CRITICAL CARE

Editors: Hannah Kieffer
Faculty Editor: Todd Rice, MD

Definition of Shock

Author: Jessica Reed

Shock is the clinical syndrome defined by inadequate tissue perfusion and oxygenation leading to cellular and organ dysfunction.

Shock Subtypes (further characterized in sections below)

Type	Examples
Distributive	Septic, anaphylactic, neurogenic, and rarely endocrine emergencies (adrenal crisis, hypothyroidism)
Cardiogenic	Cardiomyopathies, arrhythmias, severe valvular diseases, acute MI
Hypovolemic	Bleeding, volume deplete states
Obstructive	PE, tension PTX, cardiac tamponade

Clinical Signs of Shock and Key Diagnostic Findings

Shock = Hypotension¹ + Signs of Hypoperfusion² + Laboratory Markers³

Systolic BP <90 mm Hg or mean arterial pressure (MAP) <60 mm Hg for more than 30 minutes (sustained), or the requirement of vasopressors to maintain SBP ≥90 mm Hg or MAP ≥60 mm Hg. Often, but not always, with associated tachycardia pending underlying etiology
Clinical signs of tissue hypoperfusion:
Neurologic: AMS, decreased mentation with possible obtundation, disorientation or confusion
Cutaneous: Cool extremities, clammy skin w/peripheral vasoconstriction and cyanosis, and poor cap refill (note: distributive shock often has warm extremities with some signs of vasodilation)
Renal: Urine output <30 mL/h or of <0.5ml/kg of body weight/hr
Hyperlactatemia (which indicates abnormal cellular oxygen metabolism) and other markers of organ dysfunction such as impaired renal function (AKI), elevated liver function tests (shock liver), and metabolic acidosis

Management of Shock

Author: Brian Haimerl

Cardiogenic Shock

Background:

Pathophysiology: Primary insult (see etiologies) -> CO/CI decreased -> systemic hypoperfusion -> compensatory mechanisms including increased SVR and fluid retention -> further reduction of CO
PA catheter findings: Typically, high PCWP >15mmHg (can be low/normal in right heart failure), low CO (CI <2.8 L/min/m²), high SVR (>1400 dynes/sec/cm⁵) and SvO2 <65%
Etiologies: Acute MI, cardiomyopathy (LHF, RHF or biventricular), arrhythmia, mechanical such as acute AR (ex: dissection) or MR (ex: ruptured papillary muscle), myocarditis, blunt cardiac trauma

Presentation:

"Cold and wet" - cold and clammy skin/limbs, weak/nonpalpable distal pulses, edematous, elevated JVP; narrow pulse pressure; hypoxia w/crackles and pulmonary edema on CXR; POCUS with plump, non-collapsable IVC, reduced EF, and B-lines
Patients can be normotensive and still in cardiogenic shock w/ end-organ hypoperfusion

Management

See "cardiogenic shock" in the Cardiology section

Distributive Shock

Background:

Pathophysiology: Severe, peripheral vasodilation
CO/CI increased, SVR decreased, PCWP and RAP normal to low, SvO2 >65%
Etiologies: Sepsis (most common), anaphylaxis, neurogenic, adrenal insufficiency, pancreatitis

Signs/symptoms:

Sepsis: Localizing signs of infection; tachycardia, tachypnea, may be hypo/hyperthermic; POCUS with hyperdynamic cardiac function
Anaphylaxis: History of anaphylaxis; urticaria, edema, diarrhea, wheezing on exam
Neurogenic: History of CNS trauma; focal neurologic deficits on exam, associated bradycardia
Adrenal insufficiency: History of chronic steroid use, may have GI symptoms, hyponatremia (common), hyperkalemia (rare), hypoglycemia, hypo/hyperthermia, NAGMA
Pancreatitis: Abdominal pain with radiation to back, elevated lipase, evidence on CT scan

Management:

Sepsis: See "Sepsis" in Infectious Disease
Anaphylaxis: 0.3mg IM epinephrine (0.01mg/kg, max 0.5mg) ASAP to be repeated q5-15min x 3; IVF boluses for supportive treatment; after third IM epi, consider epi gtt (1-10 mcg/min) if persistent hypotension. Adjuncts: Albuterol nebs for bronchospasm, H1 and H2 blockers, glucocorticoids (methylprednisolone 1mg/kg). EPINEPHRINE SAVES LIVES.
Neurogenic: Caution with IVF resuscitation, can worsen cerebral and spinal cord edema; preferred pressor is norepinephrine; for neurogenic shock 2/2 spinal cord pathology, consider higher MAP goal 85-90 mmHg for 7 days to improve spinal cord perfusion
Adrenal insufficiency: Stress dose steroids with hydrocortisone – initial dose of 100mg IV followed by 50mg q6h. IVF resuscitation.
NOTE: Adrenal crisis NEVER comes out of nowhere; look for precipitating factor (missed medication, infection, trauma, surgery, or stressors)
Pancreatitis: IVF + pressors; trend H/H, BUN, and Ca; treat complications (necrotizing pancreatitis, abdominal compartment syndrome); address underlying etiology (see "Acute Pancreatitis" in GI section)

Hypovolemic Shock

Background

Etiologies: Hemorrhagic and non-hemorrhagic

Signs/symptoms:

Hemorrhagic: Common sources include GI, retroperitoneal (*needs high index of suspicion), traumatic, intraabdominal, thighs, thorax.
Non-hemorrhagic: 2/2 GI losses or decreased PO intake
POCUS with thin, collapsible IVC

Management (Hemorrhagic)

Ensure good access with two large-bore (at least 18G) IVs ideally in AC or above; Cordis or MAC CVC (can also use dialysis catheter, if necessary)
Hyperacute bleed:
1:1:1 ratio FFP:Plt:RBC (balanced resuscitation), trauma blood (fastest way to get RBCs); massive transfusion protocol (MTP)
Monitor iCa and replete (citrated blood products will deplete Ca)
Minimize crystalloid if possible, w/primary use to prevent immediate hemodynamic collapse (contributes to coagulopathy, hypothermia, acidemia, trauma/surgery)
Permissive hypotension until source control/transfusions with arterial bleeds (high MAP/SBP -> clot destabilization); trend POC lactate/exam to guide
Acute traumatic arterial bleed or post-partum hemorrhage consider TXA (1-2g bolus)
Reverse anticoagulation, if applicable
Vasopressors -> generally poorly effective, would start with norepinephrine
Source control -> GI, IR, or EGS
Variceal bleed: See GI Bleeding section for specific management

Management (Non-Hemorrhagic)

Aggressive IVF resuscitation (balanced crystalloid); target MAP ≥65
Can support BP during resuscitation with pressors (usually norepinephrine)

Obstructive Shock

See dedicated section below

Obstructive Shock

Author: Hannah Kieffer

Background

Obstructive shock occurs when there is increased resistance to forward blood flow. This can occur due to:
Resistance in the pulmonary/cardiovascular circuit (i.e., pulmonary embolism, intracardiac mass)
Extrinsic compression on the heart and decreased diastolic filling (i.e., pericardial tamponade, tension pneumothorax, dynamic hyperinflation (auto-PEEP))

Risk factors vary based on the underlying pathology:

PE: Known DVT, prothrombotic conditions, malignancy, recent orthopedic surgery or prolonged travel; family history of clots/thrombophilia
Pneumothorax: Recent chest trauma/thoracic procedures, mechanical ventilation, COPD/emphysema, endobronchial valve placement
Tamponade: Recent cardiac procedure, ESRD, cancer, trauma, rheumatologic diseases

Approach in the Hemodynamically Unstable Patient

Initial workup:

Evaluate the patient at bedside and bring an ultrasound if available to perform POCUS
Orders: STAT CBC, CMP, EKG, BNP, troponin, VBG, lactate, d-dimer, CXR

Supportive measures:

Consider fluid administration, especially if concerned that patient is preload dependent (e.g. cardiac tamponade)
Perform passive leg test (compare cardiac output/blood pressure between patient lying at 45 degrees and patient to lying back with both legs raised) or trial small fluid bolus to test for fluid responsiveness
Try to avoid vasopressors since increasing afterload could aggravate obstructive shock. However, if vital, can consider norepinephrine vs vasopressin to maintain lowest necessary MAP (both thought to have lesser effect on pulmonary vasculature)
If ventilated, aim for low volume and low PEEP settings to minimize afterload on the right ventricle

Clinical Signs/Symptoms:

General: Hypotension, tachycardia, hypoxemia, elevated JVP, cold extremities
Tension pneumothorax: Unilateral breath sounds, asymmetrical chest rise, CXR with one lung collapsed, tracheal deviation/mediastinal shift away from the pneumothorax
Pulmonary embolism: Chest pain, hypoxia, sense of impending doom. On EKG: Most common is sinus tachycardia but look for right heart strain (right axis deviation, S1Q3T3, ST depressions in inferior leads/precordial leads, new RBBB)
Cardiac tamponade: Beck's Triad (distant heart sounds, JVD, and hypotension), electrical alternans, low amplitude on EKG, pulsus paradoxus (drop in systolic blood pressure by >10 mmHg during inspiration)

POCUS findings:

PE: Distended IVC, RV dilation, McConnell's sign, Septal D sign, underfilled LV
Pneumothorax: Lack of lung sliding
Cardiac tamponade: Diastolic collapse of the RV, large pericardial effusion

Further Evaluation and Management by most common etiologies:

Pulmonary Embolism

Evaluation: STAT CTA PE

Management: - Supportive measures: vasopressors, supplemental O2 - Start high-dose therapeutic heparin gtt if high suspicion even before clot has been identified/confirmed, with heparin bolus unless contraindicated (i.e., recent GI bleed) - NOTE: First line is LMWH due to faster onset of action and longer time in therapeutic range. At VUMC, we often start heparin gtt first because if pt is going for EKOS, they need to be able to turn off AC quickly. We recommend starting heparin gtt until decision for EKOS has been made. If no EKOS, switch to LMWH - If massive PE, activate PERT (PE Response Team) for discussion regarding mechanical thrombectomy or chemical thrombolysis - Call "1-1111" and state "that your pt has a massive PE"/"activate PERT" - Look for the source for the embolism (four extremity dopplers) - If no risk factors for VTE are identified, consider a benign hematology outpatient referral for a hypercoagulable work-up - See "Pulmonary Embolism" in Cardiology section for more information

Cardiac tamponade:

