Defibrillator Modes – Study Notes

1. Overview

• Defibrillator = critical crash cart equipment.

• Modes:

  1. Defibrillation

  2. Synchronized cardioversion

  3. Transcutaneous pacing (TCP)

• Pads preferred over paddles: safer, easier, allow ECG monitoring.

• Pad placement:

  • Anterior-apex: below clavicle + left lateral chest.

  • Anterior-posterior: front of chest + between scapula (preferred).

2. Defibrillation

• Definition: Delivers an unsynchronized electrical shock to completely depolarize the myocardium → allows SA node to restart normal rhythm.

• Indications:

  • Ventricular fibrillation (VF).

  • Pulseless ventricular tachycardia (pVT).

• Not for: Asystole or PEA (pulseless electrical activity).

• Timing: Every minute delay ↓ success by 7–10%.

• Energy settings:

  • Monophasic: 360 J (older, rare).

  • Biphasic (modern):

    • ZOLL: 120 → 150 → 200 J.

    • Philips: 150 J (all shocks).

    • LifePak 15: 200 → 300 → 360 J.

  • Internal paddles: much lower (5–10 J, escalate).

• Steps: Attach pads → select energy → charge → clear patient → shock → resume CPR.

3. Synchronized Cardioversion

• Definition: Shock delivered in sync with the R wave (avoids T wave → prevents VF).

• Indications: Tachyarrhythmias with a pulse when unstable.

  • SVT.

  • Atrial fibrillation.

  • Atrial flutter.

  • Ventricular tachycardia with a pulse.

• Stable patients: try meds first (adenosine, rate/rhythm control).

• Energy settings:

  • Monophasic: 100 → 200 → 360 J.

  • ZOLL: 75 → 120 → 150 J.

  • Philips: 100 → 150–200 J.

  • LifePak 15: 100 → 200 → 300 J.

  • For SVT/flutter: may start as low as 50 J.

• Steps:

  • Sedate if possible.

  • Attach pads → select sync mode → confirm R-wave markers → charge → press & hold shock until delivered.

4. Transcutaneous Pacing (TCP)

• Definition: External pacing by delivering impulses through pads to stimulate ventricular contraction.

• Indications:

  • Symptomatic bradycardia unresponsive to atropine.

  • High-degree AV block (Mobitz II, third-degree).

  • Temporary measure until transvenous or permanent pacemaker.

• Setup:

  • Use anterior-posterior pad placement.

  • Attach ECG leads for monitoring (pads only deliver impulses).

• Steps:

  1. Select pacer mode.

  2. Set rate (usually 60 bpm).

  3. Start at lowest output → gradually increase until capture.

     • Capture = pacing spike followed by wide QRS.

  4. Increase slightly above capture threshold (safety margin).

5. High-Yield Reminders

• Defibrillation = VF/pulseless VT only (unsynchronized).

• Cardioversion = tachyarrhythmia with pulse (synchronized).

• TCP = bradycardia/high-degree block when atropine fails.

• Always clear patient before shocks.

• Resume high-quality chest compressions immediately after defibrillation.

ECG Findings – Study Notes

1. Sinus Rhythm

• Normal rhythm: regular P waves followed by QRS complexes.

• PR interval constant.

• QRS = ventricular depolarization, normally narrow (80–100 ms).

• Sinus bradycardia: rate < 60 bpm.

• Sinus tachycardia: rate > 100 bpm.

2. Atrial Fibrillation (AF)

• No distinct P waves, chaotic atrial activity.

• QRS complexes not preceded by P waves.

• Irregularly irregular rhythm (variable R–R intervals).

• Substrate: atrial dilation.

• Trigger: ectopic foci (often pulmonary veins).

• AF with RVR: rate > 100 bpm.

• AF with slow VR: rate < 60 bpm.

3. Atrial Flutter

• Re-entry circuit in atria → coordinated atrial contractions.

• Atrial rate ≈ 300 bpm.

• Narrow complex tachycardia.

• ECG: Sawtooth waves (inverted P waves in inferior leads).

• Conduction ratio: usually 2:1 (ventricular rate ≈ 150 bpm).

  • Higher ratios = more AV block.

  • 1:1 conduction → unstable, risk of VF.

• May mimic AF if conduction ratio varies.

4. Premature Contractions

Premature Ventricular Contractions (PVCs)

• Origin: His–Purkinje system.

• Wide QRS (>120 ms).

• Compensatory pause follows.

• Benign if isolated; risk if frequent (>10–30/hr).

• Patterns:

  • Bigeminy (every other beat).

  • Runs of PVCs = ventricular tachycardia.

Premature Atrial Contractions (PACs)

• Abnormal P wave morphology (different from sinus).

• Narrow QRS follows.

• May appear as a pause but timing matches expected P wave.

• Usually benign.

5. Bundle Branch Blocks (BBB)

• General: QRS >120 ms.

• Left BBB:

  • Deep S in V1 (“W”).

  • Broad R in V6 (“M”).

  • Mnemonic: WiLLiaM (W in V1, M in V6).

• Right BBB:

  • RSR’ in V1 (“M”).

  • Deep S in V6 (“W”).

  • Mnemonic: MaRRoW (M in V1, W in V6).

• Note: ST segments altered → difficult ischemia interpretation.

6. AV Blocks

First Degree

• PR interval > 200 ms.

• Usually benign.

Second Degree

• Mobitz I (Wenckebach): Progressive PR prolongation → dropped beat.

• Mobitz II: Dropped beat without PR prolongation.

  • Structural issue.

  • Risk of progression to complete block.

Third Degree (Complete Heart Block)

• No association between P waves and QRS.

• Atrial rate > ventricular rate.

• Ventricular escape rhythm → bradycardia.

• Regular P waves + regular QRS, but independent.

7. Ventricular Tachycardia (VT)

• Broad complex tachycardia (>120 ms).

• Monomorphic VT: uniform QRS morphology.

• Polymorphic VT: varying QRS morphologies.

• Torsades de Pointes: polymorphic VT in prolonged QT.

• Features suggestive of VT:

  • Very broad complexes (>160 ms).

