STAT Stitch Deep Dive Podcast Beyond The Bedside

STAT Stitch Deep Dive Podcast Beyond The Bedside

by Regular Guy

Courses Life Sciences

Season 20

PALS | Pediatric Shock Extended

. Core Physiology & Definition Definition: 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 Continuum Compensated Shock: Body mechanisms (tachycardia, elevated SVR, venoconstriction) maintain normal SBP despite hypoperfusion56. Key signs: tachycardia, delayed refill, cool skin, oliguria67. Hypotensive Shock: Compensatory mechanisms fail, causing low SBP and imminent arrest7. Hypotension is a late finding in most shock types, except septic shock where SVR drops early7. Progression: Compensated shock can last hours, but hypotensive shock deteriorates in minutes8. 3. The 4 Shock Types: Differential Pattern Recognition A. Hypovolemic Shock (Most Common) Mechanism: Intravascular volume loss (fluid loss) causing low preload and CO9. Signs: "Quiet tachypnea" (rapid breathing without retractions), narrow pulse pressure, pale/cool skin, delayed refill, weak pulses910. B. Distributive Shock Mechanism: Vasodilation causing blood maldistribution and relative hypovolemia110. Septic Shock: Commonest form11. Warm Shock: Low SVR, bounding pulses, flushed skin, wide pulse pressure1213. Cold Shock: High SVR, weak pulses, cool skin1213. Anaphylactic Shock: Histamine release causes bronchospasm, upper airway edema (stridor), hives, vasodilation14. Neurogenic Shock: High spinal injury causes loss of sympathetic tone hypotension without tachycardia (normal HR or bradycardia)15. C. Cardiogenic Shock Mechanism: Primary pump failure with low contractility, high afterload. Signs: Tachypnea with increased work of breathing (retractions, grunting, crackles), hepatomegaly, cyanosis1617. D. Obstructive Shock Mechanism: Physical restriction of venous return or cardiac outflow18. Tension Pneumothorax: Tracheal deviation, hyperresonance, absent breath sounds19. Cardiac Tamponade: Muffled heart sounds, pulsus paradoxus (>10 mmHg SBP drop on inspiration)20. Ductal Lesions: Neonatal presentation with differential pre/post-ductal SBP/SpO221. Massive PE: Systemic venous congestion and RV failure22.

PALS | Respiratory Distress & Failure Extended

During the copy past its throwing a lot of weird symbols. I think the information is still helpful PALS Respiratory Distress & Failure: 80/20 Core Summary 1. Core Pathophysiology & Definitions Respiratory 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, failure rapidly leads to cardiac arrest if uncorrected13. Hypoxemia: $\text{SpO}_2 < 94\%$ on room air4. Caused by V/Q mismatch, hypoventilation, diffusion defects, or shunts6. Early signs: tachypnea, tachycardia, agitation; late signs: bradypnea, bradycardia, seesaw breathing, lethargy7. Hypercarbia: Elevated $\text{PaCO}_2$ resulting in respiratory acidosis5. Lacks visual signs like cyanosis; suspect when agitation converts to decreased consciousness despite oxygen therapy5. 2. Four Clinical Types of Respiratory Problems Upper Airway Obstruction (Croup, foreign body aspiration, epiglottitis)8:Key Signs: Inspiratory stridor, barking cough, hoarseness, inspiratory retractions, and poor air entry89. Lower Airway Obstruction (Asthma, bronchiolitis)810:Key Signs: Expiratory wheezing, prolonged expiratory phase with active effort, and tachypnea910. Lung Tissue Disease (Pneumonia, pulmonary edema, ARDS)10:Key Signs: Grunting (glottic closure maintaining PEEP), crackles (rales), diminished breath sounds, and severe hypoxemia9more_horiz. Disordered Control of Breathing (Seizures, head injury, drug overdose)11:Key Signs: Variable/irregular pattern (alternating tachypnea/bradypnea), central apnea, shallow respirations, and altered mental status911. 3. Severity Spectrum: Distress vs. Failure Early recognition prevents progression from distress to failure and cardiac arrest19: Airway Patency: Open and maintainable $\rightarrow$ Not maintainable9. Rate & Effort: Tachypnea & increased effort $\rightarrow$ Bradypnea, inadequate effort, or apnea9. Air Movement: Good air entry $\rightarrow$ Poor to absent air movement9. Heart Rate: Tachycardia (compensatory) $\rightarrow$ Bradycardia (critical late sign of impending arrest)79. Skin Appearance: Pallor/mottling $\rightarrow$ Cyanosis3more_horiz. Mental Status: Anxiety & agitation $\rightarrow$ Lethargy & unresponsiveness5more_horiz. 4. High-Yield 80/20 Clinical Pearls Bradycardia is a Red Flag: Hypoxia-induced bradycardia indicates imminent cardiopulmonary arrest79. Grunting Mechanism: Glottic closure during expiration preserves PEEP to prevent alveolar collapse11. Decreased Effort $\neq$ Recovery: Reduced work of breathing with depressed mental status signals fatigue and failure39.

