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3 criteria for decision to intubate

1. Failure to maintain or protect airway - pt's ability to swallow/handle secretions

2. Failure of ventilation/oxygenation - clinical status, oxygen saturation, ventilatory pattern

3. Anticipated clinical course and likelihood of deterioration - moderate/high likelihood of predictable airway deterioration or need for intubation to facilitate pt's evaluation and treatment


LEMON mnemonic for evaluation of difficult direct laryngoscopy

L - Look externally for signs of difficult intubation

E-Evaluate 3-3-2 rule

M-Mallampati scale


N-Neck mobility


Cormack and Lehane grading system for glottic view (1-4) during direct laryngoscopy

1 and 2: Vocal cords visualized; high chance of success

3 and 4: Cannot visualize glottic aperture, success less likely


Mallampati scale (class I-IV)

I: visualize soft palate, uvula, fauces, pillars

II: soft palate uvula, fauces

III: soft palate, base of uvula

IV: only hard palate


7 P's of rapid sequence intubation

Paralysis + induction
Placement of tube
Postintubation management


Indications for necessity for pretreatment agents for rapid sequence intubation

1. Reactive airway disease -- Albuterol 2.5mg by nebulizer. If time doesn't permit albuterol, give lidocaine 1.5mg/kg IV

2. CV disease -- Fetanyl 3 µg/kg to mitigate sympathetic discharge

3. Elevated ICP -- Fentanyl 3µg/kg to mitigate sympathetic discharge and attendant rise in ICP

** give 2-3 min before induction and paralysis


Appropriate amount of preoxygenation in RSI

Administration of 100% oxygen for 3 minutes of normal tidal volume breathing in normal healthy adult → adequate oxygen reservoir to permit 6-8min of safe apnea before desat to >90%

If time is insufficient, 8 vital capacity breaths with high-flow oxygen can achieve saturations and apnea times that match traditional preoygenation.


Depolarizing neuromuscular blocking agent used for RSI:

Time to onset?
Side effects?

Succinylcholine 1.5mg/kg
Onset: <45s
Duration: 6-10min
Side effects: Bradycardia (?atropine in peds), hyperkalemia in pts with up-regulation of ACh-receptors, fasiculations/muscle pain masseter spasm, malignant hyperthermia


Conditions associated with hyperkalemia after succinylcholine administration

Burns >10% BSA, >5 days since injury until healed

Crush injury, >5 days since injury until healed

Denervation (stroke, spinal cord injury), >5 days since event until 6mo post injury

Intraabdominal sepsis, >5 days since onset until resolution

NM disease (ALS, MS, MD), onset and indefinitely


Competitive/Non-depolarizing neuromuscular blocking agent used for RSI

Side effects?

Rocuronium 1-1.2 mg/kg
Onset: 60s
Duration: 50min
No real side effects or contraindications.
Long duration of action may not be desirable in pts requiring frequent neuro checks.


Induction agent options for RSI




Side effects?

Etomidate 0.3mg/kg IV
No adverse hemodynamic effects
Decreases ICP, cerebral blood flow without adversely affecting systemic MAP and cerebral perfusion pressure

May ↓ serum coritsol levels transiently and blunt adrenal response to ACTH (?worse survival with sepsis)



Side effects?

Ketamine 1-2mg/kg
Onset: 30s-1min
Duration: 10-15min
Protective airway reflexes and ventilatory drive usually preserved
Good with acute severe asthma.
Less propensity to exacerbate hemodynamic instability
May ↑ cerebral metabolic rate, ICP, CBF
May ↑ BP and catecholamine release - avoid in TBI and HTN
Emergency phenomena



Induction dose?
Side effects?

Propofol 1.5mg/kg IV, reduced in older pts or those with hemodynamic compromise or poor cardiovascular reserve

Can cause hypotension through vasodilation and direct myocardial depression

Delivered in soybean oil and lecithin vehicle - avoid with anaphylaxis to egg proteins

Pain at site of administration - use proximal vein and/or pretreat with lidocaine/opioids/ketamine



Induction dose?