  • Extreme axis deviation.

  • No BBB morphology.

• Dangerous: can lead to VF or cardiac arrest.

8. Ventricular Fibrillation (VF)

• No P waves or QRS complexes.

• Chaotic electrical activity, varying amplitudes.

• Minimal cardiac output → lethal without defibrillation.

• Shockable rhythm in cardiac arrest.

9. Cardiac Arrest Rhythms

• Shockable: VT, VF.

• Non-shockable: Pulseless electrical activity (PEA), asystole.

10. ST Elevation

• ST segment: between end of S wave and start of T wave.

• Elevation > 1 mm (except V2–V3 need >1.5 mm).

• Causes:

  • STEMI (most important).

  • Pericarditis, LBBB, LVH, benign early repolarization.

• Localization:

  • Lateral = I, aVL, V5–V6.

  • Inferior = II, III, aVF.

  • Anterior/septal = V1–V4.

  • Posterior = V7–V9.

• Reciprocal changes: ST depression in opposite leads.

High-Yield Mnemonics

• BBB: WiLLiaM (LBBB), MaRRoW (RBBB).

• AF: “Irregularly irregular.”

• Flutter: “Sawtooth.”

• Torsades: Polymorphic VT + long QT.

Regional Anesthesia – High-Yield ITE Review Notes

1. Patient-Controlled Analgesia (PCA)

• Components: Basal rate, bolus/demand dose, lockout interval, patient limits.

• Routes: IV or epidural.

• Basal infusion: Only for cancer pain or opioid-tolerant patients. ↑ total opioid use, constipation, respiratory depression.

• Benefits: Better analgesia, higher satisfaction vs. nurse-administered.

• Risks: ↑ opioid consumption, ↑ pruritus.

• Special populations:

  • Geriatric → ↓ doses due to ↑ opioid sensitivity.

  • Pediatric → Safe if patient understands use; basal rate more acceptable (though no proven benefit).

2. Pharmacology of Local Anesthetics

• Structure: Lipophilic benzene ring + hydrophilic amine, linked by amide or ester.

• Classes:

  • Amides: Lidocaine, mepivacaine, ropivacaine.

    • Metabolized by liver (hepatic carboxylases).

    • Allergies often due to preservative (methylparaben).

  • Esters: Benzocaine, cocaine, chloroprocaine, procaine, tetracaine.

    • Metabolized by plasma cholinesterases.

    • Contraindicated in atypical pseudocholinesterase.

    • Byproduct: PABA (common allergen).

• Special toxicity: Methemoglobinemia → prilocaine, benzocaine (also tetracaine, lidocaine).

• Mechanism: Bind intracellular voltage-gated Na⁺ channels → ↓ sodium influx → block neuronal transmission. Prefer open/inactive states.

3. Properties of Local Anesthetics

• pKa:

  • Closer to physiologic pH (7.4) → faster onset.

  • Low pKa = fast onset (lidocaine, mepivacaine).

  • Exception: Chloroprocaine → rapid onset due to high concentration used.

• Lipid solubility: ↑ solubility → ↑ potency (bupivacaine, ropivacaine strongest).

• Protein binding: ↑ binding → ↑ duration (bupivacaine, ropivacaine > lidocaine).

4. Differential Blockade

• Order of loss: Autonomic → sensory → motor.

• Fiber susceptibility: Smaller myelinated > larger/unmyelinated.

  • B fibers (autonomic) → blocked first.

  • A-delta (pain/temp/touch).

  • A-alpha, beta, gamma (motor/proprioception) → harder to block.

  • C fibers (unmyelinated, dull pain) → resistant.

5. Local Anesthetic Adjuncts

• Epinephrine: ↓ absorption, prolongs block, some analgesia (α2 action).

• Bicarbonate: ↑ pH, ↑ non-ionized fraction, faster onset (esp. lidocaine).

• α2-agonists (clonidine): Prolong block (~+2 hrs), risk hypotension/bradycardia.

• Steroids (dexamethasone): ↑ block duration (up to +50%).

• Opioids: Synergistic, faster onset, ↑ quality of block.

6. Systemic Absorption (Site-Dependent)

Mnemonic: ICE Head-to-Toe

• Intercostal (highest) > Caudal > Epidural > Brachial plexus > Lower extremity.

7. Local Anesthetic Systemic Toxicity (LAST)

• Neuro signs: AMS, agitation, tinnitus, perioral numbness, seizures → coma.

• CV signs: Hypotension, AV block, ↓ contractility, arrhythmias. Pediatrics may show peaked T waves.

• Treatment:

  • Stop drug.

  • Benzodiazepines for seizures. Avoid propofol (↓ SVR, contractility).

  • ACLS: epinephrine <1 mcg/kg. Avoid vasopressin, CCBs, lidocaine. Amiodarone for refractory arrhythmias.

  • Lipid therapy: Bolus 1.5 mL/kg → infusion 0.25 mL/kg/min. Repeat bolus ×2, double infusion if collapse persists.

8. Neuraxial Anesthesia – Approaches

• Midline: Skin → SQ → supraspinous → interspinous → ligamentum flavum → epidural.

• Paramedian: Skin → SQ → ligamentum flavum → epidural.

• Needles:

  • Spinal → smaller, cutting (Quincke) vs. pencil-point.

  • Epidural → larger, curved, allows catheter.

9. Epidural Space Anatomy

• Posterior: Ligamentum flavum.

• Anterior: Posterior longitudinal ligament.

• Lateral: Pedicles.

• Superior/Inferior: Foramen magnum → sacrococcygeal ligament.

• Epidural not continuous with CNS → no total spinal possible.

10. Pediatric vs Adult Differences

• Cord end: Adult L2; child L3.

• Dural sac: Adult S2; child S3.

• CSF volume: Child ~4 mL/kg vs adult ~1.5 mL/kg.

• Myelination: Looser → faster onset.

• Duration: Shorter in children.

• Risk: Higher cephalic spread → apnea is early sign (<5 yrs).

