Chapter 27 - Alteration In Pulmonary Function Flashcards
Ventilation
Movement of air in and out of lungs
Oxygenation
Loading oxygen molecules onto. Hemoglobin
Respiration
O2 and co2 exchange of alveoli and systemic capillaries
Perfusion
Delivery of blood to a capillary bed in tissue
Dyspnea
Breathlessness
-subjective
-work of breathing is greater than actual result
Signs of dyspnea
-flaring of nostrils
-use of accessory muscles
-head bobbing in children
Paroxysmal nocturnal dyspnea
Pulmonary condition that wakes you up gasping for breath in the middle of the night
Sputum
Color provides information about progression of disease
-microscopic appearance allows microorganism identity
Hemoptysis
Coughing up blood (usually indicates infection of inflammation of bronchiole)
-if severe can indicate cancer
Normal breathing
Rhythmic and effortless
-includes short expiratory pause with each breath
Sighs
1.5 to 2 times normal tidal volume
Abnormal breathing patterns
Patterns of breathing automatically adjust to minimize WOB
Purpose of sigh
-twice tidal volume, 10 times per hour
-help maintain normal breathing
-equals out oxygen consumption and CO2 expulsion
Hyperpnea: kussmaul respiration
Occurs with strenuous exercise
-inc ventilation rate and tidal volume
-no pause
Cheyne stokes respiration
Alternating deep and shallow breathing
-periods of apnea
Periods of apnea
15 to 60 seconds
-followed by inc volume ventilations
-eventually returned to normal, triggering another period of apnea
Cause for cheyne stokes
Reduced blood flow to brain
-reduced brain impulses to respiratory center
Both of what can be determined by blood gases
Hypoventilation and hyperventilation
Hypoventilation
Inadequate ventilation
Hypoventilation issue
Co2 removal doesn’t keep up with co2 production
Hypoventilation result
Hypercapnia
-inc co2 in blood stream
Hyperventilation
Alveolar ventilation exceeding needs
Hyperventilation issue
Removal of more co2 than is produced
Hyperventilation result
Hypocapnia
-reduced co2 in blood stream
Cyanosis
-bluish discolouration of skin
Cause of cyanosis
develops when 5 grams of hemoglobin is desaturated
Cyanosis is not evident until is is severe =
Insensitive indicator of respiratory failure
Peripheral cyanosis
Poor circulation in fingers and toes due to peripheral vasoconstriction
-best seen in nail beds
Central cyanosis
Decreased arterial oxidation (low PaO2) from pulmonary disease
-best detected in buccal mucosa membranes and lips
Clubbing
Bulbous formations at end of fingertips and toes
Clubbing is from
Diseases that disrupt pulmonary circulation causing hypoxemia
-rarely reversible
Pain from pulmonary disorders
-where is it located
-what sound does it make
Almost always localized in chest wall
-can be pinpointed by unique sound called pleural friction rub
Pleural friction rub
Pleural walls rub together due to reduced fluid in pleural cavity
Pain can be reproduced by
Pressing on sternum or ribs
Hypercapnia
Increased co2 in blood
-caused by Hypoventilation of alveoli
-increased PaCO2
Hypoventilation causes
-decreased drive to breath
-depression of respiratory center
-disease to medulla oblong at a
Effects of Hypoventilation
-electrolyte imbalances
-dysrhythmia
-in severe cases comatose
Hypoventilation is often overlooked, why?
It can appear normal
-it is important then to obtain blood gases to confirm
Hypoxemia
Decreased PaO2 in arterial blood
What are the two possible causes of hypoxemia
- Related to issues with delivery of O2 to alveoli and delivery to lung
- Thickening of alveolar membrane or destruction of alveoli
Diffusion of O2 from alveoli to blood is dependant upon two factors
- Amount of air entering alveoli
- Amount of blood perfusion capillaries around alveoli
What is the most common cause of hypoxemia
Abnormal ventilation/perfusion ratio
(V/Q)
V=
Ventilation
Q=
Amount of blood perfusion capillaries around alveoli
Shunt
Normal perfusion but Inadequate ventilation
-blocked, collapsed alveolus
Alveolar dead space
Normal ventilation but inadequate perfusion
Shunt causes
Very low V/A
-hypoxemia
Alveolar dead space causes
High V/Q
-hypoxemia
Acute respiratory failure: levels of PaO2
Is less than 60 mmHg
(TX = supplemental oxygen)
Acute respiratory failure: levels of PaCO2
Is greater than 50
(TX = ventilatory support)
Acute respiratory failure: pH levels
Less than or equal to 7.25
Normal pH
7.40
Acute respiratory failure is a potential complication of
Any major surgical procedure
How to prevent Acute respiratory failure:
Frequent turning and position changes
-deep breathing exercises
-early ambulating
CWR or chest wall restrictions (cause)
Deformity
-obesity, neuromuscular disease
CWR or chest wall restrictions (result)
Increased work of breathing
-usually decrease in tidal volume
CWR or chest wall restrictions (surgical/injury complications)
Can cause such pain that causes Hypoventilation
CWR:
Decreased tidal volume, increased breathing rate, can lead to respiratory failure
