Respiratory System Study Guide

Respiratory Anatomy & Physiology

Upper Airway

• Functions: Filtration, warming, humidification of inspired air
• Protective reflexes: Gag reflex, swallow reflex (CN IX & X)
• Impaired reflexes (stroke, sedation) increase aspiration risk
• Structures: Nose, pharynx, larynx (vocal cords)

Lower Airway

• Trachea: Shares posterior wall with esophagus (risk of TE fistula)
• Carina: Bifurcation of trachea, rich in cough receptors
• Right mainstem bronchus: Straighter, larger - common aspiration site
• Bronchioles: Smooth muscle, responsive to beta-2 agonists
• Alveoli: Gas exchange units (~300 million, ~800 sq ft surface area)
• Type I pneumocytes: Gas exchange
• Type II pneumocytes: Produce surfactant (reduces surface tension)

Pulmonary Circulation

• Low-pressure system compared to systemic circulation
• Pulmonary arteries carry deoxygenated blood
• Hypoxic pulmonary vasoconstriction: Redirects blood away from poorly ventilated areas
• Pulmonary capillaries: Single RBC width for optimal gas diffusion

Ventilation & Oxygenation

Ventilation Parameters

• Tidal Volume (Vt): Volume per breath (~500 mL or 6-8 mL/kg IBW)
• Respiratory Rate (RR): Normal 12-20 breaths/min
• Minute Ventilation (MV) = Vt × RR (normal 5-10 L/min)
• Alveolar Ventilation = (Vt - Dead Space) × RR
• Dead space: Areas ventilated but not perfused (normal ~150 mL)

Oxygenation Concepts

• FiO2: Fraction of inspired oxygen (room air = 21%)
• PaO2: Partial pressure of oxygen in arterial blood (normal 80-100 mmHg)
• SaO2/SpO2: Oxygen saturation (normal >95%)
• P/F Ratio: PaO2 ÷ FiO2 - assesses oxygenation efficiency
• Normal P/F: ~500, Mild ARDS: 200-300, Moderate: 100-200, Severe: <100

Oxyhemoglobin Dissociation Curve

• Shows relationship between PaO2 and hemoglobin saturation
• Right shift (releases O2 easier): Acidosis, fever, increased 2,3-DPG, hypercapnia
• Left shift (holds O2 tighter): Alkalosis, hypothermia, decreased 2,3-DPG
• Remember: "Right = Release" for conditions that increase oxygen delivery to tissues

Hypoxemia vs Hypoxia

• Hypoxemia: Low oxygen in blood (PaO2 <60 mmHg)
• Hypoxia: Inadequate oxygen at tissue level
• Types of hypoxia: Hypoxemic, Anemic, Circulatory, Histotoxic (cyanide)
• Hypoxemia causes: V/Q mismatch, shunt, diffusion impairment, hypoventilation

ABG Interpretation

Normal ABG Values

• pH: 7.35-7.45
• PaCO2: 35-45 mmHg (respiratory component)
• HCO3: 22-26 mEq/L (metabolic component)
• PaO2: 80-100 mmHg
• Base excess: -2 to +2

Step-by-Step ABG Analysis

• Step 1: Look at pH - Acidemia (<7.35) or Alkalemia (>7.45)?
• Step 2: Identify primary disorder
• - If pH and CO2 move opposite: Respiratory cause
• - If pH and HCO3 move together: Metabolic cause
• Step 3: Check for compensation
• - Respiratory compensation happens in hours
• - Metabolic compensation takes 3-5 days

Common ABG Patterns

• Respiratory Acidosis: pH↓, CO2↑ (hypoventilation, COPD, sedation)
• Respiratory Alkalosis: pH↑, CO2↓ (hyperventilation, anxiety, PE)
• Metabolic Acidosis: pH↓, HCO3↓ (DKA, lactic acidosis, renal failure)
• Metabolic Alkalosis: pH↑, HCO3↑ (vomiting, diuretics, NG suction)

Anion Gap

• Formula: Na - (Cl + HCO3) = Normal 8-12
• Elevated AG acidosis: MUDPILES - Methanol, Uremia, DKA, Propylene glycol, INH/Iron, Lactic acid, Ethylene glycol, Salicylates
• Normal AG acidosis: Diarrhea, RTA, saline administration

ARDS

Berlin Definition Criteria

• Timing: Within 1 week of known insult or new/worsening symptoms
• Imaging: Bilateral opacities not explained by effusion, collapse, or nodules
• Origin: Not fully explained by cardiac failure or fluid overload
• Oxygenation (P/F ratio on PEEP ≥5): Mild 200-300, Moderate 100-200, Severe <100

