Critical care Flashcards
Give an approach to the various types of shock based on pathophysiology
1.

What are the main causes of distributive, hypovolemia, cardiogenic and obstructive shock?

What are the normal values for mixed venous gas and central venous gas?
- Central venous gas: 60-65%
- Mixed venous gas: 65-70%
What is the expected central venous gas in sepsis
High flow state: >80%
What is the expected central venous gas in cardiogenic shock
<65%, poor forward flow
What is the definition of SIRS based on the SIRS criteria?
- 2/4:
- WBC >12 or <4 or >10% bands
- Temp >38 or <36
- HR>90
- RR>20 or PCO2<32
What is the definition of sepsis based on the SIRS criteria?
SIRS + Infection
What is the definition of severe sepsis based on the SIRS criteria?
- Sepsis+end organ dysfunctin
- End organ dysfunction
- AKI
- Hypotension
- Shock liver
- high lactate
- Decreased LOC
- End organ dysfunction
What is the definition of septic shock based on the SIRS criteria?
- BP not responsive to 30cc/kg of IVF challenge and requiring vasopressors
What is the definition of sepsis as per qSOFA?
- 2/3 of :
- RR>22
- SBP<100
- Changes in LOC
What is the mortality in qSOFA sepsis?
10%
What is the definition of septic shock based on qSOFA
- Requries both
- Lactate >2
- Pressors required to keep MAP >65 despite adequate fluid resuscitation
What is the mortality in qSOFA septic shock
35-40%
Which criteria should be used, SIRS or qSOFA
Neither is particularly helpful on its own. Can both be used to alert clinicians
Use a combo of both scores + Lactate + clinical acumen
What test can be done to help rule in and rule out sepsis/septic shock
Lactate
Within what timeline should a patient with septic shock be admitted to the ICU if it is deemed that they need ICU level care?
6 hrs
*Associated with decreased mortality, increased proper treatment, reduced ventilation and shorter ICU and hospital LOS
What should be done within 1 hour of presentation to triage in patients with sepsis and septic shock?
- Measure lactate. Repeat in 2-4hrs if >2
- Obtain cultures (ideally before ABx
- Administer broad-spectrum ABx
- Begin rapid administration of at least 30mls/kg (IBW) cristalloids within 1st 3hrs
- Apply vasopressors for MAP≥65 if hypotensive
What should you do if you suspect sepsis but can’t confirm an infection
- If sepsis is suspected/likely
- Give antibiotics within 1hr
- Rapid assessment of infectious and non-infectious etiologies
- D/C ABx if alternate diagnosis is made
- If sepsis is “possible” and patient is not in shock
- Do rapid investigations for diagnosis
- Can delay antibiotics up to 3hrs while you decide if this is septic
- Constant reassessment
- Do not use procalcitonin
How can you predict fluid responsiveness?
- Dynamic assessment
- Passive leg raise
- Fluid bolus challenge
- Pulse pressure variation
- SV or SVV
- IVC
- Intubated + ventilated: distensibility index >15-20% predicts fluid responsiveness
- Intubated + breathing spontaneously: cannot use
- Not intubated: IVC<2cm with >50% variation predicts fluid responsiveness
- Lactate level
- Cap refil
- Abnormal >3 sec
Which fluid should be used for rescucuitation
- Balanced cristalloids
- Albumin if patient receives large volumes of IVF
In what order should you add vasopressors in septic shock?

When should steroids be started in septic shock
Norepi or epi ≥0.25 mcg/kg/min for ≥4hrs
What dose of steroids should be used for septic shock?
- Hydrocortisone 50mg IV q6 OR continuous infusion 200mg over 24hrs
After what time does mortality increase if source control is not achieved in septic shock?
6-12 hrs
When should patients with septic shock be transfused
Hb<70
What should be done for DVTp in septiic shock
LMWH>UFH for all unless CI
When should ulcer prophylaxis be considered in patients with septic shock?
- Coagulopathy
- Shock
- Liver disease
- Intubated patients
What are the BG targets in septic shock and what should be done if BG is elevated
- 8-10
- if above 10 give insulin
what is the indication for Bicarb in septic shock
- pH≤7.2 and AKI (AKIN score 2 or 3)
- *Do not give bicarb to improve hemodynamics or reduce pressor requirements in hypoperfusion-induced lactic acidosis
When should feeds be considered in septic shock patients?
- Within 72hrs
- Not if escalating pressor requirements
What are treatments to avoid in septic shock
- Ig
- Polymyxin
- Vitamin C
- Angiotensin II
- APC
- Liberal oxygen
What are the indications for HFNC?
- Should probably be used for
- Over conventional O2 therapy or NIV for type 1 resp failure
- Over COT for NIV breaks
- Over COT in non-surgical patients after extubation when they are at low/mod risk for extubation failure
- Use HFNC or COT in post-op patients at low risk of resp complications
- HFNC or NIV in post op patients at high risk for resp complications
When should HFNC probably not be used?
- After extubation for patients at high risk of extubation failure
- Acute hypercapnic resp failure 2/2 COPD (trial of NIV before HFNC)
Compare and contrast CPAP and BIPAP

