines, we strive for FiO2 < 0.60, but wish to focus particular interest in the ARDS pathway when FiO2 >= 0.75 (i.e., increased sedation, paralysis, proning, inhaled vasodilator and ECMO consultation).

Lower limit goals for PaO2 / SpO2 are widely debated; PaO2 > 55 and SpO2 >88% are also commonly used. Our rationale relies on evidence for lack of benefit from conservative PaO2 goals in clinical trials (e.g. PaO2 > 55) and past association between lower PaO2 and cognitive impairment, although the evidence is not definitive (Barrot et al; Mikkelsen et al). Many clinicians use PaO2/FiO2 (called the P/F ratio) to guide oxygenation as it is a shorthand way of assessing the A/a gradient for the patient and seeing if their oxygenation is improving.

  • If FiO2 >60%; patient requires ventilator optimization (ask a specialist). If persistent, see the Refractory Hypoxemia pathway.
  • It is reasonable to put a desaturating patient temporarily on 100% FiO2, but remember to wean oxygen as rapidly as possible

Adjusting oxygenation parameters:

  1. Typically, set PEEP and FiO2 according to the ARDSnet Tables:
  1. Within half an hour of initial ventilation settings (typically PEEP 5 for BMI <40 and PEEP 10 for BMI >40) reset PEEP and FiO2 to target oxygenation SpO2 92-96% using the following tables:

BMI < 40: ARDSnet LOW PEEP table:





























BMI ≥ 40: ARDSnet HIGH PEEP table































Higher levels of PEEP can cause hypotension. It is important to monitor blood pressure when increasing PEEP.

  1. Readjust Frequently
  1. PEEP and Fi02 should be adjusted if:
  1. SpO2 <92% or >96% (do not use more oxygen or PEEP than is needed)
  2. PaO2 <65 or >100
  3. pPlat >30 (see this pathway)
  1. PEEP Optimization (If Needed and Familiar):
  1. In the setting of persistent hypoxemia, elevated plateau pressures, or for provider preference, PEEP optimization strategies could be considered. There is little data for how to determine optimal PEEP, and it is recommended that these be conducted by people familiar with the methods.
  1. Best PEEP trial
  2. Pressure Volume Tools
  3. Esophageal balloons. Special cases (e.g. morbid obesity, burns) may need extra diagnostics, such as esophageal balloons, which we do not recommend for routine use given limited resources and infection risk.
  4. Stress index (Video)

Mechanics: Plateau Pressure and ComplianceCopy Link!

Tool: How to Check Plateau Pressure and Compliance

Plateau Pressure:

It is important to avoid elevated plateau pressures (with goal ≤ 30) which can indicate relative lung overdistention (Slutsky et al).

  1. Check plateau pressure with every change in tidal volume, PEEP, or clinical deterioration (worsening oxygenation) but not as part of routine practice. In order to accurately measure plateau pressure, the patient must be passive (i.e. not actively breathing) on AC/VC mode with a constant flow delivery (as opposed to decelerating flow delivery).
  2. If plateau pressure is >30 cm H20, then decrease tidal volume by 1 mL/kgIBW (minimum 4 mL/kgIBW)
  3. If plateau pressure is < 25 cm H20 and tidal volume < 6 mL/kgIBW, then increase tidal volume by 1 mL/kgIBW until plateau pressure is > 25 cm H2O or tidal volume = 6 mL/kgIBW
  4. If plateau pressure is < 30 cm H20 and patient is breath stacking or dyssynchronous, then increase tidal volume in mL/kgIBW increments to 7 mL/kgIBW or 8 mL/kgIBW while plateau pressure is < 30 cm H20


Compliance measures can give an indication about whether a patient’s lung stiffness is improving or declining over time, and can help with prognostication and management.

Assessing Ventilator SynchronyCopy Link!

This section is forthcoming

TroubleshootingCopy Link!

Resistance: Troubleshooting increased Peak Inspiratory Pressure due to high resistance: Work outside (machine) to inside (alveoli); circuit problem, ETT kink/occlusion/biting, ETT obstructed/malpositioned, large airway obstruction (mucous plug), small/ medium airway obstruction (bronchospasm); auscultation & passing a suction catheter can quickly eliminate many of these.

Compliance: Troubleshooting increased Peak Inspiratory Pressure due to reduced compliance: Work outside (patient extra-pulmonary factors) to inside (alveoli): Patient dyssynchrony requiring increased sedation (or temporary paralysis if refractory); intra-abdominal process; ET tube malpositioned (into a single tube); pneumothorax; auto-PEEP (due to incomplete exhalation, typically in setting of bronchospasm), parenchymal and alveolar process (flash pulmonary edema, pulmonary hemorrhage).

Other Modes of VentilationCopy Link!

PSVCopy Link!

This section is forthcoming

APRVCopy Link!

There exists significant practice variation around the use of bilevel ventilatory modes. APRV should only be used by providers with experience and familiarity with this mode. There are no data to support the superiority of APRV in ARDS patients, including those with COVID-19.

Prone VentilationCopy Link!

Updated Date: December 20, 2020
Literature Review (Proning):
Gallery View, Grid View

Early proning in COVID-associated ARDS requires intensive management but can significantly improve oxygenation. Pronation is one of the only interventions shown to improve mortality in ARDS (PROSEVA) (Guérin et al).

For proning of non-intubated patients, please see Awake Proning.

Timing and CandidacyCopy Link!

Timing: We recommend early proning in severe ARDS (<36 hrs) and prefer to initiate proning prior to use of continuous paralytics (or inhaled pulmonary vasodilators), despite the fact that in the PROSEVA trial over 95% of patients in both the intervention and the control arm were on continuous paralytics.

  • We particularly recommend proning if a patient requires an FiO2 ≥ 60% to achieve an SpO2 ≥ 92% (or PaO2 ≥ 65) with a P:F ≤ 150 (Guérin et al).

Eligibility: The only absolute contraindications are spinal cord injury, open chest, and unstable airway. Patient size is not a contraindication. Other relative contraindications should be discussed by the clinical team .

  • For patients with a tracheostomy, we recommend that patients have their tracheostomy replaced by oral endotracheal intubation (ETT) when possible, while recognizing that decannulating a tracheostomy and placing an ETT poses an infectious risk to staff.
  • Renal replacement therapy can be performed while prone, typically via a femoral line.
  • Monitor for complications: Prone ventilation can lead to increased incidence of brachial plexopathy in the context of increased pressure to anterior portions of the arm and shoulder (Scholten; Goettler). Prone positioning for surgery has been associated with abdominal or limb compartment syndromes, or rhabdomyolysis (Kwee).

Intubated Proning ProtocolCopy Link!

Tool: BWH MD MICU Proning Protocol

Tool: NEJM Video.

For proning of non-intubated patients, please see Awake Proning.

