(1)
Divisions of Critical Care Medicine and Infectious Diseases, Department of Medicine, University of Alberta, Edmonton, AB, Canada
Intensive Care Issues
ICU Admission Criteria
NEED FOR FREQUENT OR CONTINUOUS MONITORING
—post-high-risk surgery, high risk for clinical deterioration
HIGH INTENSITY OF NURSING CARE
LIFE SUPPORT THERAPY
—mechanical ventilation, vasoactive drugs, continuous renal replacement, artificial liver support
Preventative Strategies
VENTILATOR-ASSOCIATED PNEUMONIA
—remove endotracheal tube as soon as possible, orotracheal intubation unless contraindicated, strict hand hygiene, oral and dental hygiene (chlorhexidine rinse), semi-recumbent positioning (head of bed at 30°), rotational bed therapy, subglottic suctioning, drainage of condensate from ventilator circuits, minimize gastric acid suppression therapy (proton pump inhibitors) when possible
GASTROINTESTINAL STRESS ULCERATION
—risk factors include mechanical ventilation and/or coagulopathy. Prophylaxis with H2 blockers (e.g. ranitidine 50 mg IV q8h or 150 mg PO/NG q12h) preferred unless high risk as use of proton pump inhibitors is associated with increased risk of ventilator-associated pneumonia
VENOUS THROMBOEMBOLISM
—particularly in patients with trauma and prolonged bed rest. Prophylaxis includes heparin SC, LMWH, fondaparinux, or pneumatic compression stockings
Sedation, Analgesia, Paralysis in the ICU
SEDATION/AMNESIA
—propofol 0.5 mg/kg/h initial infusion, titrate to 0.5–3.0 mg/kg/h by continuous IV infusion, typical infusion range 0–300 mg/h. Appropriate for short-term sedation, monitor for acidosis and increased CK with prolonged use, rapid onset, short duration; midazolam 0.03 mg/kg loading dose, then 0.02–0.1 mg/kg/h IV infusion, typical infusion range 0–10 mg/h, rapid onset, short duration; lorazepam 0.5–10 mg IV q2–4 h PRN, load with 0.5–2 mg q15min, avoid continuous infusion as propylene glycol solvent may accumulate. Use for intermediate to prolonged sedation, longer duration than midazolam, most potent amnestic
ANALGESIA
—fentanyl 50–100 μg q5min IV load to effect, then 1–4 μg/kg/h by continuous IV infusion, typical infusion range 50–300 μg/h, 100× more potent than morphine. Used in patients with hemodynamic instability, rapid onset, short duration (but highly lipophilic; may accumulate with prolonged infusion); morphine 0.05 mg/kg IV load, then 4–15 mg/h. May cause hypotension due to histamine release; hydromorphone 0.5 mg IV initially, then 1–2 mg q1h or 0.5–2 mg/h infusion, 5× more potent than morphine
NEUROMUSCULAR BLOCKAGE
—rocuronium 0.5 mg/kg IV PRN, onset 1 min, duration 30 min; pancuronium 0.06–0.15 mg/kg IV PRN, onset 2–3 min, duration 60–120 min, may run continuous infusion 0.01–0.05 mg/kg/h, vagolytic effect may cause tachycardia; cisatracurium 0.15–0.2 mg/kg IV PRN, onset 2–3 min, duration 30 min, may run continuous infusion 3 μg/kg/min, undergoes Hoffman degradation; succinylcholine 0.5–1.5 mg/kg IV, onset 1 min, duration ~10 min, metabolized by pseudocholinesterase, many contraindications
Differential Diagnosis for Weakness in the ICU
ENCEPHALOPATHY
—hypoxic/ischemic, septic, hepatic, uremic, hypoglycemic, iatrogenic (drugs)
MYELOPATHY
—hypoxic/ischemic, traumatic
NEUROPATHY
—critical illness polyneuropathy, Guillain–Barré syndrome, motor neuron disease, compression, hypophosphatemia
NEUROMUSCULAR JUNCTION
—blocking agents, Eaton–Lambert, myasthenia gravis, hypomagnesemia, hypocalcemia, organophosphates, botulism
MYOPATHY
—critical illness myopathy, acute necrotizing myopathy, hypokalemia, hypophosphatemia, hypocalcemia, hypomagnesemia, steroid, muscular dystrophy, polymyositis
Procedures
RADIAL ARTERIAL LINE INSERTION (NEJM 2006 354:E13)
landmark—palpate radial artery immediately proximal to scaphoid. Insert 20-gauge (48 mm length) catheter at 30°
FEMORAL ARTERIAL LINE INSERTION
landmark—femoral artery is midway between ASIS and pubic symphysis. Puncture and insert catheter over the wire, never dilate an artery!