Midazolam 0.2-0.3mg/kg IV
Onset: 30-120s
Duration 15-20min

Negative inotrope; use with caution in hemodynamically compromised and older patients


Precedex (Dexmedetomidine)

Loading dose?

Precedex (Dexmedetomidine)

Loading dose 1mg/kg IV over 5-10min

Minimal effect on respiratory drive or protective airway reflexes

Limited by bradycardia and hypotension


Specific RSI for status asthmaticus

Preoxygenation - ↓ TV and RR to prevent breath stacking

Pretreatment - albuterol 2.5mg nebulized, or Lidocaine 1.5mg/kg IV

Paralysis - Succinylcholine 1.5mg/kg IV
Induction - Ketamine 1.5mg/kg (bronchodilation)


Specific RSI for elevated ICP

Pretreatment - fentanyl 3µg/kg (slowly)

Paralysis - Succinylcholine 1.5mg/kg IV
Induction - Etomidate 0.3mg/kg

Postintubation - Propofol to permit frequent neuro exams


Specific RSI for hypotension and shock

Preparation - Isotonic fluid boluses/blood products

Pretreatment - Phenylephrine HCl (Neosynephrine) 50-100µg IVP (if still hypotensive after IV fluids)

Paralysis - Succinylcholine 1.5mg/kg IV

Induction - Ketamine 0.5-0.75mg/kg OR Etomidate 0.1-0.15mg/kg IV


Cardiovascular effects of positive pressure ventilation (PPV)

PPV → diminished venous return → ↓ cardiac output → ↓ pressure gradient between LV and aorta → hypotension

** may be exaggerated in pts with clinical hypovolemia or vasodilatory states


Pressure controlled ventilation (PCV)

Set parameters?

Variable parameters?

Clinical implications?

Clinical conditions?

Set: Pressure target, inspiratory time, RR, PEEP

Variable: Tidal volume, inspiratory flow rate

Implications: controls airway pressure, but TV becomes function of compliance. Allows estimation of end-inspiratory alveolar pressure based on vent settings. Variable inspiratory flow helpful for pts with high respiratory drive.

Conditions: severe asthma, COPD, salicylate toxicity


Volume controlled ventilation (VCV).

Set parameters?

Variable parameters?



Set: tidal volume, RR, inspiratory flow pattern, inspiratory flow time

Variable: PIP, end-inspiratory alveolar pressure

Implications: guaranteed delivery of tidal volume, but may result in high/injurious lung pressures. End-inspiratory alveolar pressure can't be reliably estimated and must be measured (plateau pressure)

Conditions: ARDS, obesity, severe burns


Ventilator mode: Assist-control (A/C) aka continuous mechanical ventilation (CMV)

Parameters set by provider?

Clinical scenario?

Assist-control (A/C) aka continuous mechanical ventilation (CMV)

Parameters set by provider: Pressure or volume control, RR

Clinical scenario: paralyzed/deeply sedated, sedated pts with intermittent spontaneous respiratory effort; can lead to hyperventilation


Ventilator mode: Synchronized intermittent mandatory ventilation (SIMV)

Parameters set by provider?

Clinical scenario?

Synchronized intermittent mandatory ventilation (SIMV)

Parameters: Pressure or volume control, RR (backup rate)

Scenario: pts with regular but poor spontaneous respiratory effort; if used in deeply sedated pts, set RR will need to be higher


Ventilator mode: Pressure-support ventilation (PSV)

Parameters set by provider?

Clinical scenario?

Pressure-support ventilation (PSV)

Parameters: Level of pressure support, PEEP

Scenario: Spontaneously breathing pts with good respiratory effort requiring minimal ventilatory support


Purpose of PEEP

Adverse effects?