PALS | Pedi Bradycardia & Tachycardia Extended

80/20 Core Need-to-Know Principles Cardiac 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 < normal for age (typically <60/min) with cardiopulmonary compromise (hypotension, altered mental status, shock)3. If HR stays <60/min with poor perfusion despite ventilation, start CPR immediately3. QRS Classification: Tachyarrhythmias are divided by QRS width into narrow ($\le$0.09 s) and wide (>0.09 s)45. Wide QRS tachycardias are assumed to be Ventricular Tachycardia (VT) unless proven otherwise67. Bradycardia & AV Blocks Etiology: Primary bradycardia stems from intrinsic pacemaker/conduction disease (congenital defects, surgery, myocarditis)1. Secondary bradycardia results from noncardiac causes (hypoxia, acidosis, hypotension, hypothermia, drugs)1. ECG Features: Slow rate, variable P waves, narrow/wide QRS, and potential AV dissociation2. AV Block Spectrum:First-degree: Prolonged PR interval; asymptomatic8. Second-degree Mobitz I (Wenckebach): Progressive PR prolongation until a P wave drops89. Second-degree Mobitz II: Intermittent dropped P waves without PR prolongation (often 2:1 block); risks syncope89. Third-degree (Complete): Complete AV dissociation with independent P waves and QRS complexes; causes fatigue and syncope89. Tachyarrhythmias: Narrow vs. Wide Complex Hemodynamic Impact: Rapid rates shorten diastole, reducing stroke volume and coronary perfusion, causing heart failure and shock4. Sinus Tachycardia (ST) vs. SVT:Sinus Tachycardia: Normal response to stress, fever, or hypovolemia5. HR <220/min in infants, <180/min in children5. Shows rate variability, normal P waves, gradual onset5more_horiz. Supraventricular Tachycardia (SVT): Reentry mechanism arrhythmia11. HR $\ge$220/min in infants, $\ge$180/min in children12. Shows abrupt onset, absent/abnormal P waves, constant rate without variability6more_horiz. Atrial Flutter: Narrow-complex rhythm with atrial rate >300/min and sawtooth P waves10. Ventricular Tachycardia (VT): Wide-complex rhythm (>0.09 s), rate $\ge$120/min, AV dissociation7.Monomorphic VT: Uniform QRS complexes13. Polymorphic VT / Torsades de Pointes: QRS twists around baseline; linked to long QT, hypomagnesemia, hypokalemia, or drugs, deteriorating into VF713.

