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Critical Care

Substance Abuse Disorders

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Alcohol Withdrawal –

  • Tremors start around 6 hours, seizures around 12 hours, but can occur 3-5 days later.
  • Mortality can be as high as 35%.
  • 3 Ts – Increase temp, tremor and tachycardia
  • Treatment: correct electrolyte imbalances, benzos, can use propofol or barbiturates in refractory cases, magnesium, alpha 2 agonists, Beta blockers, calcium channel blockers
  • Avoid: tramadol, meperidine, Thorazine, bupropion, TCAs, fluoroquinolones, carbapenems, theophylline, romazicon (huge risk of seizure in chronic user)
  • Use Clinical Institute Withdrawal Assessment for Alcohol scale (CIWA-Ar): 0-67, higher is worse. Treat if 8-10.
  • Benzos are main treatment:
    • Lorazepam: 2-4 mg every 6 hours (preferred, no active metabolites, no liver interactions)
    • Diazepam: 10-20 mg every 5 hours (lower in liver failure)
    • Chlordiazepoxide: 50-100 mg every 6 hours (long-acting, decrease dose in liver issues
  • Thiamine: prevent Wernicke-Korsakoff syndrome
  • Magnesium: Check labs to see if needed
  • Electrolyte labs, such as potassium
  • Vitamins: Patients are usually undernourished
  • Fluid therapy: patients are initially overhydrated, then dehydrated, usually give 5% dextrose
  • Hallucinations can be controlled by BZDs or haloperidol
  • Beta-blockers: can control tremor, heart rate and blood pressure
  • Alpha-agonist: clonidine can help with withdrawal
  • Can use disulfiram, naltrexone, acamprosate for chronic therapy.  All are liver toxic.  Naltrexone is better in liver dysfunction.

Opioid Dependence –

  • Maintenance with methadone, naltrexone, buprenorphine.  Opioid withdrawal is not fatal (flu-like symptoms).  Methadone must be tapered to 30 mg daily or less before discontinued.

Tobacco –

  • 10+ cigarettes a day = 21 mg patch, decrease in 2 weeks
  • <10 cigarettes a day = 14 mg patch, decrease in 6 weeks
  • Gum: max = 24 pieces a day, use at least 9 pieces per day.  > 24 cigarettes a day = 4mg gum, all others use 2 mg gum
  • Lozenges – people who smoke within 30 minutes of waking use 4 mg, all others use 2 mg.
  • Bupropion – start at least 7 days before quitting.  Treat at least 8 weeks, up to 6 months.
  • Varenicline: start 7 days prior to quitting, use at least 12 weeks (can use up to 24 weeks).  Black box warning for psychosis.  Can be combined with bupropion or a patch.

Acid-Base Disturbances

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Summary of Acid-Base Disturbances

 pH (7.3 – 7.4)H+HCO3 (22-26)pCO2 (34-45)K+
metabolic acidosis↓↑↓↓↓↓↑
metabolic alkalosis↑↓↑↑↑↑↓
respiratory acidosis↓↑↑↑↑↑↑
respiratory alkalosis↑↓↓↓↓↓↓

Multiple arrows means it is a compensatory mechanism.

  • PCo2 is usually 1.5 times the bicarb + 8, if it’s higher it’s compensated
  • Gap = Sodium – (Cl + Bicarb) = normal is 6-12, greater than 12 is metabolic acidosis
  • Normal respiratory rate is 12-20

Acidosis: pH < 7.38

  • PCO2 < 38 – metabolic acidosis with respiratory compensation.  “Hyperventilation” compensates (blowing off carbon dioxide, which is an acid), decrease in bicarb
  • PCO2 38-42 – pure metabolic acidosis
  • PCO2 > 42 – primary respiratory acidosis. Need bicarb to say if primary metabolic acidosis (HCO3 < 24) or compensated respiratory acidosis (HCO3 > 28).

Alkalosis: pH < 7.42

  • PCO2 <38 – primary respiratory acidosis.  Need bicarbonate to see if the patient has primary metabolic acidosis too (HC03 > 28)
  • PCO2 38-42 – primary alkalosis without respiratory compensation
  • PCo2 > 42 – primary metabolic acidosis with respiratory compensation

Causes of Anion Gap Acidosis:

  • MUDPILES – methanol, uremia, diabetic ketoacidosis, paraldehyde, iron, isoniazid, inhalants, lactic acidosis, ethylene glycol (the propylene glycol in lorazepam can cause it too), ethanol and salicylates
  • or MULEPAKS: methanol, uremia, lactic acidosis, ethylene glycol, paraldehyde, aspirin, ketoacidosis, starvation

How to work an acid-base problem:

  1. Assess pH (acid or base)
  2. Determine if it’s respiratory or metabolic (pCO2 and HCO3)
  3. Calculate anion gap (can help determine cause).