Evaluation: Cardiac POCUS, follow up with formal echo

Management: - Supportive measures: Support preload; IV fluid bolus to temporarily improve cardiac output. AVOID diuretics, venodilators, and proning - If un-stable, STAT consult cardiothoracic surgery for procedural management (pericardiocentesis vs drain) - If stable, consult cardiology and/or cardiothoracic surgery

Tension pneumothorax:

Evaluation: Chest POCUS (look for lack of lung sliding), STAT CXR

Management: - If acutely unstable: Emergent needle decompression - 14-16 gauge needle (7-8cm long) in 5th intercostal space at the mid-axillary line (5th ICS-MAL) vs 2nd intercostal space mid-clavicular line (2nd ICS-MCL) - ATLS guidelines recommend 5th ICS-MAL since some studies suggest improved success rate and lower risk of complications (hitting major vessel) but data is not definitive - Can consider 2nd ICS-MCL when left sided if small body habitus and c/f cardiac puncture - Otherwise, urgent chest tube placement with pulmonology (if at the VA overnight, ED attending can place one) - Once stabilized, consult to pulmonology for chest tube placement is indicated in large, hemodynamically significant pneumothorax to ensure resolution. - For more on chest tubes, see "Chest Tubes" in Pulmonary

Sepsis

Authors: Jacob Lee, Jessica Reed

Definitions (Sepsis 3):

Sepsis: Organ dysfunction (change in total SOFA score ≥ 2 points) from dysregulated host response to infection
Septic shock: Sepsis + vasopressor requirement to maintain MAP ≥ 65 mmHg + serum lactate > 2 mEq/dL despite adequate volume resuscitation

Evaluation: Early screening for/identification of infection

Screening: preferably incorporate multiple - SIRS, NEWS, MEWS superior to qSOFA as single-agent-screening tools (more sensitive) - SIRS: - RR >20/min - T <36°C or > 38°C - HR >90 bpm - WBC <4 or >12x10⁹/L or >10% bands - SOFA (less sensitive, more specific): PaO2/FiO2, Thrombocytopenia, Hyperbilirubinemia, Hypotension, AMS, Kidney Injury, UOP.

Source Evaluation: - Cultures before starting antibiotics is preferred. However, do not delay antibiotics for cultures if unable to obtain them promptly. - Blood cx x2 (preferably from peripheral veins via venipuncture), Urine cx. Culture from central access points if present and patient is newly being admitted - Consider sputum cx, wound cx, other body fluid cx (thoracentesis, paracentesis, LP, joint aspiration) based on clinical picture - Make sure to do a full body physical exam to assess for SSTI/obvious wounds. - Provide source control as soon as possible; Limitations to source control: lines, drains, catheters, ports, hardware, etc.

Labs: Lactate, CBC w/ diff, BMP, HFP - Consider DIC labs for septic shock if clinical suspicion (LDH, Haptoglobin, Fibrinogen, PT, PTT, INR)

Imaging: X-ray, CT, or US depending on suspected source

Management: After screening, early antibiotic administration and fluid resuscitation

Antibiotics: Earlier = better (septic shock – within 1 hour; sepsis alone – within 3 hours)

Empiric treatments: should target organisms based on suspected source

MRSA coverage: Vancomycin/daptomycin (unless PNA suspected)/linezolid/ceftaroline
Risk factors for MRSA: Previous MRSA infection, known MRSA colonization, close contact with MRSA, cavitation on CXR, dialysis, immunosuppressed, recent antibiotics, recent hospitalization, recent influenza illness
Pseudomonas coverage: Piperacillin-tazobactam/cefepime/gentamicin
Preferred for sicker patients with MDR risk factors (recent antibiotics, recent hospitalization, immunosuppression, hemodialysis)
Fungal coverage: Fluconazole/micafungin
Fluconazole/micafungin: If high risk for candida (neutropenic, receiving TPN, abdominal surgery, recent antibiotic usage, >1 site of colonization)
Voriconazole/itraconazole: If high risk for aspergillus (asthma with hemoptysis, nodules/cavitations on lung imaging)
Liposomal amphotericin if high risk for mucor/Rhizopus or disseminated crypto (uncontrolled DM with sinus pain/proptosis, uncontrolled HIV, immunosuppression with nodules on lung imaging)
MDR coverage: if prior MDR infection (-penem) or high risk (dual Gram-Negative coverage)
During the day, will need ID attending approval. Overnight, can order one dose but will need ID approval for following doses
Anaerobic coverage: Metronidazole/Piperacillin-tazobactam/Ampicillin-sulbactam/Clindamycin
Recommended for lung abscess or empyema and intra-abdominal infections
Generally, not recommended for aspiration PNA (low quality evidence, guidelines mixed). Consider if poor dentition and higher likelihood of anaerobic involvement
Atypical coverage: Consider if concern for community respiratory source (Azithromycin/Levofloxacin/Doxycycline); should be given to any patient admitted to ICU for community-acquired pneumonia

Source Control: If unable to find source despite routine imaging, could consider PET vs tagged WBC scan

De-escalation: When source control obtained, use susceptibilities, MRSA nasal swab results, and clinical evaluation to decide how and when to de-escalate and discontinue antimicrobials; procalcitonin trend may also be helpful in certain clinical situations

Fluids:

Initial resuscitation with at least 30 mL/kg (ideal body weight) of balanced IV crystalloid fluid (prefer LR > NS), given within the first 3 hours. - Assess fluid responsiveness with an intravascular volume assessment (leg raise, US IVC, pulse pressure) - Blood: When Hb < 7 or active and large volume bleed (Hb <8 for CAD, brisk bleed suspected)

Post-Resuscitation Management:

Access:

Arterial line: Preferred for hemodynamic monitoring when in shock
Central line: For pressor administration
Can run peripherally if line is above the AC, levophed is running less than 15 mcg/min, and if needing for <48 hours

Vasopressors: Start if MAPs persistently < 65 mmHg after fluid resuscitation

Via CVC, PICC, or Port, or sometimes briefly peripherally (see above)
Target MAP ≥ 65 mmHg. Use lactic acid, mentation, and urine output as guides to adequate perfusion
1st Line NE, 2nd Line Vasopressin, 3rd Line Epi, 4th Line Ang II/Dopamine
SOAP II Trial: NE > Dopamine (less arrhythmias)
Other options:
Phenylephrine - May be useful in tachyarrhythmias to slow HR. Also comes in the code cart which makes this a good option if other pressors aren't immediately available
Ang II - Contraindicated in patients with CHF, VTE/hypercoagulable, thrombocytopenia <50k, severe bronchospasm
- Needs approval from MICU director for order
Low CO: Dobutamine + NE OR Epi single agent
Need ulcer prophylaxis w/ PPI or H2 blocker (preferably PO if possible)

Steroids: Persistent septic shock w/ ongoing pressor requirements, consider IV corticosteroids (particularly beneficial in ARDS, severe CAP)

Hydrocortisone 100 mg q8 or 50 mg q6 IV +/- fludrocortisone 50 µg (if concerned for adrenal insufficiency) enteral daily for 7 d or until out of shock

Additional management:

NaHCO3 – may be useful if pH ≤ 7.1
Early enteral nutrition (within 72 hours) if possible, would start at a trickle / trophic rate

AVOID beta-blockers unless you think HR compromising cardiac output by limiting diastolic filling/lack of atrial kick in afib; this is a physiologic compensatory response

Acute Respiratory Distress Syndrome (ARDS)

Author: Jessica Reed

Background

ARDS is a form of non-cardiogenic pulmonary edema characterized by acute onset (<7 days), bilateral pulmonary infiltrates, and severe hypoxemia as a result of diffuse systemic inflammation which damages the alveoli/capillary endothelium interface causing fluid and protein accumulation within the interstitium and alveoli leading to impaired gas exchange, decreased lung compliance, and pulmonary hypertension

Diagnostic Criteria, The Berlin Definition:

Timing: Onset within one week of a known clinical insult or new/worsening respiratory symptoms
Chest Imaging: Bilateral opacities on CXR/CT and/or consolidations on US. Not fully explained by effusions, atelectasis, or nodules/masses
Origin of Edema: Respiratory failure not fully explained by cardiac failure or fluid overload
Oxygenation: Diagnosis defined with PaO2:FiO2 ≤ 300 or SpO2:FiO2 ≤ 315 with respiratory support of PEEP ≥5 or HFNC ≥ 30L. Severity based on PaO2/FiO2 ratio with PEEP or CPAP ≥ 5cm H2O (see below)

Triggers of ARDS

Direct	Indirect
- Pneumonia (viral and bacterial) - Aspiration - Lung contusion d/t trauma - Direct inhalation injury - Primary Graft dysfunction of transplant	- Non-pulmonary Sepsis (most common cause) - Massive Blood Transfusion/TRALI - Hematopoietic stem cell transplantation - Drugs (Opioids, TCAs, ASA, cocaine, amiodarone, chemotherapy, salicylates) - Pancreatitis - Burns - Radiation

Evaluation:

Severity:

Based on PaO2/FiO2 ratio ("the P to F ratio") with PEEP ≥ 5 cm H2O (as above) - PaO2 - arterial pressure of O2 (Obtained by ABG) - FiO2 - Fraction of inspired oxygen (expressed as a decimal between 0.21 and 1.0)

Severity	PaO2/FiO2 ratio	SpO2/FiO2 (if SpO2 ≤ 97%)	PEEP or HFNC (Optiflow)
Mild	300-201	246-315	≥5 or ≥30L
Moderate	200-101	149-245	≥5 or ≥30L
Severe	<100	<148	≥5 or ≥30L

Management:

Frequently requires intubation as non-invasive ventilation is not often effective.