  1. Prepare for Proning
  1. Hold tube feeds for 1 hour prior to proning or supinating
  2. Assemble all necessary tools (pillows, props, additional persons to assist)
  1. Place Patient in Proned (“swimmer”) Position (some places have rotary beds)
  1. Have one person hold ET tube and lines to assure they are not dislodged and continuous medications are not disrupted
  1. Measure effect of proning. 1 hour post-initiation of prone ventilation:
  1. Obtain ABG. Compare pre-pronation PaO2/FiO2 to post-pronation PaO2/FiO2. Ideally there should be a 0.1 change in FiO2 (maintaining the same SpO2) or >10% change in PaO2 / FiO2. However, a lack of improvement may not be considered an absolute indication to abandon proning.
  2. Measure compliance and Plateau Pressure, PEEP, and FiO2
  3. Assess tidal volume and Adjust Ventilation Parameters
  1. If patient demonstrates improvement on proning:
  1. Prone ≥16 hrs per 24 hrs. Supine ≥ 4 hrs per 24 hrs. Repeat every day. There is no day limitation for maintaining prone ventilation and it should be repeated every day while beneficial.
  2. Discontinue neuromuscular blockade if initiated for dyssynchrony and re-assess.
  1. If patient does not improve on proning:
  1. Resupinate. Consider trying again the next day, as sometimes recruitability of lung tissue will change over time.
  1. Consider discontinuing proning
  1. If patient has improved and meets the goals listed below after supine for >4 hrs. If patients do not meet criteria for supine ventilation then recommend ongoing prone ventilation.
  1. FiO2 < 60% to meet an SpO2 ≥ 92% (or PaO2 ≥ 65)
  2. Plateau pressure < 30
  3. pH > 7.25
  1. Return to supine position emergently, if:
  1. Unscheduled extubation
  2. Endotracheal tube obstruction
  3. Severe or significantly worsening hypoxemia, e.g. Sp02 <85% and consideration of ECMO if available
  4. Hemodynamic instability

Refractory HypoxemiaCopy Link!

Updated Date: December 20, 2020

Refractory HypoxemiaCopy Link!

If patient is hypoxic (PaO2 <75) despite PEEP optimization as above); and FiO2 > 0.6 or PaO2/FiO2 ratio < 150 then consider trying each of the following

  1. Proning: Initiate early (if not already done)
  2. PEEP: Adjust PEEP as above and request expert optimization if needed
  3. Diuresis: Assess volume status. Diurese or remove volume by renal replacement therapy if indicated.
  4. Synchrony (Paralysis): Assess Ventilator Synchrony and Sedation to achieve ventilator synchrony. If still dyssynchronous, consider Neuromuscular Blockade.
  1. Assess for improvement in oxygenation (stable oxygenation metrics while being able to reduce FiO2 by 0.1)
  2. Try stopping neuromuscular blockade daily if possible, and discontinue completely if the patient maintains PaO2>75 with FiO2<0.75 without it.
  1. Inhaled pulmonary vasodilators: consider trial of continuous Inhaled Pulmonary Vasodilators. Note however that there is no evidence of survival benefit of inhaled vasodilators in ARDS.
  2. ECMO consultation: if available at your institution, if no improvement despite the above steps, no contraindications, and any of :
  1. Persistent PaO2 < 75 requiring FiO2 > 0.75
  2. Plateau pressure >30
  3. Refractory hypercapnia and pH < 7.2

Recruitment ManeuversCopy Link!

A recruitment maneuver is the deliberate administration of a high airway pressure for protocolized periods of time to open collapsed alveoli There are multiple protocols for performing recruitment maneuvers. Studies have shown that recruitment maneuvers are associated with a temporary increase in oxygen levels but do not impact clinical outcomes. (Brower et al; Meade et al; Oczenski et al). A more recent study of recruitment maneuvers in combination with best PEEP trials found an association with increased mortality (Calvacanti et al). Recruitment maneuvers can increase intrathoracic pressure enough to affect blood return to the heart and thus hemodynamics. We do not recommend regular use of recruitment maneuvers in the management of refractory hypoxemia.

Inhaled Pulmonary VasodilatorsCopy Link!

Literature Review: Gallery View, Grid View

There is no evidence of survival benefit of inhaled vasodilators in ARDS, and it can demand significant respiratory therapist resources (Fuller; Gebistorf et al,; Afshari et al). There is currently no evidence of the survival benefit in COVID ARDS, though data are still very limited. There is limited evidence from small studies that in about half of patients PaO2 to FiO2 ratios may be improved by >10%. In a retrospective cohort study of BWH intubated COVID-19 patients, inhaled epoprostenol did not significantly alter PaO2/FiO2. PaO2/FiO2 increased by >10% in 40% of patients (N=38), but clinical outcomes were not changed. 11 patients who failed to respond to inhaled epoprostenol were trialed on inhaled nitric oxide (iNO). On iNO, PaO2/FiO2 increased by >10% in 60% of patients (N=11). There was no change in outcome. This study was limited by a small sample size and retrospective design (DeGrado et al).

Epoprostenol Instructions:

  1. Exclude contraindications: Alveolar hemorrhage (epo has mild antiplatelet effect), LV systolic or diastolic CHF (vasodilators cause ↑ pulm blood flow → ↑ LV filling pressure → ↑ pulmonary edema & ↓ PaO2 → consider CHF if pt gets worse after starting).
  2. Measure baseline ABG for PaO2
  3. Start continuous nebulization at 0.05 mcg/kg/min based on IBW (MDcalc Online Calculator). Do not change ventilator settings, sedation, paralysis, patient position or other care that could affect oxygenation.
  4. Re-check ABG 2 hours after initiation of inhaled epoprostenol.
  • If PaO2 increased by >10% from baseline, continue inhaled epoprostenol.
  • If PaO2 not increased by >10% from baseline, discontinue inhaled epoprostenol.
  1. Weaning:
  • Attempt to wean off daily. Wean inhaled epoprostenol by decreasing 0.01mcg/kg/min every hour. Monitor SpO2 and hemodynamics.
  • Re-check ABG 2 hours after weaned off. If PaO2 worsened by >10%, restart inhaled epoprostenol.

Inhaled Nitric Oxide: Limited in vitro data notes that iNO at high doses inhibits replication of SARS-CoV, but this has not been studied in vivo (Akerstrom et al; Gebistorf et al) although clinical trials are in progress. iNO acts as a pulmonary vasodilator and can be used instead of epoprostenol. Depending on setting, continuous use of iNO can be logistically-challenging and cost-prohibitive.
Literature Review (Inhaled NO): Gallery View, Grid View

ECMO and Mechanical Cardiac SupportCopy Link!

Literature Review: Gallery View, Grid View

Respiratory failure:

In facilities where it is available, the veno-venous Extracorporeal Membrane Oxygenation (ECMO) team should be consulted for respiratory failure despite all other measures:

  • Persistent PaO2 / FiO2 ratio < 75 mmHg despite optimized ARDS management (optimized PEEP, neuromuscular blockade, proning, inhaled vasodilator).
  • Plateau pressure > 30 cm H2O on ARDSnet ventilation.
  • pH < 7.2
  • No potentially reversible causes (e.g. pulmonary edema, mucus plug, abdominal compartment syndrome)

Cardiogenic Shock:

In facilities where it is available, the veno-arterial ECMO or mechanical support team should be consulted for cardiogenic shock:

  • Dobutamine drip at 5mcg/kg/min (or unable to tolerate dobutamine due to tachyarrhythmias) and ScvO2 < 60% or CI < 2.2
  • Lactate > 4 after medical therapy


The criteria for ECMO and other mechanical circulatory support varies among centers and are difficult to develop even under typical circumstances. For the purposes of general education, a hypothetical set of inclusion criteria for VA ECMO or MCS could cover:

  • Younger age
  • Expected life expectancy >6 months pre-hospitalization
  • No evidence of solid or liquid malignancy
  • Able to tolerate anticoagulation
  • Platelets >50,000 or ANC > 500
  • Absence of severe peripheral arterial disease
  • No evidence of irreversible neurological injury
  • Able to perform ADLs at baseline prior to illness
  • BMI (for some devices there are BMI limitations, for others there are not)
  • No major conditions or multisystem organ failure that would preclude a reasonable chance of recovery.