FEMORAL CENTRAL VENOUS CATHETER (NEJM 2008 358:E30)
landmark—femoral artery is midway between ASIS and pubic symphysis. Femoral vein is medial to artery. Insert introducer needle through skin at 45° toward umbilicus, about 1 cm below the inguinal ligament, then use Seldinger technique to place catheter
complications—arterial puncture (9–15%), hematoma (4%), infection (6–20%)
SUBCLAVIAN CENTRAL VENOUS CATHETER (NEJM 2007 357:E26)
landmark—subclavian vein is directly underneath clavicle. Insert introducer needle through skin at 20° 2 cm lateral and 2 cm caudal to the middle third of clavicle aiming toward sternal angle. When needle hits clavicle, apply downward pressure (so needle is parallel to clavicle) and slide it under inferior surface to puncture subclavian vein
key points—place patient in Trendelenburg position and occlude hubs at all times to avoid air embolism
complications—arterial puncture (6.3–9.4%), hematoma (<2.2%), pneumothorax (<0.2%), infection (0.12%)
removal—place patient in Trendelenburg position and ask him/her to perform a Valsalva maneuver when removing the catheter to prevent air embolism
INTERNAL JUGULAR CENTRAL VENOUS CATHETER (NEJM 2007 356:E21)
landmark—locate carotid pulse. Internal jugular is immediately lateral to carotid. Consider ultrasound guided internal jugular central venous catheter insertion to identify aberrant anatomy. Insert introducer needle through skin at 20° toward ipsilateral nipple, slightly superior to the apex of the triangle
key points—place patient in Trendelenburg position, avoid significant contralateral rotation as it may increase incidence of artery/vein overlap and decrease venous return, occlude hubs at all times to prevent air embolism
complications—arterial puncture (6.3–9.4%), hematoma (<2.2%), pneumothorax (<0.2%), infections (0.45%)
removal—place patient in Trendelenburg position and ask him/her to perform a Valsalva maneuver when removing the catheter to prevent air embolism
NEJM 2003 348:12
Central Venous Saturation
ARTERIAL OXYGEN CONTENT (CaO2)
CaO2 = O2 carried by hemoglobin + O2 dissolved in blood
CaO2 = 1.36 × Hb × SaO2 + 0.003 × PaO2 where SaO2 = arterial Hb saturation
VENOUS OXYGEN CONTENT (CvO2)
CvO2 = O2 carried by hemoglobin + O2 dissolved in blood
CvO2 = 1.36 × Hb × SvO2 + 0.003 × PvO2 where SvO2 = mixed venous Hb saturation (ScvO2 if using central venous saturation)
OXYGEN FLUX (DO2)
DO2 = amount of oxygen delivered to tissues/min
DO2 = CO × CaO2, where CaO2 ~ 1.36 × Hb × SaO2 since 0.003 × PaO2 is negligible
OXYGEN CONSUMPTION (VO2)
VO2 = the arteriovenous oxygen content difference multiplied by cardiac output
VO2 = CO × (CaO2 – CvO2) ≈ constant (the body normally extracts ~25% of the delivered oxygen except in fever, sepsis, hyperthyroidism, i.e. VO2/DO2 = 0.25)
INTERPRETATION
As CO ×(CaO2 – CvO2) ≈ constant, ↓ CvO2 suggests ↓ CO or ↓ O2 consumption from end-stage shock
SvO2 is about 75% saturated. A mixed venous saturation of <50% is alarming, <25% is usually unsustainable
Prognostic Issues
ACUTE PHYSIOLOGIC AND CHRONIC HEALTH EVALUATION (APACHE) II SCORE
—predicts hospital mortality, web-based programs are available. The latest version is APACHE IV
