Brigham and Women's Hospitals

Critical Care

Updated: August 4, 2020

Undifferentiated Shock

Overview

  1. Definition:
  1. Acute onset of new and sustained hypotension (MAP < 65 or SBP < 90) with signs of hypoperfusion requiring IVF or vasopressors to maintain adequate blood pressure
  1. Time course:
  1. Patients rarely present in shock on admission
  1. Natural history seems to favor the development of shock after multiple days of critical illness.
  1. Etiology:
  1. The range of reasons for shock is wide and more variable than for most patients and may includes:
  1. Myocardial dysfunction
  2. Secondary bacterial infection
  3. Cytokine storm

Workup

  1. Assess for severity of end organ damage:
  1. UOP, mental status, lactate, BUN/creatinine, electrolytes, LFTs
  1. Obtain a FULL infectious/ septic workup, which includes all of the following:
  1. Labs: CBC 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, N Engl J Med, 2020). Two sets of blood cultures, LFTs (for cholangitis/acalculous cholecystitis), urinalysis (with reflex to culture), sputum culture (if safely obtained via inline suctioning, do not perform bronchoscopy or sputum induction), procalcitonin at 0 and 48h (do not withhold early antibiotics on the basis of procalcitonin alone), urine Strep and legionella antigens
  2. Portable CXR (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 and Perloff, JAMA, 1989)
  4. Perform POCUS, if able, to assess for gross LV/RV dysfunction (upload to PACS/Centricity)
  1. For TTE protocols see Other Tests
  1. Labs: Obtain an SCV02 or MV02 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. Obtain cardiology consultation 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 (see Cytokine Storm” below)
  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 Shock

This video is a helpful tutorial.

Type of Shock

Cardiac Output

SVR

CVP/Wedge

ScvO2, MvO2

Other features

Cardiogenic

Distributive (sepsis,cytokine, anaphylaxis)

Obstructive

Hypovolemic

Neurogenic

/normal

Decreased HR

Sepsis

Incidence

  1. The reported rates of sepsis and septic shock are not reported consistently in currently available case series
  1. Secondary bacterial infections are reported:
  1. 20% of non-survivors (Zhou et al, Lancet, 2020)
  2. 16% of non-survivors (Ruan et al, Intensive Care Med, 2020)
  3. 12-19% In H1N1 epidemic (MacIntyre et al, BMC Infect Dis, 2018)
  1. Concurrent Pneumocystis pneumonia has been reported in at least one case (possibly due to lymphopenia)

Management

  1. Antibiosis:
  1. Early empiric antibiotics should be initiated within 1 hour (see “Antibiotics”)
  1. Pressors and Fluid Management:
  1. Goal MAP > 65mmHg
  1. While there is emerging data that lower MAP thresholds may be beneficial, we recommend following this threshold for now.
  1. Pressors
  1. Start Norepinephrine while determining the etiology of undifferentiated shock
  2. Unless new evidence emerges, standard choices for distributive shock (i.e., norepinephrine then vasopressin) are recommended, with high vigilance for the development of cardiogenic shock, addressed in the next section
  1. Conservative fluid management:
  1. Do not give conventional 30cc/kg resuscitation
  1. 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, Crit Care Med, 2015; Famous et al, Am J Respir Crit Care Med, 2017; Silversides et al, Int Care Med, 2017)
  2. Conservative fluid management is also part of the most recent WHO guidelines. WHO, COVID-19 Interim guidance, March 2020).
  1. Instead, give 250-500cc IVF and assess in 15-30 minutes for:
  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
  4. For further guidance, Conservative Fluid Management protocols are available from from FACCT Lite trial (Grissom et al, Crit Care Med, 2015).
  1. Corticosteroids
  1. See “Systemic Corticosteroids” section
  2. Stress dose hydrocortisone should still be considered in patients on > 2 pressors.

Cardiogenic Shock

Incidence and clinical course

  1. Etiology: See “Acute Cardiac Injury”.
  1. Mechanism is unknown, potentially direct viral toxicity, ACS, stress or inflammatory cardiomyopathy
  1. Incidence:
  1. Heart failure or cardiogenic shock was observed
  1. In 23% (n=44 of 191) of hospitalized patients in one case series (Zhou et al, Lancet, 2020).
  1. There were higher rates in non-survivors (52%, n=28) compared to survivors (12%, n=16),
  1. In 33% of patients admitted to an ICU in Washington State 33% (n=7 of 21) (Arentz et al, JAMA, 2020).
  1. These patients tended to be older with more comorbidities and had a high mortality (11 of the 21 died).
  1. Prognostic implication:
  1. Heart failure or myocardial damage contributed to death
  1. In 39% (n=29) of deaths in a series of 68 patients in Wuhan. Most (n=22 of 29) had concomitant respiratory failure (Ruan et al, Intensive Care Med, 2020).
  1. Time course:
  1. Cardiogenic shock may present late in the course of illness even after improvement of respiratory symptoms, and manifest as a precipitous clinical deterioration in the setting of an acute decline in LVEF (see “Acute Cardiac Injury”)