Pathophysiology

• Direct injury: Pneumonia, aspiration, inhalation injury, pulmonary contusion
• Indirect injury: Sepsis, pancreatitis, trauma, transfusion (TRALI)
• Inflammatory cascade damages alveolar-capillary membrane
• Increased permeability → non-cardiogenic pulmonary edema
• Surfactant dysfunction → alveolar collapse → refractory hypoxemia

ARDS Management

• Low Tidal Volume Ventilation (LTVV): 6 mL/kg IBW
• Plateau pressure goal: <30 cmH2O
• Higher PEEP to recruit alveoli and improve oxygenation
• Permissive hypercapnia acceptable if pH >7.20
• Prone positioning: For moderate-severe ARDS (P/F <150), 16+ hours/day
• Conservative fluid management once hemodynamically stable
• Neuromuscular blockade in severe cases first 48 hours

COPD & Asthma

COPD Overview

• Chronic airflow limitation that is not fully reversible
• Two phenotypes: Chronic bronchitis ("Blue bloater"), Emphysema ("Pink puffer")
• Risk factors: Smoking (#1), occupational exposure, alpha-1 antitrypsin deficiency
• Diagnosis: Spirometry showing FEV1/FVC <70%

COPD Exacerbation Management

• Bronchodilators: Short-acting beta agonists (albuterol), anticholinergics (ipratropium)
• Corticosteroids: Reduce inflammation, shorten recovery
• Antibiotics: If increased sputum purulence or volume
• Oxygen: Target SpO2 88-92% (avoid suppressing hypoxic drive)
• NIV (BiPAP): First-line for respiratory acidosis, reduces intubation rate

Asthma & Status Asthmaticus

• Reversible airway obstruction, inflammation, hyperresponsiveness
• Triggers: Allergens, exercise, cold air, infections, aspirin
• Status asthmaticus: Severe attack unresponsive to initial treatment
• Danger signs: Silent chest, altered mental status, cyanosis
• Treatment: Continuous nebs, IV steroids, magnesium sulfate, possibly intubation
• If intubating: Low RR, long expiratory time to prevent air trapping

Pulmonary Embolism

Pathophysiology

• Obstruction of pulmonary vasculature (usually thrombus from DVT)
• Virchow's Triad: Stasis, Endothelial injury, Hypercoagulability
• Results in V/Q mismatch (ventilated but not perfused = dead space)
• Large PE can cause right heart strain and cardiogenic shock

Clinical Presentation

• Dyspnea (most common), pleuritic chest pain, tachycardia, tachypnea
• Hemoptysis, syncope (suggests massive PE)
• Signs of DVT: Unilateral leg swelling, calf tenderness
• Massive PE: Hypotension, right heart failure

Diagnosis

• D-dimer: Sensitive but not specific (rules out PE if low probability)
• CT Pulmonary Angiography (CTPA): Gold standard diagnostic test
• V/Q scan: Alternative if contrast contraindicated
• ECG findings: Sinus tachycardia, S1Q3T3 pattern, right heart strain
• Echo: RV dilation, McConnell sign

Treatment

• Anticoagulation: Heparin, then warfarin or DOAC
• Thrombolytics: For massive PE with hemodynamic instability
• Embolectomy: Surgical or catheter-based for massive PE
• IVC filter: If anticoagulation contraindicated or recurrent PE despite therapy
• Supportive: Oxygen, pressors if needed, avoid fluid overload

Mechanical Ventilation

Ventilator Modes

• Volume Control (VC): Set Vt, flow; variable pressure
• Pressure Control (PC): Set pressure, inspiratory time; variable Vt
• Assist-Control (AC): Delivers set breath for every patient trigger + backup rate
• SIMV: Set number of mandatory breaths, patient can breathe between
• Pressure Support (PS): Patient-triggered, pressure-augmented spontaneous breaths

Initial Ventilator Settings

• Tidal Volume: 6-8 mL/kg ideal body weight
• Rate: 12-16 breaths/min (adjust for PaCO2)
• FiO2: Start 100%, wean to <60% to avoid oxygen toxicity
• PEEP: 5 cmH2O baseline, increase for hypoxemia/ARDS
• Goal: Plateau pressure <30 cmH2O to prevent barotrauma

Ventilator Troubleshooting

• High peak pressure + Normal plateau = Airway resistance (secretions, bronchospasm, kinked tube)
• High peak + High plateau = Decreased compliance (ARDS, pneumothorax, edema)
• Fighting the vent: Check synchrony, sedation, pain, underlying cause
• Auto-PEEP: Incomplete exhalation, reduce rate or increase expiratory time

Weaning & Extubation

• Prerequisites: Underlying cause resolved, hemodynamically stable, adequate oxygenation
• Spontaneous Breathing Trial (SBT): T-piece or low PS for 30-120 minutes
• RSBI (Rapid Shallow Breathing Index): RR/Vt - <105 predicts success
• Cuff leak test: Assesses for laryngeal edema before extubation
• Post-extubation: Monitor for stridor, respiratory distress