Pulmonary Disorders & Treatment Lecture Notes PDF

Pulmonary Disorders & Treatment Kristen Bolton – Fall 2024 Objectives Review Anatomy & Physiology Explore Assessment/Diagnostics Examine Pulmonary Disorders and their effects on gas exchange Explore Chest Tubes  Overview Pulmonary System Thorax Conducting airwa...

Pulmonary Disorders & Treatment Kristen Bolton – Fall 2024 Objectives Review Anatomy & Physiology Explore Assessment/Diagnostics Examine Pulmonary Disorders and their effects on gas exchange Explore Chest Tubes  Overview Pulmonary System Thorax Conducting airways Respiratory airways Pulmonary blood flow Primary Function of Pulmonary System Ventilation Respiration  Thorax Thoracic cage - Rigid but flexible 12 thoracic vertebrae, each with a pair of ribs Thorax Lungs Lobes and segments Mediastinum Pleura Muscles of ventilation Too allow for inhalation/exhalation Accessory muscles  Conducting Airways Upper airways Nasal and oral cavities Pharynx Larynx Epiglottis Trachea Bronchial tree Left bronchus Right bronchus  Conducting Airways Defense Mechanisms Mucociliary escalator The mucus, which floats atop the cilia, traps foreign particles Ciliary movement propels the entire mucous blanket and any trapped particles upward toward the pharynx Cough reflex Excessive amounts of foreign particles in the trachea and bronchi can initiate the cough reflex Conducting & Respiratory Airways  Respiratory Airways Respiratory Bronchioles Alveolar Ducts Alveoli  Pulmonary Blood Supply Pulmonary circulation (Normally a low pressured system) Alveolar–capillary membrane (Blood oxygenation occurs here)  Ventilation Inhalation Air moves into the lungs Diaphragm descends causing a decrease in intra-pleural pressure Gas flows from an area of high pressure to low pressure (atmosphere into the lungs) Exhalation Air leaves the lungs Occurs as the diaphragm recoils back Air goes from lungs to atmosphere Ventilation  Ventilation vs. Gas Exchange Alveolar ventilation = total ventilation that participates in gas exchange Anatomic dead space = (conducting airways) ventilated but not perfused – do not participate in gas exchange = normal Alveolar dead space = alveoli are ventilated fully but not perfused = not normal  Respiration Diffusion: gases move across the alveolar-capillary membrane to the pulmonary capillary bed The difference in the concentrations of the gases is referred to as the driving pressure. Factors affecting the rate of diffusion - Thickness of the alveolar–capillary membrane (fluid) - The surface area of the membrane (atelectasis)  Ventilation/ Perfusion Relationships Ventilation (V): movement of air in and out of the lungs; normal 4L/min Perfusion (Q): alveolar capillary blood flow; normal 5L/min Normal ventilation/perfusion ratio (V/Q) is 4:5, or 0.8 Ventilation/Perfusion Relationships  Ventilation/ Perfusion Relationships Ventilation/perfusion mismatch​ Alveolar dead space (E)​ Intrapulmonary shunting (A)​  Assessment History Presenting illness General respiratory status General health status Family and social background Current symptoms Physical Examination: Inspection Palpation Percussion Auscultation  Diagnostics Laboratory Studies Sputum cultures Bronchoscopy (Indications - Diagnostic & Therapeutic) Thoracentesis  Diagnostics Chest radiography (X-ray) Bones Mediastinum Diaphragm Pleural space Lung tissue Tubes, wires/lines  Acute Lung Failure Pulmonary system fails to maintain adequate gas exchange Approximately 56% of patients in the ICU experience Acute Lung Failure One third of patients with Acute Lung Failure require mechanical ventilation  Acute Lung Failure ALF usually occurs secondary to another disorder that has altered the normal function of the pulmonary system Ventilatory drive Muscle strength Chest wall elasticity Lung’s capacity for gas exchange Airway resistance Metabolic oxygen requirements  Acute Lung Failure Description Type I: low PaO2, normal PaCO2 (Failure to oxygenate) Type II: low PaO2, high PaCO2 (Failure to ventilate) Etiology Extrapulmonary: disorders