Flail chest
Fracture of consecutive ribs with or without sternum damage
Result of flail chest
Chest wall instability = paradoxical movement of chest when breathing
Paradoxical breathing (inspiration)
Unstable portion of chest wall moves inward
-normal movement would be outward
Paradoxical breathing expiration
Portion moves outward
-normal movement would be inward
PaO2 rule of thumb for normal ventilation
80-100 mmHg
Severe hypoxemia PaO2 levels
<40 mmHG
Pneumothorax (cause and result)
Air or gas in pleural space
-due to rupture to visceral pleural
-lungs tend to collapse
Pleural effusion
Fluid in pleural space
-can be blood or lymph
How do you diagnosis a pleural effusion
-chest xray
-thoracentesis (needle aspiration)
Empyema
Infected pleural effusion by microorganism
What is the indication of empyema
Pus in pleural space
Cause of empyema
Pulmonary lymphatic tissue becomes blocked
-contaminated lymphatic fluid moves into pleural space
empyema is the result of
Surgery, or bronchial obstruction
TX for empyema
Antibiotics and drainage of pleural space with chest tube
Restrictive lung diseases have difficulty with
Inspiration
-expanding lungs
Obstructive lung diseases have difficulty with
Expiration
Restrictive lung diseases
Decreased lung compliance
-increased work of breathing at tidal volume
Aspiration
Passage of fluids or solids into lungs
Aspiration caused by
Abnormal swallowing mechanism
-cough reflex impaired
-lead to pneumonia
CNS or PNS abnormalities
Aspiration TX
Bronchoscopy
-failure to remove results in inflammation
Atelectasis
Collapse of lung
Atelectasis: compression
Caused by external pressure e
-tumour of fluid
Atelectasis: surfactant impairment
Decreased production of surfactant
Atelectasis tends to occur
After surgery when using general anaesthetic
Atelectasis: TX
Deep breathing exercises promotes ciliary removal of secretion
Bronchiectasis
Perisistent abnormal dilation of bronchi
Obstruction cause in Bronchiectasis
- Inflammation due to mucus plugs
- Chronic inflammation = destruction of elastic/muscular bronchi wall = permanent dilation
Symptoms for Bronchiectasis
Chronic productive cough
-large amount of foul smelling sputum
Bronchiolitis
Inflammatory obstruction of small airways
Bronchiolitis obliterans
Fibrosis of airways = scaring
BOOP
Alveoli becomes filled with connective tissue
Manifestations of Bronchiolitis
Rapid ventilatory rate and dry non productive cough
Pulmonary fibrosis
Excessive amount of fibrous and connective tissue at alveoli
Pulmonary fibrosis cause
Scar tissue left from previous disease
-example tuberculosis
Result of Pulmonary fibrosis
Decreased lung compliance and external respiration (O2/CO2 exchange)
-due to multiple injuries at different lung sites associated with abnormal healing
Symptoms of Pulmonary fibrosis
Dyspnea on exertion
Pulmonary Edema
Excessive water on lungs
-normal lung is dry
Cause of pulmonary edema
Left side heart disease
-reduced CO, blood backed up from heart into lungs, inc bp in pulmonary capillaries, fluid into interstitial space, fluid flow exceeds lymph system = pulmonary edema
COVID 19
Manifested as viral pneumonia induced acute respiratory distress syndrome
Post mortem studies of COVID 19
Mortality patients had undetectable viral loads
-cytokines effects of virus not main cause of death
-death caused by hosts runaway immune response
Management of COVID 19
Incubation
Restrictive lung disease have difficulty with
Inspiration
Obstructive lung diseases have difficulty with
Expiration
S/s of obstructive lung diseases
Dyspnea and wheezing
Asthma
Chronic inflammatory disorder of bronchial mucosa
Asthma inflammation =
Restriction of airways
-hyper immune response to irritants
Early asthmatic attack: classic immune response
Dendritic cells, helper T cells, B cell
Result of early asthmatic attack
Inflammation, inc capillary permeability, inc fluid
Late asthmatic attack
Begins 4-8 hours after early attack
-latent release of inflammatory mediators from original site
Result of late asthmatic attack
Inc damage of epithelial cells = scaring
-inc mucus forming plugs and airway resistance
Manifestation of asthma
Individuals normal between attacks
-pulmonary function tests are normal
If bronchospams are not reversed by usual treatment they are considered
Status asthmaticus
If PaCO2 (asthma) is greater than ___ it means
70 mm HG
-sign of impending death
TX asthma
-short acting inhalers, or inhaled corticosteroids
asthma (1)
Inhaled antigen passes epithelial layer
Asthma (2)
Antigen binds to mast cells
-releasing mediators
Asthma (3)
Mediators
-mucus production in airway
-bronchi spams
-edema from inc capillary permeability
Asthma (4)
Dendritic cels present antigen to helper T cells
-activate B cells, and release antibodies
Asthma (5)
Helper T cells also activate eosinophil
-neutrophils activated
-inflammation from both results in airway obstruction
COPD
Composed of chronic bronchitis and emphysema