Sedation and Ventilator SynchronyCopy Link!

Updated Date: December 20, 2020
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Achieving Ventilator SynchronyCopy Link!

  1. Start analgesia and sedation immediately:
  1. Ensure analgesia/sedation infusion is at bedside prior to intubation. The sedative boluses used during intubation will wear off long before the paralytic and the patient must be sedated while paralyzed. Assume at least 60 minutes of sustained neuromuscular blockade for rocuronium (longer in renal or liver dysfunction) and cisatracurium, and 10 minutes for succinylcholine.
  1. Assess patient synchrony with the ventilator:
  1. After neuromuscular blockade has worn off, assess synchrony (e.g, signs of breath-stacking, double triggering, other ventilator alarms)
  1. If synchronous, lighten sedation to the lowest level that maintains synchrony, ideally Richmond Agitation Sedation Scale (RASS) score 0 to -1.
  2. If not synchronous: First adjust ventilator settings (including flow settings, trigger settings, and modest liberalization of settings within ARDSnet criteria [Vt 4-8ml/kgIBW]). Then escalate sedation as needed to achieve synchrony
  1. If dyssynchronous despite deep sedation (RASS -4 to -5):
  1. First discuss additional ventilator changes with someone very familiar with mechanical ventilation (respiratory therapist or intensivist) if available
  2. Try Neuromuscular Blockade if unable to achieve with the above

Sedation: Pain, Agitation, Delirium ModelCopy Link!

Typical regimen in a ventilated ARDS patient: Generally ARDS patients require a period of continuous IV sedation and analgesia to establish ventilator synchrony. Assess and treat pain, agitation, and delirium in that order (sedating a patient who is in pain is typically less effective and less humane).

Detailed instructions on dosing, adjuncts, and enteral options for all three of these categories are available in the BWH Sedation Section.

  1. Pain: Low-dose opioids, in bolus or enteric form whenever possible, with adjuncts to reduce doses.
  1. First line agents are fentanyl or hydromorphone
  2. Second line agents is morphine
  1. Agitation:
  1. First line is continuous propofol in post patients
  1. Dexmedetomidine is generally reserved for patients approaching ventilation liberation; tachyphylaxis (diminishing response to the medication with repeated exposure) may occur with prolonged use
  1. Benzodiazepines can be used, but carry a high risk of delirium
  1. Delirium: If patients are agitated on daily Sedation Interruption (SAT), positive on the CAM-ICU screen, or receiving continuous sedation for >48hrs, we recommend delirium treatments.
  1. First line is nonpharmacologic mechanisms
  2. Second line is an antipsychotic (Haloperidol, Quietapine)
  3. Second line is alpha-2 agonists or mood stabilizers

Tool: BWH Detailed Sedation Recommendations including Dosing and Alternatives




Assess and Document

If able to self report → Numeric Rating Scale (0-10) (NRS)

If unable to Self Report → Critical Care Pain Observation Tool (CPOT) (0-8)

Richmond Agitation Sedation Scale (RASS) (-5 to +4)

Bispectral Index (BIS) in patients receiving Neuromuscular Blockade

CAM ICU-modified (+ or -)


At least every 8 hours on all patients

If receiving intermittent or continuous analgesia or sedation, every 2 hours

At least every 8 hours on all patients

If receiving intermittent or continuous analgesia or sedation, every 2 hours

At least every 8 hours on all patients


Patient is in significant pain if:

  • NRS > 4
  • CPOT > 3

Sedation/agitation depth defined according to RASS scale

Usual goal RASS is 0 to -1

Delirium present if: CAM-modified is positive


First line: Fentanyl or Hydromorphone

Second line: Morphine

First line: Propofol

Second line: Dexmedetomidine or benzodiazepines

First line: non-pharmacologic

Second line: antipsychotics

Third line: Alpha-2 agonists and mood stabilizers

Strategies to Minimize Medication ShortagesCopy Link!

  1. Boluses of benzodiazepines and opioids are preferred to continuous infusions. If continuous infusions are used, boluses should be administered prior to starting the infusion as well as when infusions are up-titrated. Bolus doses are typically 50-100% of the hourly infusion dose.
  2. Use the lowest dose that can achieve the desired effect
  3. Change IV medications to enteral medications if appropriate, especially as patients are weaning.

Strategies to Avoid Prolonged SedationCopy Link!

  1. Daily SAT:
  1. We recommend a daily spontaneous awakening trial/sedation interruption unless contraindicated.
  1. Wean quickly, while monitoring for withdrawal:
  1. Patients who have been on continuous sedation for less than 7 days can be weaned rapidly with minimal concern for withdrawal.
  2. Otherwise, wean sedation and analgesics by at least 20% per day
  1. Faster weaning is frequently possible due to drug accumulation in tissues
  2. Consult a pharmacist (if available) if concerns for withdrawal
  1. Use adjuncts:
  1. Adjuncts including alpha-2 blockers, antipsychotics, enteral agents, and non-pharmacologic delirium prevention can facilitate weaning
  2. Try ventilator adjustments to facilitate Ventilator Synchrony.

Neuromuscular BlockadeCopy Link!

When to use: Neuromuscular blockade (NMB) is often used as a last measure to achieve ventilator synchrony in patients on Assist Control or Mandatory ventilation modes to help reduce lung injury from ventilator dyssynchrony. It should be used after alternative approaches to achieving ventilator synchrony have been pursued (see Ventilator Synchrony above). It has also been used as part of standard therapy for moderate-severe ARDS, although recent data have brought this practice into question (NHLBI).

Neuromuscular blockade should always be administered with adequate sedation and for the shortest possible duration.

Use when Proning: NMB is usually not required for proning, as most patients can be proned with deep sedation alone, however, it can be used in boluses prior to proning or supination.

Safety and Monitoring:

  1. Always use analgesia and sedation: Neuromuscular blockers have no sedative or analgesic properties. Patients receiving neuromuscular blockade must be on medications for both analgesia (e.g. an opioid) and sedation (e.g. propofol or a benzodiazepine) to avoid having a patient who is paralyzed but wakeful. This must be initiated prior to starting NMB.
  1. Monitoring Sedation: Ideally you should use RASS to measure sedation before initiating neuromuscular blockade and a BIS monitor after. RASS cannot be used to assess sedation after initiating of neuromuscular blockade.
  1. Before Initiating NMB: Target sedation scale to RASS - 4 to -5
  1. Where BIS monitoring is used to assess level of sedation, it may not be reliable before neuromuscular blockade is initiated due to facial muscle activity. Some institutions do not routinely use BIS.
  1. After initiating NMB: Target BIS of 40-60 (RASS cannot be used in paralyzed patients). If BIS is not available, continue deep sedation with the dose of sedative and analgesic that had been required to achieve RASS -5 prior to starting NMB.
  1. Closely monitor heart rate and blood pressure. Unexplained high heart rates and/or hypertension may be a sign that the patient is under-sedated. Patients require higher doses of opioids or sedatives over time to achieve the same level of sedation, so assess this daily.
  1. Even if BIS is available, monitoring is imperfect, and can be falsely low in the setting of edema or hypotension or falsely high with ketamine administration.
  1. After stopping NMB: Washout time for paralytics should be allowed (and, if using, “Train of Four” with a peripheral nerve stimulator should be 4/4) before sedation weaning (see tool for using “Train of Four” below)
  1. Use the lowest effective dose for the shortest possible time: Prolonged neuromuscular blockade may contribute to weakness, prolonged weaning, and delayed recovery. Corticosteroids may increase risk of severe myopathy.
  1. Monitoring paralysis: Use the minimum dose needed for intended effect
  1. Ventilator synchrony should be the primary indicator of when a patient is adequately paralyzed. Consider bolus, not continuous, dosing for intermittent dyssynchrony.
  2. Some institutions use a peripheral nerve stimulator (“Train of Four”) to assess paralytic effect and minimize doses. The goal is still vent synchrony not a number of twitches. Use the minimal amount of paralytic necessary for synchrony. (See tool for using “Train of Four” below)
  1. Stopping NMB: Try stopping neuromuscular blockade after 48 hours (earlier if synchrony can be achieved by other means) and daily thereafter unless the patient is too unstable.
  1. Only continue neuromuscular blockade if a substantive improvement in oxygenation occurs (SpO2 and PaO2 similar with reduction in FiO2 by 0.1). Discontinue if the patient maintains PaO2>75 with FIO2<0.75.

Tool: Train of Four Monitoring (Winnipeg Regional Health Authority)

Dosing Strategy:

  1. Try bolus dosing before continuous dosing:
  1. Use boluses to facilitate pronation/supination or for intermittent ventilator dyssynchrony in adequately sedated patients
  2. Convert to a drip if there is persistent ventilator dyssynchrony requiring >3 bolus doses in 2 hours, with re-evaluation every 24-48 hours.
  1. First line agents:
  1. Cisatracurium (Preferred in renal or hepatic dysfunction, though supplies globally are limited)
  1. Dosing - Intermittent Bolus: 0.1-0.2 mg/kg Infusion: 0-5 mcg/kg/min
  1. If Cisatracurium is not available, Rocuronium is often used.
  1. Dosing - Intermittent Bolus: 0.6-1.2 mg/kg Infusion: 0-20 mcg/kg/min Start infusion at 3-5 mcg/kg/min
  1. If concerns for tachyphylaxis (decreasing effect with prolonged exposure), consider rotating to an alternative agent (vecuronium or atracurium)





Duration/Recovery (min)





Renal excretion (%)

Hoffman Elimination

Hoffman Elimination



Effect of renal failure

No change

No change

Increased, especially metabolites


Hepatic excretion (%)

Hoffman Elimination

Hoffman Elimination


< 75

Effect hepatic failure

No change

No change

Variable, mild


Histamine release


Dose dependent



Liberation from the VentilatorCopy Link!

Updated Date: December 20, 2020
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Spontaneous Awakening and Breathing Trials (SAT/SBT)Copy Link!

Tool: SCCM Guide on Spontaneous Awakening and Breathing Trials (SAT/SBT)

Tool: Adult Ventilator Protocols and Order Set Templates (OCC). This includes sample ARDS Net lung protective ventilation as well as orders for spontaneous breathing trials (SBTs), difficult to wean patients and cuff leak tests.

Aim to liberate the patient from mechanical ventilation as soon as safe and feasible. Prolonged intubation is associated with ventilator-associated pneumonia (VAP) with median-time to VAP onset of 8 days in a retrospective study of 191 COVID patients in Wuhan (Zhou).

All patients with improving or stable respiratory disease should have FIO2 and PEEP titrated at least daily and should have a Spontaneous Awakening trial (see below) to assure that their neurologic status remains intact, even if they are not yet a candidate for extubation.

Daily spontaneous awakening trial (SAT): all patients on mechanical ventilation should be assessed daily for whether they meet criteria for SAT:

  1. Is the patient on high ventilator settings, proned, paralyzed within the last 6 hours, hemodynamically unstable typically HR > 120 or unstable arrhythmia or, MAP < 65, or vasopressor requirement equivalent of norepinephrine > 10 mcg/min, though none of these is absolute? Have they had recent myocardial ischemia, elevated intracranial pressure, or are they sedated for non-intubation medical reasons (e.g. seizure)? If so, do not attempt an SAT
  2. Otherwise, stop sedatives (and analgesics not needed for pain) until a RASS of 0 is achieved
  3. Ask the patient to do the following (ideally they should do 3 of 4, though this is not absolute): If the patient becomes highly agitated they may not be able to follow commands but could still be able to be extubated if they are able to take large breaths. This is common in young people.
  1. Open their eyes
  2. Look at their caregiver,
  3. Squeeze the hand
  4. Put out their tongue
  1. Check the patient’s hemodynamics for 5 minutes. The patient should have none of the following issues:
  1. RR >35?
  2. No spontaneous breaths initiated in 5 minutes
  3. SpO2 <88% for 5 minutes
  4. Acute arrhythmia?
  5. Marked work of breathing or agitation.
  1. If the patient passes part b and c, then move on to SBT
  1. If a patient fails, sedatives are started at half the prior dosage and titrated up as needed. Often patients will need a longer washout time, or better Management of Delirium.

Spontaneous breathing trial (SBT): all patients on mechanical ventilation and passing SAT should be assessed daily for SBT (adapted from AHRQ).

  1. Does the patient meet these criteria?:
  1. FiO2 ≤ 50%, PEEP ≤ 10cmH2O for BMI ≤ 40 (or ≤ 16 cmH2O for BMI > 40 at provider discretion) with SpO2 ≥ 92% in the supine position
  2. Hemodynamically stable (defined as HR < 120, MAP > 65, and vasopressor requirement of norepinephrine < 10 mcg/min and no unstable tachyarrhythmias)
  3. No other medical contraindications to increased respiratory effort or decreased sedation
  1. If so, change their ventilator settings:
  1. SBT consists of Pressure Support ventilation mode with a pressure support = 5cmH2Oand PEEP = 5cmH2O (consider PEEP of 10cmH2O for BMI > 40)
  2. SBT is discontinued (patient is re-sedated and ventilator settings changed) if the patient develops:
  1. Evidence of increased work of breathing with RR > 30
  2. Hypoxia (SpO2 < 92%)
  3. Hemodynamic instability
  4. Rapid shallow breathing index (RSBI) = respiratory rate/tidal volume > 105
  1. If not terminated for the above reasons, terminate all SBTs after 30 minutes.
  1. If the patient does well and the medical team deems them ready to be extubated (see below), proceed with extubation.
  2. If the patient does not do well or is not ready to be extubated, they can be returned to their prior mode of ventilation or to a new mode. Typically we choose:
  1. AC/VC if ARDS is ongoing and the clinicians anticipates >1 day of need for ongoing intubation
  2. PSV (with higher pressure support) if the clinicians believe the patient may be able to be extubated within a day or deems it appropriate

ExtubationCopy Link!