Workup

  1. All cardiogenic shock cases require cardiovascular medicine consult
  1. PA catheters may be placed bedside by experienced providers, with preference for use only in mixed shock or complex cases with cardiology guidance
  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. CvO2 < 60% (PvO2 < 35 mm Hg), or
  3. POCUS or echocardiogram with depressed LV and/or RV function
  1. Rule out ACS and complete the initial work up as described in “Acute Coronary Syndromes”.
  2. Ongoing monitoring:
  1. Labs: Trend troponins to peak, SCvO2 (obtained by upper body CVC) or MvO2 q8-12h or with clinical change, Lactate q4-6h, LFTs daily (for hepatic congestion)
  2. Daily EKGs or prn with clinical deterioration
  3. Trend troponin to peak

Management

  1. Close collaboration with the cardiovascular medicine consultation service is recommended.
  1. Goals: MAPs 65-75, CVP 6-14, PCWP 12-18, PAD 20-25, SVR 800-1000, SCvO2 > 60%, CI > 2.2
  1. Note: Achieving MAP goal is first priority, then optimize other parameters
  1. How to achieve goals:
  1. Continue titration of norepinephrine gtt for goal MAP 65-75
  2. Initiate diuretic therapy for CVP > 14, PCWP >18, PAD > 25
  3. Initiate inotropic support:
  1. Dobutamine gtt for SCvO2 < 60%, CI < 2.2 and MAP > 65. Start at 2mcg/kg/min. Up-titrate 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.

Mechanical Support

  1. The benefit of mechanical circulatory support in COVID-19 is not yet clear.
  2. Patients who experience the following should prompt an immediate call to the cardiovascular medicine consult service for consideration of mechanical support:
  1. Dobutamine gtt at 5mcg/kg/min (or unable to tolerate dobutamine due to tachyarrhythmias) and ScvO2 < 60% or CI < 2.2
  2. Lactate > 4 after medical therapy
  1. The criteria for VA ECMO and other mechanical circulatory support varies among centers and are difficult to develop even under typical circumstances. The unclear trajectory of the COVID-19 pandemic makes these evaluations even more difficult.
  1. VA- ECMO guidelines are available here (Partners login required)
  2. For the purposes of general education, a hypothetical set of inclusion criteria for VA ECMO or MCS could cover:
  1. Younger age
  2. Expected life expectancy >6 months pre-hospitalization
  3. No evidence of solid or liquid malignancy
  4. Able to tolerate anticoagulation
  5. Platelets >50,000
  6. Absence of severe peripheral arterial disease
  7. No evidence of irreversible neurological injury
  8. Able to perform ADLs at baseline prior to illness
  9. Cannot have profound respiratory failure (defined as requiring prone ventilation at time of consult for MCS or having PaO2:FiO2 ratio < 150) (for MCS other than ECMO)

