STAT Stitch Deep Dive Podcast Beyond The Bedside

15:34

CC | Stroke [CVA] Additional Information

STAT Stitch Deep Dive Podcast Beyond The Bedside ·

2026/10/05

this episode goes over the 4 kinds of stokes from a high level overview

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2:28

CC CJM | Intro

STAT Stitch Deep Dive Podcast Beyond The Bedside ·

2026/10/05

the intro episode to the clinical judgement model

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54:41

CC CJM | Burns

STAT Stitch Deep Dive Podcast Beyond The Bedside ·

2026/10/05

Burn Classification & TBSA Assessment Burn severity depends on depth, extent (TBSA), location, and patient risk factors[1]. Depth is classified as partial-thickness (epidermal/dermal; painful, red, blistered) or full-thickness (dermal destruction, painless, leathery eschar, visible thrombosed vessels)[2]. TBSA is estimated using the Rule of Nines for adults or the Lund-Browder chart for children[6]. Referral to a burn center is indicated for partial-thickness burns >10% TBSA,

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65:12

CC CJM | Chronic Neurological Disorders

STAT Stitch Deep Dive Podcast Beyond The Bedside ·

2026/10/05

Primary Headaches[1]Tension (TTH): Bilateral, dull bandlike pressure[1][2]. No nausea[2]. Tx: NSAIDs[3][4]. Prev: Amitriptyline[3][5].Migraine: Unilateral throbbing, ± aura[1][6]. Triggers: stress, red wine[6][7]. Acute: Triptans (sumatriptan; contraindicated in CAD, ischemic stroke, uncontrolled HTN)[5]. Prev: Topiramate, β-blockers, Botox[3].Cluster: Severe unilateral orbital pain in clusters[1][4]. ptosis, tearing[1][4]. Tx: High-flow 100% O2 (7-12 L/min)[3][8], triptans[8]. Prev:

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53:28

CC CJM | Stroke [CVA]

STAT Stitch Deep Dive Podcast Beyond The Bedside ·

2026/10/05

80/20 Clinical Stroke SummaryCore Concepts & Emergency Recognition A stroke is an emergency where cell death occurs due to ischemia (inadequate blood flow, 87% of cases) or hemorrhage (bleeding, 13%)[1][2]. Interruption of blood flow alters brain metabolism in 30 seconds, stops it in 2 minutes, and causes cell death in 5 minutes[3]. The FAST protocol is critical for rapid recognition: Face drooping, Arm weakness/drift, Speech difficulties, and Time of symptom onset (critical for determining

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53:24

CC CJM | CKD v AKI

STAT Stitch Deep Dive Podcast Beyond The Bedside ·

2026/10/05

80/20 Clinical Summary: Renal Failure (AKI vs. CKD)1. PathophysiologyAKI: Sudden, potentially reversible decline in GFR[1].Prerenal: Decreased perfusion (hypovolemia, shock, HF). Oliguria occurs without tissue damage; reversible with fluids[1][2].Intrarenal: Direct tissue damage, 90% from Acute Tubular Necrosis (ATN) (ischemia, sepsis, nephrotoxins)[2].Postrenal: Mechanical obstruction (BPH, calculi) causing urine reflux[3].CKD: Gradual, irreversible nephron loss (GFR <60 for >3 months)[4]

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55:45

CC CJM | Neuro Assessment

STAT Stitch Deep Dive Podcast Beyond The Bedside ·

2026/10/05

80/20 Neurological Assessment & Physiology Summary1. Structure & Cellular BiologyOrganization: The CNS consists of the brain, spinal cord, and CN I-II[1]. The PNS contains CN III-XII, spinal nerves, and the ANS[1].Cells & Myelin: Neurons conduct action potentials via saltatory conduction across nodes of Ranvier, accelerated by myelin[2]. Astrocytes form the blood-brain barrier and create scar tissue (gliosis) upon injury[2]. Oligodendrocytes myelinate CNS axons; Schwann cells myelinate

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40:44

CC CJM | Blood Disorders

STAT Stitch Deep Dive Podcast Beyond The Bedside ·

2026/10/05

Clinician’s 80/20 Hematologic & Anemia SummaryCore Clinical Concepts Blood disorders disrupt homeostasis. Key pathological threads include:Fatigue: Secondary to tissue hypoxia (anemia, cancer).Infection Risk: Compromised immunity and risk for infection is a major concern in hematologic cancers and a common side effect of therapy.Pain: Common and classic in sickle cell disease (SCD) and oncology.Perfusion & Clotting: Excessive clotting impairs perfusion; inadequate clotting causes blood loss

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44:36

CC CJM | DKA v HHS

STAT Stitch Deep Dive Podcast Beyond The Bedside ·

2026/10/05

. DM Classification & Core DiagnosticsType 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

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36:17

CC CJM | GU

STAT Stitch Deep Dive Podcast Beyond The Bedside ·

2026/10/05

Urinary System: 80/20 Summary1. Anatomy & Blood Supply The upper urinary tract has two retroperitoneal, bean-shaped kidneys (T12–L3) and 2 ureters[1]. The lower tract comprises the bladder and urethra[1]. Each kidney is shielded by a fibrous capsule and cushioned by fat[1]. The functional unit is the nephron (~1 million), consisting of a glomerulus, Bowman's capsule, and tubule system (PCT, loop of Henle, DCT, and collecting ducts)[2]. Blood flow is ~1200 mL/min (20-25% of cardiac output) via

