pulmonary function Flashcards
central respiratory center
controls the rate of breathing
central chemoreceptors
sensitive to changes in PaCO2 and pH
peripheral chemoreceptors
located in the carotid and aortic bodies
sensitive to changes in PaO2 and PaCO2
anatomic “dead space”
all of the airways that do not contain alveoli for gas exhange
alveolar “dead space”
alevoli that are filled with air, but gas exchange is not occuring
airway resistance determined by:
length of the tube
radius of the tube
viscosity (thickness) of substance flowing through the tube
what is consistent in the airway regarding resistance
lenth and viscosity is constant so changes in the radius is primary force influcencing resistance
a change in airway radius results in
a fourfold. hange in airway constriction
types of change that can alter airway radius
bronchoconstriction
inflammation (swelling)
mucus production
tissue resistance is influenced by the balance of what two factors?
compliance and elastance
compliance
ease of inflation of alveoli
elastance
ease of alveolar recoil
la places law
smaller spheres are more difficult to inflate
surfactant
mixture of proteins and phospholipids
secreted by Type 2 alveolar cells
what does surfactant do?
reduce surface tension = helpping them inflate
prevent water from coming into the alveoli
what happens if we have surfactant deficiency?
decreases the compliance of the alvoli (more difficult to inflate)
would allow water from the interstitial space to enter then alveoli
ventilation (V) and perfusion (Q) relationship
(dont need to know but know the ups and downs)
normal pulmonary perfusion=5 lpm
normal alveolar ventilation=4 lpm
normal V/Q ration=0.8-0.9
4lpm alveolar ventilations
———————————— = 0.8
5lpm pulmonary perfusion
low V/Q ratio
(vascular shunt)
Perfusion without Ventilation
problems with pumonary ventilation (inadequate oxygen in the alveoli)
(most pulmonary disorders are from this)
high V/Q ratio
(alveolar dead space)
ventilation without perfusion
problem with pulmonary perfusion
blood flow through pulmonary vasculature is inadequate
(pulmonary cascular defects)
how chronic elevation of paCO2 levels in a pt with chronic lung disease can cause a “resetting” of the homeostatic set point of the central chemoreceptors for CO2
↑paCO2 and normal pH is (compensated respiratory acidosis) so we have the secondary monitors (peripheral chemoreceptors)
paO2 becomes main indicator because paCO2 is always elevated
why use caution when administering oxygen to pt with chronic lung disease
they are sensitive to oxygen
may cause them to stop breathing
hypoxia induced pulmonary vasoconstriction
(alveolar oxygen issue)
local ↓ in alveolar oxygenation leads to a responsive vasocontriction
this increases resistance and decreases blood flow through pulmonary vessels
this increases the work load of the right side of the heart and can lead to right sided heart failure
work of beathing
amount of energy expended to support ventilations
pt with pulmonary disease have ↑ work of breathing
if there is not enough energy to perform work of breathing what happens
respiratory failure
forced expiratory volume (FEV)
volume of air expired in the first second of FVC (full volume capacity or full inspiration)
(this measures airway resistance)
what do we do if FEV is low?