Cytokine Storm Syndrome

Pathophysiology

  1. Categories of Cytokine Storm Syndrome (CSS). 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. However, treatment is similar. These fall into four main categories (reviewed in Henderson et al, Arthritis Rheumatol, 2020):
  1. Familial hemophagocytic lymphohistiocytosis (fHLH) - associated with genetic mutations in granule-mediated cytotoxicity by NK cells and CD8 T cells (Brisse et al, Br J Haematol, 2016)
  2. Secondary HLH, also called macrophage activation syndrome (MAS), seen in patients with systemic juvenile idiopathic arthritis and other systemic autoimmune diseases and malignancies (Brisse et al, Br J Haematol, 2016)
  3. Chimeric antigen receptor (CAR) T-cell therapy (Fitzgerald et al, Crit Care Med, 2018, Shimabukuro-Vornhagen et al, J Immunother Cancer, 2018)
  4. Viral infections, especially EBV and influenza but also others (Schulert et al, J Infect Dis, 2016)
  1. Cytokine storm contributing to ARDS has been implicated in SARS and MERS (Kim et al, J Korean Med Sci, 2016)
  1. Cytokine Storm Syndrome in COVID. A subgroup of patients with severe COVID-19 have an immune hyperactivation that resembles CSS (Mehta et al, Lancet, 2020, Henderson et al, Arthritis Rheumatol, 2020).
  1. 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, Lancet, 2020, Chen, JCI, 2020)
  1. Mechanisms underlying Cytokine Storm Syndrome. (Mangalmurti and Hunger, Immunity, 2020, Vabret et al, Immunity, 2020, Henderson et al, Arthritis Rheumatol, 2020, Tay, Nature Reviews Immunology, 2020)
  1. 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
  1. CSS usually originates from dysfunctional interactions between the innate immune system and the adaptive immune system as follows:
  1. The adaptive immune system fails to kill activated innate immune cells. Why this happens is not yet clear. It is likely that SARS-CoV-2, like other viruses, expresses factors that suppress the innate immune system, creating an asynchrony in the normal course of the immune response. (Illustrated in Subbarao and Mahanty, Immunity, 2020)
  1. 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. 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
  2. The immune response fails to move toward the resolution phase and instead causes amplification of the immune response, especially systemic inflammatory cytokine production.
  3. 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.
  1. Cytokine storm syndrome has a number of downstream clinical consequences, including:
  1. Fever
  2. Hypotension/distributive shock
  3. Respiratory failure/ARDS
  4. Renal failure
  1. Secondary to hypotension/AKI/ATN, microthrombi, or other mechanisms
  1. Thrombosis - both microthrombi and larger clots
  2. Disseminated intravascular coagulation
  3. Cytopenias (especially lymphopenia and thrombocytopenia)
  4. Cardiac injury/heart failure
  5. Liver injury

Workup

  1. Diagnosis: Suspect cytokine storm in patients with the following lab findings, paired with severe illness due to SARS-CoV2 infection, manifested by one or more of the following:
  1. Escalating supplemental oxygen requirement or work of breathing
  2. Shock/septic physiology
  3. Unexplained myocardial dysfunction
  4. ICU admission
  1. Lab work-up:
  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. D-dimer is an acute phase reactant and can be elevated even in the absence of VTE. However, given the thrombotic propensity of patients with COVID-19, imaging or other studies to evaluate for DVTs or other clots should be considered.
  2. 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. Readily available inflammation markers: Elevated C-reactive protein (CRP), ESR, ferritin (all of these markers are non-specific)
  1. CRP
  1. CRP is predominantly regulated by IL-6, so it is a good surrogate marker of IL-6 signaling pathways.
  2. After IL-6 blocking therapy (e.g. tocilizumab or sarilumab), CRP levels usually drop by about 50% each day, reflecting its half-life of about 19 hours (Pepys and Hirschfield, JCI, 2003).
  1. ESR
  1. ESR tends to change more slowly than CRP - days to weeks, not hours to days
  2. It is affected by a number of factors relevant in COVID-19, including fibrinogen levels, anemia, renal function, immunoglobulin levels, which makes it a little more difficult to interpret
  1. Ferritin
  1. In CSS in COVID-19, ferritin levels are only moderately elevated, even in severe cases (typically no higher than low 1000s).
  2. This is in contrast to other types of CSS, including macrophage activation syndrome, where ferritin can be >10,000.
  1. Targeted immune cell activation markers:, sIL2R (sCD25), IL-6
  1. These tests may take several days to result and should not delay clinical care.
  2. Large serum cytokine panels are commercially available but are not recommended for patients with COVID-19 due to the turnaround time and the uncertainty of how to interpret the results, as serum cytokine levels often do not correlate with their importance in pathogenic mechanisms
  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
  1. Screening: All hospitalized patients with COVID-19 should receive laboratory screening for CSS
  1. Please see Inpatient Laboratory Workup for screening recommendations
  2. There are currently no validated risk calculator to predict risk of CSS in COVID-19.
  3. CSS may show up in the labs before it appears clinically, and suggestive lab findings merit early consideration of immunomodulators as patients with laboratory evidence of CSS exhibit higher risk of progression to ARDS, shock, and multiorgan failure (Chen et al, Lancet, 2020).
  1. 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
  1. Some patients may not meet these cut-offs
  1. 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 dif, 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

  1. The management of CSS in COVID-19 is actively evolving.
  2. Corticosteroids are now recommended for patients with COVID who require supplemental oxygen.
  1. The mechanism through which steroids provide benefit is not clear, but it is likely that they help prevent cytokine storm.
  1. If there is suspicion of developing or ongoing cytokine storm, discuss with ID, Rheumatology, and/or Pulmonary/Critical Care about the use of other immunomodulatory agents
  1. Currently, Anti-IL6 Agents and Anti-IL1 Agents are most commonly used, but trials are underway to test a number of different compounds (e.g. complement inhibitors, Jak inhibitors (Seif, Int. Arch. All. Imm, 2020)).
  2. The timing and choice of immunomodulators for CSS in COVID-19 is still under investigation.
  1. Preliminary results of several clinical trials have been mixed.
  2. Pending further data, the specific details of each case should be discussed with Rheumatology of Pulmonary/Critical Care.
  3. More information is available in appendix A of the ID treatment guidelines (only accessible on the BWH internal network).

