What is the immediate management algorithm for Acute Ischemic Stroke in the Emergency Department (Door-to-CT, tPA/Tenecteplase inclusion/exclusion criteria, BP targets, and Mechanical Thrombectomy window)?

1) Determine exact 'Last Known Well' time, check fingerstick Blood Glucose immediately (hypoglycemia is the #1 reversible stroke mimic!), and obtain a Non-Contrast Head CT within 20 minutes of ED arrival (interpret within 45 min) to RULE OUT intracranial hemorrhage; 2) If non-contrast CT shows no hemorrhage and symptom onset is within <= 3.0 hours (or <= 4.5 hours in eligible patients), administer IV Alteplase (tPA, 0.9 mg/kg, max 90 mg, 10% bolus over 1 min + 90% over 60 min) or Tenecteplase with Door-to-Needle <= 60 min — PROVIDED Blood Pressure is lowered to < 185/110 mmHg BEFORE starting fibrinolysis (using IV Labetalol or Nicardipine) and maintained < 180/105 mmHg for 24 hours after tPA (if NOT receiving tPA, allow 'permissive hypertension' up to 220/120 mmHg to perfuse the ischemic penumbra); 3) Perform CT Angiography and proceed to Endovascular Mechanical Thrombectomy for anterior circulation Large Vessel Occlusion (ICA or proximal M1 MCA) up to 6–24 hours from last known well.

In a patient with a Chest Tube (Water-Seal Drainage System), what do 'Tidaling' versus 'Continuous Bubbling' in the Water-Seal Chamber and 'Gentle Bubbling' in the Suction Control Chamber indicate?

1) Tidaling (rise and fall of the fluid level in the water-seal chamber with inspiration and expiration): NORMAL finding indicating the chest tube is patent and transmitting intrapleural pressure swings (tidaling stops when the lung has fully re-expanded OR if the tubing is kinked/occluded); 2) Intermittent bubbling in the water-seal chamber during exhalation/coughing in a pneumothorax: expected as pleural air escapes, whereas CONTINUOUS bubbling in the water-seal chamber indicates an active AIR LEAK (either a persistent bronchopleural fistula in the patient or a loose connection in the external tubing); 3) Gentle continuous bubbling in a wet Suction Control Chamber: NORMAL when wall suction is attached; if the chest tube disconnects from the drainage unit, submerge the distal tube end in 2 cm of sterile water (creating a temporary water seal), and NEVER clamp a chest tube during transport (risks tension pneumothorax!).

Compare the receptor profiles and clinical indications of the major ICU Vasopressors and Inotropes: Norepinephrine, Epinephrine, Phenylephrine, Dopamine, Dobutamine, and Milrinone.

1) Norepinephrine (α1 >> β1): first-line vasopressor in septic, cardiogenic, and hypovolemic shock (raises SVR and MAP with minimal tachycardia); 2) Epinephrine (β1 = β2 > α1 at low dose; α1 predominates at high dose): first-line for Anaphylactic shock (IM), Cardiac Arrest (IV push), severe symptomatic bradycardia/post-arrest shock; 3) Phenylephrine (pure α1 agonist, zero β activity): raises SVR and induces baroreceptor reflex bradycardia (used in anesthesia-induced hypotension or hypotensive tachyarrhythmias/HOCM); 4) Dopamine (dose-dependent D1 -> β1 -> α1; largely replaced by norepinephrine due to higher tachyarrhythmia rate); 5) Dobutamine (β1 > β2): inodilator that increases Cardiac Output and slightly lowers SVR in Cardiogenic Shock (can cause mild hypotension/tachycardia); 6) Milrinone (PDE3 inhibitor -> increases cardiac & vascular cAMP independently of beta-receptors): inodilator increasing contractility and reducing pulmonary/systemic vascular resistance in HFrEF (even in patients on chronic beta-blockers; causes hypotension and is cleared renally).

What happens if a peripheral IV infusion of a potent alpha-1 vasopressor (such as Norepinephrine, Dopamine, or Phenylephrine) extravasates into subcutaneous tissue, and what is the immediate antidote?

Intense local alpha-1 vasoconstriction causes severe tissue ischemia, blanching, coldness, and sloughing/necrosis; immediately STOP the infusion, leave the IV cannula in place briefly to aspirate any residual drug, elevate the extremity, apply warm compresses, and infiltrate the extravasated site subcutaneously in a ring pattern with the alpha-adrenergic antagonist Phentolamine (5–10 mg diluted in 10 mL normal saline).

What are the components of the Surviving Sepsis Campaign Hour-1 / 3-Hour Resuscitation Bundle for Sepsis and Septic Shock?

1) Measure Serum Lactate level (and remeasure within 2–4 hours if initial lactate > 2.0 mmol/L); 2) Obtain Blood Cultures (at least 2 sets: aerobic + anaerobic) PRIOR to administering antibiotics (without delaying antibiotic administration); 3) Administer broad-spectrum Intravenous Antibiotics within 1 hour of recognition of septic shock (or within 3 hours if sepsis without shock); 4) Rapidly infuse 30 mL/kg of IV Balanced Crystalloid fluid (Lactated Ringer's or Normal Saline) within the first 3 hours for hypotension (MAP = 4.0 mmol/L; 5) Apply Vasopressors (first-line: Norepinephrine) during or after fluid resuscitation if hypotensive to maintain MAP >= 65 mmHg.

What are the '5 Hs and 5 Ts' (reversible causes of Cardiac Arrest, particularly Pulseless Electrical Activity [PEA] and Asystole) in ACLS?

The 5 Hs: 1) Hypovolemia (hemorrhage/dehydration -> IV crystalloid/blood bolus), 2) Hypoxia (airway obstruction/apnea -> 100% O2 and advanced airway), 3) Hydrogen ion / Acidosis (severe metabolic/respiratory acidosis -> ventilation and IV NaHCO3), 4) Hypokalemia or Hyperkalemia (check K+ -> IV CaCl2/Ca-gluconate + insulin/D50/NaHCO3 for hyperkalemia), and 5) Hypothermia (rewarming). The 5 Ts: 1) Tension Pneumothorax (needle decompression + chest tube), 2) Tamponade, cardiac (bedside ultrasound + pericardiocentesis), 3) Toxins (drug overdose -> specific antidotes/lipid emulsion/NaHCO3), 4) Thrombosis, pulmonary (Massive PE -> systemic fibrinolysis tPA), and 5) Thrombosis, coronary (Massive STEMI -> emergent PCI).

What does a LOW Mixed Venous Oxygen Saturation (SvO2 80%) signify in a critically ill patient?

By the Fick equation, SvO2 reflects the balance between systemic Oxygen Delivery (DO2 = CO × CaO2) and tissue Oxygen Consumption (VO2): a LOW SvO2 ( 80%) indicates impaired cellular oxygen utilization / microvascular shunting, seen in hyperdynamic Septic Shock, Cyanide toxicity (histotoxic hypoxia), or left-to-right vascular shunts.

What are the immediate Post-Cardiac Arrest Care (ROSC) targets for Oxygenation, Ventilation, Blood Pressure, 12-Lead ECG, and Targeted Temperature Management (TTM)?

1) Airway & Oxygenation: secure endotracheal airway (confirm with waveform capnography) and titrate FiO2 to maintain SpO2 92%–98% (avoid hyperoxia [SpO2 100% / PaO2 > 300], which generates reactive oxygen species and worsens reperfusion brain injury); 2) Ventilation: maintain normocarbia (PETCO2 35–40 mmHg, PaCO2 35–45 mmHg; avoid hyperventilation, which causes cerebral vasoconstriction); 3) Hemodynamics: maintain Systolic BP > 90 mmHg and MAP >= 65 mmHg with IV crystalloid bolus and Norepinephrine/Epinephrine infusion; 4) Obtain immediate 12-Lead ECG and proceed to emergent Coronary Angiography/PCI if STEMI or high suspicion of acute coronary occlusion; 5) Targeted Temperature Management (TTM) for any patient who remains COMATOSE (unable to follow verbal commands) after ROSC: actively maintain a constant core temperature between 32°C and 37.5°C (strictly preventing fever > 37.7°C) for at least 24 hours.

