Exam 2 - pulmonary Flashcards
Term: Ventilation
gas transport in and out of the lungs during inspiration and expiration
Term: respiration
gas exchanges across alveoli-capillary tissue
Term: perfusion
circulation of blood through tissues
Mech of ventilation: inspiration
all due to pressure changes
-inspiration = pressure in alveolar is LOWER than atmospheric
***diaphragm ACTIVELY lowers, thorax raises and expands
mech of ventilation: expiration
pressure changes result in air flow
- exhale = alveolar pressure is HIGHER than atmospheric
**diaphragm relaxes and PASSIVELY elevates, thorax lowers to resting position
mech of ventilation: compliance
- distensibility of the lungs
- relates to ease of inflation and chest wall expansion during inspiration
mech of ventilation: elasticity
- recoil, tendency to return to original size
- elastin and collagen fibers, surface tension
mech of ventilation: surface tension
- contributes to elasticity by acting to collapse the alveoli
- surfactant acts to reduce surface tension
Mech of ventilation: airway resistance
- Flow = delta P / R
- resistance = 8 micro l/(pi r^4)
upper airways - responsible for most airway resistance
bronchial smooth muscle innervated by
ANS
inhale vs exhale: airways open or close
inhale = airways are pulled open
Exhale = airways collapse and increase resistance
how does gas exchange occur in the lungs?
diffusion
diffusion of gases across alveolar membrane affected by??? (3 things)
1) pressure/concentration gradients (high to low)
2) surface area (total amount of alveolar-capillary interface)
3) thickness of membrane (thickness can impede exchange)
Ventilation perfusion ratio
- gas exchange is optimized when ventilation matches perfusion
- actual V:Q (ventilation:blood flow) = ~.8
- gravity, position, and dysfunction affect ratio
- generally, vent and perfusion are greatest in gravity dependent areas
Dead space (lungs)
when perfusion < ventilation (PE)
Shunting (lungs)
when perfusion > ventilation (alveolar collapse from secretions)
Gas transport: O2
- dissolved in plasma (PO2)
- bound to hemoglobin (pulse ox toys! - ~97%)
Gas transport: CO2
- dissolved in plasma (PCO2)
- bound to hemoglobin (30%)
- bicarbonate (60%)
Acid-base balance of breathing
- breathing removes acid from blood in from of CO2
(inc breathing = reduce CO2 = reduce H+ = increase in pH)
(dec breathing = increase CO2 = increase H+ = dec pH)
Acid - base breathing equation
CO2 + H20 H2CO3 H+ +HCO3-
Neural - respiratory control
-automatic and voluntary
automatic = brainstem voluntary = cerebral cortex
Chemical - respiratory control
chemoreceptors in carotids and aortic arch
- CO2, H+ ions, and O2
Non-chemical (respiratory control)
-coughing, sneezing, bronchoconstriction, and mucus secretion occur in lungs as protective reflexes to irritants
Restrictive dysfunction (gen def)
abnormal reduction in pulmonary ventilation
Obstructive dysfunction (gen definition)
-diseases of the airways, producing obstruction to expiratory airflow
Restrictive dysfunction: characterized by
- decreased chest wall or lung compliance
- dec lung volumes and capacities
- inc work of breathing (inc pressures required for normal TV, inc energy expenditure, dec TV and inc RR)
Signs and symptoms of restricted lung dysfunction
- rapid, shallow breathing
- tachypnea
- hypoxemia
- accessory muscle use
- diminished breath sounds
- dec lung vol and capacities
- crackles
- dyspnea
- cough
- weight loss
- muscle wasting
Restricted lung dysfunction eventually may lead to
- pulmonary hypertension
- cor pulmonale
- severe hypoxia
- ventilatory or cardiac failure
Restrictive conditions (main categories)
pulmonary connective tissue musculoskeletal neuromuscular other (cancer, surgery, etc)
Restrictive lung dysfunction TREATMENT
- correct underlying cause if possible
- supportive (supplement O2, antibiotic therapy, interventions for ventilation or prevent accum of secretions, good nutrition)
Pulmonary fibrosis (what it is)
Interstitial lung disease
- inflam process involving alveolar wall
- leads to progressive scarring (fibrosis)
