CCRN (Adult)

The respiratory system consists of conducting airways and gas exchange surfaces. Conducting airways include the nasopharynx, trachea, bronchi, and bronchioles down to the terminal bronchioles. Gas exchange occurs in respiratory bronchioles, alveolar ducts, and alveoli.

Alveoli are thin-walled structures surrounded by capillary networks. Type I pneumocytes provide the surface for gas exchange. Type II pneumocytes produce surfactant which reduces surface tension and prevents alveolar collapse. Approximately 300 million alveoli provide 70 square meters of gas exchange surface.

Ventilation is the movement of air into and out of the lungs. Inspiration occurs when the diaphragm and intercostal muscles contract, creating negative intrathoracic pressure. Expiration is normally passive through elastic recoil. Minute ventilation equals tidal volume multiplied by respiratory rate.

Oxygenation depends on matching ventilation to perfusion. Normal V/Q ratio is approximately 0.8. Dead space ventilation occurs when ventilated areas lack perfusion (high V/Q). Shunt occurs when perfused areas lack ventilation (low V/Q or zero V/Q).

Gas exchange occurs by diffusion across the alveolar-capillary membrane. Oxygen diffuses from alveoli into capillary blood. Carbon dioxide diffuses from capillary blood into alveoli. Diffusion capacity depends on membrane thickness, surface area, and driving pressure gradient.

Oxygen transport occurs primarily bound to hemoglobin. Each hemoglobin molecule can carry four oxygen molecules. Oxygen saturation reflects the percentage of hemoglobin binding sites occupied. Oxygen content includes both bound and dissolved oxygen.

The oxyhemoglobin dissociation curve describes the relationship between PaO2 and oxygen saturation. The curve shifts right (decreased affinity) with increased temperature, PCO2, H+ (acidosis), and 2,3-DPG. Right shift facilitates oxygen unloading to tissues. Left shift occurs with opposite conditions and impairs tissue oxygen delivery.

Carbon dioxide transport occurs in three forms: dissolved, bicarbonate, and carbamino compounds. Most CO2 is transported as bicarbonate. Carbonic anhydrase in red blood cells catalyzes CO2 hydration. Ventilation primarily regulates CO2 elimination.

Arterial blood gas analysis provides information about oxygenation, ventilation, and acid-base status. Normal values include pH 7.35 to 7.45, PaCO2 35 to 45 mmHg, PaO2 80 to 100 mmHg, HCO3 22 to 26 mEq/L, and base excess -2 to +2.

Systematic interpretation involves evaluating pH, primary disorder, and compensation. Acidemia is pH below 7.35 while alkalemia is pH above 7.45. Respiratory disorders involve PaCO2 changes while metabolic disorders involve HCO3 changes.

Respiratory acidosis results from hypoventilation with elevated PaCO2. Acute respiratory acidosis changes pH by 0.08 for every 10 mmHg change in PaCO2. Chronic respiratory acidosis shows metabolic compensation with elevated bicarbonate. Causes include COPD exacerbation, drug overdose, and neuromuscular weakness.

Respiratory alkalosis results from hyperventilation with decreased PaCO2. Causes include anxiety, pain, hypoxemia, sepsis, and mechanical overventilation. Compensation involves decreased bicarbonate reabsorption.

Metabolic acidosis is characterized by decreased bicarbonate and negative base excess. Anion gap calculation helps determine the cause. Normal anion gap acidosis results from bicarbonate loss or chloride excess. Elevated anion gap acidosis results from acid accumulation.

Metabolic alkalosis results from acid loss or bicarbonate gain. Causes include vomiting, nasogastric suctioning, diuretic use, and excessive bicarbonate administration. Chloride-responsive alkalosis improves with saline administration. Chloride-resistant alkalosis requires treatment of underlying cause.

Mixed acid-base disorders occur when multiple primary disturbances exist simultaneously. Winter's formula predicts expected PaCO2 in metabolic acidosis. If measured PaCO2 differs significantly from expected, a mixed disorder is present.

Acute respiratory failure is the inability to maintain adequate oxygenation or ventilation. Type I (hypoxemic) failure involves PaO2 below 60 mmHg with normal or low PaCO2. Type II (hypercapnic) failure involves PaCO2 above 50 mmHg. Mixed failure combines both abnormalities.

Hypoxemic respiratory failure results from V/Q mismatch, shunt, diffusion impairment, or hypoventilation. Causes include pneumonia, pulmonary edema, ARDS, and pulmonary embolism. Treatment targets the underlying cause while providing supplemental oxygen.

Hypercapnic respiratory failure results from inadequate alveolar ventilation. Causes include COPD exacerbation, drug overdose, neuromuscular disease, and chest wall abnormalities. Treatment may require mechanical ventilatory support.

Clinical assessment includes respiratory rate, work of breathing, accessory muscle use, and mental status. Tachypnea above 30 breaths per minute suggests significant distress. Paradoxical breathing pattern indicates diaphragmatic fatigue. Altered mental status may indicate severe hypoxemia or hypercapnia.