What is the Rapid Shallow Breathing Index (RSBI), and what clinical and ABG parameters indicate a patient is ready for Extubation from mechanical ventilation?

RSBI = Respiratory Rate (breaths/min) / Tidal Volume (in Liters), measured during a 30–120 minute Spontaneous Breathing Trial (SBT on minimal pressure support 5–8 cmH2O / PEEP = 90–92% (PaO2 >= 60 mmHg) on FiO2 10–15 mL/kg.

How is Hypertensive Emergency distinguished from Hypertensive Urgency (Severe Asymptomatic Hypertension), and what is the safe blood pressure reduction rule (plus the two major exceptions)?

Both typically present with BP > 180/120 mmHg, but ONLY Hypertensive Emergency has acute Target-Organ Damage (hypertensive encephalopathy, intracranial hemorrhage/ischemic stroke, acute coronary syndrome, acute cardiogenic pulmonary edema, aortic dissection, acute kidney injury/microangiopathic hemolytic anemia, or eclampsia). Hypertensive Urgency (no end-organ damage) is treated by restarting/adjusting ORAL antihypertensives over 24–48 hours. Hypertensive Emergency requires ICU admission and titratable IV antihypertensives (Nicardipine, Clevidipine, Labetalol, Esmolol, Fenoldopam, or Nitroprusside): lower MAP by NO MORE than 15%–25% in the first hour (then to ~160/100 over the next 2–6 hours) to prevent watershed cerebral or coronary ischemia — WITH TWO CRITICAL EXCEPTIONS: 1) Acute Aortic Dissection: rapidly reduce Systolic BP to < 120 mmHg and Heart Rate to < 60 bpm within 20 minutes using an IV Beta-Blocker FIRST (Esmolol or Labetalol to reduce dP/dt shear stress) followed by IV Nicardipine/Nitroprusside; 2) Severe Preeclampsia / Eclampsia or Pheochromocytoma crisis: lower SBP < 140–160 mmHg acutely (plus IV Magnesium Sulfate in preeclampsia).

What are the normal reference ranges for Cardiac Output (CO), Cardiac Index (CI), Stroke Volume (SV), Systemic Vascular Resistance (SVR), and Mixed Venous Oxygen Saturation (SvO2)?

Cardiac Output (CO = HR × SV): 4.0–8.0 L/min; Cardiac Index (CI = CO / Body Surface Area, normalizes CO for patient size): 2.5–4.0 L/min/m² (cardiogenic shock is CI = 70%).

What are the evidence-based ARDSnet Lung-Protective Mechanical Ventilation targets that reduce mortality in ARDS?

1) Low Tidal Volume (Vt) ventilation: 4–8 mL/kg (target 6 mL/kg) of Predicted/Ideal Body Weight (calculated from height and sex, NOT actual body weight) to prevent volutrauma; 2) Plateau Pressure (measured during an end-inspiratory hold pause) strictly = 7.20–7.25); and 5) Early Prone Positioning (>= 16 hours/day) when PaO2/FiO2 < 150 mmHg.

How do you calculate Mean Arterial Pressure (MAP), what is its normal range, and what is the minimum MAP target required to maintain vital organ (cerebral, coronary, renal) perfusion in shock?

MAP = [(2 × Diastolic BP) + Systolic BP] / 3, or Diastolic BP + 1/3(Pulse Pressure); normal MAP is 70–100 mmHg, and the minimum resuscitation target in shock/sepsis is MAP >= 65 mmHg.

What is the physiological mechanism and hemodynamic timing of an Intra-Aortic Balloon Pump (IABP) in Cardiogenic Shock?

Positioned in the descending thoracic aorta just distal to the left subclavian artery and proximal to the renal arteries, synchronized to the ECG or arterial pressure waveform for 'counterpulsation': the balloon INFLATES at the onset of Diastole (on the dicrotic notch of the arterial waveform / middle of the T wave), augmenting diastolic aortic pressure to increase CORONARY ARTERY PERFUSION and cerebral blood flow; the balloon DEFLATES just prior to Isometric Ventricular Systole (on the R wave peak), creating a vacuum effect in the aorta that reduces Left Ventricular AFTERLOAD and myocardial oxygen consumption (Note: strictly contraindicated in moderate-to-severe Aortic Regurgitation or aortic dissection!).

How is Waveform Capnography (End-Tidal CO2 / PETCO2) used during ACLS Cardiopulmonary Resuscitation?

1) Gold-standard confirmation of proper Endotracheal Tube placement in the trachea (continuous square-wave capnogram with PETCO2 > 0 mmHg, eliminating esophageal intubation); 2) Real-time monitor of CPR chest compression quality: target PETCO2 >= 10–20 mmHg during CPR (if PETCO2 is persistently = 35–40 mmHg) indicates spontaneous cardiac output has resumed even before the next pulse check.

How do you calculate Cerebral Perfusion Pressure (CPP), what are the normal ICP and CPP reference ranges, and what are the tiered interventions for Elevated Intracranial Pressure (ICP > 20–22 mmHg)?

CPP = Mean Arterial Pressure (MAP) - Intracranial Pressure (ICP); Normal ICP is 5–15 mmHg (sustained ICP > 20–22 mmHg requires treatment), and target CPP in traumatic brain injury is 60–70 mmHg. Tiered ICP Management: 1) Elevate Head of Bed to 30 degrees with head/neck in strictly neutral midline alignment (prevents internal jugular vein compression and promotes cerebral venous drainage), 2) Maintain normothermia, adequate sedation/analgesia, normocarbia (PaCO2 35–40 mmHg; brief hyperventilation to PaCO2 30–35 mmHg is ONLY a temporary bridge for acute impending herniation because cerebral vasoconstriction worsens ischemia!), 3) CSF drainage via External Ventricular Drain (EVD), and 4) Hyperosmolar therapy with IV Mannitol (0.25–1 g/kg; monitor serum osmolality < 320 mOsm/kg) OR Hypertonic Saline (3% or 23.4% NaCl).

How is the Glasgow Coma Scale (GCS) scored across Eye Opening (E1–E4), Verbal Response (V1–V5), and Motor Response (M1–M6), and what total score mandates endotracheal intubation?

Total GCS ranges from 3 (deepest coma; never 0!) to 15 (fully alert): Eye Opening (4): 4 = Spontaneous, 3 = To speech/voice, 2 = To pain/pressure, 1 = None; Verbal Response (5): 5 = Oriented, 4 = Confused conversation, 3 = Inappropriate words, 2 = Incomprehensible sounds/moaning, 1 = None; Motor Response (6 — most prognostic component): 6 = Obeys commands, 5 = Localizes pain, 4 = Withdraws from pain (normal flexion), 3 = Abnormal flexion (Decorticate posturing), 2 = Abnormal extension (Decerebrate posturing), 1 = None (flaccid). Severity: Mild TBI = 13–15; Moderate TBI = 9–12; Severe TBI / Coma = <= 8 ('GCS <= 8, Intubate!' to protect the airway).

What is the difference between Synchronized Cardioversion and Unsynchronized Defibrillation, and for which rhythms is each used?