When should NIV definitely and probably be used?
- Definitely
- Mild-severe acidotic COPD patients
- RR> 20-40
- pH<7.35
- PaCO2≥45
- Cardiogenic pulmonary edema
- excluding cardiogenic shock and acute MI
- Mild-severe acidotic COPD patients
- Probably
- Prophylaxis for post-extubation resp failure in high risk patients
- High risk = ≥65 with underlying cardiac disease or resp failure
- Post-op patients with ARF
- Palliative patients if dyspneic from terminal cancers
- Immunocompromised patients with ARF
- Prophylaxis for post-extubation resp failure in high risk patients
When should NIV probably not be used?
- Failed extubation
- prevention of hypercapnia in COPDe
In what conditions are there no recomendations regarding NIV?
- Asthma exacerbation
- De novo resp failure
- Hypoxemia NYD
- ARDS
List contraindications to NIV
- Facial surgery, trauma, obstruction
- Decreased LOC *relative
- Inability to clear secretions
- Respiratory arrest
- HD instability (reduces preload)
- Indication for intubation (e.g. airway protection)
*remember that it is an AGMP
What surgeries are eligible for NIV
- Supra-diaphragmatic surgery
- GI surgery
- Pelvic surgery
*Ask surrgeon first (? anastomotic leak concern)
What are the diagnostic criteria for ARDS?
- Timing- within 1 week of known clinical insult
- Origin oof the edema-Not explained by heart failure or fluid overload
- CXR-Bilateral opacities not fully explained by effusions, lobar/lung collapse or nodules
-
Severity *All with PEEP<5*
- Mild PF 200-300
- Mod PF 100-200
- severe PF<100
How should vent settings be set in ARDS?
- Select volume control
- Tidal volume 6ml/kg PBW
- If PPlat>30mmhg devrease TV to 4-5
- Set RR to maintain minute ventilation
- Maintain pH 7.3-7.45
- do not exceed 35 bpm
- Dont let CO2 get under 25
- Set I:E ration 1:1 -1:3
- Change if breath stacking or CO2 retention)
- Set PEEP and FiO2 to maintain sats 88-95 or PaO2 55-80 using PEEP table