Extubation should be considered if patient:

  1. Passes SAT and SBT
  2. Is able to follow commands (with RASS ideally 0 to -1)
  3. Coughs on deep suctioning and has a gag reflex
  4. Does not require deep suctioning more than every 2 hours
  5. Does not need any other medical interventions prior to extubation
  6. The patient has enteric access if needed.
  1. We recommend placing an NG or Dobhoff tube (with bridle if possible) prior to extubation for patients intubated for >48h given the frequency of swallowing issues post-extubation in these patients and the challenges in obtaining swallowing evaluations in ICU extubation

Extubation Procedure:

  1. Clarify goals of care if the patient fails extubation and whether reintubation should be attempted.
  1. Make sure adequate supplies for Reintubation and Airway Management are available and nearby if needed.
  1. Use airborne precautions, don appropriate PPE, minimize staff
  2. Place the patient on 1.0 FiO2 on the ventilator
  3. Ensure the selected supplemental oxygen device that the patient will use after extubation is at bedside. Optimal selection may help reduce the risk of reintubation. The selection of devices varies widely depending on practice patterns. One suggestion is that patients who have hypercapnia be extubated to NIPPV. Other patients at high risk for reintubation may get NIPPV or HFNC where available. Patients with prolonged intubation should be extubated to HFNC where possible. Other oxygen delivery devices are often adequate, but prepare for the potential to increase oxygen delivery rapidly if needed (Hernández et al; Oulette et al; Hernández et al).
  4. Place bed pad or towel on patient chest. Consider placing a drape on top of the patient to prevent exposure to any coughing that may occur.
  5. Secure the feeding tube to nose.
  6. Suction mouth and loosen tape securing ETT to patient.
  7. Turn all gas flows to “OFF” (may still have some O2 flow as a safety mechanism for most machines)
  8. Deflate the ET tube cuff, and extubate the patient.
  9. Immediately place the oxygen delivery device on the patient (typically at a high flow or FiO2 rate).
  10. Immediately discard ETT, absorbent pad or towel, and drape
  11. Ensure the patient is adequately oxygenating and ventilating (Sp02, respiratory rate)
  1. Consider blood gas half an hour after extubation
  1. Doff PPE and ensure adequate air turnover in the room before taking off airborne precautions. Assuming an air changeover of 6 times an hour, this is 47 minutes.

Barriers to LiberationCopy Link!

Weaning can fail in the setting of the following conditions (address appropriately) (Boles et al)

  1. Respiratory factors:
  1. Ongoing pneumonia or pulmonary inflammation
  2. Bronchoconstriction
  3. Glottic and airway edema, sputum production, impaired cough
  1. Cardiac factors:
  1. Cardiac dysfunction or shock
  1. Neuromuscular factors
  1. Weakness and prolonged immobility
  2. Effects of steroids or neuromuscular blockade
  1. Neuropsychological factors
  1. Delirium
  2. Sedating medications
  1. Metabolic factors
  1. Malnutrition
  2. Electrolyte disturbances (hypophosphatemia, etc)

Tracheostomy ManagementCopy Link!

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  1. For tracheostomy procedure, see BWH guide on Tracheostomy
  2. This section is in development

ShockCopy Link!

Updated Date: December 20, 2020

Undifferentiated ShockCopy Link!

Definition: Acute onset of new and sustained hypotension (MAP < 65 or SBP < 90) with signs of hypoperfusion requiring intravenous fluids or vasopressors to maintain adequate blood pressure

Time course: Patients rarely present in shock on admission. Natural history seems to favor the development of shock after multiple days of critical illness.

Etiology: The range of reasons for shock in COVID is broad, and includes

  1. Myocardial dysfunction
  2. Secondary bacterial infection
  3. Cytokine Storm Syndrome
  4. Sedation effects in intubated patients


  1. Assess for severity of end organ damage:
  1. Urine output, mental status, lactate, BUN/creatinine, electrolytes, liver function tests
  1. Obtain a FULL infectious/ septic workup, which includes all of the following:
  1. Labs: CBC (FBC) with differential. Note that most COVID patients are lymphopenic (83%). However, new leukocytosis can occur and left-shift can be used as a part of clinical picture (Guan et al). Two sets of blood cultures, liver function tests (for cholangitis/acalculous cholecystitis), urinalysis (with reflex to culture), sputum culture (if it can be safely obtained), procalcitonin at 0 and 48h if available (do not withhold early antibiotics on the basis of procalcitonin alone), urine Strep pneumo and legionella antigens if available
  2. Portable chest xray (avoid CT unless absolutely necessary)
  3. Full skin exam
  1. Assess for cardiogenic shock
  1. Assess extremities: warm or cool on exam
  2. Assess patient volume status: JVP, CVP, edema, CXR
  3. Assess pulse pressure: If < 25% of the SBP, correlates highly with a reduction in cardiac index to less than 2.2 with a sensitivity of 91% and a specificity of 83% (Stevenson et al).
  4. Perform point of care ultrasound, if available, to assess for gross LV/RV dysfunction
  1. For transthoracic echocardiography (TTE) protocols see Advanced Cardiac Diagnostics.
  1. Labs: Obtain a central venous O2 sat or mixed venous O2 sat if the patient has central access, troponin x2, NT proBNP, A1c, lipid profile, TSH
  2. EKG (and telemetry)
  3. Calculate estimated Fick Cardiac Output
  1. MDcalc online calculators: Fick CO, BSA
  1. Consult cardiologist if available if any suspicion of cardiogenic shock
  1. Assess for other causes of shock:
  1. Vasoplegia:
  1. Run medication list for recent cardiosuppressive medications, vasodilatory agents, antihypertensives
  1. Adrenal insufficiency:
  1. Unless high pretest probability of adrenal insufficiency, we recommend against routine cortisone stimulation testing
  1. Obstruction:
  1. PE (given the elevated risk of thrombosis)
  2. Tamponade (given elevated risk of pericarditis)
  3. Obstruction from PEEP
  1. Cytokine Storm Syndrome
  2. Allergic reactions to recent medications
  3. Neurogenic shock is uncommon in this context
  4. Hypovolemia:
  1. Bleeding
  2. Insensible losses from fever
  3. Diarrhea/vomiting

Differentiating ShockCopy Link!

Tool: Differentiating Shock

Type of Shock

Cardiac Output



ScvO2, MvO2

Other features






Distributive (sepsis,cytokine, anaphylaxis)


















Low or normal


Decreased HR

Septic ShockCopy Link!

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The rates of sepsis and septic shock are not reported consistently in currently available case series. One meta-analysis of 21 studies (47,344) found that 4.7 % of patients developed shock (95CI 0.9–8.6 %), though this was pooled septic and other forms (Hu et al). Sepsis can be caused by the coronavirus itself (viral sepsis), multisystem organ failure, or by Secondary Bacterial Infection.

We recommend instituting early empiric antibiotics for suspected septic shock and following a conservative fluid management strategy.

AntibiosisCopy Link!

  • Early empiric antibiotics should be initiated within 1 hour (see Antibiotics)
  • Choice of agent varies widely depending on local bacterial epidemiology and the availability of antibiotics. For septic shock it should include broad gram positive and gram negative coverage.

Pressors and Fluid Management:Copy Link!

Pressors. Goal MAP > 65mmHg. While there is emerging data that lower MAP thresholds may be beneficial, we recommend following this threshold for now.

