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ICU and OSCE Critical Care High-Yield Reference
Guide
Emergency Response & Decompensation (ACLS & Rapid Response)
Primary Survey (ABCDEF): In any decompensation or code situation, immediately assess Airway, Breathing, Circulation, Disability (neuro status), Exposure, and Fingerstick glucose. Ensure airway patency (consider jaw thrust or intubation if needed), provide 100% oxygen via bag-mask, and check pulses and blood pressure. Initiate CPR if no pulse, and attach defibrillator/monitor. Simultaneously, call for the Rapid Response/Code Team and bring the crash cart. Obtain a fingerstick glucose (hypoglycemia is a reversible cause of altered mental status). ACLS Cardiac Arrest Algorithm: If the patient is pulseless, follow ACLS protocols for adult cardiac arrest: o High-Quality CPR: Start chest compressions immediately (100-120/min, 2-2.4 inches deep, full recoil). Minimize interruptions; rotate compressor every 2 minutes to avoid fatigue. o Rhythm Check: After 2 minutes of CPR, analyze rhythm: Shockable (VF/VT): Deliver one shock (biphasic ~200J, or manufacturer recommended). Immediately resume CPR for 2 min, then re-check rhythm. After second shock, give epinephrine 1 mg IV/IO and continue CPR. Repeat epinephrine every 3- minutes during arrest. After third shock, give amiodarone 300 mg IV/IO bolus (antiarrhythmic) for refractory VF/pulseless VT, followed by a second dose of 150 mg if neededncbi.nlm.nih.gov. Alternatively, lidocaine 1-1.5 mg/kg IV can be used (max 3 mg/kg). Continue CPR between shocks, and address reversible causes (the “H’s & T’s”). Non-Shockable (Asystole/PEA): Do NOT defibrillate. Continue CPR and give epinephrine 1 mg IV as soon as possible (q3-5 min). Every 2 minutes, do a brief rhythm check (<10 seconds). If organized rhythm appears, check pulse (if pulse, ROSC care; if no pulse, continue CPR). Continue cycles of CPR with epinephrine every 3-5 min. Search for reversible causes (see below). o Advanced Airway: If bag-mask ventilation is inadequate or prolonged arrest, intubate with minimal interruption to compressions. Once advanced airway in place, give continuous compressions and ventilate 10 breaths/min (1 breath q6 seconds). Confirm ET tube placement with end-tidal CO₂ (ETCO₂); a persistent ETCO₂ < 10 mmHg suggests poor CPR quality or need to reassess efforts. o Reversible Causes (Hs & Ts): Continuously consider and treat potential causes of arrest. The 5 H’s: Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypo-/hyperkalemia, Hypothermia. The 5 T’s: Tension pneumothorax, Tamponade (cardiac), Toxins, Thrombosis (pulmonary embolism), Thrombosis (myocardial infarction). For example, if PEA and suspected tamponade or tension pneumothorax , perform emergency pericardiocentesis or needle decompression, respectively. If hyperkalemia is suspected (e.g., dialysis patient), give IV calcium, insulin/glucose, and bicarbonate. Correct hypoxia with ventilation and 100% O₂, hypovolemia with IV fluids, etc. o ROSC (Return of Spontaneous Circulation): If pulse returns, begin post-cardiac arrest care. Optimize oxygenation (titrate O₂ to keep SpO₂ 92-98%), and ventilation (target PaCO₂ 35- mmHg). Treat hypotension (IV fluids, vasopressors to keep MAP ≥ 65). Obtain a 12- lead ECG to identify STEMI (consider emergent cath lab for coronary reperfusion). Initiate targeted temperature management (TTM) if the patient remains comatose, cooling to 32-36°C for 24 hours to improve neurologic outcomes. Consider ICU therapies such as mechanical ventilation and vasopressors, and investigate causes of arrest.
ACLS Arrhythmia Management (Adult): Recognize and intervene on pre-arrest arrhythmias: o Tachyarrhythmias (With Pulse): Evaluate patient condition – unstable tachycardia (hypotension, acutely altered mental status, ischemic chest pain, signs of shock) requires synchronized cardioversion immediately (e.g., 100-200J for narrow regular, up to 200J biphasic for irregular). For stable tachycardias , determine QRS width: Narrow QRS (<0.12 sec): Likely SVT or atrial fibrillation/flutter. SVT (Paroxysmal Supraventricular Tachycardia): Attempt vagal maneuvers (Valsalva, carotid sinus massage if no bruits) first. If ineffective, give adenosine 6 mg rapid IV push followed by flush; if no conversion, 12 mg IV can be given (for regular narrow complex SVT). If still in SVT, rate control with beta-blocker or calcium channel blocker (e.g., diltiazem 15-20 mg IV over 2 min for atrial fibrillation with RVR). Atrial Fibrillation/Flutter: If rapid ventricular rate and patient is stable, control rate with IV diltiazem (0.25 mg/kg IV bolus) or beta-blocker (e.g., metoprolol 5 mg IV). Consider anticoagulation if duration >48 hrs or high stroke risk (not usually an acute OSCE decision unless scenario includes known status). If WPW with AF (irregular wide complex tachycardia), avoid AV nodal blockers – use procainamide. Wide QRS (≥0.12 sec): Could be ventricular tachycardia or SVT with aberrancy. Stable Ventricular Tachycardia (monomorphic): Give antiarrhythmics. First- line: Amiodarone 150 mg IV over 10 minutes (may repeat if VT recurs; then maintenance infusion 1 mg/min). Alternative: Procainamide 20-50 mg/min IV until arrhythmia suppressed or hypotension ensues (max 17 mg/kg). Avoid procainamide if prolonged QT or CHF. Sotalol 100 mg (1.5 mg/kg) IV over 5 minutes is another option (avoid if prolonged QT). If at any point the patient becomes unstable, perform synchronized cardioversion. Torsades de Pointes: (Polymorphic VT usually due to prolonged QT) – treat with Magnesium sulfate 2 g IV push and immediate defibrillation if pulseless. o Bradyarrhythmias: Identify inadequate perfusion (hypotension, confusion, chest pain). If unstable from bradycardia, begin atropine 1 mg IV bolus , may repeat every 3-5 minutes to a total of 3 mgncbi.nlm.nih.gov. If atropine is ineffective (e.g., high-degree AV block or infranodal block likely), prepare for transcutaneous pacing (place pads, set rate ~70 and increase mA until capture). Consider starting epinephrine infusion (2-10 μg/min) or dopamine infusion (5- μg/kg/min) if pacing is delayed or ineffective. For refractory cases (e.g., Mobitz II or complete heart block), transvenous pacing by cardiology may be required. Acute Decompensation (Respiratory or Circulatory): If a patient on the ward decompensates (e.g., severe hypotension, respiratory failure), call a Rapid Response. Simultaneously, apply the ABCDE approach : o Airway/Breathing: Give high-flow oxygen; if respiratory distress or low consciousness, prepare for intubation (see Procedures). Use bag-valve mask if necessary. Check for lung sounds (wheezing for asthma, crackles for pulmonary edema, absent on one side for pneumothorax, etc.) and manage accordingly (e.g., bronchodilators for wheezing, needle decompression for tension pneumothorax). o Circulation: Place IVs (2 large-bore IVs), draw STAT labs including ABG, lactate, basic metabolic panel, troponin, CBC, coags. Attach monitors (ECG, pulse ox, NIBP). Give IV fluid bolus (e.g., 1-2 L crystalloid) if hypotensive, unless pulmonary edema present. If suspect sepsis, start broad-spectrum antibiotics quickly. If shock persists (MAP < 65) despite fluids, start vasopressors (e.g., norepinephrine for most shocks, or epinephrine for anaphylaxis). o Disability (Neuro): Check responsiveness, pupils, gross neuro status. If GCS <8, intubation is indicated (coma). Check for stroke signs (FAST exam) or seizure activity. If glucose is low, give IV dextrose (D50). If opioid overdose suspected (pinpoint pupils, etc.), give naloxone 0.4 mg IV.
