physiology / pathology of the pulmonary system

7/22/2019 PHYSIOLOGY / PATHOLOGY OF THE PULMONARY SYSTEM

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PHYSIOLOGY / PATHOLOGYOF

THE PULMONARY SYSTEM

Michael Guerra, PA!C, MS

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Contact MePlease feel free to contact me if you have any questionsor comments about today’s lecture.

[email protected]

[email protected]

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mailto:[email protected]






Objectives

Part 1

• Understand normal pulmonary physiology

• Ventilation: transport of gas to alveoli

• Respiration: alveolar-capillary gas exchange• Pulmonary Defense mechanisms

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Objectives

Part 2

• Understand common pathology affectinglungs

• Gas transport problems

• Gas exchange problems

• Pulmonary Defense mechanism failures

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Function of Pulmonary System

• Provides O2

• Eliminates CO2

• Regulate H+ concentration (body pH)

• Phonation

• Defense

• Controls enzymes

• Dissolves blood clots

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Anatomy of AirwaysConducting airways

• Upper airways

• Nasopharynx

• Oropharynx

Larynx

• Connects upper and lowerairways

Lower airways

• Trachea

• Bronchi

• Terminal bronchioles

• Alveoli 6

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Airway Anatomy

• Upper Airway

• Transition

• Lower Airway

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Conducting Airways

• Defenses: cough, sneeze, mucocilliary

elevator traps and eliminates microbes,chemicals foreign matter

• Warms and humidifiers air

• Low resistance pathway to alveoli

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Ventilation -vs- Respiration

Conducting Airways (ventilation)

• Trachea, bronchi, bronchioles, terminal

bronchioles

Airways that exchange gases (respiration)

• Respiratory bronchioles• Alveolar ducts

• Alveoli9

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Histology of Airways

• MOST airway

resistance is in larger

(non-respiratory)

conducting airways

• Respiratory (small)

airways offer LEASTairway resistance--

why?

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Ventilation

• Movement of gas or air into and outof the lungs (your text definition)

• Not necessarily reflected in observedresp. rate

1) Provides O2 for respiration2) Eliminates CO2 fromrespiration

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Respiration

• The exchange of oxygen and carbon

dioxide during cellular metabolism (your

text definition)

• Occurs in the “Respiratory Bronchioles”

and Alveoli

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Respiration

Respiration

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The Alveoli

• 300 million: surface area = tennis court

• Type 1 Alveolar cells: epithelial, flat onecells

• Type 2 Alveolar cells: thicker, surfactantproducing cells

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Alveoli Histology

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Alveoli Histology

alveolar air : alveolar capillary separated by 0.2 microns

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Surfactant

• Reduces

cohesion of H2O

• Reduces surface

tension

• Increases lungcompliance (makes

easier to inflate)

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Mechanics of Ventilation

• 2 layers pleura: visceral

and parietal

• Pleura separated by thinlayer (intra-pleural fluid)

• Diaphragm

• Intra-pleural pressure is

subatmospheric--why is

this useful?

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Ventilation Physiology• Air moves from high (gas in mouth) to low (gas

in alveoli) pressure

• Flow is proportional to change in pressure

between high and low points

• Flow is inversely proportional to airway

resistance (most affected by diameter of airways)

• Pressures in lungs are at atmosphericpressure (760 mmHg at sea level)

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Boyle’s Law

• Volume of a container

and Pressure within

that container are

inversely related (at

constant temp.)

• Lung expansion (inc.volume container) will

decrease pressure of

gas in lungs19

expiration

inspiration

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Mechanics of Ventilation

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Elasticity / Compliance(opposing forces)

• Compliance

(stiffness) is a

measure of lungand chest

distensibility

• Elasticity is a

measure of recoil

property of lungs(think rubber band) 21

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Pneumothorax

• Elastic recoil of lung will collapse if sub-

atmospheric intrapleural pressure is lost

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Pulmonary Circulation• Hypoxic vasoconstriction (low PAO2)

• Blood is shunted to well-ventilated portions of

the lungs

• Better ventilation-perfusion matching

• Excessive pulmonary hypoxia all segments of

the lungs--may result in vasoconstriction and

pulmonary hypertension

• Acidemia also causes pulmonary artery

constriction

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Neurolgy of Ventilation

Neurochemical control

• Lung receptors

• Irritant receptors

• Stretch receptors

• J-receptors

Chemoreceptors

• Central chemoreceptors

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Neurolgy of Ventilation

• Inspiration: burst of action potentials

in nerves to respiratory muscles

• Insp. neurons primarily in Medulla

• Synchrony of Insp. and Exp. is

complex autonomic control:

• Central chemoreceptors (medulla)

• Peripheral chemoreceptors (carotid / aortic

bodies)

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Summary of Inspiration• Diaphragm and inspiratory muscles contract

• Thorax expands

• Increase pressure gradient: mouth > lungs

• Pressure in lungs becomes

subatmospheric

• Lungs expand

• Air flows into alveoli

IN

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Summary of Expiration

• Diaphragm and inspiratory muscles STOP

contracting

• Thorax contracts

• Increase pressure gradient: lungs > mouth

• Lungs recoil (due to elasticity)• Air flows out of alveoli

OUT

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h



Atmospheric Gases

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21%

78%

Earth Barometric Pressure = 760mmHg (sea level)

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Dalton’s Law of Partial Pressure

159mmHg

592mmHg

Earth Barometric Pressure = 760mmHg (sea level)

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Al l G



Alveolar Gases

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R i i



Respiration

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A G di t



A-a Gradient(Alveolar-arterial Gradient)

• Reflects difference between Alveolar

oxygen and arterial blood oxygen

• Average is 5-10mmHg

• e.g. 105 PAO2– 95 PaO2• = A-a gradient of 10mmHg A=105

a=9532

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F ff i R i i



Factors affecting Respiration

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F ff i R i i




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F ff i R i i




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Al l O2



Alveolar O2

• Factors that result in changes in PAO2

are:

• PACO2

• Inspired Oxygen concentration (room air

versus enriched O2)• Ventilation

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Al l CO2



Alveolar CO2

• Factor which results in changes inPACO2 is:

• Ventilation

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H i



Hypoxemia (low arterial O2)

• Resting PaO2 normally > 70mmHg

• A PaO2 of 60mmHg is lower limit of safety

• Decreases in PaO2 occur with:

• aging

• Intracardiac shunt

• Intrapulmonary shunt

• V/Q mismatch

• Alveolar hypoventilation (high CO2)36

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C f H i



Causes of Hypoxemia

• 1) Decreased O2 content (think high altitude)

• 2) V/Q (ventilation/perfusion) mismatch)

• 3) Shunt (R to L)

• 4) Diffusion problem

• 5) Hypoventilation (this means HIGH CO2 NOT

decreased resp. rate--think COPD)

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C Hi h t i l CO2



Causes High arterial CO2• Anything that impairs normal

ventilation

• Acute and chronic respiratory failure

• Respiratory arrest

• COPD

• Neuromuscular diseases

• V/Q mismatching

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O h l bi Di i ti C



Oxyhemoglobin-Dissociation Curve

Many

reasons for normal

curve to

shift leftleft or rightright

Carbon Monoxide poisoning

Fever

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Causes of Low arterial CO2



Causes of Low arterial CO2

• Anything that increases ventilation

• Acute anxiety (hyperventilation)

• Compensatory responses to: Metabolic

problems

• Hypoxemia (think asthma andpneumonia)

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Review Questions



Review Questions1) Surfactant is produced by type 2 alveolar cells, and allows alveoli to inflate at

LOWER intra-pulmonary gas pressure.

• a) TRUE

• b) FALSE

2) A patient in DKA (Diabetic Ketoacidosis) presents with a RR of 40 breaths per

minute. Given this information, you may assume this patient has:

• a) hypoxemia

• b) hypoventilating

• c) an arterial CO2 that is likely high

• d) an arterial CO2 that is likely low

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Review Questions



Review Questions

3) BOTH O2 and CO2 have similar diffusion coefficients (diffuse through alveoli to

capillary with equal ease).

• a) TRUE

• b) FALSE

4) Premature birth (before development of type 2 cell development) will result in an

infant with:

• a) increased lung compliance

• b) decreased lung compliance

• c) no impairment of normal lung compliance

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Review Questions



Review Questions

5) Elasticity of the lungs is DECREASED in patients with advanced emphysema.

• a) TRUE

• b) FALSE

6) The MOST influential factor influencing ventilation in otherwise healthy humans

is:

• a) peripheral chemoreceptors

• b) central chemoreceptors

• c) J-receptors

• d) Lung stretch receptors

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Review Questions



Review Questions7) Diaphragmatic relaxation and the lung recoil account for expiration while breathing normally at rest.