Interventions with proven mortality benefit:

Low tidal volume (Vt) ventilation (LTVV): - Goal Vt is 4-8 mL/kg of ideal body weight - Target plateau pressure of ≤ 30 cm H2O - Oxygenation goal: PaO2 55-80 mmHg or SpO2 88-95% - Slowly titrate PEEP and FiO2 concurrently to achieve oxygenation goals - pH goal: ≥ 7.20; "permissive hypercapnia"; titrate respiratory rate to target as normal pH as possible - Treat ventilator dyssynchrony

Proning: - Can be considered if moderate to severe ARDS and oxygenation does not improve with LTVV - PROSEVA study (2013) demonstrated mortality benefit to early and prolonged proning (16 hours per day) in patients with moderate to severe ARDS (most significant benefit for severe)

Interventions that probably won't hurt the patient but less data to support them:

Conservative fluid management and IV diuresis as needed (at risk for pulmonary edema d/t vascular leak); goal of net even or negative.
Note: FACTT study demonstrated 2 more days alive and off the ventilator with aggressive diuresis, but no mortality difference
Glucocorticoids in ARDS d/t septic shock, COVID, CAP, steroid-responsive conditions; may shorten time on ventilator but may also result in some neuromuscular weakness

American Thoracic Society Guidelines of 2024 placed emphasis on early ECMO involvement and neuromuscular blockade in severe ARDS patients. Two trials on neuromuscular blockade (ACURASYS and ROSE) with conflicting results. EOLIA suggest benefit to ECMO in patients with P/F <80 or hypercapnic respiratory acidosis.

Intubation and Extubation

Author: Jacob Lee

Intubation

This section will discuss how an ideal intubation will work; intubations during codes are emergent scenarios where this process will differ

Indications:

Respiratory failure – hypoxic and/or hypercapnic; NOTE hypercapnia with a normal pH is not a reason to intubate, this is well compensated
Respiratory distress – angioedema or anaphylaxis with impending airway compromise, significantly increased work of breathing and pending ventilatory failure due to exhaustion
Airway protection – altered mental status without ability protect airway (prevent aspiration and clear secretions); GCS <8 -> intubate
Although recent study (NICO trial in JAMA) suggests that not intubating patients with acute overdose and GCS<8 is better (fewer complications, shorter ICU and hospital LOS) than intubation
Airway trauma – damage or penetrating injuries to larynx

Contraindications:

Airway trauma/obstruction preventing safe placement of ETT; if definitive airway is needed in these cases, consider tracheostomy/cricothyrotomy
Not within goals of care. Confirm code status with patient, family, or surrogate

Considerations:

Will the patient be able to be extubated? Is the underlying cause necessitating intubation treatable/reversible (severe, progressive neuromuscular disease)? Would a tracheostomy be within their goals of care?
Is the intubation high risk? Difficult airway anatomy, physiologic instability, underlying comorbidities (pulmonary hypertension) increase the chance further decompensation with intubation

If overnight, Airway team must be called. See the following "Anesthesia Airway" section chapter

Checklist

Assess the patient: - Airway predictors for difficult intubation: Mallampati ≥ III, neck circumference > 40 cm, thyromental distance < 6cm, head-neck extension <30°, mouth unable to open > 34cm - High risk comorbidities: pulmonary hypertension with RV failure, angioedema, variceal hemorrhage, hemodynamic instability

Prepare the patient: - Two large bore IVs - Position in the supine sniffing position, pre-oxygenate with 100% FiO2 and NIV if patient not actively vomiting - Optimize medical status: Give appropriate resuscitation, temporize anemia (hgb >7) /electrolyte abnormalities (hyperkalemia)

Prepare the equipment: - Monitoring: SpO2, end-tidal CO2 monitor (capnography), continuous BP cycling, telemetry - Airway: Bag-valve mask, 2 endotracheal tubes (check cuffs prior to utilization), direct laryngoscope, video laryngoscope, bougie/stylet, suction device (on and functional), supraglottic and oropharyngeal airway as backup

Prepare the medications: - Paralytic (succinylcholine or rocuronium), sedative - induction (etomidate or ketamine) and maintenance (propofol), analgesic for intubation (fentanyl) - Should have fluids, pressors, inotropes hanging in the room. Push-dose pressors (Neostick's=syringe of phenylephrine) also valuable

NOTE: we are currently doing a clinical trial on sedatives and paralytics to see if there is a superior regimen

Paralytic Agents: - Succinylcholine – depolarizing agent, faster onset (45-60 seconds), shorter duration (5-10 minutes) but should be avoided in hyperkalemia, burns, crush injuries, and neuromuscular disease (PD, MG, ALS) - Rocuronium – non-depolarizing agent, longer onset (45-90 seconds) longer duration (30-60 minutes) safer in CKD patients, as well as in NMD patients. Note, longer duration of action may outlast the duration of the induction sedative - risk for paralysis awareness

Induction sedatives: - Etomidate – hemodynamically stable to slight hypotension - Ketamine – hemodynamically stable, can be dually helpful for bronchospasm - Propofol – associated with hypotension

Prepare the team: - First and second intubators, RT, RN to prepare meds, RN to give meds, someone to monitor hemodynamics, someone with hand on the pulse - Run through the plan: meds to be given, meds available as backup

Rapid-sequence intubation (RSI):

Simultaneous administration of a sedative and paralytic to reduce patient movement and airway reflexes and quickly achieve optimal intubation conditions
Goal is to intubate within 60 seconds of paralysis onset
Preferred method of induction; associated with increased first-attempt success, reduced aspiration risk, reduced gastric insufflation, and even improved extubation rates

Post-intubation:

Ensure correct ETT placement: End-tidal CO2 color change (gold standard), bilateral breath sounds, and chest rise, absence of gastric sounds, CXR
Secure the ETT with tape and/or tube holder
Ventilate patients according to condition

Complications:

Airway trauma (oropharyngeal, laryngeal/vocal cords)
Aspiration: Suction airway (ideally prior to initiation of PPV). Mixed data re whether cricoid pressure during intubation (i.e. Selleck maneuver) decreases risk of this.
Desaturation/Hypoxia: Caused by inadequate preoxygenation, PTX, mucous plugging. Rescue maneuvers with bag-mask ventilation if necessary. Stat CXR
Hypercapnia: Assess for cuff leaks - if underinflated or defective can lead to poor ventilation
Cardiovascular collapse: intubation increases intrathoracic pressure and thus decreases venous return and CO; sedation vasodilates and decreases BP, sympathetic surge may trigger arrhythmia leading to cardiogenic shock. Manage with fluids/pressors if need, rule out other causes (ex: hypoxia, PTX)
Mechanical injury: Dental, soft tissue, tracheal, laryngeal. Retrieve any dislodged teeth, suction blood

Anesthesia Airway

Editors: Mercede Erickson, MD, Camille Adajar, MD
Faculty Editor: Brandon Pruett, MD

Call/text Airway Phone: (615) 887-7369

Provides direct contact with the on-call resident/Airway Team (we also respond to all overhead STATs for airway management)
Utilized during MICU night shifts or when the MICU attending is unavailable
If the Airway Team is consulted for intubation, the anesthesia attending and residents will perform the intubation sequence and intubation – other team members are not permitted to intubate under these circumstances per Anesthesiology Department protocol

Extubation

Patients should be assessed for extubation readiness on a daily basis with SAT/SBT trials

Spontaneous Awakening Trial (SAT)

Contraindication: seizures, alcohol withdrawal, agitation, paralytics, MI, or increased ICP
Pass: Patient is able to follow commands without significant anxiety, agitation, or respiratory distress as evidenced by vital signs. Precedex can be used if having trouble with agitation or anxiety
Fail: Unable to cooperate/follow commands, clinically significant VS changes (new or worsening arrhythmia, tachypnea, hypoxia)
If failed, restart sedation at reduced dose and titrate to RASS 0 (unless otherwise specified)

Spontaneous Breathing Trial (SBT)

Once SAT is passed
Trial of pressure support (PS); PEEP ≤7.5cm H2O and FiO2 ≤ 50% for at least 30 minutes (ideal settings: PS 5cm H2O and PEEP 5cm H2O with FiO2 40%)
Pass: No evidence of respiratory distress (tachypnea, bradypnea, hypoxia)
Fail: Tachypnea (RR>35), bradypnea (RR <8), hypoxia (O2 sat < 88%), respiratory distress, cardiac arrhythmia, worsening hypotension; new hypertension (demonstrates increased work to maintain adequate breathing on SBT)

Additional considerations prior to extubation:

Has the underlying cause of their respiratory failure or need to be intubated improved?
Is the patient able to protect their airway (coughing) and handle secretions?
What does the patient need to be extubated to? (RA, LFNC, BiPAP)
Preventative post-extubation BiPAP not routinely used in all pts but consider in select populations at high risk for failure: severe COPD with preexisting chronic hypercarbia, cardiogenic pulmonary edema, NMD, baseline airway regimen
Is there a cuff leak, or lack thereof which will require pretreatment with steroids?

Cuff leak test:

Set ventilator to AC/VC and measure the TV. Deflate the ETT cuff completely, observe for an audible leak, and measure the difference in TV between delivered and exhaled breaths over 6 breathing cycles. Average the 3 lowest expiratory TV values

Positive cuff leak: can hear audible leak, TV difference of >110-130 mL or > 10% between delivered and exhaled breath; significant variability in criteria
A negative cuff leak test (lack of cuff leak) is not very accurate, but can indicate possible laryngeal edema and post-extubation airway obstruction/stridor
Negative cuff leak is not an absolute CI to extubation. Will likely require steroids to minimize airway swelling
IV Solumedrol 20 mg IV Q4hrs for 4 doses prior to extubation

For borderline cases, calculate a Rapid Shallow Breathing Index (RSBI): - RR/TV (L) during their SBT or while on PS - RSBI > 105 is indicative of higher likelihood of reintubation; higher score = greater risk

Post-Extubation:

Consider ABG/VBG 20-30 mins after extubation to ensure adequate ventilation
Airway clearance therapy should be available for patients with NMD, COPD/bronchiectasis, and those with heavy secretion burdens
Extubating to BiPAP as described above has data supporting its use in certain scenarios. Note, rescue BiPAP to prevent re-intubation has not been shown to be beneficial and only found to delay reintubation. Exception: patient has known hypercapnea - then rescue BIPAP may actually rescue patients from re-intubation

Complications:

Laryngeal Edema/Stridor: Can occur even if positive cuff leak - Risk factors: Prolonged intubation ≥7 days, large ETT, repeated or traumatic intubation attempts, tracheal stenosis or upper airway mass, history of angioedema or anaphylaxis, cardiogenic pulmonary edema, ARDS - Treatment: 40 mg IV Solumedrol, inhaled racemic epinephrine and reassess in 60 minutes. If still present or patient has respiratory distress, consider re-intubation

Post-extubation respiratory failure: hypoxic or hypercapnic - Risk factors: ARDS, PNA, Volume Overload, Sepsis - Consider blood gas 20-30 minutes post-extubation. Unless select high risk population discussed above, rescue BiPAP not shown to prevent re-intubation. If showing signs of respiratory distress, consider re-intubation.