Oxygen delivery devices vary in FiO2 capability. Nasal cannula delivers 24 to 44% oxygen at 1 to 6 L/min. Simple face mask delivers 35 to 50% at 5 to 10 L/min. Non-rebreather mask delivers 60 to 90% at 10 to 15 L/min. High-flow nasal cannula delivers up to 100% at flows up to 60 L/min.

ARDS is acute inflammatory lung injury with bilateral pulmonary infiltrates and severe hypoxemia. Berlin definition criteria include acute onset within one week, bilateral opacities on imaging, respiratory failure not fully explained by cardiac failure or fluid overload, and PaO2/FiO2 ratio abnormality.

Severity classification uses PaO2/FiO2 ratio with PEEP at least 5 cmH2O. Mild ARDS has ratio of 201 to 300 mmHg. Moderate ARDS has ratio of 101 to 200 mmHg. Severe ARDS has ratio of 100 mmHg or below.

Common causes include sepsis, pneumonia, aspiration, trauma, and pancreatitis. Direct lung injury occurs from pneumonia, aspiration, and inhalation injury. Indirect lung injury occurs from sepsis, pancreatitis, and transfusion-related injury.

Pathophysiology involves alveolar epithelial and capillary endothelial injury. Exudative phase features pulmonary edema, hyaline membrane formation, and atelectasis. Proliferative phase shows type II pneumocyte hyperplasia and fibroblast proliferation. Fibrotic phase may develop with persistent inflammation.

Lung protective ventilation is the cornerstone of management. Target tidal volume is 4 to 8 mL/kg predicted body weight. Plateau pressure should remain below 30 cmH2O. PEEP titration improves oxygenation and prevents atelectrauma.

Prone positioning improves oxygenation and reduces mortality in moderate to severe ARDS. Recommended duration is at least 16 hours per day. Improvements in V/Q matching and lung recruitment explain the benefit. Contraindications include spinal instability, open abdomen, and hemodynamic instability.

Neuromuscular blockade may benefit patients with severe ARDS. It improves patient-ventilator synchrony and reduces oxygen consumption. Duration should be limited to 48 hours when possible. Continuous train-of-four monitoring guides dosing.

Conservative fluid management reduces pulmonary edema and ventilator days. Target CVP below 4 mmHg or PAWP below 8 mmHg when hemodynamically stable. Diuretics achieve negative fluid balance. Avoid aggressive fluid restriction in shock states.

ECMO provides rescue therapy for refractory ARDS. Venovenous ECMO provides gas exchange support without cardiac support. Referral criteria include PaO2/FiO2 below 80 despite optimization. Survival rates have improved with increasing experience.

Indications for mechanical ventilation include acute respiratory failure, airway protection, and anticipated clinical deterioration. Goals include maintaining oxygenation, ensuring adequate ventilation, and reducing work of breathing.

Pressure-controlled ventilation delivers flow until set pressure is reached. Tidal volume varies based on compliance, resistance, and inspiratory time. Decelerating flow pattern may improve gas distribution. Risk of hypoventilation exists with changing lung mechanics.

Positive end-expiratory pressure maintains alveolar recruitment at end-expiration. It improves oxygenation by increasing functional residual capacity. Excessive PEEP may cause overdistention and hemodynamic compromise. Optimal PEEP balances recruitment and overdistention.

Assist-control mode provides full ventilatory support. Every breath receives the set tidal volume or pressure. Patient triggering initiates additional breaths. High minute ventilation may result from patient-ventilator dyssynchrony.

Synchronized intermittent mandatory ventilation provides set number of mandatory breaths. Spontaneous breaths occur between mandatory breaths. Weaning occurs by gradually reducing mandatory rate. Increased work of breathing may occur with spontaneous breaths.

Pressure support ventilation augments spontaneous breaths with set pressure. Patient controls rate, inspiratory time, and tidal volume. It is commonly used during weaning. Level is titrated to achieve adequate tidal volume with acceptable work of breathing.

Ventilator-associated pneumonia is a significant complication. Prevention bundles include head of bed elevation, daily oral care with toothbrushing, daily sedation interruption, and daily assessment of readiness to extubate. Early mobility reduces VAP risk and improves outcomes.

• Head of the bed at 30 to 45 degrees
• Daily sedation interruption and assessment of readiness to extubate
• Oral care
• Subglottic secretion drainage and cuff pressure of 20 to 30 cmH₂O
• Early mobility
• Change the ventilator circuit only when it is soiled or malfunctioning

Weaning readiness assessment evaluates resolution of underlying condition, adequate oxygenation, hemodynamic stability, and ability to protect airway. Spontaneous breathing trial is the definitive weaning test. Rapid shallow breathing index below 105 predicts successful extubation.

Auto-PEEP (intrinsic PEEP) occurs when expiration is incomplete before the next breath. It is common in obstructive lung disease and with high minute ventilation. Consequences include breath stacking, hemodynamic compromise, and triggering difficulty. Management includes reducing respiratory rate and tidal volume, increasing expiratory time, and treating bronchospasm.