- progressive, stead decline in lung funct, often with acute exacerbations
- poor prognosis
Pulmonary fibrosis (what causes it)
- idiopathic (2/3 of cases. risk factors = environmental, genetic, age over 50 usually)
- other causes: infectious agents, environ and occupational inhalants, drugs, healing scar tissue
Pulmonary Fibrosis TREATMENT
- lack of evidence supporting most treatments
- response to treatment is unpredictable
- lung transplant is the ONLY definitive therapy
Pneumoconiosis (general and risk severity)
-lung diseases resulting from inhalation of industrial substances (dusty lungs)
risk depends on many things (type/duration/intensity of exposure, presence of underlying pulmonary disease, smoking history, particle size and water solubility)
Pneumoconiosis (most common population)
- among miners, sandblasters, stonecutters, asbestos workers, insulators, and agriculture workers
Pneumoconiosis (pathogenesis)
- variable
- may be rapid onset or last years without clinical manifestations
- dust particles taken up by macrophages
- may activate and/or damage macrophages causing release of mediators
- macrophages containing particles may accumulate in nodules or lesions in the lung, connective tissue, and lymphatic tissues.
- can lead to excessive fibrosis and scarring of lung tissue
Systemic sclerosis or scleroderma (what it is)
- autoimmune disease
- excessive collagen deposition in the skin, but can affect internal organs including the lungs
- inflammation leads to fibrosis
- with progression of fibrosis, capillaries become involved causing pulmonary hypertension and cor pulmonale
systemic sclerosis or scleroderma (disease course, treatment)
- unpredictable disease course
- treatment = immunosuppressive medications and drugs targeting pulmonary HTN (although could be bad drugs)
- lung transplant may be an option for some
Most common cause of death from scleroderma
Lung disease
Atelectasis (definition)
collapse/incomplete expansion of alveoli in part or all of a lung
obstructive.
non-obstructive (collapse, compression)
Atelectasis (what does it result from)
- hypoventilation or ineffective secretion clearance
- inactivity
- thoracic or abdominal incisional pain
- compression of lung
- diaphragm weakness/paralysis
- pneumonia
- foreign body obstruction
Types of lung cancer
-small cell lung cancer (20%)
-non-small cell lung cancer (80%
squamous cell, adenocarcinoma = most common, large cell)
Most common type of non-small cell lung cancer
adenocarcinoma
Most cases of lung cancer are linked to what?
cigarette smoking (~80%)
Most common site of lung cancer metastases?
Adrenal
**also the lungs are a common site of metastases from other types of cancer
Lung cancer (symptoms)
symptoms = productive cough, dyspnea, hemoptysis, recurrent infection
May also have fatigue, weight loss, weakness (vague systemic symptoms) or bone pain, headaches, jaundice (metastasis)
Lung cancer (treatment and prognosis)
Treatment and prognosis depends on stage
treatments can be: chemotherapy, radiation, surgery, and hormone therapies
Pulmonary edema: inc pulmonary capillary hydrostatic pressure
L sided heart failure
PE
= transudate
Pulmonary edema: inc pulmonary capillary membrane permeability
ARDS
pna
infection
=exudate
Pulmonary edema: dec plasma protein
liver cirrhosis
=transudate
Pulmonary edema: inc fluid accum in interstitial space and alveoli
- inc hydrostatic pressure
- inc membrane permeability
- dec plasma protein
- altered lymphatic function
ARDS
“Acute respiratory distress syndrome”
- acute respiratory failure that follows systemic or pulmonary insult (severe trauma, sepsis, burns, aspiration, embolism, etc)
- diffuse alveolar damage
ARDS clinical manifestations
- respiratory distress
- dyspnea
- hyperventilation
- atelectasis
- hypoxia and cyanosis
ARDS treatment
- first aimed at underlying pathology (sepsis, pneumonia)
- supportive therapy (ventilation)
- high mortality rate (>40%)
- **many recover pulmonary func but may have physical or cognitive impairments (some get scarring and interstitial fibrosis)
