STAT Stitch Deep Dive Podcast Beyond The Bedside

STAT Stitch Deep Dive Podcast Beyond The Bedside

di Regular Guy

Corsi Scienza della vita

Stagione 7

CC | Chronic Neurological Complications

Primary Headaches Tension (TTH): Bilateral, dull bandlike pressure. No nausea. Tx: NSAIDs. Prev: Amitriptyline. Migraine: Unilateral throbbing, ± aura. Triggers: stress, red wine. Acute: Triptans (sumatriptan; contraindicated in CAD, ischemic stroke, uncontrolled HTN). Prev: Topiramate, β-blockers, Botox. Cluster: Severe unilateral orbital pain in clusters. ptosis, tearing. Tx: High-flow 100% O2 (7-12 L/min), triptans. Prev: Verapamil. Medication Overuse (MOH): Daily headache from analgesic overuse. Tx: Stop drug. Seizure Disorders Def: ≥2 unprovoked seizures >24h apart. Classes: Generalized (bilateral hemispheres, e.g., tonic-clonic with LOC) vs. Focal (1 hemisphere, aware vs. impaired). Status Epilepticus (SE): Seizure >5 min or recurrent; emergency. Tx: IV Lorazepam, then fosphenytoin. Nursing Care: Airway, turn on side, do not restrain, never insert objects in mouth, pad rails, record phases. Restless Legs Syndrome (RLS) Leg paresthesias, worse at rest/night, relieved by movement. Basal ganglia dopamine dysfunction. Tx: Dopamine agonists (ropinirole), gabapentin. Degenerative Neurologic Disorders Multiple Sclerosis (MS): Autoimmune T-cell CNS demyelination. Signs: optic neuritis, spasticity, ataxia, bladder dysfunction. Tx: DMDs (interferons), steroids for relapses. Parkinson's (PD): Substantia nigra DA neuron loss; DA/ACh imbalance. Key: resting tremor ("pill-rolling"), cogwheel rigidity, bradykinesia (masked facies, shuffling gait), postural instability. Tx: Levodopa/Carbidopa (avoid protein meals), DA agonists, DBS. Myasthenia Gravis (MG): Autoimmune AChR antibody destruction. Fluctuating weakness (ptosis/diplopia; worsens with activity, improves with rest). Dx: Edrophonium test (atropine bedside).Myasthenic Crisis: Respiratory failure; Tx: IVIG, plasmapheresis. Cholinergic Crisis: Excess anticholinestase; SLUDGE signs; Tx: hold drugs, atropine. Tx: Pyridostigmine. Amyotrophic Lateral Sclerosis (ALS): Upper/lower motor neuron degeneration; cognition spared. Wasting, bulbar signs. Death: respiratory failure. Tx: Riluzole. Huntington's (HD): Autosomal dominant CAG repeats. ACh/GABA deficit, excess DA. Key: chorea, psychiatric decline, dementia. Caloric needs: 4000-5000 kcal/day. Tx: Tetrabenazine.

CC | Burns

Burn Classification & TBSA Assessment Burn severity depends on depth, extent (TBSA), location, and patient risk factors. Depth is classified as partial-thickness (epidermal/dermal; painful, red, blistered) or full-thickness (dermal destruction, painless, leathery eschar, visible thrombosed vessels). TBSA is estimated using the Rule of Nines for adults or the Lund-Browder chart for children. Referral to a burn center is indicated for partial-thickness burns >10% TBSA, chemical/electrical burns, inhalation injury, or burns of the face, hands, feet, genitalia, perineum, or joints. Face, neck, and circumferential torso burns threaten ventilation. Circumferential limb burns impair perfusion, requiring escharotomy. Emergent Phase Pathophysiology & Resuscitation The emergent phase (first 72 hours) prioritizes burn shock and gas exchange. Loss of capillary seal triggers a massive fluid shift from the intravascular to the interstitial space (third spacing), causing severe hypovolemia, hemoconcentration, high blood viscosity, and increased peripheral resistance. Damaged cells release potassium (hyperkalemia), and sodium moves into the interstitium (hyponatremia). Inhalation injuries (carbon monoxide, above/below glottis) cause mucosal edema, obstruction, and pneumonia (the leading cause of death). Myoglobinuria (from electrical muscle damage) can block renal tubules, causing acute kidney injury (AKI). Priority care includes early intubation, 100% humidified O2, and resuscitation. The ABA formula dictates 2–4 mL Lactated Ringer's per kg per % TBSA in the first 24 hours (half in the first 8 hours). Target clinical parameters are MAP >65 mmHg, HR <120 bpm, and adult urine output of 0.5–1 mL/kg/hr (75–100 mL/hr for electrical burns). Acute, Rehabilitative & Psychosocial Care The acute phase begins with diuresis and ends when wounds are nearly healed. Sepsis, often from gram-negative bacteria or Candida, is a leading cause of death during this immunosuppressed period. Stress-induced hypermetabolism causes protein catabolism and transient hyperglycemia, requiring early enteral nutrition and insulin. Excision and grafting (autograft, CEA, or Integra) are vital for full-thickness wounds. Pain is managed with continuous IV opioids, procedural breakthrough doses, and anxiolytics. Continuous physical therapy and splinting prevent contractures. In the rehabilitation phase, hypertrophic scars are minimized using custom-fitted pressure garments worn up to 23 hours daily for 12–18 months. Hydration and antihistamines help relieve severe itching. Older adults face higher mortality due to thinner skin, delayed healing, and co-morbidities. Support groups and psychiatric interventions address emotional needs, body image changes, and PTSD.

