Forefront in Medical And Traumatic Emergencies

Modesto T. Kapuno, MD, CSEE, MNSA

BU College of Nursing December 16, 2004

Respiratory System

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

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

Respiratory System Divisions

• Upper tract– Nose, pharynx and

associated structures

• Lower tract– Larynx, trachea,

bronchi, lungs

Nose and 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

Nasal Cavity and Pharynx

1 2

3

4

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

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

Pseudo stratified ciliated columnar epithelium with

goblet cells

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

Tracheobronchial Tree

1

2

3

4

5

6

7

Respiratory zone

Conducting zone

Bronchioles and Alveoli

12

34

5

Alveolus and Respiratory Membrane

Gas Exchange

Lungs

• Two lungs: Principal organs of respiration– Right lung: Three lobes– Left lung: Two lobes

• Divisions– Lobes, bronchopulmonary segments, lobules

Thoracic WallsMuscles of Respiration

1

2

Inspiration

Active process involving thediaphragm and intercostal muscles

Expiration

Usually passive -can become active using internal intercostals and abdominal muscles

Elasticity

• Lungs are compliant- they have the ability

to stretch and recoil like a balloon

Apnea and Dyspnea

• Apnea- absence or cessation of breathing

• Dyspnea- difficulty of breathing

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

Alveolar Membrane

1) Surfactant and water layer2) Alveolar wall- Simple squamous

epithelium3) Basement membrane of alveolar wall4) Interstitial space5) Capillary wall- Simple squamous

epithelium6) Basement membrane of cap wall

Alveolar Capillary Membrane

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

Blood flow through the lungsTwo 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.

Pleura

• Pleural fluid produced by pleural membranes– Acts as lubricant– Helps hold parietal and visceral pleural

membranes together

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

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

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

Pulmonary Volumes• Tidal 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

Pulmonary Capacities

• Inspiratory 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

Respiratory ProblemsAll respiratory problems can be

categorized as:

Impacting ventilation,

Diffusion, or

Perfusion

Management can be initiated once this can be established

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

Diffusion

• Inadequate O2

• Alveolar pathology

• Interstitial space pathology

• Capillary bed pathology

• Fire, CO poisoning

• Lung disease, inhalation injury

• Pulmonary edema, drowning

• Severe artherosclerosis

Perfusion

• Inadequate blood volume/ Hgb

• Impaired circulation

• Capillary wall pathology

• Shock, anemia

• Pulmonary embolus

• Trauma

Interventions

• Ensure that the upper and lower airways are open and unobstructed

• Provide assisted ventilations

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

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

Interventions

• Provide high flow O2

• Reduce inflammation of interstitial space

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

Perfusion

• Refers to the process of circulating blood through the pulmonary capillary bed

Interventions

• Ensure adequate circulating volume and Hgb levels

• Optimize left sided heart function

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

Assessment Review

• Scene size up

• Wide variety of toxic environments resulting in deficient O2

• Initial Assessment

• Recognition of life threats

• Focused history

• Physical exam

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

Focused History• Dyspnea• Chest pain• Productive/ nonproductive cough• Hemoptysis• Wheezes• Infection- fever, sputum• Previous experience• Patient’s description of severity• Medications

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

• 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

Sputum

• Infection/pneumonia- thick, green, brown

• Allergies/inflammatory- yellow, pale grey

• Pulmonary edema- pink, frothy

Chronic Obstructive Airway Disease

• Chronic bronchitis

• Emphysema

• Asthma

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

• “Blue bloaters”- appear cyanotic,decreased pO2 due to altered ventilation-perfusion

• Polycythemia common secondary to chronic hypoxemia

• Increased airway resistance during inspiration and expiration

Signs and Symptoms

• Typically overweight

• Productive cough with sputum

• Coarse rhonci

• Mild chronic dyspnea

• Resistance on inspiration and expiration

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

• 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

Signs and Symptoms

• Thin, barrel chested

• Nonproductive cough

• Wheezing, rhonchi

• Pink complexion

• Extreme DOE

• Prolonged expiration

• Pursed lips

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

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

• 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

Signs and Symptoms of Severe Asthma

• Obtundation

• Diaphoresis and pallor

• Retractions

• One, two word sentences

• Poor muscle tone

• HR > 130, RR >30

Management• High flow O2, IV-rehydration, CM• Nebulized Beta agonists• Albuterol 2.5-5.0mg• Alupent• Corticosteroids- solumedrol• Aminophylline• MgSO4• Epinephrine- SQ 0.3-0.5mg• Ketamine