Post-MI complications: Be vigilant for arrhythmias (VF, VT, bradyarrhythmias from AV block), acute mechanical defects (papillary muscle rupture – acute MR, VSD, free wall rupture – tamponade), and heart failure. Treat arrhythmias per ACLS. Acute MR or VSD may present with shock and new murmur
- emergent surgical intervention needed. Tamponade (free wall rupture) causes PEA arrest – attempt pericardiocentesis if suspected (often fatal). Manage pericarditis pain (Dressler’s syndrome) with high- dose aspirin.
Arrhythmias (Non-Arrest)
Atrial Fibrillation (AF) with RVR: If new onset AF in ICU, assess stability. In a stable patient, control rate with diltiazem (e.g., 15-20 mg IV over 2 min, then infusion 5-15 mg/hr) or beta-blocker (e.g., metoprolol 5 mg IV push up to 15 mg). Target HR < 110 (lenient control) or < 80 if feasible. If EF is reduced (<40%), avoid calcium blockers; use beta-blocker cautiously or amiodarone. If patient is unstable (hypotension, pulmonary edema, ischemia) due to AF RVR, perform synchronized cardioversion (e.g., 100-200J biphasic). Anticoagulation should be considered if AF duration >48h or unknown (heparin in hospital, then evaluate need for long-term anticoagulation via CHA₂DS₂-VASc score). For known WPW with AF (irregular wide QRS), procainamide is preferred; avoid AV node blockers. Atrial Flutter: Typically sawtooth atrial rate ~300 with 2:1 block (ventricular ~150). Management similar to AF (rate control with diltiazem or beta-blocker). Unstable flutter -> synchronized cardioversion (50-100J often effective). Paroxysmal SVT (AVNRT/AVRT): Patient may have sudden onset palpitations, narrow QRS ~150- 220 bpm. If stable, attempt vagal maneuvers (Valsalva, carotid massage). If unsuccessful, adenosine 6 mg IV rapid push (flush immediately); can give 12 mg if no conversion. Adenosine will transiently block AV node – patient may feel chest tightness or flushing. If adenosine fails, use AV nodal blockers (diltiazem or beta-blocker). Unstable SVT -> synchronized cardioversion. Ventricular Tachycardia (VT) with Pulse: Monomorphic VT (regular wide QRS tachycardia) can sometimes have a pulse. If unstable , do immediate synchronized cardioversion (if pulseless, treat as cardiac arrest). If stable, use IV amiodarone 150 mg over 10 minutes or procainamide infusion as noted above. Prepare for cardioversion if drugs fail. Obtain expert consultation if recurrent; consider overdrive pacing or anti-tachycardia pacing if available (ICD interrogation in those with devices). Ventricular Fibrillation/Pulseless VT: (Typically in arrest scenarios) – see ACLS above; defibrillation is key. Torsades de Pointes: Polymorphic VT associated with prolonged QT. Causes include drugs (QT- prolonging meds), hypokalemia, hypomagnesemia. Treat unstable torsades with defibrillation. Give Magnesium 2 g IV as first-line even if Mg level is normal. Overdrive pacing or isoproterenol infusion can help shorten QT if persistent. Remove offending causes (stop QT-prolonging drugs, correct electrolytes). Bradycardia & AV Block: Sinus bradycardia is common in ICU (e.g., sedated patients, beta-blocker use). Treat if hemodynamic compromise (hypotension, poor perfusion): atropine 1 mg IV push (may repeat q3-5 min up to 3 mg)ncbi.nlm.nih.gov. If ineffective or Mobitz II or 3° AV block, initiate transcutaneous pacing and/or epinephrine infusion (2-10 μg/min) or dopamine infusion (5- 20 μg/kg/min). Transvenous pacing may be needed if persistent high-grade block. Identify reversible causes (e.g., beta-blocker overdose – treat with glucagon; hyperkalemia – calcium, etc.). Pulseless Electrical Activity (PEA): Organized rhythm without a pulse (not VT/VF) – manage as in ACLS with CPR and epinephrine, and correct reversible causes (Hs & Ts). Common PEA etiologies: hypovolemia (flat veins – give fluid), tamponade (do ultrasound – pericardiocentesis), tension PTX (decompress), massive PE (thrombolysis), acidosis (ABG, give bicarbonate if severe acidosis), hyperkalemia (see Electrolytes section for treatment), etc. Asystole: Flatline – verify in two leads to rule out fine VF. Immediately start CPR, epinephrine, search causes. Generally poor prognosis unless a reversible cause is found (like hypothermia or massive hyperkalemia – sometimes treat with pacing but usually ineffective).
Post-Arrest Care Arrhythmias: After ROSC, patients may have reperfusion arrhythmias. Treat as needed, but for non-sustained VT or isolated PVCs post-thrombolysis or reperfusion, often no intervention is needed if patient stable. Maintain electrolytes in normal range (K ~4, Mg ~2) to prevent arrhythmias.