  1. Norepinephrine is the preferred initial vasopressor for undifferentiated shock and septic shock.
  1. If norepinephrine is not available, we recommend epinephrine (Myburgh et al).
  1. Dopamine should only be used as an initial pressor if other pressors are unavailable
  1. When norepinephrine requirement is above 10, we recommend adding a second agent (typically vasopressin if available).
  1. If vasopressin is unavailable, epinephrine should be used as a second pressor
  1. Sometimes phenylephrine is also needed, though this should be used with caution if there is concern for cardiogenic shock.
  2. Corticosteroids. Consider increasing from COVID-dosing Corticosteroids to stress-dose hydrocortisone at 50mg IV every 6 hours in patients on > 2 pressors. If hydrocortisone is not available, equivalent steroids with both

Conservative Fluid Management:

Literature Review (Intravenous Fluids): Gallery View, Grid View

Do not give conventional 30cc/kg resuscitation. COVID-19 clinical reports indicate the majority of patients present with respiratory failure without shock. ARDS is mediated in part by pulmonary capillary leak, and randomized controlled trials of ARDS indicate that a conservative fluid strategy is protective in this setting (Grissom et al; Famous et al; Silversides et al). Conservative fluid management is also part of the most WHO guidelines.

If vasopressors are unavailable or limited, a conservative fluid strategy may not be possible for patients with shock. In these situations, fluid management should be guided by focusing on either shock (i.e. fluid resuscitation) or respiratory failure (i.e. conservative fluid strategy), depending on which is the most immediately life-threatening problem. Seeking expert opinion is also recommended.

  1. Give 250-500cc IVF and assess in 15-30 minutes for response:
  1. Increase > 2 in CVP
  2. Increase in MAP or decrease in pressor requirement
  1. Use isotonic crystalloids; Lactated Ringer’s solution is preferred where possible. Avoid hypotonic fluids, starches, or colloids
  1. Repeat 250-500cc IVF boluses; Use dynamic measures of fluid responsiveness
  1. Pulse Pressure Variation: can be calculated in mechanically ventilated patients without arrhythmia; PPV >12% is sensitive and specific for volume responsiveness
  2. Straight Leg Raise: raise legs to 45° w/ supine torso for at least one minute. A change in pulse pressure of > 12% has sensitivity of 60% & specificity of 85% for fluid responsiveness in mechanically ventilated patients; less accurate if spontaneously breathing
  3. Ultrasound evaluation of IVC collapsibility should only be undertaken by trained personnel to avoid contamination of ultrasound

Tool: Conservative Fluid Management protocols are available from from FACCT Lite trial (Grissom et al).

Cardiogenic ShockCopy Link!

Cardiogenic shock occurs in hospitalized COVID-19 patients, can occur late in the course, and portends a poorer outcome. The mechanisms are still being researched but potentially include direct viral toxicity, acute coronary syndrome, stress or inflammatory cardiomyopathy. Please see here for more information on Acute Cardiac Injury, Acute Coronary Syndromes, and Myocarditis.

Time course: Cardiogenic shock may present late in the course of illness even after improvement of respiratory symptoms.

WorkupCopy Link!

  1. Significant concern for cardiogenic shock if any of the following are present with evidence of hypoperfusion (e.g. elevated lactate):
  1. Elevated NT-proBNP OR
  2. ScvO2 < 60% (PvO2 < 35 mm Hg) OR
  3. Point of care ultrasound or echocardiogram with depressed LV and/or RV function
  1. Rule out acute coronary syndrome and complete the initial work up as described in Acute Coronary Syndromes.
  2. Ongoing monitoring:
  1. Labs: ScvO2 (central venous O2 sat obtained by upper body central line) or ScvO2 (mixed venous O2 sat) every 8-12 hours or with clinical change, lactate every 4-6 hours, liver function tests daily (for hepatic congestion)
  2. Daily EKGs or as needed with clinical deterioration
  3. Trend troponin to peak
  1. All cardiogenic shock cases require cardiology consult if available.
  1. PA catheters may be placed bedside by experienced providers, with preference for use only in mixed shock or complex cases with cardiology guidance

ManagementCopy Link!

Close collaboration with a cardiologist is recommended if possible.


  • Mean Arterial Pressure 65-75, Central Venous Pressure 6-14, SCvO2 > 60%
  • If invasive monitoring is used: PCWP 12-18, PAD 20-25, SVR 800-1000, CI > 2.2
  • Note: Achieving MAP goal is first priority, then optimize other parameters

How to Achieve Goals:

  1. Continue titration of norepinephrine infusion for goal MAP 65-75. If norepinephrine is not available, then epinephrine (adrenaline) can be used.
  2. Initiate diuretic therapy for CVP > 14, PCWP >18, PAD > 25
  3. Initiate inotropic support:
  1. Dobutamine drip for SCvO2 < 60%, CI < 2.2 and MAP > 65. Start at 2mcg/kg/min. Increase by 1-2mcg/kg/min every 30-60 minutes for goal parameters. Alternative strategies should be considered once dose exceeds 5mcg/kg/min. Maximum dose is 10mcg/kg/min.
  1. Ensure negative inotropes such as beta blockers, calcium channel blockers and antihypertensives are discontinued.
  2. If the patient is failing to meet goals despite the above, consider mechanical support if it is available.

Cytokine Storm SyndromeCopy Link!

Updated Date: November, 2020
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MechanismCopy Link!

Also called cytokine release syndrome, CSS is an umbrella term used for many different cytokine-driven illnesses that share certain aspects of pathophysiology but differ in serum cytokine patterns, timing, and other factors (Henderson et al). Viral infections, especially EBV and influenza, are a known cause of cytokine storm, and it has been implicated in SARS and MERS-associated ARDS as well (Schulert et al, Kim et al).

Cytokine Storm Syndrome in COVID: A subgroup of patients with severe COVID-19 have an immune hyperactivation that resembles CSS (Mehta et al, Henderson et al).

  • Evidence of cytokine storm syndrome in COVID-19 includes correlation of elevated D-dimer, ferritin (a marker of macrophage activation), and soluble IL-2 receptor (a marker of T lymphocyte activation) with severe disease course (Zhou).

Mechanisms: Cytokine storm reflects impaired control of immune responses, leading to leukocyte activation and release of cytokines such as IL-1, IL-6, and IFN-gamma (Mangalmurti et al; Vabret et al; Henderson et al; Tay et al). CSS usually originates from dysfunctional interactions between the innate immune system and the adaptive immune system as follows: (See illustration in Subbarao et al). The adaptive immune system takes 5-7 days to respond to a new antigen, which may explain why CSS usually occurs around/after this timepoint in the course of disease:

  1. The adaptive immune system fails to kill activated innate immune cells.
  2. If the innate immune cells are not shut down, both the innate cells (especially monocytes and macrophages) and adaptive cells continue to produce pro-inflammatory cytokines, activating positive feedback loops
  3. The immune response fails to move toward the resolution phase and instead causes amplification of the immune response, especially systemic inflammatory cytokine production.
  4. These inflammatory cytokines cause upregulation of complement proteins, clotting factors, and other substances that can cause target cell damage. This in turn leads to further inflammation.

Consequences: Cytokine storm syndrome has a number of downstream clinical consequences, including:

  • Fever
  • Hypotension/distributive shock
  • Respiratory failure/ARDS
  • Renal failure
  • Secondary to hypotension/AKI/ATN, microthrombi, or other mechanisms
  • Thrombosis - both microthrombi and larger clots
  • Disseminated intravascular coagulation
  • Cytopenias (especially lymphopenia and thrombocytopenia)
  • Cardiac injury/heart failure
  • Liver injury

ManagementCopy Link!