clinical—age, GCS, organ failure (biopsy-proven cirrhosis, NYHA class IV, severe COPD, chronic hemodialysis, immunocompromise), procedure (non-surgical, elective, emergency operation)
vitals—HR, RR, MAP, temp
ABG—pH, A-a gradient or PaO2
CBC—Hct, WBC
chemistry—Na, K, Cr
VENTILATION
—95% of patients with acute respiratory failure can be weaned within 7 days of intubation. 5% are unable to be weaned from the ventilator and require tracheostomy and long-term ventilatory support
Cardiopulmonary Resuscitation
CONDITIONS ASSOCIATED WITH NEGLIGIBLE CHANCE OF SURVIVING CPR
—decompensated diseases (cancer, sepsis, pre-arrest hypotension or hypoxia, anemia, chronic renal failure), poor baseline function (dependent on ADLs), scene of CPR (>10 min of CPR without the return of at least a single vital sign, unwitnessed arrest)
PROGNOSIS
—respiratory arrest better than cardiac arrest. VT/VF/bradycardia better than asystole/PEA (patients with VF/VT witnessed arrest and response within 5 min of resuscitation have the highest probability of survival to discharge). Outcomes most favorable if resuscitated promptly; however, many have neurologic impairment, particularly if out-of-hospital arrest. Survival to discharge 1–5% for out-of-hospital CPR and 15% for in-hospital CPR
Brain Death
EXAMINATION OF THE UNRESPONSIVE PATIENT
vitals—including GCS
5 N—neurological, noggin, neck, nose, needle
eyes—fundoscopy, pupillary reflex, corneal reflex, oculocephalic reflex, oculovestibular reflex
others—gag reflex, cough reflex, tone, limb reflexes, Babinski
GLASGOW COMA SCALE
eyes opening—1 = none, 2 = to pain, 3 = to voice, 4 = voluntary
language—1 = none, 2 = sounds, 3 = words, 4 = disorganized sentences, 5 = organized sentences/oriented
motor—1 = none, 2 = extension to pain (decerebrate), 3 = flexion to pain (decorticate), 4 = withdraws, 5 = localizes to pain; 6 = obeys commands
consider intubation—if GCS <8, unable to protect airway
OCULOCEPHALIC REFLEX
doll’s eyes response—avoid this test in patients with suspected cervical spine injury. Move the patient’s head from side to side. Conjugate eye movement in the opposite direction to head movement is expected in the comatose patient, while it may be absent/asymmetric if the patient has brain stem injury or if psychogenic
OCULOVESTIBULAR REFLEX
caloric testing—instillation of ice-cold water into the ear canal on one side (ensure tympanic membrane intact prior to performing). Conjugate eye movement to the irrigated side is expected in the comatose patient (without nystagmus), while it may be absent or asymmetric if the patient has brain stem injury. In a conscious patient, nystagmus will be seen with the slow phase toward irrigated side and the fast phase toward the opposite side. Warm water instillation produces the opposite effect (★COWS★ In conscious patient instilled with Cold water, nystagmus fast phase moves toward Opposite side; with Warm water, nystagmus fast phase moves toward Same side)
ANOXIC BRAIN INJURY SPECTRUM
1.
Good recovery (mild disability)
2.
Moderate disability (independent with ADLs)
3.
Severe disability (dependent for ADLs)
4.
Persistent vegetative state (unawareness but awake at times)
5.
Persistent coma (unawareness at all times but potentially reversible)
6.