CC | DKA & HHS

1. DM Classification & Core Diagnostics Type 1 DM: Autoimmune β-cell destruction (HLA-DR3/DR4) causing absolute insulin deficiency; presents abruptly with classic 3 Ps (polyuria, polydipsia, polyphagia), weight loss, and DKA risk[1][2]. Type 2 DM: Insulin resistance combined with relative β-cell deficiency and inappropriate hepatic glucose production[3]. Onset is gradual[4]. Diagnostic Criteria: A1C ≥6.5%, Fasting Plasma Glucose ≥126 mg/dL, 2-hr OGTT ≥200 mg/dL, or Random Glucose ≥200 mg/dL with classic symptoms[5]. Glycemic target A1C is <7.0%[6]. 2. High-Yield Pharmacotherapy & Insulin Dynamics Insulin Types: Rapid-acting (lispro, aspart; onset 10–30 min, mealtime bolus), Short-acting (Regular; onset 30–60 min, only IV insulin), Intermediate (NPH; peaks 4–12 hr, cloudy), Long-acting (glargine, detemir; peakless basal)[7]. Basal-Bolus Strategy: Optimal plan mimicking normal endogenous insulin secretion[7]. Key Oral Agents: Metformin (Biguanide) reduces hepatic glucose output[10]. Safety Alert: Discontinue metformin 48 hr before/after IV contrast to prevent acute kidney injury and lactic acidosis[10][11]. Sulfonylureas (glipizide) stimulate insulin release and carry high hypoglycemia risk[11][12]. 3. Hyperglycemic Emergencies: DKA vs. HHS DKA (T1DM): Absolute insulin deficiency → uncontrolled lipolysis → ketone bodies → metabolic acidosis (pH <7.30, HCO₃⁻ <16 mEq/L), Kussmaul respirations, fruity breath, glucose >250 mg/dL[13][14]. HHS (T2DM): Enough circulating insulin prevents ketosis, but severe hyperglycemia (>600 mg/dL) causes osmotic diuresis, hyperosmolality, and profound neurologic deficits (coma, seizures)[15][16]. Emergency Treatment Protocol:IV Fluids: First priority. 0.9% NaCl (1 L/hr) to maintain urine output (30–60 mL/hr)[14][15]. Add 5%–10% dextrose when glucose reaches ~250 mg/dL to prevent hypoglycemia and cerebral edema[14][15]. Potassium: Check K⁺ BEFORE starting insulin. Insulin shifts K⁺ intracellularly, causing life-threatening hypokalemia if uncorrected[15]. Continuous IV Regular Insulin: 0.1 U/kg/hr; target glucose reduction of 36–54 mg/dL/hr[15]. 4. Hypoglycemia & Chronic Complications Hypoglycemia (<70 mg/dL): Treat via Rule of 15 (15–20g fast-acting carbs, recheck in 15 min)[16][17]. Unconscious: 20–50 mL 50% Dextrose IV or 1 mg Glucagon IM/SQ (turn on side to prevent aspiration)[17]. Chronic Complications: Driven by angiopathy[18]. Macrovascular (CVD, stroke, PAD) managed via BP (<140/90) and lipid control[19]. Microvascular annual screening: Retinopathy (dilated eye exam), Nephropathy (urine albumin/creatinine; treat with ACEi/ARBs), and Neuropathy (monofilament test, daily foot inspection)[20].

