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Modesto T. Kapuno, MD, CSEE, MNSA
Forefront in Medical And Traumatic Emergencies BU College of Nursing December 16, 2004 Modesto T. Kapuno, MD, CSEE, MNSA
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Respiratory System
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Respiration Ventilation: Movement of air into and out of lungs
External respiration: Gas exchange between air in lungs and blood Transport of oxygen and carbon dioxide in the blood Internal respiration: Gas exchange between the blood and tissues
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Respiratory System Functions
Gas exchange: Oxygen enters blood and carbon dioxide leaves Regulation of blood pH: Altered by changing blood carbon dioxide levels Voice production: Movement of air past vocal folds makes sound and speech Olfaction: Smell occurs when airborne molecules drawn into nasal cavity Protection: Against microorganisms by preventing entry and removing them
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Respiratory System Divisions
Upper tract Nose, pharynx and associated structures Lower tract Larynx, trachea, bronchi, lungs
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Nose and Pharynx Pharynx Nose
External nose Nasal cavity Functions Passageway for air Cleans the air PSCCE w/goblet cells Humidifies, warms air Smell Along with paranasal sinuses are resonating chambers for speech Pharynx Common opening for digestive and respiratory systems Three regions Nasopharynx Oropharynx Laryngopharynx
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Nasal Cavity and Pharynx
1 2 3 4
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Vocal Folds Functions Maintain an open passageway for air movement (thyroid and cricoid) Epiglottis and vestibular folds prevent swallowed material from moving into larynx Vocal folds are primary source of sound production
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Trachea Windpipe Divides to form Primary bronchi Carina: Cough reflex
Dense regular connective tissue and smooth muscle reinforced with c-shaped cart. on the ant. surface. Post. Trachea consists of elastic lig. and a bundle of muscle called the trachealis muscle The lining of the trachea is pseudo stratified ciliated columnar epithelium with goblet cells
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Pseudo stratified ciliated columnar epithelium with goblet cells
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Tracheobronchial Tree
Conducting zone Trachea to terminal bronchioles which is ciliated for removal of debris Passageway for air movement Cartilage holds tube system open and smooth muscle controls tube diameter Respiratory zone Respiratory bronchioles to alveoli Site for gas exchange
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Tracheobronchial Tree
1 2 Conducting zone 3 4 5 6 Respiratory zone 7
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Bronchioles and Alveoli
1 2 3 4 5
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Alveolus and Respiratory Membrane
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Gas Exchange
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Lungs Two lungs: Principal organs of respiration Divisions
Right lung: Three lobes Left lung: Two lobes Divisions Lobes, bronchopulmonary segments, lobules
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Thoracic Walls Muscles of Respiration
1 2
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Inspiration Active process involving the
diaphragm and intercostal muscles
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Expiration Usually passive
-can become active using internal intercostals and abdominal muscles
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Elasticity Lungs are compliant- they have the ability
to stretch and recoil like a balloon
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Apnea and Dyspnea Apnea- absence or cessation of breathing
Dyspnea- difficulty of breathing
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Negative Intrapleural Pressure
-2 to -4 mm Hg pressure maintained in the pleural space to aid in… Keeping lungs expanded Return of blood to the heart
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Alveolar Membrane Surfactant and water layer
Alveolar wall- Simple squamous epithelium 3) Basement membrane of alveolar wall 4) Interstitial space 5) Capillary wall- Simple squamous epithelium 6) Basement membrane of cap wall
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Alveolar Capillary Membrane
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The factors that effect rate of gas exchange
Partial pressure gradients of O2 and CO2 Surface area of alveolar membrane Thickness of capillary-alveolar membrane Ventilation- perfusion mismatch
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Blood flow through the lungs
Two blood flow routes of the heart exist: Major rout brings deoxygenated blood to the lungs via the pulmonary artery, to pulmonary capillaries, is oxygenated and returns to the heart through the pulmonary veins. The second rout brings oxygenated blood to the tissues of the bronchi, down to the respiratory bronchioles. Oxygenated blood flows through the aorta, through bronchial arteries capillaries, where O2 is released. Deoxygenated blood from the proximal part of the bronchi returns to the heart through the bronchial vein and the azygose venous system.