How can you manage refractory hypoxia in ARDS
- Optimize lungs
- Diuresis
- R/O PNA
- R/O pneumothorrax
- Optimize PEEP
- Off load lungs
- NG To succion
- Elevate head of bed
- Increase sedation
- Prone patient
- Consider if P:F<150
- Consider paralysis
- Recommended against if ventilation not optimized, mild ARDS, achieving lung protective ventilation
- Consider inhaled NO
- No mortality benefit
- May improve oxygenation
- Bridge to transplant?
- ECMO
- Call and ask
- Steroids
- Depends on the situation
Do not give statins or do high frequency oscillation
When should O2 be started in covid patients
SpO2 < 92-90
In COVID PNA, SpO2 should be maintained no higher than ?
96%
What should you do in patients with COVID who are hypoxic despite COT
HFNC
*NIV reasonable if no HFNC
How should COVID pneumonia be treated
Same as ARDS
What are the indications for Dexamethasone in COVID
If requiring O2/hospitalized/intubated
What are the indications for Remdesivir in COVID
Requiring O2 but not intubated
What are the indications for Tocilizumab in COVID
If requiring O2/intubation with systemic inflammation (CRP>75) and worsening despite 24-48hrs of steroids
Shoould antibiotics be started empirically in convid pneumonia?
No
What are the steps to follow in cases of acute desaturation of a ventilated patient in the ICU?
- Check the vent: Are connections intact, is the O2 connected
- Disconnect ETT from vent and bag ventilate
- Increased resistance?
- Airway=blocked ETT
- Airspace= Pus, blood, water, cells, proteinn
- Pleura=pneumothorax, effusion, hemothorax
- Vascular=PE
- Increased resistance?
- Deep succionn
- Auscultate and ensure trachea is midline
- Check other vitals
- R/O hypoperfusion (hypoTn? tachycardia?)
- CXR
- Review Hx
- New line=R/O pneumothorrax
- New blood transfusion= R/O TACO TRALI
- ACS/bolus=R/O pulm edema
- No DVT Px= R/O PE
What is found on physical exam in the case of a migrated ETT
- Left trachea displacement
- R if mainstem intubation
- Air entry decreased on L
- Percussion decreased on L
What is found on physical exam in the case of pneumothorax
- Trachea displaced away from affected lung
- Air entry decreased on affected siide
- Percussion increased on affected side
- Possible subQ emphysema if trauma involved
What is found on physical exam in the case of a collapsed lung?
- Trachea displaced towards the affected lung
- Air entry decreased on the affected side
- percussion decreased on the affected side
How is the intrinsic PEEP measured
end expiratory breath hold
How is gas trapping detected
- Flow curve doesn’t come back to 0 before next breath
- Volume curve doesn’t come back to 0 before next breath is given
- Higher PIP and PPlat
What are signs and symptoms of gas trapping in patients on a ventilator?
- Increased WOB
- Wheeze
- Increased chest distention
- Decreased chest expansion
- Bilateral decreased air entry
- Increased CO2
- Increased intrathoracic pressures
- Decreased venous return and HD instability
List causes of gas trapping
- Machine factors
- Kinked ET tube
- ETT clogged by sputum
- Patient biting on ETT
- Vent settings
- High RR
- High I:E ratio
- Patient
- Bronchospasm
- Increased RR
How is gas trapping managed?
- Patient changed
- Reverse anything reversible
- Bronchodilators, steroids…
- Suction ETT and ensure it is patent
- Reverse anything reversible
- Vent changes
- Longer I:E ratio
- lower RR
- Dectrease Vt
- Apply PEEP to counter the increased WOB
- Last line measures
- Disconnect vent and press on chest
- Heliox
- ECCOR2
- High frequency oscillation
List the procedure (in 5 stages) of extubation management