Synchronized Cardioversion delivers an electrical shock timed ('synchronized') to land directly on the peak of the R wave (ventricular depolarization), strictly AVOIDING the vulnerable relative refractory period of the T wave (which would induce R-on-T Ventricular Fibrillation); it is used for any UNSTABLE Tachyarrhythmia WITH A PULSE (Unstable Atrial Fibrillation, Atrial Flutter, Supraventricular Tachycardia, or Monomorphic Ventricular Tachycardia with a pulse). Unsynchronized Defibrillation fires immediately upon pressing the shock button (because there is no organized R wave to synchronize to or the rhythm is polymorphic); it is used for PULSELESS VT, Ventricular Fibrillation (VF), and Unstable Polymorphic VT (even if a faint pulse is present, because polymorphic QRS morphology prevents reliable R-wave synchronization).

How do you calculate the Parkland Formula for 24-hour fluid resuscitation in a major Thermal Burn (> 20% Total Body Surface Area using the Rule of Nines), and how is resuscitation adequacy monitored?

Adult Rule of Nines (only count partial-thickness [2nd-degree] and full-thickness [3rd-degree] burns; EXCLUDE superficial 1st-degree erythema): Head & neck = 9%, Anterior trunk = 18%, Posterior trunk = 18%, Each upper extremity = 9% (×2), Each lower extremity = 18% (×2), Perineum = 1%. Parkland Formula: Total 24-hour Lactated Ringer's (LR) volume = 4 mL × Body Weight (kg) × % TBSA Burned; administer ONE-HALF (50%) of this total volume over the FIRST 8 HOURS (timed from the moment of the burn injury, NOT time of ED arrival!) and the remaining ONE-HALF (50%) over the NEXT 16 HOURS; however, formulas are only a starting estimate — titrate the hourly LR infusion rate to maintain Urine Output of 0.5–1.0 mL/kg/hr (30–50 mL/hr) in adults (or 1.0–1.5 mL/kg/hr in children or electrical burns with myoglobinuria).

What are the immediate bedside diagnostic signs and life-saving needle decompression / procedural treatments for Tension Pneumothorax and Cardiac Tamponade?

Tension Pneumothorax (one-way valve traps air in pleural space, collapsing ipsilateral lung and shifting mediastinum/vena cava to the opposite side): hypotension, JVD, unilaterally ABSENT breath sounds, hyperresonance to percussion, and tracheal deviation AWAY from the affected side -> do NOT wait for a chest X-ray; perform immediate Needle Thoracostomy (2nd intercostal space at the midclavicular line or 4th–5th intercostal space at the anterior axillary line, inserting over the SUPERIOR border of the rib to avoid the intercostal neurovascular bundle) followed by Tube Thoracostomy (chest tube). Cardiac Tamponade (Beck triad: hypotension, JVD, muffled heart sounds + pulsus paradoxus > 10 mmHg and electrical alternans on ECG): immediate ultrasound-guided Pericardiocentesis or surgical pericardial window (with temporary IV fluid bolus to maintain RV filling).

Where should the Phlebostatic Axis transducer be leveled when zeroing an Arterial Line or Central Venous / Pulmonary Artery Catheter, and how does transducer malpositioning affect pressure readings?

Level the transducer stopcock at the Phlebostatic Axis: the intersection of the 4th intercostal space and the mid-axillary line (corresponding to the anatomical level of the right atrium); if the transducer is positioned TOO LOW (below the right atrium), hydrostatic weight produces a FALSELY HIGH pressure reading; if the transducer is positioned TOO HIGH (above the right atrium), it produces a FALSELY LOW pressure reading.

How do the four major Shock Categories (Hypovolemic, Cardiogenic, Distributive/Septic, and Obstructive) differ across Preload (CVP/PAWP), Cardiac Output (CO/CI), Afterload (SVR), and Mixed Venous O2 (SvO2)?

1) Hypovolemic Shock (hemorrhage, severe dehydration, burns): LOW CVP/PAWP, LOW CO/CI, HIGH compensatory SVR, and LOW SvO2; 2) Cardiogenic Shock (massive MI, end-stage HFrEF, myocarditis, acute valve rupture): HIGH CVP and HIGH PAWP (> 18 mmHg), LOW CO/CI (< 2.2 L/min/m²), HIGH compensatory SVR, and LOW SvO2; 3) Distributive Shock — Septic/Anaphylactic ('warm shock'): LOW CVP/PAWP, HIGH (or normal) CO/CI early, markedly LOW SVR (< 800 dynes·sec/cm⁵ due to systemic vasodilation), and normal-to-HIGH SvO2; 4) Obstructive Shock (Cardiac Tamponade, Massive PE, Tension Pneumothorax): HIGH CVP (with equalization of diastolic pressures CVP ≈ RVEDP ≈ PADP ≈ PAWP ~18–20 mmHg in tamponade; or high CVP/PAP with low/normal PAWP in massive PE), LOW CO/CI, HIGH SVR, and LOW SvO2.

How is Septic Shock formally defined (Sepsis-3 criteria), what is the First-Line Vasopressor, what is the Second-Line agent added if MAP remains < 65 mmHg, and when are IV Corticosteroids added?

Sepsis is life-threatening organ dysfunction (increase in SOFA score >= 2 points) caused by a dysregulated host response to infection; Septic Shock is sepsis in which, despite adequate volume resuscitation (30 mL/kg crystalloid), the patient requires Vasopressors to maintain MAP >= 65 mmHg AND has a Serum Lactate > 2.0 mmol/L. First-line vasopressor: Norepinephrine (Levophed — potent alpha-1 vasoconstrictor with modest beta-1 inotropy); Second-line adjunct: add Fixed-dose Vasopressin (0.03 units/min via V1 receptors) when norepinephrine doses escalate; if septic shock remains refractory to norepinephrine + vasopressin, add IV Hydrocortisone (200 mg/day) and/or Epinephrine (or Dobutamine if myocardial dysfunction/low CO persists).

What are the AHA High-Quality Adult Basic Life Support (BLS) CPR parameters for Compression Rate, Depth, Recoil, Compression-to-Ventilation Ratio, and Ventilation Rate with an Advanced Airway?

1) Compression Rate: 100 to 120 compressions per minute; 2) Compression Depth: at least 2 inches (5 cm) but not exceeding 2.4 inches (6 cm) in adults (at least 1/3 anteroposterior chest depth in children [~2 in] and infants [~1.5 in]); 3) Allow complete chest wall recoil after each compression (do not lean on chest) and minimize interruptions ( 80%); 4) Compression-to-Ventilation Ratio WITHOUT an advanced airway: 30:2 for 1 or 2 rescuers in adults (15:2 for 2-rescuer pediatric/infant CPR); 5) ONCE an Advanced Airway (ETT or supraglottic airway) is in place: deliver continuous compressions at 100–120/min without pauses and give 1 breath every 6 seconds (10 breaths/min), avoiding excessive ventilation.

What are the critical nursing safety rules for inflating the balloon of a Swan-Ganz (Pulmonary Artery) Catheter to measure Pulmonary Artery Wedge Pressure (PAWP)?

1) Never inflate the balloon with more than 1.5 mL of air using the dedicated volume-limited syringe; 2) Keep the balloon inflated for no longer than 8–15 seconds (2–3 respiratory cycles) and measure PAWP at END-EXPIRATION; 3) Immediately allow the balloon to deflate PASSIVELY and verify on the bedside monitor that the damped 'wedge' waveform has returned to a pulsatile Pulmonary Artery waveform (prolonged wedging or overinflation can cause catastrophic Pulmonary Artery Rupture or Pulmonary Infarction!).

How do you clinically and hemodynamically distinguish Acute Respiratory Distress Syndrome (ARDS — non-cardiogenic pulmonary edema) from Acute Decompensated Left Heart Failure (cardiogenic pulmonary edema)?