give bronchodilator med
check PFT again
Peak Expiratory Flow Rate (PEFR)
measure how fast you breath out (measuring degree of airway resistance to the outflow of air)
same as FEV but it is the rate of flow not a volume of air exhaled
use a peak flow meter to measure the resistance
hypoxemia
decreased O2 level in arterial blood
hypoxia
decreased O2 in tissues
hypercarbia (hypercapnea)
increased CO2 in arterial blood
acute respiratory failure
Lab values
ABG values:
primarily hypoxemic : paO2 50mmHg or less
Primarily hypercarbic: paCO2 50 or more (with ↓ pH)
These pt will need to be oxygenated
Upper respiratory tract infections
Common cold
Rhinosinusitis (rhinitis and sinusitis)
Laryngitis
Upper and lower respirator tract infection
Influenza
Effects both upper and lower
We worry about it getting lower
Lower respiratory tract infection
Acute bronchitis (bronchi)
Bronchiolitis (bronchioles)
Pneumonia (alveoli)
Tuberculosis
Pneumonia
Causes: bacteria, viral, fungi
Agent depends where the pneumonia was acquires
Hospital or community acquired pnemonia
Lobar pneumonia
Where got it
Where located
Xray
Usually HAI
Infection within a lobe of the lung
Appears on xray as consolidation of a lobe
Bronchopneumonia
Where got it
Where located
Xray
Usually community aquired
Infection spread throughout the lungs
*particularly where the bronchioles connect to avloli
Appears on xray as patchy areas throughout
Pluritis (pleurisy)
Pluritis and Pleuritic pain may occur with pneumonia
*sharp stabbing pain on inspiration
Typical pattern of pneumonia
Infection within alvoli
Most bacterial
Neutrophil response
Atypical pattern pneumonia
Infection within interstitial spaces
Most viral
Lymphocyte response
Stages of bacterial pneumonia
Edema
Red hepatization
Grey hepatization
Resolution
Edema
(Stage of bacterial pneumonia)
Frothy, pink sputum
Red hepatization
(Stage of bacterial pneumonia)
Consolidation of alveoli with RBCs, neutrophils
Rust colored sputum (may be present in both red and grey hepatization)
Grey hepatization
(Stage of bacterial pneumonia)
Immune process production of fibrin and immune molecules
Tuberculosis
Cause : mycobacterium tuberculosis
Resistant to destruction alvolar macrophages (infects the macrophages)
Tb induce a Type IV cell-mediated hypersensitivity response
TB Type IV cell mediated hypersensitivity response
Results in production of t cytotoxic cells specific for the TB organism
TB healing
Healing by granuloma formation
Ghon Foci/ Ghon Complex
Tb is walled off in granuloma
Fungal resp tract infections
Most common in immune compromised persons
*opportunistic infections
Usually persent as lower resp infections but its really not
Very serious and difficult to cure
Malignancies of the resp tract
Laryngeal cancer
Lung cancer (bronchogenic carcinoma)
Tobacco is a common cause
Pulmonary disorders in children
Airways are small
Since their radius is already small then small changes to the radius can rapidly lead to resistance of their air flow
Airway obstructions are a common issue
Serious resp tract infection in children
Acute bronchitis
Acute laryngotracheobrhonchitis (Croup)
*barkey cough
Bronchiolitis
*more severe in children due to small airways
Epiglotitis
Epiglotitis in children
Inflammation of the epiglottis
Can cause complete obstruction of airway
May need intubation
Neonatal respiratory distress syndrome
(Hyaline membrane disease) HMD
Pink membranes that form in the alveoli
Cause: developmental deficiency of surfactant (born too early)
*Type II alvolar cells too immature to produce enough surfactant
Most common in preterm newborn infants
Bronchopulmonary dysplasia
Iatrogenic type of chronic lung disease
*began due to treatment
Occurs in infants treated with mechanical ventilation for congential pulmonary problems
*pressure of ventilations damages cell
The dysplastic changes cause scarring and fibrosis of airway and pulmonary tissue
Classification of lung disorders
Disorders of lung inflation
Obstructive lung disorders
Interstitial lung disorders
Pulmonary vascular disorders
Disorders of lung inflation
Aspiration
Atelectasis
Pulmonary edeam
Pleural disorders:
-pnemothorax
-pleural effusion
-pleuritis (pleurisy)
Flail chest
Acute lung injury and acute respiratory distress syndrome (ARDS)
Aspiration
Inhalation of foreign substances into the lungs
Risks of aspiration:
-Airway obstruction prevent gas exchange
-Aspiration pneumonia
(aspiration into right mainstem bronchus is more common due to anatomy)
High risk population for aspiration
-young children
-person who conditions that disrupt the ability to protect airway
*swallowing dysfunction neuro problems
*⬇️ level of consciousness
Atelectasis
Compression atelectasis :
something outside lungs push against the alvoli and prevent them from inflating
Absorption atelectasis:
Alveoli reabsorb air causing atelectasis
Pulmonary edema
Fluid into alveoli
Due to :
-increased capillary hydrostatic pressure in pulmonary capillaries due to left sided HF
S/s:
Frothy pink sputum
Crackles possibly
Pleural disorder: pneumothorax
Air in pleural space due to:
-External trama to chest
-Internal pulmonary injury:
*chronic lung disease
*iatrogenic consequences of mechanical ventilation
Spontaneous pneumothorax occurs particularly in?
