Pulmonary Lecture

7/29/2019 Pulmonary Lecture

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Pulmonary

Disorders

Bill Buron, PhD, RNC, GNP/FNP-BC



Signs and Symptoms of

Pulmonary Disease

Dyspnea- subjective sensation of uncomfortable breathing

Dyspnea on exertion Orthopnea- dyspnea when a person is lying

down

Paroxysmal nocturnal dyspnea

Abnormal breathing patterns Kussmaul respirations- hyperpnea

Cheyne-Stokes respirations




Pulmonary Disease

Hypoventilation

Hypercapnia

Hyperventilation

Hypocapnia

Cough- acute vs chronic

Hemoptysis

Pain

Pleural friction rub




Pulmonary Disease

Cyanosis

Clubbing

Abnormal sputum



Oxygen Transport to the Tissues

Ventilation

Distribution

Perfusion

Exchange at the blood-gas barrier



Ventilation-Perfusion

Relationships Nomenclature

Va= gas flow (usually inliters/minute)

Q= blood flow (usually in ml /

minute)



Perfusion

In upright position, gravity causes

less blood flow to reach the higher,

upper lobes than the lower lobes

Upper alveoli receive moderate

ventilation with decreased or littleblood flow, creating a high Va/Q ratio



Perfusion

Lower alveoli receive moderately

increased ventilation and greatly

increased blood flow, creating a lower Va/Q ratio

Va/Q ratios decrease from top tobottom



Perfusion

Blood flow to lungs changes with

exercise and position



Va/Q Mismatching

Abnormal

distribution of

ventilation andperfusion

Most common

cause of

hypoxemia



Va/Q Mismatch

Hypoxia caused by

Inadequate ventilation

of well-perfused areas

of lung causes a lowV/Q

Poor perfusion of well-

ventilated areas

causes a high V/Qcalled alveloar dead

space



Acute Respiratory Failure

Inadequate gas exchange

PaO2 < 50 mmHg

PaCO2 > 50 mmHg

pH < 7.25



Pulmonary Edema



Pulmonary Edema Clinical

Manifestations

Dyspnea

Hypoxemia

Increased work of breathing

Inspiratory crackles

Dullness to percussion over lung bases

Frothy sputum (late sign)

PaCO2 increases



Aspiration

Passage of fluid and/or

solid particles into the

lungs Patients at high risk

CNS abnormalities

Decreased LOC

Altered cough/swallowingmechanism

Children



Aspiration Clinical Manifestations

Sudden onset of choking, cough

Vomiting

Dyspnea

Wheezing

Development of a chemical pneumonitis



Restrictive Patterns of

Respiratory Disease Characterized by increased stiffness

of the lungs or thorax or both

Due to decreased compliance and

reduction in all lung volumes

Causes decrease in:

Total lung capacity

Vital capacity



Restrictive Patterns of

Respiratory Disease Increased WOB

Rapid, shallow breathing noted

Alveolar hypoventilation

Inability to maintain normal blood gas

tensions



Classification of Restrictive

Patterns of Respiratory Disease: Diseases of the pleura and lung

parenchyma

Extra pulmonary Disorders



Diseases of the Pleura and Lung

Parenchyma Atelectasis:

“imperfect

expansion”Involvescollapse of a

previouslyexpandedalveoli.




Parenchyma Compression atelectasis:

compression of lung tissue from a

source outside the alveoli.

Pneumothorax/hemothorax

Pleural effusionTumors within the thorax




Parenchyma Absorption atelectasis: Obstruction of the airway

prevents air from entering the alveoli distal tothe obstruction. Absorption of gas form the

alveoli, causing the lung to collapse.

Intrinsic causes- most common isretention of secretions or exudates

Extrinsic pressure on a bronchuscommonly results form neoplasm, lymphnode enlargement, aneurysm, or scar formation



Obstruction Atelectasis



Obstructive Atelectasis



Pathogenesis of Atelectasis

Collateral ventilation- air can pass form one lung

acinus to another by other than the normal

airways. Small pores, called the pores of Kohn, between

the alveoli provide a path for collateral

ventilation to help prevent atelectasis

Prolonged atelectasis may lead to replacementof lung tissue with fibrous tissue.