Diagnosis: Suspect cytokine storm in patients with the following lab and clinical findings.

  1. Clinical findings of severe COVID-19:
  1. Escalating supplemental oxygen requirement or work of breathing
  2. Shock/septic physiology
  3. Unexplained myocardial dysfunction
  4. ICU admission
  1. Labs suggestive of possible cytokine storm:
  1. General markers: neutrophilia, lymphopenia, elevated hepatic transaminases, elevated LDH
  2. Disseminated Intravascular Coagulation markers: elevated D-dimer, thrombocytopenia, falling fibrinogen, prolonged PT / PTT.
  1. Fibrinogen is also an acute phase reactant, so it may be elevated in CSS. If fibrinogen levels fall rapidly from baseline, or fall below the normal range, consider active DIC.
  1. General inflammation markers: Elevated C-reactive protein (CRP), ESR, ferritin (all of these markers are non-specific)
  1. Ferritin even in severe CSS in COVID-19 is only moderately elevated (typically no higher than low 1000s), in contrast to other types of CSS.
  1. Targeted immune cell activation markers: soluble IL-2 receptor (sCD25), IL-6
  1. These tests may not be available, or may take several days to result and should not delay clinical care.
  1. Keep in mind that procalcitonin is downstream of IL-6 and IL-1, so it is not a specific marker of infection in the setting of cytokine storm

Screening: All hospitalized patients with COVID-19 should receive laboratory screening for CSS. Please see Lab Monitoring for recommendations

  1. CSS may show up in the labs before it appears clinically, and suggestive lab findings merit early consideration of immunomodulators given higher risk of progression to ARDS, shock, and multiorgan failure (Chen).
  2. CSS should be considered if the following lab parameters are met (though some patients may not meet these cut-offs):
  1. CRP >50mg/L
  2. At least two of the following:
  1. Ferritin >500 ng/mL
  2. LDH >300 U/L
  3. D-dimer >1000 ng/mL

Monitoring: Patients with suspected or confirmed CSS should receive the following monitoring labs:

  1. CRP and fibrinogen are dynamic and should be checked daily, along with daily basic labs (CBC with diff, BMP)
  2. D-dimer, ferritin, LDH, LFTs tend to change more slowly and can therefore be checked every 2 days
  3. sIL2R and IL-6 can be monitored 1-2 times per week
  1. Keep in mind that serum IL-6 levels often go up after tocilizumab and sarilumab, likely because the cytokine is displaced or blocked from the receptor by the IL-6 receptor-blocking antibody. Therefore, monitoring IL-6 after tocilizumab or sarilumab is not clinically useful.

Management: The management of CSS in COVID-19 is actively evolving. If there is suspicion of developing or ongoing cytokine storm, the patient should be started on Corticosteroids (if they are not already on them). If they are worsening, they should be discussed with infectious disease, rheumatology, and/or pulmonary/critical care specialists before initiating other immunomodulatory agents (IL-1 and IL-6 agents typically).

Cardiac ArrestCopy Link!

Updated Date: November, 2020
Literature Review:
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In-Hospital Cardiac Arrest ManagementCopy Link!

Out-of-hospital cardiac arrest (OHCA) is not covered in this guide, only in-hospital (IHCA). Because lay people and emergency responders often initiate chest compressions, risk to bystanders is a concern. Follow local guidance.

Tool: BWH Hospital Cardiac Arrest Code Quick Guide

Cardiac Arrest OutcomesCopy Link!

In a study of 5019 critically ill patients across 68 U.S. hospitals, 14% had a cardiac arrest, and 57% of those received CPR. The most common rhythms were PEA (49.8%) and asystole (23.8%). Only 12% of the patients who underwent CPR survived to hospital discharge (Hayek et al).

Early Goals of Care ConversationsCopy Link!

To avoid unnecessary codes in patients with an irreversible underlying condition leading to cardiac arrest, patients should all have goals of care discussions on admission. Those who are at high-risk for acute decompensation should be identified early and code status confirmed with the patient and family. In some places and circumstances it may be appropriate to not offer resuscitation if there is no reasonable chance of recovery or if there are no critical care resources to care for the patient if ROSC is achieved. Rules, laws, regulations, as well as cultural and religious values about code status vary widely and local laws must be obeyed.

Minimizing Healthcare Worker ExposureCopy Link!

Code Responses to COVID-19 patients are high-risk events for healthcare worker exposure due to aerosolization with chest compressions and intubation

  • Use PPE:
  • CDC guidelines recommend N95 respirator, face shield, gown and gloves be used by all code responders during code events (CDC Guidelines, 2020).
  • Minimize personnel:
  • Use an automated compression device where available to minimize personnel.
  • Cover the patient’s face:
  • If it does not interfere with oxygen equipment, place a surgical facemask and/or a blanket over the patient’s face prior to chest compressions while awaiting a definitive airway.
  • Prepare code equipment:
  • To limit transmission of virus while passing meds/supplies into the patient’s room from the code cart, consider creating Code Bags inside the Code Cart pre-packed with necessary code meds (Epinephrine, Bicarbonate, Calcium etc.) and IV/lab supplies.

Cardiopulmonary ResuscitationCopy Link!


  1. Shock early: If the patient is on monitoring and has shockable rhythm (VF/VT), defibrillate as soon as possible (even if this means pausing compressions before 2 minutes is complete)
  2. Proned patients: If a patient has been proned for ventilatory purposes and they develop cardiac arrest, a decision should be made by the medical and nursing team whether to de-prone the patient.
  1. If the patient is able to be safely de-proned in an efficient manner, the medical team should do so
  2. If the patient is not able to be de-proned due to limited staff, or concerns about extubation or line/tubing entanglements, the team should proceed with reverse precordial compressions, also called Reverse CPR (Brown et al).
  1. Reverse precordial compressions are performed by placing a clenched fist beneath the sternum while administering compressions to the midthoracic spine between the inferior scapulae (Sun et al). This is optimally performed with one person administering compressions and one person holding counter-pressure beneath the sternum.


  1. Avoid bag valve mask or rescue breathing: Until a definitive airway is obtained, compression-only CPR with passive oxygen delivery should be performed. Multiple studies have shown that compression-only CPR is non-inferior to standard CPR (Svensson et al).
  1. If the patient is already on high-flow nasal cannula or non-invasive ventilation (CPAP, BiPAP) these can be continued
  1. Proceed with Rapid Sequence Intubation as early as possible if the patient does not have a shockable rhythm,
  1. To maximize the success rate for intubation, airway interventions should be carried out by experienced individuals and chest compressions should be stopped briefly during intubation (Cheung). Pausing compressions is a deviation from usual cardiac arrest care, however this is acceptable to maintain the safety of code responders and minimize attempts at intubation. See intubation. Chest compressions should resume once the endotracheal tube (ETT) cuff is inflated.
  2. If the pause in chest compressions is excessive and endotracheal intubation does not seem likely, consider a laryngeal mask or other extraglottic airway device.
  1. Initial Ventilator Settings
  1. Patients should be placed on the following settings, consistent with AHA ACLS guidelines (Edelson et al) unless the patient was already on the ventilator (in which case they should not be disconnected) or clinical information suggests different ventilator settings be used:
  1. Vt 500 cc, RR 10, PEEP 5cm H20, FiO2 100%
  2. Post-return of spontaneous circulation patients should be placed on Lung Protective Ventilation