Acute Heart Failure & Cardiogenic Pulmonary Edema
Recognition: Acute decompensated heart failure (ADHF) presents with dyspnea, tachypnea, hypoxia, often hypertension (acute pulmonary edema), or hypotension if cardiogenic shock. Signs: jugular venous distension, S3 gallop, diffuse crackles, wheezing (cardiac asthma), frothy pink sputum, peripheral edema. On CXR: pulmonary vascular congestion, interstitial edema, pleural effusions. Initial Management: Position patient upright, give 100% O₂ (consider noninvasive ventilation). In acute cardiogenic pulmonary edema, use NIPPV (BiPAP) early to improve oxygenation and reduce work of breathing. BiPAP decreases preload and afterload by positive pressure, often rapidly improving pulmonary edema. Reduce Preload and Afterload: Give IV Nitroglycerin (if systolic BP > 90-100). Start with sublingual nitro then IV infusion (e.g., 20-100 μg/min, titrate) to vasodilate and reduce cardiac filling pressures – this is very effective for pulmonary edema. If hypertensive, consider IV nitroprusside carefully (potent vasodilator). Diuretics: Administer IV loop diuretic (e.g., furosemide 40 mg IV if naïve, or higher if on chronic diuretics) to reduce fluid overload. Monitor urine output. If already on outpatient furosemide, initial IV dose should be equal or higher than their total daily PO dose. Watch BP and renal function. Inotropic Support: If signs of low perfusion (cold extremities, low urine output, mental status changes) and hypotension (cardiogenic shock), consider inotropes. Dobutamine (β1 agonist) 2-20 μg/kg/min can improve contractility and reduce afterload (β2 effect) – useful if SBP > 90. If hypotension severe, norepinephrine can be used to maintain BP while still providing some inotropy. Dopamine is an option in bradycardic hypotensive patients (5-10 μg/kg/min has inotropic and some vasoconstrictive effect; >10 μg/kg/min mainly vasoconstricts). Titrate to maintain MAP ~65 and adequate end-organ perfusion. Monitor for arrhythmias with inotropes. Ultrafiltration: In refractory pulmonary edema with renal dysfunction or diuretic resistance, consider emergent dialysis or ultrafiltration to remove fluid. Identify Cause: Evaluate for precipitant of ADHF (e.g., ischemia – get ECG and troponin, arrhythmia like AF RVR, uncontrolled hypertension, dietary or medication noncompliance, valvular issue like acute MR or aortic stenosis). Treat the cause: e.g., acute MI – urgent reperfusion; tachyarrhythmia – rate/rhythm control or cardioversion; severe hypertension – aggressive afterload reduction. Cardiogenic Shock & Mechanical Support: If cardiogenic shock from pump failure (e.g., large MI, acute VSD, fulminant myocarditis), consider mechanical circulatory support devices. An intra-aortic balloon pump (IABP) can augment coronary perfusion and reduce afterload in acute MI with cardiogenic shock, especially if mechanical defect like VSD or MR while awaiting surgery. More advanced options include percutaneous ventricular assist devices (Impella) or venoarterial ECMO for severe cardiogenic shock. These require specialized centers. In the interim, optimize medical therapy (vasopressors/inotropes) and get cardiology/cardiothoracic consults. Acute Right Heart Failure: Often due to RV infarct or massive PE. Treat the cause (restore RV perfusion in RV MI by fixing LV infarct, thrombolysis or thrombectomy in PE). Support BP; fluids can be helpful in RV infarct (to stretch RV and maintain output) but not in left HF. Avoid excessive vasodilators in RV infarct; maintain preload. Inotropes like dobutamine may help RV. In PE, avoid aggressive fluids (worsens RV wall stress); use vasopressors (norepi) early if hypotensive. Chronic Heart Failure Management: (Beyond acute scope) – ensure optimal long-term therapy (ACEi/ARB/ARNI, beta-blocker, mineralocorticoid antagonist, etc.), but these are usually addressed after stabilization.
o Adequate PEEP: Apply PEEP (Positive End-Expiratory Pressure) to improve oxygenation and prevent alveolar collapse. Use ARDSnet PEEP/FiO₂ tables to titrate: e.g., if FiO₂ 0. required, set PEEP ~14-18 cm; if FiO₂ 0.5, PEEP ~8-10 cm, etc. The goal SpO₂ is 88-95% (PaO₂ ~55-80 mmHg) to avoid oxygen toxicity while ensuring sufficient oxygenation. Higher PEEP in moderate-severe ARDS can improve oxygenation at the cost of barotrauma or hemodynamic effects; balance carefully. o Respiratory Rate: Adjust to maintain minute ventilation. Since Vt is low, need higher RR (often 20-35) but beware of auto-PEEP. Monitor pH; allow permissive hypercapnia if needed. o Driving Pressure: Monitor plateau minus PEEP (driving pressure) and keep it <15 cm if possible (to limit lung stress). Adjunctive Therapies: o Prone Positioning: For severe ARDS (PaO₂/FiO₂ < 150) , early prone positioning at least 16 hours/day improves oxygenation and has mortality benefit. Proning recruits posterior lung units and improves V/Q matching. o Neuromuscular Blockade: In moderate-severe ARDS, consider early short-term paralysis (e.g., cisatracurium infusion for 48 hours) to improve ventilator synchrony and oxygenation. This can also reduce oxygen consumption and patient fighting the vent. o Conservative Fluids: Avoid fluid overload – a conservative fluid strategy (aim for euvolemia or even slight negative balance if possible) helps minimize pulmonary edema, unless contraindicated by other organ needs. o Inhaled Pulmonary Vasodilators: In refractory hypoxemia, inhaled nitric oxide or epoprostenol can transiently improve oxygenation by dilating pulmonary vessels in ventilated areas (thus improving V/Q matching). These don’t improve mortality but are rescue measures. o ECMO: In extreme cases of refractory hypoxemia or hypercapnia (especially young patients with potentially reversible cause), consider venovenous ECMO (Extracorporeal Membrane Oxygenation) if available, at specialized centers. Sedation: ARDS patients often require deep sedation to tolerate ventilation settings. Use propofol or dexmedetomidine infusions, or benzodiazepine if needed. Titrate to RASS goal (e.g., - 4 to -5 if paralyzed). Underlying Cause: Always address the cause of ARDS. For example, give broad antibiotics and source control for sepsis/pneumonia, pancreatitis management, etc. Monitoring: Frequent ABGs and pulse oximetry. Watch plateau pressures on ventilator. CXR daily to check for lung status, pneumothorax (from barotrauma), ETT position. Ensure DVT prophylaxis and stress ulcer prophylaxis. Physical therapy and early mobilization if possible.
Pulmonary Embolism (PE)
Recognition: Suspect PE in acute onset dyspnea, pleuritic chest pain, tachycardia, hypoxemia, especially with risk factors (immobilization, recent surgery, known DVT, cancer, etc.). Massive PE can present with obstructive shock (hypotension, distended neck veins) or PEA arrest (one of the ACLS T’s). Signs can include RV strain on ECG (new RBBB, S1Q3T3 pattern) and elevated JVP. Bedside echo may show RV dilation or dysfunction in massive PE. Diagnosis: If hemodynamically stable, order a CT pulmonary angiogram (CTA chest) which is the gold standard for diagnosis. If CTA contraindicated (renal failure, contrast allergy) and patient stable, a V/Q scan is alternative. If unstable (suspected massive PE with shock), do bedside ultrasound : signs like RV enlargement, McConnell’s sign (akinesia of mid RV wall with apical sparing) support PE diagnosis. Also check for DVT via leg ultrasound. In extremis, may treat based on clinical suspicion. Risk Stratification: o Massive PE: Defined by hemodynamic compromise (SBP <90 or drop >40 mmHg from baseline) – this requires aggressive treatment.