Modes of Oxygen Delivery

Author: Jacob Lee

Definitions:

Entrainment – the process of oxygen being mixed with ambient air that impacts the true fraction of inspired oxygen delivered to the patient

Non-Invasive modes of oxygenation augmentation

These modes of oxygen delivery focus on oxygenation as opposed to ventilation

System	L/min	% O2	Comments
Blow by (ex: Trach collar)	Depends on O2 delivery device	21-100%	Used for patients who cannot tolerate more direct devices (agitated, cuffed tracheostomy tubes); how snug the trach collar is determines the degree of entrainment
Nasal cannula	1-6	24 – 45%	Add 3-4% to Room Air FiO2 (21%) for each liter of supplemental oxygen administered. Flows in excess of 6 L/min will not appreciably increase the FiO2
Large bore nasal cannula	Up to 15	Up to 80%	This is NOT high flow nasal cannula (HFNC) although it may be documented in the chart as such. The nasal cannula prongs have a larger radius allowing for additional flow that will reliably increase flow rate up to 15 L/min
Venturi mask	2 to 15	Up to 60%	Color-coded adaptors allow for specific entrainment that deliver more accurate FiO2 delivery at given flows. Actual FiO2 is dependent on pt effort
Non-rebreather	10 to 15	60-90%	Reservoir bag is filled with pure oxygen, with one-way valves that prevent patient from breathing ambient air. Often used as a bridge to a higher tier of oxygen delivery
HFNC: Optiflow, AirVo, Vapotherm	50-60	30-100%	Used for hypoxic respiratory failure; although does deliver roughly 0.6-1.2 cm/H2O of PEEP per 10L of flow, not typically used for hypercapnic respiratory failure

Non-invasive positive pressure ventilation

Deliver set pressures by adjusting flow. Note, while flow and pressure are inter-related, they cannot be inter-converted. Pressure is maintained by regulating flow dynamically based on patient effort and lung mechanics
Supplemental flow and FiO2 can be delivered into the tubing or blended into the machine (bled in) to give FiO2 reliably up to 60% (outpatient with oxygen bled in) or close to 100% (inpatient using high-flow devices)

System	Settings	Indications	Comments
CPAP	Pressure (CPAP), FiO2	OSA, Tracheomalacia	FiO2 delivery varies due to leaks, mask type, and patient breathing pattern. Not indicated solely for oxygen delivery but can bleed oxygen in if hypoxia is also present
BiPAP	IPAP, EPAP (nomenclature is IPAP/EPAP), FiO2, RR	Hypoxic and/or hypercapnic respiratory failure, cardiogenic pulmonary edema, OSA, obesity hypoventilation syndrome, prevention of post-extubation respiratory failure in high-risk patients	Delta between IPAP and EPAP = driving pressure (higher driving pressure improves ventilation not oxygenation). Increasing EPAP can improve oxygenation by increased mean airway pressure but will not improve ventilation. FiO2 delivery varies due to pressure cycling, leaks, and inspiratory flow changes. Generally contraindicated if patient unable to remove mask themself, vomiting, or lots of secretions

All of the above oxygen delivery systems are used in spontaneously breathing patients

Invasive positive-pressure ventilation

See "Intubation and Extubation" chapter (chapter prior to this one) for indications
See "Introduction to Ventilator Management" below for ventilator modes

Introduction to Vent Management

Author: Seth Alexander

See "Intubation and Extubation" for the clinical criteria to initiate or discontinue mechanical ventilation.

Ventilator Settings:

Trigger: what initiates a breath; time, flow, or pressure - Patient-initiated triggers are flow and pressure - Ventilator breaths are triggered by time

Cycle: what terminates a breath

Mode	You set	Not set	Comments
Pressure support (PS)	PEEP PS above PEEP FiO2	TV RR Inspiratory flow	- Used for spontaneous breathing trials (see intubation and extubation) and vent weaning - Patient is breathing on their own and will trigger each breath, setting their own flow, RR and TV - PS added to overcome the inherent resistance of the circuit
Volume Control (AC/VC)	PEEP RR TV Inspiratory flow FiO2	Inspiratory pressure	- Patient or ventilator can trigger a breath; the breath is initiated when a preset tidal volume is delivered - Pros: Guarantees a minute ventilation and low tidal volume; will limit volutrauma - Cons: Pressure varies and may lead to lower mean airway pressure and thus less alveolar recruitment; if lungs become less compliant, the pressure needed to deliver set tidal volumes can become dangerously high causing risk of barotrauma
SIMV Synchronized Intermittent Mandatory Ventilation	PEEP RR FiO2 If vent triggered breaths, TV If pt triggered breaths, PS above PEEP		- Vent provides a set number of breaths at a set tidal volume. Patient can trigger breaths above this rate that are only supported by designated PS/PEEP (no set TV) - The ventilator tries to synchronize with the patient's breathing effort Pros: more comfortable, allows for spontaneous breathing Cons: Increased work of breathing if patient is tachypneic but not getting adequate TV with spont breaths, breath stacking if async w vent, does not guarantee MV - Numerous RCTs demonstrated that it's worse for vent weaning – associated with longer weans and fewer liberations
Pressure Control (AC/PC)	RR Inspiratory Pressure PEEP Inspiratory Time (or I:E ratio) FiO2	TV	- Patient or ventilator can trigger breaths. All breaths supported. The breath is cycled when the preset inspiratory time is reached - The ventilator maintains a constant pressure during inspiration (flow decreases as the lungs fill with air) Pros: theoretically better for oxygenation - maintains a more consistent mean airway pressure, limits barotrauma Cons: Tidal volume, and therefore, MV is not guaranteed, requires close monitoring as TV and MV may drop if lung compliance decreases (need to increase low MV alarm threshold manually)
PRVC Pressure Regulated Volume Control	PEEP RR TV Inspiratory flow Pressure max FiO2		- Attempts to reach a set volume by adjusting the pressure (same triggers and cycles as AC/VC) - Vent will average the preceding few breaths to try and deliver a desired tidal volume at the lowest possible pressure Pros: Tries to limit both volutrauma and barotrauma Cons: If conflict between the VC and PC aspects (e.g. ARDS), PC will supersede - cannot guarantee MV. The more work the patient does, the less the ventilator does and patients may be prone to 'tiring out' – should monitor PCO2 with blood gases
APRV / Bilevel	PEEP (PLow) Pressure High Time Low Time High FiO2	TV	- The ventilator cycles between P(high) and P(low) based on preset times but the patient is allowed to breathe spontaneously at any time - Usually, long periods of inspiratory holds with brief expirations - Pros: Used for refractory hypoxemia - increases mean airway pressure and alveolar recruitment - Cons: Does not guarantee MV, risk of air trapping and hyperinflation due to auto-PEEP and breath-stacking, often difficult to ventilate patients

Static Ventilator Readouts:

Plateau pressure (Pplat): Measured with an inspiratory hold (assesses lung compliance)
Auto-PEEP: Measured with an expiratory hold; occurs when volume of previous breath is not entirely expelled before the next breath is initiated

Dynamic Ventilator Readouts:

Measured RR: In most modes, patients may trigger breaths more frequently than the set RR; if set and measured RR match, consider ↓ respiratory drive (sedation, neurologic injury) or iatrogenic over-ventilation
Tidal volume of inspiration (VTi) and expiration (VTe)
VTi should approximately equal VTe. If not, then assess for an air leak (e.g. cuff leak or pneumothorax) or auto-PEEP
Minute ventilation: calculated from VTe x RR; higher MV = more CO2 clearance
Peak (Inspiratory) pressure (PIP): Highest pressure reached in the entire ventilator cycle

Critical non-ventilator hemodynamic readouts:

SpO2: If poor waveform or discordant with measured PaO2, exchange the probe or consider serial ABGs
HR: Can be an indicator of emergencies such as pneumothorax, PE, ventilator disconnection
Blood pressure: Positive pressure ventilation decreases preload and has mixed effects on afterload (pulmonary vascular resistance vs. systemic afterload) by altering intrathoracic pressure gradients.
Depending on the patient's pathophysiology, increases in positive pressure may be detrimental or beneficial for BP

It is helpful, when you first have a ventilated patient, to review the equipment that makes up the "circuit" from the ventilator to the patient and back with an RT or bedside nurse. - Key things to know: How to inline suction, perform an inspiratory hold, reconnect/disconnect the circuit to the ETT if needing to bag the patient, etc.

Troubleshooting vent alarms:

Alarm Type	What is causing the alarm?	Troubleshooting
High Peak Pressure	Dynamic compliance issue (resistance of the circuit when there is air flowing) vs. Static compliance issue (stretch of the lung - doesn't change with airflow)	Step 1: Check plateau pressure by performing inspiratory hold. Must be in VC mode. High Peak and Low Plateau: Dynamic compliance issue → High Resistance Work outside -> in: - Check if pt is biting on the ETT - Incline suction to clear secretions or proximal mucous plug - Check circuit tubing for excess water condensation, mucous plug, or a kink. Ask RT to disconnect and clear circuit - Auscultate for wheezing/stridor to indicate bronchospasm or obstruction → give bronchodilators High Peak and High Plateau: Static compliance issue → Worsening alveolar process Emergencies: tension PTX, mainstem intubation Work Outside -> in: - Obesity/chest wall rigidity - Abdominal Compartment syndrome/ascites - Single Lung: mucous plug, large pleural effusion/atelectasis - Worsening alveolar process - pulmonary edema, PNA, DAH, ARDS - CXR, b-lines on US, tracheal aspirate, bronchoscopy, etc.
Low Tidal Volume/Low Minute Ventilation (VE)	Patient is not getting the desired (set) tidal volume/VE. The alarm reports exhaled VE. This may cause inadequate ventilation, CO2 retention, and potentially hypoxia.	1. Put patient back on VC, assess for high peak pressures (-> low volume in certain vent modes) 2. Compare inspiratory tidal volumes (Vti) with expiratory tidal volumes (Vte) on the ventilator. If Vti>Vte, check for a leak in the system: - Check circuit for connection leaks w RT - Listen for a cuff leak – can have RT check a cuff pressure and if low re-inflate → sometimes need to do an ETT exchange - Ensure ETT not high or out 3. Consider disconnecting vent and bagging pt If normal resistance: - Leak in ventilator, tubing, or Y-adapter If low resistance: - Cuff leak, ETT above cords, or bronchopleural fistula If low tidal volumes and no leak (ie. Vti = Vte) and RR WNL: - Patient may need more support (i.e. switching to a different vent mode (PS to PRVC)). Discuss with RT or fellow If low RR and no leak and Vt at goal: - Patient may be over-sedated - May need to increase set/back-up ventilator respiratory rate
Apnea	No breaths are being triggered by the vent… in other words, your pt is NOT breathing → this is an emergency…	*Check that the patient hasn't self-extubated, their trach hasn't fallen out, or they haven't been unhooked from vent* If self-extubated or tracheostomy decannulated, then immediately start bagging the pt (may need to bag from trach stoma if s/p laryngectomy) Have nurse call staff assist for re-intubation if necessary or have trach team called to replace a fresh (<7 days old) trach

