Renal/urologic disorders involve infection, inflammation, obstruction, and immune-mediated damage to the urinary system. UTIs (cystitis, urethritis, pyelonephritis) occur when bacteria—mainly E. coli—enter the urinary tract. Risk factors include female anatomy, obstruction (BPH, stones), retention, catheter use, pregnancy, diabetes, and immunosuppression. Symptoms include dysuria, frequency, urgency, suprapubic pain, foul/cloudy urine, and hematuria. Older adults may only show confusion 🧠. Diagnosis uses UA + culture; treatment uses antibiotics like TMP-SMX, nitrofurantoin, fosfomycin. Teaching: hydration, wipe front-to-back, void after sex, complete antibiotics 🌊.

Pyelonephritis is infection of the renal parenchyma. Acute cases present with fever, chills, CVA tenderness, N/V, systemic toxicity 🤒. Labs show WBCs, bacteria, possible casts. Treat with broad-spectrum IV or PO antibiotics and hydration. Chronic pyelonephritis leads to fibrosis, CKD, and renal scarring.

Urethritis often arises from bacterial or STI causes, presenting with dysuria and discharge. Treat based on organism.

Interstitial cystitis/painful bladder syndrome causes chronic pelvic pain, urinary frequency, and urgency without infection. No cure—management includes diet changes (avoid citrus, caffeine, alcohol), stress reduction, and bladder analgesics.

🧬 Glomerular Disorders

Glomerulonephritis (GN) results from immunologic inflammation of the glomeruli. Triggers include infections (post-strep GN), autoimmune diseases (SLE), hypertension, diabetes, drugs, and toxins. S/S: hematuria (tea-colored urine), proteinuria, edema, hypertension, flank pain. APSGN follows strep infection; treat with rest, sodium/fluid restriction, antihypertensives, and sometimes diuretics or antibiotics 🎯.

Nephrotic syndrome results from massive protein loss (≥3.5 g/day). Causes: diabetes, SLE, infections, drugs. Symptoms: severe edema, ascites, foamy urine, hyperlipidemia, hypoalbuminemia. Treatment: ACEIs/ARBs, corticosteroids, statins, diuretics, low-sodium diet. Risk for DVT/PE due to hypercoagulability ⚠️.

🪨 Urinary Tract Calculi

Stones form when solutes supersaturate urine. Types: • Calcium oxalate 🧊 • Calcium phosphate • Uric acid • Struvite (infection) • Cystine (genetic)

Risk factors: dehydration, high sodium, high animal protein, hyperparathyroidism, immobility, UTIs. Symptoms: sudden severe flank pain radiating to groin, N/V, hematuria, restlessness. Diagnosis: CT, ultrasound. Management: fluids, tamsulosin, pain control, strain urine. Procedures: lithotripsy, ureteroscopy, stent placement.

🚑 Renal Trauma & Vascular Disorders

Renal trauma occurs from blunt injuries (MVCs, falls). Assess flank bruising, hematuria. Management ranges from observation to surgery.

Vascular conditions include nephrosclerosis, renal artery stenosis, and thromboembolism—may require antihypertensives or revascularization.

🧬 Polycystic Kidney Disease (PKD)

Autosomal dominant disorder → multiple renal cysts → enlarged kidneys, flank pain, hematuria, HTN, progressive renal failure. No cure; manage BP, treat infections, prepare for dialysis/transplant. Tolvaptan may slow progression. Counseling is essential due to hereditary risk. 🧬

Renal/urologic disorders involve infection, inflammation, obstruction, and immune-mediated damage to the urinary system. UTIs (cystitis, urethritis, pyelonephritis) occur when bacteria—mainly E. coli—enter the urinary tract. Risk factors include female anatomy, obstruction (BPH, stones), retention, catheter use, pregnancy, diabetes, and immunosuppression. Symptoms include dysuria, frequency, urgency, suprapubic pain, foul/cloudy urine, and hematuria. Older adults may only show confusion 🧠. Diagnosis uses UA + culture; treatment uses antibiotics like TMP-SMX, nitrofurantoin, fosfomycin. Teaching: hydration, wipe front-to-back, void after sex, complete antibiotics 🌊.