According to the Berlin Definition, ARDS presents within 1 week of a clinical insult (sepsis, pneumonia, aspiration, trauma, pancreatitis) with bilateral chest radiograph opacities not fully explained by cardiac failure/fluid overload and a normal Pulmonary Artery Wedge Pressure (PAWP = 5 cmH2O by PaO2/FiO2 ratio: Mild (201–300), Moderate (101–200), and Severe ( 18 mmHg, elevated BNP (> 400 pg/mL), JVD, S3 gallop, and cardiomegaly.

In the AHA Adult ACLS Cardiac Arrest Algorithm, which two rhythms are 'Shockable' versus 'Non-Shockable', and what are the exact timing of Defibrillation, Epinephrine, and Amiodarone/Lidocaine?

Shockable Rhythms: 1) Ventricular Fibrillation (VF) and 2) Pulseless Ventricular Tachycardia (pVT) -> Immediately deliver 1 unsynchronized Biphasic Defibrillation shock (120–200 J; or 360 J monophasic) and immediately resume 2 minutes of CPR (5 cycles of 30:2) before checking rhythm/pulse; administer IV/IO Epinephrine 1 mg every 3–5 minutes starting AFTER the 2nd shock, and administer IV/IO Amiodarone 300 mg bolus (1st dose) after the 3rd shock (followed by a second dose of 150 mg if refractory; or Lidocaine 1–1.5 mg/kg first dose, 0.5–0.75 mg/kg second dose). Non-Shockable Rhythms: 3) Asystole and 4) Pulseless Electrical Activity (PEA) -> DO NOT defibrillate; perform immediate continuous 2-minute cycles of CPR, administer IV/IO Epinephrine 1 mg AS SOON AS POSSIBLE (and repeat every 3–5 minutes), and aggressively search for and treat reversible causes ('Hs and Ts').

What are the two categories of Endotracheal Mechanical Ventilator Alarms: High-Pressure Limit Alarms ('DOPE') versus Low-Pressure / Low-Exhaled-Volume Alarms?

High-Pressure Alarms (triggered by increased airway resistance or decreased lung compliance): Secretions/mucus plug in ETT (suction patient), Patient biting on ETT (insert oral bite block), Kinked ventilator tubing or water condensation in circuit, Coughing/gagging/fighting the ventilator (patient-ventilator dyssynchrony -> check sedation/analgesia), Bronchospasm, or Right Mainstem Bronchus migration / Tension Pneumothorax ('DOPE' = Displacement, Obstruction, Pneumothorax, Equipment failure). Low-Pressure / Low-Minute-Ventilation Alarms: Disconnection of ventilator tubing from the endotracheal/tracheostomy tube, ETT cuff leak, or accidental self-extubation (if unable to troubleshoot a ventilator alarm immediately, disconnect the patient from the ventilator and manually ventilate with a Bag-Valve-Mask [Ambu bag] connected to 100% O2!).

What are the normal reference ranges for Central Venous Pressure (CVP / Right Atrial Pressure), Right Ventricular Pressure, Pulmonary Artery Pressure (PAP), and Pulmonary Artery Wedge Pressure (PAWP / PCWP)?

Central Venous Pressure (CVP / RAP — right ventricular preload): 2–8 mmHg (or 2–6 mmHg); Right Ventricular (RV) Pressure: 15–25 mmHg systolic / 0–8 mmHg diastolic; Pulmonary Artery Pressure (PAP): 15–30 mmHg systolic / 8–15 mmHg diastolic (Mean PAP 10–20 mmHg; pulmonary hypertension is Mean PAP > 20 mmHg); Pulmonary Artery Occlusion/Wedge Pressure (PAWP / PCWP — reflects Left Atrial Pressure and Left Ventricular End-Diastolic Pressure / LV preload): 6–12 mmHg (cardiogenic pulmonary edema typically occurs when PAWP > 18–20 mmHg).

What are the components of the 'ABCDEF' (and 'VAP Prevention') ICU Liberation & Ventilator Care Bundle?

VAP Prevention Bundle: 1) Elevate Head of Bed 30 to 45 degrees, 2) Daily Sedation Vacation (spontaneous awakening trial) + Daily Assessment of Readiness to Extubate (spontaneous breathing trial), 3) Peptic ulcer disease prophylaxis (PPI or H2 blocker), 4) Deep vein thrombosis (DVT) prophylaxis, and 5) Oral care with Chlorhexidine / subglottic suctioning. ABCDEF ICU Bundle: Assess/prevent/manage Pain, Both Spontaneous Awakening Trials (SAT) and Spontaneous Breathing Trials (SBT), Choice of analgesia and sedation (prefer dexmedetomidine/propofol over benzodiazepines), Delirium assessment/management (CAM-ICU), Early mobility and exercise, and Family engagement.

What is the AHA ACLS Adult Bradycardia with a Pulse Algorithm when heart rate is < 50 bpm?

First assess whether the bradycardia is causing hemodynamic instability / poor perfusion ('5 signs': Acutely altered mental status, Ischemic chest discomfort, Acute heart failure / pulmonary edema, Hypotension, or Signs of shock): if the patient is ASYMPTOMATIC and hemodynamically stable, simply monitor and observe (no treatment needed, except evaluate Mobitz Type II or 3rd-degree AV block for permanent pacemaker); if SYMPTOMATIC / UNSTABLE: 1) First-line drug is IV Atropine 1 mg bolus every 3–5 minutes (up to a maximum total dose of 3 mg); 2) If Atropine is ineffective (note: Mobitz Type II and Complete 3rd-degree infranodal AV blocks and denervated heart transplants typically do NOT respond to Atropine!), immediately initiate Transcutaneous Pacing (with sedation/analgesia) AND/OR start a continuous IV infusion of Dopamine (5–20 mcg/kg/min) or Epinephrine (2–10 mcg/min) while preparing for Transvenous Pacing.

How does Neurogenic Shock (distributive shock from spinal cord injury above T6) differ hemodynamically from Septic/Anaphylactic Shock and Hypovolemic Shock?

Like other distributive shocks, Neurogenic shock has LOW CVP/PAWP and LOW SVR (loss of sympathetic alpha-1 vascular tone causing warm, dry skin and venous pooling); however, because sympathetic cardioaccelerator fibers (T1–T4) are also severed, Neurogenic shock uniquely presents with BRADYCARDIA (unopposed vagal tone) and low CO, whereas all other shock states present with reflex TACHYCARDIA.

Hemodynamic Monitoring (CVP, PAP, PAWP, CO/CI, SVR, MAP), Shock States, Sepsis Bundles & ACLS/BLS Critical Care Algorithms

Swan-Ganz catheter pressures, MAP/CO/SVR formulas, hypovolemic/cardiogenic/obstructive/distributive shock profiles, Surviving Sepsis 1-hr bundle & ACLS cardiac arrest

Level: advanced
Languages: en → en
Cards: 32
Markdown: Hemodynamic Monitoring (CVP, PAP, PAWP, CO/CI, SVR, MAP), Shock States, Sepsis Bundles & ACLS/BLS Critical Care Algorithms (.md)

Flashcards (32)