• a) TRUE

• b) FALSE

8) The partial pressure of oxygen varies according to barometric pressure (BP) of the

surrounding atmosphere. What would be the approximate partial pressure of O2 at a

BP of 600mmHg.

• a) about 160mmHg

• b) about 200mmHg

• c) about 126mmHg

• d) about 760mmHg

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Review Questions



Review Questions9) Ventilation is the single MOST important factor regarding changes in Alveolar

CO2.

• a) TRUE

• b) FALSE

10) Arterial PaO2 in a blood gas sample is noted to be 59mmHg. You correctly

conclude that the corresponding O2 saturation (think dissociation curve) is about:

• a) 100%

• b) 90%

• c) 80%

• d) 70%

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BREAK!



BREAK!

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Pulmonary Pathophysiology



y p y gy(when things go wrong)

Michael Guerra, PA!C, MS

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Definitions



Definitions

Dyspnea: subjective sense of SOB oruncomfortable breathing

• Subjective: the patient tells you they feel(not

the clinician’s perception)

• Many etiologies

• Mechanism unclear: possibly due to changesin chest wall / lungs / chemoreceptors:

afferents stimulate CNS DYSPNEA

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Definitions



Definitions

• Hypoxemia: low arterial blood oxygen

• Hypoxia : low cellular oxygen (mitochondria)

• Hypercapnia: elevated arterial CO2 (hypoventilation)

• Hypocapnia: low arterial CO2 (hyperventilation)

• Atelectasis: alveolar collapse

• compression vs absorption

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Definitions



Definitions• Orthopnea: dyspnea associated with position of lying

down (many causes)

• PND (Paroxysmal Nocturnal Dyspnea): acute

positional (lying) dyspnea; often awakens pt. from sleep(think CHF)

• Hypoventilation: inadequate alveolar ventilation

(elevated CO2)

• Hyperventilation: excessive alveolar alveolar

ventilation (low CO2)

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Definitions



Definitions

• Cyanosis: bluish skin discoloration due

to desaturated hemoglobin.

• Desaturate 5g of available Hb todemonstrate clinical cyanosis

• Many etiologies

• LATE objective evidence ofhypoxemia

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Definitions



Definitions

• Cyanosis: bluish skin discoloration due

to desaturated hemoglobin.

• Desaturate 5g of available Hb todemonstrate clinical cyanosis

• Many etiologies

• LATE objective evidence ofhypoxemia

Can a patient be cyanotic and NOT have hyoxemia?

5151

Cough



CoughAcute: (< 3 wks duration);

• is usually inflammatory; URI, pneumonia, acute

asthma attack

Chronic: ( > 3wks duration);

• in non-smokers usually post-nasal drainage

• in smokers usually chronic bronchitis• also think about: GERD, CHF, Asthma, CA,

• Drugs: ACE and Beta Blockers

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Pulmonary Pain



Pulmonary PainMay originate in parietal pleura, airways or chest wall

• 1) Pleural pain: worse with respiratory motion (pleurodynia)

• acute pleurisy, PE or infarct

• 2) Airways: central or global chest pain

• acute bronchitis and pneumonia

• 3) Chest Wall: soft tissue, muscle, rib

• often reproducible on PE (costochondritis)

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Digital Clubbing



Digital ClubbingCauses

• idiopathic

• many secondary

causes:cardiopulmonary

diseases: CA, COPD

• Mechanism of clubbingunknown

• ? circulating vasoldilator

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Lung Pathology



Lung Pathology

• MOST lung

pathology is

associated with a

pathologic change

represented in this

illustration.

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Acute Pulmonary Disease



y

• Bronchitis

• Bronchiolitis• Pneumonia

• Pulmonary Embolism (PE)

• Pulmonary Edema

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Bronchitis / Bronchiolotis



/Bronchiolotis (“happy wheezers”)

• Inflammatory obstruction of the small airways

• Most common in children

• Occurs in adults with chronic bronchitis, in association with a viralinfection, or with inhalation of toxic gases

• Acute Bronchitis

• acute bronchial inflammation; usually viral and SELF LIMITED

• cough, chest discomfort, fever: often follows URI (cold)

• unlike pneumonia, no signs lung consolidation--would you expect pt.

to c/o dyspnea?