PALS | Pedi Bradycardia and Tachycardia Management Extended

80/20 Summary: Pediatric Arrhythmia Management & Algorithms[1] 1. Core Assessment & Stability Principles Hemodynamic 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 Algorithm (With Pulse & Poor Perfusion) Primary Trigger: HR < 60/min with poor perfusion despite adequate oxygenation and ventilation[2][4]. Immediate Action (CPR): Start high-quality CPR (100–120 compressions/min; depth ≥1/3 AP chest diameter: ~2 in [5 cm] in children, ~1.5 in [4 cm] in infants; complete recoil; minimal interruptions)[2][4]. Medications for Persistent Bradycardia:Epinephrine: 0.01 mg/kg IO/IV (0.1 mL/kg of 0.1 mg/mL); repeat every 3–5 min. (ET dose: 0.1 mg/kg)[2][5]. Atropine: 0.02 mg/kg IO/IV (min 0.1 mg, max single dose 0.5 mg; repeat once in 5 min) for increased vagal tone or primary AV block[2]. Cardiac Pacing: Consider for complete AV block or sinus node dysfunction[2][6]. Pulseless Arrest: If pulses are lost, switch immediately to the Cardiac Arrest Algorithm[7]. 3. Pediatric Tachycardia Algorithm (With Pulse) Classify by QRS width: Narrow (≤0.09 sec) vs Wide (>0.09 sec)[8][9]. A. Narrow QRS (≤0.09 sec) Sinus Tachycardia (ST): HR <220/min (infants) or <180/min (children); P waves present; variable R-R[8][9]. Action: Treat underlying cause (fever, pain, dehydration)[8][9]. Supraventricular Tachycardia (SVT): HR ≥220/min (infants) or ≥180/min (children); P waves absent/abnormal; abrupt onset[8][9].Stable SVT:Vagal Maneuvers: Ice bag to upper face (15–20 sec) or straw blowing[10][11]. Adenosine: 0.1 mg/kg IV/IO rapid bolus (max 1st dose: 6 mg) via 2-syringe flush. 2nd dose: 0.2 mg/kg (max: 12 mg)[8][11]. Unstable SVT: Synchronized Cardioversion at 0.5–1 J/kg (up to 2 J/kg). If IV/IO available, give adenosine first without delaying shock[12]. B. Wide QRS (>0.09 sec) Ventricular Tachycardia (VT):Unstable VT: Synchronized Cardioversion at 0.5–1 J/kg (up to 2 J/kg)[12]. Stable VT: Expert consult. Amiodarone 5 mg/kg IV/IO over 20–60 min OR Procainamide 15 mg/kg IV/IO over 30–60 min (do not combine)[15]. Adenosine may be tried if monomorphic[11][13]. Magnesium for Torsades de Pointes[19].

PALS | Management of Pedi Resp. Arrest Extended

80/20 Summary: Pediatric Respiratory Emergency Management Respiratory 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 Management Rescue 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 comfort or perform head tilt-chin lift (jaw thrust if trauma suspected)[3]. Suction secretions; insert an OPA only if unresponsive without a gag reflex, or an NPA if a gag is present (avoid NPA in facial trauma)[3][4]. Breathing & Circulation: Provide high-flow O2 via nonrebreathing mask; assist bag-mask ventilation (BMV) if needed[3]. Monitor SpO2, HR, BP, and establish IV/IO access[3]. 2. Targeted Management by Etiology Category Upper Airway Obstruction Croup: Mild cases get dexamethasone[5]. Moderate-to-severe require humidified O2, nebulized epinephrine, and dexamethasone[5]. Impending failure needs high-flow O2, BMV, dexamethasone, and ET intubation with a tube 0.5 size smaller[5]. Anaphylaxis: Give IM epinephrine q10–15 min[6]. Give IV methylprednisolone, albuterol, antihistamines, and 20 mL/kg IV fluid boluses for hypotension[6]. FBAO: Infants (<1 yr) get 5 back slaps + 5 chest thrusts; children (≥1 yr) get abdominal thrusts[7]. If unresponsive, start CPR; inspect mouth before breaths (no blind finger sweeps)[7]. Lower Airway Obstruction Hyperventilation Risks: Avoid hyperventilation during BMV to prevent gastric distension, pneumothorax, and severe air trapping[8]. Bronchiolitis: Suctioning; bronchodilator trial; O2 for SpO2 < 94%[8]. Acute Asthma: Give O2, albuterol, and steroids[9]. Severe cases get continuous albuterol, ipratropium, IV steroids, and IV magnesium sulfate[9]. Lung Tissue Disease Pneumonia: Give antibiotics within 1 hour, albuterol for wheezing, and CPAP/NIV[10]. Cardiogenic Edema: Support with PEEP, diuretics, and inotropes[11]. ARDS: Use permissive hypercapnia, low tidal volume (5–8 mL/kg), and PEEP[12]. Avoid succinylcholine in neuromuscular disease[13]. Disordered Control of Breathing Increased ICP: Head midline, avoid hyperventilation (PaCO2 < 30 mmHg causes vasoconstriction), give hypertonic saline/mannitol[14]. Poisoning: Contact Poison Control, maintain airway, give antidotes (naloxone)[13]. 3. Key Takeaways Stabilize ABCs First: Restore oxygenation before advanced therapy[2][3]. Select Right Adjunct: OPA for no gag; NPA for intact gag[4]. Avoid Over-Ventilation: Prevents barotrauma and reduced cardiac output[8].