that affect the brain, spinal cord, neuromuscular system, thorax, pleura, upper airways Intrapulmonary: affect lower airways and alveoli, pulmonary circulation, alveolar-capillary membrane  Acute Lung Failure Change in mental status occurs Hypoxemia Compensatory mechanisms fail Auscultation- Adventitious sounds Assessment of cardiac status - hypoxia will initially cause tachycardia and increased BP ABG analysis - Decreased PaO2/Potentially increasing PaCO2  Acute Lung Failure Treat underlying cause - Improve oxygenation and ventilation Oxygenation Supplemental oxygen administration – low flow or high flow systems Ventilation Noninvasive and invasive mechanical ventilation May need positive pressure to open collapsed airways Pharmacology Bronchodilators (beta2-agonists and anticholinergic agents) Steroids Sedation or neuromuscular paralysis may be necessary to assist with maintaining adequate ventilation  Acute Lung Failure Correct Acidosis Hypoxemia = impaired tissue perfusion = production of lactic acid = metabolic acidosis Impaired ventilation = accumulation of carbon dioxide = respiratory acidosis Nutrition support Monitor for cardiac dysrhythmias Venous thromboembolism prophylaxis Gastrointestinal bleeding Acute Lung Failure  Pulmonary Embolism What is it? Occurs when a blood clot or other matter lodges in the pulmonary arterial system Most thrombotic emboli arise from the pelvic and deep leg veins (DVT) Non-thrombotic emboli can be from fat, tumors, amniotic fluid, air, and foreign bodies. Pulmonary Embolism  Pulmonary Embolism The pulmonary circulation has an enormous capacity to compensate for a PE Pathophysiology Increase in alveolar dead space -> “wasted ventilation” Bronchoconstriction – (occurs in areas not being perfused) Compensatory Shunting – unaffected lung areas must accommodate to the entire CO Pulmonary Embolism  Pulmonary Embolism Hemodynamic consequences of a PE Pulmonary hypertension Right ventricular failure Decreased preload in left ventricle Decreased cardiac output  Pulmonary Embolism Signs & Symptoms Tachycardia Tachypnea Dyspnea Pleuritic chest pain Cough Hypoxemia Diagnosis Evidence of DVT D-dimer CXR Spiral CT V/Q scan Doppler (extremities)  Pulmonary Embolism Management Prevention/DVT prophylaxis Clot dissolution - Fibrinolytic therapy – (massive PE and hemodynamically unstable) Promoting gas exchange Supplemental O2 Intubation and mechanical ventilation Pneumonia An acute inflammation of the lung caused by an infectious agent that can lead to alveolar consolidation A lower respiratory tract infection Pneumonia  Pneumonia Community-Acquired Pneumonia Occurs outside of the hospital or within 48 hours of admission to the hospital Hospital-Acquired Pneumonia (including VAP) Occurs while in the hospital for at least 48 hours Health Care-associated Pneumonia Acquired in health care environments outside of the traditional hospital setting  Pneumonia Organism accumulates in the lower respiratory tract (normally competent defense mechanisms become overwhelmed) Most common method of bacterial invasion is Aspiration of oropharyngeal organisms Inhalation of aerosols or particles Spread from another infected site into the lungs  Ventilator Acquired Pneumonia (VAP) Definition: Pneumonia in patients that have been ventilated for at least 48 hours and at least 2 consecutive days Incidence: 10-20% of patients receiving mechanical ventilation > 48 hours  Pneumonia Assessment – What might we find with our assessment? Diagnostic Tests – What might they show?  