#	Front (Term / Question)	Back (Definition / Answer)
1	What is the immediate management algorithm for Acute Ischemic Stroke in the Emergency Department (Door-to-CT, tPA/Tenecteplase inclusion/exclusion criteria, BP targets, and Mechanical Thrombectomy window)?	1) Determine exact 'Last Known Well' time, check fingerstick Blood Glucose immediately (hypoglycemia is the #1 reversible stroke mimic!), and obtain a Non-Contrast Head CT within 20 minutes of ED arrival (interpret within 45 min) to RULE OUT intracranial hemorrhage; 2) If non-contrast CT shows no hemorrhage and symptom onset is within <= 3.0 hours (or <= 4.5 hours in eligible patients), administer IV Alteplase (tPA, 0.9 mg/kg, max 90 mg, 10% bolus over 1 min + 90% over 60 min) or Tenecteplase with Door-to-Needle <= 60 min — PROVIDED Blood Pressure is lowered to < 185/110 mmHg BEFORE starting fibrinolysis (using IV Labetalol or Nicardipine) and maintained < 180/105 mmHg for 24 hours after tPA (if NOT receiving tPA, allow 'permissive hypertension' up to 220/120 mmHg to perfuse the ischemic penumbra); 3) Perform CT Angiography and proceed to Endovascular Mechanical Thrombectomy for anterior circulation Large Vessel Occlusion (ICA or proximal M1 MCA) up to 6–24 hours from last known well.
2	In a patient with a Chest Tube (Water-Seal Drainage System), what do 'Tidaling' versus 'Continuous Bubbling' in the Water-Seal Chamber and 'Gentle Bubbling' in the Suction Control Chamber indicate?	1) Tidaling (rise and fall of the fluid level in the water-seal chamber with inspiration and expiration): NORMAL finding indicating the chest tube is patent and transmitting intrapleural pressure swings (tidaling stops when the lung has fully re-expanded OR if the tubing is kinked/occluded); 2) Intermittent bubbling in the water-seal chamber during exhalation/coughing in a pneumothorax: expected as pleural air escapes, whereas CONTINUOUS bubbling in the water-seal chamber indicates an active AIR LEAK (either a persistent bronchopleural fistula in the patient or a loose connection in the external tubing); 3) Gentle continuous bubbling in a wet Suction Control Chamber: NORMAL when wall suction is attached; if the chest tube disconnects from the drainage unit, submerge the distal tube end in 2 cm of sterile water (creating a temporary water seal), and NEVER clamp a chest tube during transport (risks tension pneumothorax!).
3	Compare the receptor profiles and clinical indications of the major ICU Vasopressors and Inotropes: Norepinephrine, Epinephrine, Phenylephrine, Dopamine, Dobutamine, and Milrinone.	1) Norepinephrine (α1 >> β1): first-line vasopressor in septic, cardiogenic, and hypovolemic shock (raises SVR and MAP with minimal tachycardia); 2) Epinephrine (β1 = β2 > α1 at low dose; α1 predominates at high dose): first-line for Anaphylactic shock (IM), Cardiac Arrest (IV push), severe symptomatic bradycardia/post-arrest shock; 3) Phenylephrine (pure α1 agonist, zero β activity): raises SVR and induces baroreceptor reflex bradycardia (used in anesthesia-induced hypotension or hypotensive tachyarrhythmias/HOCM); 4) Dopamine (dose-dependent D1 -> β1 -> α1; largely replaced by norepinephrine due to higher tachyarrhythmia rate); 5) Dobutamine (β1 > β2): inodilator that increases Cardiac Output and slightly lowers SVR in Cardiogenic Shock (can cause mild hypotension/tachycardia); 6) Milrinone (PDE3 inhibitor -> increases cardiac & vascular cAMP independently of beta-receptors): inodilator increasing contractility and reducing pulmonary/systemic vascular resistance in HFrEF (even in patients on chronic beta-blockers; causes hypotension and is cleared renally).
4	What happens if a peripheral IV infusion of a potent alpha-1 vasopressor (such as Norepinephrine, Dopamine, or Phenylephrine) extravasates into subcutaneous tissue, and what is the immediate antidote?	Intense local alpha-1 vasoconstriction causes severe tissue ischemia, blanching, coldness, and sloughing/necrosis; immediately STOP the infusion, leave the IV cannula in place briefly to aspirate any residual drug, elevate the extremity, apply warm compresses, and infiltrate the extravasated site subcutaneously in a ring pattern with the alpha-adrenergic antagonist Phentolamine (5–10 mg diluted in 10 mL normal saline).
5	What are the components of the Surviving Sepsis Campaign Hour-1 / 3-Hour Resuscitation Bundle for Sepsis and Septic Shock?	1) Measure Serum Lactate level (and remeasure within 2–4 hours if initial lactate > 2.0 mmol/L); 2) Obtain Blood Cultures (at least 2 sets: aerobic + anaerobic) PRIOR to administering antibiotics (without delaying antibiotic administration); 3) Administer broad-spectrum Intravenous Antibiotics within 1 hour of recognition of septic shock (or within 3 hours if sepsis without shock); 4) Rapidly infuse 30 mL/kg of IV Balanced Crystalloid fluid (Lactated Ringer's or Normal Saline) within the first 3 hours for hypotension (MAP < 65, SBP < 90) or Lactate >= 4.0 mmol/L; 5) Apply Vasopressors (first-line: Norepinephrine) during or after fluid resuscitation if hypotensive to maintain MAP >= 65 mmHg.
6	What are the '5 Hs and 5 Ts' (reversible causes of Cardiac Arrest, particularly Pulseless Electrical Activity [PEA] and Asystole) in ACLS?	The 5 Hs: 1) Hypovolemia (hemorrhage/dehydration -> IV crystalloid/blood bolus), 2) Hypoxia (airway obstruction/apnea -> 100% O2 and advanced airway), 3) Hydrogen ion / Acidosis (severe metabolic/respiratory acidosis -> ventilation and IV NaHCO3), 4) Hypokalemia or Hyperkalemia (check K+ -> IV CaCl2/Ca-gluconate + insulin/D50/NaHCO3 for hyperkalemia), and 5) Hypothermia (rewarming). The 5 Ts: 1) Tension Pneumothorax (needle decompression + chest tube), 2) Tamponade, cardiac (bedside ultrasound + pericardiocentesis), 3) Toxins (drug overdose -> specific antidotes/lipid emulsion/NaHCO3), 4) Thrombosis, pulmonary (Massive PE -> systemic fibrinolysis tPA), and 5) Thrombosis, coronary (Massive STEMI -> emergent PCI).
7	What does a LOW Mixed Venous Oxygen Saturation (SvO2 < 60%) versus a HIGH SvO2 (> 80%) signify in a critically ill patient?	By the Fick equation, SvO2 reflects the balance between systemic Oxygen Delivery (DO2 = CO × CaO2) and tissue Oxygen Consumption (VO2): a LOW SvO2 (< 60%) means tissues are extracting a higher fraction of oxygen because either O2 delivery is inadequate (low Cardiac Output [cardiogenic/hypovolemic shock], anemia [low Hgb], or hypoxemia [low SaO2]) OR O2 demand is increased (fever, shivering, seizures, pain); a HIGH SvO2 (> 80%) indicates impaired cellular oxygen utilization / microvascular shunting, seen in hyperdynamic Septic Shock, Cyanide toxicity (histotoxic hypoxia), or left-to-right vascular shunts.
