Pulm Pathophysiology Powerpoint to Word Doc PDF

Document Details

Harmony.Alexis_

Uploaded by Harmony.Alexis_

University of Texas Health Science Center

Tags

pulmonary diseases pathophysiology respiratory system health

Summary

The document contains information about obstructive sleep apnea (OSA), chronic obstructive pulmonary disease (COPD), and pulmonary hypertension. It details the pathophysiology, incidence, clinical features, treatment, and anesthetic management for these conditions. It's likely intended for students in health sciences or medicine.

Full Transcript

**Obstructive Sleep Apnea (OSA)** Obstructive Sleep Apnea (OSA): mechanical obstruction secondary to reduction in pharyngeal muscle tone during sleep Obesity Hypoventilation Syndrome (OHS): obesity/sleep-disordered breathing/daytime hypoventilation with no mechanical, neuromuscular, or metabolic e...

**Obstructive Sleep Apnea (OSA)** Obstructive Sleep Apnea (OSA): mechanical obstruction secondary to reduction in pharyngeal muscle tone during sleep Obesity Hypoventilation Syndrome (OHS): obesity/sleep-disordered breathing/daytime hypoventilation with no mechanical, neuromuscular, or metabolic etiology **Incidence, Outcomes, and Etiology (OSA)** Obesity is most significant risk factor 40% of obese patients  80% of patients presenting for bariatric surgery  Increasing prevalence in pediatric patients  OSA is associated with increased morbidity/mortality in hospitalized patients **Pathophysiology (OSA)**  OSA results in chronic hypoxemia and hypercarbia  Chronic hypoxemia and hypercarbia lead to inflammatory state  OSA decreases FRC  Decreased apneic oxygen reserve, contributes to hypoxemia and hypercarbia **Clinical Features and Diagnosis (OSA)** Hallmark -- daytime somnolence due to habitual snoring and fragmented sleep Polysomnography provides *definitive* objective diagnosis and gradation of severity  Apnea Plus Hypopnea (AHI) Index -- number of abnormal respiratory events per hour of sleep STOP-Bang is easily used during preoperative evaluation Sensitivity \~100%, specificity \~40% **OSA -- STOP-Bang (need three of the following)** S- snoring B- Body mass index \>35 kg/m^2^ T- Tiredness A- Age \> 50 years O- Observed apnea N- Neck circumference \> 40 cm P- High blood pressure G- Gender, male **Treatment** Lifestyle- weight loss Medical- CPAP, airway devices, medications (modafinil, methylxanthines, tricyclic antidepressants) Surgical- adenotonsillectomy, uvulopalatopharyngoplasty, hypoglossal nerve stimulator **Anesthetic Management** [Preoperative Considerations]  Bring CPAP on day of surgery Airway examination- anticipate difficult mask ventilation/laryngoscopy Mallampati and neck circumference Consider regional anesthesia or multimodal analgesia (minimize need for meds that produce sedation) Minimize/avoid sedatives (patient with OSA may be more sensitive to sedative effects) [Induction] Anticipate difficult mask ventilation/laryngoscopy decreased FRC= decreased apneic oxygen time Elevate head and shoulders (ramping) Have airway adjuncts (LMA/videolaryngoscope) available [Maintenance] N/A [Emergence] Consider awake extubation [Postoperative Considerations]  Monitor ventilation and oxygenation  Consider CPAP in PACU Consider prolonged monitoring (6 -24 hours) **Chronic Obstructive Pulmonary Disease (COPD)** "...preventable and treatable disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases..." -- American Thoracic Society/European Respiratory Society **Chronic Bronchitis** Obstruction of expiratory airflow by excess mucous secretion Occurs most days for at least three months per year for at least two successive years **Emphysema** Permanent abnormal enlargement of air spaces distal to the terminal bronchioles accompanied by irreversible destruction of alveolar walls Centrilobular- predominantly affects respiratory bronchioles in upper lung lobes Panlobular- widespread destruction of acini **Incidence, Outcomes, and Etiology** Cigarette smoking is the most significant risk factor Environmental pollutants, genetics Third leading cause of death; \~5% of American adults Death may be secondary to respiratory failure or related comorbidities (e.g., heart disease, lung cancer) **Pathophysiology**  Inflammatory reaction in the lungs leads to progressive airflow obstruction (i.e., decreased FEV~1~)  Decrease in intrinsic size of bronchial lumina Increase in