Clinical Manifestations

Dyspnea

Tachycardia

Cough

Fever

Decreased chest wall expansion Hypoxemia



Diagnostic

Blood gases show hypoxemia,

hypercapnia, and a decreased pH

Chest film



Infectious Diseases

Bacterial

pneumonia-

characterizedby an intra-

alveolar

suppurativeexudates with

consolidation



Pneumococcal pneumonia

(streptococcus pneumonia) Common bacterial infection of the

lung, responsible for 30-80% of

community-acquired pneumonia

Malnutrition, alcoholism and aging

are risk factors



Pneumococcal pneumonia

(streptococcus pneumonia) Pathogenesis: an acute inflammatory response

leads to consolidation (leukocytes and fibrin) of the involved area

Clinical manifestations- sudden onset of symptoms

Fever

Cough Pleuritic chest pain

Production of rusty-colored or blood-streakedsputum



Viral or Mycoplasma Pneumonia

Characterized by an interstitial

inflammation with accumulation of an

infiltrate in the alveolar walls,although, the alveolar spaces

themselves are free of exudate and

there is no consolidation



Viral or Mycoplasma Pneumonia

Mycoplasmal pneumonia is a self -

limiting disease that is a common

cause of respiratory tract infections

Viral pneumonia is usually mild and

self-limiting in adults but may be

rapidly proliferative and be fatal in

children (usually under the age of 2)



Mycobacterium Tuberculosis

Causes patchy distribution of

granulomas, which undergo caseous

necrosis with the development of cavities



Tuberculosis Granuloma



Advanced Tuberculosis



Tuberculosis



Pneumonias

Nosocomial infections- acquired within the

hospital

More likely to be gram-negativebacteria or Staphylococcus aureus

and less likely to be caused by

pneurmococci or mycoplasma

Community based infections



Aspiration Pneumonia

Inhalation of gastric contents, food,

water, or blood into the

tracheobronchial system.

Pneumonia results when the

material is propelled into the alveolar

system. Chemical irritation form the

aspirant leads to bronchospasm,necrosis, and fibrosis of airways.



Aspiration Pneumonia

Clinical manifestations

Abrupt signs of bronchospasm

Dyspnea

Tachycardia

TachypneaCyanosis



Pneumocystis Pneumonia



Traumatic Injuries of the Chest

Wall Simple rib fracture

Fracture of several ribs (flail chest,

fluid chest)



Pleura Disorders

Pneumothorax- Air in the pleural

space form an opening in the chest

wall (through parietal pleura) or formthe lungs (through the visceral pleura)

Spontaneous Pneumothorax

Tension Pneumothorax



Pneumothorax Clinical

Manifestations Dyspnea

Chest pain

Tracheal deviation with a mediastinalshift toward the unaffected side

Unequal chest expansion

Reduced breath sounds on theaffected side



Pneumothroax



Pneumothorax



Pneumothorax



Pleural Disorders

Pleural Effusion: The accumulation

of excess fluid in the pleural cavity,

resulting from trauma or disease



Related terminology

Transudate: accumulation of fluid due to arise in pulmonary venous pressure,hypoproteinemia, or pressure form atumor on the vena cava

Hydrothorax- accumulation of pleuraltransudate

Empyema- effusion contains purulentmaterial



Related terminology

Fibrothorax- fibrous fusion of the

lung and chest wall

Hemothorax- frank blood in the

pleural fluid (trauma)

Exudate-fluid that has a higher specific gravity and protein content



Respiratory Diseases Caused by

Exposure to Organic and Inorganic Dust

Silicosis-An industrial disease (seenin masons, potters, sandblasters)

resulting form inhalation of silicondioxide

Coal Workers’ Pneumonconiosis

(black lung disease) Asbestosis



Asbestosis



Structural Restriction of Thoracic

Excursion Skeletal deformities

Compression may decrease lung

volume and cause atelectasis

Compliance and total lung capacity are

reduced



Structural Restriction of Thoracic

Excursion Pulmonary vascular bed is reduced,

causing increased work of ventilation,alveolar hypoventilation, and hypoxemia

Kyposcoliosis

Pectus Excavtum (funnel chest

Pectus Carinatum (pigeon chest) Picwickian syndrome



Obstructive Patterns of

Respiratory Disease Acute Obstructive Airway Disease

Acute bronchitis

Asthma Chronic Obstructive Airway Disease

Bronchiectasis

Cystic fibrosis Chronic bronchitis

Pulmonary emphysema



Acute Bronchitis

Caused by infection and inhalants

Inflammation of mucosal lining of tracheobronchial tree

Characterized by:

Increased secretions of mucus

Bronchial swelling

Dysfunction of cilia leading to increased resistance to

expiratory airflow



Clinical Manifestations of Acute

Bronchitis Recent history of upper respiratory infection

Chronic lung disease

Smoking

Exposure to respiratory irritants

Mucoid- viral

Mucopurulent- bacterial

Mucopurulent productive congestion Fever below 101oF

Wheezing



Asthma

Episodic disorder characterized by recurrentparoxysm of wheezing and dyspnea notattributable to other diseases