What should be the RASS targets in ventilated patients
-2 to +1
What medications should preferentially be used to sedate patients in the ICU
- Propofol
- dexmedetomidine
*Dont use a benzo
How should delirium be prevented in the ICU
- Non-pharm
- Optimize sleep, mobility, hearing, vision
- Reorientation (clocks in the room)
How should delirium be managed in the ICU once it is present?
- Use non-pharmacological interventions
- Reduce modifiable risk factors (i.e. minimize benzos and trransfusions)
- Improve cognition
- Optimize sleep, mobility, hearing, and vision
- Do not use atypical antipsychotics, Haldol or a statin to treat delirium
- Exceptions (for haldol or an atypical antipsychotic)
- Significant distress secondary to symptoms of delirium
- Agitation at risk of harming themselves
- Exceptions (for haldol or an atypical antipsychotic)
What is the best medication to use for agitation preventing weaning and extubation?
Dexmedetomidine
What interventions and medications can be used for sleep in the ICU?
- Non-pharm
- Ear plugs
- eyeshades
- Relaxing music
- Avoid sleep disruptions
- No recommendations on melatonin or dexmedetomedine
- DO NOT use propofol for sleep
What can be used for pain treatment in the ICU
- Utilize good pain practicies
- Acetaminophen, NSAIDs if appropriate
- Opioids
- Adjuncts
- Low dose ketamine
- Lidocaine
- Neuropathic pain
- Gabapentin
- Pregabalin
- Carbamazepine
- Regional anesthesia adjuncts
- Epidural anesthesia for trauma, laparotomy
- Peripheral nerve block for trauma
What elements of the history should be obtained in a patient with a suspected OD?
- What did the patient take?
- How long ago?
- How much
- Co-ignestions
- EtOH
- ASA
- Acetaminophen
- Environmental exposures: CO risk factors
What should be checked for on physical exam in a suspected OD?
- look for toxidromes
- Vitals, GCS
- Pupils
- Skin
What stat investigations should be sent when suspecting an overdose NYD?
- CBC. lytes, extended lytes, bic, Cr, LFTs, CK, troponins, glucose
- ABG, lactate
- Serum osmolality, urea
- beta-HCG
- Urine/serum tox
- ALWAYS ask for EtOH, ASA, Aceta
- 12-lead ECG
- UA (pH), R+M (cristals)
- Consider CT head
How is an anion gap calculated
Na-Cl-bicarb
How is an osmolar gap calculated?
Sosm-Cosm
What is the formula to calculate Cosm?
2Na+gluc+BUN
What is the management of OD NYD?
- ABC, IV, Continuous cardiac monitor, O2, foley
- C-Colar if unwitnessed LOC
- Consider DONT
- Dextrose
- Oxygen
- Naloxone
- Thiamine
- Toxicity specific treatment
- Decrease absorption
- Increase elimination
- Antidote
- Always call poison control and psychiary
What are the signs and symptoms of TCA overdoses
- CVS
- Hypotension
- Arrhythmias
- sinus tach
- As QRS widens VT/VF
- CNS
- Decreased LOC
- Agitation
- Psychosis
- Delirium
- Seizures
- Anticholinergic toxicity
- red as a beet
-
dry as a bone
- Urinary retention
-
mad as a hatter
- Sedation, confusion, delirium, hallucinations
-
blind as a bat
- mydriasis: dilated pupils not responding to light
-
hot as a desert
- hyperthermic
-
stuffed as a turnip
- Absent bowel sounds
- seizures
What are the lab findings in TCA overdose
- TCA level not usefull
- Resp acidosis from decreased LOC
- ECG changes
What ECG changes are associated with TCA overdoses?
- QRS > 100
- >100 26% get seizures
- >160 50% get arrythmias
- Tall R wave in AVR
- Deep slurred S in 1 and AVL
- R/S ratio >0.7 AVR
- Type 1 Brugada
- RBBB
- Downsloping ST depression in V1-V3
How are TCA overdoses generally managed?
- Decontamination
- Consider activated charcoal if present within 1-2 hrs unless decreased LOC, gut perforation, bowel obstruction
- No increased elimination
- No antidote
When should a person be intubated following a TCA OD?
- GCS≤8
How should seizures be treated following TCA OD
- Ativan, diazepam. Midaz infusion if refractory
- Propofol infusion if refractory
- Then barbituates
- Do not use phenytoin, increases toxicity
How should hypotension be treated following TCA OD
- NS or bicarb bolus
- Norepi or phenylephrine if refractory
How should wide complex tachycardia be treated following TCA OD
- Sodium bicarb IV bolus. If narrows, start infusion
- If fails, give MgSO4
- If fails give lidocaine
- If fails and unstable, lipid emulsion
What are the indications for bicarb in TCA OD? What pH should be targetted
- QRS > 100
- Ventricular arrythmia
- hypotension
Target pH 7.50-7.55
In what is ethylene glycol and methanol found
- Antifreeze
- Wiper fluid
- cleaners
- fuels
- moonshine
- solvents
- hastily made “alcohol based hand sanitizers”
What are symptoms and signs of ethylene glycol toxicity?
- Decreased LOC
- Frank hematuria, flank pain, oliguria
- Oxalate cristals
- HypoCa
- Cranial nerve palsies
What are symptoms and signs of methanol toxicity?
- Decreased LOC
- Retinal injury leading to blindness
- Afferent pupillary defect
- Mydriasis
- Retinal sheen
- Hyperemia of the optic disc
What happens to the AG and the OG over time in alcohol toxicity