CC | Acute Neurological Disorders

Core Intracranial Dynamics (The 20%) Volume Distribution: The enclosed skull holds 78% brain tissue, 12% blood, and 10% CSF[1][2]. Monro-Kellie Doctrine: Intracranial volume is constant; an increase in any component requires compensatory displacement of others to maintain constant volume within the skull[2]. Key Clinical Target Values: Normal ICP is 5–15 mm Hg (sustained >20 mm Hg is abnormal)[2]. Normal CPP is 60–100 mm Hg (CPP = MAP − ICP)[3]. A CPP <50 mm Hg causes cerebral ischemia, while <30 mm Hg is incompatible with life[3]. Cerebral autoregulation maintains constant blood flow between a MAP of 70–150 mm Hg[2]. PaCO2 Impact: Elevated PaCO2 causes potent cerebral vasodilation, increasing blood volume and ICP[4]. 2. Essential Recognition & Red Flags LOC: Change in level of consciousness is the most sensitive and reliable indicator of neurological decline[5]. Cushing's Triad: Systolic hypertension with widening pulse pressure, bradycardia, and irregular respirations signify brainstem compression and impending herniation[5]. Pupils & Motor Response: A fixed, unilateral dilated pupil indicates ipsilateral CN III compression[6]. Decerebrate posturing (extensor) reflects midbrain/brainstem damage and is more severe than decorticate (flexor) posturing[6]. Compliance Loss: A ventriculostomy waveform where P2 is higher than P1 indicates compromised compliance[7][8]. 3. High-Yield Condition Comparisons Epidural Hematoma (EDH): Arterial tear (middle meningeal artery) causing rapid compression; presents with unconsciousness → lucid interval → rapid decline[9]. Requires emergency surgical evacuation[9]. Subdural Hematoma (SDH): Venous tear (bridging veins) progressing slower; chronic forms are common in older adults due to brain atrophy[9][10]. Basilar Skull Fracture: Marked by Battle's sign, raccoon eyes, and CSF otorrhea/rhinorrhea (verified via halo sign or positive glucose)[11][12]. Bacterial Meningitis: Presents with fever, severe headache, and nuchal rigidity[13]. Diagnostic LP reveals decreased CSF glucose, elevated protein, and high neutrophils[13][14]. 4. Priority Clinical Actions Airway & Position: Secure airway (GCS ≤8 requires intubation)[15]. Maintain HOB elevated 30 degrees with head midline to optimize venous drainage and CPP[16]. Avoid extreme neck or hip flexion[16]. Medical Interventions: Administer Mannitol or Hypertonic Saline to draw edema from tissue into circulation[17]. Give prompt IV antibiotics right after cultures for meningitis[14]. Critical Contraindications: Lumbar puncture is contraindicated with elevated ICP due to herniation risk[18]. Avoid NG tubes and nasotracheal suctioning in basilar fractures/CSF leaks[15][19]. Enforce respiratory isolation for meningococcal meningitis[20].

