BCCCP cheat sheet

MAP = DBP + 1/3(SBP − DBP), equivalently (SBP + 2 × DBP)/3; the usual resuscitation target is MAP ≥65 mmHg in septic shock.

Cardiac index = cardiac output / body surface area; normal 2.5–4.0 L/min/m². Low CI with adequate MAP indicates a need for an inotrope such as dobutamine 2.5–20 mcg/kg/min.

Norepinephrine is first-line in septic shock (0.05–0.1 mcg/kg/min titrated); add vasopressin 0.03 units/min or epinephrine when norepinephrine requirement exceeds 0.25–0.5 mcg/kg/min.

Refractory VF or pulseless VT: amiodarone 300 mg IV bolus, then 150 mg; post-arrest infusion 1 mg/min for 6 hours, then 0.5 mg/min for 18 hours.

Stable SVT: adenosine 6 mg rapid IV push, then 12 mg if needed; avoid in irregular wide-complex rhythms such as pre-excited atrial fibrillation.

NSTE-ACS unfractionated heparin: 60 units/kg bolus (max 4000 units) then 12 units/kg/h (max 1000 units/h), titrated to aPTT.

Aneurysmal subarachnoid hemorrhage: nimodipine 60 mg PO or NG every 4 hours for 21 days; hypotension is managed with dose reduction (30 mg every 4 hours), not discontinuation.

Sodium bicarbonate is not routine in cardiac arrest; it is reserved for hyperkalemia, sodium channel blocker toxicity, or pre-existing severe metabolic acidosis.

ARDS Berlin criteria: onset within 1 week, bilateral opacities, not primarily cardiogenic, PaO2/FiO2 ≤300 on PEEP ≥5 cmH2O; mild 201–300, moderate 101–200, severe ≤100.

Lung-protective settings: tidal volume 6 mL/kg predicted body weight (range 4–8), plateau pressure ≤30 cmH2O, driving pressure (Pplat − PEEP) ≤15 cmH2O.

Predicted body weight: male 50 + 2.3 × (height in inches − 60) kg; female 45.5 + 2.3 × (height in inches − 60) kg.

Static compliance = tidal volume / (plateau pressure − PEEP); typical ventilated adult values are 50–70 mL/cmH2O.

Prone positioning for at least 16 hours per day reduces mortality in moderate-to-severe ARDS with PaO2/FiO2 <150.

Permissive hypercapnia is tolerated to a pH of about 7.20; treat the acidosis if pH <7.15 or if intracranial hypertension is present.

Auto-PEEP management in obstructive disease: reduce respiratory rate, shorten inspiratory time, treat bronchospasm, and avoid large tidal volumes.

NIV for COPD exacerbation uses bilevel IPAP 10–15 cmH2O and EPAP 4–8 cmH2O; heliox 70:30 lowers turbulent flow in upper airway obstruction.

CPP = MAP − ICP; target CPP 60–70 mmHg and ICP <20–22 mmHg in severe traumatic brain injury.

Hyperosmolar therapy: mannitol 0.25–1 g/kg IV bolus (hold if osmolality >320 mOsm/kg) or 3% saline 150–250 mL bolus targeting sodium 145–155 mEq/L.

Avoid hypotonic fluids (0.45% NaCl, D5W) in cerebral edema; 0.9% sodium chloride is the default maintenance fluid.

Dexamethasone is indicated for vasogenic edema from tumors or abscesses, not for traumatic brain injury.

Seizure prophylaxis after traumatic brain injury uses phenytoin/fosphenytoin or levetiracetam for 7 days; prophylaxis beyond 7 days does not prevent late posttraumatic epilepsy.

Convulsive status epilepticus: lorazepam 0.1 mg/kg (max 4 mg) IV, then fosphenytoin 20 phenytoin equivalents/kg or levetiracetam 60 mg/kg (max 4500 mg).

Brief hyperventilation to PaCO2 30–35 mmHg is a temporizing bridge for herniation; sustained hyperventilation risks cerebral ischemia.

