Pulmonary Physiology PDF

VENTILATION — movement into & out of lungs DIFFUSION — movement of gases between air spaces in lungs & blood stream PERFUSION — movement up blood into & out of capillary beds of lungs to body organs & tissues upper airways (nasopharynx & oropharynx) — warms & humidifies air larynx — connects upper &...

VENTILATION — movement into & out of lungs DIFFUSION — movement of gases between air spaces in lungs & blood stream PERFUSION — movement up blood into & out of capillary beds of lungs to body organs & tissues upper airways (nasopharynx & oropharynx) — warms & humidifies air larynx — connects upper & lower airways lower airways (trachea, bronchi, terminal bronchioles) carina — ridge where trachea divides to R & L bronchi hila — where R & L bronchi enter lungs along with blood & lymph vessels goblet cells — produce mucus cilia — hairlike structures acinus — gas-exchange airways alveoli — primary was exchange units minute ventilation — total amount of air moved into and out of respiratory system per minute MV = TV x RR MV = 500 x 12 = 6000mL or 6L/min respiratory rate or frequency — number of breaths taken per minute anatomic dead space — part of respiratory system where gas exchange does not take place; normal 150mL alveolar ventilation — how much air per minute enters the parts of the respiratory system, in which gas exchange takes place AV = RR x (TV - dead space) AV = 12 x (500 - 150) = 4200mL or 4.2L/min determinants of arterial oxygenation — rate of O2 transport to tissues in blood; rate at which O2 is used by tissues retaining too much, CO2 will cause an increase in respiratory rate/ventilatory rate 60% venous CO2 is in bicarbonate form 90% arterial CO2 is in bicarbonate form TV — tidal volume: volume of air inspired or expired with each normal breath (~500mL) IRV — inspiratory reserve volume: extra volume of air that can be inspired, over and above the normal title volume when the person inspires with full force (~3000mL) ERV — expiratory reserve volume: max extra volume of air that can be expired by forceful expiration after end of normal title expiration (~1100mL) RV — residual volume: volume of air remaining in lungs after the most forceful expiration (~1200mL) FRC — functional residual capacity IC — inspiratory capacity VC — vital capacity: amount of air exchange from max inspiration to max expiration TLC — total lung capacity: total amount of air in lung after forced inspiration Pulmonary circulation has lower pressure (18 mmHg) than systemic circulation (90mmhg) high pressure = low flow = bronchial circulation low pressure = high flow = pulmonary circulation chest well includes the skin, ribs, and intercostal muscles pleura — serous membrane that adheres firmly to lungs pressure in pleural space — negative or subatomospheric (-4 to -10 mmHg); keeps lungs from collapsing perfuse lungs enabling the organs and tissues of the body to receive blood that is rich in oxygen and low in CO2 alveolar surface tension — attraction of water molecules at air dash water enter surface; trying to contract results in an attempt to force air out of Avola and them trying to collapse surfactant — detergent like substance secreted by type II alveolar epithelial cells in lungs that keep alveoli open and free of fluid and pathogens (collectins) dorsal respiratory group — set, basic automatic rhythm; receives impulses from referral chemo, receptors in carotid & aortic bodies; detect the PaCO2 & amount of oxygen in arterial blood ventral respiratory group — contains inspiratory & expiratory neurons; active when increased ventilatory effort is required pneumotaxic & apeustic centers — located in the pons; modifiers of inspiratory depth & rate are established by medullary centers central chemoreceptors — reflex PaCO2, stimulated by H in cerebral spinal fluid (pH), increases respiratory depth & rate peripheral chemoreceptors — located in aorta & carotid bodies, stimulated by hypoxemia (Pa02), responsible for all of increase in ventilation that occurs in response to arterial hypoxia effective gas exchange needs approximately even distribution of gas/ventilation & blood/perfusion in all portions of lungs oxygen delivery — ventilation of lungs, diffusion of oxygen from alveoli to capillary blood, perfusion of systemic capillaries with oxygenated blood, diffusion