PEEP - positive end-expiratory pressure

Maintains positive airway pressure after completion of passive expiration → ↑ functional residual capacity (FRC) → ↑ oxygenation → ↓ intrapulmonary shnting

Also reduces portions of nonaerated lung that may contribute to development of VILI

PEEP increases intrapulmonary and intrathoracic pressures

Adverse effects: ↓CO, lung overdistention, pneumothorax


Relative contraindications to NPPV

Decreased level of consciousness
Lack of respiratory drive
Increased secretions
Hemodynamic instability
Facial trauma


Initial IPAP and EPAP settings

IPAP 10cm H2O
EPAP 5cm H2O


Effects of increasing IPAP

↑ IPAP → ↓ Hypercarbia

by ↑ tidal volume and minute ventilation


Effects of increasing EPAP

↑ EPAP → ↑ Oxygenation

by ↑ alveolar recruitment and ↓ atelectasis


Initial vent settings for an intubated pt in the ED:


TV 6-8mL/kg of ideal body weight
(if PCV, adjust target pressures to get ideal TV)

RR 12-14/min

Initial pressure targets should not exceed 30cm H2O

FiO2 should be set at 1.0 saturation of 90% or greater

PEEP 5cm H2O


Causes of respiratory distress on ventilator:
Acutely unstable
Improves with removal from ventilator

Likely iPEEP - resume mechanical ventilation with ↓ RR and ↑ expiratory time


Causes of respiratory distress on ventilator:
Acutely unstable
Does not improve with removal from ventilator

Presumptive treatment for tension pneumothorax with needle decompression.
If pt remains unstable, other diagnoses should be pursued, including PE


Causes of respiratory distress on ventilator:
Not acutely unstable
ETT in proper place
PIP elevated
Plateau pressure normal

↑ PIP with normal Pplat = increased airway or circuit resistance

Worsening airway obstruction from underlying pathology
New bronchospasm (e.g. allergic reaction)
ETT obstruction
Ventilator circuit obstructed


Causes of respiratory distress on ventilator
Not acutely unstable
ETT in proper place
PIP elevated
Plateau pressure elevated

↑ PIP with ↑ Pplat = decreased respiratory system compliance

Worsening lung compliance from underlying pathology
Abdominal distension
Inadequate sedation
Ventilatory dyssynchrony


Vent settings for acute COPD exacerbation

Focus: improve gas exchange while minimizing iPEEP

↓ airway resistance with bronchodilators and corticosteroids
Ensure adequate expiratory time by ↓RR, ↓ TV, and ↓inspiratory time
Reduce minute ventilation (permissive hypercapnia)
Inspiratory:expiratory (I/E ratio) should initially set at 1:4
PEEP set at 5cm H2O
Avoid NBMAs + corticosteroids, increased risk for polymyopathy of critical illness and subsequent increased mortality


Vent settings for status asthmaticus

Airway obstruction less dynamic than COPD and predominantly in large airways. Inflammatory changes lead to ↓ lung compliance which has direct impact on lung pressures during ventilation.

Low RR with emphasis on maximizing expiratory time

VCV with TV 6-8ml/kg IBW
RR 10-15/min
PEEP 0-5cm H2O

Decrease inspiratory time by increasing inspiratory flow rate


Vent settings for ARDS

6mL/kg IBW



Loading dose for acute severe pain?

IV vs PO dosing?

Metabolism and metabolites?


Loading dose for acute severe pain: 0.1 mg/kg IV of ideal body weight.

10mg = 50mg PO (20% of ingested morphine reaches tissues after 1st pass metabolism)

Hepatic conjugation to three- and six- conjugation forms.
- Three-conjugate (normorphine) no opioid anagesic activity, rarely assoc with CNS side effects (greatest in older pts with renal insufficiency)
- Six-conjugate - strong mu and delta receptor agonist


Common side effect after infusion of IV opioids?

IV opioids → histamine release from opioid receptors on mast cells → urticaria, pruritus, orthostatic hypotension

** not an allergy



Equivalence to morphine?

Loading dose?




1mg Hydromorphone = 7mg Morphine

Loading dose: 0.015mg/kg

Administered in active form, metabolized to inactive by liver. ** Good for hepatic dysfunction pts because it doesn't require activation by liver.