Brain death (unawareness at all times and irreversible)
DEFINITION OF BRAIN DEATH
history—documentation of cause and irreversibility, absence of drug intoxication or poisoning, absence of hypothermia, absence of metabolic causes for encephalopathy
physical —core temperature ≥34 °C [≥93.2 °F], absence of motor response to painful stimulus, absence of brain stem reflexes (corneal, pupillary, gag, cough, doll’s eyes, calorics), apnea testing
imaging —perfusion scan (most sensitive test), cerebral angiogram, EEG, transcranial doppler ultrasound, somatosensory evoked potentials (SSEPs)
criteria —need history, physical features and apnea testing to confirm brain death clinically. If apnea testing cannot be performed or indeterminate, ancillary testing required (cerebral blood flow most reliable ‘stand alone’ test)
brain death mimics —locked-in syndrome (focal injury to pons), hypothermia (light reflex lost 28–32 °C [82.4–89.6 °F], other brain stem reflexes lost <28 °C [82.4 °F]), drug intoxication, Guillain–Barré syndrome
Related Topics
Dialysis Issues (p. 96)
Critical Illness Neuromuscular Disorders (p. 378)
Palliative Care (p. 439)
Resuscitation Status (p. 440)
APNEA TESTING
1.
Obtain ABG just prior to test
2.
Pulse oximetry on, ventilator off, 100% oxygen 6 L/min into trachea or place patient on bagger
3.
Observe for respiratory movements. Obtain ABG after 8 min. Reconnect ventilator immediately and draw ABG if SBP <90 mmHg, marked decrease in SaO2, or arrhythmia
4.
Apnea present if respiratory movements are absent, PaCO2 ≥60 mmHg or increased ≥20 mmHg above baseline
RATIONAL CLINICAL EXAMINATION SERIES: IS THIS PATIENT DEAD, VEGETATIVE, OR SEVERELY NEUROLOGICALLY IMPAIRED (ASSESSING OUTCOME FOR COMATOSE SURVIVORS OF CARDIAC ARREST)?
LR+ | LR– | |
|---|---|---|
Clinical signs that predict death or poor neurological outcome | ||
Absent corneal reflexes at 24 h | 12.9 | 0.60 |
Absent pupillary response at 24 h | 10.2 | 0.8 |
Absent withdrawal response to pain at 24 h | 4.7 | 0.2 |
No motor response at 24 h | 4.9 | 0.6 |
No motor response at 72 h | 9.2 | 0.7 |
APPROACH—“simple physical examination maneuvers strongly predict death or poor outcome in comatose survivors of cardiac arrest. The most useful signs occur at 24 h after cardiac arrest and earlier prognosis should not be made by clinical examination alone. These data provide prognostic information, rather than treatment recommendations, which must be made on an individual basis incorporating many other variables”
JAMA 2004 291:7
Hypoxemia
Differential Diagnosis
R TO L SHUNT
(unresponsive to supplemental O2, V/Q <1)—ARDS, HF, pneumonia, alveolar hemorrhage, atelectasis, pulmonary arteriovenous malformation, intracardiac shunt (ASD, VSD, PFO)
V/Q MISMATCH
(V/Q >1)—pneumonia, ARDS, asthma, COPD, fibrosis, pulmonary embolism, tumor-filled alveoli, atelectasis, HF
DIFFUSION DEFECTS
—interstitial lung disease, PJP, atypical pneumonia
HYPOVENTILATION (A-a normal)
CNS—sedating drugs, tumor, stroke, sleep apnea
neuromuscular —botulism, Guillain–Barré, ALS, myxedema
upper airway obstruction —epiglottitis, laryngospasm
lower airway obstruction —COPD, asthma
dead space ventilation —COPD
LOW O2 PARTIAL PRESSURE
(A-a normal)—high altitude
Pathophysiology
DEFINITION OF HYPOXEMIA
—PaO2 < 60 mmHg. Note that hypoxia refers specifically to decreased oxygen supply to tissues and organs
Investigations
BASIC
labs —CBCD, lytes, urea, Cr, troponin/CK, lactate
imaging —CXR, CT chest
ABG
ECG
Diagnostic Issues
OXIMETRY
normal —>90% is normal. Dyspnea may occur ~85%. Pulmonary hypertension may develop from chronic alveolar hypoxia if saturations <80%
accuracy —between 70 and 100% saturation error is ±2%. Saturation values <70% may not be valid. Most reliable when applied to well-perfused, warm, and motionless extremities. Nail polish, darkly pigmented skin, carboxyhemoglobin, methemoglobin may all affect readings. Co-oximetry required for accurate results (run ABG). Continuous oximetry is better than spot measurements
correlation —SpO2 50% = PaO2 27 mmHg, 75% = 40 mmHg, 90% = 60 mmHg, 92% = 80 mmHg, 95% = 90 mmHg. ABG is the gold standard for diagnosing hypoxemia
OVERALL APPROACH TO DETERMINING THE CAUSE OF HYPOXEMIA
1.