of oxygen from systemic capillaries into cells carbon dioxide removal — diffusion of CO2 from cells into systemic capillaries, perfusion of pulmonary capillary bed by venous blood, diffusion of CO2 into alveoli, removal of CO2 from by ventilation diffusion depends on partial pressure of gas Haldane effect ventilation–perfusion ratio — normal 0.8 Lowering V/Q ratio = low PaO2 & high PaCO2; low ventilation, high perfusion Increasing V/Q ratio = higher Pa02 & lower PaCO2; high ventilation, low perfusion perfusion exceeds ventilation in the bases of the lungs because of gravity ventilation exceeds perfusion in the apices of the lungs NORMALIZING THE RATIO hypoxic vasoconstriction — when ratio is low this can occur & cause blood coming into area to be directed to other parts of lung decreasing perfusion of hypoxic region which raises ratio & brings ABG closer to what we expect; most important cause of pulmonary artery constriction is low PaO2 bronchoconstriction — high ratio bronchi will constrict slightly to increase resistance & decrease amount of ventilation coming into area that is not well perfused Measures lung & chest wall distensibility; represents relative ease with which the structures can be stretched. Reciprocal of elasticity. Low = increase work of inspiration (stiff lungs). High = increased work of expiration (easy to inflate; lost some elastic recoil) bronchoconstriction — increases airway resistance bronchodilation — decreases airway resistance tendency of lung in chest while to return to the resting state after inspiration; elastic recoil forces of the lungs & chest wall are in opposition and pull on each other creating the normally negative pressure of the plural space Pulmonary Alterations Dyspnea – subjective sensation of uncomfortable breathing Kussmaul respirations (hyperpnea) – slightly increased ventilatory rate, very large tidal volume, and no expiratory pause Cheyne-Stokes respirations – alternating periods of deep and shallow breathing; apnea lasting 15 to 60 seconds, followed by ventilations that increase in volume until a peak is reached, after which ventilation decreases again to apnea Hypoventilation – leads to respiratory acidosis from hypercapnia Hyperventilation – leads to respiratory alkalosis from hypocapnia Peripheral cyanosis – most often caused by poor circulation ○ Best observed in the nail beds Central cyanosis – caused by decreased arterial oxygenation (low partial pressure of oxygen – PaO2) ○ Best observed in buccal mucous membranes and lips Pleural pain ○ Is the most common pain caused by pulmonary diseases ○ Is usually sharp or stabbing in character ○ Infection and inflammation of the parietal pleura (pleuritis or pleurisy) can cause pain when the pleura stretches during inspiration and is accompanied by a pleural friction rub. Chest wall pain ○ Might be from the airways. ○ Might be from muscle or rib pain. Hypercapnia – increased carbon dioxide (CO2) in the arterial blood ○ Occurs from decreased drive to breathe or an inadequate ability to respond to ventilatory stimulation Hypoxemia (NOT hypoxia) ○ Ventilation-perfusion abnormalities – most common cause; shunting blood to areas that are better ventilated Acute respiratory failure ○ Gas exchange is inadequate (hypoxemia). ○ PaO2 is ≤50 mm Hg. ○ Hypercapnia occurs, during which partial pressure of carbon dioxide (PaCO2) is ≥50 mm Hg ○ pH is ≤7.25. ○ Important post op consideration or complication, smokers at increased risk. ○ Chronic disease patient also at increased risk Chest wall restriction ○ Chest wall is deformed, traumatized, immobilized, or made heavy by fat; work of breathing is increased, and ventilation may be compromised because of a decrease in tidal volume. ○ Impaired respiratory muscle function is caused by neuromuscular disease. Flail chest ○ Instability of a portion of the chest wall from rib or sternal fractures. ○ Causes paradoxical movement of the chest with breathing. ○ Causes pain, dyspnea, unequal chest expansion, hypoventilation and hyoxemia Pneumothorax ○ Presence of air or gas in the pleural space ○ primary (spontaneous) – occurs unexpectedly in healthy individuals. ○ secondary – caused by disease, trauma, injury, or condition. ○ iatrogenic – caused by medical treatments, especially transthoracic needle aspiration. ○ Open – air is NOT trapped ○ Tension – air is trapped; life-threatening Pleural effusion – presence of fluid in the pleural space ○ Transudative effusion – watery and diffuses out of the capillaries. ○ Exudative effusion – less watery and contains high concentrations of white blood cells and plasma proteins. ○ Chylothorax – chyle exudate ○ Hemothorax – blood exudate ○ Clinical manifestations – Dyspnea and pleural pain Empyema – infected pleural effusion; pus in the pleural space ○ Clinical manifestations – cyanosis, fever, tachycardia, cough, and pleural pain Restrictive lung disease – the compliance of the lung is reduced; increases the stiffness of the lung and limits expansion ○ In these cases, a greater pressure (P) than normal is required to give the same increase in volume (V) ○ Common causes of decreased lung compliance are pulmonary fibrosis, pneumonia and pulmonary edema ○ Difficult to get air in ○ FEV1/FVC ratio can be normal; or increased Restrictive Lung Disorders ○ Aspiration – passage of fluid and solid particles into the lungs Right lower lobe: Is the most frequent site. Clinical manifestations – both choking and intractable cough have a sudden onset. ○ Atelectasis – collapse of lung tissue Compression atelectasis – external compression on the lung Absorption atelectasis – gradual absorption of air from obstructed or hypo-ventilated alveoli Surfactant impairment – decreased production or inactivation of surfactant Clinical manifestations – dyspnea, cough, fever, and leukocytosis ○ Pulmonary fibrosis – excessive amount of fibrous or connective tissue in the lung Idiopathic pulmonary fibrosis – no specific cause Clinical manifestations – increasing dyspnea on exertion Exposure to toxic gasses – ammonia, hydrogen chloride, sulfur dioxide, chlorine, phosgene, and nitrogen dioxide Clinical manifestations: Burning of the eyes, nose, and throat; coughing; chest tightness; dyspnea; hypoxemia ○ Oxygen toxicity – prolonged exposure to high concentrations of supplemental oxygen Severe inflammatory response mediated primarily by oxygen radicals Causes damage to alveolocapillary membranes, disruption of surfactant production, interstitial and alveolar edema, and decrease in compliance ○ Pneumoconiosis – any change in lung caused by the inhalation of inorganic dust particles; usually from the workplace Most common causes – silica, asbestos, and coal Clinical manifestations – cough, sputum production, dyspnea, decreased lung volumes, and hypoxemia ○ Systemic disorders and the lungs – several systemic diseases affect the airways, pleurae, or lung parenchyma. Granulomatous disorders, connective tissue diseases, Goodpasture syndrome Clinical manifestations of lung involvement – usually nonspecific and diagnosis is based on involvement of other organs. ○ Pulmonary edema – excess water in the lung from disturbances of capillary hydrostatic pressure, capillary oncotic pressure, or capillary permeability Most common cause of pulmonary edema – left-sided heart disease Postobstructive pulmonary edema (POPE) – negative pressure pulmonary edema Rare life-threatening complication that can occur after relief of upper airway obstruction. Clinical manifestations – dyspnea, orthopnea, hypoxemia, and increased WOB ○ Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) – forms of respiratory failure characterized by acute lung inflammation and diffuse alveolocapillary injury Injury to the pulmonary capillary endothelium Increased capillary permeability Inflammation Surfactant inactivation Edema and atelectasis ARDS clinical manifestations in order: 1. Dyspnea and hypoxemia with poor response to oxygen supplementation 2. Hyperventilation and respiratory alkalosis 3. Decreased tissue perfusion, metabolic acidosis, and organ dysfunction 4. Increased work of breathing, decreased tidal volume, and hypoventilation 5. Hypercapnia, respiratory acidosis, and worsening hypoxemia 6. Decreased cardiac output, hypotension, death Obstructive lung disease – airway obstruction causes an increase in resistance ○ During normal breathing, the pressure volume relationship is no different from in a normal lung. However, when breathing rapidly, greater pressure is needed to overcome the resistance to flow, and the volume of each breath gets smaller ○ Common obstructive diseases include asthma, bronchitis, and emphysema. ○ Difficult to