CC | Epidural v Subdural Hematomas

An Epidural Hematoma (EDH) and a Subdural Hematoma (SDH) are two distinct forms of focal intracranial bleeding caused by head trauma[1][2]. They differ significantly in anatomical location, primary bleeding source, clinical progression, and at-risk populations[2][3]. 1. Side-by-Side Comparison FeatureEpidural Hematoma (EDH)Subdural Hematoma (SDH)Anatomical LocationBetween the dura mater and the inner surface of the skull[2][4].Between the dura mater and the arachnoid layer of the meninges[2][4].Primary Vessel InvolvedUsually arterial (most commonly a tear of the middle meningeal artery beneath the temporal bone)[2][5]. Can occasionally be venous from a dural venous sinus tear[2].Usually venous (tear of bridging veins draining from the brain surface into the sagittal sinus)[2]. Can occasionally be arterial[2].Rate of Bleeding & OnsetRapidly developing due to high-pressure arterial expansion; considered a critical neurologic emergency[2].Usually slower to develop due to lower-pressure venous bleeding[2]. Divided into acute, subacute, and chronic forms[2][3].Classic Clinical PresentationUnconsciousness at the scene → brief lucid interval → rapid neurologic deterioration and decreased level of consciousness (LOC)[2].Symptoms of progressive increased intracranial pressure (ICP) and brain compression: headache, drowsiness, confusion, decreasing LOC, and ipsilateral fixed/dilated pupil[2].Associated Etiology & Risk FactorsFrequently associated with linear skull fractures crossing major dural arteries (e.g., temporal bone fractures)[2][5].Older adults (due to brain atrophy stretching bridging veins), alcohol use (risk of falls), and anticoagulant therapy[2][3].Surgical TreatmentRapid surgical evacuation via craniotomy or burr-hole decompression to prevent brain herniation[2][6].Surgical evacuation, decompression, or membranectomy (craniotomy or burr holes) depending on size and impairment[2]. 2. Key Clinical Nuances The EDH Lucid Interval: The hallmark of an arterial EDH is a patient who temporarily regains clarity after an initial knockout, only to rapidly deteriorate as arterial blood expands inside the closed skull[2]. Emergency surgical intervention is required before herniation occurs[2][6]. Subdural Subtypes (Acute, Subacute, Chronic):Acute SDH: Manifests within 24–48 hours of severe trauma with immediate deterioration[2]. Subacute SDH: Appears within 48 hours to 2 weeks post-injury; blood breakdown products draw fluid into the subdural space, causing late expansion[2][3]. Chronic SDH: Develops over weeks or months (often >20 days) after a seemingly minor or forgotten head injury[2][3]. Diagnostic Pitfalls in Older Adults: Chronic SDH in older adults is frequently misdiagnosed as dementia, a transient ischemic attack (TIA), or a stroke because symptoms present as subtle confusion, memory loss, and lethargy rather than acute ICP spikes[3].

Stagione 19

ACLS | ACS and Preventing Arrest

Rapid Response System (RRT) Triggers Over half of in-hospital cardiac arrests (IHCAs) stem from respiratory failure or hypovolemic shock[1]. RRS activates based on adult criteria[1]: Airway & Breathing: Airway compromise; respiratory rate <6/min or >30/min[1]. Circulation: Heart rate <40/min or >140/min; SBP <90 mmHg; symptomatic hypertension[1]. Neurological & Renal: Unexpected drop in consciousness; unexplained agitation; seizures; significant urine output drop[1]. Subjective: Clinician concern regarding patient deterioration[1]. II. ACS Classification & Triage The initial 12-lead ECG is central to classifying ACS into two major categories[2]: STEMI: ST elevation in ≥2 contiguous leads (≥2 mm in V2–V3 for men ≥40, ≥2.5 mm for men <40, ≥1.5 mm for women; ≥1 mm in other leads) or new LBBB[4]. Indicates complete coronary occlusion requiring immediate reperfusion[5]. NSTE-ACS: ST depression (≥0.5 mm), dynamic T-wave inversion, transient ST elevation, or normal/nondiagnostic ECG[2][4]. III. Initial Medications & Critical Traps ED assessment within 10 minutes targets ischemia relief and risk triage[3]: Aspirin: Administer 162 to 325 mg (chewed) immediately to inhibit COX-1 and thromboxane A2[4][7]. Suppositories (300 mg) for severe nausea/vomiting[7]. Contraindicated in true allergy or active/recent GI bleed[4][7]. Oxygen: Give (4 L/min) only if SpO2 <90%, dyspneic, hypoxemic, or showing heart failure signs; withhold in normoxic patients[4][7]. Nitroglycerin: Give 1 sublingual dose every 3–5 minutes (max 3 doses)[7][8]. Contraindications: SBP <90 mmHg (or ≥30 mmHg drop below baseline), severe bradycardia (<50/min), tachycardia (>100/min), or RV infarction[4][7]. Morphine: IV for pain unalleviated by nitroglycerin; caution in hypotension or RV infarction[4][7]. Can decrease oral antiplatelet absorption[4]. NSAID Contraindication: NSAIDs (except aspirin) are strictly avoided due to increased risk of mortality, reinfarction, and myocardial rupture[9]. IV. STEMI Reperfusion Timelines Reperfusion within 12 hours of onset limits myocardial necrosis[5][10]: Primary PCI: Preferred strategy[10]. FMC-to-balloon goal ≤90 minutes (≤120 minutes if transferred to PCI facility)[10]. Fibrinolysis: Door-to-needle goal ≤30 minutes[10]. Most effective within 1 hour of symptom onset (reduces mortality by 47%)[5][10]. Not recommended if symptoms >12 hours; contraindicated >24 hours or for ST depression without posterior MI[8]. V. NSTE-ACS & Adjunctive Care High-Risk NSTE-ACS: Early invasive strategy indicated for refractory ischemia, recurrent ST deviation, VT, instability, or heart failure[4][6]. IV Nitroglycerin: For recurrent ischemia, hypertension, or pulmonary edema; titrate maintaining SBP >90 mmHg[8][11]. Heparin: Routine adjunct for PCI and fibrinolysis[8].