11. Systemic Effects of Neuraxial Block

• CV: Vasodilation → hypotension; CO often maintained/increased. HR ↑ (reflex) or ↓ (T1–T4 block).

• Pulmonary: Dyspnea from blocked proprioception; apnea if phrenic blocked. Minor ↓ FVC, FEV1 if T6+.

• GI: N/V (opioids, hypoperfusion); ↑ motility from sympathectomy.

• GU: Urinary retention (afferent inhibition).

12. Complications

• Backache: Multiple attempts, dural puncture.

• Post-dural puncture headache (PDPH): Due to CSF loss → venodilation. Risk: female, pregnant, young, low BMI, large/cutting needles. Positional headache, resolves <1 wk. Tx: hydration, analgesics, epidural blood patch (definitive).

• Other: Low-frequency hearing loss, high/total spinal (rare, 1:4000), permanent injury (trauma, abscess, hematoma, hypoperfusion).

13. Neuraxial Opioids

• Hydrophobic (fentanyl, sufentanil): Rapid onset, short duration, less cephalic spread, less late respiratory depression.

• Hydrophilic (morphine, hydromorphone): Slow onset, long duration, more cephalic spread, ↑ side effects.

• Side effects:

  • Pruritus (dose-dependent, not histamine; treat with naloxone/naltrexone).

  • N/V (trigger zone stimulation, esp. morphine).

14. Spread of Subarachnoid Block

• Drug factors:

  • Baricity:

    • Hyperbaric (with dextrose) → flow with gravity (dependent regions).

    • Hypobaric (with water) → float to non-dependent regions.

    • Hyperbaric = more consistent block.

  • Dose/volume: ↑ → ↑ spread.

• Patient factors:

  • Position during/after injection.

  • Pregnancy: ↑ spread (↓ CSF volume).

  • Age: ↑ → slower onset, longer duration (no effect on extent).

15. Anticoagulation (ASRA Guidelines)

• Hold/restart times for common anticoagulants must be observed for neuraxial procedures & catheter removal (reference table provided in lecture).

Summary:
High-yield regional anesthesia review covered PCA, local anesthetic pharmacology, key physiologic properties (pKa, solubility, protein binding), adjuncts, systemic toxicity, neuraxial techniques, anatomy, pediatric/adult differences, systemic effects, complications, neuraxial opioids, subarachnoid block spread, and anticoagulation safety.

Airway Management Quick Study Notes

Airway Management – Emergency Medicine Study Notes

Core Principles

• Airway management is a life-saving skill in EM; failure has immediate consequences.

• EM physicians are the airway experts in the hospital (anesthesia excels in controlled settings; EM must manage the uncontrolled, emergent airway).

• Early recognition of impending respiratory failure is critical: intervention before collapse prevents the need for emergent intubation.

Oxygen Delivery (Non-Invasive Options First)

1. Nasal Cannula

   • Delivers ~24–30% FiO₂.

2. Venturi Mask

   • Allows precise FiO₂ titration (e.g., 27%).

   • Useful for COPD (avoids suppressing hypoxic drive).

3. Simple Face Mask

   • Should be avoided in EM practice (unreliable).

4. Non-Rebreather Mask (NRB)

   • Max FiO₂ ≈ 55–60% (not truly 100%).

   • One-way valves prevent entrainment of room air.

5. Bag-Valve-Mask (BVM)

   • Delivers near 100% FiO₂ when used with a reservoir and good seal.

   • Can be used to assist spontaneous breathing.

6. High-Flow Nasal Cannula (HFNC)

   • Provides heated, humidified O₂ at high flow.

   • Indicated for hypoxemic respiratory failure (not hypercapnia).

Non-Invasive Ventilation (NIV)

• Revolutionary in EM → prevents intubation in 50–90% of cases (esp. CHF, COPD).

• Modes & Terms:

  • NPPV = Non-Invasive Positive Pressure Ventilation.

  • PEEP = Positive End-Expiratory Pressure.

  • CPAP = Continuous, single pressure.

  • BiPAP (Bi-Level PAP) = Different inspiratory (IPAP) & expiratory (EPAP) pressures.

• Typical starting settings:

  • 8/3 or 10/5 (IPAP/EPAP).

  • ↑ both if persistent hypoxemia.

  • ↑ IPAP only if persistent hypercapnia.

• Special case: acute pulmonary edema

  • Start high (15/10 or 18/13) to push fluid back into interstitium.

• Patient selection:

  • Must be cooperative & able to protect airway.

  • Initiate early, not as a last resort.

• Key Indications:

  • COPD exacerbation (first-line, decreases mortality).

  • Acute pulmonary edema (dramatic improvement).

  • Obesity hypoventilation syndrome.

  • Palliative/end-of-life care (alternative to intubation).

Transition to Invasive Airway

Ask 4 questions before deciding to intubate:

1. Is the patient unable to oxygenate despite best efforts?

2. Is the patient unable to ventilate?

3. Can they protect their airway?

4. Will their condition worsen inevitably (overdose, transport, progressive illness)?

If yes → prepare for invasive airway management.

Intubation Techniques

Direct Laryngoscopy (DL):

• Backup airway skill – should be mastered by all EM providers.

• Always pre-oxygenate before attempting.

Positioning:

• Goal: external auditory canal aligned horizontally with sternal notch.

• “Ramping” (shoulder and head elevation) improves view in all patients, not just obese.

Technique Pearls:

• Insert laryngoscope midline, not sweeping from the side.

• Angle slightly toward the patient’s left foot to maximize space.

• Use bimanual laryngoscopy (externally manipulate thyroid cartilage to optimize view).

Adjuncts & Backups

1. Bougie (introducer):

   • Essential, cheap, life-saving.

   • Especially useful if only epiglottis is seen (“epiglottis = airway is just beyond”).

   • Feels “tracheal clicks” when in trachea.

   • Keep laryngoscope in place while passing tube over bougie.

2. Extraglottic devices:

   • LMAs, i-gels → temporizing options if intubation fails.

3. Definitive fallback:

   • Cricothyrotomy – always possible if all else fails.