-most common
Characteristics of COPD
-persistent airflow limitation
-chronic inflammatory response to noxious partials or gas
-progressive
COPD: chronic bronchitis defined
As hypersecretion of mucus
-chronic cough for at least 3 months of the year for 2 consecutive years
Cause of COPD: chronic bronchitis
Inspired irritant-> inflammation and thickening of mucous membrane
-reduced radius of airways causing obstruction
Initially COPD: chronic bronchitis affects
Large airways and eventually all airways
COPD: chronic bronchitis airways collapse
Early in exhalation
-air trapped in distal portions of lungs
-hyperinflation = Hypoventilation
COPD: emphysema
Permanent enlargement of gas exchange airways
-destruction of alveolar walls
-obstruction due to destroyed walls of alveoli
COPD: emphysema does not
Mucus production of inflammation
COPD: emphysema destruction =
Large alveolar spaces = greatly inc diffusion distance between alveoli and capillary
Result of COPD: emphysema
-reduced O2 and CO2 diffusion
-expiration becomes difficulty because of loss of recoil of normal alveoli
Symptom difference between chronic bronchitis and emphysema
B- frequent couch with mucus
E- shortness of breath
Acute bronchitis
Acute infection and inflammation of airways
-self limiting
-occurs due to viral infection
Symptoms of acute bronchitis
Similar to pneumonia
-non productive cough, aggravated by cold, dry, dusty air
TX for acute bronchitis
Rest, aspirin, cough, suppressant, antibiotics
Pneumonia
Infection of lower respiratory tract caused by microorganisms
HAP pneumonia
Hospital acquired pneumonia
CAP pneumonia
Community acquired pneumonia
HAP or CAP is the second most common health care associated infection
HAP
Pneumonia most common pathogen
S.pneumoniae
Pathophysiology of HAP pneumonia
In hospitals suctioning tubes can become colonized with bacterial biofilms and suction results in seeding lungs with bacteria
Guardian cells of lower respiratory tract
Cellular alveolar macrophages
Macrophages present antigens to
Adaptive immune system = activation T and B cells
resulting immune response can
Fill alveoli with debris
Further damage is caused when
Microorganisms release toxins
Tuberculosis
Infection caused by M.tuberculosis
-leading cause of death although curable
How is TB spread
person to person via airborn droplets
TB pathophysiology
-pathogen reaches lung and is engulfed by macrophages
-survives and multiplies
-reproduction causes chemotactic response and more macrophages respond causing tubercul formation
Macrophage start to die and release (TB)
Pathogen, this form a centers in tubercle (dormant stage)
Tubercle center enlargens… (TB)
Enlargement fills with air, aerobic pathogen starts to multiply outside macrophage
Liquifidcation continues (TB)
Tubercle ruptures and pathogen sdisseminate throughout lung
Pulmonary vascular diseases
Pulmonary blood flow disrupted causing occlusions
-destroys vascular bed
When pulmonary blood flow is disrupted it causes
Dramatic alterations in perfusion and ventilation ratios
Pulmonary embolism
Occlusion of portion of pulmonary vascular bed by embolus
Effect of pulmonary embolism depends on
-extent of pulmonary blood flow
-size
-nature of embolus
-secondary effects
Pulmonary artery hypertension
Mean pulmonary artery pressure greater than 25 mmHG at rest
Endothelial dysfunction (pulmonary artery hypertension)
Overproduction of vasoconstrictiors
pulmonary artery hypertension: increased growth factors
=fibrosis=thickening of vessel walls=narrowing of vessels and gas exchange is reduced
pulmonary artery hypertension: inc pulmonary artery pressure
Increased pressure in right ventricle = right ventricle hypertrophy = failure
Cor pulmonale
Right ventricle enlargement due to hypertrophy or dilation or birth
-result of pulmonary artery hypertension
In cor pulmonale there is an increased
Work of right ventricle = increased hypertrophy of normally thin walled heart muscle
pulmonary artery hypertension: pressure overload
=dilation/hypertrophy= failure of right ventricle
Laryngeal cancer: Primary risk factor
Smoking
-increased when smoking combined with alcohol consumption
What pathogen is linked to laryngeal cancer
HPV or human papilloma virus
Pathphysioloy of laryngeal cancer
Carcinoma of vocal cords (most common site)
-metastsis occurs in lymph nodes, but distant is rare
Manifestation of laryngeal cancer
Hoarseness, dyspnea, cough
-cough following swallowing
Diagnosis and TX for laryngeal cancer
Biopsy, radiation, chemotherapy
Lung cancer
Tumours on respiratory tract in epithelium
-leading cause of death in Canadians
Msot common cause of lung cancer
Smoking, gas exposure, second hand smoke exposure
Pathophysiology of lung cancer
Bronchial mucosa suffers hits from tobacco smoke = epithelial damage
-metastasis to brain, bone marrow and liver
Tobacco smoke
Contains 30 carcinogens
-90% of lung cancers
Tumour in lung cancer is result of
Growth factors and free radicals