get air out ○ FEV1/FVC ratio decreased Obstructive Disease ○ Asthma – chronic inflammatory disorder of the bronchial mucosa. Causes bronchial hyperresponsiveness, constriction of the airways and variable airflow obstruction that is reversible. One half of all cases develop during childhood; a familial disorder – over 100 genes have been identified Reversible bronchoconstriction Leads to vasodilation, increased capillary permeability, mucosal edema, bronchial smooth muscle contraction (bronchospasm), and thick mucous secretions. ○ Chronic bronchitis – hypersecretion of mucus and chronic productive cough that lasts at least 3 months of the year and for at least 2 consecutive years ○ Emphysema – abnormal permanent enlargement of the gas-exchange airways accompanied by the destruction of the alveolar walls without obvious fibrosis Loss of elastic recoil Primary emphysema – inherited deficiency of the enzyme α1-antitrypsin Secondary emphysema – cigarette smoke Panacinar (Panlobular) – involves the entire acinus; damage is more randomly distributed Involves lower lobes of the lung ○ Cystic fibrosis – autosomal recessive multisystem disease Chloride transport is a fundamental abnormality Chronic inflammation leads to hyperplasia of goblet cells, bronchiectasis, pneumonia, hypoxia, and fibrosis, among other conditions Pneumococcal pneumonia – ALI, resulting in inflammatory cytokines and cells, causes alveolar edema. ○ Edema creates a medium for the multiplication of bacteria and aids in the spread of infection into adjacent portions of the lung ○ Involved lobe undergoes consolidation ○ Four phases: 1. Consolidation 2. Red hepatization 3. Gray hepatization 4. Resolution Viral pneumonia – seasonal; usually mild and self-limiting. ○ Can set the stage for a secondary bacterial infection. Provides an ideal environment for bacterial growth and by damaging ciliated epithelial cells, which normally prevent pathogens from reaching the lower airways. Most common form: Influenza ○ Clinical manifestations: preceded by an upper respiratory infection, ough, dyspnea, fever, chills, malaise, and pleuritic chest pain Abscess – circumscribed area of suppuration and destruction of lung parenchyma ○ Follows consolidation of lung tissue, in which inflammation causes alveoli to fill with fluid, pus, and microorganisms ○ Necrosis (death and decay) of consolidated tissue – abscess empties into the bronchus, leaving a cavity ○ Cavitation – process of abscess emptying and cavity formation ○ Most common cause – aspiration ○ Clinical manifestations – fever, cough, chills, sputum production, pleural pain, bronchus involvement (severe cough, copious amounts of often foul-smelling sputum, and occasionally hemoptysis) Pulmonary embolism – occlusion of a portion of the pulmonary vascular bed by a thrombus, embolus, tissue fragment, lipids, or air bubble ○ Pulmonary emboli commonly arise from the deep veins in the thigh ○ Virchow triad – venous stasis, hypercoagulability, and injuries to the endothelial cells that line the vessels ○ Clinical manifestations – sudden onset of pleuritic chest pain, dyspnea, tachypnea, tachycardia, and unexplained anxiety Pulmonary artery hypertension (PAH) – mean pulmonary artery pressure above 25 mm Hg at rest ○ Clinical manifestations – masked by primary pulmonary or cardiovascular disease First indication – chest radiograph (enlarged pulmonary arteries and right heart border) or an ECG that shows right ventricular hypertrophy Laryngeal cancer ○ Risk factors – tobacco smoke, heightened with smoking and alcohol consumption, GERD, HPV ○ Clinical manifestations – hoarseness, dyspnea, and cough Non-small-cell lung cancer ○ Squamous cell carcinoma – nonproductive cough or hemoptysis ○ Adenocarcinoma – tumor arising from glands; asymptomatic or pleuritic chest pain and shortness of breath ○ Large cell carcinoma (undifferentiated) – chest wall pain, pleural effusion, cough, sputum production, hemoptysis, airway obstruction resulting in pneumonia Neuroendocrine – small cell carcinoma (oat) ○ Worst prognosis – rapid growth, metastasize early ○ Arise from neuroendocrine tissue so there ectopic hormone secretion which results in paraneoplastic syndromes Hyponatremia (ADH), Cushing syndrome (ACTH), hypocalcemia (calcitonin), gynecomastia (gonadotropins) and carcinoid syndrome (serotonin)