o Submassive PE: Normotensive but with signs of RV strain (echo showing RV dysfunction, elevated troponin/BNP, significant hypoxemia). o Low-risk PE: Normal hemodynamics and no RV strain. Treatment: o Anticoagulation: Unless contraindicated, start anticoagulation in any moderate or high suspicion of PE while awaiting confirmation. Use IV unfractionated heparin (especially if considering thrombolysis or if renal failure) or SC LMWH (enoxaparin) 1 mg/kg. This prevents clot extension and further emboli. o Thrombolysis: In massive PE with shock , administer thrombolytic therapy immediately (e.g., Alteplase 100 mg IV over 2 hours is standard for PE) – this can be life-saving by dissolving the clot. In cardiac arrest from presumed PE, you can give 50-100 mg alteplase as a bolus during CPR. For submassive PE , thrombolysis is controversial; consider it if there's severe RV dysfunction or deteriorating condition (some protocols use half-dose tPA in submassive, but this is case-by-case weighing bleeding risk). o Mechanical interventions: If thrombolysis is contraindicated (e.g., recent surgery, hemorrhagic stroke) or unsuccessful and patient is in shock, options include catheter-directed thrombolysis or thrombectomy (catheter or surgical pulmonary embolectomy) if available, especially in massive PE. o Oxygenation & Support: Give supplemental O₂ to maintain SpO₂ > 90%. Intubation may be needed for severe hypoxemia, but positive pressure can further strain the RV – if necessary, do it with caution (avoid drops in preload or systemic BP). In hypotension, use vasopressors – norepinephrine is often preferred in massive PE to support BP and modestly improve cardiac output. Dobutamine or epinephrine can also be considered to support the failing RV (inotropic support plus some vasoconstriction with epi). o IVC filter: Consider placing an inferior vena cava filter if there is a contraindication to anticoagulation or if recurrent PE despite anticoagulation. Monitoring: ICU for massive or submassive PE. Follow hemodynamics, oxygenation, signs of bleeding from lytic. Echo can be repeated to monitor RV function improvement. Transition to long-term anticoagulation (usually at least 3-6 months for provoked, indefinite for unprovoked or high-risk).
COPD and Asthma Exacerbations
COPD Exacerbation: Often triggered by infection or irritant, presents with increased sputum, dyspnea, wheezing, CO₂ retention. o Oxygen: Titrate O₂ carefully (target SpO₂ ~88-92%) to avoid knocking out hypoxic drive in CO₂ retainers; however, in acute distress, do not withhold oxygen – treat hypoxemia. o Bronchodilators: Give short-acting bronchodilators : e.g., albuterol (β₂-agonist) via nebulizer q1-2h as needed, plus ipatropium (anticholinergic) nebulizer q4h. In moderate exacerbation, do duoneb (albuterol + ipatropium) treatments. o Corticosteroids: Give systemic steroids to shorten recovery: e.g., methylprednisolone 40- mg IV or prednisone 40-60 mg PO daily. Short courses (5-7 days) are usually sufficient. o Antibiotics: Many COPD exacerbations are due to infection. If sputum is purulent or signs of pneumonia, start antibiotics (coverage for typical respiratory pathogens: e.g., azithromycin or doxycycline or if more severe, a respiratory fluoroquinolone or ceftriaxone + macrolide). In ICU or risk for Pseudomonas (advanced COPD with frequent exacerbations), cover with levofloxacin or pip/tazo as appropriate. o Ventilatory Support: If CO₂ retention (rising PaCO₂, falling pH) or severe work of breathing, start NIV (BiPAP). BiPAP often prevents intubation in COPD exacerbation by improving ventilation and resting fatigued respiratory muscles. Criteria for intubation: unable to tolerate BiPAP, severe acidosis (pH <7.25), respiratory arrest, or other organ failures. If intubated, use lung-protective settings but allow longer exhalation (to prevent air trapping). Set initial tidal
o PEEP: Start at 5 cm H₂O (physiologic PEEP) if lungs normal. If hypoxemic (like pulmonary edema or ARDS), start higher (8-10) to improve oxygenation. Adjust with FiO₂ together (use PEEP/FiO₂ table if ARDS). o FiO₂: Start at 100% FiO₂ when intubated for safety, then rapidly titrate down based on SpO₂ to avoid oxygen toxicity. Aim for FiO₂ ≤ 0.6 as soon as possible while maintaining SpO₂ > 90%. Use PEEP to allow lower FiO₂. o Flow and I:E: Common initial I:E ratio is 1:2. In obstructive disease (asthma/COPD) do 1:3-1: to allow full exhalation. In ARDS, sometimes inverse ratio ventilation (I:E 2:1) is used to improve oxygenation (but needs deep sedation/paralysis). o Pressure Control alternative: For ARDS or when worried about pressures, AC/PC mode could be used to directly control peak pressures. Ventilation Goals: o Oxygenation: Adjust PEEP and FiO₂ to target PaO₂ ~ 60-80 mmHg or SpO₂ 90-96%. Avoid 100% FiO₂ for prolonged periods (risk of O₂ toxicity). o Ventilation (CO₂ removal): Adjust RR and Vt to achieve pH 7.30-7.45 (PaCO₂ usually 35-45). In ARDS or obstructive disease, permissive hypercapnia is acceptable (pH >7.15) as long as hemodynamics permit. o Pressure Limits: Keep Plateau pressure < 30 cm H₂O (check by inspiratory hold). High plateau indicates poor lung compliance (ARDS, fibrosis, etc.). If plateau >30, reduce tidal volume or adjust PEEP. o Alarm Settings: Set appropriately (high pressure alarm ~40 cm; if it alarms, check for causes: coughing/biting tube, secretions needing suction, or true decreased lung compliance or pneumothorax). ABG Interpretation Quick Guide: Arterial Blood Gas helps assess ventilation (CO₂) and oxygenation (O₂) and acid-base status:
- Look at pH: Normal 7.35-7.45. pH <7.35 = acidemia, >7.45 = alkalemia.
- Look at PaCO₂: Normal 35-45 mmHg. CO₂ is an acid; high CO₂ causes acidosis, low CO₂ causes alkalosis. If pH is acidotic and CO₂ is high (>45), this is a primary respiratory acidosis (e.g., hypoventilation). If pH is alkalotic and CO₂ is low (<35), this is primary respiratory alkalosis (hyperventilation).
- Look at HCO₃ :⁻ Normal ~22-26 mEq/L. If pH is acidotic and HCO₃ ⁻is low (<22), that’s primary metabolic acidosis. If pH alkalotic and HCO₃ ⁻ high (>26), primary metabolic alkalosis.