collapsibility of bronchial walls  Decrease in elastic recoil of the lungs  COPD is a combination of both emphysema and chronic bronchitis **Clinical Features and Diagnosis**  Hallmark -- chronic productive cough and progressive exercise limitations  Clinical Manifestations -- dyspnea, wheezing  Pulmonary Function Testing (i.e., GOLD Classification) FEV~1~ ≥80% = mild FEV~1~ 50%-79% = moderate FEV~1~ 30%-49% = severe FEV~1~ \ Propofol \> Etomidate/Barbiturates [Maintenance]  Consider use of sevoflurane, least irritating volatile anesthetic  Avoid atracurium, mivacurium, morphine, B-antagonists, Hemabate, NSAIDs [Emergence]  Consider deep extubation  Consider use of Sugammadex; anticholinesterase reversal agents have risk of bronchospasm Verify adequate reversal of neuromuscular blockade **Intraoperative Bronchospasm** 1\. Administer additional anesthetic agents 2\. Increase FiO~2~ to 1.0 (100%) 3\. Administer short acting B~2~-agonist (albuterol) 4\. Consider administering epinephrine 10 mcg/kg 5\. Administer a corticosteroid (hydrocortisone 2-4 mg/kg) 6\. Consider administering aminophylline **Pulmonary Hypertension**  Mean Pulmonary Artery Pressure \>25 mm Hg **Incidence, Outcomes, and Etiology** Rapid disease progression; 5-year mortality rate is 79% May be caused by COPD, connective tissue disorders, sarcoidosis, drug effects, and genetics/idiopathic **Pathophysiology** Increased vascular tone Growth and proliferation of pulmonary vascular smooth muscle  Right ventricular overload culminating in cor pulmonale **Clinical Features and Diagnosis** Hallmark- dyspnea/ exercise intolerance  Diagnosis **Anesthetic Management** [Perioperative Considerations] Consider ECG, echocardiogram, chest x-ray and ABG Continue medications for PAH Consider regional anesthesia [Induction]  N/A [Maintenance] Neuraxial anesthesia may cause significant hemodynamic alterations Etomidate or high-dose opioids may be preferable to minimize cardiac depression  Consider arterial blood pressure monitoring  Consider central venous catheter for major procedures [Emergence]  N/A **Cor Pulmonale** Right heart failure secondary to pulmonary pathology **Incidence, Outcomes, and Etiology**  Cor pulmonale is third most common cardiac disorder in people greater than 50 years of age Five times more prevalent in males Cor pulmonale may be acute or chronic  Acute -- PE Chronic -- COPD **Pathophysiology**  Right ventricular dysfunction develops in response to pulmonary hypertension  Rate at which right ventricular dysfunction develops is dependent on the severity and progression of pulmonary hypertension **Clinical Features and Diagnosis**  Clinical Manifestations -- cough, dyspnea, weakness, fatigue, hemoptysis, jugular venous distension, S~3~ gallop, S~4~ heart sound, murmur, hepatomegaly, ascites, dependent edema  Doppler echocardiography -- velocity of tricuspid regurgitation correlates with invasive PAP measurements  Cardiac catheterization -- provides information about pressures in the pulmonary system and heart **Treatment** Lifestyle- N/A Medical- Administer O~2~, Medications (prostanoids, endothelin receptor antagonists, phosphodiesterase inhibitors, diuretics) Surgical- heart/lung transplant **Anesthetic Management** [Preoperative Considerations]  Consider regional anesthesia [Induction] N/A [Maintenance]  Maintain adequate oxygenation  Avoid acidosis Avoid stimuli that increase sympathetic tone Avoid hypothermia [Emergence]  N/A **Pulmonary Embolism (PE)** Occlusion of pulmonary blood flow by embolic material, resulting in obstruction of pulmonary blood flow and resultant mismatch of ventilation and perfusion **Incidence, Outcomes, and Etiology**  Occurs in \~1% of surgical patients Occurs in up to 30% of orthopedic surgical patients  Usually caused by a DVT from the iliofemoral vessels  DVT, air, CO~2~, tumor, bone, fat, catheter fragments  Virchow's Triad  Venous stasis, venous injury, hypercoagulable state **Pathophysiology**  Thrombus formation Release of thrombus into circulation Occlusion of pulmonary circulation Increased PVR proximal to occlusion, decreased perfusion distal to occlusion V/Q mismatch Alveolar damage **Clinical Features and Diagnosis**  Hallmark -- sudden-onset dyspnea; sudden decrease in EtCO~2~  Clinical Manifestations -- hypotension, tachycardia, hypoxemia, wheezing, tachypnea **Treatment** Lifestyle- N/A Medical- thrombolytic agents, anticoagulation