PALS | Pedi Cardiac Arrest Extended

80/20 Summary: Pediatric Cardiac Arrest Recognition & Management 1. 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 assessed in ≤10 seconds[4][5]. Begin CPR immediately within 10 seconds if uncertain[1][5]. 2. High-Quality CPR & Airway Management Sequence & Ratios: Use C-A-B[6]. Without an advanced airway, compression-to-ventilation ratio is 30:2 (1 rescuer) and 15:2 (2+ rescuers)[7]. With an advanced airway, give continuous compressions at 100–120/min with 1 breath every 6 seconds (10 breaths/min)[7][8]. Compression Technique: Rate is 100–120/min[7]. Depth is at least 1/3 chest AP diameter (~1.5 in / 4 cm in infants; ~2 in / 5 cm in children)[7]. Allow full recoil and limit chest compression pauses to <10 seconds[7][9]. Rotate compressors every 2 minutes[8][10]. CPR Monitoring: PETCO₂ goal is >10–15 mmHg; a jump to >40 mmHg indicates Return of Spontaneous Circulation (ROSC)[9][11]. 3. Cardiac Arrest Algorithms & Electrical Therapy Nonshockable Rhythms (Asystole / PEA): Most common initial pediatric arrest rhythms (~85–95%)[3][5]. Pathway: Start CPR → Give Epinephrine ASAP → Reassess rhythm every 2 minutes → Treat reversible H's & T's[12]. Shockable Rhythms (VF / pVT): Occurs in 5–15% initially[3]. Pathway: Deliver 1st shock at 2 J/kg → CPR 2 min → Recheck rhythm → If persistent, 2nd shock at 4 J/kg + Epinephrine → CPR 2 min → 3rd shock (≥4 J/kg, max 10 J/kg) + Amiodarone or Lidocaine[10]. Paddle Sizes: Adult paddles (8–13 cm) for >10 kg (≥1 yr); infant paddles (4.5 cm) for <10 kg (<1 yr)[16]. 4. Critical Resuscitation Medications Epinephrine: Dose is 0.01 mg/kg (0.1 mL/kg of 0.1 mg/mL) IV/IO every 3–5 minutes[12][17]. ET dose is 0.1 mg/kg[12][17]. Amiodarone: 5 mg/kg IV/IO bolus (max 300 mg) for refractory VF/pVT, repeatable up to 2 times[12][15]. Lidocaine: 1 mg/kg IV/IO loading dose[12][15]. Magnesium Sulfate: 25–50 mg/kg (max 2 g) for Torsades de Pointes or hypomagnesemia[15][18]. Vascular Access Order: IV → IO (obtain within 30–60 sec) → Endotracheal (ET) as last resort[19][20]. 5. Reversible Causes (H's and T's) H's: Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypoglycemia, Hypo-/Hyperkalemia, Hypothermia[4][21]. T's: Tension pneumothorax, Tamponade (cardiac), Toxins, Thrombosis (pulmonary), Thrombosis (coronary)[4][21].