Confirm ABG shows low PaO2
2.
Exclude diffusion defects and low partial pressure of O2
3.
Check PaCO2. If normal or low, then hypoventilation is excluded. This leaves either shunt or V/Q mismatch, which can be distinguished with response to O2 (absence of response suggests shunt. V/Q mismatch should respond to O2)
4.
If high PaCO2, then hypoventilation is present. Check A-a gradient to determine if co-existing shunt or V/Q mismatch (presence of A-a gradient suggests yes and should check response to O2 to distinguish between these two possibilities)
ALVEOLAR-ARTERIAL (A-a) O2 GRADIENT
normal —A-a gradient < age/4 + 4, or <0.4 × age. Usually <15 mmHg in young, up to ~30 mmHg in elderly
calculation —A-a gradient = PAO2 – PaO2 = [(PB–47) × 0.21– PaCO2/0.8] – PaO2, where PB = barometric pressure ≈760 mmHg if at sea level
interpretation —calculation used when FiO2 is 21% (room air). Normal range changes with supplemental oxygen. If A-a gradient normal, consider hypoventilation or low inspired O2 as causes of hypoxemia. If A-a gradient high, consider V/Q mismatch, R to L shunt, and/or diffusion defects
PaO2/PAO2 RATIO
—when FiO2 >21% (i.e. on supplemental O2 therapy), PaO2/PAO2 ratio should be used instead of A-a gradient
normal —PaO2/PAO2 ≥0.99 – (0.003 × age), usually >0.82
interpretation —unlike A-a gradient, PaO2/PAO2 ratio decreases in the presence of V/Q mismatch, R to L shunt, or diffusion defects
Management
ACUTE
—ABC, O 2 , IV, mechanical ventilation if severe respiratory failure (invasive or non-invasive)
TREAT UNDERLYING CAUSE
Treatment Issues
AVOID OVER-CORRECTING O2 SATURATION IN HYPOVENTILATION
—O2 displaces CO2 from Hb, causing elevated CO2 in blood. In addition, O2 may change V/Q relationship and may decrease hypoxic drive. For patients with chronic hypoventilation (↑ HCO3), O2 to keep saturation between 88 and 92% only
Specific Entities
HYPOXEMIC RESPIRATORY FAILURE
(PaO2 < 50 mmHg even with FiO2 > 50)—failure to oxygenate, see DIFFERENTIAL DIAGNOSIS OF HYPOXEMIA
HYPERCARBIC RESPIRATORY FAILURE
(PaCO2 greater than baseline with concomitant acidosis)—failure to ventilate, see hypoventilation under DIFFERENTIAL DIAGNOSIS OF HYPOXEMIA
Acute Respiratory Distress Syndrome
Differential Diagnosis
PULMONARY EDEMA
cardiogenic —ischemic cardiomyopathy, valvular disease
non-cardiogenic —ARDS, toxic inhalation, drug reaction, aspiration, fat embolism
INFECTION
—bacterial, viral, mycobacterial, fungal
HEMORRHAGE
—pulmonary embolism, pulmonary contusion, bleeding diathesis, DIC, anticoagulation, vasculitis (granulomatosis with polyangiitis, Goodpasture’s, SLE)
Pathophysiology
DEFINITION OF ARDS
(Berlin Definition, JAMA 2012 307:23)
acute onset —new (or worsening) respiratory symptoms <1 week
bilateral alveolar infiltrates —usually asymmetric/patchy, peripheral > central
moderate to severe hypoxemia (with peep or cpap ≥5 cmH 2 O)—mild: PaO2/FiO2 > 200 mmHg but ≤300 mmHg; moderate: PaO2/FiO2 100–200 mmHg; severe: PaO2/FiO2 ≤ 100 mmHg
absence of cardiac failure or fluid overload —objective assessment to exclude hydrostatic pulmonary edema (e.g. echocardiography) required if no risk factors for ARDS present
INFLAMMATION IN ARDS
—ARDS is a clinical syndrome of severe lung injury due to systemic inflammation. Cytokine release results in capillary membrane permeability and protein-rich fluid exudation into the alveolar space, impairing oxygenation. Ongoing inflammation may lead to extensive fibrosis