Intubation• Support patient’s

failing ventilation efforts- does not solve problem

• Irritation due to intubation may increase bronchospasm

• Increased air trapping• Poor compliance

Medical Respiratory Conditions/Diseases

1. Hyperbaric—Bends, Decompression2. Pneumonia3. Hypoxia4. Hyperventilation5. High Altitude6. Emphysema7. Tuberculosis8. Lung Cancer9. Cystic Fibrosis10. Asthma

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

Left lung with pneumonia

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

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

High Altitudes

• Low air density, low oxygen pressure

• Increases RBC production

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

Bronchitis

• Chronic obstructive pulmonary disease

• Inhale irritants, causes mucous production to increase

• Inflammation

• Obstruct airways

• Less air flow

Tuberculosis

• Bacteria

• Spread by cough

• Live in alveoli in lungs

• Antibiotics for 12 month to cure

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

Cystic fibrosis:

• Oversecretion of mucous that clogs respiratory passageways

Asthma:• External factors cause• Allergy• Respiratory passages swell• Bronchioles constrict

Traumatic and Medical Respiratory Emergencies

PneumothoraxMassive Hemothorax

Hemoptysis Flail Chest

Pulmonary Embolism

Pneumothorax

• Accumulation of air within the pleural space

• Secondary collapse of the lung

Etiology1. Rupture of visceral

pleura with secondary leak of air from the lung (Tension pneumothorax)

2. Loss of integrity of chest wall (open pneumothorax)

3. Mixed (tension-open pneumothorax)

Rupture of bronchus or trachea

Rupture of esophagus

Pathology Presentation

Presentation

Asymptomatic . life-threatening

Sudden-onet Dyspnea, dry cough,

ipsilateral pleuritic chest pain

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

Pathophysiology

Apex to base pressure gradient ↓

Lung compliance ↓ FRC ↓ Ventilation ↓ Oxygenation ↓

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

Diagnosis

• Clinical assessment - Chest radiograph - AP CXR - PA and lateral CXR• Expiratory PA CXR• CT imaging of the chest

Visceral pleuralsurface of lungAbsence of lung

markings

Chest Radiograph

Chest Radiograph

Classification

Spontaneous - Primary spontaneous - Secondary spontaneous Traumatic - Chest wall

- Tracheobronchial airway injury - Disruption of lung visceral surface Iatrogenic Other

Tension ornon-tension

General Management (c)ABC Suspected tension pneumothorax –

emergency decompression of the pleural space

Large-bore (14 -16 gauge) angiocatheter inserted into the second intercostal space in the midclavicular line followed immediately by,

Tube thoracostomy In extremis? Consider bilateral

pleural space decompression

Angiocath and Chest Tube Insertion

1. Use blade to cut skin only

2. Blunt dissection through interspace with Kelly and/or gloved finger (avoid trocars)

3. Explore pleural space with gloved finger and then insert tube 20 cm

4. Attach chest tube to a pleural drainage system and apply – 20 cm H2O pressure

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• 25 - 35% risk of recurrence by 5 years

(most in the 1st year)• Recurrence – (1st) 25%, (2nd) 50%,

(3rd) 80%

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

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

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

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 (>50 - 60% by 5 years)

Significant risk of mortality

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

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

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

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.