Pressors and Ionotropes

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Drug NameReceptor affectedHRBPCOUses
Norepinephrineα, β1↔↑↑↑↔ or ↑cardiogenic shock
Epinephrineα, β1, β2↑↑↑↑↑↑↑↑↑cardiogenic shock  and anaphylaxis
epi activates everything)
Dopamineα, β1, dopaminergic↑↑↑↑↑cardiogenic and neurogenic
shock, if not tachy
Phenylephrineα↔ or ↓↑↑↑↓septic shock only, can use if tachy
Vasopressinvasopressin–↑↑↑ – or ↑septic only
Isoproterenolβ1, β2↑↓↑ 
Dobutamineβ1, β2 (less β2
than isoproterenol		↑↓↑cardiogenic and septic shock   At high doses, causes headaches, paresthesias, and muscle cramps Doesn’t work well if the patient on beta blocker, milrinone is similiar choice
Milrinoneinotrope, vasodilation,
PDE (phosphodiesterase
inhibitor)		↑↑–↑ 

α = smooth muscle contraction

β1 = positive chronography, dromotropic and ionotropic

β2 = smooth muscle relaxation

Remember:

  • BP = SBP/DBP
  • MAP = [SBP + (2 * DBP)]/3    (normal is 70-100)
    • Map is largely based off of DBP because most of cardiac cycle is in diastole (filling)
  • Cardiac Output (CO) = Sv + HR

Which pressor when:

  • Septic shock: norepinephrine is first line, +/- vasopressin +/- dopamine
  • Cardiogenic shock: dobutamine is first line, +/- IABP (intra-aortic balloon pump) +/- milrinone.
  • Post-op: phenylephrine
  • Post-code:epinephrine

I like these graphics, which came from here:

Shock

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Hypovolemic shock:

  • Restore intravascular volume and oxygen carrying capacity.
  • If hemoglobin < 7, administer blood products.
  • Patients may need pressers.

Obstructive shock:

  • Must treat actual obstruction.
  • Fluids may improve end-organ perfusion temporarily.

Vasodilatory shock:

  • Usually sepsis

Septic Shock:

Treat with sepsis bundles.

  • Within 3 hours:
    • Obtain labs.
    • Start broad-spectrum antibiotics, ideally within the first hours (obtain cultures first if possible, but do not wait if not)
    • Measure lactate.
    • Administer crystalloids for hypotension or lactate > 4.  Use of balanced crystalloids (Ringers, plasmalyte) leads to less acute kidney injury.  Avoid hydroxyethyl starches, +/- albumin. Usually 30mL/kg fluid bolus.
  • Within 6 hours:
    • Check on what you did initially.  See if it worked.
    • Vasopressors if hypotension not improved to keep MAP > 65.
      • Norepinephrine is drug of choice (vasopressin or dopamine may be considered)
      • Phenylephrine is not recommended unless CO is high and BP is low.
      • Vasopressin added to norepinephrine may improve outcomes
    • Recheck lactate, monitor CVP or SCVOO2.
  • Empiric antibiotics: usually vancomycin and cefepime, pip/tazo or imipenem or meropenem +/- antifungal.  Change with cultures.
    • Procalcitonin levels can give guidance to the effectiveness of empiric therapy.  Decreasing levels suggests response.
  • Corticosteroids if not responding to IV fluids.  Hydrocortisone is preferred. Avoid fludrocortisone.