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Pleura Pleural fluid produced by pleural membranes Acts as lubricant
Helps hold parietal and visceral pleural membranes together
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Ventilation Movement of air into and out of lungs
Air moves from area of higher pressure to area of lower pressure Pressure is inversely related to volume
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Changing Alveolar Volume
Lung recoil Causes alveoli to collapse resulting from Elastic recoil and surface tension Surfactant: Reduces tendency of lungs to collapse Pleural pressure Negative pressure can cause alveoli to expand Pneumothorax is an opening between pleural cavity and air that causes a loss of pleural pressure
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Compliance Measure of the ease with which lungs and thorax expand
The greater the compliance, the easier it is for a change in pressure to cause expansion A lower-than-normal compliance means the lungs and thorax are harder to expand Conditions that decrease compliance Pulmonary fibrosis Pulmonary edema Respiratory distress syndrome
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Pulmonary Volumes Tidal volume Inspiratory reserve volume
Volume of air inspired or expired during a normal inspiration or expiration Inspiratory reserve volume Amount of air inspired forcefully after inspiration of normal tidal volume Expiratory reserve volume Amount of air forcefully expired after expiration of normal tidal volume Residual volume Volume of air remaining in respiratory passages and lungs after the most forceful expiration
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Pulmonary Capacities Inspiratory capacity Functional residual capacity
Tidal volume plus inspiratory reserve volume Functional residual capacity Expiratory reserve volume plus the residual volume Vital capacity Sum of inspiratory reserve volume, tidal volume, and expiratory reserve volume Total lung capacity Sum of inspiratory and expiratory reserve volumes plus the tidal volume and residual volume
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Respiratory Problems All respiratory problems can be categorized as:
Impacting ventilation, Diffusion, or Perfusion Management can be initiated once this can be established
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Ventilation Upper airway obstruction Lower airway obstruction
Chest wall impairment Neurogenic dysfunction Foreign body, epiglottitis Asthma, airway edema Trauma, muscular dystrophy CNS depressant drugs, stroke
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Diffusion Inadequate O2 Alveolar pathology
Interstitial space pathology Capillary bed pathology Fire, CO poisoning Lung disease, inhalation injury Pulmonary edema, drowning Severe artherosclerosis
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Perfusion Inadequate blood volume/ Hgb Impaired circulation
Capillary wall pathology Shock, anemia Pulmonary embolus Trauma
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Interventions Ensure that the upper and lower airways are open and unobstructed Provide assisted ventilations
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Ventilation Requirements
Neurological control to initiate ventilation Nerves between the brain stem and the muscles of respiration Functional diaphragm and intercostal muscles Alveoli that are functional and noncollapsed
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Diffusion Process of gas exchange between the air-filled alveoli and the pulmonary capillary bed Gas exchange is driven by simple diffusion in which gases move from areas of high concentration of low concentration until equal
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Interventions Provide high flow O2
Reduce inflammation of interstitial space
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Diffusion Requirements
Alveolar and capillary walls that are not thickened Interstitial space between the alveoli and capillary wall that is not enlarged or filled with fluid
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Perfusion Refers to the process of circulating blood through the pulmonary capillary bed
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Interventions Ensure adequate circulating volume and Hgb levels
Optimize left sided heart function
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Perfusion Requirements
Adequate blood volume Adequate Hgb in the blood Pulmonary capillaries that are not occluded Properly function left heart that provides smooth flow of blood through pulmonary capillary bed
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Assessment Review Scene size up
Wide variety of toxic environments resulting in deficient O2 Initial Assessment Recognition of life threats Focused history Physical exam
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Signs of Life Threats Altered LOC Severe cyanosis Absent BS
Audible stridor One or two word dyspnea Tachycardia Pallor and diaphoresis Retractions/ accessory muscle use
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Focused History Dyspnea Chest pain Productive/ nonproductive cough
Hemoptysis Wheezes Infection- fever, sputum Previous experience Patient’s description of severity Medications
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Physical Exam Position, respiratory effort, skin color, ability to speak Tachycardia- hypoxemia/ sympathomimetic medications Bradycardia- severe hypoxemia & imminent arrest Hypertension- sympathomimetics Respiratory rate may not be accurate indicator; extremely slow- exhaustion