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

Approach to Hemoptysis

(c)ABC’s↓

History↓

Physcial Exam↓

CXR/Lab Evaluation↓

Special Procedures↓

Therapeutic Intervention↓

Evaluation of Response

Sputum analysis

BronchoscopyCT imaging of

the chestV/Q scanning

BronchscopyEmbolizationMedical therapySurgery

Stabilization: (c)ABC

Airway and Breathing:Position patient sitting upright or with the affected lung dependentSupplemental oxygenSuctioning of secretionsIntubation and ventilation if necessaryCough suppression (codeine or other narcotics)

Intubation and ventilation:Facilitates airway suctioningImproves ventilation and gas exchange (PEEP)Facilitates fiberoptic bronchoscopyAllows for sedation/patient comfortCan 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

Stabilization: (c)ABC

Circulation:Obtain 2 large-bore IV’sCrossmatchImmediate fluid esuscitation with crystalloidUse packed RBC’s and/or fresh frozen plasma as necessaryMonitor hemodynamics frequently (HR, BP, urine output, central venous pressure)

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

Life-Threatening Hemoptysis

Hemoptysis

> 100 ml/houror,> 400 - 600ml/day

Immediatelylife-threatening

(massive)Not

immediatelylife-threatening

Judgment

Confirmation and Localization

Hemoptysis vs. hematemesis vs. pseudohemoptysisFocal vs. diffuse hemoptysis

History and physicalImaging

Endoscopy, otherManagement and prognosis varies considerably for each of these clinical conditions

Etiology

TB is the most common cause worldwideAcute 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

Etiology

PneumoniaAbscessTBBronchiectasisFungus (aspergilloma)

Infections

Other Cancer

VascularPulmonary embolism with infarction of lung tissueHeart failureMitral stensisVasculitisCoagulopathies

Bronchogenic carcinomaCarcinoid tumorsMetastasesAdenomas (children)

TraumaCystic fibrosisDrugs (cocaine)IatrogenicEndometriosisParasitesIdiopathic (15 – 30%)

Chest Radiography

Bronchial ArteryAngiography/Embolization

Angiography can be used for both diagnostic and therapeutic purposesEmbolization (coils or beads) will achieve temporary control of bleeding in 90% of patientsBleeding 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 electivelyControl of bleeding in patients with limited cardiopulmonary reserve

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 solutionSurgery 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 pneumonectomyElective surgery is better than emergency surgery

Pulmonary ThromboembolicDisease

Experienced clinicians can synthesize information from history, physical, and routine lab data into a meaningful pre-test probability (PTP) for DVT/PE

Deep Venous Thrombosis

Contrast venography is the gold standardDoppler venous ultrasonography has excellent predictive values and fewer complications

Pulmonary Embolism: CXR

NormalNonspecificUnilateral volume loss/elevation of hemidiaphragmAtelectasisRegional oligemia (Westermark’s sign)Peripheral wedge-shaped density due to infarction of tissue (Hampton’s hump)Enlargement of pulmonary arterial shadowPleural effusion

Pulmonary Embolism: Diagnosis

Helical CT imaging or CT angiographyIdentification of alternative diagnosisSensitivity for PE 80 – 98%; high specificity<2% risk of subsequent PE if CT is negative and clinical suspicion is lowPulmonary angiography (remains the gold standard) Multimodality algorithms

Pulmonary Embolism: Treatment

Prevention of DVT/PE is criticalLook for hypercoagulability (history, physical, lab)Supportive therapy; empiric treatment is often necessaryUnfractionated or LMW heparin for at least 5 days followed by,Warfarin to keep INR 2.0 – 3.0Overlap 2 – 4 daysThrombolytic therapy remains controversial (massive PE with hemodynamic instability despite IV fluids and pressor agents; in consultation with critical care)

Pulmonary Embolism: Treatment

IVC interruption as a last resort

Reversible risk: 3 – 6 months Idiopathic DVT/PE: 6 - 12 months; evidence suggests that >6 months is better Ongoing risk or life threatening: indefinite

• 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

CPR

Head tilt-chin lift

Jaw thrust

• 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

CPR

• Breathing (cont’d)– Mouth-to-mouth technique

CPR

• Breathing (cont’d)– Barrier devices

• Face shields

• Face masks

–Cephalic technique

–Lateral technique

CPR

• Breathing (cont’d)– Bag-mask respiration

CPR

Thank you…

Questions shall now be entertained…