After aneurysmal subarachnoid hemorrhage maintain euvolemia; prophylactic hypervolemia and hemodilution worsen outcomes without preventing vasospasm.

Sepsis-3: suspected infection plus an acute rise in SOFA ≥2 points; septic shock adds vasopressor requirement for MAP ≥65 mmHg and lactate >2 mmol/L despite fluids.

Give broad-spectrum antibiotics within 1 hour of recognizing septic shock, and within 3 hours for possible sepsis without shock.

Crystalloid 30 mL/kg within the first 3 hours for sepsis-induced hypoperfusion or lactate ≥4 mmol/L; balanced solutions are preferred over 0.9% saline.

Vancomycin: loading dose 25–30 mg/kg for severe MRSA infection; target AUC24/MIC 400–600, or trough 15–20 mg/L when AUC monitoring is unavailable.

Piperacillin-tazobactam 4.5 g every 6 hours as a 4-hour extended infusion for Pseudomonas coverage; meropenem 1 g every 8 hours over 3 hours, or 2 g every 8 hours for CNS infection.

Cefepime accumulates in renal impairment and causes encephalopathy and myoclonus; adjust the dose and consider an alternative in neurocritically ill patients.

Candidemia: echinocandin first-line (micafungin 100 mg daily; caspofungin 70 mg load then 50 mg daily), stepping down to fluconazole for susceptible isolates in stable patients.

Procalcitonin trends plus clinical response support antibiotic de-escalation; source control (drainage, debridement, catheter removal) matters as much as drug selection.

Enteral nutrition is preferred over parenteral and starts within 24–48 hours in the hemodynamically stabilized critically ill patient; trophic feeding is appropriate during shock.

Caloric goal 25–30 kcal/kg/day with protein 1.2–2.0 g/kg/day (up to 2.5 g/kg in burns or continuous renal replacement therapy).

Refeeding syndrome: start at 10–20 kcal/kg/day, give thiamine before feeding, and check phosphate, potassium, and magnesium daily for the first 72 hours.

Hepatic encephalopathy: lactulose titrated to 2–3 soft stools per day; rifaximin 550 mg twice daily reduces recurrence after an overt episode.

Spontaneous bacterial peritonitis: ascitic PMN ≥250 cells/mm³; treat with IV cefotaxime 2 g every 8 hours plus albumin 1.5 g/kg on day 1 and 1 g/kg on day 3.

Acute variceal hemorrhage: octreotide 50 mcg bolus then 50 mcg/h for up to 5 days, ceftriaxone 1 g daily, and endoscopic band ligation; propranolol plus isosorbide mononitrate for secondary prophylaxis.

Stress ulcer prophylaxis is indicated for mechanical ventilation >48 hours, coagulopathy, or prior GI bleeding; PPIs are preferred when bleeding risk is high.

Acute pancreatitis: early enteral nutrition and goal-directed lactated Ringer's; prophylactic antibiotics are not recommended without infected necrosis.

Acute liver failure: N-acetylcysteine for acetaminophen and non-acetaminophen etiologies, avoid benzodiazepines, treat intracranial hypertension, and refer early for transplant.

KDIGO AKI stage 1 = creatinine 1.5–1.9 × baseline or a rise ≥0.3 mg/dL within 48 hours, or urine output <0.5 mL/kg/h for 6 hours.

KDIGO stage 2 = 2.0–2.9 × baseline or urine output <0.5 mL/kg/h for ≥12 hours; stage 3 = 3.0 × baseline, creatinine ≥4.0 mg/dL, or initiation of renal replacement therapy.

FENa = (urine Na × plasma creatinine) / (plasma Na × urine creatinine) × 100; <1% suggests a prerenal state, but diuretics, CKD, and contrast make it unreliable.

Continuous renal replacement therapy is preferred over intermittent hemodialysis when the patient is hypotensive or has raised intracranial pressure, because solute and volume shifts are gentler.

Drugs cleared by hemodialysis require a supplemental dose after each session; assess vancomycin, aminoglycosides, and other renally eliminated agents.