Goals of Airway Intervention

1. Correct hypoxemia.

2. Reduce work of breathing / improve ventilation.

3. Optimize strength of the respiratory “pump.”

Bottom Line:

• Master non-invasive options first (often avoid intubation).

• Intubate with preparation, positioning, and backups ready.

• Always respect the gravity of “taking away someone’s ability to breathe.”

Syncope- Study Notes

Definition:

• Syncope = transient global cerebral hypoperfusion → transient loss of consciousness (LOC) with spontaneous, rapid recovery to baseline.

• Key point: always due to reduced cerebral perfusion.

Major Categories of Syncope

1. Reflex (neurally mediated) syncope

   • Vasovagal

   • Situational

   • Carotid sinus hypersensitivity

2. Orthostatic syncope

3. Cardiogenic syncope

   • Arrhythmogenic

   • Mechanical

1. Reflex Syncope (Neurocardiogenic)

Mechanism

• Trigger → ↑ vagal outflow (cranial nerve X).

• Vagal effects:

  • Cardioinhibitory: ↓ HR → ↓ CO → ↓ SBP.

  • Vasodepressor: vasodilation → ↓ SVR → ↓ DBP.

• Net result: ↓ BP + ↓ cerebral perfusion → transient LOC.

Subtypes

• Vasovagal syncope

  • Trigger: pain, phobia, prolonged standing.

  • History: prodrome (nausea, diaphoresis, blurry vision).

• Situational syncope

  • Triggered by straining events (coughing, micturition, defecation).

• Carotid sinus hypersensitivity

  • Trigger: carotid compression.

  • Causes: carotid sinus massage, tight collar, shaving, head turning.

2. Orthostatic Syncope

Mechanism

• Standing → ↓ venous return → ↓ preload → ↓ stroke volume → ↓ CO → ↓ BP → ↓ cerebral perfusion → LOC.

Causes

1. Volume depletion

   • Vomiting, diarrhea, diuretics, bleeding, burns, excessive sweating.

2. Vasodilation

   • Medications: calcium channel blockers (amlodipine, nifedipine), α1-blockers (tamsulosin, prazosin, doxazosin).

3. Autonomic neuropathy

   • Failure of sympathetic vasoconstriction (e.g., diabetic neuropathy).

3. Cardiogenic Syncope

Mechanism

• Primary cardiac problem → ↓ cardiac output → ↓ BP → ↓ cerebral perfusion → LOC.

Causes

1. Arrhythmias

   • Tachyarrhythmias (e.g., VT >150 bpm → ↓ diastolic filling).

   • Bradyarrhythmias (e.g., AV block, sinus node dysfunction → ↓ HR).

2. Mechanical

   • ↓ Contractility: MI, severe HF.

   • ↓ Filling: cardiac tamponade, tension pneumothorax.

   • ↑ Afterload/obstruction:

     • Hypertrophic cardiomyopathy (HCM).

     • Aortic stenosis.

     • Pulmonary embolism.

Clinical Features

• Sudden onset, often no prodrome.

• May occur with exertion (classic for HCM, aortic stenosis).

Clinical Differentiation:

• Reflex syncope: prodrome (nausea, diaphoresis, blurry vision).

• Orthostatic syncope: positional change (supine/seated → standing).

• Cardiogenic syncope: sudden, exertional, or without warning.

Diagnostic Approach

1. Initial tests

   • Orthostatic vitals:

     • ↓ SBP ≥20 mmHg or ↓ DBP ≥10 mmHg = orthostatic syncope.

   • 12-lead ECG:

     • Arrhythmias (e.g., AV block, VT).

2. Further evaluation

   • Holter monitor / EP study → occult arrhythmia.

   • Echocardiography → structural/mechanical causes (HCM, aortic stenosis, EF, tamponade).

   • Carotid sinus massage → diagnostic if SBP ↓ >50 mmHg or asystole >3 sec.

   • Tilt table test → vasovagal/situational.

3. Rule out seizure

   • Seizure features: tonic-clonic activity, aura, tongue biting, incontinence, postictal confusion.

   • Syncope: prodrome, transient LOC, rapid recovery, no postictal state.

Management

• Reflex syncope: avoid triggers.

• Orthostatic syncope:

  • Rehydrate, treat hypovolemia.

  • Stop vasodilator drugs.

  • Pharmacologic: midodrine (vasoconstrictor), fludrocortisone (↑ Na+/water retention).

• Cardiogenic syncope:

  • Arrhythmias: ICD (VT/VF), pacemaker (bradyarrhythmias).

  • Mechanical: treat underlying cause (valve replacement, HF management, PE treatment, pericardiocentesis for tamponade).

The Takeaways

• Syncope = transient global cerebral hypoperfusion.

• Categorize: reflex, orthostatic, or cardiogenic.

• Prodrome → reflex, positional → orthostatic, sudden/exertional → cardiogenic.

• Always distinguish from seizure.

• Management is cause-specific.

Acid–Base Balance – Study Notes Normal Blood pH

 Acid–Base Balance – Study Notes

Normal Blood pH

• Normal range: 7.35 – 7.45

• <7.35 = Acidosis

• >7.45 = Alkalosis

• pH measures H⁺ (hydrogen ion) concentration.

Key Chemical Equation

CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻

• CO₂ = Respiratory component (lungs).

• HCO₃⁻ (bicarbonate) = Metabolic component (kidneys).

• H⁺ = Determines pH.

Seesaw Concept:

• ↑ CO₂ → ↑ H⁺ → ↓ pH (acidosis).

• ↓ CO₂ → ↓ H⁺ → ↑ pH (alkalosis).

Respiratory Disorders

1. Respiratory Acidosis

   • Cause: Hypoventilation → CO₂ retention.

   • Mechanism: ↑ CO₂ → ↑ H⁺ → ↓ pH.

   • Example: COPD, respiratory depression.

2. Respiratory Alkalosis

   • Cause: Hyperventilation → CO₂ loss.

   • Mechanism: ↓ CO₂ → ↓ H⁺ → ↑ pH.

   • Example: Anxiety, early sepsis, high altitude.