8	What are the immediate Post-Cardiac Arrest Care (ROSC) targets for Oxygenation, Ventilation, Blood Pressure, 12-Lead ECG, and Targeted Temperature Management (TTM)?	1) Airway & Oxygenation: secure endotracheal airway (confirm with waveform capnography) and titrate FiO2 to maintain SpO2 92%–98% (avoid hyperoxia [SpO2 100% / PaO2 > 300], which generates reactive oxygen species and worsens reperfusion brain injury); 2) Ventilation: maintain normocarbia (PETCO2 35–40 mmHg, PaCO2 35–45 mmHg; avoid hyperventilation, which causes cerebral vasoconstriction); 3) Hemodynamics: maintain Systolic BP > 90 mmHg and MAP >= 65 mmHg with IV crystalloid bolus and Norepinephrine/Epinephrine infusion; 4) Obtain immediate 12-Lead ECG and proceed to emergent Coronary Angiography/PCI if STEMI or high suspicion of acute coronary occlusion; 5) Targeted Temperature Management (TTM) for any patient who remains COMATOSE (unable to follow verbal commands) after ROSC: actively maintain a constant core temperature between 32°C and 37.5°C (strictly preventing fever > 37.7°C) for at least 24 hours.
9	What is the Rapid Shallow Breathing Index (RSBI), and what clinical and ABG parameters indicate a patient is ready for Extubation from mechanical ventilation?	RSBI = Respiratory Rate (breaths/min) / Tidal Volume (in Liters), measured during a 30–120 minute Spontaneous Breathing Trial (SBT on minimal pressure support 5–8 cmH2O / PEEP <= 5 cmH2O): an RSBI < 105 breaths/min/L predicts successful extubation (~80% positive predictive value), along with: reversal of underlying respiratory failure, awake/following commands with intact gag and cough reflexes (cuff-leak test positive if laryngeal edema suspected), hemodynamic stability (no or minimal vasopressors), SpO2 >= 90–92% (PaO2 >= 60 mmHg) on FiO2 <= 0.40 and PEEP <= 5–8 cmH2O, Negative Inspiratory Force (NIF/MIP) stronger than -20 to -30 cmH2O, and Vital Capacity > 10–15 mL/kg.
10	How is Hypertensive Emergency distinguished from Hypertensive Urgency (Severe Asymptomatic Hypertension), and what is the safe blood pressure reduction rule (plus the two major exceptions)?	Both typically present with BP > 180/120 mmHg, but ONLY Hypertensive Emergency has acute Target-Organ Damage (hypertensive encephalopathy, intracranial hemorrhage/ischemic stroke, acute coronary syndrome, acute cardiogenic pulmonary edema, aortic dissection, acute kidney injury/microangiopathic hemolytic anemia, or eclampsia). Hypertensive Urgency (no end-organ damage) is treated by restarting/adjusting ORAL antihypertensives over 24–48 hours. Hypertensive Emergency requires ICU admission and titratable IV antihypertensives (Nicardipine, Clevidipine, Labetalol, Esmolol, Fenoldopam, or Nitroprusside): lower MAP by NO MORE than 15%–25% in the first hour (then to ~160/100 over the next 2–6 hours) to prevent watershed cerebral or coronary ischemia — WITH TWO CRITICAL EXCEPTIONS: 1) Acute Aortic Dissection: rapidly reduce Systolic BP to < 120 mmHg and Heart Rate to < 60 bpm within 20 minutes using an IV Beta-Blocker FIRST (Esmolol or Labetalol to reduce dP/dt shear stress) followed by IV Nicardipine/Nitroprusside; 2) Severe Preeclampsia / Eclampsia or Pheochromocytoma crisis: lower SBP < 140–160 mmHg acutely (plus IV Magnesium Sulfate in preeclampsia).
11	What are the normal reference ranges for Cardiac Output (CO), Cardiac Index (CI), Stroke Volume (SV), Systemic Vascular Resistance (SVR), and Mixed Venous Oxygen Saturation (SvO2)?	Cardiac Output (CO = HR × SV): 4.0–8.0 L/min; Cardiac Index (CI = CO / Body Surface Area, normalizes CO for patient size): 2.5–4.0 L/min/m² (cardiogenic shock is CI < 2.2 L/min/m²); Stroke Volume (SV): 60–100 mL/beat; Systemic Vascular Resistance (SVR = [(MAP - CVP) / CO] × 80 — left ventricular afterload): 800–1,200 dynes·sec/cm⁵; Mixed Venous Oxygen Saturation (SvO2 drawn from the distal pulmonary artery port; or Central Venous ScvO2 from SVC): SvO2 65%–75% (ScvO2 >= 70%).
12	What are the evidence-based ARDSnet Lung-Protective Mechanical Ventilation targets that reduce mortality in ARDS?	1) Low Tidal Volume (Vt) ventilation: 4–8 mL/kg (target 6 mL/kg) of Predicted/Ideal Body Weight (calculated from height and sex, NOT actual body weight) to prevent volutrauma; 2) Plateau Pressure (measured during an end-inspiratory hold pause) strictly <= 30 cmH2O (and driving pressure [Pplat - PEEP] < 15 cmH2O) to prevent barotrauma; 3) Titrated higher PEEP (Positive End-Expiratory Pressure) to recruit collapsed alveoli and prevent atelectrauma; 4) Permissive hypercapnia (accepting PaCO2 elevation as long as pH >= 7.20–7.25); and 5) Early Prone Positioning (>= 16 hours/day) when PaO2/FiO2 < 150 mmHg.
13	How do you calculate Mean Arterial Pressure (MAP), what is its normal range, and what is the minimum MAP target required to maintain vital organ (cerebral, coronary, renal) perfusion in shock?	MAP = [(2 × Diastolic BP) + Systolic BP] / 3, or Diastolic BP + 1/3(Pulse Pressure); normal MAP is 70–100 mmHg, and the minimum resuscitation target in shock/sepsis is MAP >= 65 mmHg.
14	What is the physiological mechanism and hemodynamic timing of an Intra-Aortic Balloon Pump (IABP) in Cardiogenic Shock?	Positioned in the descending thoracic aorta just distal to the left subclavian artery and proximal to the renal arteries, synchronized to the ECG or arterial pressure waveform for 'counterpulsation': the balloon INFLATES at the onset of Diastole (on the dicrotic notch of the arterial waveform / middle of the T wave), augmenting diastolic aortic pressure to increase CORONARY ARTERY PERFUSION and cerebral blood flow; the balloon DEFLATES just prior to Isometric Ventricular Systole (on the R wave peak), creating a vacuum effect in the aorta that reduces Left Ventricular AFTERLOAD and myocardial oxygen consumption (Note: strictly contraindicated in moderate-to-severe Aortic Regurgitation or aortic dissection!).
15	How is Waveform Capnography (End-Tidal CO2 / PETCO2) used during ACLS Cardiopulmonary Resuscitation?	1) Gold-standard confirmation of proper Endotracheal Tube placement in the trachea (continuous square-wave capnogram with PETCO2 > 0 mmHg, eliminating esophageal intubation); 2) Real-time monitor of CPR chest compression quality: target PETCO2 >= 10–20 mmHg during CPR (if PETCO2 is persistently < 10 mmHg after 20 minutes of CPR, cardiac output generated by compressions is inadequate — improve compression depth/recoil or switch compressors); and 3) Earliest physiological indicator of Return of Spontaneous Circulation (ROSC): a sudden, abrupt jump in PETCO2 to normal/supranormal values (>= 35–40 mmHg) indicates spontaneous cardiac output has resumed even before the next pulse check.
16	How do you calculate Cerebral Perfusion Pressure (CPP), what are the normal ICP and CPP reference ranges, and what are the tiered interventions for Elevated Intracranial Pressure (ICP > 20–22 mmHg)?	CPP = Mean Arterial Pressure (MAP) - Intracranial Pressure (ICP); Normal ICP is 5–15 mmHg (sustained ICP > 20–22 mmHg requires treatment), and target CPP in traumatic brain injury is 60–70 mmHg. Tiered ICP Management: 1) Elevate Head of Bed to 30 degrees with head/neck in strictly neutral midline alignment (prevents internal jugular vein compression and promotes cerebral venous drainage), 2) Maintain normothermia, adequate sedation/analgesia, normocarbia (PaCO2 35–40 mmHg; brief hyperventilation to PaCO2 30–35 mmHg is ONLY a temporary bridge for acute impending herniation because cerebral vasoconstriction worsens ischemia!), 3) CSF drainage via External Ventricular Drain (EVD), and 4) Hyperosmolar therapy with IV Mannitol (0.25–1 g/kg; monitor serum osmolality < 320 mOsm/kg) OR Hypertonic Saline (3% or 23.4% NaCl).