Inactive form (hydromorphone-3-glucuronide, H3G) renally excreted -- some risk of neurotoxicity after prolonged exposure to H3G accumulation in renal insufficiency patients



Loading dose?

Routes of administration?



Side effects?


Loading dose: 1.5 µg/kg

Administration: IV, transmucosally, transdermally, nebulized/intranasal

Hepatic P450 metabolism into inactive metabolites.

Benefits - short duration (good for frequent/serial examinations), titratable, ↓ bronchospasm

Side effects - more frequently associated with respiratory depression, high/repeated doses → muscle rigidity/ACUTE CHEST SYNDROME (usually with doses > 15µg/kg.

Tx for acute chest syndrome = naloxone, NM blockade may be necessary if not successful



Loading dose?




Loading dose 0.15mg/kg oral

Hepatic metabolism to oxymorphine; strong opioid agonist that principally accounts for its analgesic effects

CYP2D6 metabolism; competes with neuroleptics, TCAs, and SSRIs; may → serotonin syndrome



Loading dose?



Loading: 0.2mg/kg PO

No known neurotoxic/active metabolites. High bioavailability.

Strong opioid agonist, N-methyl-d-aspartate antagonist, SSRI effects.

Slow elimination 1/2 life 2/2 lipophilicity and tissue distribution.

6-8 hours analgesic effect, 24 hours until onset of withdrawal 2/2 biphasic elimination of the drug and its redistribution





Side effects?



Weak mu agonist, some SSRI/SNRI

Should not cause physiologic dependence

CYP450 metabolism to M1 with greater mu receptor affinity

Appears to have effects on GABA, NE and serotonin receptors and reuptake of the neurotransmitters. May → activation of descending pain modulation pathways.

SE: n/v, dizziness, orthostatic hypotension






Analgesia with little/no respiratory depression or abuse potential

Agonist action at kappa receptors + mu antagonist to prevent respiratory depression.


COX 1 inhibition vs COX 2

COX 1 inhibition → ↑ thromboxane inhibition (antiplatelet activity) vs prostacyclin inhibition → CARDIOPROTECTIVE

COX 2 inhibition ↑ prostacyclin vs throboxane → prothrombotic and ↑ CV risk


Pathophysiology of development of ulcers from NSAIDS

COX promotes production of prostacyclin, a vasodilator that increases GI mucosal perfusion

In the stomach, COX 1 increases bicarbonate and mucous production, important for protecting the mucosal lining.

Inhibition of COX 1 compromises these protective functions, predisposing patients to ulcerations and bleeding, which are exacerbated by concomitant NSAID-induced platelet dysfunction.


Pathophysiology of renal insufficiency from NSAIDS

COX 1 produces prostaglandins → renal vasodilation → maintenance of renal blood flow and GFR

Inhibition, especially in volume-depleted patients → ↓ GFR and acute renal insuffiency.

Na and H2O retention, HTN, hyperK, and ARF ensue, particularly in pts with CHF


Drug interactions with NSAIDS (6)

1. ASA - NSAIDs may impair the cardioprotective effect of ASA

2. Oral AC - antiplatelet effects + anticoagulant properties of warfarin compounds risk of significant bleeding complications. NSAIDs also displace protein-bound warfarin and cause subsequent ↑ PT at constant warfarin dose.

3. ACE - may impair renal function and anti-hypertensive effects of ACE

4. Diuretics - ↑ risk of development of renal failure 2/2 NSAID-mediated decreased renal blood flow. Natriuretic response to diuretics also depends in part on prostaglandin-mediated vasodilation.