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Pneumonia (CAP)



( )

Pneumonia Facts

• 7th leading cause death• MOST common lethal infection US

• About 5 million cases annually

• 1 million hospitalizations annually

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Pneumonia Pathophysiology



p y gy

Routes of Infection

• 1) Aspiration• 2) Inhalation

• 3) Hematogenous

• 4) Direct Inoculation

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p y gy

Routes of Infection

• 1) Aspiration• 2) Inhalation

• 3) Hematogenous


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Routes of Infection

• 1) Aspiration

• 2) Inhalation

• 3) Hematogenous


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Pneumonia Microbiology



gy

2) H. Influenza

3) Morexella

4) Staphylcoccus5) Klebsiella

6) Pseudomonas

7) Pneumocystis jiroveci

8) T.B.

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1) Pneumococcus Pneumonia (Strep. Pneumoniae)

• Encapsulated bacteria

• Many strains (>80)

• Virulence related to capsule strain

• Antibiotic resistance related to PBPon capsule (polysaccharide)

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Inflammation Cascade

• Alveolar macrophage

activation

• Complement, antibodies,cytokines

• Consolidation of air spaces

with inflammation; fluid

(exudate)

• Pulmonary vascular

congestion

• Anatomic shunt created

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Pneumonia Presentation



• Cough (rusty / bloody

sputum--think Pneumococcus)

• Fever / Chills

• Dyspnea

• Chest Pain

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Pneumonia PE Findings



Signs of consolidation:

• Rales (crackles)

• Egophony

• Bronchial breath sounds

• Fremitus• Dullness to percussion

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Pneumonia CXR



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Pneumonia CXR



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Pulmonary Embolism (PE)



• Acute blood clot in pulmonary vessel(s)

• Most common cause: DVT (deep vein thrombosis) from thigh

• Embolism may be: Blood, air, fat or tissue

Pathophysiology:

• occlusion of pulmonary circulation

• hypoxic vasoconstriction / inflammation

• atelectasis

• V/Q mismatch

• arterial hypoxemia

• clinical manifestations--death

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Acute PE



• Acute dyspnea

• Tachycardia

• Tachypnea

• Chest pain

• Low PaO2• Can be difficult Dx to make!

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Acute Pulmonary Edema



• Excess lung water (edema)

• Acute CHF (left heart failure) most common cause

• ARDS (Adult Resp. Distress Syndr.)

• capillary injury

• increased capillary permeability (leaky)• edema

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Pulmonary Edema Pathophysiology



Left Heart (pump)Failure

• increased pulmonary hydrostatic

pressure

• capillary hydrostatic > capillary

oncotic pressure

• fluid moves from interstitial

space to alveoli

• lymphatics overwhelmed

• clinically apparent edema

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Pulmonary Edema Presentation



• PND (Paroxysmal Nocturnal Dyspnea)

• Orthopnea

• Cough / wheezing (“cardiac asthma”)

• Exertional dyspnea

• Hypoxemia

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SUMMARY ALGORITHMPulmonary Edema



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Acute Pulmonary Edema



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ARDS



• Fulminant form of respiratory failure :acute lung inflammation and diffuse

alveolar-capillary injury

• Injury to: pulmonary capillary

endothelium

• Increased capillary permeability

(leaky)

• Inflammation / Platelet activation

• Surfactant inactivation

• Atelectasis

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ARDS Presentation



• Tachypnea

• Severe dyspnea

• Hypoxemia (unresponsive to

enriched O2 delivery)

• Decreased lung compliance

• Hypoventilation

• Decreased cardiac output

Death

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Pleural Disease



Pneumothorax

• Open pneumothorax

• Tension pneumothorax

• Spontaneous pneumothorax

• Secondary pneumothorax

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Acute Pneumothorax



Spontaneous Pneumothorax

• pleural integrity (parietal or visceral is violated)

• normal sub-atmospheric intrapleural pressure is

lost

1) OPEN Pneumothorax

• pleural space openly communicates withexternal environment and barometric pressure

between pleura and environment are equal

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Acute Pneumothorax



2) TENSION Pneumothorax

• one way-valve flap: airflow into pleural space

during inspiration BUT closed during expiration

• “tension” created by increasing pleural pressures

with each breath

• cardiovascular compromise / mediastinal shift due

to unilateral increase in tension

• life-threatening emergency requires immediate relief

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Open Pneumothorax



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Tension Pneumothorax



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Pleural Disease



Pleural effusion

• fluid in pleural space

1) Transudative effusion (watery): CHF, orhypoproteinemia (liver/kidney disease)