Refractory Hypoxemia

Author: Hannah Kieffer

Background

Inadequate arterial oxygenation despite high levels of inspired O2 or the development of barotrauma in mechanically ventilated pts
Oxygen index (MAP × FiO2 × 100/PaO2) < 40
Consider work up/interventions below if needing FiO2 >80%

Differential:

Always first consider worsening of primary underlying process
Consider recent injuries/interventions, e.g., smoke inhalation, opioid administration and check dose, recent blood transfusion, etc.
Altered alveolar permeability/V-Q mismatch:
PE, pneumothorax, fluid overload (severe pleural effusion/pulmonary edema), ventilator-associated pneumonia (VAP), new ARDS, diffuse alveolar hemorrhage
Shunting:
Large lung consolidation, bronchus obstruction, intracardiac shunt, intrapulmonary shunt (pulmonary AVMs)

Evaluation:

Always get CXR STAT if pt has new or worsening O2 requirement
Consider CT chest if patient stable enough
CBC, ABG
POCUS:
Lack of lung sliding; pneumothorax
RV enlargement/septal bowing/McConnell's sign; RV strain in PE
TTE if stable and concerned for intracardiac shunt/acute HF decompensation
Bronchoscopy if concerned for mucous plug

Management Algorithm for refractory hypoxemia

Initial triaging maneuvers: - If at any point the pt is rapidly decompensating, you can always disconnect them from the vent and bag them until they recover/while calling for help - Troubleshoot ventilator – see "Introduction to Vent Management" for more information - Optimize fluid status; consider diuresis/dialysis if not making significant urine - Reposition patient – elevated HOB, position "good lung" down

Consider higher PEEP strategy: - Increased PEEP -> higher mean airway pressure. Generally, improves oxygenation especially with diffuse pulmonary pathologies - Exceptions may include certain focal/shunt pathologies (e.g. dense lobar PNA) - Worsening oxygenation may occur with overdistension of alveoli -> increased dead space ventilation; generally determined empirically at the bedside - Titrate up slowly; generally, do not exceed PEEP 18 - Limited by high plateau pressures/barotrauma, overdistension/dead space ventilation, decreased preload/venous return - ARDS net FiO2/PEEP Tables: At VUMC we typically use the Lower PEEP table - Note - Updated 2024 guidelines conditionally recommend use of higher PEEP (reduced mortality and fewer ventilator days) without prolonged lung recruitment maneuvers (higher mortality)

Lower PEEP/higher FiO2

FiO2	0.3	0.4	0.4	0.5	0.5	0.6	0.7	0.7
PEEP	5	5	8	8	10	10	10	12

FiO2	0.7	0.8	0.9	0.9	0.9	1.0
PEEP	14	14	14	16	18	18-24

Higher PEEP/lower FiO2

FiO2	0.3	0.3	0.3	0.3	0.3	0.4	0.4	0.5
PEEP	5	8	10	12	14	14	16	16

FiO2	0.5	0.5-0.8	0.8	0.9	1.0	1.0
PEEP	18	20	22	22	22	24

Inhaled vasodilators: Distribute preferentially to well-ventilated alveoli ->local vasodilation -> improved V/Q matching - VUMC formulary preference: Inhaled epoprostenol (aka Flolan) - Alternatives: Inhaled milrinone, inhaled nitric oxide - Data suggest they improve PaO2/FiO2; large RCT without evidence for mortality benefit

Deep sedation (RASS -4 or -5) - Promotes ventilator synchrony

Neuromuscular blockade (paralysis) – call your fellow before doing this - Maximal vent synchrony (eliminates residual chest wall/diaphragm tone) - Pt MUST be RASS -5 (need analgesia + sedation) - Trial one time IV push of vecuronium 0.1 mg/kg - If improved vent synchrony/oxygenation, consider cisatracurium (Nimbex) drip - Data are mixed; ACURASYS 2010 (improved 90-day mortality but underpowered likely overestimating benefit); ROSE 2019 (no difference in 90-day mortality)

Prone positioning (Need attending approval) - Pts with moderate to severe ARDS (PaO2/FiO2 ratio < 150) - At VUMC, we use regular ICU beds and manually flip pts; cycle prone 16h/supine 8h - When proning or supining a pt, always have a provider who can intubate in the room in case unplanned extubation occurs - Considerations: need a team of people to reposition, high risk of ET tube malposition, difficult to access lines/perform procedures, high risk of pressure injuries - Data: PROSEVA 2013 - proning improved 28-day mortality; note study c/b imbalances between groups

Alternative ventilator modes (usually PC or APRV/BiLevel/BiVent) - APRV/BiVent should be avoided in people with bad obstructive lung dx, hemodynamic instability, refractory hypercarbia - No data that demonstrates superiority of any one ventilator mode over another

Venovenous (V-V) ECMO - CONSULT EARLY if a pt may be a candidate; allows ECMO team to assist with evaluation - Hypoxemia related indications: - PaO2/FiO2 < 50 with FiO2 >80% for >3h OR - PaO2/FiO2 < 80 with FiO2 >80% for >6h - PaO2 <40 mmHg despite maximal ventilator support - Murray Score ≥ 3 - Absolute Contraindications: - Poor short-term prognosis/non-survival comorbidity (e.g. metastatic cancer) - Irreversible, devastating neurologic pathology - Irreparable cardiac damage and unsuitable for transplant/VAD - Chronic respiratory insufficiency without the possibility for transplant - Limitation of care orders (DNR) - Can calculate RESP score; predicts in-hospital survival with ECMO - Data: - Included in updated 2024 ATS practice guidelines - CESAR 2009: Improved 6-month survival without severe disability - EOLIA 2018: No mortality benefit but 28% crossover from control to ECMO arm dilutes potential effects. ECMO group had a significant increase in ventilator-free days

Refractory Hypercapnia

Author: Hannah Kieffer

Background:

Definition: Inadequate clearance of CO2 leading to respiratory acidosis (pH ≤ 7.20) despite maximum RR&TV (i.e. minute ventilation) tolerated without causing barotrauma or autoPEEP
Common causes:
Obstructive lung disease (COPD, emphysema, asthma)
Hypoventilation syndromes (congenital central hypoventilation, brainstem injury, sleep apnea, obesity, sedative medications (i.e. opiates), neuromuscular weakness, chest wall trauma, ascites/pleural effusion)
Increased CO2 load (shock, sepsis, malignant hyperthermia)
Presentation:
Shortness of breath, AMS, somnolence, hypoxemia, tachycardia, HTN (in some cases)

Evaluation:

Physical exam, mental status, recent medications
ABG or VBG
Respiratory acidosis: Expect high CO2; normal pH suggests chronic condition with compensation vs low pH suggests more acuity
If increased PCO2 and normal pH, always treat the pH and not the PCO2 (i.e., if compensated chronic hypercarbia, decreasing CO2 below what the patient has adapted to -> decreased respiratory drive, cerebral vasoconstriction, Bohr effect)

Management Algorithm:

Maximize conventional ventilation strategies: - Consider HFNC or BiPAP if safe - If refractory (PaCO2 >60 mmHg for >6 hours w pH <7.25), consider ECCO2R - Consider escalation to V-V ECMO

Special considerations: - If history of OSA, make sure they are on home CPAP/BiPAP - If opiate related, trial Narcan - If reactive airway disease contributing, bronchodilators

BiPAP: - Contraindicated if pt unable to remove BiPAP mask independently - Increase MV by increasing Δ between IPAP/EPAP or increasing RR

Mechanical ventilation: - Allows you to control rate and TV (in VC modes) - To increase MV and CO2 clearance: - Increase RR: - Up to ~30-35 breaths/min - Need to keep in mind I/E time to avoid breath stacking/autoPEEP - Evidence of autoPEEP: Increased WOB/vent dyssynchrony, worsening hypotension, and failure of the expiratory limb on the flow waveform on the vent to return to zero - Possible corrective measures: Lower RR, decrease inspiratory time, increase expiratory phase time - Increase TV: - Usually start at 4-6mL/kg PBW. Can consider increasing to 8mL/kg PBW as long as plateau pressures remain < 30 cm H2O - Goal peak pressures ≤ 35 cmH2O / plateau pressures ≤ 30 cmH2O - If ARDS, allow for permissive hypercapnia (goal pH ≥ 7.2)

V-V ECMO / Extracorporeal carbon dioxide removal (ECCO2R): - Indications for ECMO for hypercapnia: - Severe dynamic hyperinflation and/or severe respiratory acidosis - pH ≤ 7.20 with PaCO2 ≥ 60 for 6h with RR at 35/min and TV increased to target maximum MV while keeping plateau pressure ≤ 32 cmH2O - Similar considerations and contraindications as refractory hypoxemia (see above) - Benefits: Reduces work of breathing, promotes early ventilator weaning/extubating -> allows early mobilization and recovery

Tracheostomy

Author: Alice Kennedy

Indications for Tracheostomy:

Prolonged mechanical intubation and weaning (typically consider ~ day 14)
Prior failed extubation attempt(s)
Tracheal stenosis
Upper airway obstructions (e.g., head and neck cancers, severe infections, congenital obstructions)
Trauma
Neuromuscular disease

Benefits of Tracheostomy vs ET tube:

Lower risk of laryngeal and vocal cord damage
Improved ability to communicate (i.e. speaking valve)
Improved pt comfort and decreased need for sedation
Lower airway resistance -> reduced work of breathing
May reduce time to wean from the vent and hospital LOS (mixed data)
Potential improvement in patient mobility
Easier access to trachea for suctioning/airway hygiene
May decrease risk of ventilator associated pneumonia (Mixed data)