5. Glucocorticoids + NSAIDS = ↑ risk of PUD

6. Lithium - NSAIDs enhance lithium reabsorption and may ↓ excretion → ↑ lithium levels → CNS symptoms, cardiac dysrhythmias, QRS widening


Cautions with NSAID therapy (6)

1. Pts with dehydration/hypovolemia or impaired renal function are at ↑ risk for ↓ renal function or renal failure

2. Liver disease/CHF - in particular those already on ACE/ARB/diuretic - in whom liver or heart conditions may worsen

3. Older patients with ↑ risk of GI and renal events

4. Pts with asthma and known ASA hypersensitivity are at ↑ risk for bronchospasm

5. Women in 3rd trimester of pregnancy - NSAIDs may prolong gestation or prematurely close ductus arteriosus

6. Patients who use tobacco/EtOH with h/o gastritis or PUD are at ↑ risk for peptic ulcer/GIB


Maximum doses (w/wo epi):



Lidocaine 3-5mg/kg w/o epi, 7mg/kg with epi

Bupivacaine 1.5mg/kg w/o epi, 3mg/kg with


Equipment required for procedural sedation and anesthesia (8)

1. High-flow O2 source
2. Suction
3. Airway management equipment
4. Monitoring (pulse ox, ECG monitor, defibrillator, transcutaneous pacer, BP monitor, capnography)
5. Vascular access equipment
6. Reversal agents
7. Resuscitation drugs
8. Adequate staff


Pathogenesis of hemorrhagic shock

Rapid ↓ in intravascular blood volume → ↑ in strength of cardiac contraction and HR → baroreceptor activation and peripheral vasoconstriction

Typically slight ↑ in DBP → ↓ PP → ↓ ventricular filling and CO → ↓ SBP

Blood flow directed away from non-critical organs/tissues → production of lactic acid (Acidemia precedes any significant ↓ in CO)

Hypotension + overwhelmed buffering mechanisms → acidosis → activation of HPA axis → stress hormone release → glycogenolysis, lipolysis, mild hypokalemia


Expected labs in hemorrhagic shock --


Lactate <4
PaCO2 <35
Mild hyperglycemia (150-170)
Mild hypoK (3.5-3.7)

** Although hemorrhagic hypotension reduces lung perfusion, arterial hypoxemia shouldn't be attributed to blood loss


Second phase of organ injury from hemorrhagic shock

Occurs during resuscitation

Acute phase of hemorrhage initiates inflammatory cascade. Resuscitation unleashes volatile inflammatory mediators on the body → organ injury

During resuscitation, neutrophils become more aggressive → bind to lung endothelium → capillary leakage → ARDS


Three major phases of septic shock that must be addressed by resuscitation

1. Hypovolemia
Absolute -- GI loss, tachypnea, sweating, ↓ fluid intake
Relative -- ↑ venous capacitance + ↑ capillary leak and resultant loss of intravascular volume into third spaces

2. Cardiovascular depression - cardiac contractility and mechanical function becomes impaired early in the course of septic shock, even in hyperdynamic stages

3. Induction of systemic inflammation - circulating mediators, myocardial cellular injury from inflammation, and deranged metabolism interact synergistically to injure heart during septic shock


Cardiogenic shock


>40% of the myocardium becomes dysfunctional from ischemia, inflammation, toxins, or immune injury

** When shock results from pure cardiac cause, severe LV dysfunction will be evident on echocardiography early in the course


Neurogenic shock

Interrupted sympathetic and parasympathetic input from the spinal cord to the heart and peripheral vasculature

Typically results from acute traumatic injury

Described as peripheral vasodilation + bradycardia

Although, ED pts with shock from acute spinal injury may manifest range of HR and pVR, most likely dt variable location of the injury and balance between disrupted efferent sympathetic and parasympathetic tone


Empiric criteria for diagnosis of circulatory shock (6)

Four criteria must be met:

1. Ill appearance or AMS
2. HR >100bpm
3. RR >20 or PaCO2 <32
4. Arterial base deficit 4
5. Uop <0.5mL/kg/h
6. Arterial hypotension >30 min duration, continuous


Definition/Criteria for septic shock (SIRS → Severe sepsis → Septic shock)

2+ of the following:
- Temp >38°C or <36°C
- HR >90
- RR > 20 or PaCO2 <32
- WBC > 12 or <4 or >10% neuts

Severe Sepsis:
SIRS + confirmed infection + assoc organ dysfunction (lactic acidosis, oliguria, AMS) or hypotension