Indications for intubation include failure to maintain airway patency, failure to protect airway from aspiration, anticipated clinical course requiring intubation, failure of noninvasive ventilation, and refractory hypoxemia.

Rapid sequence intubation involves preoxygenation, induction agent, and neuromuscular blocker in rapid succession. Preoxygenation maximizes oxygen reserve and extends safe apnea time. Induction agents include etomidate, propofol, and ketamine. Succinylcholine and rocuronium are common neuromuscular blockers.

Direct laryngoscopy visualizes the glottis using a laryngoscope blade. Macintosh (curved) and Miller (straight) blades are most common. Proper positioning includes sniffing position with neck flexion and head extension. Cormack-Lehane classification grades laryngoscopic view.

Video laryngoscopy improves glottic visualization. It is particularly useful for difficult airways. Hyperangulated blades may provide better views but require different insertion technique. Learning curve is generally shorter than direct laryngoscopy.

Confirmation of endotracheal tube placement requires multiple methods. Continuous waveform capnography is the gold standard. Bilateral breath sounds, chest rise, and absence of gastric sounds support proper placement. Chest radiography confirms depth of insertion.

Tracheostomy provides long-term airway access. Timing decisions balance risks of prolonged translaryngeal intubation against procedural complications. Percutaneous dilational technique can be performed at bedside. Benefits include improved comfort, easier oral care, and facilitated weaning.

Chronic obstructive pulmonary disease exacerbation presents with increased dyspnea, cough, and sputum production. Common triggers include respiratory infections and environmental factors. Spirometry shows reduced FEV1/FVC ratio.

Bronchodilators are first-line therapy. Short-acting beta-agonists provide rapid relief. Short-acting anticholinergics add bronchodilation through different mechanism. Combination therapy is more effective than single agents.

Antibiotics are indicated when purulent sputum is present. Coverage targets common pathogens including Haemophilus, Moraxella, and Streptococcus. Macrolides, fluoroquinolones, or amoxicillin-clavulanate are appropriate choices.

Noninvasive positive pressure ventilation reduces intubation rates and mortality. It is indicated for moderate to severe exacerbations with respiratory acidosis. Contraindications include impaired consciousness, hemodynamic instability, and inability to protect airway. Initial settings include IPAP 10 to 15 cmH2O and EPAP 4 to 6 cmH2O.

Status asthmaticus is a severe asthma exacerbation unresponsive to initial therapy. Clinical features include inability to speak full sentences, use of accessory muscles, and silent chest. Peak flow below 25% of predicted indicates severe obstruction.

Continuous nebulized beta-agonists provide sustained bronchodilation. Ipratropium adds anticholinergic bronchodilation. Systemic corticosteroids reduce airway inflammation. Magnesium sulfate provides smooth muscle relaxation in severe cases.

Heliox (helium-oxygen mixture) reduces airway resistance through lower gas density. It may be considered for severe obstruction not responding to conventional therapy. Intubation should be avoided if possible due to difficult ventilation. Permissive hypercapnia is acceptable in mechanically ventilated asthmatics.

Community-acquired pneumonia presents with cough, fever, dyspnea, and pleuritic chest pain. Physical examination reveals crackles, bronchial breath sounds, and dullness to percussion. Chest radiography shows infiltrate. Severity scoring guides site of care decisions.

CURB-65 score predicts mortality: Confusion, Uremia, Respiratory rate above 30, Blood pressure below 90/60, and age 65 or older. Scores of 0 to 1 suggest outpatient management. Scores of 2 suggest hospitalization. Scores of 3 or higher suggest ICU consideration.

Empiric antibiotic therapy covers likely pathogens. Streptococcus pneumoniae is the most common bacterial cause. Atypical organisms include Mycoplasma, Chlamydia, and Legionella. Severe CAP regimens include beta-lactam plus macrolide or respiratory fluoroquinolone.

Hospital-acquired pneumonia develops 48 hours or more after admission. Ventilator-associated pneumonia is a subset occurring after endotracheal intubation. Common pathogens include gram-negative bacilli and Staphylococcus aureus. MRSA coverage is added based on risk factors.

Aspiration pneumonia results from inhalation of oropharyngeal contents. Impaired consciousness, dysphagia, and poor oral hygiene are risk factors. Typical location is dependent lung segments. Anaerobic coverage may be considered for severe cases.

Pneumothorax is air in the pleural space causing lung collapse. Primary spontaneous pneumothorax occurs without underlying lung disease. Secondary spontaneous pneumothorax occurs in patients with lung disease. Traumatic pneumothorax results from chest injury or iatrogenic causes.

Clinical presentation includes sudden dyspnea, pleuritic chest pain, and decreased breath sounds. Tracheal deviation away from affected side suggests tension physiology. Hyperresonance to percussion is characteristic.

Treatment depends on size and symptoms. Small asymptomatic pneumothorax may be observed with supplemental oxygen. Symptomatic or large pneumothorax requires chest tube drainage. Placement is typically at fourth or fifth intercostal space anterior to midaxillary line.