Note: No proven reduction in short-term mortality

Timing of Tracheostomy:

Generally performed after 2 weeks of intubation (timing not backed by data)
Pts that might get tracheostomy earlier: Anticipated prolonged mechanical ventilation (i.e. those with acute neurologic injury affecting spinal cord)
Research: No benefit in 30-day mortality rates or hospital length of stay for early (day 4) vs late (day 10) tracheostomy in TracMan trial (Tracheostomy Management trial, 2013)
*NOTE: Many patients in late trach group did not end up requiring one

Tracheostomy Tubes:

Most common in hospital = Portex (Previously Shiley)
Components:
Faceplate/Flange: Keeps tube in place, has the model and size on it
Inner cannula: Can be removed, cleaned, and replaced in case of obstruction
Cuff (may or may not have): Allows for pt to be ventilated; may prevent some aspiration. Pressure needs to be assessed qshift and kept <30mmHg
Fenestration (i.e. holes in the cannula) (may or may not have): Allow speaking without valve
Obturator/Trocar: Kept at the bedside to assist with trach insertion/removal
Common sizes:
Initial: 8-0; Standard downsizing: 6-0 (Sizing: Comparable to ETT size for Portex)
Lengths: Standard vs. larger XLT (P = longer proximal end, D = longer distal end)
Presenting on ICU rounds = size/cuff status/brand (e.g. 8-0 cuffed Portex)
"Trach collar" means pt is receiving just humidified O2/room air, cuff should be down

Speaking Valves:

Passy Muir Valve (PMV): One-way valve placed on the outer portion of the trach; air moves in with inspiration but is blocked and thus funneled up around/outside the trach and through the vocal cords during exhalation allowing for phonation
Contraindications: Severe upper airway obstruction or aspiration risk, copious secretions, decreased cognitive status, severe medical instability, or inability to tolerate cuff deflation
IMPORTANT SAFETY PRINCIPLE: Cuff must be deflated when PMV is on. Since air needs to be able to travel back up the airway, if the cuff is not deflated and you put the PMV on then pt cannot exhale. Must remove when asleep.

Maintenance of Tracheostomy Tubes:

Inner cannula should be cleaned 2-3 times per day or swapped (disposable)
Daily stoma care to prevent pressure ulcers and stoma infections
As needed suctioning for secretions

Complications and airway emergencies in a tracheostomy pt:

Hemorrhage (mild bleeding from surface vessels and granulation tissue is common, major bleeding is rare - think erosion into brachiocephalic [innominate] artery)
Causes for alarm: Drop in sats/Hgb, new tachycardia or hypotension, increasing PIP, new/worsening bleeding, or large clots
Airway damage - subglottic or tracheal stenosis, tracheobronchitis
Fistulas (tracheoarterial, tracheoesophageal)
Unintended tracheostomy tube dislodgement:
All pts with trachs have a yellow sign above bed with date, type, size of trach as well as a replacement trach with obturator in the room
- Fresh trach (≤ 14 days): do NOT replace due to risk of misplacement into the mediastinum and loss of airway; airway management from above
- Older trach: can be replaced at bedside with obturator by trained staff
In the case of an EMERGENCY:
- Bag mask (use hand/gauze to occlude stoma) or intubate from above (i.e. through the mouth); if complete laryngectomy then must use stoma
- Contact Surgical Airway Emergency Team +/- Team that placed it

Secretion Management:

Respiratory hygiene ("pulmonary toilet"): heated vent, guaifenesin (may not have an effect), hypertonic saline, DuoNebs, cough assist device, appropriate suctioning (too much -> worsens secretions), acapella, IS

Decannulation:

Candidates: Need to protect their airway and be on minimal FiO2 settings
Should pass capping trials and tolerate PMV for most of the day
Avoid if imminently discharging/planning for procedures

ABCDEF (A2F) Bundle

Author: Kaele Leonard

Background

Post-Intensive Care Syndrome (PICS): complex constellation of cognitive, physical, and psychological impairments that impact most survivors of critical illness, leading to disability, frailty, and poor quality of life
Predicted by (1) duration of immobility and (2) delirium
Both are reduced by >80% compliance with ABCDEF (A2F) Bundle concepts
ABCDEF (A2F) Bundle: Interprofessional, evidence-based safety bundle of care principles to help reduce LOS, mortality, bounce-backs, and the duration of ICU delirium and coma
Goal: allow pt to "prove us wrong" about readiness for liberation from devices, sedatives, etc.

Assess, prevent, and manage pain

Tools to assess pain using facial expressions, body movements, muscle tension, compliance with ventilator, or vocalization for extubated pts
Ex: Critical Care Pain Observation Tool (CPOT): scale 0-8, uncontrolled pain >=3
Uncontrolled pain increases risk for delirium, limits inspiratory effort & weaning from ventilator, and limits ability to mobilize
Treatment: multi-modal: parenteral opioids, neuropathic meds (e.g., gabapentin, ketamine), adjunctive non-opioids analgesics (e.g., acetaminophen, NSAIDs), nonpharmacologic interventions (repositioning, heat/cold)

Both spontaneous awakening trials (SATs) and spontaneous breathing trials (SBTs)

SATs = daily sedative interruptions - RN-driven protocol involving safety checklist: no active seizures, alcohol withdrawal, agitation, paralytics, myocardial infarction, or increased ICP - If pass SAT, proceed to SBT - If fail SAT (anxiety, agitation, pain, resp distress) → restart sedation at ½ doses

SBTs = PS ventilation (Fi02 ≤ 50%, PEEP ≤ 7.5; typically 40% and 5/5) for ≥ 30 minutes - RT or physician/APP-driven protocol with safety screen: passed SAT, O2 sat ≥ 88%, inspiratory efforts, no myocardial ischemia, no/low vasopressor support - If pass SBT, physician/APP judgment on extubation - If fail SBT (RR > 35 or < 8, O2 sat < 88%, resp distress, mental status change) → restart full ventilatory support

Evidence: - Liberated pts from mechanical ventilation 3 days sooner, decreased ICU and hospital length of stay by 4 days, and 14% absolute reduction in mortality at 1 year

Choice of analgesia and sedation

Richmond Agitation-Sedation Scale (RASS): sedation & level of arousal assessment tool
Target light sedation of RASS -1 to 0 with goal of (1) pt following commands without agitation and (2) limiting immobilization
Over-sedation: hold sedatives till target, then restart at ½ prior dose
Analgosedation with focus on treating pain first and then adding sedation meds PRN
Sedatives: dexmedetomidine (dex) or propofol >>> benzodiazepines (increased delirium risk)

Delirium - assess, prevent, and manage

Screening for delirium: q4h using CAM-ICU
Affects 60-80% of ventilated pts and associated with increased morbidity and mortality, longer ICU and hospital length of stay, long-term cognitive dysfunction
Risk factors and treatment: see Delirium section in Psychiatry

Early mobility and exercise

Prolonged immobilization during critical illness leads to ICU-acquired weakness, associated with worse outcomes: ↑ mechanical ventilation, increased hosp length of stay, greater mortality, and greater disability
Consult PT/OT to initiate rehab at the beginning of critical illness
Can be done safely in pts receiving advanced support

Family engagement and empowerment

Especially important when pts are unable to communicate themselves
Incorporate family at the bedside and on rounds to learn pt preferences and values, engage in shared decision making, and address questions and concerns

ICU Delirium

Author: Phil Schmitt

Background

Delirium is a DSM-V diagnosis based on acute-onset fluctuating attention and awareness, unlike the chronic changes seen in dementia. It is largely interchangeable with Encephalopathy.
This becomes more difficult to assess when patients are sedated, intubated, etc. in the ICU
Very well-studied at VUMC, more resources found at: https://www.icudelirium.org
Associated with higher morbidity and mortality compared to those who do not experience delirium and duration of delirium also associated with higher morbidity and mortality.

Evaluation

Can present as either hyperactive (agitated, trying to leave bed, etc.) or hypoactive (somnolent, minimally interactive, etc.).
Do neuro exam to rule out focal deficits. Basic ICU/coma neuro exam:

Component	Assessment
Level of consciousness	If not alert and oriented, test if they are redirectable/open eyes to loud voice
CN II (also III)	Pupillary light reflex - check pupillary size + rate of constriction, symmetry
CN III/IV/VI	Eye tracking to voice, roaming around room
CN V/VII	Corneal blink reflex - can use NS syringes to drop water into eyes
CN VIII (also III + VI)	Oculocephalic reflex - turn head left/right, eyes should compensate to fix in forward position
CN IX/X	Cough/Gag - Can test with tongue depressor. If intubated, can advance/retract OG tube for gag and endotracheal tube suction catheter for cough
CN XI	Difficult in delirious/intubated patients, can check for Shoulder shrugging with pain response
CN XII	Difficult in delirious/intubated patients, can monitor for Spontaneous tongue movements
Extremities	+Withdrawal to pain: Pt appears to voluntarily, non-stereotypically withdraw limbs to vigorous nailbed pressure, sternal rub, trapezius pinch +Localization of pain: Pt will attempt to reach to side of painful stimulus +Muscle Tone: relaxed at baseline, no abnormal flexion/extension IE posturing +Presence of abnormal reflexes: Unilateral hyper-/hypoactive reflexes, rapid & transient stereotyped movements to noxious stimuli IE triple flexion, up-going Babinski, ankle clonus

For ICU Patients, consider sedation when doing neuro exam - propofol and other anesthesia dampens brainstem + peripheral reflexes
Always remember patients can be encephalopathic and evolve another acute neurological syndrome. Follow up any odd/changing exam findings.
Perform the CAM-ICU for scoring – ICU nurses perform this q4h as part of routine ICU care
See RASS scoring table in ABCDEF Bundle Critical Care chapter.

Differential Diagnosis for ICU Delirium

Most typically due to changes in environment, alterations in sleep cycle, reduced cognitive reserve from critical illness, dementia, neurodegeneration, etc.