ACLS | Resp Arrest Extended

Clinical Recognition & Assessment Respiratory Arrest Definition: Patient is unconscious and unresponsive with a perfusing pulse, but respirations are absent or inadequate[1]. Agonal gasps do not indicate adequate breathing[1]. Distress vs. Failure: Normal adult respiration is 12–20 breaths/min with a tidal volume of 6–8 mL/kg[1]. Distress shows tachypnea (>20/min), accessory muscle use, or agitation[1]. Failure is inadequate oxygenation/ventilation marked by severe bradypnea (<12/min), cyanosis, or stupor[1][2]. Rate <6/min requires assisted ventilation with 100% oxygen[1]. 2. Ventilation Protocol & Critical Rules Ventilation Rate: Deliver 1 breath every 6 seconds (10 breaths/min) using a bag-mask device or advanced airway[3][4]. Deliver each breath over 1 second to produce visible chest rise[3][5]. Tidal Volume: Provide 500–600 mL (6–7 mL/kg)[2][5]. Adult bag-mask devices often deliver excess volume; caution is advised, and a pediatric bag-mask may be considered[2]. Pulse Reassessment: Recheck pulse every 2 minutes for 5–10 seconds[3]. If no pulse, start CPR immediately[3]. Oxygenation Targets: Give 100% oxygen in arrest[1][4]. Maintain SpO2 ≥95% generally, 90% for ACS, and 92–98% for post-cardiac arrest care[4]. Avoiding Hyperventilation: Excessive ventilation increases intrathoracic pressure, decreases venous return, lowers cardiac output, causes cerebral vasoconstriction, and leads to gastric inflation and aspiration[3]. 3. Airway Opening & Adjuncts Airway Opening: Tongue displacement due to lost muscle tone is the primary cause of obstruction[4]. Perform head tilt-chin lift, or jaw-thrust without head extension for suspected cervical trauma[4][5]. Bag-Mask Technique: Two-rescuer BVM using the E-C clamp technique is preferred[5]. Single rescuers should use a pocket mask if available[5]. OPA (Oropharyngeal Airway): Use only in unresponsive patients without a cough/gag reflex[4][6]. Size from corner of mouth to angle of mandible[6]. Insert curved upward toward palate, then rotate 180°[6]. NPA (Nasopharyngeal Airway): Suitable for conscious, semiconscious, or unconscious patients[7]. Size length from nose tip to earlobe[7]. Lubricate and insert perpendicular to face[7]. Caution with facial trauma due to cribriform plate fracture risk[7]. 4. Suctioning Standards Vacuum & Flow: Wall-mounted units must provide >40 L/min airflow and >-300 mmHg vacuum[8]. Catheter Types: Rigid Yankauer for thick secretions/oropharynx; soft flexible catheter for thin secretions, NPA, or ET tube[8]. Procedure: Measure catheter and do not insert beyond tongue[8]. Apply suction while withdrawing with a rotating motion, limiting attempts to ≤10 seconds[8].