Pneumonia Treatment Medications (Antibiotic therapy, Bronchodilators) Oxygen therapy for hypoxemia Mechanical ventilation if ALF develops Fluid management for hydration Nutritional support  Acute Respiratory Distress Syndrome vs. Acute Lung Failure Acute respiratory distress syndrome (ARDS) is a type of respiratory failure where the lungs stiffen and lose the ability to make surfactant (Characterized by widespread inflammation in the lung) Acute Lung Failure (ALF) is the inability of an individual to breathe or carry out ventilation on their own (Characterized by inadequate gas exchange by the respiratory system)  ARDS systemic process characterized by noncardiac pulmonary edema and disruption of the alveolar–capillary membrane as a result of injury to either the pulmonary vasculature Acute or the airways Respiratory Criteria Distress -Acute onset within one week of clinical injury Syndrome -Bilateral pulmonary opacities not explained by other conditions (ARDS) - Pulmonary edema – Respiratory Failure is not fully explained by heart failure or fluid overload -Altered PaO2/FiO2 ratio  Mild, moderate, or severe : based on the severity of hypoxemia Etiology Direct injuries: the lung epithelium ARDS sustains a direct insult Indirect injuries: the insult occurs elsewhere in the body, and mediators are transmitted via the blood stream to the lungs  Exudative phase: (first 72h) Damage to pulmonary capillaries leads to hypoxemia Pulmonary HTN, decreased CO Tachypnea, restlessness ARDS: Fibroproliferative phase: Three Fibrotic alveoli, scarred pulmonary capillaries Phases Stiff lungs, increased pulmonary HTN, worsening hypoxemia fatigue, excessive accessory muscle use, fine crackles Resolution phase: Several weeks  Focus - promote gas exchange, support tissue oxygenation, treat underlying cause, prevent complications Ventilation -Use of ventilator settings that decrease lung tissue trauma ARDS - Oxygen therapy - Lowest level possible Management Positive end-expiratory pressure (PEEP) Prone Positioning - Shifts perfusion from posterior base to anterior portion with improved ventilation Chest tubes  Pleural Anatomy Pleural membrane has 2 layers: Visceral pleura (pulmonary pleura) lines the lungs Parietal pleura lines the thoracic cavity  Pleural Anatomy -Two membranes are separated only by the lubricating fluid (pleural fluid), allowing the pleura to slide easily during breathing Pleural cavity is between the visceral and parietal pleura which seal the cavity Pathophysiology - Pleural space has a negative pressure = keeps the two pleurae together and allows the lung to expand and contract Changes to the Pleural Pressure When air (Pneumothorax) or fluid (Pleural Effusion) enters the pleural space between the parietal and visceral pleura, the pressure gradient that normally keeps the lung against the chest wall is gone and the lung collapses Chest Tubes When do we use chest tubes? - When negative pressure in the pleural cavity is disrupted by presence of air or fluid (Pulmonary compromise) What is their purpose? - To drain air or fluid from the pleural space Image result for thopaz chest drainage Image result for pleur evac Thoracotomy - An incision into the pleural space of the chest to gain access to the thoracic organs, most commonly the heart, lungs, esophagus or thoracic aorta.  Tumors or Malignancies Trauma Reasons Abscesses or Cysts Bronchopleural Fistula Repair for Surgery Infection Tuberculosis Lobectomy The removal of one or more lobes of the lung Lesion/Tumor confined to lobe of the lung Pneumonectomy Removal of the entire lung Completed when the tumour is found in both lobes of the left lung, or if it has spread to the central airways (involving main stem bronchi or the bronchus to a different lobe) Open Pneumothorax - Opening in the chest wall (with or without lung puncture) - Allows atmospheric air to enter the pleural space - Penetrating trauma: stab, gunshot, impalement Closed Pneumothorax - Chest wall is intact - Rupture of the lung and visceral pleura (or airway) allows air into the pleural space Pleural Effusion - Fluid that collects in the pleural space when there are fluid shifts in the body from conditions such as CHF, malnutrition, renal and liver failure Hemothorax Occurs after thoracic surgery and many traumatic injuries Negative pressure between the pleurae is disrupted, and the lung will collapse to some degree, depending on the amount of blood Empyema - Defined as a collection of pus in the pleural cavity, gram-positive, or culture from the pleural fluid.