Other differentials fit in a modified VITAMINS PO mnemonic:

Category	Differential Diagnoses
Vascular	Ischemic stroke, CNS hemorrhage, arrhythmia, carotid stenosis
Infectious	+Any severe illness, UTI & PNA are most common +Also consider meningitis/encephalitis
Trauma	Falls, TBI, etc.
Autoimmune	Autoimmune encephalitis, SLE, CNS vasculitis among others
Metabolic	+Constipation +Hypo/hyperthyroidism, hypoglycemia, AKI, hypercalcemia, hyperammonemia (IE hepatic encephalopathy), severe hyponatremia, Uremia among many others +Vitamin deficiencies - thiamine and B12 especially
Ingestion	+Illicits, Opiates, Benzos, barbiturates, anti-psychotics, anti-cholinergics, cefepime +Withdrawal syndromes - EtOH/benzos/opioids especially, also SSRI's/daily psych meds
Neoplasm	Brain mets, primary CNS tumors, CA associated with paraneoplastic syndromes (SCLC, Multiple myeloma, ovarian teratoma, etc.)
Seizure
Pain	Always important to consider, especially in geriatric pts
Oxygenation	Hypoxia

Management

Initial toxic/metabolic/infectious workup can include: CBC, CMP, TSH, Folate, Vitamin B12, UA, blood cultures, CT Head w/o. Look through med list to see if there are any sedating medications that could be contributing and try to minimize as much as possible.
Definitive treatment is addressing underlying etiology.
First-line symptomatic treatment includes delirium precautions, such as keeping blinds open during daytime, limiting daytime naps, redirection when agitated, lights on during day, TV on during day, family at bedside (opposite of these at night). There is an order in Epic called Nursing: Delirium Care, which can be found as part of the Geriatric Delirium Care order set, that has all these precautions listed out.
Although they do not provide mortality benefit in ICU delirium patients (and debatably worsen mortality), antipsychotics can be used if needed for more severe agitation IE pulling at lines, physical aggression. Start with one-time dose of zyprexa 2.5 mg or 5 mg, can escalate to 1 mg haldol if refractory. Check an EKG for QTc prolongation (>440ms) prior to giving.

Brain Death

Author: Anna Berry

Background

Brain death = complete and permanent loss of brain function. Defined by coma with loss of capacity for consciousness, brainstem reflexes, and the ability to breathe independently

Checklist for Determination of Brain Death (American Academy of Neurology)

1. Prerequisites (all must be checked)

Coma, irreversible and cause known
Neuroimaging explains coma – usually CT or MRI
Absence of CNS depressing drugs
No evidence of residual paralytics (electrical stimulation if paralytics used)
Absence of severe acid-base, electrolyte, endocrine abnormality
Normothermia or mild hypothermia (core temp >36°C)
SBP ≥100 mmHg
No spontaneous respirations

2. Examination (all must be checked) – Attending MUST be present for brain death exam

See: Greer DM, Determination of Brain Death. NEJM. 2021;385;2554-61. doi: 0.1056/NEJMcp2025326

3. Apnea testing (all must be checked) – Attending MUST be present

Pt is hemodynamically stable
Ventilator adjusted to provide normocarbia (PaCO2 35–45 mmHg)
Preoxygenate with 100% FiO2 and PEEP of 5 cmH2O for >10 min to PaO2 >200 mmHg
Provide oxygen via a suction catheter to the level of the carina at 6 L/min or attach T-piece with continuous positive airway pressure (CPAP) at 10 cmH2O
Disconnect ventilator
Spontaneous respirations absent
Arterial blood gas drawn at 8–10 minutes, pt reconnected to ventilator
PCO2 ≥60 mmHg, or 20 mmHg rise from normal baseline value; OR:
Apnea test aborted due to spontaneous respirations present, hemodynamic instability, or hypoxia

4. Ancillary testing (Order one test if clinical examination cannot be fully performed due to pt factors or if apnea testing inconclusive/aborted)

Cerebral angiogram
HMPAO SPECT (Single photon emission computed tomography)
EEG & TCD (transcranial Doppler)

Organ donation caveats

Discussions about organ donation should take place between Tennessee Donor Services (TDS) and the surrogate. You SHOULD NOT be having conversations with the surrogate about donation. Direct questions to TDS

MICU/CCU Drips

Author: Patrick Barney

Most have order sets in Epic. Typically choose "Titration Allowed" in ICU

Vasopressors

Drug	Dose	Receptors	Indications	Considerations
Norepinephrine (Levophed)	1 – 100 mcg/min	α₁ > β₁	1st line septic shock	Peripheral ischemia, skin necrosis
Phenylephrine (Neosynephrine)	Bolus: 0.05 – 0.5 mg q 10-15 min Infusion: 40-360 mcg/min	α₁	Periprocedural hypotension (Neostick), pts w/ tachyarrhythmias, Critical AS or HOCM with severe LVOT obstruction and shock	Reflex bradycardia, Peripheral ischemia, skin necrosis
Epinephrine	1 – 40 mcg/min	α₁=β₁=β₂	Post PEA arrest, Anaphylaxis, Septic shock (severe), Cardiogenic shock	Tachyarrhythmias, Peripheral ischemia, skin necrosis
Vasopressin	0.04 U/min (no titration)	V1, V2, V3	2nd line septic shock, Right heart failure	Hyponatremia, Bradycardia
ANG II *needs approval MICU leadership	20 – 40 ng/kg/min	ANG II	Refractory vasodilatory shock	Thrombosis → pt MUST have chemical DVT ppx. Contraindicated in heart failure
Dopamine	2 – 20 mcg/kg/min	Dopamine (1-5 mcg) > β₁ (5-10 mcg) >α₁ (>10mcg)	Hypotension, Cardiogenic shock	Tachyarrhythmias, Peripheral ischemia, skin necrosis
Dobutamine	2.5 – 20 mcg/kg/min	β₁ >>> β₂	Cardiogenic shock	Vasodilation Hypotension, Tachycardia, Tachyphylaxis
Milrinone	0.375 – 0.75 mcg/kg/min	PDE-3	Cardiogenic shock	Hypotension, Renally cleared

Sedatives/Anxiolytics:

Drug	Dose	Class	Metabolism	Side Effects
Propofol	Infusion: 5 – 150 mcg/kg/min	General anaesthetic (GABA R agonist)	Hepatic, Renal (minor)	Severe hypotension, bradycardia, hypertriglyceridemia, propofol infusion syndrome (rare) Monitor for toxicity with q4 day TGs and CK
Dexmedetomidine (Precedex)	Infusion: 0.1 – 1.5 mcg/kg/h	Central α₂ agonist	Hepatic	Hypotension, bradycardia
Midazolam (Versed)	Push: 0.5 – 5 mg Infusion: 0.25 – 5 mg/h (no max dose)	Benzodiazepine	Hepatic & Renal	Hypotension, risk of BNZ withdrawal if used for long periods with sudden discontinuation
Lorazepam (Ativan)	Push: 0.5 – 10 mg Infusion: 0.5 – 5 mg/h (no max dose)	Benzodiazepine	Hepatic	Hypotension. Propylene glycol carrier – AGMA
Ketamine	Push: 1-2mg/kg Infusion: 0.2mg/kg/h, titrate by 0.1 q15min	NDMA antagonist	Hepatic	Delirium/hallucination – use caution in pts with psychiatric hx, hypertension, tachycardia Pretreat with 0.4mg IV glycopyrrolate to avoid hyper-salivation

Analgesic:

Drug	Dose	Metabolism	Side effects
Fentanyl	Push: 25 – 100 mcg Infusion: 25 – 400 mcg/h	Hepatic	Hypotension, Serotonin syndrome, chest wall rigidity at high doses
Morphine	Push: 1 – 5 mg q1-2h prn Infusion: 1 – 5 mg/h	Hepatic/Renal	Hypotension (profound), itching, constipation, HA; avoid in renal failure
Hydromorphone (Dilaudid)	Push: 0.25–1mg q1-2h prn Infusion: 0.5–3 mg/h	Hepatic	Hypotension, respiratory depression, itching

Anti-Arrhythmics

Drug	Dose	Indications	Side effects	Comments
Adenosine	6 – 12 mg IV rapid push and flush; may repeat x2	PSVT conversion	Complete AV nodal blockade	10 second half-life Must have continuous EKG/tele monitor
Amiodarone	ACLS: 300 mg IV push Non-emergent: 150 mg over 10 min then 0.5 mg/min	Vtach/Vfib, Afib	Pulm, ophthalmic and thyroid toxicity w/ chronic use	Less hypotension than other agents, safe in heart failure. May chemically cardiovert pts, caution if off therapeutic AC
Diltiazem	Push: 10 – 20 mg q15 min x 2 if no response Infusion: 5 – 15 mg/h	Afib, Aflutter, PSVT	Bradycardia, hypotension	Avoid use in pts with HfrEF
Lidocaine	ACLS: 1 mg/kg x 1 Infusion: 1 – 4 mg/min	Vtach	Bradycardia, Heart block	Avoid use in liver failure/ Okay for HfrEF. Often 1st line CCU med for VT/ May need to check levels if using for longer than 24 hours
Procainamide	15 mg/kg over 30 min then 1 – 6 mg/min	Vtach, refractory afib	Bradycardia, hypotension	Drug-induced lupus, cytopenias

Anti-hypertensives

Drug	Class/MOA	Dose	Indications	Side effects	Comments
Esmolol	Beta blocker	Bolus: 1mg/kg over 30s Infusion: 50-300mcg/kg/min (max 300)	Aortic dissection, HTN emergency	Bradycardia, hypotension	Titrate to desired BP or HR. Caution in HfrEF
Nicardipine	CCB	Infusion: 5-15mg/h (max 15)	HTN emergency	Bradycardia, hypotension	Titrate to desired BP, avoid in HfrEF
Nitroprusside	Metabolized to NO → vasodilatory effect (arterial roughly = venous)	Infusion: 0.3mcg/kg/min; titrate q2min to max 10mcg/kg/min	HTN E, flash pulmonary edema, HfrEF for afterload reduction	Hypotension, cyanide toxicity	Contraindicated in hepatic and renal failure
Nitroglycerin	NO mediated venous > arterial vasodilation	Infusion: start 0.25mcg/kg/min, titrate by 1mcg/kg/min q15min (max 10mcg/kg/min)	Refractory angina, flash pulmonary edema, HTN emergency	Hypotension, headache, palpitations	Contraindicated in severe RHF and concurrent use of PDE-5 inhibitor

Running Codes

Author: Hannah Kieffer

Arrival to a Code:

Questions to ask when you arrive: Who is running this code? Have we confirmed the pt's code status?
Calmly take charge: Establish if anyone is actively running the code. If someone is running the code, introduce yourself and ask how you may be helpful. If someone is NOT, assume responsibility for running the code