Septic Shock:
Severe Sepsis + hypotension despite adequate fluid resuscitation requiring vasopressor support


Definition/criteria of hemorrhagic shock (Simple hemorrhage → hemorrhage + hypoperfusion → hemorrhagic shock)

Simple Hemorrhage: suspect bleeding with HR <100bpm, normal RR, normal BP, normal base deficit

Hemorrhage + Hypoperfusion: suspect bleeding + base deficit 100

Hemorrhagic shock: suspect bleeding with at least 4 of the following:
- Ill appearance/AMS
- HR >100
- RR >20 or PaCO2 <32
- Base deficit 4
- Uop < 0.5ml/kg/h
- Hypotension >30min, continuous


Definition/criteria for cardiogenic shock (cardiac failure → cardiogenic shock)

Cardiac failure: clinical evidence of impaired forward flow of the heart -- dyspnea, tachycardia, pulmonary edema, peripheral edema, cyanosis

Cardiogenic shock:
Cardiac failure + at least 4 of the following:
- Ill appearance/AMS
- HR >100
- RR >20 or PaCO2 <32
- Base deficit 4
- Uop < 0.5ml/kg/h
- Hypotension >30min, continuous


Clinical management guidelines for hemorrhagic shock (6)

1. Ensure adequate ventilation and oxygenation

2. Provide immediate control of hemorrhage when possible, obtain urgent consultation as indicated for uncontrollable hemorrhage

3. Judicious infusion of isotonic crystalloid (10-20mL/kg)

4. With evidence of poor perfusion + 30min anticipated delay to hemorrhage control, begin PRBCs (5-10mL/kg)

5. With suspected massive hemorrhage, immediate PRBC transfusion may be preferable as initial resuscitation fluid.

6. Treat coincident dysrhythmias (eg Afib, with synchronized cardioversion)


Clinical management guidelines for cariogenic shock (4)

1. Ameliorate ↑ work of breathing; provide oxygen and PEEP for pulmonary edema

2. Begin vasopressor or inotropic support; NE (0.5 µg/min) and dobutamine (5 µg/kg/min) are common empirical agents.

3. Seek to reverse insult (eg thrombolysis, percutaneous transluminal angioplasty)

4. Consider IABP conterpulsation for refractory shock


Clinical management guidelines for septic shock (4)

1. Ensure adequate oxygenation; remove work of breathing

2. Administer 20mL/kg of crystalloid, or 5mL/kg of colloid (albumin), and titrate based on dynamic indices, volume responsiveness, and/or Uop

3. Begin antimicrobial therapy; attempt surgical drainage or debridement

4. Begin PRBC infusion for Hgb <7.

** If volume restoration fails to improve organ perfusion, begin vasopressor support with NE, infused at 0.5 µg/min


Initial volume replacement in shock

Rapid infusion of 20-25mL isotonic crystalloid per kilogram


Indications for administration of blood products

In setting of hemorrhage or Hgb <7 + criteria for shock despite crystalloid infusion, transfuse 1-2U PRBCs in adults or 5-10ml/kg in children.

** Fully crossmatched preferred, unless pt's need considered sufficiently urgent to justify uncrossed - usually those with hemorrhagic shock with persistent severe hypotension and massive/uncontrolled hemorrhage
** O-neg in all women of childbearing age, O-pos in everyone else
** If pts require >2U, do balanced resuscitation of PRBCS:FFP:plts in 1:1:1 ratio



Head CT:
Compressed basal cisterns
Diffuse sulcal effacement
Diffuse loss of differentiation between gray/white matter

Elevated ICP


Initial management of elevated ICP --


MAP >65
CPP 50-70
ICP <20


Methods to manage elevated ICP (8)

