Cardiac

Common cardiac causes of dyspnea in the PACU include acute coronary syndrome (ACS) and an acute exacerbation of congestive heart failure. Postoperative patients are at an increased risk for ACS given the hypercoagulable state following surgical intervention. An electrocardiogram (ECG), cardiac enzymes, and a chest X-ray can aid in the diagnosis of cardiogenic causes of dyspnea. Treatment for ACS involves increasing the oxygen supply to the heart while decreasing myocardial oxygen demand. Treatment for congestive heart failure involves decreasing lung congestion through fluid restriction and diuresis. The PACU provider should have a clear understanding of intraoperative and postoperative fluid administration, as well as preoperative cardiac function, while assessing these patients. Careful consideration should also be paid to chronic medications that may or may not have been administered preoperatively.

Pulmonary

Dyspnea due to pulmonary etiology in the PACU may be attributed to many conditions ranging from pre-existing pulmonary pathophysiology such as asthma and chronic obstructive pulmonary disease (COPD) to acute postoperative issues such as anaphylaxis, pulmonary embolism (PE), pneumothorax, mechanical obstruction, or inability to efficiently clear mucus. A focused physical exam and medical history can lead to the diagnosis.

Underlying pulmonary pathophysiology may be exacerbated and present as dyspnea in the PACU. Patients may arrive for surgery with pulmonary disease that has not been medically optimized. Endotracheal intubation and manipulation of the trachea and larynx during intubation are risk factors for bronchospasm especially among patients with a prior history of asthma and COPD. These patients may present in the PACU with dyspnea, cyanosis, cough, wheeze, and increasing oxygen requirements. Arterial blood gas may reveal an increased PaCO₂ and a decreased PaO₂. Patients with chronic COPD may have an elevated PaCO₂ at baseline, making extubation criteria complicated. Nebulized bronchodilators such as albuterol and ipratroprium should be administered during an acute COPD exacerbation along with supplemental O₂ to maintain adequate blood oxygenation levels as measured by pulse oximetry or serial arterial blood gas samples. Inhaled corticosteroids have not proven to be effective in an acute exacerbation of COPD.^[1] To decrease postoperative pulmonary complication, patients should be advised to stop smoking at least 4 to 8 weeks preoperatively.^[2] In addition, early ambulation and deep breathing, combined with incentive spirometry, intermittent positive-pressure breathing, and effective analgesia, may decrease postoperative complications.^[3]

During an acute asthma attack, wheezing may or may not be heard depending upon the severity of the exacerbation. Patients will typically rely on accessory muscles of respiration and may present with tachycardia and tachypnea. Treatment involves delivering oxygen via nasal cannula or facemask until a SaO₂ greater than 90% is achieved.^[1] β₂ agonists such as albuterol and inhaled agents such as ipratropium should be administered via metered dose inhaler or nebulizer. In refractory cases, inhaled or intravenous (IV) epinephrine may be administered, and intubation and mechanical ventilation should be considered.

PE commonly results from lower-extremity deep venous thrombosis, stressing the importance of preventative measures throughout the perioperative period. In addition to dyspnea, common signs and symptoms of PE include chest pain, tachycardia, cyanosis, acute desaturation, and a decrease in end-tidal CO₂ (ETCO₂) in an intubated patient. Imaging studies offer definitive diagnosis with the gold standard being a pulmonary angiogram. However, CT offers a non-invasive alternative and should be used as first-line study in most patients.^[2]

Pneumothorax presents with absent breath sounds on the ipsilateral side. Signs and symptoms also include chest pain, cyanosis, confusion, hypotension, hyperresonance to chest percussion, tracheal deviation, subcutaneous emphysema, and narrowed pulse pressure. Immediate treatment depends on the hemodynamic status of the patient. For a simple pneumothorax in a spontaneously breathing patient, increasing the inspired FiO₂ often allows for adequate tissue oxygenation until chest X-ray can be obtained and surgical consultation can be performed to determine the necessity of a tube thoracostomy. In the case of tension pneumothorax in a hemodynamically compromised patient, immediate needle decompression prior to imaging is indicated. Should pneumothorax be suspected in the PACU, extreme caution should be taken with positive pressure ventilation as a simple pneumothorax can rapidly convert to tension pneumothorax resulting in hemodynamic collapse.