CSC Cardiac Surgery Certification Exam

The respiratory system comprises the conducting airways and the gas exchange surfaces. The trachea divides into right and left mainstem bronchi, with the right bronchus more vertical and wider, predisposing to right-sided aspiration and intubation. Bronchi subdivide progressively into bronchioles and terminal bronchioles, ending in alveoli where gas exchange occurs.

Alveoli are lined with type I pneumocytes, thin cells facilitating gas diffusion, and type II pneumocytes, which produce surfactant to reduce surface tension and prevent alveolar collapse. The alveolar-capillary membrane, approximately 0.5 micrometers thick, permits rapid oxygen and carbon dioxide exchange.

Ventilation refers to the movement of air into and out of the lungs. Tidal volume (TV) is the volume of air moved with each breath, typically 6-8 mL/kg of ideal body weight. Minute ventilation equals tidal volume multiplied by respiratory rate. Dead space ventilation includes anatomic dead space in conducting airways and physiologic dead space in poorly perfused alveoli.

Perfusion describes blood flow through the pulmonary vasculature. Ventilation-perfusion (V/Q) matching optimizes gas exchange. V/Q mismatch, where ventilated alveoli receive inadequate perfusion or perfused alveoli receive inadequate ventilation, impairs oxygenation. Hypoxic pulmonary vasoconstriction diverts blood flow away from poorly ventilated lung regions, partially compensating for V/Q mismatch.

Oxygen transport depends on hemoglobin concentration, oxygen saturation, and cardiac output. Each gram of hemoglobin carries 1.34 mL of oxygen when fully saturated. The oxyhemoglobin dissociation curve describes the relationship between partial pressure of oxygen (PaO2) and hemoglobin saturation. Factors shifting the curve rightward (acidosis, hyperthermia, increased 2,3-DPG) facilitate oxygen unloading at tissues but may impair loading at the lungs.

Carbon dioxide transport occurs primarily as bicarbonate ions, with smaller amounts dissolved in plasma or bound to hemoglobin as carbaminohemoglobin. Carbon dioxide diffuses across the alveolar membrane more readily than oxygen.

Atelectasis, the collapse of alveoli, is nearly universal following cardiac surgery due to general anesthesia, pain-limited inspiration, diaphragmatic dysfunction, and pleural fluid accumulation. Atelectasis manifests as decreased breath sounds, hypoxemia, and opacity on chest radiograph. Prevention and treatment include incentive spirometry, early ambulation, adequate analgesia, and positive pressure therapy.

Pneumonia complicates 2-10% of cardiac surgical cases. Risk factors include prolonged intubation, aspiration, immunocompromise, and poor pulmonary toilet. Ventilator-associated pneumonia (VAP) develops in patients mechanically ventilated for more than 48 hours. Prevention bundles include head-of-bed elevation of 30 to 45 degrees, daily oral care with toothbrushing, daily sedation interruption paired with spontaneous breathing trials, and early mobility; routine chlorhexidine oral care is no longer recommended for cardiac surgery patients beyond the immediate perioperative period. Empiric antibiotic coverage should address common pathogens including gram-negative organisms and Staphylococcus aureus.

Acute respiratory distress syndrome (ARDS) is acute hypoxemic respiratory failure with bilateral opacities not fully explained by cardiac failure or fluid overload, with a PaO2/FiO2 ratio of 300 or less on PEEP of at least 5 cm H2O (mild 201–300, moderate 101–200, severe 100 or less). ARDS may result from direct lung injury (aspiration, pneumonia) or indirect injury (sepsis, transfusion, prolonged bypass). Management includes lung-protective ventilation with tidal volumes of 6 mL/kg predicted body weight, plateau pressure of 30 cm H2O or less, adequate PEEP, conservative fluids once perfusion is restored, and prone positioning for severe cases.

Air-leak syndromes after cardiac surgery include pneumothorax, pneumomediastinum, pneumopericardium, and subcutaneous emphysema, usually from barotrauma, pleural entry, or central line placement. A tension pneumothorax or tension pneumopericardium causes obstructive shock and needs immediate decompression.

Pleural effusions commonly develop after cardiac surgery from surgical manipulation, cardiopulmonary bypass inflammation, and impaired lymphatic drainage. Small effusions may be observed. Large effusions causing dyspnea or respiratory compromise require thoracentesis or chest tube drainage. Chylothorax, the accumulation of lymphatic fluid in the pleural space from thoracic duct injury, presents as milky effusion with high triglyceride content and requires dietary modification or surgical intervention.