1st Minute: Check in on ABCDE

A: Airway – Check that patient is receiving breaths; do they need an airway adjunct?
B: Breathing – Is someone bagging the patient effectively?
C: Compressions – Has someone started chest compressions? Have 2-3 people in line to take over during pulse checks
D: Defibrillation – Are there pads on the patient?
E: Epinephrine – Make sure first dose has been given

2nd Minute: Set up your room

You/the code leader stands at the foot of the bed. Do not move.
One person on chest compressions; 2-3 people in a line behind to take over during pulse checks
Airway manager at head of bed. Have second person to assist/hold the mask
Someone monitoring femoral pulse
Medication administrator
Timer/Recorder

Be clear and remove extra people out of the room

Now that your code is running:

Access: IV access preferred, if no immediate IV access, place IO
Obtain a brief medical history and events surrounding the code

Interventions with proven mortality benefit:

Strong ACLS: - Check that high quality CPR with minimal interruptions (<10s) - Change compressors during pulse checks to decrease interruptions - Q2min - pulse check, rhythm check, shock? - Do NOT pause compressions for intubation - Restart CPR immediately after defibrillation - do not check pulse until after 1 additional round of CPR after defibrillation, even if possible perfusing rhythm returns

Early Defibrillation: Assess the rhythm - If Vfib/VT, immediately shock - For polymorphic VT, this is ischemia until proven otherwise unless the pt is on a large amount of QTc prolonging medications - If PEA/Asystole - resume compressions

Epinephrine: Given every 3-5mins during CPR

Consider Advanced Airway: - Intubation is not proven to increase survival over bag-mask ventilation - Remember chest compressions save lives, not intubation. Do NOT stop compressions for intubation

H's and T's: - Treat Reversible Factors - Some of the fellows here will empirically give 2 grams of magnesium, 1 amp of D50, 1 amp of bicarb, and 1g calcium chloride at the onset of the code irrespective of presenting rhythm

Treatable Causes of Cardiac Arrest:

H's	T's
Hypoxia	Toxins
Hypovolemia	Tamponade
H+	Tension Pneumothorax
Hypo/Hyper K	Thrombosis: Pulmonary
Hypothermia	Thrombosis: Coronary

Miscellaneous Advice:

Closed Loop communication - continue giving instructions, minimize interruptions
It can be helpful to maintain a constant verbal running summary of the course of the code and interventions that have been tried
Have a member of the team locate an ultrasound for line placement and diagnostics
Once code is underway, you have more time to understand specifics of patient. Ask bedside nurse for more past medical and more immediate history. Have someone look up most recent labs in Epic (looking for recent hyperK, acidosis). Can send Labs – ask for a "loaded gas"
Allow family to be present if they want. Very Important: If family present, ensure that a healthcare provider (nurse, APP, resident, attending) is with the family (to answer questions, explain what is going on)

Terminating a Code

Consider initial rhythm, pt comorbidities, cardiac vs non-cardiac arrest, bedside echo findings. ROSC or rhythm changes during code?
Persistent ETCO2 < 10 mmHg after 20min CPR has minimal survival
Ask your team if they have any other therapies that they feel would be indicated
Ask if anyone remains in favor of continuing CPR
When unanimous, terminate the code and announce time of death. Thank your team. Take a moment of silence for the deceased patient

Post-Arrest Care

Immediately following ROSC is the most dangerous point of ACLS
Airway: Secure airway if not done during code. Avoid hypoxia AND hyperoxia
BP: MAPs < 65, IVF and/or pressors if needed
If on floor, prioritize moving pt to a unit for ongoing care once hemodynamically stable enough for transfer. Would not delay for other diagnostics/interventions (lines, CXR, etc)
Cardiac: Obtain EKG. Assess if urgent cardiac intervention is required for STEMI vs unstable cardiogenic shock vs VT storm or Vfib
Neuro: If not following commands, consider Targeted Temperature Management. TTM is still performed at VUMC with a strict protocol and inclusion criteria. If there is any question about TTM eligibility, page the CCU fellow
Send rainbow labs (CBC, CMP, Mg, coags, trop, lactate, VBG/ABG). Treat rapidly reversible causes
CXR
Propofol/fentanyl infusion if the pt is intubated. Pressor of choice post ROSC is usually levophed
If not done during the code, obtain central access and an arterial line

Resident Roles:

Intern: Grab yellow IO kit before leaving ICU for the code. Discuss learning opportunities with senior prior to codes; consider holding femoral pulse, placing IO if needed, chest compressions if no prior experience
Resident: Ask the fellow in advance if you can run the code with them standing next to you for support and assistance. This is a very important experience.

Temperature Abnormalities

Author: Soibhan Kelley

Hypothermia

Background

Core temperature <35°C (95°F). Mild 32-35C (90-95F), moderate 28-32C (82-90F), or severe <28C (82F) +/- pulseless
Ensure thermometer is "low-reading," standard thermometers not accurate
Core temperature can be measured w/ bladder catheter probe or esophageal probe (may be falsely ↓ if heated oxygen being delivered). Rectal temp can be used but is less accurate
Etiologies:
Heat loss: environmental, burns, iatrogenic (CRRT, cold IVF, massive transfusion protocol), vasodilatory drugs/toxins
Decreased heat production: endocrinopathies (hypothyroidism, adrenal insufficiency, hypopituitarism, hypoglycemia), thiamine deficiency
Impaired regulation: Spinal cord injury, hypothalamic lesions, drugs (classes including antihyperglycemics, beta blockers, sedatives, ETOH, alpha agonists, general anesthetics)
Multiple mechanisms: sepsis, pancreatitis, DKA

Evaluation

Infectious work-up
POC blood glucose, TSH/FT4, cortisol, lipase, UA, UDS, EtOH level, additional tox as appropriate, DKA work-up if relevant
Physical exam + history for exposures and trauma
CBC, CMP, Lactate, ABG, CK, PT/PTT, Fibrinogen
EKG

Management

Treat underlying cause [see appropriate sections]
Mild hypothermia:
Passive external rewarming (PER): blankets, increase ambient temperature
Note that PER requires sufficient underlying physiologic reserve to generate heat. This is often impaired in elderly pts, malnutrition, sepsis
Moderate hypothermia, refractory mild hypothermia, or cardiovascular instability:
Active external rewarming (AER): forced warm air (ie Bair Hugger), heated blankets, heat lamps, hot packs (consider burn risk)
Severe hypothermia or refractory moderate hypothermia:
Active core rewarming: Warmed IV crystalloid (limited rewarming potential unless large volume but will decrease ongoing losses), warmed humidified inspired air, warmed bladder lavage
More extreme methods such as peritoneal/thoracic lavage more likely to be used in severe environmental cases in ED
Pulseless severe hypothermia ("You aren't dead unless you are warm and dead"):
Continue CPR until re-warmed as severe hypothermia is neuroprotective and pts can have good neurologic outcomes despite hours of CPR
ACLS medications and shocks will have poor effectiveness; prioritize circulation (i.e. chest compressions) and rewarming
Consider ECMO (likely venoarterial if pulseless); would need transfer to CVICU
Identify and manage complications: bradycardia/heart block, arrhythmias, shock, coagulopathy/DIC, rhabdomyolysis; rebound hyperkalemia/hypoglycemia with rewarming

Fever and Hyperthermia

Background

Fever: T >38.0°C (100.4°F) driven by hypothalamus activity in response to systemic triggers (i.e. cytokines); may use lower threshold for immunocompromised pts
Hyperthermia: T >41.0 C (105.8°F) uncontrolled heat production with failure of thermoregulation
Infectious etiologies:
Considerations in the ICU include central-line associated blood stream infection, catheter-associated UTI, pneumonia (including ventilator-associated), sinusitis (esp. in pts with NGT or ETT), clostridium difficile, acalculous cholecystitis
Non-infectious etiologies:
Drug fever:
- Difficult to distinguish from other causes; Can begin hrs-wks after starting a drug
- Sources: antibiotics (penicillins, cephalosporins, sulfonamides), anticonvulsants (phenytoin, carbamazepine, phenobarbital), allopurinol, heparin, dexmedetomidine
- Drugs of abuse with sympathomimetic activity (cocaine, meth, ecstasy)
- Anticholinergic or salicylate intoxication
Idiosyncratic drug reactions:
- Serotonin syndrome
- Neuroleptic malignant syndrome
- Malignant hyperthermia
Transfusion reactions
PE/DVT
Endocrine: hyperthyroidism/thyroid storm, adrenal insufficiency
CNS pathology (intracranial bleed/stroke, particularly hypothalamic region)
Malignancy
Heat stroke (exertional or non-exertional)
Other inflammatory states: Pancreatitis, gout, pericarditis, pneumonitis

Evaluation

Infectious work-up +/- LP; may consider pan-scan if unable to identify source
POC glucose, BMP, LFT, Mg/Phos, CBC w/diff
Consider coags + fibrinogen (DIC), CK/UA (rhabdo), UDS, acetaminophen and salicylate levels, TSH/FT4, cortisol, lipase, ABG
Review medication list: antibiotics, serotonergic drugs, anti-psychotics, recent sedation for OR, or recently intubated with succinylcholine, dexmedetomidine
Consider CT/MRI head

Management

Treat underlying etiology [see appropriate sections]
Serotonin syndrome -> stop serotonergic drugs; add cyproheptadine
Malignant hyperthermia ->activate malignant hyperthermia team; add dantrolene
Cooling:
Target <38.0°C (100.4°F)
Surface cooling: Ice (bath, or ice packs more likely in our MICU), evaporative cooling with misted lukewarm water and fan
Internal cooling: Cold IV fluids, dry ventilation (evaporative) with non-humidified nasal cannula or vent circuit
Avoid shivering -> give opiates (except in serotonin syndrome), precedex, propofol, benzos, ketamine
Antipyretics:
Acetaminophen, NSAIDs
Block prostaglandin-mediated temperature elevations
Effective for most causes of fever- infection, pancreatitis, DVT/PE, pneumonitis
AVOID for true hyperthermia (ineffective and potentially harmful) -> neuroleptic malignant syndrome, malignant hyperthermia, serotonin syndrome, heat stroke
Monitor for complications:
Rhabdomyolysis, DIC, arrhythmias
If high suspicion for infection and not improving on antibiotics, consider other infectious etiologies including fungal (e.g., candida)