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Pursed lips- helps maintain pressure within airways even during exhalation to support bronchial walls internally that have lost their external support as a result of disease Accessory muscle use- quickly result in respiratory fatigue JVD- right heart failure in severe pulmonary congestion Barrel chest- long standing COPD Clubbing- enlargement of distal phalanges; long standing chronic hypoxemia Peripheral cyanosis- excess deoxygenated Hgb Carpopedal spasm- hypocapnia
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Sputum Infection/pneumonia- thick, green, brown
Allergies/inflammatory- yellow, pale grey Pulmonary edema- pink, frothy
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Chronic Obstructive Airway Disease
Chronic bronchitis Emphysema Asthma
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Chronic Bronchitis Inflammatory changes and excessive mucus production in bronchial tree Hyperplasia and hypertrophy of mucus producing glands that result from prolonged exposure to irritants Hypoventilation, hypercapnia, hypoxemia, increases pCO2 Frequent infections, scarring, irreversible changes bronchiectasis- bronchi dilation
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“Blue bloaters”- appear cyanotic,decreased pO2 due to altered ventilation-perfusion
Polycythemia common secondary to chronic hypoxemia Increased airway resistance during inspiration and expiration
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Signs and Symptoms Typically overweight Productive cough with sputum
Coarse rhonci Mild chronic dyspnea Resistance on inspiration and expiration
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Emphysema Permanent abnormal enlargement of air spaces beyond terminal bronchioles, destruction of alveoli, failure of supporting structures to maintain alveolar integrity Reduces alveolar functional surface area, elasticity resulting in air trapping Residual volume increases while vital capacity remains the same
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Reduced pO2 leads to increased RBC production and polycythemia- elevated Hct
“Pink puffer”- increased airway resistance only on expiration, calorie consumption Decrease in alveolar membrane surface area & number of pulmonary capillaries Decrease in area for gas exchange and increased resistance to pulmonary blood flow Air trapping due to loss of elastic recoil
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Signs and Symptoms Thin, barrel chested Nonproductive cough
Wheezing, rhonchi Pink complexion Extreme DOE Prolonged expiration Pursed lips
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Management High flow O2, IV,CM
Beta agonists- relieve bronchospasms and reduce constricted airways metaproterenol- Alupent albuterol- Albuterol Corticosteroids- Solumedrol Xanthine-bronchodilation and stimulation of respiratory drive Aminophylline MgSO4- smooth muscle relaxer
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Asthma Reversible airflow obstruction caused by smooth muscle contraction Hypersecretion of mucus resulting in mucus plugging Inflammatory changes in bronchial walls Increased resistance air flow, alveolar hypoventilation Ventilation-perfusion mismatch resulting in hypoxemia and CO2 retention stimulating hyperventilation
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Inspiratory obstruction and marked expiratory obstruction results in auto-PEEP due to air trapping
Increased airway resistance, increased respiratory drive, air trapping results in excessive demand on respiratory muscles Excessive positive thoracic pressure may decrease left ventricular preload resulting in a transient reduction in CO and SBP, pulsus paradoxus Hypoxemia, hemodynamic alterations, death
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Signs and Symptoms of Severe Asthma
Obtundation Diaphoresis and pallor Retractions One, two word sentences Poor muscle tone HR > 130, RR >30
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Management High flow O2, IV-rehydration, CM Nebulized Beta agonists
Albuterol mg Alupent Corticosteroids- solumedrol Aminophylline MgSO4 Epinephrine- SQ mg Ketamine
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Intubation Support patient’s failing ventilation efforts- does not solve problem Irritation due to intubation may increase bronchospasm Increased air trapping Poor compliance
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Medical Respiratory Conditions/Diseases
Hyperbaric—Bends, Decompression Pneumonia Hypoxia Hyperventilation High Altitude Emphysema Tuberculosis Lung Cancer Cystic Fibrosis Asthma
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Hyperbaric: High pressure
Force more oxygen into patient’s blood Use for carbon monoxide, circulatory shock, asphyxiation Gangrene, tetanus—bacteria causing these can not live at high pressures or high oxygen levels Oxygen toxicity (>2.5-3 atm) NS disturbances, coma, death Nitrogen narcosis: high pressure forces nitrogen into blood Bends—ascend gradually ok Fast ascent—pressure of nitrogen gas decreases fast, boils from tissue into blood, gas bubble in blood—emboli Decompression sickness—joint, pain, mood, numbness Air emboli—ascend without exhaling Air under less pressure, expands, alveoli rupture