Newborn infants (pressure of first breaths)
Marfan syndrome (connective tissues weakened)
2 presentations of pneumothorax
Communicating pneumothorax (open)
*can get air in and out
Tension pneumothorax
*only have air coming in not out
Pleural effusion
Types
Liquid in lungs
Transudative pleural effusion (serous fluid)
*due to HF
Exudative pleural effusion (infectious/inflammatory exudate) (most common)
*empyema
Chylothroax (lymphatic fluid)
Hemothroax (blood)
Pleuritis (plurisy)
(Other pleural abnormalities)
Inflammation within pleural space
Characteristic pattern of sharp/stabbing inspiratory pain (pleuritic pain)
Flail chest
Chest injury with fracture of a segment of ribs
Paradoxical (opposite) free floating movement
Rib segment moves in when chest moves out
Creates high risk for pneumothroax
Acute respiratory distress syndrome (ARDS)
Severe hypoxemia
ARDS is secondary to various critical illnesses or injury
Severe inflammatory response with widespread destruction of alveoli
Too much stuff in alveoli and decreased surfactant
Neonatal RDS
Primary developmental deficiency of surfactant so you can treat with surfactant
Preterm infants
Obstructive pulmonary disorders
Obstruction to the outflow of air during expiration
Asthma (bronchial asthma)
Chronic obstructive pulmonary disease (COPD)
*chronic obstructive bronchitis
*emphysema
Cystic fibrosis
Bronchiectasis
Asthma (bronchial asthma)
Reactive airway disease (RAD)
No cure but can reverse symptoms (makes it unique)
S/s:
Edema
Mucus secretion
Bronchoconstriction
Characteristics of asthma
Chronic inflammatory disorder
⬆️ bronchial hyperresponsiveness to “triggers”
Difficulty with expiration
S/s:
Wheezing, breathlessness, chest tightness, coughing
Common at night or early morning
Pathophysiology of asthma
Small airway
Inflammation leads to
Small airway especially affected:
⬆️ smooth muscle
Little supporting cartilage
Airway inflammation leads to:
Edema
Mucus plug
Airway hyperresponsiveness
Bronchospasm
Hyperexpansion of alveoli
Airtrapping in asthma
Breathing:
Inspiratory phase is active
Expiratory phase is passive
Air can enter alveoli when airway is dilated with inspiration bc its active and using muscles
BUT
Air gets trapped when it relaxes on expiration bc no muscles being used
Triggers of asthma symptoms
Allergic vs non allergic triggers
(Early vs late response)
Extrinsic vs intrinsic triggers
(Extrinsic: external origin)
(Intrinsic: internal origin (stress)
Childhood vs adult onset
Immune responses in allergic asthma
Early phase:
Degranulation of mast cells with IgE
Causes release of inflammatory mediators
Late phase:
Leukocyte responses with more inflammatory cytokines
Clinical manifestation of asthma
Cough
Expiratory wheezing (may be absent)
Chest tightness
⬆️ work of breathing with fatigue
⬇️ peak expiratory flow rate (PEFR)
⬇️ forced expiratory volume in 1 second (FEV1)
Chest xray usually normal
Chronic obstructive pulmonary disease (COPD)
Two different disorders but may occur seperately
*chronic bronchitis
*emphysema
Neither are reversible or curable
Pathophysilogy of chronic bronchitis
Inflamed and swollen airway with increased mucus secretion
Narrowed ariway with mucus plugs cause air trapping like asthma
Clinical manifestation of chronic bronchitis
Excessive bronchial secretions=airway obstruction