Analgesics

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 MorphineFentanylHydromorphone
Onset (min)5-101-25-10
Duration (h)2-41-52-6
Prolonged in renalyesnono
Prolonged in hepaticyesyesyes
T 1/2 in hours1-42-52-3
Active metabolitesyesnono
Hypotensionyesnoyes
Flushingyesnoyes
Bronchospasmyesnono
Constipationyesyesyes

Neuromuscular Blockade and Sedation

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Assessment Tools:

  • Critical Care Pain Observation Tool (CPOT) (0-8)
  • Behaviour Pain Scale (BPS)
  • Sedation is Richmond Agitation Sedation Scale (RASS) or Sedation-Agitation Scale (SAS)

Sedation Agents:

  • Propofol:
    • Rapid onset (1-2 minutes)
    • Short duration (3-5 minutes).
    • Avoid prolonged infusions greater than 50 mcg/kg/min.
    • Monitor BP, triglycerides, adjust lipid calories
    • Monitor for propofol infusion syndrome: metabolic acidosis, hemodynamic instability, cardiac failure, arrhythmias, cardiac arrest, rhabdomyolysis, hypertriglyceridemia, kidney failure, and hyperkalemia
      • Usually for infusion rates higher than 75-83 mg/kg/min for more than 48 hours.
    • Causes respiratory depression, must be intubated.
  • Dexmedetomidine: Dexmedetomidine is a highly selective α2-adrenergic receptor agonist. It has effects similar to other α2-adrenergic receptor agonists (think clonidine) and is used as a sedative
    • Rapid onset (5-15 minutes)
    • Short duration (2-hour half-life)
    • Can cause bradycardia and hypotension (again think clonidine). However, initial titrations can cause a vasoconstrictive rise in BP (temporary and usually not clinically significant). It can also have EKG effects.
    • Can affect blood sugar.
    • Can be used to decrease intracranial pressure.
    • Low incidence of delirium.
    • Does not cause respiratory depression.
    • Dexmedetomidine can have withdrawal symptoms if used long term (1-2 days). Rebound increase in heart rate and blood pressure and increased anxiety unless titrated.
    • Adverse effects are mostly additive effects with other sedatives or medications that lower heart rate and blood pressure.
  • Ketamine –
    • Analgesic and sedative properties.
    • Risk of delirium.
    • Adverse effects: hypertension, tachycardia, and delirium.
    • No respiratory depression
  • Delirium
    • CAM-ICU Scale – Confusion Assessment Scale for ICU
    • ICDSC: Intensive Care Delirium Screening Checklist
    • Best course is prevention, including minimizing BZD doses, opioids, and anticholenergic medications.
    • Can treat with: haloperidol, quetiapine, olanzapine, risperidone, ziprasidone.  Olanzapine and risperidone have the lowest risk of QTc prolongation.

Neuromuscular Blockade

  • Never use a neuromuscular blocker on someone who is not sedated and doesn’t have analgesia.
  • Drugs/Electrolytes that potentiate block: corticosteroids, aminoglycosides, clindamycin, tetracyclines, polymixin, calcium channel blockers, Type 1a antiarrhythmics, furosemide, lithium, hypocalcemia, hypermagnesemia, hypokalemia
  • Drugs/Electrolytes that antagonize block: aminophylline, theophylline, carbamazepine, phenytoin, hyperkalemia, hypercalcemia
  • Succinylcholine and atracurium cause direct mast cell release.  Pancuronium, rocuronium, and vecuronium cause the least.  This is not anaphylaxis.
  • When neuromuscular blockers are used in combination with steroids, it increases the risk of acute quadriplegic myopathy syndrome.
  • Reverse non-depolarizing agents with neostigmine or edrophonium (acetylcholinesterase inhibitors). DO NOT USE THESE WITH succinylcholine.  They make succ induced paralysis worse.
 OnsetDurationT 1/2 
Succinylcholine30-60 sec4-6 m < 1minSucc is the only depolarizing agent.
Do NOT use neostigmine with succ.
Atracurium2-3 m20-35 m2-20 m no renal or hepatic dosing
Pancuronium2-3 m60-100 m110 mthe longest duration of action
Rocuronium1-2 m30 m60-70 mcaution in pulmonary HTN
Vecuronium3-5 m45-65 m65-70 m 
Cisatracurium2-3 m20-35 m22-29 m does not release histamine

Hypersensitivity Reactions

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Type 1 Hypersensitivity is IgE mediated.  It’s anaphylaxis and the one we’re most concerned with in critical care.

Treatment:

  • Epinephrine, Benadryl, albuterol or racepinephrine, IV fluids, and pressors
  • Steroids will help biphasic reaction, but not acute reaction.
  • Monitor for 4-6 hours. Keep overnight if you have to re-intervene.
  • Send home with 2 epi-pens, oral steroids for 3-5 days, H2RA antihistamines and Benadryl
  • A biphasic reaction can happen within 24-48 hours.  Symptoms are rash and swelling. This is a medical emergency. Call 9-1-1-.