Which toxins give you a high anion gap and a normal osmolar gap
- Ketones
- Tylenol
- Salicilate
- Lactic acidosis
Which toxins give you a high AG and OG?
- Ethylene glycol
- Methanol
- Ethanol
- DKA
- Propylene glycol
- ESRD with no HD
Which toxins give you a normal AG and a high OG?
- Isopropyl alcohol
- Ethanol
- Severe hyperproteinemia, hyperlipidemia
How are toxic alcohol intoxications treated?
- Decontamination
- No role
- Elimination
- Bicarb
- Acidemia allows toxic metabolites to penetrate tissues
- Aim for pH 7.35
- Bicarb
- Inhibition of alcohol dehydrogenase
- Fomipezole or ethanol
- Blocks the conversion of alcohols to their toxic metabolites
- Fomipezole or ethanol
- Hemodialysis
- Clear the alcohol and their metabolites
What are the indications for fomipezole in toxic alcohol OD?
- Serum methanol >6.2 or ethylene glycol > 3.2
- Documented or recent Hx of ingestion of toxic amounts of methanol or ethylene glycol + osmolar gap >10
- Suspicion of ingestion and 2 of the following
- pH<7.3
- Bicarb<20
- OG>10
- Urine oxalate cristals
What are the indications for HD in patients with toxic alcohol toxicity
- Any end organ damage
- Coma
- seizure
- Visual defects
- renal failure
- pH≤7.15
- persistent metabolic acidosis
- High AG metabolic acidosis
- Very high level of parent alcohol
What levels of ethanol are considered toxic?
4-10
How is EtOH intoxication taken into account in the OG
Cosm=2Na+gluc+BUN+(1.25xEtOH)
How is isopropyl alcohol intoxication treated?
Treatment is supportive only
List sources of salicilate

What symptoms are associated with salicilate toxicity

What are the laboratory values in Salicilate toxicity
- Toxicity with levels >2.9-3.6
- ABG/VBG
- First resp alkalosis because of direct stimulation of the resp centre
- Then AG metabolic acidosis because of uncoupling of oxidative phosphorylation
- Common to see a mixed acid-based disturbance
What should be considered if respiratory acidosis is present in salicilate toxicity
- ALI
- CNS depression
- Mixed OD
- Benzos
- EtOH
How is salicilate toxicity treated
- Decontaminate
- Activated charcoal within 2 hrs if not somnolent
- Can consider whole bowel irrigationfor massive ingestion, enteric coated tabs, bezoar (ask poison control)
- Enhanced elimination
- Alkalanize urine and blood
- Blood pH7.4-7.5
- Do not go above 7.55 and urine pH 7.5-8
- Use bicarb bolus and infusion
- Watch lytes (K, Ca, Na)
- Correct hypokalemia before alkalinization
- Blood pH7.4-7.5
- Alkalanize urine and blood
- HD
When is HD indicated for salicilate toxicity?
- levels >7.2 with normal kidney function
- Hypoxemia requiring supplemental O2
- a change in mental status
- Renal failure (and levels >6.5)
- Progressive deterioration of vital signs
- Severe acid-base or electrolyte imbalance despite appropriate treatment (pH<7.2)
- Hepatic compromise with coagulopathy
- Volume overload preventing the administration of Bicarb
What two main toxidromes cause hyperthermia
NMS
SS
What are the signs and symptoms of serotonin syndrome
- Autonomic
- Tachycardia
- hypertension
- Vomit
- fever
- diarhhea
- diaphoresis
- Neuromuscular hyperactivity
- tremor
- rigidity (lower>upper)
- Myoclonus
- hyperreflexia
- bilateral babinskis
- Occular clonus
- Change in mental status
- anxiety
- agitation
- restlessness
- disoriented
What are the signs and symptoms of NMS?
- Tetrad:
- Fever (temp>38, can be >40)
- Autonomic -Tachy, labile BP, arrhythmia, diaphoresis
-
Rigidity - lead pipe, cogwheel
- no clonus
- hyporeflexia
- Mental status change - agitated, delirium, catatonia, coma
Compare and contrast the time of onset and duration of serotonin syndrome and NMS
- SS
- Onset within 24hrs
- Off after 24hrs
- NMS
- Onset days to weeks
- off after 2 weeks
What medications cause serotonin syndrome?
- SSRIs, SNRI, TCAs, NDRIs
- Acetaminophen, cocaine, MDMA, levodopa
- Tramadol, meperidine
- St. John’s wart, Valproic acid
- MAOI
- Direct serotonin agonists
- Triptans
- Ergots
- Fentanyl
- buspirone
What medications cause NMS
All classes of neuroleptic drugs
Antiemetic agents (domperidone, metoclopramide, prochloperazine)
What are the diagnostic criteria for serotonin syndrome?
- Hunter criteria
- Serotoninergic agent and one of:
- Spontaneous clonus
- Ocular clonus
- Inducible clonus+diaphoresis or agitation
- Tremor + hyperrreflexia
- Hypertonic + temp>38+occular or inducible clonus
- Serotoninergic agent and one of:
What are the diagnostic criteria for NMS?
Noone exist
How is serotonin syndrome treated?
- Stop the offending agent(s)
- Support
- Sedate with benzos
- Eliminate agitation, hypertonia, normalize vitals
- Cyproheptadine if benzos fail
How is NMS treated?
- Stop offending agent
- Support
- cooling blankets
- Benzos are mainstay
- Dantrolene and bromocriptine are adjuncts
How do the following drugs affect your HR, SVR, CO and PCWP?
- Phenylephrine
- Norepineohrine
- Dopamine
- Epinephrine
- Dobutamine
- Milrinone
- Vasopressin