Metabolic Disorders

1. Metabolic Acidosis

   • Causes:

     • ↑ H⁺ (e.g., lactic acidosis, ketoacidosis).

     • ↓ HCO₃⁻ (e.g., diarrhea, renal failure).

   • Lab: ↓ HCO₃⁻, ↓ pH.

2. Metabolic Alkalosis

   • Causes:

     • ↑ HCO₃⁻ (e.g., vomiting, excess antacids).

     • ↓ H⁺ (e.g., diuretic use, hypokalemia).

   • Lab: ↑ HCO₃⁻, ↑ pH.

Compensation

• Respiratory system compensates quickly by changing ventilation.

• Metabolic (renal) system compensates slowly by adjusting HCO₃⁻ reabsorption or H⁺ excretion.

• Compensation attempts to return pH toward normal, but the primary disorder is identified by the initial abnormality in CO₂ or HCO₃⁻.

Quick Diagnostic Guide

1. Check pH:

   • <7.35 = Acidosis

   • 7.45 = Alkalosis

2. Check PaCO₂ (respiratory):

   • ↑ CO₂ = Acidosis

   • ↓ CO₂ = Alkalosis

3. Check HCO₃⁻ (metabolic):

   • ↓ HCO₃⁻ = Acidosis

   • ↑ HCO₃⁻ = Alkalosis

4. Determine if compensation is present.

Summary Table

Disorder	pH	CO₂	HCO₃⁻	Common Causes
Respiratory Acidosis	↓	↑	Normal/↑	COPD, hypoventilation, drug OD
Respiratory Alkalosis	↑	↓	Normal/↓	Anxiety, hyperventilation, altitude
Metabolic Acidosis	↓	Normal/↓	↓	DKA, lactic acidosis, renal failure
Metabolic Alkalosis	↑	Normal/↑	↑	Vomiting, diuretics, antacid excess

Mechanical Ventilation – Study Notes

Basics

• Mechanical ventilation = machine delivers breaths (positive pressure ventilation, PPV).

• Normal breathing = negative pressure (diaphragm pulls air in).

• PPV dangers:

  • Barotrauma (lung damage from overinflation).

  • Can cause pneumothorax (popped lung).

Suctioning (most tested NCLEX topic)

1. Suction OUT only – never on insertion.

2. <10 seconds per pass.

3. Pre-oxygenate 100% O₂ for 30 seconds before suction.

4. Avoid suctioning before ABGs – wait ≥20 min.

5. Never suction routinely – only when needed (risk of trauma).

Key terms: acute lung injury, assess before intervention.

Oral Care & VAP (Ventilator-Associated Pneumonia)

• Prevention measures:

  1. Reposition q2h.

  2. Oral care with chlorhexidine q2h.

• Best indicators of VAP: sputum culture (+), fever >100.3°F, new infiltrates on CXR.

• Prevention protocols:

  • Daily sedation vacations & weaning trials.

  • HOB ≥30–45°.

  • Oral care.

  • Strict hand hygiene.

NG Tube & Stress Ulcers

• No bolus feedings → aspiration risk. Use continuous feedings.

• Stress ulcers (from gastric secretions). Prevent with PPIs or H₂ blockers.

Complications

• Dropping O₂ sat → always assess first.

  • Auscultate lungs, check for mucus plugs/secretions → suction.

  • If unresolved → manual ventilation (ambu bag).

• Pneumothorax: from high PEEP/barotrauma.

• Hypotension: PPV compresses thoracic vessels → ↓ cardiac output.

Extubation

• Risks: airway obstruction, respiratory distress.

• Post-extubation care:

  • Humidified O₂ mask.

  • Oral care with sponges (no ice chips).

  • NPO initially.

  • High Fowler’s.

• Watch for:

  • Atelectasis → encourage IS, turn/cough/deep breathe.

  • Stridor (squeak) = airway emergency → report immediately.

Tracheostomy Care

• New trach (<7 days): check tie tightness (1 finger under tie). Priority = maintain airway.

• If dislodged:

  • Mature trach (>7 days) → reinsert with obturator/hemostat.

  • New trach (<7 days) → cover with sterile occlusive dressing + bag-mask ventilation.

Ventilator Alarms

• Low pressure alarm (low tidal volume) = disconnection, cuff leak, tube displacement.

• High pressure alarm (high blockage) = secretions, kinked tube, biting tube, coughing, pulmonary edema, pneumothorax.

Ventilator Modes

• AC (Assist Control) = full machine control (life support, post-CPR).

• SIMV (Synchronized Intermittent Mandatory Ventilation) = weaning mode, pt initiates some breaths.

Ventilator Settings

• VT (tidal volume): 500–800 mL (air per breath).

• RR (respiratory rate): 12–20/min.

• FiO₂: 35–100% (“feed me O₂”).

• PEEP: keeps alveoli open; watch for barotrauma/pneumothorax.

• PS (pressure support): helps spontaneous breaths.

Monitoring

• VE (minute ventilation) = air delivered per minute.

• PIP (peak inspiratory pressure) = max pressure during inspiration.

• Plateau pressure (Pplat) = measures lung compliance (↑ in ARDS/stiff lungs).

Key NCLEX Traps

• Always assess before intervening.

• Priority is airway, not infection prevention/dressing changes.

• High PEEP → barotrauma/pneumothorax.

• Stridor after extubation = emergency.

• No bolus feeds in intubated patients.

Mechanical Ventilation – Ventilator Settings & Initial Setup

Definition

• Ventilator settings = controls on a ventilator that determine how much ventilation (removing CO₂) and oxygenation (O₂ delivery) a patient receives.

• Adjusting settings = more or less support depending on patient need.

Core Ventilator Settings

1. Ventilator Modes

• Defines how the ventilator assists with inspiration (full vs partial support).

• Common modes:

  • Assist Control (AC) → full support.

  • SIMV → partial support, weaning.

  • Pressure Support Ventilation (PSV) → assists spontaneous breaths.

  • CPAP → continuous positive airway pressure.