Cardiac Arrest

Minimizing Healthcare Worker Risk of Exposure

  1. Code Responses to COVID-19 patients are high-risk events for healthcare worker exposure due to the aerosolization that occurs with chest compressions and intubation
  1. Use PPE:
  1. CDC guidelines recommend N95 respirator, face shield, gown and gloves be used by all code responders during code events (CDC Guidelines, 2020) as well as Face Shield, Gown and Gloves).
  1. Minimize personnel:
  1. Use an automated compression device where available to minimize personnel.
  1. Prepare code equipment:
  1. 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.

Early goals of care conversations

  1. To avoid unnecessary codes in patients with an irreversible underlying condition, patients who are at high-risk for acute decompensation should be identified early and appropriate steps should be taken to confirm code status and initiate early goals of care conversations with the patient and family.

Out-of-Hospital Cardiac Arrest Management

  1. Emergency Department Out-of-Hospital Cardiac Arrest Code Protocol

In-Hospital Cardiac Arrest Management

  1. Code Protocol One-Pager is available here.
  2. Efforts should be made to minimize the total number of Code responders in the room to 7-8.
  1. Code responders inside the patient’s room who should don full PPE prior to entering the patient’s room:
  1. Code Leader (1)
  2. Code RN (1)
  3. Scribe RN (Primary RN or NIC) (1)
  4. Respiratory Therapist (1)
  5. Anesthesiologist (1)
  6. 2 Chest Compressors, resting compressor holds femoral pulse (2)
  7. If needed for surgical procedures, Surgical Responder (1)
  1. Code responders outside the patient’s room should not don PPE unless called upon in the room:
  1. Additional unit nurses (2-3) (supplies, meds from omnicell, code cart)
  2. Code Cart
  3. Pharmacist (1)
  4. Additional medical resident/MDs (2) (Medical resident on computer outside the room placing orders, calling consults, and providing code leader with patient information)
  5. Additional Code Responders (3-4) Surgery and Anesthesia team if not needed in the room
  6. Security
  7. Observer (for PPE observation)
  1. Circulation
  1. Until a definitive airway is obtained, compression-only CPR should be performed. Multiple studies have shown that compression-only CPR is non-inferior to standard CPR (Svensson et al, NEJM, 2010).
  2. If the patient has shockable rhythm (VF/VT), defibrillate as soon as possible.
  3. 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 de-prone the patient and begin supine chest compressions.
  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, Resuscitation, 2001).
  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, Anesthesiology, 1992).
  2. This is optimally performed with one person administering compressions and one person holding counter-pressure beneath the sternum.
  1. Airway
  1. Initial Airway Management, Prior to Intubation:
  1. Prior to securing a definitive airway, oxygen should be applied via a non-rebreather mask at 15L/min without humidification
  2. Avoid BVM ventilation, high-flow nasal cannula, and non-invasive ventilation (CPAP, BiPAP) to minimize aerosolized virus (Cheung, Lancet Resp Med, 2020; Tran et al, PLoS One, 2012).
  3. If passive oxygen is not available, place a surgical face-mask and a blanket over the patient’s face prior to chest compressions.
  4. If the patient does not have a shockable rhythm, proceed with Rapid Sequence Intubation as early as possible to limit aerosolization
  1. Endotracheal Intubation
  1. Endotracheal intubation is the procedure that subjects the rescuer to the highest risk of infection during resuscitation. To maximize the success rate for intubation, airway interventions should be carried out by experienced individuals and chest compressions should be stopped (Cheung, Lancet Resp Med, 2020). This may deviate from usual cardiac arrest care leading to a pause in chest compressions, however this is acceptable to maintain the safety of code responders. Please see “Intubation” chapter.
  2. Chest compressions should resume once the endotracheal tube (ETT) cuff is inflated and the ETT is connected to the ventilator.
  3. If the pause in chest compressions is excessive and endotracheal intubation does not seem likely, consider LMA or other extraglottic airway device.
  4. Code responders should distance themselves from the head of the bed during the intubation procedure (6 ft distance).
  5. Continuous capnography device should be used to monitor ventilation (Cheung, Lancet Resp Med, 2020).
  6. Depending on institutional policies, anesthesia and respiratory therapy may don higher levels of PPE including PAPR hoods for the intubation procedure.
  1. Breathing
  1. Initial Ventilator Settings
  1. Patients should be placed on the following settings, consistent with AHA_ACLS guidelines (Edelson et al, Circulation, 2020) unless clinical information suggests different ventilator settings be used
  1. Vt 500 cc, RR 10, PEEP 5cm H20, FiO2 100%
  1. Post-ROSC patients should be placed on lung protective ventilation with the lowest FiO2 to maintain adequate oxygenation.
  2. If the patient is on the ventilator during the code event, they should remain on the ventilator, as disconnecting to BVM may risk exposure.
  1. Etiologies to Consider
  1. Data from a retrospective study in Wuhan (Ruan et al, Intensive Care Med, 2020) revealed cause of death to be:
  1. Respiratory failure (53%)
  2. Heart failure with respiratory failure (33%)
  3. Myocardial damage (7%)
  4. Unknown cause (7%)
  1. It is important to attempt to identify and treat reversible causes (5H’s, 5T’s) before stopping the code.
  1. Cardiac Arrest Outcomes
  1. Early outcomes from China for in-hospital cardiac arrest with attempted resuscitation (n=136; 113 in general ward, 23 in ICU) (Shao, Resuscitation, 2020):
  1. Did not achieve ROSC: 118
  2. Achieved any ROSC: 18
  3. Of those who achieved ROSC, 14 died in hospital, 4 survived at 30-days
  1. Initial rhythm of patients with cardiac arrest was
  1. Asystole 89%
  2. PEA 4.4%
  3. VF/VT 5.8%
  1. Factors associated with ROSC and 30-day survival were initial rhythm and location of arrest (ICU patients did better than ward patients).
  1. Terminating Resuscitative Efforts
  1. Avoid prolonged resuscitation if there is no easily reversible etiology identified.
  2. No one factor alone, or in combination, is predictive of outcome during cardiac arrest, however it is reasonable to stop resuscitation efforts if return of spontaneous circulation (ROSC) has not been achieved within 30 minutes.
  3. 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, Circulation, 2015)
  1. Post-Resuscitation Care
  1. Dispose of, or clean, all equipment used during CPR. Any work surfaces used for airway/resuscitation equipment will also need to be cleaned.
  2. After the resuscitation has ended adhere to strict doffing procedure to limit exposure.
  3. If ROSC is achieved, provide usual post-resuscitation care consistent with current recommended guidelines including targeted temperature management (Donnino et al, Circulation, 2015).