Hyperkalemia with ECG changes: IV calcium gluconate or calcium chloride first to stabilize the myocardium, then insulin with dextrose, nebulized albuterol, and definitive removal by diuresis or dialysis.

Rhabdomyolysis: aggressive isotonic fluid resuscitation targeting urine output 200–300 mL/h, with monitoring of potassium, phosphate, and calcium.

Prevention of contrast-associated AKI relies on isotonic crystalloid expansion and minimizing contrast volume; N-acetylcysteine has not shown consistent benefit.

0.9% NaCl contains Na 154 and Cl 154 mEq/L (osmolarity 308 mOsm/L); lactated Ringer's contains Na 130, K 4, Ca 3, Cl 109, and lactate 28 mEq/L.

Balanced solutions (lactated Ringer's, Plasma-Lyte) reduce hyperchloremic metabolic acidosis compared with large-volume 0.9% saline; lactated Ringer's is relatively hypotonic and is avoided in traumatic brain injury.

Anion gap = Na − (Cl + HCO3), normal 8–12 mEq/L; a delta-delta ratio of 1–2 indicates pure high-anion-gap acidosis, while <1 indicates a concurrent hyperchloremic acidosis.

Winter's formula: expected PaCO2 = 1.5 × HCO3 + 8 ± 2; a value outside this range indicates an additional respiratory disorder.

Hypernatremia free water deficit = 0.6 × weight (kg) × (Na/140 − 1); correct sodium by no more than 10 mEq/L per 24 hours to avoid cerebral edema.

Hyponatremia correction should not exceed 8–10 mEq/L per 24 hours; overly rapid correction risks osmotic demyelination.

Peripheral IV potassium generally should not exceed 10 mEq/h (up to 20 mEq/h centrally with continuous monitoring); each 10 mEq raises serum potassium roughly 0.1 mEq/L.

Sodium bicarbonate is used to alkalinize urine in salicylate and tricyclic toxicity (target urine pH 7.5–8.0) and as an adjunct in severe hyperkalemia, not as first-line therapy.

DKA: glucose >250 mg/dL, arterial pH <7.3, bicarbonate <18 mEq/L, anion gap >10–12, and positive ketones. HHS has glucose >600 mg/dL and osmolality >320 mOsm/kg with minimal ketosis.

DKA resuscitation: 15–20 mL/kg (about 1–1.5 L) isotonic crystalloid in the first hour, then 250–500 mL/h; insulin infusion 0.1 units/kg/h once potassium is ≥3.3 mEq/L.

Add dextrose when glucose falls below 200–250 mg/dL in DKA (250–300 mg/dL in HHS) while continuing insulin until the anion gap closes.

Corrected sodium = measured sodium + 1.6 × (glucose − 100)/100; a rising corrected sodium during DKA treatment suggests free water replacement is inadequate.

Thyroid storm: thionamide first (propylthiouracil 500–1000 mg load, then 250 mg every 4 hours), iodine at least 1 hour later, plus propranolol or esmolol and hydrocortisone 100 mg every 8 hours.

Myxedema coma: IV levothyroxine 200–400 mcg loading dose then 50–100 mcg daily; give hydrocortisone first if adrenal insufficiency is possible.

Adrenal crisis: hydrocortisone 100 mg IV bolus then 50 mg every 6 hours (or 200 mg/24 h infusion) with isotonic fluid and dextrose; do not delay steroids for confirmatory testing.

Etomidate suppresses adrenal steroidogenesis and should be avoided for induction in septic shock when an alternative agent is available.

HIT: platelet decline >50% from baseline typically 5–10 days after heparin initiation; the 4Ts score stratifies probability; stop all heparin and start a non-heparin anticoagulant.

Argatroban 2 mcg/kg/min (0.5 mcg/kg/min with hepatic impairment or heart failure), titrated to aPTT 1.5–3 times baseline; bivalirudin is an alternative, including for cardiac surgery.