Pneumothorax may result from central line placement, barotrauma, or surgical injury. Tension pneumothorax causes hemodynamic compromise requiring emergent needle decompression followed by chest tube placement. Simple pneumothorax may be observed if small or treated with chest tube drainage.

Diaphragmatic dysfunction results from phrenic nerve injury during internal mammary artery harvest or from cold injury during topical cardiac cooling. Unilateral diaphragmatic paralysis may be asymptomatic or cause dyspnea, particularly when supine. Bilateral paralysis causes respiratory failure. Diagnosis is made by fluoroscopic or ultrasound observation of paradoxical diaphragm movement. Most cases recover spontaneously over months. Persistent symptomatic paralysis may be treated with diaphragmatic plication.

Pulmonary embolism (PE) risk increases with immobility, central venous catheters, and hypercoagulable states. Symptoms include sudden dyspnea, pleuritic chest pain, and hemodynamic instability in massive PE. CT pulmonary angiography confirms the diagnosis. Treatment includes anticoagulation, with thrombolysis or embolectomy reserved for massive PE with hemodynamic compromise.

Physical examination includes inspection for respiratory rate, pattern, and work of breathing. Accessory muscle use, nasal flaring, and paradoxical abdominal movement indicate respiratory distress. Auscultation reveals normal vesicular breath sounds or abnormal findings including crackles (atelectasis, pulmonary edema, pneumonia), wheezes (bronchospasm), and diminished sounds (effusion, pneumothorax).

Arterial blood gas (ABG) analysis provides definitive assessment of oxygenation and ventilation. pH indicates acid-base status. PaCO2 reflects ventilation, with elevated values indicating hypoventilation. PaO2 reflects oxygenation, with values below 60 mmHg indicating hypoxemia. Bicarbonate and base excess indicate metabolic acid-base status. The alveolar-arterial (A-a) gradient, normally less than 15 mmHg, increases with V/Q mismatch or diffusion impairment.

Pulse oximetry provides continuous noninvasive monitoring of oxygen saturation. Limitations include inaccuracy with poor perfusion, nail polish, skin pigmentation, and inability to detect hypercarbia or differentiate oxyhemoglobin from carboxyhemoglobin or methemoglobin.

Chest radiography reveals pulmonary pathology including consolidation, effusion, pneumothorax, and pulmonary edema. Comparison with prior images identifies interval changes. Portable radiographs obtained in the ICU have technical limitations affecting interpretation.

Pulmonary function tests measure lung volumes and airflow. Forced vital capacity (FVC) is the total volume exhaled forcefully after maximal inspiration. Forced expiratory volume in one second (FEV1) reflects airflow. The FEV1/FVC ratio below 70% indicates obstructive disease. Reduced FVC with normal ratio suggests restrictive disease.

Chronic obstructive pulmonary disease (COPD) increases perioperative risk due to impaired pulmonary reserve, infection susceptibility, and air trapping. Preoperative optimization includes smoking cessation, bronchodilator therapy, and treatment of acute exacerbations. Intraoperative management minimizes auto-PEEP through adequate expiratory time. Postoperative care emphasizes aggressive pulmonary toilet and early mobilization.

Asthma predisposes to bronchospasm, particularly with airway manipulation. Preoperative control should be optimized with inhaled corticosteroids and bronchodilators. Intraoperative triggers include histamine-releasing drugs and airway instrumentation. Treatment includes inhaled beta-agonists and systemic corticosteroids.

Pulmonary hypertension increases right ventricular afterload, predisposing to right heart failure. Cardiac surgery, particularly procedures involving cardiopulmonary bypass, may exacerbate pulmonary hypertension through endothelial dysfunction and vasoactive mediator release. Management includes avoiding hypoxia, hypercarbia, and acidosis, which increase pulmonary vascular resistance. Pulmonary vasodilators including inhaled nitric oxide, inhaled epoprostenol, and sildenafil may be required.

Obstructive sleep apnea (OSA) increases risk of difficult airway, postoperative respiratory depression, and arrhythmias. Continuous positive airway pressure (CPAP) should be continued perioperatively. Enhanced monitoring and judicious opioid use are essential.