Respiratory Review PDF

RESPIRATORY REVIEW Douglas Massey II, DNP, CRNA NURS 6413  Arterial Perfusion Superior thyroid artery, derived from external carotid artery Inferior thyroid artery, derived from the thyrocervical trunk of...

RESPIRATORY REVIEW Douglas Massey II, DNP, CRNA NURS 6413  Arterial Perfusion Superior thyroid artery, derived from external carotid artery Inferior thyroid artery, derived from the thyrocervical trunk of subclavian artery Larynx – Innervation Ganglion nodosum of vagus nerve (CN X) Neurovascu Superior laryngeal nerve External branch of the superior laryngeal nerve – lar inferior constrictor muscle of pharynx, cricothyroid muscles Internal branch of the superior laryngeal nerve – Structures interarytenoid muscles, sensory innervation between inferior aspect of epiglottis and true vocal cords Inferior laryngeal nerve (i.e., recurrent laryngeal nerve [RLN]) – all intrinsic laryngeal muscles except cricothyroid muscles and part of interarytenoid muscles, sensory innervation between true vocal cords and trachea Boyle’s Law Inspiration Contraction of inspiratory muscles increases the volume of the thoracic cavity, resulting in decreased alveolar pressure (i.e., negative pressure ventilation) Increased atmospheric pressure (i.e., positive pressure ventilation) can also drive air into the lungs Expiration Relaxation of the diaphragm causes the lungs to contract (i.e., increases pressure), driving air out of the lungs Pleural, Alveolar, and Transpulmonary Pressures Pleural pressure (Ppl) Continuous negative pressure favoring lung expansion Ppl during inspiration: - 7.5 cm H2O Ppl during expiration: -5 cm H2O Alveolar pressure (Palv) Fluctuates to drive movement of gas Palv at rest: 0 cm H2O Palv during inspiration: -1 cm H2O Palv during expiration: +1 cm H2O Transpulmonary pressure Under normal physiologic conditions, transpulmonary pressure is always positive and is a measure of elastic force Reynold’s Number Re – Reynold’s number Indicates whether flow is laminar or turbulent Turbulent – Re >2300 Laminar – Re < 2300  Poiseuille’s Law describes resistance to laminar Poiseuille’s flow According to Poiseuille’s Law, laminar flow is: Law directly proportional to the pressure gradient, directly proportional to the radius of the tube inversely proportional to the viscosity, and (Hagen-Poiseuille Equation) inversely proportional to the length of the tube Spirometry – measurement of the volume movement into and out of the lungs Lung Volumes Name Definition Volume Tidal Volume amount of air inspired or expired with 500 mL each normal breath Inspiratory Reserve Volume extra amount of air that can be inspired 3000 mL when the person inspires with full force Expiratory Reserve Volume extra amount of air that can be expired 1100 mL by forceful expiration after the end of a normal tidal expiration Residual Volume amount of air remaining in the lungs 1200 mL after the most forceful expiration Lung Capacities Name Definition Formula Volume Inspiratory Capacity amount of air that a person can IC = VT + IRV 3500 mL breathe in, beginning at the normal expiratory level and distending the lungs to the maximum amount Functional Residual amount of air that remains in FRC = ERV + RV 2300 mL Capacity the lungs at the end of normal expiration Vital Capacity maximum amount of air a VC = ERV + VT + IRV 4600 mL person can expel from the lungs after first filling the lungs to their maximum extent and then expiring them to the maximum extent Total Lung Capacity maximum amount of air that TLC = RV + ERV + VT 5800 mL the lungs can contain with the + IRV Pulmonary Circulation Bronchial Pulmonary circulation High-pressure (i.e., systemic), low-flow (i.e., 2% of CO) circulation Low-pressure (i.e., pulmonary), high-flow (i.e., all of CO) circulation circulation Supplies oxygenated blood to the conducting zone of Supplies deoxygenated blood to respiratory zone for the respiratory system gas exchange Thoracic aorta → bronchial arteries → … → bronchial Right ventricle → pulmonary arteries → … → pulmonary veins → azygos, hemiazygos, posterior intercostal, veins → left atrium pulmonary veins Vessels of the pulmonary arterial system are shorter, wider, and more distensible than systemic arteries, resulting in large compliance and low pulmonary vascular resistance (PVR)  Ventilation-Perfusion Ratio – VENTILATIO normally 0.8 Describes the distribution of N- ventilation (i.e., airflow) relative to PERFUSION perfusion (i.e., blood flow) V/Q varies in different regions of the lung RELATIONSH Ventilation > Perfusion (i.e., V/Q = ∞) IP IN THE Alveoli that are ventilated but not perfused result in dead space