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Pneumonia Fluid in lungs, inflammation of lungs, less oxygen in blood, cells no work Causes: RBC not in pulmonary capillaries long enough for gas exchange, low oxygen in blood Due to respiratory membrane thickening due to fluid, gases not diffuse fast enough through thick membrane Bacteria, virus, fungi, chemical cause Decreased immunity—inflamed air sacs, lungs will with fluid Bacteria—antibiotics cure, cough, green mucous Viral-dry cough, little mucous in cough Mycoplasma (fungi)—violent cough attacks, little mucous, vomiting, antibiotics speed recovery
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Left lung with pneumonia
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Hypoxia: Low oxygen supply to tissues
Cyanide poisoning—cells no use oxygen even though delivered Carbon monoxide—competes with oxygen to bind to hemoglobin, better than oxygen by 200x, displaces oxygen, cells no get oxygen and die
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Hyperventilation: Rate of breathing increased
Flushes carbon dioxide out of blood Increase blood pH Ends when blood carbon dioxide levels restored Occurs when take quick shallow breaths, carbon dioxide levels decrease Breath into bag, increase carbon dioxide levels Respiratory alkalosis (pH increase) CO2 + H20 H + HCO3
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High Altitudes Low air density, low oxygen pressure
Increases RBC production
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Emphysema: Gradual disease Chronic obstructive pulmonary disease
Smoke, labored breathing, cough Destroys elastin fibers, less recoil of lungs, breathlessness—less expand and constrict Airways collapse during expiration—obstruct outflow
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Bronchitis Chronic obstructive pulmonary disease
Inhale irritants, causes mucous production to increase Inflammation Obstruct airways Less air flow
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Tuberculosis Bacteria Spread by cough Live in alveoli in lungs
Antibiotics for 12 month to cure
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Lung Cancer: 1/3 of cancer deaths 90% smoker patients Low cure rate
Caused by a decrease in protective organs Nasal hairs, cilia, mucous Mucous cells grow wildly and lose function and structure
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Cystic fibrosis: Oversecretion of mucous that clogs respiratory passageways
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Asthma: External factors cause Allergy Respiratory passages swell
Bronchioles constrict
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Traumatic and Medical Respiratory Emergencies
Pneumothorax Massive Hemothorax Hemoptysis Flail Chest Pulmonary Embolism
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Pneumothorax Accumulation of air within the pleural space
Secondary collapse of the lung
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Etiology Rupture of visceral pleura with secondary leak of air from the lung (Tension pneumothorax) Loss of integrity of chest wall (open pneumothorax) Mixed (tension-open pneumothorax) Rupture of bronchus or trachea Rupture of esophagus
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Pathology Presentation
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Presentation Asymptomatic . life-threatening Sudden-onet
Dyspnea, dry cough, ipsilateral pleuritic chest pain
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Physical Examination Anxiety, diaphoresis, “respiratory distress”
Tachypnea, tachycardia, hyper- or hypotension Cyanosis Elevated JVP Tracheal deviation Subcutaneous emphysema Asymmetric/decreased excursion of chest, abnormal tactile fremitus, hyperresonance , diminished breath sounds
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Pathophysiology Apex to base pressure gradient ↓ Lung compliance ↓
FRC ↓ Ventilation ↓ Oxygenation ↓
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Tension Pneumothorax Life threatening
One-way flow of air due to “ball-valve” and/or positive pressure ventilation Progressive increase in pressure within the pleural space Progressive shift of the mediastinum Decreased oxygenation and ventilation Decreased venous return to the heart ¨ obstructive shock
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Diagnosis Clinical assessment - Chest radiograph - AP CXR
- PA and lateral CXR Expiratory PA CXR CT imaging of the chest Visceral pleural surface of lung Absence of lung markings
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Chest Radiograph
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Chest Radiograph
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Classification Tension or non-tension Spontaneous
- Primary spontaneous - Secondary spontaneous Traumatic - Chest wall - Tracheobronchial airway injury - Disruption of lung visceral surface Iatrogenic Other Tension or non-tension
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General Management (c)ABC
Suspected tension pneumothorax – emergency decompression of the pleural space Large-bore ( gauge) angiocatheter inserted into the second intercostal space in the midclavicular line followed immediately by, Tube thoracostomy In extremis? Consider bilateral pleural space decompression
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Angiocath and Chest Tube Insertion
Explore pleural space with gloved finger and then insert tube 20 cm Attach chest tube to a pleural drainage system and apply – 20 cm H2O pressure Use blade to cut skin only Blunt dissection through interspace with Kelly and/or gloved finger (avoid trocars)