1. Elevate head of bed by 30°
2. Maintain neutral head and neck position to avoid jugular venous compression
3. Treat fever
4. Minimize triggers of ↑ ICP -- treat pain (fentanyl 25-50 µg q5min PRN), cough/bucking of vent (propofol → ↓ cerebral metabolic activity → ↓ CBF, rapidly clears for neurologic assessments
5. Initiate osmolar therapy (mannitol 0.5-1g/kg q6h, 30mL of 23.4% NS q6h to max serum Na 160)
6. Treat refractory ↑ ICP not amenable to previous therapies -- Barbiturates (pentobarbital 10mg/kg loading dose x1h → 0.5-1mg/kg/h to get EEG suppression -- often requires vasopressors to maintain adequate CPP
7. Mild induced hypothermia (temp 32°-36°C) and avoid rapid rewarming
8. Surgical treatment (decompressive craniectomy and evacuation of intracranial hematoma, hemicraniectomy)


Evidence based guidelines for cooling of unconscious adult patients after cardiac arrest

33° for 12-24h

** 2 multicenter prospective, RCTs of mild hypothermia have shown marked improvements in neurologic outcome in comatose survivors of out-of-hospital cardiac arrest.

NNT to have 1 additional pt with good neurologic outcome was only about 7


Indicators of adequate blood flow during CPR:

Palpable carotid/femoral pulse

Coronary perfusion pressure > _____?

Arterial relaxation (diastolic) pressure > ______?

Partial pressure of CO2 in exhaled air at the end of expiration (PETCO2) > _____?

Central venous oxygen saturation > ______?

Palpable carotid/femoral pulse

Coronary perfusion pressure > 15mmHg

Arterial relaxation (diastolic) pressure > 20-25mmHg

Partial pressure of CO2 in exhaled air at the end of expiration (PETCO2) > 10mmHg

Central venous oxygen saturation > 40%


Utility of PETCO2 during CPR

What value is desired?

PETCO2 - partial pressure of exhaled air at end of expiration

Reliable indicator of CO during CPR

Depends on CO2 production, alveolar ventilation, and pulmonary blood flow (i.e. CO), and correlates well with coronary and cerebral perfusion pressure during CPR

When minute ventilation is constant and no exogenous CO2 is introduced (eg no NaHCO3), only ↑ CO during CPR and ROSC significantly increase PETCO2

** Resuscitation after cardiac arrest is likely to fail if PETCO2 values of 10mmHg or more are not achieved during CPR.


Utility of SCVO2 during CPR

What value is desired?

SCVO2 - Central venous oxygen saturation

Represents oxygen remaining in blood after systemic extraction.

Oxygen consumption, SaO2, Hgb remains relatively constant during CPR, therefore changes in SCVO2 reflects changes in O2 delivery by means of changes in CO.

Normal SCVO2 is 60-80%
During cardiac arrest/CPR, SCVO2 25-35% due to greatly enhanced oxygen extraction of tissues owing to inadequacy of oxygen delivery during CPR.

SCVO2 also detects ROSC rapidly without interruption of chest compressions, bc ROSC will result in rapid increase in SCVO2 as O2 delivery to tissues dramatically increases

** Failure to achieve SCVO2 of >40% during CPR has NPV for ROSC of almost 100%


Definition of PEA

Causes of PEA

PEA = pulseless electrical activity -- coordinated electrical activity of the heart (other than VT or VF) without palpable pulse.

True electromechanical dissociation (EMD) - no myocardial contractions
Pseudo electromechanical dissociation (pseudo-EMD) - myocardial contractions occur, but are inadequate and no pulse can be palpated


True electromechanical dissociation (EMD)

Appearance on monitor?
Possible causes?

True EMD:
Primary disorder of electromechanical coupling in myocardial cells.

Abnormal automaticity and conduction → bradycardia and wide QRS

Mechanism of uncoupling is unclear, but usually associated with global myocardial energy depletion and acidosis resulting from ischemia or hypoxia.

Typically occurs after defibrillation following prolonged VF and is associated with:
- Hyperkalemia
- Hypothermia
- Drug overdose


Pseudo-electromechanical dissociation (pseudo-EMD)

Possible causes?

Appearance on monitor?

Electromechanical dissociation in which myocardial contractions occur but are inadequate.