- Determine Primary vs Compensation: Usually one system is primary disorder, the other is compensatory. For example, in metabolic acidosis (low HCO₃ ), expect respiratory⁻ compensation (lower CO₂ via hyperventilation). In acute settings, the compensation won’t fully normalize pH (expect pH to move toward normal but still abnormal). Winters’ formula: Expected CO₂ in metabolic acidosis = (1.5 * HCO₃ ) + 8 ± 2. If⁻ measured CO₂ is higher than expected, there is a concomitant respiratory acidosis; if much lower, concomitant respiratory alkalosis. Metabolic alkalosis compensation: CO₂ increases ~0.6 mmHg for each 1 mEq rise in HCO₃ .⁻ Acute respiratory acidosis: HCO₃ ⁻rises ~1 mEq for each 10 mmHg CO₂ acute increase (chronic ~3.5 per 10). Acute respiratory alkalosis: HCO₃ ⁻drops ~2 mEq per 10 mmHg CO₂ acute decrease (chronic ~5 per 10).
- Anion Gap: For metabolic acidosis, calculate AG = Na - (Cl + HCO₃). Normal ~8-12. If AG > 12, there’s a high anion gap metabolic acidosis (MUDPILES causes: Methanol, Uremia, DKA, Propylene glycol, INH/Iron, Lactic acidosis, Ethylene glycol, Salicylates). Check also the ΔAG to ΔHCO₃ to see if a mixed disorder exists (e.g., if AG increased by more than HCO₃ dropped, there’s concurrent metabolic alkalosis, etc.).
- Clinical correlation: Combine ABG info with patient status. Example: pH 7.25, CO₂ 55, HCO₃ 24 indicates primary respiratory acidosis with no metabolic compensation yet (e.g., acute hypoventilation, maybe drug overdose or COPD exacerbation). pH 7.25, CO₂ 25, HCO₃ 10 indicates primary metabolic acidosis (AG likely) with respiratory alkalosis compensation (hyperventilation). Adjusting Vent Settings by ABG: If PaCO₂ is high (and pH low), increase ventilation (increase RR or Vt) unless obstructive (where you may need to tolerate some CO₂). If PaCO₂ too low (pH high), reduce RR or Vt. If PaO₂ is low, increase FiO₂ or PEEP. If PaO₂ too high (and FiO₂ >0.5), try reducing FiO₂ first if possible or PEEP if FiO₂ already moderate and concern for overdistension. Weaning & Extubation: Once cause of respiratory failure improves, and patient is awake, start weaning trials. Use spontaneous breathing trials (SBT) on minimal support (e.g., CPAP 5 or T-piece, or pressure support 5) to test if patient can breathe unassisted. Check for adequate oxygenation (PaO₂ > 60 on FiO₂ ≤ 40%, PEEP ≤ 5-8), and good mental status, airway protection. Perform cuff leak test if concerned about airway edema. For successful SBT (e.g., 30-120 min tolerating), prepare for extubation: have patient cough, suction airway, extubate to supplemental O₂ and monitor.
Neurological Emergencies
Stroke (CVA)
Stroke Types: Differentiate Ischemic stroke (~85% of strokes) from Hemorrhagic stroke (~15%). Ischemic can be thrombotic or embolic. Hemorrhagic can be intracerebral hemorrhage (ICH) or subarachnoid hemorrhage (SAH). Transient ischemic attack (TIA) is stroke symptoms that resolve within 24h (usually <1h) without infarction but warning for future stroke. Initial Actions for Suspected Stroke: Use FAST (Face droop, Arm weakness, Speech difficulty, Time) for recognition. Note time “last known well” (onset time). Immediate actions: o Activate Stroke Code/Team. Aim to get CT scan within 20 minutes of arrival. o IV Access, Labs: Check glucose ASAP (hypoglycemia can mimic stroke; if low, correct and reassess). Draw CBC, BMP, PT/INR, PTT, cardiac enzymes, type & screen. o NIH Stroke Scale assessment for baseline deficit (scored 0-42). o Emergent Non-Contrast CT Head: to distinguish ischemic vs hemorrhagic. Ischemic changes may be subtle early, but CT mainly to rule out hemorrhage before giving thrombolytic. Ischemic Stroke Management: o tPA (Alteplase): If patient is a candidate, administer IV fibrinolysis with alteplase (tPA). Criteria: Time window: ≤ 4.5 hours from symptom onset ( ≤3 hours for certain patient groups is standard; 3-4.5h extended window in some cases except if age >80, NIHSS >25, diabetic with prior stroke, etc.). BP < 185/110 mmHg: If higher, carefully lower BP with IV labetalol or nicardipine infusion to below 185/110 before tPA. Contraindications: hemorrhage on CT; history of intracerebral bleed; recent major surgery or head trauma (<3 months); recent GI bleeding (<21 days); coagulopathy (INR
1.7, platelets <100k); use of direct thrombin or Xa inhibitors (unless labs normal or 48h since last dose); active bleeding; very large infarct on CT; etc. If any present, tPA is contraindicated. Dose: Alteplase 0.9 mg/kg (max 90 mg) IV – 10% given as bolus over 1 minute, rest over 60 min. Monitoring: After tPA, admit to ICU. Neuro checks q15 min for 2h, then q30 min for 6h, then hourly. Strict BP control: keep SBP < 180 and DBP < 105 for 24h. No antiplatelets or anticoags for 24h post-tPA. Watch for signs of intracerebral hemorrhage
(typically days 3-14 after SAH) via transcranial Doppler or clinical changes; treat vasospasm with “triple-H” historically (hypertension, hypervolemia, hemodilution) but now mainly induced hypertension if no cardiac contraindications, and endovascular therapies (intra-arterial vasodilators or angioplasty). o Manage ICP: Similar measures (head up, ventriculostomy if hydrocephalus is present). o Seizures: Consider prophylactic anticonvulsants in SAH for at least short-term (though practice varies). o Watch for complications: Rebleeding (highest risk in first day if unsecured aneurysm – hence early intervention), hydrocephalus (often needs EVD if acute, or shunt if chronic), hyponatremia (from SIADH or cerebral salt wasting).
Seizures and Status Epilepticus
Initial treatment of a seizure: Ensure patient safety (padding, airway protection). Check glucose (treat hypoglycemia with IV dextrose if needed). Most single seizures <2 minutes will self-terminate; afterward, postictal state is common (transient confusion). Status Epilepticus: A seizure lasting >5 minutes or recurrent seizures without regaining consciousness in between. This is a neurological emergency that can cause brain injury. Management protocol:
- Stabilization: ABCs – position patient on side to avoid aspiration, give oxygen, start IVs, connect to monitors. If airway compromise or persistent status, intubation will be needed (prefer rapid sequence intubation with propofol or benzodiazepine and succinylcholine/rocuronium to secure airway, but note that paralytic drugs will stop motor activity without stopping seizure electrical activity, so continuous EEG may be needed after intubation).
- First-line (within 0-5 min): Benzodiazepines. Give IV Lorazepam 0.1 mg/kg (usually ~4 mg) slowly, may repeat once after 5 min. Alternatively, IV diazepam 5-10 mg. If no IV access, give IM Midazolam 10 mg (midazolam IM is as effective as IV lorazepam), or rectal diazepam in children.
