Pulmonary Pathophysiology

MEHighfield
credit to: Peggy Kalowes, RN, MSN, CNRN, CNS

n     Provides the Body With O2

n     Removes CO2---Waste Product of Cellular Metabolism

n     Regulates Acid-base Balance

GAS EXCHANGE AIRWAYS
ALVEOLI---MOST IMPORTANT STRUCUTRES IN GAS EXCHANGE

 

ALVEOLAR CELLS

TYPE I

     Gas exchange

TYPE II

     Secrete surfactant

             ROLE OF PULMONARY                                           SURFACTANT

è Reduction of Surfactant makes lung expansion more difficult; the greater the surface tension, the greater the pressure needed to overcome it

PHYSIOLOGY OF RESPIRATION

n      VENTILATION- refers to the movement of air into & out of the lungs

n     MECHANICS OF VENTILATION

â  Elasticity

â  Compliance

â  Resistance

â  Pressure

PHYSIOLOGY OF RESPIRATION: COMPLIANCE

 PHSIOLOGY OF RESPIRATION: RESISTANCE

Age effects

n     Children have

u  Higher elasticity & compliance

u  Smaller, “softer airways

n     Older adults

u  Lower lung volumes

u  Less elasticity & compliance

u  Increase curvature of vertebrae

Pulmonary Function Tests: Measurements of Lung Volumes and Capacities

n      Tidal volume

n      Expiratory reserve volume

n      Inspiratory reserve volume

n      Vital Capacity = Tidal + ERV + IRV

n      Residual volume

n      Total lung capacity = all

n      Inspiratory capacity = Tidal+IRV

n      Functional residual capacity = ERV + RV

PULMONARY BLOOD &
LYMPH SUPPLY

 

   2 Vascular Systems +  Lymphatic System =  Pulmonary Blood & Lymph Supply.

n      PULMONARY- provides lungs with blood for gas exchange around alveoli

n      BRONCHIAL-provides oxygen to the bronchi & other pulmonary tissues.

VENTILATION & PERFUSION

FACTORS AFFECTING ALVEOLAR-CAPILLARY GAS EXCHANGE

Functional Components

n     Mechanism of breathing

n     Gas Transport

n     Regulation of respiration: neurochemical control

n     Control of pulmonary circulation

Mechanism of Breathing

n     Respiratory muscles

n     Elastic properties of lung and chest wall: elasticity, elastic recoil, compliance

n     Resistance to air flow

n     Ventilation pressure: atmospheric, intrapleural, intrapulmonic

u  Inhalation/inspiration

u  Exhalation/expiration

Regulation of Respiration

n     An excess of CO2 lowers the blood pH. A low pH causes the medulla to increase respirations in an effort to blow off more CO2 and thus raise the pH to normal

n     Chemoreceptors in major vessels sense low 02 & send signals to increase respirations to raise 02.

Alteration in Pulmonary Dysfunction: S/S of Pulmonary Disease

n     Dypnea, Orthopnea, Paroxymal Nocturnal Dyspnea (PND)

n     Cough

n     Hemoptysis

n     Cyanosis

n     Chest wall or pleural pain

n     Clubbing

n     Abnormal sputum

Abnormal Breathing Patterns

n     Kussmaul respirations

n     Labor or obstructed breathing

n     Restricted breathing

n     Cheyne-stokes

n     Hypo-/hyper-ventilation

Restrictive Disease

n    Difficulty inhaling

u Atelectasis: 2 types

u Pulmonary edema

u Flail chest

u Pneumothorax

u Pleural effusion

Acute respiratory failure

n     ARDS

u  Insult

u  Inflammation

u  Pulmonary edema

u  Type II pneumocyte damage

(H&M p. 751)

Obstructive Disease

n     Difficulty Exhaling

u  Asthma

u  Bronchitis

u  Emphysema

u  COPD

Obstructive Pulmonary Disease: Asthma

n     Lung disease characterized by airway obstruction, airway inflammation, airway hypperresponsiveness, and episodic of bronchospasm.

Asthma

n     The scheme for asthma classification has been revised in the U.S. from one based on etiology and pathophysiology to one based on clinical severity.