PHASES OF ARDS
—<10 days = exudative phase, 10–14 days = fibroproliferative/fibrotic phase
HYPOXEMIA IN ARDS
—caused mainly by right to left shunt, thus the PaO2/FiO2 ratio is low. V/Q mismatch and hypoventilation may also contribute
CAUSES
—over 80% of ARDS caused by infection, aspiration, and trauma
pulmonary —pneumonia (bacterial, viral, fungal including PJP, mycobacterial), aspiration, drowning, inhalation injury (O2, smoke, NO2), reperfusion injury (post-lung transplant or cardiopulmonary bypass)
GI—acute pancreatitis
CNS—neurogenic (intracerebral hemorrhage)
systemic —sepsis, transfusion reaction, major trauma, drugs (heroine, cocaine, aspirin, chemotherapy)
Investigations
BASIC
labs —CBCD, lytes, urea, Cr, troponin/CK, urinalysis, lactate
microbiology —blood C&S, sputum Gram stain/C&S/AFB, urine C&S
imaging —CXR, CT chest, echocardiogram
ABG
ECG
pulmonary artery catheterization
Diagnostic and Prognostic Issues
PROGNOSIS OF ARDS
—overall mortality rate ~45%. Mortality increases with additional organ failure (>99% if three system failures)
Management
ABC
—O 2 to keep SpO2 85–95%, IV access
MECHANICAL VENTILATION
lung-protective ventilation (low tidal volumes to minimize ventilation-induced lung injury)—set tidal volume ~4–8 mL/kg, based on ideal body weight, maintain plateau pressure ≤30 cmH2O
peep —should be employed to keep FiO2 in presumed non-toxic range (<0.60). Increase PEEP by increments of 3–5 cm (maximum = 15–20 cm) to ↑ mean airway pressure, recruit alveoli (preventing alveolar collapse and ventilator-induced lung injury) and ↑ functional residual capacity (may be harmful)
recruitment —recruitment maneuvers may be used to keep alveoli open; e.g. 40 cmH2O PEEP for 40 s
permissive hypercapnia —generally tolerate pH >7.25, may need to run HCO3 infusion to maintain pH
salvage/alternate modes of ventilation —APRV (airway pressure release ventilation), HFOV (high-frequency oscillatory ventilation), prone positioning (only salvage technique with mortality benefit; NEJM 2013 368:23)
MEDICATIONS
—no effective pharmacologic therapy for ARDS. There is limited evidence regarding steroid use for treatment of ARDS and no evidence for prophylaxis. Some clinicians still use in non-resolving cases (start 7–14 days after onset. Methylprednisolone 2 mg/kg load, then 2 mg/kg/day from days 1 to 14, then taper by 50%/week to 0.125 mg/kg/day, monitor for infection). Inhaled nitric oxide or epoprostenol (Flolan) selectively dilate pulmonary vessels of ventilated alveoli, improving V/Q matching. Reduce pulmonary artery pressures and intrapulmonary shunting with an increase in PaO2/FiO2
TREAT UNDERLYING CAUSE
Ventilation Issues
Mechanical Ventilation
INDICATIONS FOR MECHANICAL VENTILATION
decreased compliance (stiff lungs)—pulmonary fibrosis, pulmonary edema, ARDS
increased resistance (narrowed airways, air trapping)—status asthmaticus, COPD exacerbations, bronchial tumor, excessive secretions
mechanical failure —spinal cord injury, Guillain–Barré
lack of respiratory drive —neurologic disease, drug overdose
NON-INVASIVE POSITIVE PRESSURE VENTILATION (NIPPV)
conditions in which NIPPV is used —COPD, HF, asthma, postoperative respiratory failure, postextubation in select situations. If no improvement after 30 min-1 h, should intubate
indications—pH 7.2–7.3, RR >25, use of accessory muscles, and cooperative