- Second-line (5-15 min): If seizure continues, administer an AED (antiepileptic drug) IV loading dose : Fosphenytoin (preferred over phenytoin due to safer infusion): 20 mg phenytoin equivalents (PE) per kg IV at 150 mg PE/min. (For a 70 kg patient, ~1.4 grams PE). Alternatively, Phenytoin 20 mg/kg IV at 50 mg/min (watch for hypotension, arrhythmia). Levetiracetam (Keppra) 40-60 mg/kg IV (max 4500 mg, commonly 1500-3000 mg dose) over 5-10 min – often chosen for fewer side effects and no need for cardiac monitoring. Valproate 40 mg/kg IV (max ~3000 mg) can be used especially if idiopathic or primary generalized seizures (avoid in young women or if concern for hepatic issues). One of these agents is given; there isn’t an absolute hierarchy, institutional preferences vary.
- Third-line (≥ 20 min, Refractory Status): If still seizing after benzo + AED load, this is refractory status. Intubate if not already done. Initiate continuous IV sedation with EEG monitoring : Options: Midazolam infusion (e.g., 0.2 mg/kg bolus then 0.1 mg/kg/hr infusion, titrate up to stop seizures on EEG), or Propofol infusion (e.g., 2 mg/kg bolus then 5- mg/kg/hr, titrate; watch for hypotension and propofol infusion syndrome if prolonged/high dose). Thiopental or Pentobarbital infusion is another option (barbiturate coma) if above fail. Goal: Achieve burst-suppression or complete suppression of seizures on EEG for 24-48h before slow wean.
o Identify Cause: While treating, investigate causes of status: head CT (rule out hemorrhage, mass), labs (electrolytes, calcium, magnesium, renal/hepatic function, toxicology). Common causes: noncompliance with AEDs, alcohol withdrawal (treat with benzos, phenobarb), stroke, hypoglycemia, infection (meningitis/encephalitis – do LP and add antibiotics if suspected), eclampsia (pregnant – give magnesium 4-6g IV). o Other considerations: If eclampsia (pregnant or postpartum with seizures and HTN), give Magnesium sulfate 4-6 g IV immediately (even before benzos often). If INH toxicity (status in a patient treated for TB), give pyridoxine (Vitamin B6). For hypoglycemia, dextrose as mentioned. For hyponatremic seizures, hypertonic saline 100-150 mL 3% IV. o After stabilization: Arrange EEG to confirm seizure cessation or detect non-convulsive status (which can occur especially if patient paralyzed/intubated). Also consider MRI and neurology consult for further workup.
Altered Mental Status (Delirium/Coma)
General Approach (AEIOU TIPS): Altered mental status (AMS) has many causes. Use the mnemonic A E I O U T I P S for differential: o A: Alcohol (intoxication or withdrawal), Acidosis. o E: Endocrine (hypoglycemia, DKA, thyroid crisis, adrenal crisis), Electrolytes , Encephalopathy (hepatic encephalopathy). o I: Infection (sepsis, meningitis, encephalitis, UTI, pneumonia – especially in elderly delirium). o O: Overdose/O₂ (CO₂ retention hypercapnia, or hypoxia), Opiates (toxidrome pinpoint pupils, etc.). o U: Uremia (renal failure). o T: Trauma (head injury, intracranial hemorrhage), Tumor (increased ICP), Temperature (hyperthermia or hypothermia). o I: Insulin (hypoglycemia, DKA we had), Intussusception (peds) – not applicable in adult OSCE, Psych (primary psychiatric cause, diagnosis of exclusion). o P: Poisoning (any toxin ingestion, medication side effect), Pharmacologic (e.g., anticholinergic delirium, polypharmacy in elderly). o S: Stroke (ischemic or hemorrhagic), Seizure (postictal state or non-convulsive status epilepticus). Initial Evaluation: Check vitals (fever suggests infection, high or low BP could be stroke or sepsis, bradycardia in opioid or elevated ICP Cushing reflex). Check fingerstick glucose right away (treat if <60 mg/dL). Assess pupil size/reactivity (pinpoint = opioids or pontine stroke; blown unilateral pupil = herniation; dilated fixed = severe brain damage or anticholinergic toxidrome). Check meningismus (stiff neck -> meningitis/SAH). Look for signs of trauma (head bruising, Battle’s sign, etc.). Evaluate mental status (level of consciousness on GCS, orientation, any focal deficits). Immediate Interventions (“Coma Cocktail”): Often if immediate cause unclear: administer Dextrose (D50 IV) if hypoglycemia can’t be ruled out, Thiamine 100 mg IV (for possible Wernicke’s encephalopathy, especially if malnourished or alcoholism, give before glucose if possible), and Naloxone 0.4-2 mg IV if opioid overdose suspected (pinpoint pupils, respiratory depression). Also give oxygen if hypoxic. These interventions can be life-saving and diagnostic. Workup: Based on differential: o Labs: CBC (infection?), CMP (electrolytes, LFTs for hepatic encephalopathy, renal function for uremia), ABG (especially if CO₂ retention suspected), serum osm (for intoxications), toxicology screen (opiates, benzos, barbs, stimulants, acetaminophen level, salicylate level, alcohol levels, etc.), TSH (myxedema coma can cause AMS, also severe hyperthyroid (thyroid storm) can cause agitation), cortisol (adrenal crisis can present with AMS and shock). o Imaging: Noncontrast CT head for structural causes (stroke, hemorrhage, large mass). In a comatose patient with no obvious cause, CT is almost always indicated urgently. If CT negative
Maintain CPP (Cerebral Perfusion Pressure) = MAP - ICP. Keep CPP ~60-70 mmHg (so if ICP is high, may need to keep MAP higher with vasopressors). Avoid hypotension (SBP <90) at all costs in TBI. Monitoring: If invasive ICP monitor is in place, goal ICP < 22 mmHg typically. Continue neuro checks (pupils, motor response).
Neuromuscular Emergencies (briefly)
While not a separate section, note critical neuromuscular causes of respiratory failure: o Myasthenic Crisis: Rapid muscle weakness in myasthenia gravis leading to respiratory failure. Treat with plasmapheresis or IVIG and intubation if needed; avoid exacerbating meds. o Guillain-Barré Syndrome: Ascending paralysis; watch for respiratory muscle involvement – may need intubation if vital capacity drops. Treat with plasmapheresis or IVIG. o Stroke involving brainstem or high spinal cord injury (C3-5): can 】 Adult Suspected Stroke Algorithm (American Heart Association). This flowchart illustrates the emergent evaluation of stroke, including rapid EMS assessment, immediate neurologic assessment with CT imaging, and treatment pathways for ischemic vs hemorrhagic stroke. For ischemic stroke, it emphasizes checking for tPA criteria and administering alteplase if within the time window, whereas for hemorrhagic stroke it prompts initiation of intracranial hemorrhage
protocol 】.