ACLS | Stroke Extended

1. Core Epidemiology & Stroke Types Ischemic Stroke (87%): Resulting from arterial occlusion; prime candidate for rapid reperfusion therapies (IV alteplase and endovascular therapy)[1]. Hemorrhagic Stroke (13%): Caused by cerebral vessel rupture; IV fibrinolytics and anticoagulants are strictly contraindicated[1]. Ischemic Penumbra: Dysfunctional but viable brain tissue surrounding the central infarct core that reperfusion strategies aim to preserve[2][3]. 2. Prehospital Assessment & The 8 D's of Stroke Care The 8 D's: Detection, Dispatch, Delivery, Door, Data, Decision, Drug/Device, and Disposition[4]. Prehospital Screening (CPSS): Evaluates Facial Droop, Arm Drift, and Abnormal Speech. A single abnormal finding yields a 72% stroke probability[5]. Critical EMS Actions: Assess ABCs, check point-of-care blood glucose (treat hypoglycemia <60 mg/dL)[5][6], establish Last Known Normal (LKN) time[5][7], provide hospital prenotification, and bypass ED to CT suite[7][8]. 3. In-Hospital Time Targets (NINDS & Target: Stroke) Door-to-Assessment: Immediate general assessment within 10 minutes; neurologic exam within 20 minutes[9]. Door-to-CT/MRI: Noncontrast CT acquired within 20 minutes; expert scan interpretation within 45 minutes[9]. Door-to-Needle (Alteplase): Administer within 60 minutes of arrival (Target: Stroke III goal: ≥85% within 60 min)[7][9]. Door-to-Device (EVT): First pass within 90 minutes (direct arrival) or 60 minutes (transfers)[7][9]. Treatment Windows:IV Alteplase: Within 3 hours (extended to 4.5 hours for select eligible patients)[1]. Endovascular Therapy (EVT): Up to 24 hours from onset for confirmed Large Vessel Occlusion (LVO)[9][11]. 4. Blood Pressure Thresholds & Pharmacotherapy Pre-Alteplase BP Goal: Lower blood pressure to ≤185/110 mmHg before initiating IV alteplase[12]. Post-Reperfusion Goal: Maintain BP ≤180/105 mmHg for at least 24 hours post-alteplase[12]. First-Line IV Antihypertensives: Labetalol (10–20 mg IV), Nicardipine (5–15 mg/h IV), or Clevidipine (1–2 mg/h IV)[7][12]. 5. Key Contraindications & Stroke System Levels Absolute Exclusions: Intracranial Hemorrhage (ICH) on NCCT/MRI[2][13], severe head trauma or ischemic stroke within 3 months[13], prior history of ICH[13], active GI bleed within 21 days[13], or coagulopathy (platelets <100k, INR >1.7, aPTT >40s)[14]. Stroke Facility Levels: Acute Stroke Ready (ASRH), Primary (PSC), Thrombectomy-Capable (TSC), and Comprehensive Stroke Centers (CSC)[15][16].

ACLS | Bradycardia and Tachycardia Extended

Core Assessment & Stability Hallmarks Prioritize identifying whether the rhythm causes hemodynamic instability [1]. Symptomatic bradycardia occurs at HR <50/min [1][4], and symptomatic tachycardia at HR ≥150/min [5][6]. 5 Instability Signs: Hypotension, altered mental status, signs of shock, ischemic chest discomfort, acute heart failure [2]. First Actions: Patent airway, assist ventilation/O2 if hypoxemic, monitor/BP/oximetry, IV access, 12-lead ECG [2]. Never delay electrical therapy for a 12-lead ECG in unstable patients [8]. 2. Bradycardia Algorithm (HR <50/min) Stable: Monitor and observe [2][4]. Unstable:Atropine (1st Line): 1 mg IV bolus every 3–5 min (max total: 3 mg) [4][9]. Doses <0.5 mg may slow HR [9]. Atropine Gotchas: Avoid in Mobitz II 2nd-degree or 3rd-degree AV block with wide QRS [9], acute MI [9], or heart transplant patients (Class III: Harm; use TCP/dopamine/epinephrine) [9]. 2nd Line (If Atropine Fails): TCP: Rate 60–80/min; output 2 mA above capture threshold [10]. Sedate conscious patients if possible [11][12]. Contraindicated in severe hypothermia [12]. Don't check carotid pulse for capture [12]. Infusions: Dopamine IV (5–20 mcg/kg/min) [2] or Epinephrine IV (2–10 mcg/min) [2]. 3. Tachycardia Algorithm (HR ≥150/min) Unstable: Immediate Synchronized Cardioversion (consider sedation) [3]. For regular narrow complex, consider Adenosine 6 mg IV [3][6]. Stable Narrow QRS (<0.12 s):Regular (SVT): Vagal maneuvers → Adenosine 6 mg IV push + flush [6][14]. If unconverted in 1–2 min, give 12 mg IV [6][14]. Follow with β-blockers or CCBs [6][14]. (Use 3 mg Adenosine in heart transplants/central lines; avoid in asthma/COPD) [14]. Irregular (Afib/Flutter): Rate control with β-blockers or CCBs [14][15]. Stable Wide QRS (≥0.12 s):Regular & Monomorphic: Adenosine 6 mg IV only if regular and monomorphic [6][16]. Antiarrhythmic Infusions: Procainamide (20–50 mg/min, max 17 mg/kg; avoid in prolonged QT/CHF) [6][16], Amiodarone (150 mg IV over 10 min) [6][16], or Sotalol (100 mg over 5 min) [6][16]. 4. Electrical Therapy & Critical Traps Defibrillation (Unsynchronized): Pulseless (VF/pVT), polymorphic VT, or severe deterioration [13]. Cardioversion (Synchronized): Unstable tachycardia with pulse [13]. Reactivate sync mode after each shock [17]. AV Nodal Blocker Trap: Do NOT give AV nodal blockers (adenosine, CCBs, β-blockers, digoxin) in pre-excited Afib/flutter (WPW), as it risks triggering VF [14][15]. Avoid combining CCBs and β-blockers due to severe bradycardia [15].