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Primary Spontaneous Pneumothorax (PSP)
No known pre-existing lung disease Rupture of subpleural bleb(s) at lung apex Younger (20’s); tall and thin; male > female; smokers 5% tension; 10% bilateral Decreased PaO2; normal or low PaCO2 % risk of recurrence by 5 years (most in the 1st year) Recurrence – (1st) 25%, (2nd) 50%, (3rd) 80%
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PSP – Initial Management
Oxygen and observation – select few; small asymptomatic pneumothorax; resolving; reliable patient with good follow-up Tube thoracostomy – most common and safe management strategy; ambulatory or hospital; lung must be re-expanded Small bore pleural catheters are often as effective
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PSP – Surgical Management
First episode: Prolonged airleak Incomplete re-expansion of lung Bilateral Tension Hemopneumothorax Occupational hazard Absence of facilities Second episode: Ipsilateral recurrence Contralateral after a first episode Resect blebs Obliterate the pleural space - apical pleurectomy - pleural abrasion
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PSP – Chemical Pleurodesis
Involves the introduction of talc or doxycycline into the pleural space Brisk pleural inflammation → pleural adhesions → reduced risk of recurrence In the setting of PSP, chemical pleurodesis is reserved for high-risk patients who refuse surgery
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Secondary Spontaneous Pneumothorax (SSP)
Often older; pre-existing lung disease – COPD, HIV/AIDS with PCP, CF, TB, interstitial lung disease, asthma, etc. Hypoxemia and hypercapnia is common Failure of lung to re-expand and/or persistent air leak (bronchopleural fistula) is common Very high risk of recurrence (> % by 5 years) Significant risk of mortality
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SSP - Management Chest tube insertion
Adequate trial of conservative management before surgery Prolonged chest tube drainage by means of a Heimlich valve (outpatient) Many patients ultimately require more aggressive intervention (incomplete re-expansion and/or persistent air leak) Chemical pleurodesis via the chest tube* if the lung re-expands and the air leak stops Surgical intervention *This could affect the patient’s ability to have a future transplant
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Traumatic Pneumothorax
Often there is blood and air in the pleural space (hemopneumothorax) Emergency insertion of a large bore (34 – 36 French) chest tube ATLS-guided management and referral to a trauma center Iatrogenic pneumothorax: observation +/- O2, aspiration, chest tube, surgery
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Flail Chest Develops when there are multiple segment fractures of 3 or more adjacent ribs with or without an associated costochondral separation or with a fracture of the sternum. The classic finding is paradoxical respiration. Management consists of temporary stabilization of the flail segment which may be achieved by laying the patient on the affected side. In several cases incubation and positive pressure ventilation may be necessary. Blunt Thoracic Injury is often complicated by pulmonary contusion
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Massive Hemothorax Conditions when hemothorax may be so massive and may cause ventilatory embarrassment. The lung is reexpanded by draining the blood by a thoracostomy tube. The blood should be collected in sterile container for possible autologous transfusion.
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Hemoptysis Expectoration of blood from the lower respiratory tract – below the vocal cords Frightening to the patient Often a manifestation of serious underlying disease Massive hemoptysis is immediately life-threatening
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Approach to Hemoptysis
(c)ABC’s ↓ History Physcial Exam CXR/Lab Evaluation Special Procedures Therapeutic Intervention Evaluation of Response Sputum analysis Bronchoscopy CT imaging of the chest V/Q scanning Bronchscopy Embolization Medical therapy Surgery
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Stabilization: (c)ABC
Airway and Breathing: Position patient sitting upright or with the affected lung dependent Supplemental oxygen Suctioning of secretions Intubation and ventilation if necessary Cough suppression (codeine or other narcotics) Intubation and ventilation: Facilitates airway suctioning Improves ventilation and gas exchange (PEEP) Facilitates fiberoptic bronchoscopy Allows for sedation/patient comfort Can be used to prevent contamination of normal regions of lung with blood (selective intubation or dual-lumen tube) Control of airway and breathing prevents cardiovascular compromise in most cases
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Stabilization: (c)ABC
Circulation: Obtain 2 large-bore IV’s Crossmatch Immediate fluid esuscitation with crystalloid Use packed RBC’s and/or fresh frozen plasma as necessary Monitor hemodynamics frequently (HR, BP, urine output, central venous pressure)
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Quantification Severity varies from minor streaking of the sputum to life-threatening, large volume hemorrhage (asphyxia, cardiovasular collapse) Whether hemoptysis is life-threatening depends upon: The rate of bleeding into the airway The patient’s ability to expectorate the blood The underlying cardiopulmonary status of the patient