Neuromuscular Emergencies Note: Acute neuromuscular failures can also cause respiratory crises. For example, Myasthenic Crisis (in myasthenia gravis) causes severe weakness leading to respiratory failure – treat with plasmapheresis or IVIG and intubation as needed. Guillain-Barré Syndrome (acute polyradiculoneuropathy) can progress to diaphragmatic paralysis – monitor vital capacity and consider early intubation plus IVIG or plasmapheresis. Always consider these in ICU patients with rapidly progressive weakness or paralysis.
Infectious Disease Emergencies
Sepsis and Septic Shock
Recognition: Sepsis is life-threatening organ dysfunction due to dysregulated infection response (often defined as increase in SOFA score ≥2). Septic shock is sepsis with persisting hypotension requiring vasopressors to maintain MAP ≥65 and lactate >2 mmol/L despite fluids. Common sources: pneumonia, UTI/pyelo, abdominal infections, skin/soft tissue, lines/devices. Initial Bundle (First 1-3 Hours): Early identification and treatment greatly improve outcome】. The Surviving Sepsis Campaign recommends the following (Hour-1 bundle):
- Measure Lactate: Elevated lactate (>2) can indicate hypoperfusion and is associated with worse prognosi】. Recheck lactate if initial is >2.
- Obtain Cultures: Draw blood cultures (at least 2 sets) before antibiotics (if no significant delay) to help identify pathogen. Culture other sites as indicated (urine, sputum, etc.).
- Broad-Spectrum Antibiotics: Start IV antimicrobials promptly – within 1 hour for septic shock, and ideally within 3 hours for sepsis without shoc】. Use broad coverage tailored to suspected source:
For unknown source in ICU: use broad gram-negative and gram-positive coverage (e.g., piperacillin-tazobactam + vancomycin , or carbapenem + vancomycin ). Add MRSA coverage (vancomycin) especially for catheter-related, skin, or pneumonia sources. Consider double coverage for Pseudomonas (e.g., add aminoglycoside or fluoroquinolone) if neutropenic or resistant risk. If intra-abdominal, ensure anaerobe coverage (pip-tazo or add metronidazole). If suspected fungal (immunosuppressed or TPN or central line candida), consider echinocandin. Tailor antibiotics once cultures result.
- Fluid Resuscitation: Give 30 mL/kg IV crystalloid for hypotension or lactate ≥4 mmol/L as a bolus as fast as possibl】 (usually within the first 3 hours). Typically use lactated Ringer’s or Normal Saline (balanced crystalloids like LR preferre】). Reassess volume status after initial bolus (exam: JVP, lung sounds, ultrasound IVC, etc.). Additional fluid boluses can be given in smaller aliquots (e.g., 500 mL) based on response (blood pressure, urine output, lactate clearance】.
- Vasopressors: If patient remains hypotensive (MAP < 65) after fluids, start vasopressors. Norepinephrine is first-line for septic shocaafp.org】. Titrate to MAP ≥ 65. If needing high dose NE (>0.3-0.5 μg/kg/min), add vasopressin 0.03 U/min to augment and allow NE dose reductioaafp.org】. Epinephrine can be added or substituted if additional support needed. Dopamine is an alternative in highly selected cases (e.g., bradycardic shock, but it has more arrhythmias). Consider dobutamine if cardiac output is low (persistent hypoperfusion despite MAP goal, high filling pressures). Maintain adequate arterial pressure and perfusion.
- Reassessment: After initial resuscitation, evaluate tissue perfusion: normalize lactate, capillary refill, mental status, urine output (>0.5 mL/kg/hr). Use dynamic measures (passive leg raise, fluid challenge) to decide if more fluid will hel】. Place invasive lines if needed: an arterial line for continuous BP monitoring is recommended in shocaafp.org】. Adjunctive Therapy: Apply vasopressor through central line when possible (but do not delay via peripheral IV if central not yet placeaafp.org】). If hypotension is refractory to fluids and high-dose pressors, consider hydrocortisone 200 mg/day (e.g., 50 mg IV q6h) for possible relative adrenal insufficiency (especially if vasopressor requirement remains high). Start within first 24-48h if needed. Source Control: Remove infection sources (drain abscess, remove infected lines, debride necrotic tissue) as early as possible. Glucose control: Avoid severe hyperglycemia – aim glucose < mg/dL with insulin drip if needed (but avoid hypoglycemia). DVT prophylaxis and stress ulcer prophylaxis in ICU unless contraindicated. Nutrition: Start enteral feeding when feasible in 24-48h. Monitoring: ICU care with frequent vitals and volume status checks. Repeat lactate 2-4h after resuscitation; improving lactate suggests better perfusion. Monitor kidney function (U/O and creatinine), liver function, mentation. Use vasopressor doses guided by continuous BP. If SvO₂ monitoring available, aim for >70%, but not mandatory. If patient intubated with ARDS, manage as above. Septic Shock Pearls: Target MAP ~65; higher MAP (75-85) may be needed in known hypertensive patients, but generally no benefit to very high BP targetaafp.org】. Norepi can cause peripheral ischemia at high doses – adding vasopressin at fixed low dose is recommended rather than escalating norepi indefinitelaafp.org】. Watch for pulmonary edema with large fluids – if oxygenation worsens, consider intubation and ventilation. Consider advanced hemodynamic monitoring (e.g., cardiac output monitors, echo) if shock not responding as expected.
Severe Pneumonia
Community-Acquired Pneumonia (CAP): Common ICU admission diagnosis if severe (respiratory failure or sepsis). Pathogens: Streptococcus pneumoniae most common, also Legionella, H. influenzae, Staph aureus (especially post-influenza), gram-negatives, etc.