17	How is the Glasgow Coma Scale (GCS) scored across Eye Opening (E1–E4), Verbal Response (V1–V5), and Motor Response (M1–M6), and what total score mandates endotracheal intubation?	Total GCS ranges from 3 (deepest coma; never 0!) to 15 (fully alert): Eye Opening (4): 4 = Spontaneous, 3 = To speech/voice, 2 = To pain/pressure, 1 = None; Verbal Response (5): 5 = Oriented, 4 = Confused conversation, 3 = Inappropriate words, 2 = Incomprehensible sounds/moaning, 1 = None; Motor Response (6 — most prognostic component): 6 = Obeys commands, 5 = Localizes pain, 4 = Withdraws from pain (normal flexion), 3 = Abnormal flexion (Decorticate posturing), 2 = Abnormal extension (Decerebrate posturing), 1 = None (flaccid). Severity: Mild TBI = 13–15; Moderate TBI = 9–12; Severe TBI / Coma = <= 8 ('GCS <= 8, Intubate!' to protect the airway).
18	What is the difference between Synchronized Cardioversion and Unsynchronized Defibrillation, and for which rhythms is each used?	Synchronized Cardioversion delivers an electrical shock timed ('synchronized') to land directly on the peak of the R wave (ventricular depolarization), strictly AVOIDING the vulnerable relative refractory period of the T wave (which would induce R-on-T Ventricular Fibrillation); it is used for any UNSTABLE Tachyarrhythmia WITH A PULSE (Unstable Atrial Fibrillation, Atrial Flutter, Supraventricular Tachycardia, or Monomorphic Ventricular Tachycardia with a pulse). Unsynchronized Defibrillation fires immediately upon pressing the shock button (because there is no organized R wave to synchronize to or the rhythm is polymorphic); it is used for PULSELESS VT, Ventricular Fibrillation (VF), and Unstable Polymorphic VT (even if a faint pulse is present, because polymorphic QRS morphology prevents reliable R-wave synchronization).
19	How do you calculate the Parkland Formula for 24-hour fluid resuscitation in a major Thermal Burn (> 20% Total Body Surface Area using the Rule of Nines), and how is resuscitation adequacy monitored?	Adult Rule of Nines (only count partial-thickness [2nd-degree] and full-thickness [3rd-degree] burns; EXCLUDE superficial 1st-degree erythema): Head & neck = 9%, Anterior trunk = 18%, Posterior trunk = 18%, Each upper extremity = 9% (×2), Each lower extremity = 18% (×2), Perineum = 1%. Parkland Formula: Total 24-hour Lactated Ringer's (LR) volume = 4 mL × Body Weight (kg) × % TBSA Burned; administer ONE-HALF (50%) of this total volume over the FIRST 8 HOURS (timed from the moment of the burn injury, NOT time of ED arrival!) and the remaining ONE-HALF (50%) over the NEXT 16 HOURS; however, formulas are only a starting estimate — titrate the hourly LR infusion rate to maintain Urine Output of 0.5–1.0 mL/kg/hr (30–50 mL/hr) in adults (or 1.0–1.5 mL/kg/hr in children or electrical burns with myoglobinuria).
20	What are the immediate bedside diagnostic signs and life-saving needle decompression / procedural treatments for Tension Pneumothorax and Cardiac Tamponade?	Tension Pneumothorax (one-way valve traps air in pleural space, collapsing ipsilateral lung and shifting mediastinum/vena cava to the opposite side): hypotension, JVD, unilaterally ABSENT breath sounds, hyperresonance to percussion, and tracheal deviation AWAY from the affected side -> do NOT wait for a chest X-ray; perform immediate Needle Thoracostomy (2nd intercostal space at the midclavicular line or 4th–5th intercostal space at the anterior axillary line, inserting over the SUPERIOR border of the rib to avoid the intercostal neurovascular bundle) followed by Tube Thoracostomy (chest tube). Cardiac Tamponade (Beck triad: hypotension, JVD, muffled heart sounds + pulsus paradoxus > 10 mmHg and electrical alternans on ECG): immediate ultrasound-guided Pericardiocentesis or surgical pericardial window (with temporary IV fluid bolus to maintain RV filling).
21	Where should the Phlebostatic Axis transducer be leveled when zeroing an Arterial Line or Central Venous / Pulmonary Artery Catheter, and how does transducer malpositioning affect pressure readings?	Level the transducer stopcock at the Phlebostatic Axis: the intersection of the 4th intercostal space and the mid-axillary line (corresponding to the anatomical level of the right atrium); if the transducer is positioned TOO LOW (below the right atrium), hydrostatic weight produces a FALSELY HIGH pressure reading; if the transducer is positioned TOO HIGH (above the right atrium), it produces a FALSELY LOW pressure reading.
22	How do the four major Shock Categories (Hypovolemic, Cardiogenic, Distributive/Septic, and Obstructive) differ across Preload (CVP/PAWP), Cardiac Output (CO/CI), Afterload (SVR), and Mixed Venous O2 (SvO2)?	1) Hypovolemic Shock (hemorrhage, severe dehydration, burns): LOW CVP/PAWP, LOW CO/CI, HIGH compensatory SVR, and LOW SvO2; 2) Cardiogenic Shock (massive MI, end-stage HFrEF, myocarditis, acute valve rupture): HIGH CVP and HIGH PAWP (> 18 mmHg), LOW CO/CI (< 2.2 L/min/m²), HIGH compensatory SVR, and LOW SvO2; 3) Distributive Shock — Septic/Anaphylactic ('warm shock'): LOW CVP/PAWP, HIGH (or normal) CO/CI early, markedly LOW SVR (< 800 dynes·sec/cm⁵ due to systemic vasodilation), and normal-to-HIGH SvO2; 4) Obstructive Shock (Cardiac Tamponade, Massive PE, Tension Pneumothorax): HIGH CVP (with equalization of diastolic pressures CVP ≈ RVEDP ≈ PADP ≈ PAWP ~18–20 mmHg in tamponade; or high CVP/PAP with low/normal PAWP in massive PE), LOW CO/CI, HIGH SVR, and LOW SvO2.
23	How is Septic Shock formally defined (Sepsis-3 criteria), what is the First-Line Vasopressor, what is the Second-Line agent added if MAP remains < 65 mmHg, and when are IV Corticosteroids added?	Sepsis is life-threatening organ dysfunction (increase in SOFA score >= 2 points) caused by a dysregulated host response to infection; Septic Shock is sepsis in which, despite adequate volume resuscitation (30 mL/kg crystalloid), the patient requires Vasopressors to maintain MAP >= 65 mmHg AND has a Serum Lactate > 2.0 mmol/L. First-line vasopressor: Norepinephrine (Levophed — potent alpha-1 vasoconstrictor with modest beta-1 inotropy); Second-line adjunct: add Fixed-dose Vasopressin (0.03 units/min via V1 receptors) when norepinephrine doses escalate; if septic shock remains refractory to norepinephrine + vasopressin, add IV Hydrocortisone (200 mg/day) and/or Epinephrine (or Dobutamine if myocardial dysfunction/low CO persists).
24	What are the AHA High-Quality Adult Basic Life Support (BLS) CPR parameters for Compression Rate, Depth, Recoil, Compression-to-Ventilation Ratio, and Ventilation Rate with an Advanced Airway?	1) Compression Rate: 100 to 120 compressions per minute; 2) Compression Depth: at least 2 inches (5 cm) but not exceeding 2.4 inches (6 cm) in adults (at least 1/3 anteroposterior chest depth in children [~2 in] and infants [~1.5 in]); 3) Allow complete chest wall recoil after each compression (do not lean on chest) and minimize interruptions (< 10 seconds for rhythm checks; chest compression fraction > 80%); 4) Compression-to-Ventilation Ratio WITHOUT an advanced airway: 30:2 for 1 or 2 rescuers in adults (15:2 for 2-rescuer pediatric/infant CPR); 5) ONCE an Advanced Airway (ETT or supraglottic airway) is in place: deliver continuous compressions at 100–120/min without pauses and give 1 breath every 6 seconds (10 breaths/min), avoiding excessive ventilation.