Compare the motor, sensory andf reflex finding in critical illness myopathy, critical illness polyneuropathy and glucocorticoid-induced myopathy

What are the risk factors for critical illness myopathy
- 25% of patients who are vented for 7 days
- COPD/asthma
- liver transplant
- ARDS
- IV steroids
- Hyperglycemia
- hyperT4
- SIRS
Differentiate Brain death, persistent vegetative state, Minimal conscious state and locked-in syndrome
- Brain death
- irreversible cessation of cerebral and brainstem function
- Persistent vegetative state
- Severe anoxic brain injury progressive to a state of wakefulness without awareness
- No purposeful responses, sleep wake intact
- Minimally conscious state
- Limited interaction with environment with visual tracking +/- simple commands
- Intelligible verbalization or sometimes yes/no but not always appropriate
- Locked in
- Retained alertness, cognitive abilities, can move eyes and blink voluntarily, paralysis of limbs and oral structures
What are the minimum clinical criteria to determine someone to be braindead
- 24hrs after cardiac arrest
- 2 physicians
- Established etiology compatible with NDD
- Absence of confounding factor
- Absent brainstem reflexes:
- Pupillary response
- corneal
- gag
- cough
- occulovestibular (caloric)
- *Dont have to do doll’s eyes
- Absent movements: spontaneous + noxious stimuli
- Bilaterally
- Above and bellow clavicles
- EXCLUDES spinal reflexes
- Apnea testing
List confounding factors in NDD?
- Hypothermia
- T<34
- Electrolyte imbalances
- PO4<0.4
- Ca<1
- Mg<0.8
- Na>160 or <125
- Glucose <4
- Neuromuscular blockers
- Un-resuscitated shock
- Peripheral nerve or muscle dysfunction
- GBS botulism, MG
- Inborn errors of metabolism
- Drugs
- Hypoxic-ischemic encephalopathy
- Need 24hrs post cardiac arrest
What ancillary tests can be sent to confirm neurological death when there are confounding factors?
- Radionucleotide angiography
- CT angio
- Traditionnal 4-vessel angiography
- MR angiography
*EEG not accepted
How is apnea testing conducted?
- Pre-oxygenate patient
- PaCO2: 35-45
- pH:7.35-7.45
- Disconnect from ventilator
- Have inline catheter with O2 flow 10L/min and FiO2 1
- Monitor for resp efforts
- Serial ABGs at 5,10 and 15 minutes
What are the thresholds for completion of an apnea test?
- PaCO2 >60 AND >20mmHg above baseline AND
- pH<7.28
What are the findings with the highest positive likelihood ratios associated with poor neurological outcomes?
*Motor score
- M4: Responding to command
- M3: Localizing to pain
- M2: Flexion to pain
- M1: Extensor posturing
- M0: No response or generalized status

What are the adaptations to CPR that should be done in a pregnant patient?
- Detatch all fetal monitors
- Defibrillate as you normally would
- Move the gravid uterus off the IVC once fundus is at or above the umbilicus (20 weeks)
- IV above the diaphragm
- If getting IV Mg, stop and give Calcium
- Focus on early intubation
- ++ hypoxia
- Rescuscitation should not be overshadowed by postmortem C/S
- Consider @ 5 minutes in the later half of pregnancy
How should patients be managed once ROSC is attained?