Surgical- embolectomy (thromboendartectomy, rheolytic embolectomy, rotational embolectomy, suction embolectomy), IVC filter insertion **Anesthetic Management** [Induction] Etomidate Avoid Ketamine and N~2~O [Maintenance]  Consider high FiO~2~  Consider monitoring CVP/PAP [Emergence]  N/A **Intraoperative Pulmonary Embolism** 1\. Increase FiO~2~ to 1.0 (100%) 2\. Discontinue administration of anesthetic agents 3\. Administer sympathomimetics and fluid/blood as needed 4\. Administer lidocaine or amiodarone in the presence of ventricular dysrhythmias 5\. Prepare for thrombolysis or pulmonary embolectomy 6\. Consider cardiopulmonary bypass as a temporizing measure **Restrictive Pulmonary Disease (Pulmonary Edema)**  Conditions that interfere with normal lung expansion during inspiration Acute intrinsic (e.g., pulmonary edema, aspiration pneumonitis, ARDS)  Chronic intrinsic (e.g., idiopathic pulmonary fibrosis, sarcoidosis, radiation injury)  Chronic extrinsic (e.g., flail chest, pneumothorax, pleural effusion) **Incidence, Outcomes, and Etiology** Pulmonary edema refers to accumulation of excess fluid in interstitium and alveoli  Negative-pressure pulmonary edema may result from acute airway obstruction **Pathophysiology** Imbalance of Starling's forces leads to pulmonary edema  Cardiogenic - high pulmonary capillary pressure  Non-cardiogenic - increased permeability of the alveolar-capillary membrane  Sepsis, ARDS **Clinical Features and Diagnosis**  Hallmark -- pink, frothy sputum  Clinical Manifestations -- tachypnea, accessory muscle use, tachycardia, hypertension, diaphoresis, basilar crackles on auscultation  Chest X-Ray  Enlargement of cardiac silhouette  'White-out' appearance **Treatment** Lifestyle- N/A Medical- administer O~2~, consider CPAP or mechanical ventilation, restrict fluid administration, medications (morphine, nitroprusside, inotropes) Surgical- N/A **Aspiration Pneumonitis** Movement of gastric contents from the stomach to the lungs that results in chemical injury to the lung tissue **Incidence, Outcomes, and Etiology**  Overall incidence \~1/3000 anesthetics  \~1/1500 emergency anesthetics or cesarean deliveries Occurs when protective airway reflexes are inhibited; usually occurs after vomiting or gastroesophageal reflux  Risk Factors -- emergency surgery with a full stomach, bowel obstruction, pregnancy, acute trauma  Often resolves without treatment **Pathophysiology**  Immediate damage to lung parenchyma by caustic aspirate  Atelectasis develops within minutes, leading to airway closure and decreased compliance  Alveolar macrophages release inflammatory cytokines (IL-8, TNF-alpha), which attract neutrophils that in turn release oxygen radicals and proteases Secondary injury results from fibrin deposition and alveolar necrosis  Damage to alveolar-capillary membrane  Impaired gas exchange  Capillary leak  Hemodynamic changes  Myocardial ischemia and acidosis secondary to hypoxemia **Clinical Features and Diagnosis**  Hallmark -- arterial hypoxemia  Clinical Manifestations -- tachypnea, dyspnea, cyanosis, tachycardia, hypertension  Diagnosis is made by ABG and chest radiography  Chest radiography demonstrates aspirate in perihilar and dependent lung regions  Differential Diagnosis -- have high concern in an otherwise healthy patient who develops unexplained/sudden hypoxemia intra- or postoperatively **Treatment** Lifestyle- N/A Medical- ventilation (consider low FiO~2~, consider PEEP), consider steroids, consider lidocaine 1.5 mg/kg, avoid routine administration of antibiotics, avoid routine use of deep tracheal suctioning/bronchoscopy Surgical- N/A **Anesthetic Management** [Preoperative Considerations]  NPO  Recognize risk factors Pharmacologic prophylaxis  Nonparticulate antacid (sodium citrate with citric acid)  H~2~ receptor antagonist (famotidine)  PPI (pantoprazole)  antiemetics (ondansetron) [Induction] Consider RSI with cricoid pressure Consider videolaryngoscopy If vomiting, reflux, or aspiration occur during induction  Tilt the patient's head downward or turn the patient to the left side  Suction the oropharynx/ETT  Consider applying PEEP  Consider postponing surgery [Maintenance] Avoid excessive administration of sedating medication Evacuate the stomach [Emergence] Awake extubation Verify adequate reversal of neuromuscular blockade **Acute Respiratory Distress Syndrome (ARDS)** Condition occurring in