  • Other advanced modes: Volume Support, Control Mode Ventilation (CMV), APRV, MMV, IRV, HFOV.

2. Tidal Volume (VT)

• Amount of air delivered per breath.

• Normal breathing: air inhaled/exhaled each cycle.

• Volume-controlled mode: set VT directly.

• Pressure-controlled mode: VT depends on pressure applied.

• Initial setting: 5–10 mL/kg IBW (commonly 6–8 mL/kg).

3. Respiratory Rate (Frequency, f)

• of breaths delivered per minute.

• Normal range: 10–20/min.

• Sets overall minute ventilation when combined with VT.

4. FiO₂ (Fraction of Inspired Oxygen)

• % O₂ delivered (21% = room air).

• Initial setting: 30–60%, unless patient was already on higher O₂.

• Severe hypoxemia: may start at 100%, but must wean to <60% ASAP (to avoid oxygen toxicity).

5. Inspiratory Flow Rate

• Speed of gas delivery.

• Normal: 40–60 L/min (up to 120 L/min if needed).

• If too low → ventilator dyssynchrony, ↑ work of breathing.

• If too high → ↓ mean airway pressure.

6. I:E Ratio (Inspiratory:Expiratory)

• Normal: 1:2 to 1:4.

• Longer expiratory times needed in obstructive disease (prevent air trapping).

• Adjusted by: flow rate, inspiratory/expiratory time, VT, and frequency.

7. Sensitivity (Trigger)

• Determines how much negative pressure patient must generate to trigger a breath.

• Normal: –1 to –2 cmH₂O.

• If too high → auto-triggering (extra breaths).

• If too low → patient struggles to trigger breaths.

8. PEEP (Positive End-Expiratory Pressure)

• Positive pressure left in lungs at end of expiration.

• Prevents alveolar collapse → improves oxygenation.

• Common use: refractory hypoxemia unresponsive to FiO₂.

• Initial: 4–6 cmH₂O.

• Caution: excessive PEEP → barotrauma, hypotension, pneumothorax.

9. Ventilator Alarms

• High pressure: obstruction (secretions, biting, kinks, coughing, pulmonary edema, pneumothorax).

• Low pressure/volume: disconnection, leak, tube displacement.

• Other alarms: low expired volume, apnea, high/low PEEP.

Initial Ventilator Settings (General Guidelines)

1. Mode:

   • AC (full support) or SIMV (partial support).

2. Tidal Volume (VT): 5–10 mL/kg IBW (6–8 mL/kg preferred for lung protection).

3. Rate (f): 10–20/min.

4. FiO₂: 30–60% (100% if severe hypoxemia).

5. Flow Rate: 40–60 L/min.

6. I:E Ratio: 1:2 to 1:4.

7. Sensitivity: –1 to –2 cmH₂O.

8. PEEP: 4–6 cmH₂O.

Key Takeaways for Exams:

• Always use lowest FiO₂ possible to maintain O₂ sat.

• High PEEP → pneumothorax/barotrauma risk.

• Assess alarms before intervening.

• Modes: AC = full support, SIMV = weaning.

• Sensitivity too high/low → dyssynchrony.

ACLS – Study Notes

Approach in simulations:

First steps: O₂ → IV → monitor + pads.

• • If no pulse → start CPR immediately.

  • Rhythm changes every 2 min of CPR → reassess + follow algorithm.

  • Stay calm, delegate tasks, and verbalize steps.

Airway & Ventilation

• Nasopharyngeal airway → conscious with gag reflex; measure nose → earlobe.

• Oropharyngeal airway → unconscious, no gag; measure mouth → angle of jaw.

• Bag-mask ventilation:

  • 1 breath every 6 sec (10/min).

  • Each breath over 1 sec.

  • Only half the bag (avoid overventilation → ↓ venous return + cardiac output).

Bradycardia (HR <50 with pulse)

• Stable → monitor.

• Unstable (hypotension, chest pain, shock, HF, AMS):

  • 1st line: Atropine 1 mg q3–5 min (max 3 mg).

    • Works for sinus brady, 1° block, 2° type I.

    • Not effective for 2° type II or 3°.

  • If atropine ineffective or contraindicated:

    • Transcutaneous pacing (preferred).

    • Dopamine 5–20 mcg/kg/min or Epinephrine 2–10 mcg/min.

  • If refractory: Transvenous pacing (expert consult).

• Pacing rate: ~60 bpm (can go 60–80, but 60 is standard).

• Sedate if possible before pacing.

Tachycardia (HR ≥150 with pulse)

• Stable:

  • Narrow → vagal maneuvers → Adenosine 6 mg → (then 12 mg if needed).

    • Avoid in asthma/COPD (bronchospasm risk).

  • If Afib/flutter → skip adenosine; use β-blocker or Ca²⁺-channel blocker.

  • Wide → consider adenosine (if monomorphic), otherwise → antiarrhythmics:

    • Procainamide, Amiodarone (150 mg IV over 10 min), Sotalol.

• Unstable (hypotension, chest pain, shock, HF, AMS):

  • Immediate synchronized cardioversion.

  • Sedate if available.

  • Never cardiovert sinus tach.

Pulseless Rhythms

VFib / Pulseless VTach

• CPR + O₂ + IV access.

• First action = Defibrillate ASAP.

  • Shock 120 J → CPR 2 min → rhythm check.

  • Shock 150 J → CPR 2 min + give Epinephrine 1 mg.

  • Shock 200 J → CPR 2 min + give Amiodarone 300 mg (or Lidocaine 1–1.5 mg/kg).

  • Alternate Epi (1 mg) and Amio/Lido with each cycle.

  • Amio 2nd dose = 150 mg.

  • Lidocaine 2nd dose = 0.5–0.75 mg/kg (max 3 mg/kg).

• Switch compressors q2min.

• For torsades → Magnesium 1–2 g in 10 mL NS over 20 min.

PEA / Asystole

• CPR + O₂ + IV access.

• Give Epinephrine 1 mg ASAP.

• No defibrillation.

• Continue CPR cycles: Epi → nothing → Epi → nothing.