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Life-Threatening Hemoptysis
> 100 ml/hour or, > ml/day Immediately life-threatening (massive) Not immediately life-threatening Judgment
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Confirmation and Localization
Hemoptysis vs. hematemesis vs. pseudohemoptysis Focal vs. diffuse hemoptysis History and physical Imaging Endoscopy, other Management and prognosis varies considerably for each of these clinical conditions
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Etiology TB is the most common cause worldwide
Acute and chronic bronchitis accounts for at least 50% of cases in industrialized regions Do not attribute hemoptysis to AB or CB in older individuals, smokers, or those with lung disease until more sinister pathology has been ruled-out 7% of lung cancer patients present with hemoptysis
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Etiology Vascular Infections Pneumonia Abscess TB Bronchiectasis
Fungus (aspergilloma) Pulmonary embolism with infarction of lung tissue Heart failure Mitral stensis Vasculitis Coagulopathies Cancer Other Bronchogenic carcinoma Carcinoid tumors Metastases Adenomas (children) Trauma Cystic fibrosis Drugs (cocaine) Iatrogenic Endometriosis Parasites Idiopathic (15 – 30%)
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Chest Radiography
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Angiography/Embolization
Bronchial Artery Angiography/Embolization Angiography can be used for both diagnostic and therapeutic purposes Embolization (coils or beads) will achieve temporary control of bleeding in 90% of patients Bleeding often recurs weeks-to-months later unless the underlying cause can be treated definitively Conversion of acute, life-threatening hemoptysis into a controlled situation that can be managed electively Control of bleeding in patients with limited cardiopulmonary reserve
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Definitive Treatment Many cases can be managed with bronchoscopy +/- embolization + medical therapy (pneumonia; tuberculosis; pulmonary embolism with infarction) In other cases bronchoscopy + embolization + medical therapy offers only a temporary solution Surgery remains an option when there is a structural problem not responding or amenable to more conservative treatment (localized, severe bronchiectasis not responding to medical therapy) Lobectomy or pneumonectomy Elective surgery is better than emergency surgery
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Pulmonary Thromboembolic Disease
Experienced clinicians can synthesize information from history, physical, and routine lab data into a meaningful pre-test probability (PTP) for DVT/PE
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Deep Venous Thrombosis
Contrast venography is the gold standard Doppler venous ultrasonography has excellent predictive values and fewer complications
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Pulmonary Embolism: CXR
Normal Nonspecific Unilateral volume loss/elevation of hemidiaphragm Atelectasis Regional oligemia (Westermark’s sign) Peripheral wedge-shaped density due to infarction of tissue (Hampton’s hump) Enlargement of pulmonary arterial shadow Pleural effusion
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Pulmonary Embolism: Diagnosis
Helical CT imaging or CT angiography Identification of alternative diagnosis Sensitivity for PE 80 – 98%; high specificity <2% risk of subsequent PE if CT is negative and clinical suspicion is low Pulmonary angiography (remains the gold standard) Multimodality algorithms
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Pulmonary Embolism: Treatment
Prevention of DVT/PE is critical Look for hypercoagulability (history, physical, lab) Supportive therapy; empiric treatment is often necessary Unfractionated or LMW heparin for at least 5 days followed by, Warfarin to keep INR 2.0 – 3.0 Overlap 2 – 4 days Thrombolytic therapy remains controversial (massive PE with hemodynamic instability despite IV fluids and pressor agents; in consultation with critical care)
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Pulmonary Embolism: Treatment
IVC interruption as a last resort Reversible risk: 3 – 6 months Idiopathic DVT/PE: months; evidence suggests that >6 months is better Ongoing risk or life threatening: indefinite
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CPR Airway – Open the patients airway
Head tilt-chin lift - Place the palm of one hand on the victim’s forehead and tilt the head back by applying firm backward pressure. Gently lift the chin with two fingers of the other hand Jaw thrust - Lift the angles of the jaw forward without bending the neck
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Head tilt-chin lift Jaw thrust
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CPR Breathing – hold the airway open and look, listen, and feel to see if the patient is breathing. If the patient is not breathing give two slow rescue breaths
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CPR Breathing (cont’d) Mouth-to-mouth technique
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CPR Breathing (cont’d) Barrier devices Face shields Face masks
Cephalic technique Lateral technique
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CPR Breathing (cont’d) Bag-mask respiration
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Thank you… Questions shall now be entertained…
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