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27:35

CC | DKA & HHS

STAT Stitch Deep Dive Podcast Beyond The Bedside ·

2026/10/02

1. DM Classification & Core DiagnosticsType 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

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18:49

VS CC | DKA V HHS

STAT Stitch Deep Dive Podcast Beyond The Bedside ·

2026/10/02

1. DM Classification & Core DiagnosticsType 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

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24:14

VS ACLS | Lidocaine v Amiodarone

STAT Stitch Deep Dive Podcast Beyond The Bedside ·

2026/09/22

80/20 Comparative Summary: Amiodarone vs. Lidocaine1. Class & Mechanism of ActionAmiodarone (Cordarone): Class III antiarrhythmic with Class I, II, III, and IV actions[1][2]. Primarily blocks potassium channels in phases 2 and 3, delaying repolarization and prolonging effective refractory period[1]. Weakly blocks sodium channels (phase 0 upstroke), depresses SA/AV automaticity, blocks calcium channels, noncompetitively inhibits alpha/beta receptors, and causes vasodilation[2][3].Lidocaine: Class

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9:01

ACLS VS | Intro to The Comparison

STAT Stitch Deep Dive Podcast Beyond The Bedside ·

2026/09/22

this is the intro to a new segment comparing two drugs or disease processes to bring you more clarity.

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48:01

PALS | Pedi Cardiac Arrest Extended

STAT Stitch Deep Dive Podcast Beyond The Bedside ·

2026/09/14

80/20 Summary: Pediatric Cardiac Arrest Recognition & Management1. Core Pathways & Immediate Recognition (High-Impact 20%)Pathways to Arrest: Most pediatric cardiac arrests stem from progressive hypoxic/asphyxial respiratory failure or shock rather than sudden cardiac collapse[1][2]. Out-of-hospital arrest (OHCA) survival is ~8%, whereas in-hospital (IHCA) survival reaches ~43%[1][3].Immediate Recognition: Identify unresponsiveness, absent/agonal breathing, and absence of a central pulse

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56:07

PALS | Management of Pedi Resp. Arrest Extended

STAT Stitch Deep Dive Podcast Beyond The Bedside ·

2026/09/14

80/20 Summary: Pediatric Respiratory Emergency ManagementRespiratory failure causes most pediatric cardiac arrests[1]. Prompt management via the Evaluate-Identify-Intervene cycle restores oxygenation and ventilation before collapse[1][2].1. Core Life-Support & Initial ManagementRescue Breathing: For respiratory arrest with a pulse, give 12–20 breaths/min (1 breath every 3–5 seconds), each over 1 second for visible chest rise[2]. Reassess pulse every 2 minutes[2].Airway Management: Position in

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61:04

PALS | Pedi Bradycardia and Tachycardia Management...

STAT Stitch Deep Dive Podcast Beyond The Bedside ·

2026/09/14

80/20 Summary: Pediatric Arrhythmia Management & Algorithms[1]1. Core Assessment & Stability PrinciplesHemodynamic Instability: Recognized by respiratory failure, shock with poor end-organ perfusion (with or without hypotension), altered mental status/irritability, chest pain, or sudden collapse[1].Initial Actions: Support ABCs, give high-concentration O₂, attach ECG/oximetry/BP monitor, obtain IV/IO access, and record a 12-lead ECG without delaying emergency care[1].2. Pediatric Bradycardia

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38:41

PALS | Pedi Bradycardia & Tachycardia Extended

STAT Stitch Deep Dive Podcast Beyond The Bedside ·

2026/09/14

80/20 Core Need-to-Know PrinciplesCardiac Output Formula: Cardiac output equals stroke volume times heart rate ($CO = SV \times HR$)1. Because young children cannot increase stroke volume significantly, bradycardia directly drops cardiac output2.Leading Cause of Bradycardia: Tissue hypoxia from hypoxemia or respiratory failure is the main cause of symptomatic bradycardia1. Supporting airway, oxygenation, and ventilation is the initial priority1.CPR Threshold: Symptomatic bradycardia is HR <

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50:19

PALS | Respiratory Distress & Failure Extended

STAT Stitch Deep Dive Podcast Beyond The Bedside ·

2026/09/14

During the copy past its throwing a lot of weird symbols. I think the information is still helpfulPALS Respiratory Distress & Failure: 80/20 Core Summary1. Core Pathophysiology & DefinitionsRespiratory Distress: Clinical state with increased respiratory rate and effort (tachypnea, retractions, nasal flaring) while maintaining adequate gas exchange1more_horiz.Respiratory Failure: Inadequate oxygenation, ventilation, or both, causing tissue hypoxia and hypercarbia3more_horiz. In pediatrics,

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45:00

PALS | Pediatric Shock Extended

STAT Stitch Deep Dive Podcast Beyond The Bedside ·

2026/09/14

. Core Physiology & DefinitionDefinition: Shock is inadequate tissue perfusion to meet metabolic demands and oxygenation needs1. Hypotension is not required for diagnosis; shock exists with normal, high, or low SBP1.Pediatric Focus: Infants have fixed stroke volume and depend on elevated heart rate to maintain CO3.Stroke Volume: Preload (volume), Contractility (pump force), and Afterload (resistance)34.2. Severity & Compensatory ContinuumCompensated Shock: Body mechanisms (tachycardia,

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