What temperature should be considered for TTM after cardiac arrest?
33-36
COnsider 36 if arrhythmia or CV instability
After what type of arrest can TTM be managed (what rhythm)
All
For how long should TTM be continued?
24hrs
What are the good prognostic factors in in-hospital cardiac arrest?
- Poor rates of survival to hospital discharge. (6-15%)
- More likely to survive if
- Witnessed arrest
- VT/VF
- Pulse regained within 10 min
- 1 resuscitation vs multiple
What is the first line pressor in Acute or acute on chronic liver failure
Norepinephrine
How should the propensity to bleed be assessed in patients with acute or acute on chronic liver failure undergoing procedures?
Fibroelastic testing (TEG/ROTEM)
What BG targets shoudl be aimed for in acute or acute on chronic liver failure?
6-10
List the 4 stages of accidental hypothermia

How is stage 1 hypothermia managed?
- Warm environment and clothing
- Warm sweet drink
- Active movements if possible
How is stage 2 hypothermia managed?
- Cardiac monitoring
- Minimal and cautions movements to avoid arrythmias
- horizontal position and immobilization
- Full body insulation
- active external and minimally invasive rewarming techniques
- Warm environment
- chemical, electrical or forced air heating packs/blankets
- warm parenteral fluids
How is stage 3 hypothermia managed?
- Same as stage 2 plus
- Airway management as required
- ECMO or CPB if refractory cardiac instability
How is stage 4 hypothermia managed?
- Same as stage 2 and 3 plus:
- CPR
- Up to 3 doses of epinephrine
- Further doses guided by clinical response
- defibrillation
- Rewarming with ECMO or CPB or CPR with active external and alternative internal rewarming
List rewarming techniques
- Without cardiac support
- Warm environment and clothing, warm sweet drinks, active movements
- Active external and minimally invasive rewarming
- Warm environment
- chemical, electrical, forced air heating heating packs or blankets
- warm parenteral fluids
- PD
- HD
- Thoracic lavage
- Venovenous ECMO
- With cardiac support
- VA ECMO
- CPB
List causes of prolonged QT
- “antis”
- Antibiotics
- Antipsychotics
- Antiemetics
- Antidepressants (TCA)
- Ant-arrythmics
- Electrolyte abnormalitiies
- Cocaine
What can be seen on ECG in TCA overdose?
- Prolonged QT
- QRS >100
- Tachycardia
- Terminal R-wave in aVR >3mm
What can be seen on ECG in digoxin toxicity?
- Tachy (VT/VF) or brady (2o or 3o HB) arrythmias
- Accelerated junctional tachycardia (most common)
*Do not give Calcium for hyperkalemia
Categorize overdoses by how they affect pupillary size