- Global myocardial dysfunction, progression to true-EMD
- Papillary and myocardial wall rupture; ventricle continues to contract but forward flow is greatly diminished
- Primary SVT
- Hypovolemia
- Tension PTX
- Pericardial tamponade
- Massive PE

Extra-cardiac origin often has narrow complex tachycardia initially, may progress to bradycardia, with conduction abnormalities and wide QRS


Treatment of cardiac arrest

Vasopressors and doses?

Epinephrine 1mg IV/IO q3-5 min
Subsequent doses may be increased up to 0.1mg/kg

Vasopressin 40U IVP
Repeat x1 in 3min, followed by epi q3-5min


Treatment of cardiac arrest

Antiarrhythmics, doses, and when to use?

Amiodarone 300mg IVP simultaneous with epinephrine
Followed by 150mg q30min

Lidocaine if amio not available

** Use with VF/VT


Treatment of cardiac arrest with Torsades de pointes

Magnesium sulfate 1-2g IVP


Unilateral weakness:

Combination of arm/hand/leg with IPSILATERAL facial involvement


Arm/hand/leg with CONTRALATERAL facial involvement

Ipsilateral facial involvement = lesion in contralateral cerebral cortex or CSTs coursing down the corona radiata and forming the internal capsule.

Contralateral facial involvement = brainstem lesion


Short-lived (<30sec), positional, fatiguable, associated n/v.

precipitated by certain positions.
+ Hallpike or supine roll test

Benigh paroxysmal positional vertigo (BPPV)


Develops suddenly or evolves over several hours, usually increasing in intensity, then gradually subsiding over several days, but can last weeks. Can be worsened with positional change. Sometimes recent h/o viral infection. Highest incidence in 3rd-5th decades. Associated n/v.

PE: Spontaneous nystagmus beating away from side of lesion in 1st few hours. + Head impulse test. +/- hearing loss.

Vestibular neuritis (normal hearing)

Labyrinthitis (hearing loss)


Recurrent episodes of severe rotational vertigo, usually lasting hours. Abrupt onset. Attacks may occur in clusters. Long symptom-free remissions. Associated n/v, tinnitus, hearing loss.

Hearing loss
Positional nystagmus not present

Meniere's disease


New onset in pt with advanced age without obvious cause. H/o atherosclerosis. +/- neck trauma. Associated HA, neuro symptoms including dysarthria, ataxia, weakness, numbness, double vision. Tinnitus and hearing loss uncommon.

Vertebrobasilar insufficiency


Sudden onset, associated HA, vomiting, ataxia.

Dysmetria, true ataxia. Ipsilateral CN VI palsy may be present

Cerebellar hemorrhage


+ significant neuro complaints. Assoc n/v, loss of pain/temp sensation, ataxia, hoarseness.

PE: loss of pain/temp sensation on the side of the face ipsilateral to the lesion and on the opposite side of body. Paralysis of palate, pharynx, larynx. Horner's syndrome (ipsilateral ptosis, miosis, and ↓ facial sweating)

Occlusion of posterior inferior cerebellar artery (Wallenberg's syndrome)


Hallpike test

Confirms diagnosis of posterior canal BPPV

Pt sitting up, turn head 45 degrees to one side, then move to supine position with head overhanging edge of gurney.

Pt is queried for occurrence of vertigo and eyes observed for nystagmus after latency period for a few seconds.

Classic posterior canal BPPV: nystagmus 5-30sec and is combinded upbeating and ipsilateral torsional.

Pt brought back up to seated position and repeat with head to other side.

**downward ear indicates involved side



Head Impulse - rapidly turn head approx 10 deg to one side. Normal pts keep focused on examiner, if problem with vestibular nerve, eyes temporarily move along with the head and corrective saccade back to midline. (reassuring for vestibular neuritis)

Nystagmus - direction change of nystagmus on eccentric gaze. E.g. when pt looks to the left, fast component beats to the left, when to the right the fast component beats to the right. (direction changing nystagmus may indicate stroke)

Test of Skew - vertical ocular misalignment during alternate cover testing (suggests brainstem stroke)