25	What are the critical nursing safety rules for inflating the balloon of a Swan-Ganz (Pulmonary Artery) Catheter to measure Pulmonary Artery Wedge Pressure (PAWP)?	1) Never inflate the balloon with more than 1.5 mL of air using the dedicated volume-limited syringe; 2) Keep the balloon inflated for no longer than 8–15 seconds (2–3 respiratory cycles) and measure PAWP at END-EXPIRATION; 3) Immediately allow the balloon to deflate PASSIVELY and verify on the bedside monitor that the damped 'wedge' waveform has returned to a pulsatile Pulmonary Artery waveform (prolonged wedging or overinflation can cause catastrophic Pulmonary Artery Rupture or Pulmonary Infarction!).
26	How do you clinically and hemodynamically distinguish Acute Respiratory Distress Syndrome (ARDS — non-cardiogenic pulmonary edema) from Acute Decompensated Left Heart Failure (cardiogenic pulmonary edema)?	According to the Berlin Definition, ARDS presents within 1 week of a clinical insult (sepsis, pneumonia, aspiration, trauma, pancreatitis) with bilateral chest radiograph opacities not fully explained by cardiac failure/fluid overload and a normal Pulmonary Artery Wedge Pressure (PAWP <= 18 mmHg) or normal BNP/echocardiogram, categorized on PEEP >= 5 cmH2O by PaO2/FiO2 ratio: Mild (201–300), Moderate (101–200), and Severe (<= 100); Cardiogenic pulmonary edema shows an elevated PAWP > 18 mmHg, elevated BNP (> 400 pg/mL), JVD, S3 gallop, and cardiomegaly.
27	In the AHA Adult ACLS Cardiac Arrest Algorithm, which two rhythms are 'Shockable' versus 'Non-Shockable', and what are the exact timing of Defibrillation, Epinephrine, and Amiodarone/Lidocaine?	Shockable Rhythms: 1) Ventricular Fibrillation (VF) and 2) Pulseless Ventricular Tachycardia (pVT) -> Immediately deliver 1 unsynchronized Biphasic Defibrillation shock (120–200 J; or 360 J monophasic) and immediately resume 2 minutes of CPR (5 cycles of 30:2) before checking rhythm/pulse; administer IV/IO Epinephrine 1 mg every 3–5 minutes starting AFTER the 2nd shock, and administer IV/IO Amiodarone 300 mg bolus (1st dose) after the 3rd shock (followed by a second dose of 150 mg if refractory; or Lidocaine 1–1.5 mg/kg first dose, 0.5–0.75 mg/kg second dose). Non-Shockable Rhythms: 3) Asystole and 4) Pulseless Electrical Activity (PEA) -> DO NOT defibrillate; perform immediate continuous 2-minute cycles of CPR, administer IV/IO Epinephrine 1 mg AS SOON AS POSSIBLE (and repeat every 3–5 minutes), and aggressively search for and treat reversible causes ('Hs and Ts').
28	What are the two categories of Endotracheal Mechanical Ventilator Alarms: High-Pressure Limit Alarms ('DOPE') versus Low-Pressure / Low-Exhaled-Volume Alarms?	High-Pressure Alarms (triggered by increased airway resistance or decreased lung compliance): Secretions/mucus plug in ETT (suction patient), Patient biting on ETT (insert oral bite block), Kinked ventilator tubing or water condensation in circuit, Coughing/gagging/fighting the ventilator (patient-ventilator dyssynchrony -> check sedation/analgesia), Bronchospasm, or Right Mainstem Bronchus migration / Tension Pneumothorax ('DOPE' = Displacement, Obstruction, Pneumothorax, Equipment failure). Low-Pressure / Low-Minute-Ventilation Alarms: Disconnection of ventilator tubing from the endotracheal/tracheostomy tube, ETT cuff leak, or accidental self-extubation (if unable to troubleshoot a ventilator alarm immediately, disconnect the patient from the ventilator and manually ventilate with a Bag-Valve-Mask [Ambu bag] connected to 100% O2!).
29	What are the normal reference ranges for Central Venous Pressure (CVP / Right Atrial Pressure), Right Ventricular Pressure, Pulmonary Artery Pressure (PAP), and Pulmonary Artery Wedge Pressure (PAWP / PCWP)?	Central Venous Pressure (CVP / RAP — right ventricular preload): 2–8 mmHg (or 2–6 mmHg); Right Ventricular (RV) Pressure: 15–25 mmHg systolic / 0–8 mmHg diastolic; Pulmonary Artery Pressure (PAP): 15–30 mmHg systolic / 8–15 mmHg diastolic (Mean PAP 10–20 mmHg; pulmonary hypertension is Mean PAP > 20 mmHg); Pulmonary Artery Occlusion/Wedge Pressure (PAWP / PCWP — reflects Left Atrial Pressure and Left Ventricular End-Diastolic Pressure / LV preload): 6–12 mmHg (cardiogenic pulmonary edema typically occurs when PAWP > 18–20 mmHg).
30	What are the components of the 'ABCDEF' (and 'VAP Prevention') ICU Liberation & Ventilator Care Bundle?	VAP Prevention Bundle: 1) Elevate Head of Bed 30 to 45 degrees, 2) Daily Sedation Vacation (spontaneous awakening trial) + Daily Assessment of Readiness to Extubate (spontaneous breathing trial), 3) Peptic ulcer disease prophylaxis (PPI or H2 blocker), 4) Deep vein thrombosis (DVT) prophylaxis, and 5) Oral care with Chlorhexidine / subglottic suctioning. ABCDEF ICU Bundle: Assess/prevent/manage Pain, Both Spontaneous Awakening Trials (SAT) and Spontaneous Breathing Trials (SBT), Choice of analgesia and sedation (prefer dexmedetomidine/propofol over benzodiazepines), Delirium assessment/management (CAM-ICU), Early mobility and exercise, and Family engagement.
31	What is the AHA ACLS Adult Bradycardia with a Pulse Algorithm when heart rate is < 50 bpm?	First assess whether the bradycardia is causing hemodynamic instability / poor perfusion ('5 signs': Acutely altered mental status, Ischemic chest discomfort, Acute heart failure / pulmonary edema, Hypotension, or Signs of shock): if the patient is ASYMPTOMATIC and hemodynamically stable, simply monitor and observe (no treatment needed, except evaluate Mobitz Type II or 3rd-degree AV block for permanent pacemaker); if SYMPTOMATIC / UNSTABLE: 1) First-line drug is IV Atropine 1 mg bolus every 3–5 minutes (up to a maximum total dose of 3 mg); 2) If Atropine is ineffective (note: Mobitz Type II and Complete 3rd-degree infranodal AV blocks and denervated heart transplants typically do NOT respond to Atropine!), immediately initiate Transcutaneous Pacing (with sedation/analgesia) AND/OR start a continuous IV infusion of Dopamine (5–20 mcg/kg/min) or Epinephrine (2–10 mcg/min) while preparing for Transvenous Pacing.
32	How does Neurogenic Shock (distributive shock from spinal cord injury above T6) differ hemodynamically from Septic/Anaphylactic Shock and Hypovolemic Shock?	Like other distributive shocks, Neurogenic shock has LOW CVP/PAWP and LOW SVR (loss of sympathetic alpha-1 vascular tone causing warm, dry skin and venous pooling); however, because sympathetic cardioaccelerator fibers (T1–T4) are also severed, Neurogenic shock uniquely presents with BRADYCARDIA (unopposed vagal tone) and low CO, whereas all other shock states present with reflex TACHYCARDIA.