PALS | Systematic Approach To Pedi Patient

This is the first episode to the PALS material. THIS NOT A REPLACEMENT FOR READING THE BOOK OR ATTENDING CLASS

PALS | Recognition of Shock

Adequate O2 delivery depends on three components: sufficient O2 content in the blood, adequate blood flow to the tissues (cardiac output), and appropriate distribution of blood flow. Cardiac output (CO), which measures the volume of blood pumped per minute, is determined by Stroke Volume (SV) multiplied by Heart Rate (HR). SV is influenced by three factors: Preload (volume before contraction), Contractility (strength of contraction), and Afterload (resistance to ejection). Severity and Compensation The body utilizes several compensatory mechanisms to maintain O2 delivery and blood pressure (BP). These include tachycardia (increased HR), increased Systemic Vascular Resistance (SVR) via vasoconstriction, and increased contractility. Blood flow is redistributed from nonvital areas (like skin and kidneys) to vital organs (like the heart and brain). 1. Compensated Shock: The patient exhibits clinical signs of poor tissue perfusion (such as tachycardia, delayed capillary refill, and decreased urine output), but compensatory mechanisms successfully maintain the blood pressure within the normal range. 2. Hypotensive Shock (Decompensated Shock): Compensatory mechanisms are failing, leading to low blood pressure (hypotension) and evidence of severely impaired perfusion. Hypotension is considered a late finding in most types of shock and signals impending cardiac arrest. Shock progression is unpredictable, but early recognition is critical to halt the physiologic continuum from compensated to hypotensive shock and subsequent cardiac arrest. 1. Hypovolemic Shock: This is the most common type in pediatric patients and is caused by an absolute deficiency of intravascular volume. Causes include dehydration (diarrhea, vomiting), hemorrhage, and burns. Physiologically, it is characterized by decreased preload and compensatory increased afterload (SVR). Clinical findings often include pale, cool skin and weak peripheral pulses. 2. Distributive Shock: This type is characterized by the maldistribution of blood volume and flow, typically due to reduced SVR. It includes septic shock, anaphylactic shock, and neurogenic shock. These conditions often result in relative hypovolemia due to vasodilation and capillary leak. Septic shock is the most common form of distributive shock and can present as "warm shock" (low SVR, bounding pulses) or "cold shock" (high SVR, weak pulses). Neurogenic shock is unique in that the loss of sympathetic tone causes hypotension and bradycardia, a lack of the usual compensatory tachycardia seen in other forms. 3. Cardiogenic Shock: This results from reduced CO due to impaired cardiac function or pump failure. Common causes include congenital heart disease, myocarditis, and arrhythmias. It is defined by decreased contractility and high afterload (secondary to compensatory vasoconstriction). Clinical signs include evidence of congestive heart failure, such as pulmonary edema or hepatomegaly. 4. Obstructive Shock: This type is caused by a physical impairment of blood flow that limits venous return or restricts the heart's ability to pump. Etiologies include pericardial tamponade, tension pneumothorax, massive pulmonary embolism, and ductal-dependent lesions. It is characterized by normal contractility and often increased afterload, with variable preload. Tension pneumothorax is a critical cause that rapidly leads to decreased cardiac output and hypotension.