• Search for H’s & T’s (hypovolemia, hypoxia, H⁺, hypo/hyperkalemia, hypothermia, tamponade, tension pneumo, thrombosis PE/MI, toxins).

• LVAD patients may have pseudo-PEA → check hum/perfusion, not pulse.

Post-ROSC Care

• Primary survey (ABCDE):

  • Airway: intubate if needed.

  • Breathing: O₂, ventilation, ETCO₂ monitoring (goal 35–40; >10 = good CPR).

  • Circulation: ECG, BP, fluids, pressors (norepi/epi/dopamine).

  • Disability: neuro exam (pupils, LOC).

  • Exposure: look for trauma, bleeding, burns.

• Targeted Temperature Management (TTM):

  • 32–36°C for unresponsive patients post-ROSC.

• STEMI:

  • Aspirin 162–325 mg chewed.

  • Oxygen if sat <90%.

  • Nitroglycerin (avoid if hypotensive, RV infarct, PDE-5 inhibitor).

  • PCI goal: ≤90 min from first medical contact.

  • Fibrinolysis: ≤12 hrs from onset.

Stroke (ACLS adjunct)

• FAST exam: facial droop, arm drift, speech.

• Determine last known well time.

• CT head within 20 min, read by 45 min.

• tPA (alteplase): 3–4.5 hr window; BP <185/110 before giving.

• Endovascular therapy: ≤24 hrs.

• Glucose check mandatory (hypoglycemia can mimic stroke).

• Admit to stroke or neuro ICU.

Cardioversion vs Defibrillation vs Pacing

• Synchronized cardioversion: unstable tachycardia with pulse.

• Unsynchronized (defibrillation): pulseless VF/VT.

• Pacing: unstable bradycardia (2° type II or 3° block → skip atropine).

• CPR only: PEA & asystole.

Drug Quick Review

• Atropine: 1 mg q3–5 min (max 3 mg).

• Epinephrine (arrest): 1 mg q3–5 min.

• Amiodarone (arrest): 300 mg → 150 mg.

• Lidocaine: 1–1.5 mg/kg → 0.5–0.75 mg/kg (max 3 mg/kg).

• Adenosine: 6 mg → 12 mg.

• Magnesium (torsades): 1–2 g over 20 min.

• Pressors (post-ROSC): norepi, epi, dopamine.

Resuscitation Minds Notes

Emergency Mind 

Key Themes

1. Silos of Resuscitation

• Many specialties encounter resuscitation (EM, anesthesia, internal medicine, hospitalists).

• Often low frequency for each → limited expertise.

• Goal: consolidate into smaller dedicated group → develop deep skill.

• Analogy: “resuscitationist” similar to acute care surgeon in the US.

• Some clinicians drawn to resus work, others stressed by it → system should support both.

2. System Design: RACE Team

• Provincial program: Critical Care Response Team (called RACE at their hospital).

• Team = physician + RT + nurse.

• Activation: by anyone (nurse, porter, attending, patient, even self-activation).

• Key principle: low barrier + welcoming response, regardless of perceived severity.

• Builds trust, resilience, and responsiveness.

3. Team Structure & Training

• Multiple teams (cardiac arrest, trauma, RACE) → overlapping but distinct.

• Learners included → balance between autonomy and patient safety.

• Continuous cycle: respond, teach, reflect.

• Fellowship created: dedicated training in resuscitation medicine.

  • Recognized cognitive/decision-making skills as central.

  • Goes beyond EM/CCM training content.

4. Joy and Flow of Resuscitation

• Some clinicians find flow state: clarity, slowed perception, comfort in chaos.

• Not “happy” but rewarding, purposeful.

• Goal: help those who experience only stress reframe and improve performance.

• Ethical tension: we don’t wish crises on patients, but if they occur, we want to respond.

Training Under Pressure

Skill vs Trait

• Performing under pressure: partly inherent, partly trainable.

• Everyone can move along the spectrum; degree varies.

• Growth through deliberate practice, reframing, and feedback.

Why Learners Struggle

• Causes vary → needs “diagnostic workup”:

  • Learning disabilities, psychological stressors, substance use.

  • Knowledge deficits (rarely the only issue).

  • Application under pressure (cognitive load problems).

• Executive function buckets:

  1. Inhibition (suppressing emotional/system 1 response).

  2. Working memory.

  3. Cognitive flexibility (creativity, adaptability).

• Many learners overwhelmed by emotional suppression → no reserve left to think.

Comparison to Other High-Stakes Teams

• Other professions: rigorous selection under pressure → weeds out those unfit.

• Medicine: gate entry to specialty, then mostly training & support → “elevate everyone.”

• Challenge: some residents attracted to image of EM/CCM, not actual work.

• Need better systems to redirect people to niches where they thrive.

Emergency vs Critical Care Mindset

• EM/Resus: rapid decision-making with incomplete info.

• Critical Care: slower, precise, incremental gains.

• Experienced clinicians learn when to switch “gears.”

• Greatness comes from playing to strengths, but resuscitation requires both fast and slow modes.

Big Questions Raised

1. How to identify early-career physicians’ natural strengths (fast vs slow decision-making)?

2. How to train opposite skill set to ensure flexibility?

3. How to teach rapid switching between modes (fast ↔ slow thinking) during crises?

Kidney: Study notes- Super High-yield

Big-picture functions

• Regulation: water, electrolytes, acid–base, blood pressure (via RAAS).

• Excretion: urea, creatinine, drugs/toxins.

• Secretion: active transport of wastes into tubular fluid.

• Gluconeogenesis: kidney supplies glucose during fasting.

Flow of blood → filtrate → urine (terms)

• Blood → plasma → filtration → tubular fluid → urine.

• Only plasma (water + solutes) should be filtered; cells & plasma proteins normally remain in blood (too large & negatively charged).

• Reabsorption: tubule → blood (returns “good stuff”).

• Secretion: blood → tubule (adds “bad stuff”).

• Excretion: what leaves in urine = filtered − reabsorbed + secreted.