Pathophysiology

n     Allergic response to allergens which leads to mast cell degranulation and release of bronchoactive and vasoactive mediators

n     Allergic rhinitis with bronchoconstriction

n     Bronchial hyperresponsiveness: exaggerated bronchospastic response, increased functions of the inflammatory response, & degranulation of eosinophils

n     Smooth muscle contraction

n     Microvascular leakage

Clinical Manifestations

n      During full remission individuals are asymptomatic

n      Acute attack=anxiety, cyanosis, chest constriction, inspiratory and expiratory wheezing, dyspnea, non productive coughing, prolonged expiration, tachycardia, tachypnea.  With severe attacks the accessory muscles of respiration are prominent. NO wheezing if severe enuff to block air entirely.

Key factors to remember with respect to drug treatment

 

n    Airway obstruction

n    Airway hyperresponsiveness

n    Airway inflammation

Rule of Two’s:
Is asthma controlled?

n      A 'yes' answer to any of these questions indicates that the patient's asthma is not under control:

 

u  * Do you have more than two uses of rescue medication a week?

 

u  * Do you wake up because of your asthma more than two nights a month?

 

u  * Do you go through more than two canisters of rescue medication a year?

Chronic Obstructive Pulmonary Disease (COPD)

n      Pathologic lung changes

n      Characterized by abnormal tests of expiratory flow

n      Airflow limitation is worse during expiration

n      Results from inflammation and structural damage to alveoli and airway

COPD

n     Chronic Bronchitis

n     Emphysema

Epidemiology

n     4th leading cause of death in the United States

n     100,000 deaths in U.S. in 1996

n     Smoking accounts for >90% of the risk of COPD

Risk Factors

n      Passive smoke, occupational exposures

n      SES, airway hyperresponsiveness, family history, and past respiratory illness

n      Genetic enzyme deficiencies (alpha1-antitrypsin and chymotrypsin) account for only a very small percentage of the cases

Pathophysiology

n     Many  patients with COPD have characteristics of both emphysema and chronic bronchitis, with one or the other pathophysiologic processes predominating

Pathophysiology: Emphysema

n     Reduced elastic recoil resulting in expiratory airway collapse and hyperinflation; disintegration of alveolar walls and bulla formation

n     Inhibition of the activity the lung antielastases, leading to elastic fiber damage, loss of normal airway and destruction of alveolar walls

Pathophysiology: Emphysema

n     Loss of alveolar surface area

n     Airway collapse during expiration with airtrapping leads to hyperexpansion of the lung

n     Destruction of alveolar septa

Emphysema:
Clinical picture

n     History: active or passive smoke hx; occupational hx; hx of cough and dyspnea; progressive exercise limitation; possible family hx in non smoker

n     Symptoms: progressive dyspnea on exertion, paroxymal nocturnal dyspnea, pedal edema, weight loss

On Examination

n      Decreased LOC and cyanosis during severe exacerbations

n      Increased A/P chest diameter (barrel chest)

n      Use of accessory muscles of breathing

n      Decreased breath sounds

n      Prolonged expiratory phase

n      Expiratory wheezing

n      clubbing and pedal edema with advanced disease

Pathophysiology: Bronchitis

n      Chronic cough productive of phlegm for at least 3 months per year for at least 2 consecutive years

n      Increase in goblet cells in the airway mucosa with hypertrophy and hyperplasia of submucosal glands and production of copious tenacious amounts of sputum

n      Assc. with epithelial inflammation and smooth muscle hypertrophy lead to scarring

Bronchitis: Clinical picture

n     History: hx of smoking, recurrent pulmonary infections with copious sputum production of most days for least 3 months per year for at least 2 years

n     Symptoms: productive cough with episodes of increased dyspnea with production of discolored sputum; pedal edema

On Examination:

n     May be relatively normal between acute exacerbations

n     May have low grade scattered expiratory wheezing

n     On acute exacerbation: tachypnea, decreased LOC, fever, increased wheezing, cyanosis, and pedal edema

NURSING MANAGEMENT: ACUTE RESPIRATORY FAILURE

 

n     In Acute Respiratory Failure, the Respiratory System cannot carry out its two main functions:

n           Delivery of an adequate amount of O2 into arterial blood.

n           Removal of a corresponding amount of CO2

Classification of Respiratory Failure