LUNG Ventilation < Perfusion (i.e., V/Q = 0) Alveoli that are perfused but not ventilated result in shunt  Physical dissolution in plasma (0.3%) Solubility coeffieicnt of O2 in plasma is 0.003 0.003 mL of O2 is transported for every 1 mm Hg PO2 in 100 mL Oxygen Assuming a normal PaO2 of 100 mm Transport Hg, 0.3 mL of O2 is dissolved in blood Bound to hemoglobin (99.7%) 1 g Hgb can carry 1.36 mL of O2 Assuming a normal Hgb of 15 g/100 mL, 20.4 mL of O2 is bound to Hgb Oxyhemoglobin Dissociation Curve Rightward shift (i.e., enhances release of oxygen from hemoglobin) Increased H+ (i.e., decreased pH) Increased CO2 Increased temperature Increased 2,3-BPG Leftward shift (i.e., reduces release of oxygen from hemoglobin) Decreased H+ (i.e., increased pH) Decreased CO2 Decreased temperature Decreased 2,3-BPG Methemoglobin Carbon monoxide  Physical dissolution in plasma (5-10%) CO2 is approximately 20 times more soluble than O 2 Carbon Carbamino compounds (5-10%) Dioxide Bicarbonate (80-90%) CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3− Transport Catalyzed by carbonic anhydrase in RBCs HCO3- formed and diffuses out of the RBC CL- diffuses into the RBC maintaining equilibrium (i.e., Chloride shift) H+ buffered with the RBC binding to Hgb  Bohr Effect – CO2/H+ affect the affinity of Hgb for O2 Acidosis/hypercarbia facilitate release of O2 Bohr & at peripheral tissues Haldane Effect – O2 affects the affinity of Hgb Haldane for CO2/H+ Effects Deoxyhemoglobin has an increased affinity for CO2, thus facilitating transport to lungs Oxyhemoglobin has a decreased affinity for CO2, thus facilitating offloading of CO2 at alveoli OSA – Defintion Obstructive Mechanical obstruction secondary to Sleep Apnea reduction in pharyngeal muscle tone during sleep (OSA) Obesity Obesity/sleep-disordered Hypoventilati breathing/daytime hypoventilation with no mechanical, neuromuscular, or on Syndrome metabolic etiology (OHS) OSA – STOP-Bang https://www.anesthesiologynews.com/Clinical-Anesthesiology/Article/08-19/Scoring-Systems-to-Detect-Severe- OSA-Compared/55612?sub=BF677D85A65B6F432279AFF560FD1F495263D8B1E8B69BAE4CB171B569A COPD – Clinical Features and Diagnosis Hallmark – chronic productive cough and progressive exercise limitations Clinical Manifestations – dyspnea, wheezing Pulmonary Function Testing (i.e., GOLD Classification) FEV1 80% = mild FEV1 50%-79% = moderate FEV1 30%-49% = severe FEV1 25 mm Hg Pulmonary Arterial Hypertension (PAH) PAH – Definition is an increase in PVR secondary to cellular changes and proliferation in the pulmonary arteries  Induction N/A PAH & Cor Pulmonale – Maintenance Anesthetic Maintain adequate oxygenation Managemen Avoid acidosis t Avoid stimuli that increase sympathetic tone Avoid hypothermia Emergence N/A Pulmonary Embolism – 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, CO2, tumor, bone, fat, catheter fragments Virchow’s Triad Venous stasis, venous injury, hypercoagulable state Pulmonary Edema – Incidence, Outcomes, and Etiology Pulmonary edema refers to accumulation of excess fluid in interstitium and alveoli Accumulation of excess fluid is usually caused by increased pulmonary capillary hydrostatic pressure or decreased intravascular colloid oncotic pressure Negative-pressure pulmonary edema may result from acute airway obstruction Risk Factors – young patients, male gender, delayed recognition/prolonged treatment of airway obstruction, excessive administration of intravenous fluids  Aspiration Movement of gastric contents Pneumonitis – from the stomach to the lungs Definition that results in chemical injury to the lung tissue Aspiration Pneumonitis – 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 (e.g. IL- 8, TNF-), which attract neutrophils that in turn release oxygen radicals and proteases Secondary injury results from fibrin deposition and alveolar necrosis Aspiration Pneumoni tis – Fasting Guideline s https://pubs.asahq.org/anesthesiology/article/126/3/376/19733/Practice-Guidelines-for-Preoperative- Fasting-and  ARDS – Treatment Lifestyle Medical Surgical N/A Lung protective N/A ventilation Supplemental O2 Afterload reduction/inotropic support Prone positioning Inhaled nitric oxide Miscellaneous Pneumothorax – Treatment Simple Catheter aspiration Tube thoracostomy Pneumothorax Communicating Semi-occlusive dressing Supplemental O2 Pneumothorax Tube thoracostomy Tension Needle thoracostomy Tube thoracostomy Pneumothorax Tube thoracostomy Hemothorax Consider blood transfusion Atelectasis – 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, with absorption of alveolar oxygen, leading to alveolar collapse, which prevents alveolar gas exchange.