contraindications —↓ level of consciousness (but possible use if due to ↑ PCO2), respiratory arrest, facial trauma/surgery/burn, upper airway obstruction, copious secretions, aspiration risk, GI bleeding, gastroesophageal surgery, esophageal rupture, hemodynamic instability, co-existent organ failure, massive obesity, extreme anxiety
mask types —full face, nose and mouth, nasal only
ventilatory modes —CPAP or BIPAP. CPAP is mainly used for obstructive sleep apnea; however, can be used in isolated hypoxemia (ventilation adequate). BIPAP is used to assist with oxygenation and ventilation
INVASIVE MECHANICAL VENTILATION
indications —severe hypoxemia, acute hypercapnia, need for airway protection (GCS ≤8), impending airway occlusion, therapeutic hyperventilation. In general, intubate if BIPAP contraindicated or failed, or clinical status severe and likely require longer term ventilation
tubes —endotracheal tubes, tracheostomy tubes (see ARTIFICIAL AIRWAYS)
TERMINOLOGY
resistance —restriction that inhibits flow of gas in airways. May result in increased Ppeak or decreased Ve
compliance —ease with which lungs expand. Normal ~50 mL/cm H2O
tidal volume (VT)—amount of air delivered per breath. Normal ~8 mL/kg (500 mL)
minute volume (Ve)—amount of air delivered per minute. Ve (mL/min) = VT × RR
positive end-expiratory pressure (PEEP)—maintenance of positive pressure throughout exhalation. PEEP improves PaO2 mainly by augmenting mean airway pressure. Other potential mechanisms include recruitment of collapsed alveoli, increased functional residual capacity, and improvement in V/Q matching. Usually set at 5–15 cmH2O. >15 cmH2O may cause barotrauma
peak airway pressure (Ppeak)—maximal inspiratory pressure to distend alveoli and to overcome airway resistance. Ppeak is dependent on inflation volume, airways resistance, and lung/chest wall compliance. Happens about halfway through inspiration phase
plateau pressure (Pplat)—pressure to prevent lungs from deflating at end inspiration. Related to lung/chest wall compliance. Limit to ≤30 cmH2O in ARDS
rapid shallow breathing index (RSBI)—index used for weaning/liberation. The lower the better (<70 is excellent, <100 is good). RSBI = RR/tidal volume (measured in liters)
Assessment of Airway
PRIOR TO INTUBATION
—assess airway to anticipate difficulty of procedure, establish IV access (for blood pressure control and medication administration), position patient (sniffing position), remove false teeth/dentures, suction and endotracheal tube ready
SUBJECTIVE SIGNS OF DIFFICULT AIRWAY
—prominent upper incisors, short/thick neck, large tongue, micrognathia
OBJECTIVE SIGNS OF DIFFICULT AIRWAY
neck extension—atlanto-occipital extension ≤35°
thyromental distance —<6 cm [<2.4 in] (3 finger breaths)
mouth opening —<4 cm [<1.6 in] (2–3 finger breaths)
mandibular length —<9 cm [3.5 in]
Mallampati score—III/IV may indicate difficult airway for intubation
I = visualization of the soft palate, fauces, uvula, anterior and posterior pillars
II = visualization of the soft palate, fauces, and uvula
III = visualization of the soft palate and the base of the uvula
IV = soft palate is not visible at all
Artificial Airways
ORAL AIRWAYS
—used in unconscious patients without a gag reflex to prevent airway collapse/obstruction. Also allow access for suctioning and stimulation of cough. Sizes 8, 9, 10 cm in length (Guedel sizes 3, 4, 5). Insert backward along the hard palate and rotate into position. If improperly placed, may push tongue posteriorly and obstruct the airway. Can induce vomiting or laryngospasm if placed in an awake or semiconscious patient