SOB with decreased exercise tolerance
Cyanosis, hypoxemia and hypercapnea
Polycythemia due to simulation of erythropoiesis due to hypoxia
May develop right sided HF (cor pulmonale) with peripheral edema
Pathophysiology of emphysema
Destruction of alveoli and supportive tissue
Distortion of small airways (causes air trapping)
Two types of emphysema:
Centriacinar
Panacinar
Centriacinar emphysema
Occurs in smokers
Alveolar damage is due to continued exposure to toxins
Affects central bronchioles
Panacinar emphysema
Due to inherited deficiency of the enzyme Alpha 1 Antitrypsin (genetic)
distal alveoli affected first
Alpha 1 Antitrypsin opposes the action of proteolytic enzymes within lungs
Without opposing proteolytic enzymes we have destruction of alveolar tissue
Clincial manifestagtion of emphysema
-Dyspnea
-Increased work of breathing with accessory muscle use (over compensation so s/s are late)
-barrel chest due to air trapping
-pursed lip breathing
-weight loss (unique)
Chronic bronchitis vs emphysema
Chronic bronchitis: blue bloaters
Difficulty breathing and decreased O2
Turn blue
Emphysema: pink puffers
Fast breathing turn red
Cystic fibrosis
Obstructive pulmonary disorder
Autosomal recessive mutation on long arm (q) chr 7
Chloride transport issue causing production of mucus thats thick and dehydrated
Causes airway obstruction due to the mucus
Bronchiectasis
Permanent dilation of bronchi due to chronic airway damage
Destruction of bronchial muscle and supportive lung tissue
Due to several chronic lung diseases
(not a disease entity on its own)
Interstitial lung disorders
Causes:
Occupational and environmental inhalants
Side effect to drug
Immunologic lung diseases
*sarcoidosis: multisystem immune disorder (formation of granulomas in the lung)
Interstitial lung disorder
Case model
Pulmonary fibrosiss
Idiopathic pulmonary fibrosis
(fibrous tissue between alveoli effects ventilation)
Idiopathic=dont know what caused it
Pulmonary vascular disorders
Perfusion issue 🚮
Issue primary of decreased perfusion
Problem with the Adequacy of flow of blood to lungs
High V/Q ratio disorders
Pulmonary vascular disorders
Case models
Pulmonary embolism
Pulmonary hypertension
Cor pulmonale
Pulmonary embolism
(Pulmonary vascular disorders)
Fragment travels to lung
Can originate from:
A clot (DVT)
Air (iv therapy
Fat (ortho injury exposing fat)
Amniotic fluid in pregnancy
Pulmonary hypertension
(Pulmonary vascular disorders)
Elevated BP in main pulmonary artery
Primary and secondary pulmonary hypertension
Pulmonary hypertension
(Pulmonary vascular disorders)
Primary HTN
Fatal due to no tx
Increase resistance to blood flow due to narrowing in pulmonary artery
Idiopathic condition
Pulmonary hypertension
(Pulmonary vascular disorders)
Secondary HTN
1)Secondary to pulmonary disorders which causes decreased alveolar oxygen
2)hypoxia induced pulmonary vasoconstriction
3)increase resistance to blood flow thru pulmonary vessels
4)secondary elevation of BP in main pulmonary artery
Cor pulmonale
(Pulmonary vascular disorders)
Right sided HF secondary to pulmonary disease
Lung disease produces hypoxia induced pulmonary vasoconstriction leads to:
1. Increased resistance in pulmonary vessels
2. increased BP in main pulmonary artery
3. increased workload on the right side of heart
4. right sided HF