What are the causes of CO intoxication
- Fire related smoke inhalation (most common)
- Improperly vented burning devices
- Kerosene heaters
- Charcoal grills
- camping stoves
- Motor vehicles
What are the signs and symptoms of CO poisoning?
- Non-specific headache
- Malaise
- Nausea
- Dizzieness
- loss of conciousnness
- Possible to see a cherry red appearance of lips and skin
How is CO poisoning diagnosed
- Not reflected on pulse Ox or with PaO2
- CarboxyHb levels
- 3% is normal in non-smokers
- In smokers normal is 10-15%
How is CO poisoning treated?
- Half life of carboxyHb is 250-320 min
- Reduced to 90min with high flow O2 via NRB
- Most important Tx: Remove source and give high flow O2
- If comatose, may intubate and put on 100% FiO2
- Hyperbaric O2 if indicated
- *If CO poisoning after a smoke inhalation Treat for cyanide poisoning
What are the indications for hyperbaric O2 following CO poisoning
- If within 6hrs of exposure is best
- COHb >25%
- pH <7.1
- MI
- Loss of consciousness
- Pregnant women with COHb>20%
- Fetus exhibiting fetal distress
What are the indications that a patient may be suffering from cyanide poisoning?
- Smells of bitter almonds
- Cherry red skin coloring
- Decreased AV oxygen gradient “venous arterialization”
- Loss of conciousness
- Metabolic/lactic acidosis with increased AG→CV collapse→death (may happen within 15min of exposure)
What is the severity grading of cyanide toxicity
- Mild toxicity
- Nausea
- Dizzieness
- Droowsieness
- Tachypnea
- Moderate toxicity
- Loss of consciousness for a short period
- Vomiting
- Seizure
- Cyanosis
- Metabolic/lactic acidosis
- elevated AG
- Tachycardia
- Hypotension
- Severe toxicity
- Deep coma
- Dilated non-reactive pupils
- Deteriorating cardio-resp function
- Cardio-resp arrrest
How is cyanide toxicity diagnosed?
- Blood cyanide level
- Take level before giving antidote
- Level >2.4=resp depression and coma
- Level>3 death
- Venous O2 sats from SVC or PA catheter >90
- Sign of decreased O2 utilization
- Also happens in CO and hydrogen sulfide tox
- ECG is non-specific
- Blocks, brady, tachy
How is cyanide toxicity treated?
- 100% FiO2 and intubation
- Need to protect inhalation of hydrogen cyanide from the stomach
- Antidote=hydroxycobalamine
- May give 1 or 2 doses
- C.I.=Sensitivity to B12
- If inability or delay at getting antidote, then:
- Nitrites
- Aim for methemoglobin concentration 20-30%
- Carefull for hypotension
- Sodium thiosulfate
- Enhances conversion to less toxic thiocyanide
- beware of hypernatremia
- Nitrites
- Elimination
- No indication for HD
What is the therapeutic window of lithium
0.6-1.2
Is it possible to get symptoms of lithium toxicity within the therapeutic window?
yes
What are the symptoms of lithium toxicity?
- N/V/D: Earliest symptoms
- ECG: T wave flattening in precordial leads, QT prolongation, bradycardia, unmasks brugada
- Heme: increases WBC
- CNS (late finding): Dizzy, lightheadedness, orthostatic Sx, lethargy, slurred speech, ataxia, tremor, myoclonic jerks
How is lithium toxicity diagnosed
Li levels
How is lithium toxicity treated?
- Decontamination
- NOT absorbed by activated charcoal
- Whole bowel irrigation if indications
- Enhanced elimination
- HD if indicated
- Restore fluid balance (NS @ 1.5 maintenance)
- NO forced diuresis
- Salt and water depletion lead to Li retention
What are the indications for whole bowel irrigation in lithium toxicity
- Sustained release ingestion
- Symptomatic patients
- Unknown amounts ingested
- >40mg/kg ingested
- <6hrrs from ingestion
- Increasing Li levels
What are the indications for IHD in Li toxicity
- Arrythmias
- Seizures or severely abnormal mental status
- Li levels >5 (6 in some places…)
- Li level over 4 with Cr >176
Where are organophosphates found?
- Insecticides
What is the mechanism of action of organophosphate poisoning?
- Binds acetylcholinesterase and renders it nonfunctioning
- Overabundance of acetylcholine in NM junction
What are the clinical manifestations of Organophosphate poisoning
- Onset within 3hrs if oral/resp exposure. If dermal 12hrs
- Muscarinic effects
- Diaphoresis, diarhhea
- Urination
- Miotic pupils
- Bronchospasm, bradycardia, bronchorrhea
- Emesis
- Lacrimation
- Salivation
- Nicotinic effects
- Muscle weakness (paralysis)/fasciculations
- Adrenergic stimulation…midriasis
- Tachycardia
- CNS-lethargy, seizures, coma, resp depression
- HTN
- CV effects
- QTc prolongation
- MI
- CV collapse (?2/2 vasodilation)
- Resp
- Resp failure 2/2 CNS depression, NM weakness, resp secretions, bronchoconstriction
- Neuro
- Nicotinic effects
- “intermediate syndrome”
- 24-96hrs after exposure
- Neck flexion
- Decreased reflexes
- CN abnormalities
- Prox muscle weakness
- resp insufficiency
- Organophosphate agent delayed neuropathy
- 1-3 weeks post-ingestion
- painful stocking and glove paresthesia followed by a symmetrical motor polyneuropathy characterized by flaccid weakness of the lower extremities
How is organophosphate toxicity diagnosed
clinically
How is organophosphate toxicity managed?
- ABC
- 100% FiO2
- Intubate
- Reassess ability to protect airway and resp insufficiency constantly
- Avoid succs as it is cleared by acetylcholinesterase
- Can use roc but will need higher doses
- Monitor BP and HR
- Can cause HTN and tachycardia with sympathetic stim
- Decontaminate
- Wash patient
- Medical personnel wear full protection
- Well vented area
- Antidote
- Atropine
What are the indications for atropine in organophosphate poisoning?
- Miosis
- Excessive sweating
- Hypotension
- Resp distress
- Poor air entry
- Bronchorrhea
- Bronchospasm/wheeze
What are the side effects of Atropine
- Agitation
- Urinary retention
- ileus
- hyperthermia
- Tachycardia causing MI if pre-existing heart disease
- Not a CI to cholinergic toxicity-may be from hypoxia