ACLS | Post Arrest Care Extended

High-Performance CPR & Perfusion Metrics Compressions: Rate 100-120/min at a depth of ≥2 inches (5 cm) with complete chest recoil[1][2]. Chest Compression Fraction (CCF): Target >80% to maximize coronary perfusion pressure[2][3]. Capnography (PETCO₂): Continuous waveform monitoring; values <10 mmHg indicate poor CPR quality, whereas an abrupt sustained rise to ≥40 mmHg signals Return of Spontaneous Circulation (ROSC)[1]. Coronary Perfusion Pressure (CPP): Target CPP (or arterial relaxation pressure) ≥15–20 mmHg to achieve ROSC[2][5]. Adult Cardiac Arrest Algorithm (80/20 Prioritization) VF / Pulseless VT (Shockable Pathway) Defibrillation: Immediate 1 shock (Biphasic: 120-200 J; Monophasic: 360 J), then immediately resume CPR for 2 minutes[1][7]. Epinephrine: 1 mg IV/IO every 3-5 minutes starting after the second shock[1][8]. Antiarrhythmics: Amiodarone (300 mg IV/IO bolus; 2nd dose 150 mg) or Lidocaine (1–1.5 mg/kg 1st dose; 2nd dose 0.5–0.75 mg/kg) after the third shock for refractory VF/pVT[1][9]. PEA / Asystole (Non-Shockable Pathway) Immediate Action: No shock. Resume CPR for 2-minute cycles immediately[1][10]. Epinephrine: 1 mg IV/IO as soon as vascular access is available, repeated every 3-5 minutes[1][11]. Reversible Causes (H's & T's): Identify and treat Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypo-/Hyperkalemia, Hypothermia, Tension pneumothorax, Tamponade (cardiac), Toxins, Pulmonary thrombosis, or Coronary thrombosis[1]. Airway & Ventilation Strategies Unadvanced Airway: 30:2 compression-to-ventilation ratio[1][15]. Advanced Airway: Insert ETT or supraglottic airway; confirm placement with waveform capnography[1]. Ventilation Rate: 1 breath every 6 seconds (10 breaths/min) with continuous chest compressions[1]. Avoid hyperventilation to prevent reduced venous return[1]. Post-Cardiac Arrest Care (ROSC Management) Oxygenation & Ventilation: Titrate FiO₂ for SpO₂ 92–98%; maintain PaCO₂ at 35–45 mmHg[14]. Hemodynamics: Target SBP >90 mmHg or MAP >65 mmHg using fluid boluses or pressors (Norepinephrine 0.1–0.5 mcg/kg/min, Epinephrine 2–10 mcg/min, or Dopamine 5–20 mcg/kg/min)[14]. Reperfusion: 12-lead ECG; emergent PCI for STEMI or unstable cardiogenic shock[14]. Targeted Temperature Management (TTM): If comatose, maintain core temperature at 32-36°C for ≥24 hours[13]. Special Situations Pregnancy: Perform manual left lateral uterine displacement; prepare for perimortem cesarean delivery within 5 minutes if no ROSC[17][23]. LVAD: Check hum/power; perform compressions only if MAP ≤50 mmHg or PETCO₂ ≤20 mmHg and restart fails[24][25].

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