Warfarin-related major bleeding: 4-factor prothrombin complex concentrate 25–50 units/kg based on INR plus vitamin K 5–10 mg IV; do not wait for INR results in life-threatening hemorrhage.

Dabigatran reversal: idarucizumab 5 g IV (two 2.5 g doses). Factor Xa inhibitor reversal: andexanet alfa, or 4-factor prothrombin complex concentrate when andexanet is unavailable.

Heparin reversal: protamine 1 mg per 100 units of heparin given in the preceding 2–3 hours; for enoxaparin, protamine 1 mg per 1 mg reverses about 60% of anti-Xa activity.

Febrile neutropenia: start an antipseudomonal beta-lactam (cefepime 2 g every 8 hours) within 60 minutes; add vancomycin for line infection, skin/soft tissue infection, pneumonia, or hemodynamic instability.

Tumor lysis syndrome: rasburicase is contraindicated in G6PD deficiency; monitor potassium, phosphate, calcium, and uric acid, and use allopurinol prophylaxis in lower-risk patients.

TTP: plasma exchange plus corticosteroids is first-line; withhold platelet transfusion unless there is life-threatening bleeding because it can worsen microvascular thrombosis.

Parkland formula: 4 mL × body weight (kg) × %TBSA burned of lactated Ringer's over the first 24 hours from injury, half in the first 8 hours, titrated to urine output 0.5 mL/kg/h.

Adult rule of nines: head 9%, each arm 9%, anterior trunk 18%, posterior trunk 18%, each leg 18%, perineum 1%; use the Lund-Browder chart for children.

Trauma hemorrhage: tranexamic acid 1 g IV over 10 minutes within 3 hours of injury, then 1 g over 8 hours; benefit is lost when given later than 3 hours.

Permissive hypotension (SBP 80–90 mmHg) is used in hemorrhagic shock until surgical control, but is avoided in traumatic brain injury where a higher MAP is required.

Massive transfusion approximates a 1:1:1 ratio of packed red blood cells, plasma, and platelets; give cryoprecipitate or fibrinogen concentrate when fibrinogen is <150 mg/dL.

Cyanide toxicity from smoke inhalation is treated with hydroxocobalamin 5 g IV; it causes red discoloration of urine and interferes with colorimetric laboratory assays.

Carbon monoxide poisoning: 100% oxygen by nonrebreather mask; consider hyperbaric oxygen for COHb >25%, syncope, neurologic deficits, or pregnancy.

Inhalation injury: suspect with facial burns, singed nares, soot in the oropharynx, hoarseness, or stridor, and intubate early before airway edema progresses.

Target a Richmond Agitation-Sedation Scale score of −2 to 0 in most ICU patients; light sedation shortens ventilation and reduces delirium versus deep sedation.

The CAM-ICU is the validated delirium screen in ventilated patients; screen at least once per shift and document the result.

Propofol 5–50 mcg/kg/min causes hypotension and hypertriglyceridemia; propofol infusion syndrome (metabolic acidosis, rhabdomyolysis, hyperkalemia, bradycardia, lipemia) requires immediate discontinuation.

Dexmedetomidine 0.2–1.5 mcg/kg/h sedates without respiratory depression but causes bradycardia and hypotension; it is unsuitable when rapid control of severe agitation is needed.

Routine antipsychotics are not recommended for prevention or treatment of ICU delirium; reserve quetiapine or haloperidol for hyperactive delirium that endangers the patient or staff.

Hydromorphone is preferred over morphine in renal dysfunction because morphine-6-glucuronide accumulates and causes neuroexcitation; fentanyl also accumulates during prolonged infusion.

Salicylate toxicity: sodium bicarbonate to alkalinize serum and urine (urine pH 7.5–8.0), correct hypokalemia, and dialyze for levels >100 mg/dL or severe symptoms; avoid intubation-induced hypoventilation.

Tricyclic overdose: sodium bicarbonate 1–2 mEq/kg IV for QRS >100 ms or ventricular arrhythmia; avoid class IA and IC antiarrhythmics and avoid flumazenil.