ENDOTRACHEAL TUBES (NEJM 2007 356:e15)
—inserted nasally or orally, with aid of laryngoscope, bronchoscope, or glidescope. Sizes 6.0–9.0 mm in diameter. Cuff occludes airway surrounding endotracheal tube (cuff pressure <25 mmHg ideally; inflate cuff only to the point when leak disappears, i.e. use minimal occlusion pressure to avoid iatrogenic airway ischemia)
TRACHEOSTOMY TUBES
indications —long-term ventilation (>10–14 days intubation), to facilitate weaning, or to bypass an upper airway obstruction
types —Portex, Shiley (fenestrated)
components —fenestrations (openings in tracheostomy tube allowing weaker patients to tolerate plugging trials easier), disposable inner cannula (seal fenestration, allows easier exchange of tracheostomy tube if plugged), cuff (balloon that occludes airway surrounding tracheostomy tube)
plugging procedure —provide alternate source of O2 (via upper airway), suction of upper and lower airways, deflate cuff completely, remove inner cannula if present, insert plug and lock it in place, assess patient for airway patency, increased work of breathing and stridor
decannulation criteria —breathing spontaneously without ventilator assistance, consistent cough and ability to expectorate secretions, airway protected, on minimal FiO2 (<40% or <5–6 l/min), no evidence of upper airway obstruction
TRACHEOSTOMY BUTTONS
—to maintain stoma during weaning. Less resistance than plugged tracheostomy tube. Usually left in for <24 h
Ventilatory Settings
RATE
—minimal respiratory rate. Normal = 8–16
TIDAL VOLUME
—range 5–8 mL/kg of ideal body weight. Normal = 400–600 mL. In volume cycled modes only
PEAK FLOW
—determines how fast a positive pressure breath is delivered. In volume cycled modes only
PRESSURE SUPPORT
—ranges from 6 cm H2O (almost no support) to 30 cm H2O (max). Normal = 14–16 cm H2O. In pressure limited modes only
INSPIRATORY TIME
—determines duration over which the pressure is delivered. In pressure limited modes only
FIO2
—range 0.21–1.0. Normal = 0.4 or to keep SpO2 ≥92%
SENSITIVITY
—determines the degree of patient effort required to trigger a positive pressure breath
PEEP/EPAP
—generally start at 5 cm H2O, max 15–20 cm H2O (usually in ARDS)
VENTILATORY MODES
assist control (AC)—mandatory ventilator controlled breaths at set rate. Patient may breathe spontaneously (i.e. trigger the ventilator, “assist” breaths) but ventilator augments breath to reach fixed volume or pressure (VC or PC)
volume control (VC)—set tidal volume, machine-initiated inspiration
pressure control (PC)—set pressure, machine-initiated inspiration
volume support (VS)—set tidal volume, patient-initiated inspiration (no backup rate, ventilator only boosts airflow to pre-determined volume)
pressure support (PS)—set pressure, patient-initiated inspiration (no backup rate, ventilator only boosts airflow to pre-determined pressure)
synchronized intermittent mandatory ventilation (SIMV)—mandatory positive pressure breaths delivered at a preset rate and breath type (either volume cycled or pressure limited). Any other breaths patient takes are normal spontaneous breaths with or without additional pressure/volume support (i.e. patient determines size of breath)
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