critically ill patients in which fluid accumulates in the alveoli, resulting in a mismatch of ventilation and perfusion **Incidence, Outcomes, and Etiology** Risk for developing ARDS is additive 1 risk factor- 25% 2 risk factors- 42% 3 risk factors- 85%  Risk Factors  Major- sepsis, bacterial pneumonia, trauma, aspiration pneumonitis  ARDS has a mortality rate of \~50% **Pathophysiology**  Damage to the alveolar-capillary membrane leads to diffuse inflammatory response  Capillary endothelium- releases cytokines and membrane-bound phospholipids, complement system- activates leukocytes and macrophages, produces microemboli Pulmonary vasoconstriction, bronchoconstriction, altered vascular reactivity/permeability  Increased PVR with possible development of cor pulmonale **Clinical Features and Diagnosis** Hallmark -- noncardiogenic pulmonary edema  Clinical Manifestations -- dyspnea, hypoxemia, diffuse bilateral pulmonary infiltrates, decreased pulmonary compliance  ARDS is precipitated by a noxious event (e.g., trauma, bacterial pneumonia) **Treatment** Lifestyle- N/A Medical- Lung protective ventilation (supplemental O~2~), afterload reduction/inotropic support, prone positioning, iNO Surgical- N/A **Anesthetic Management** [Induction] N/A [Maintenance] Ventilation Consider V~t~ 6-8 mL/kg IBW  Consider PEEP  Avoid PIPs \>30 cm H~2~O  Avoid excessive administration of IV fluids  Consider monitoring arterial blood pressure, central venous pressure, cardiac output, urinary output [Emergence] N/A **Pneumothorax**  Simple Pneumothorax- accumulation of air in pleural space; no communication between plural space and atmosphere  Communicating Pneumothorax- accumulation of air in pleural space due to communication between pleural space and atmosphere  Tension Pneumothorax- progressive accumulation of air in pleural space that results in mediastinal shift  Hemothorax- accumulation of blood in pleural space **Incidence, Outcomes, and Etiology** Spontaneous (sneezing, coughing)  Chest trauma (rib fracture)  Barotrauma  Subclavian central line insertion Supraclavicular/infraclavicular brachial plexus block Surgical procedures (mediastinoscopy, radical neck dissection, mastectomy, axillary lymph node dissection, nehrectomy) **Clinical Features and Diagnosis**  Hallmark -- decreased SpO~2~, increased peak inspiratory pressures, tachypnea, hypotension, tachycardia  Clinical Manifestations -- asymmetric chest wall movement, tracheal shift, hyperresonance  Differential Diagnosis -- have high concern in patient with history of chest trauma who develops acute decrease in pulmonary compliance **Treatment** Simple Pneumothorax catheter aspiration  tube thoracostomy Communicating Pneumothorax semi-occlusive dressing  supplemental O~2~ tube thoracostomy Tension Pneumothorax needle thoracostomy tube thoracostomy Hemothorax tube thoracostomy consider blood transfusion **Atelectasis** Pathologic condition characterized by abnormal alveolar gas exchange due to airway collapse **Incidence, Outcomes, and Etiology**  Occurs in \~90% of patients who receive general anesthesia Develops within minutes; may persist for hours or days Most common after thoracic/upper abdominal surgery  Most common cause of postoperative respiratory dysfunction **Pathophysiology**  Blockage or obstruction of airways may result from: compression of lung tissue;  impaired surfactant, or;  absorption of oxygen from nitrogen-free alveoli.  Blockage or obstruction of airways results in:  closure of small airways, **Anesthetic Management** [Induction] N/A [Maintenance] Ventilation Conside V~t~ 6-8 mL/kg IBW Consider PEEP Consider low FiO~2~  Consider vital capacity maneuver  Consider open-lung ventilation [Emergence]  N/A [Postoperative Considerations] Incentive spirometry Consider CPAP in PACU **Pleural Effusion** Accumulation of excess pleural fluid within the pleural space, secondary to disease or pathology of adjacent structures **Pathophysiology** 1\. Blockage of lymphatic drainage from the pleural cavity 2\. Increased pulmonary capillary pressure (secondary to cardiac failure) with eventful transudation of fluid into pleural cavity 3\. Decreased plasma colloid osmotic pressure 4\. Infection/inflammation of pleura resulting in altered capillary membrane permeability **Treatment** Lifestyle- N/A Medical- N/A Surgical- tube thoracostomy, thoracentesis, pleurodesis

Use Quizgecko on...
Browser
Browser