Nutrition in ICU Patients

  1. Consult nutrition services if not already done. While awaiting nutrition input, start enteral nutrition:
  2. In most patients:
  1. Osmolite 1.5 @10mL/hr., advance by 20mL Q6h to goal 50mL/hr.
  1. If renal failure and high K or phosphorus:
  1. Nepro @ 10mL/hr, advance by 10mL Q6h to goal 40mL/hr.
  1. If on pressor support:
  1. Hold tube feeds for elevated pressors requirements d/t risk of intestinal ischemia including:
  1. Hold tube feeds if on two escalating 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 as per ICU nursing procedure ICU-31.
  1. Other:
  1. Famotidine 20mg IV BID in intubated patients; Pantoprazole 20-40mg IV daily if history of GERD or GI bleed
  2. MVI with minerals daily
  3. Thiamine 100mg daily and Folate 1mg daily x3 days
  4. Goal glucose range is 70-180.

Diabetic Ketoacidosis

  1. Please see “ICU management of hyperglycemia and DKA

Line Management

Bedside procedures

  1. See “Procedures

Arterial Line Heparin for ICU Patients

  1. In the SP-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.
  2. Patient selection:
  1. Requiring more than 1 arterial line placements (or re-wiring) due to thrombus
  2. Clinical team discretion based on patient specific factors (e.g. line access issues)
  3. Contraindications: history of HIT and/or currently on systemic anticoagulation
  1. Product and dosing:
  1. Separate Epic Order is required (see attached document) Heparin infusion in NS 2 units/mL 500 mL bag (on the BWH facility list -ERX 15847)
  2. Typical dose: 5mL/hr (10 units/hr) continuous via the arterial line

Safe Removal of Central Venous Catheters

A standard checklist for the CVC removal procedure to be used at the time of removal (Partners login required)

An EPIC smart phrase (please find under “.CVCREMOVALNOTE ”) to facilitate proper documentation of the safety steps and the CVC removal procedure