PALS | Management of Shock

1️⃣ Types of Pediatric Shock (Know These Cold) Hypovolemic 🩸: dehydration, hemorrhage Distributive 🌡️: sepsis (most common), anaphylaxis, neurogenic Cardiogenic ❤️: congenital heart disease, myocarditis Obstructive 🚫: tension pneumo, tamponade, PE 2️⃣ Universal Signs of Shock (High Yield) Tachycardia (earliest sign) Delayed cap refill > 2 sec Cool, mottled, pale skin Weak or thready pulses Altered mental status Oliguria / ↓ urine output Hypotension = late and pre-arrest 3️⃣ General Management Principles (ALL Shock Types) A. Immediate Actions 🆘 Call for help / PALS team Airway & breathing: O₂ to maintain SpO₂ > 94% Cardiac monitor + large-bore IV/IO access Check glucose (treat <70 mg/dL) B. Fluid Resuscitation ⚡ 20 mL/kg isotonic fluid bolus (NS or LR) Give rapidly over 5–10 min Reassess after each bolus Can repeat up to 60 mL/kg (except cardiogenic shock) 4️⃣ Shock-Specific Management 🩸 A. Hypovolemic Shock (Most Common) Problem: ↓ preload Treatment: 20 mL/kg boluses x3 Control bleeding Treat dehydration (fluids + electrolytes) Monitor for improvement: HR ↓, cap refill ↑ 🌡️ B. Distributive Shock (Septic, Anaphylactic, Neurogenic) 1. Septic Shock Problem: vasodilation + capillary leak Treatment: 20 mL/kg boluses (often large volumes needed) Broad-spectrum antibiotics within 1 hour Vasopressors if fluid-refractory:Epinephrine or norepinephrine Correct glucose & electrolytes Warm the child 2. Anaphylactic Shock Problem: massive vasodilation + airway obstruction Treatment: IM Epinephrine 0.01 mg/kg (1:1000) ASAP Airway support Albuterol neb for wheeze IV fluids Diphenhydramine + steroids (adjuncts) 3. Neurogenic Shock Problem: loss of sympathetic tone Treatment: Judicious fluids Vasopressors (epi or norepi) Maintain spinal precautions ❤️ C. Cardiogenic Shock Problem: ineffective pump DO NOT flood with large fluid boluses. Management Small boluses: 5–10 mL/kg Inotropes:Epinephrine Dopamine Milrinone (afterload reduction) Correct arrhythmias Treat myocarditis / congenital issues Consider cardiology consult early

PALS | Recognition of Respiratory Failure/ Distress

🌬️ PALS: Recognizing Respiratory Distress vs. Respiratory Failure — High-Yield Study Guide ⚠️ Respiratory problems are the #1 cause of pediatric cardiac arrest. Early recognition = survival. 1️⃣ Respiratory Distress — The Compensation Phase The child is still maintaining oxygenation + ventilation by working harder. 🔥 Key Signs (“WORK OF BREATHING ↑”) Tachypnea (earliest sign) Nasal flaring 👃 Retractions (intercostal, suprasternal, subcostal) Head bobbing 🧠↕️ (infants) Grunting (auto-PEEP to keep alveoli open) Wheezing or stridor (depends on upper vs. lower airway) Anxious, irritable 🫁 Breath Sounds Upper airway: stridor, barking cough Lower airway: wheezing, prolonged expirations 📈 O2 Sat Usually normal or mildly low because compensation still works. 2️⃣ Respiratory Failure — Decompensation Phase The child cannot maintain oxygenation or ventilation. CO₂ retention, hypoxemia, fatigue → arrest. 🚨 Key Signs (“WORK OF BREATHING ↓ — they are giving up”) Bradypnea (late + ominous) Apnea or gasping Weak or absent cry Silent chest ❗ Seesaw respirations Cyanosis 💙 (central) Poor muscle tone, floppy infant Decreased LOC → lethargy → unresponsiveness 🫁 Breath Sounds Very diminished or silent chest = impending arrest. 📉 O2 Sat Low despite oxygen 💀 Remember: Kids crash fast. Once they tire out, cardiac arrest follows within minutes. 3️⃣ Causes by Category (PALS Mnemonic) Upper Airway 🟥 Croup, anaphylaxis, foreign body Signs: Stridor, hoarse voice, barking cough Lower Airway 🟦 Asthma, bronchiolitis Signs: Wheezing, prolonged expiration Lung Tissue/Parenchymal 🟩 Pneumonia, pulmonary edema Signs: Crackles, hypoxemia Disordered Control of Breathing 🟨 Seizure, head injury, OD Signs: Irregular respirations, apnea 4️⃣ Nursing Management & Immediate Actions (High Yield) In Respiratory Distress: Position: sniffing or tripod Oxygen: blow-by → NC → NRB Nebulizers: albuterol, racemic epi (if indicated) Suctioning for infants Avoid agitation in upper-airway obstruction Prepare for escalation 5️⃣ Red Flags You NEVER Ignore 🚩 Silent chest Bradypnea Cyanosis unresponsive to O₂ Diminishing retractions (NOT improvement—this means fatigue) Altered mental status

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