Pyelonephritis is infection of the renal parenchyma. Acute cases present with fever, chills, CVA tenderness, N/V, systemic toxicity 🤒. Labs show WBCs, bacteria, possible casts. Treat with broad-spectrum IV or PO antibiotics and hydration. Chronic pyelonephritis leads to fibrosis, CKD, and renal scarring.

Urethritis often arises from bacterial or STI causes, presenting with dysuria and discharge. Treat based on organism.

Interstitial cystitis/painful bladder syndrome causes chronic pelvic pain, urinary frequency, and urgency without infection. No cure—management includes diet changes (avoid citrus, caffeine, alcohol), stress reduction, and bladder analgesics.

🧬 Glomerular Disorders

Glomerulonephritis (GN) results from immunologic inflammation of the glomeruli. Triggers include infections (post-strep GN), autoimmune diseases (SLE), hypertension, diabetes, drugs, and toxins. S/S: hematuria (tea-colored urine), proteinuria, edema, hypertension, flank pain. APSGN follows strep infection; treat with rest, sodium/fluid restriction, antihypertensives, and sometimes diuretics or antibiotics 🎯.

Nephrotic syndrome results from massive protein loss (≥3.5 g/day). Causes: diabetes, SLE, infections, drugs. Symptoms: severe edema, ascites, foamy urine, hyperlipidemia, hypoalbuminemia. Treatment: ACEIs/ARBs, corticosteroids, statins, diuretics, low-sodium diet. Risk for DVT/PE due to hypercoagulability ⚠️.

🪨 Urinary Tract Calculi

Stones form when solutes supersaturate urine. Types: • Calcium oxalate 🧊 • Calcium phosphate • Uric acid • Struvite (infection) • Cystine (genetic)

Risk factors: dehydration, high sodium, high animal protein, hyperparathyroidism, immobility, UTIs. Symptoms: sudden severe flank pain radiating to groin, N/V, hematuria, restlessness. Diagnosis: CT, ultrasound. Management: fluids, tamsulosin, pain control, strain urine. Procedures: lithotripsy, ureteroscopy, stent placement.

🚑 Renal Trauma & Vascular Disorders

Renal trauma occurs from blunt injuries (MVCs, falls). Assess flank bruising, hematuria. Management ranges from observation to surgery.

Vascular conditions include nephrosclerosis, renal artery stenosis, and thromboembolism—may require antihypertensives or revascularization.

🧬 Polycystic Kidney Disease (PKD)

Autosomal dominant disorder → multiple renal cysts → enlarged kidneys, flank pain, hematuria, HTN, progressive renal failure. No cure; manage BP, treat infections, prepare for dialysis/transplant. Tolvaptan may slow progression. Counseling is essential due to hereditary risk. 🧬

the recognition and management of Pedi cardiac Arrest

PALS | Management of Pedi Arrhythmias

1️⃣ Bradyarrhythmias (Slow Rhythms)

Definition: HR <60 bpm with poor perfusion = treat immediately.

🌡️ Causes

Hypoxia (MOST COMMON), heart block, vagal stimulation, hypothermia, drugs.

🫀 Sinus Bradycardia

• Recognition: P waves present, regular rhythm, slow rate.
• Peds Tip: Normal in athletes/sleeping; NOT normal with poor perfusion.

🟪 AV Blocks

1° AV Block:

• PR prolonged (>0.20s adult-equivalent), but every P → QRS.
• Usually benign; watch for progression.

2° Type I (Wenckebach):

• PR progressively lengthens → dropped QRS.
• “Longer, longer, longer, drop ▶️ Wenckebach.”
• Usually transient, often vagal.

2° Type II:

• Normal PR intervals with random dropped QRS.
• Bad. Can progress to complete block.

3° Complete Heart Block:

• Atria + ventricles beat independently.
• Regular P waves, regular QRS—but no relationship.
• Often bradycardic, poor perfusion.

2️⃣ Tachyarrhythmias (Fast Rhythms)

Definition: Above age-appropriate range (often >180 infants, >160 children).

⚡ Supraventricular Tachycardia (SVT)

• Rate: 180–300 bpm
• P waves: Absent or hidden
• QRS: Narrow
• Onset: Abrupt
• Key Tip: Infant may just appear irritable, poor feeding, or pale.