  1. It is important to attempt to identify and treat reversible causes before stopping the code. Hypoxemia, hypo/hyperkalemia, hypoglycemia, hypovolemia, acidosis, hypothermia, pulmonary embolus,acute coronary syndrome, tension pneumothorax, cardiac tamponade, toxin
  2. Cause of Death in COVID patients is largely respiratory failure (see Cause of Death)
  3. Terminating Resuscitative Efforts
  1. Legal rules on the termination of resuscitative efforts vary by location and should always be observed. Within these parameters, avoid prolonged resuscitation if there is no easily reversible etiology identified. Medically, it is reasonable to stop resuscitation efforts if return of spontaneous circulation (ROSC) has not been achieved within 30 minutes as the chance of meaningful recovery is low.
  2. In intubated patients, failure to achieve an ETCO2 of greater than 10 mm Hg by waveform capnography after 20 minutes of CPR should be considered as one component of a multimodal approach to decide when to end resuscitative efforts (Mancini et al).
  1. Post-Resuscitation Care
  1. Dispose of, or clean all equipment used and any work surfaces.
  2. Doff PPE.
  3. If ROSC is achieved, provide usual post-resuscitation care consistent with current recommended guidelines including targeted temperature management where possible (Donnino et al).

Brain Death and Targeted Temperature ManagementCopy Link!

Please see BWH guidelines for more information about diagnosing brain death and Targeted Temperature Management after cardiac arrest.

Prevention of ComplicationsCopy Link!

Updated Date: September 24, 2020

Best Practice ChecklistsCopy Link!

(As adapted from WHO interim SARI guidance)



Reduce days of invasive mechanical ventilation

  • Minimize sedation with daily interruption of sedative infusions (spontaneous awakening trial, SAT)
  • Use weaning protocols that include daily assessment for readiness to breathe spontaneously (Spontaneous breathing trial, SBT)

Reduce incidence of ventilator associated pneumonia

  • Oral intubation is preferable to nasal intubation in adolescents and adults
  • Keep patient in semi-recumbent position (head of bed elevation 30-45 degrees)
  • Use a closed suctioning system, periodically drain and discard condensate in tubing
  • Use a new ventilator circuit for each patient, once patient is ventilated, change circuit if it is soiled or damaged but not routinely
  • Change heat moisture exchanger when it malfunctions, when soiled, or every 5-7 days

Reduce incidence of venous thromboembolism

  • Use pharmacological prophylaxis. If contraindications, use intermittent pneumatic compression devices.

Reduce incidence of catheter-related bloodstream infection

  • Use checklist of steps for sterile insertion, verified by an observer in real time
  • Use a daily reminder to remove catheter if no longer needed

Reduce incidence of pressure ulcers

  • Turn patient every 2 hours

Reduce incidence of stress ulcers and gastrointestinal (GI) bleeding

  • Give early enteral nutrition (within 24-48 hours of admission).
  • If available, also give histamine-2 receptor blockers (e.g. famotidine 20mg IV BID) or a proton pump inhibitor (e.g. pantoprazole 20-40mg IV daily) if history of GERD or GI bleed

Reduce incidence of ICU - related weakness

  • Actively mobilize patient early in the course of illness when safe to do so
  • Assure nutrition and give a multivitamin with minerals, Thiamine 100mg, and Folate 1mg daily

Tool: BWH COVID-19 ICU Bundle

Critical Illness Neuropathy and MyopathyCopy Link!

ICU-acquired weakness has been observed in 25-46% of ICU patients. Duration of ventilation, corticosteroid administration, multi-organ dysfunction, sepsis, hyperglycemia, and renal replacement therapy have all been correlated with ICU-acquired weakness (De Jonghe). Data are mixed regarding correlation of steroids and NMBA administration with ICU-acquired weakness (Doughty).

Tool: BWH General Guidelines on Critical Illness Neuropathy and myopathy

Nutrition in ICU PatientsCopy Link!

Updated Date: June, 2020
Literature Review:
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Nutrition (ICU)Copy Link!

Enteral nutrition is recommended for intubated patients. It is important to maintain muscular strength and reduce stress ulcers.

  1. In most patients:
  1. Standard 1.5 calorie tube feeds (e.g. Osmolite 1.5 @10mL/hr., advance by 20mL Q6h to goal 50mL/hr)
  1. If renal failure and high K or phosphorus:
  1. Renally formulated tube feeds (e.g. Nepro @ 10mL/hr, advance by 10mL Q6h to goal 40mL/hr)
  1. If on pressor support:
  1. Hold tube feeds due to the risk of intestinal ischemia if on:
  1. Any two pressors
  2. Epinephrine > 5 mcg/min
  3. Norepinephrine > 10 mcg/min
  4. Phenylephrine >60 mcg/min
  5. Vasopressin >0.04 units/min
  1. If unable to tolerate enteral nutrition support given escalating or multiple vasopressors TPN should be considered.
  1. If paralyzed:
  1. It is safe to feed while patients are on paralytic agents such as cisatracurium
  1. If prone:
  1. Patients requiring proning may continue to receive tube feeding.
  2. The tube feeds should be held for one hour prior to turning the patient.
  3. Prokinetic agents may be beneficial during proning to enhance gastric emptying and decrease risk of vomiting.

Glucose Management (ICU)Copy Link!

Glucose Management and DKA:

  1. Goal glucose range is typically 140-180, though some places prefer tighter control
  2. Management of DKA in COVID is challenging given the frequent need for blood sugar checks and the PPE/Donning/Doffing involved. In some instances, subcutaneous insulin might be used instead of a drip.

Tool: BWH Guidelines on ICU Management of DKA for COVID Patients

Procedures and LinesCopy Link!

Updated Date: August, 2020

Arterial and Venous CathetersCopy Link!

Literature Review (Central Line): Gallery View, Grid View
Literature Review (Arterial Line):
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Placing and removing arterial and central venous catheters is the same in COVID patients as it is in others. Given the duration of time and proximity to the patient’s face, some institutions may want to consider treating these as aerosol generating procedures.

Provider should make sure to don and doff PPE properly, take only needed supplies in the room, and clean all durable equipment thoroughly on departing.

Tool: NEJM video on Arterial Lines
NEJM video on Central Venous Catheters

Arterial Line HeparinCopy Link!

In the COVID-ICU we have seen frequent arterial line thrombus formation. A possible means to prevent this is the use of heparinized saline in the arterial line pressure bag.

Patient selection:

  • Requiring more than 1 arterial line placements (or re-wiring) due to thrombus
  • Clinical team discretion based on patient specific factors (e.g. line access issues)
  • Contraindications: history of heparin-induced thrombocytopenia and/or currently on systemic anticoagulation

Product and dosing:

  • Heparin infusion in normal saline 2 units/mL 500 mL bag. Not all pharmacies will have the correct formulation of heparin for this aim.
  • Typical dose: 5mL/hr (10 units/hr) continuous via the arterial line

Nasogastric Tubes and ThoracentesesCopy Link!

Placement is standard, however given the proximity to the patient’s oropharynx and tendency to cough, treat these as aerosol generating procedures.

Tool: Tulane video on NG tubes

Tool: NEJM video on Thoracentesis

BronchoscopyCopy Link!

Literature Review (Bronchoscopy): Gallery View, Grid View
BWH COVID-specific Bronchoscopy guidelines.