2) Exudative effusion (less watery& higher

protein content): inflammatory diseases,infections, malignancies

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Pleural Effusion



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Pleural Disease



• Pleurisy: pain associated with respiratory

motion; secondary to acute inflammation

within pleura• Hemothorax (blood in pleural space): secondary to

ruptures intrathoracic aneurysm--usually fatal)

• Empyema (pus within pleural space): secondary toinfections--bacterial pneumonia, lung abscesses

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Chronic Pulmonary Disease(COPD)



• Asthma

• Bronchiectasis (chronic dilated airways)

• Chronic Bronchitis

• Emphysema

• Pulmonary Fibrosis

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Asthma



• Chronic inflammatory airway disorder

characterized by: hyper-bronchial

reactivity reversible bronchospasm• genetic predisposition strong

• clinically presents as dyspnea, wheezing and

cough

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Asthma Pathophysiology



Early Phase

• Type I hypersensitivity IgE

mediated reaction

• triggered by allergens

• inflammatory mediators

• bronchial smooth musclespasms

• eosinophil / lymphocyte

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Late Phase

• 4-8 hours after onset acute

attack

• Fresh round mediator release

• More cells; eosinophils and

leukocytes

• More edema--sustain

inflammation

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Asthma Presentation



• Acute dyspnea / cough

• Accessory muscle use

• Prolonged expiration (why?)• Thick mucus

• Decrease O2 saturation (pulse oximetry)

• What would you expect the arterial CO2 to

be during acute attack?88

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• Airway obstruction (bronchospasm, edema) leads to

increasing airway resistance: if airway

diameter decreases by 1/2, resistanceincreases by factor of 16!

• Hyperinflation, air trapping, V/Q

mismatching hypoxemia

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Chronic Bronchitis



• Hypersecretion of

mucus /chronic

productive cough for at

least 3 mos. /yr. and forat least 2 consecutive

years

• Inspired irritants,smoking major causes

• Smoking #1

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Chronic Bronchitis



• Mucus hypersecretion leads to hypertrophy

mucus glands (goblet cell metaplasia in bronchial epithelium)

• Chronic obstruction

• Recurrent infections

• Hypoventilation--Hypoxemia--Death

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Emphysema



• Irreversible enlargement ofthe gas-exchange airways

• Destruction of alveolar walls

without obvious fibrosis

• Loss of elastic recoil

• Panacinar (resp. bronchioles and

alveolar ducts) vs

• Centriacinar (involves entire acinus)

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Emphysema Cascade



• Chronic airway Inflammation (tobacco toxins)

• alpha-1 Antitrypsin inhibition (protects against

proteases) inhibited by smoking

• Destruction of elastin

• Loss of elastic recoil

• Hyperinflation (air trapping)

• Destruction alveoli / capillaries

• Hypoventilation

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Emphysema



• Dyspnea with activity (early)

• Dyspnea at rest (late)

• Accessory muscledevelopment

• Barrel chest appearance

• Prolonged expiration (why?)

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Pulmonary Hypertension(arterial)



• Mean pulmonary artery pressure 5-10 mm Hg above normal or above 20 mm

Hg (your text definition)

• pulmonary arterial vasoconstriction and remodeling of vessels

Causes:

• 1) COPD and interstitial disease

• 2) Pulmonary Embolism (recurrent)

• 3) Heart disease with L to R shunting

• 4) Idiopathic (uncommon)

• Exertional dyspnea, fatigue, JVD, and Right Ventric. Hypert. (on chest x-

ray)95

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Cor Pulmonale



• Caused by chronic pulmonary

hypertension / pulmonary disease

• Think of it as Right-sided Heart Failure

• Chest pain, exertional dyspnea, JVD,

RVH

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Lung Cancer



• Leading cause of cancer death men / women

• MOST common Cancer worldwide

• Bronchogenic is MOST common type

1) Non-Small cell carcinoma (NSCLC)

• Adenocarcinoma (located in parenchyma--now is #1--why?)

• Squamous (located in central bronchial epithelium #2)

• Large cell carcinoma

2) Small cell carcinoma (SCLA)

3) Other Lung cancers (sm. %)

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Lung Cancer



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Lung Cancer



• Cough

• Weight loss

• Hemoptysis

• Wheezing

• Chest pain• Recurrent pneumonia

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physiology / pathology of the pulmonary system

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