⚡ Atrial Flutter

• Sawtooth F-waves
• Rate often 250–350
• Rare in kids (post-op congenital heart disease)

⚡ Ventricular Tachycardia (VT)

With Pulse:

• Wide QRS, regular rhythm
• Rate usually 120–250
• May have poor perfusion

Pulseless VT:

• Treat like VF (defibrillate)

💥 Ventricular Fibrillation (VF)

• Chaotic, no identifiable waves
• No pulse → CPR + defibrillate immediately

😵 Asystole (Flatline)

• No electrical activity
• Confirm in 2 leads
• CPR + epinephrine only (NO shock)

🌪️ PEA (Pulseless Electrical Activity)

• Organized electrical rhythm without a pulse
• Causes = H’s & T’s (hypoxia, hypovolemia, hypothermia, H+ acidosis, hypo/hyperK, tension pneumo, tamponade, toxins, thrombosis)

3️⃣ How to Rapidly Recognize Rhythms (PALS Algorithm)

Step 1: Pulse Check

• Present? → Rhythm with pulse
• Absent? → Treat as cardiac arrest rhythm

Step 2: Narrow vs. Wide QRS

• Narrow (<0.08s): SVT, sinus tach, atrial flutter/fib
• Wide (>0.08–0.12s): VT, aberrancy

Step 3: Regular vs. Irregular

• Regular: SVT, VT, sinus tach
• Irregular: Atrial fibrillation/flutter with variable block, polymorphic VT

Step 4: P Waves Present?

• Yes → sinus or atrial rhythm
• No → SVT or VT

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

1️⃣ MANAGEMENT OF RESPIRATORY DISTRESS (Compensation Phase)

Goal → Support oxygenation & ventilation BEFORE fatigue sets in.

A. Airway Opening Maneuvers

• Positioning is everything
  • Infants: sniffing position
  • Older kids: tripod or chin lift / jaw thrust
• Avoid hyperextension in infants (soft trachea collapses)

B. Oxygen Administration 🫧

Start low → escalate:

1. Blow-by (infants, mild)
2. Nasal cannula
3. Simple mask / NRB
4. Humidified O₂ for croup

Target SpO₂ ≥ 94% unless chronic lung disease.

C. Treat the Underlying Problem

• Upper airway (stridor):
  • Racemic epi neb
  • Dexamethasone
  • Avoid upsetting the child ❗
• Lower airway (wheezing):
  • Albuterol ± ipratropium
  • Magnesium sulfate (severe)
  • Steroids
• Parenchymal (pneumonia):
  • Antibiotics
  • High-flow nasal cannula if hypoxemic
• Fluid overload: diuretics
• Foreign body: encourage cough; prepare for removal

D. Monitoring

• Continuous pulse ox
• Reassess work of breathing q5–10 min
• Cap refill, mental status, perfusion
• Prepare airway equipment early

E. Red Flags That Require Escalation

• Increased fatigue
• Declining retractions (NOT improvement)
• Rising CO₂ signs: headache, confusion, lethargy
• SpO₂ not improving with O₂

2️⃣ MANAGEMENT OF RESPIRATORY FAILURE (Decompensation Phase)

Goal → Ventilate & oxygenate NOW. Fatigue → arrest in minutes.

A. Call for Help / Activate PALS Team 🚨

Failure means the child cannot compensate. You need backup.

B. Immediate Bag-Mask Ventilation (The #1 lifesaving step)

• Correct size mask → seal with “EC clamp”
• Rate: 12–20/min (1 breath q3–5 sec)
• Use PEEP valve if available
• Watch chest rise and SpO₂
• Avoid over-ventilation (↓ venous return → ↓ BP)

C. Consider Airway Adjuncts

• OPA if no gag
• NPA if gag intact
• Suction PRN

D. Prepare for Intubation

Indications:

• Fatigue
• Worsening hypoxemia
• Hypercarbia
• Apnea / bradypnea
• Diminished or silent chest

Setup:

• Appropriate ETT size
• Stylet
• Suction
• BVM with PEEP
• Confirm with waveform capnography

E. Ventilation Strategy Post-Intubation

• Use lowest pressures needed
• Avoid breath stacking
• Adjust rate for CO₂ goals
• Reassess every few minutes

F. Treat the Cause (Critical)

• Anaphylaxis → IM epi, fluids
• Asthma → continuous albuterol, steroids, mag, possible ketamine
• Croup → racemic epi, steroids
• Bronchiolitis → suction, high-flow

🌬️ 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

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.

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