Empiric Antibiotics: Based on patient’s age and risk factor】: o Age 18-49 (adult): Likely organisms S. pneumoniae, N. meningitidis. Vancomycin IV (15- mg/kg q8-12h, to cover ceph-resistant Strep) + Ceftriaxone 2 g IV q12h (covers pneumococcus and meningococcus) is standar】. (Add Ampicillin if risk factors as below.) o Age ≥50 or immunocompromised (or alcoholism, pregnancy): Add Ampicillin 2 g IV q4h to cover Listeri】, in addition to * Vancomycin + Ceftriaxone 】. Listeria coverage is also indicated in <1 month old (amp + gentamicin in neonates). o Post-neurosurgery or skull trauma, or CSF shunt: Cover hospital organisms including Pseudomonas and staph: Vancomycin + Cefepime 2 g IV q8h (or Vancomycin + Meropenem). If penicillin-allergic, could use Vancomycin + Moxifloxacin (for pneumo/meningo) plus TMP- SMX for Listeria (noting moxi doesn’t cover pseudomonas). o If beta-lactam allergic (severe): Consider Chloramphenicol + Vancomycin + TMP-SMX (for Listeria) or consult ID for alternatives. Adjunct: Dexamethasone: Give IV Dexamethasone 0.15 mg/kg (10 mg) q6h for 4 days , starting
- before or with the first antibiotic dose aafp.org】. This is proven to reduce morbidity and mortality in adult pneumococcal meningitis (and hearing loss in H. influenzae meningitis in children). If pneumococcal meningitis is confirmed, continue the steroid course; if not, often dex can be stopped after culture results. Supportive Care: ICU monitoring. Manage fever with antipyretics (fever increases metabolic demand). Seizure precautions; treat seizures with benzos and load phenytoin or levetiracetam if occur (consider seizure prophylaxis in severe meningitis with seizures). Watch for signs of increased ICP – maintain adequate BP for cerebral perfusion, elevate head if needed. If profoundly altered, consider ICP monitoring. Avoid hypotonic fluids; use normal saline. CSF findings (bacterial): Elevated opening pressure; WBC very high with neutrophil predominance (thousands with >80% PMNs); low CSF glucose (<40, or CSF:serum glucose ratio <0.4); high protein (>200). Send PCR for common pathogens as needed. Neisseria meningitidis precautions: Place patient on droplet isolation. Close contacts need prophylaxis (rifampin or ciprofloxacin). Viral encephalitis consideration: If the presentation could be encephalitis (e.g., confusion, seizures, fever but maybe not as stiff neck), particularly HSV encephalitis , add Acyclovir 10 mg/kg IV q8h empirically (especially for altered mental status or focal neuro signs without bacteria on gram stain). HSV encephalitis classically causes temporal lobe seizures and high RBC count in CSF. Acyclovir is also indicated for VZV or severe unidentified viral encephalitis. Outcome: Tailor antibiotics when culture identifies organism (e.g., pneumococcus – 10-14 days therapy, meningococcus – ~7 days, Listeria – at least 21 days, etc.). Ensure appropriate follow-up (hearing tests for kids, etc.).
Infective Endocarditis
Presentation: Can be subtle – fever, chills, night sweats, weight loss, malaise in a patient with risk factors (IV drug use, prosthetic valves, recent dental work, structural heart disease). May have new or changing heart murmur, heart failure signs (if valve destroyed), or embolic phenomena: Janeway lesions (painless macules on palms/soles), Osler nodes (tender nodules on fingers/toes), Roth spots (retinal hemorrhages), splinter hemorrhages, etc. ICU scenarios include endocarditis causing septic shock, stroke (septic embolus to brain), or acute valvular regurgitation with pulmonary edema. Diagnosis: Obtain 3 sets of blood cultures from different sites, ideally before antibiotics (if patient stable enough to wait a few hours). Do a transthoracic echo (TTE) ; if negative and suspicion remains high, a transesophageal echo (TEE) is indicated (much higher sensitivity for vegetations). Endocarditis is defined by Duke criteria (major: positive blood cultures with typical organisms, evidence of endocardial involvement on echo; minor: fever, risk factors, vascular phenomena, immunologic phenomena, etc.).
Empiric Therapy: Do not delay therapy in critically ill. Initial empiric antibiotics should cover staphylococci (MSSA/MRSA), streptococci, and enterococc】: o Native Valve, unknown organism: Vancomycin IV (15-20 mg/kg q8-12h) is a good monotherapy empiric choice in most case】. It covers MRSA, MSSA (although beta-lactam is better for MSSA when known), Streptococci, and Enterococci (except VRE). o Prosthetic Valve Endocarditis: Use Vancomycin + Gentamicin + Rifampin empiricall】. Rifampin (300 mg PO/IV q8h) helps penetrate biofilms on prosthetic material (only add rifampin in prosthetic valve cases). Gentamicin (3 mg/kg/day IV in 2-3 divided doses) for synergistic kill, especially for enterococcus or staph prosthetic valve early infection. o Alternatively, some protocols for native valve (especially subacute presentation) use Ampicillin- sulbactam 3 g IV q6h + Gentamicin to cover all flora (amp-sulbactam covers strep, enterococcus, and HACEK, plus MSSA; gent adds gram-negative synergy】. o If IV drug user, staph aureus is most common (often MRSA) – vancomycin appropriate. Definitive Therapy: Tailor once cultures result: o MSSA: β-lactam like Nafcillin or Cefazolin (better than vanco for MSSA bactericidal activity). o MRSA: Vancomycin (or daptomycin if vanco MIC high or intolerance). o Streptococcus viridans or bovis: IV Penicillin G or Ceftriaxone for 4 weeks (add gentamicin for first 2 weeks in some cases for synergy). o Enterococcus: Ampicillin + gentamicin or Ampicillin + ceftriaxone (the latter is a regimen for E. faecalis). VRE: linezolid or daptomycin (consult ID). o HACEK organisms (culture-negative endocarditis common causes: Haemophilus aphrophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella): treat with Ceftriaxone IV for 4 weeks (amp-sulbactam or ciprofloxacin are alternatives). Duration: Typically 4-6 weeks IV antibiotics from first negative culture. Longer (6+ weeks) for prosthetic valves or difficult organisms (MRSA, fungi). Surgery: Early cardiothoracic surgery consult if any of the following: acute heart failure from valve destruction (e.g., acute MR or AI causing pulmonary edema or cardiogenic shock), uncontrolled infection (persistent bacteremia, abscess, or difficult-to-treat pathogen like fungi), large vegetations >10 mm especially if embolizing, or prosthetic valve endocarditis. Valve replacement may be lifesaving in these scenarios. Embolic complications: Monitor for signs of systemic emboli (stroke workup if neuro changes, spleen or kidney infarcts causing abdominal/flank pain, limb ischemia, PE if right-sided endocarditis). After stabilization, patients need evaluation for embolic phenomena and maybe prophylaxis (though anticoagulation is not routinely used in native valve endocarditis due to hemorrhagic stroke risk, except in mechanical valves per usual indications). Prophylaxis: Not for ICU care, but remember patients with prosthetic valves or prior endocarditis need antibiotics before high-risk dental or surgical procedures.
Other Notable Infections
Spontaneous Bacterial Peritonitis (SBP): Cirrhotic patient with ascites and mental status change/fever
- do paracentesis, if PMN ≥250, treat with cefotaxime 2 g IV q8h (or other 3rd-gen ceph). Add IV albumin for renal protection if creat >1 or BUN >30 or Tbili >4. Clostridioides difficile Colitis: Watery diarrhea in ICU, especially post-antibiotics. Send stool PCR/toxin. Treat severe cases with oral Vancomycin 125-250 mg QID (and add IV metronidazole if fulminant) or fidaxomicin. If ileus, consider rectal vancomycin. Watch for toxic megacolon – surgical colectomy if perforation or refractory. Necrotizing Fasciitis: Rapidly progressive soft tissue infection with pain out of proportion, crepitus, systemic toxicity. Broad antibiotics (e.g., vancomycin + pip/tazo + clindamycin for toxin suppression) and emergent surgical debridement are key.