Basic renal hemodynamics & key numbers (typical)

• Cardiac output ≈ 5 L/min; kidneys get ~20–25% → renal blood flow (RBF) ≈ 1.0–1.2 L/min.

• Renal plasma flow (RPF) ≈ RBF × plasma fraction (≈0.55) → ≈ 600–650 mL/min.

• GFR ≈ 125 mL/min (≈180 L/day).

• Filtration fraction (FF) = GFR / RPF ≈ 125 / 625 = 0.20 = 20%.

  • Example (simple numbers): if afferent plasma = 100 mL, filtered = 20 mL → GFR = 20 mL/min, FF = 20/100 = 20%.

Glomerular filtration barrier (3 layers)

1. Fenestrated endothelium (glomerular capillaries) — allows plasma but not cells.

2. Glomerular basement membrane — negatively charged (repels negatively charged proteins).

3. Podocytes (foot processes + slit diaphragms) — final sieve.
   → Net effect: plasma filters; cells & proteins return in efferent arteriole.

Starling-style forces in glomerular filtration

• Favoring filtration: glomerular capillary hydrostatic pressure ≈ 60 mmHg and Bowman’s oncotic ≈ 0 mmHg (no protein in filtrate).

• Opposing filtration: Bowman’s space hydrostatic ≈ 18 mmHg and glomerular capillary oncotic ≈ 32 mmHg.

• Compute net (digit-by-digit):

  • Opposing total = 18 + 32 = 50 mmHg.

  • Net filtration pressure = 60 − 50 = 10 mmHg (favors filtration).

Nephron anatomy & function (high-yield)

Order: Bowman's capsule → Proximal convoluted tubule (PCT) → Loop of Henle (descending → thin ascending → thick ascending) → Distal convoluted tubule (DCT) → Collecting duct → minor calyx → major calyx → renal pelvis → ureter.

Proximal convoluted tubule (PCT)

• Main jobs: bulk reabsorption (Na⁺, water, glucose, amino acids, bicarbonate) + secretion (organic acids/bases: uric acid, bile salts, drugs).

• Transport principles:

  • Basolateral Na⁺/K⁺-ATPase (primary active) pumps Na⁺ out → creates low intracellular Na⁺.

  • Apical: Na⁺ flows downhill into cell and cotransports solutes (secondary active).

  • SGLT2 (sodium–glucose cotransporter 2) on apical side reabsorbs glucose + Na⁺ (mnemonic: SGLT2 = in kidney → “2 kidneys”).

  • Basolateral glucose exit: facilitated diffusion (carrier, no ATP).

• Acid–base: carbonic anhydrase inside cells converts CO₂ + H₂O ⇄ H₂CO₃ ⇄ HCO₃⁻ + H⁺. H⁺ secreted via Na⁺/H⁺ exchanger (NHE); HCO₃⁻ reabsorbed.

Loop of Henle — countercurrent multiplier

• Descending limb: thin, permeable to water, impermeable to NaCl → tubular fluid concentrates (osmolality rises up to ~1200 mOsm in inner medulla).

• Ascending limb (thin → thick): impermeable to water, actively reabsorbs NaCl.

  • Thick ascending limb (TAL): NKCC2 = Na⁺/K⁺/2Cl⁻ cotransporter at luminal membrane (reabsorbs Na⁺, K⁺, Cl⁻).

  • TAL also drives reabsorption of Ca²⁺ & Mg²⁺ (paracellular) and is diluting segment.

• Countercurrent setup produces corticomedullary gradient → ability to concentrate urine.

Distal convoluted tubule (DCT) & Collecting ducts

• Early DCT: Na⁺/Cl⁻ cotransporter (NCC) — thiazide diuretic target; PTH acts to increase Ca²⁺ reabsorption here.

• Late DCT & collecting duct cell types:

  • Principal cells: reabsorb Na⁺, secrete K⁺; respond to aldosterone (↑ENaC, ↑Na⁺ reabsorption) and ADH (vasopressin V2 receptors) (↑aquaporin insertion → ↑water reabsorption = free water).

  • α-intercalated cells: acid–base: secrete H⁺ (via H⁺-ATPase/H⁺-K⁺-ATPase) and reabsorb HCO₃⁻ (protect against acidosis).

• Ammonium handling: NH₃ binds H⁺ → NH₄⁺ excreted (one major method for acid elimination). Also titratable acids (H⁺ buffered by phosphate) are used.

Membrane transport & routes (quick)

• Transcellular: through cells (can be active or passive).

• Paracellular: between cells (usually passive).

• Primary active: uses ATP directly (e.g., Na⁺/K⁺-ATPase).

• Secondary active: uses gradient established by primary active (e.g., SGLT2).

• Facilitated diffusion: carrier-mediated, no ATP (e.g., basolateral glucose exit).

Clinical & pharmacologic pearls

• Diuretic targets:

  • Loop diuretics → inhibit NKCC2 (TAL) → block urine concentration ability.

  • Thiazides → inhibit NCC (early DCT).

  • K⁺-sparing (amiloride, spironolactone) → act at principal cell ENaC or aldosterone receptor.

• SGLT2 inhibitors → block PCT glucose reabsorption → glucosuria (used in diabetes).

• Carbonic anhydrase inhibitors (acetazolamide) → act on PCT → reduce HCO₃⁻ reabsorption (can cause metabolic acidosis).

High-yield formulas & concepts (one-liners)

• Urine Excretion = Filtration − Reabsorption + Secretion.

• FF ≈ 20% (GFR ≈125 mL/min; RPF ≈600–650 mL/min).

• Descending = water out (concentrates). Ascending = salt out (dilutes).

• Aldosterone = “salt saver, K⁺ & H⁺ waster.”

• ADH (V2) = free water reabsorption via aquaporins.

Quick study mnemonics

• SGLT2 = “2 kidneys” → kidney SGLT.

• NKCC2 = “Na K 2 Cl” (TAL transporter — loop diuretic target).

• Principals: Aldosterone ↑Na⁺ reabsorption, ↑K⁺ & H⁺ secretion.

• α-intercalated: Acid secretors (H⁺ out) and HCO₃⁻ reabsorption.