Initiated by release of chemical mediators in anIgE mast cell interaction

Results in increased bronchial secretion,mucosal swelling and bronchospasm

Classified as

Extrinsic

Intrinsic



Clinical Manifestations of Asthma

History of childhood asthma/or positive family history

Inhalation of irritants

Respiratory infection

Psychogenic factors Tightness in chest

Dyspnea

Fatigue due to increased WOB

Tachypnea/ may have pulsus paradoxus Expiratory wheezing progressing to inspiratory and

expiratory wheezing



Status Asthmaticus

Severe episode of asthma that isrefractory to therapy

Life-threatening event with increasingmortality rates

Onset of respiratory failure may besignaled by cyanosis, decreased

wheezing with progressive hypoventilationand decreased levels of consciousness



Chronic Obstructive Pulmonary

Disease Bronchiectasis

Cystic fibrosis

Chronic bronchitis.

Pulmonary emphysema



Bronchiectasis

Disease of bronchi and broncioles

Associated with chronic infection and inflammation

Irreversible dilation of bronchial tree

Clinical manifestations Childhood onset

Initiating event- pneumonia or bronchitis

Cough

Symptoms of infection Production of large amounts of mucopurulent sputum

Occasional hemoptysis



Cystic fibrosis

Hereditary disorder affecting children

Disorder affects sweat glands, bronchi, pancreas, and

mucous-secreting glands of small intestine

Clinical manifestations related to inability to handle largequantities of viscous material

Chronic cough

Persistent lung infections-especially Pseudomonas

aeruginosa and Staphylococcus aureus

Cor pulmonale



Chronic Bronchitis

Chronic bronchial inflammation withprogressive increase in productive coughand dyspnea

Bronchial mucosa becomes thick and rigiddue to vasodilatation, congestion andedema

Excessive secretion of mucous Narrowing of the passageways



Clinical Manifestations of Chronic

Bronchitis Cigarette smoking

Generally overweight

Cough

Recurrent chest infections

Marked cyanosis and edema

Clinical Manifestations of




Chronic Bronchitis

Lungs

Mild hyperinflations

Marked hypercapnia

Severe hypoxemia Wheezes

Resonant percussion

Heart

Jugular venous distention Cardiac enlargement

Liver engorgement

Peripheral edema



Pulmonary Emphysema

Chronic pulmonary disease

May be classified with chronic bronchitis

Characterized by permanent enlargementof the acinus




Pulmonary Emphysema Cigarette smoking

Exposure to chemical irritants or air pollution

Chronic respiratory infections

Exert ional dyspnea

Cough with small sputum production

Wheezing or tightness of chest

Tachypnea at rest or with mild exertion Flushed

Purse lipped breathing




Pulmonary Emphysema Decreased PaO2 in late stage

Chronic increase in PaCO2

Increased RV

Prolonged FEV1

Acute Respiratory Distress



Acute Respiratory Distress

Syndrome

Acute lung inflammation

Diffuse alveolocapillary injury

Non cardiac pulmonary edema

Adult Respiratory Distress



Adult Respiratory Distress

Syndrome (ARDS)

Manifests within 72 hours following the

predisposing insult

Characterized by noncardiogenicpulmonary edema, collapsed and fluid-

filled alveoli and severe hypoxemia

Incidence – 200,000-250,000 cases/year Mortality 40-90%



ARDS Risk Factors

Shock

Sepsis

Hypothermia/hyperthermia

Drug overdose

DIC

Massive transfusion Cardiopulmonary

bypass

Eclampsia

Burns

Pancreatitis Severe nonthoracic

trauma

Pneumonia

Inhalation therapy

Aspiration



ARDS

Change in lung compliance

Decreased in ARDS and lungs become “stiff”

Increased accumulation of secretions andmediator-induced bronchoconstriction

Radiographic Changes

Increasing alveolar atelectasis, consolidation Development of air bronchograms



Assessment of ARDS

Tachypnea

Dyspnea

Tachycardia

Lung crackles

Refractory hypoxia

Hypercarbia- (LATE SIGN!!)

Intrapulmonary shunt



ARDS Management

Oxygenation and ventilation

Mechanical ventilation

Small tidal volumes (<10 ml/kg) to minimize airway pressures

Extracorporeal lung assist

Positioning- prone positioning being explored

Pharmacological therapy

Corticosteroids

Antibiotic therapy

Bronchodilators

Exogenous surfactant replacement

Nitric oxide

Antioxidants

Nutritional Support

Patients require 35-45 Kcal/kg/day

TPN

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