Final: Ch 23 Disorders of Ventilation & Gas Exchange Flashcards
what is ventilation
movement of air into the lungs
what is perfusion
circulation of blood through pulmonary vessels
what is diffusion
oxygen and CO2 x respiratory membrane
what is hypoxemia
low arterial PO2
symptoms of hypoxemia
mental confusion, restlessness, agitation, combativeness
cyanosis when deoxygenated Hb > 5g/dl
SNS activation
PA vasoconstriction and polycythemia when chronic
diagnosis and treatment of hypoxemia
diagnosis: ABG, pulse oximeter
treatment: correct the cause – give O2 and/or ventilate
hypercapnea, symptoms, treatment
High CO2 in blood
hypoventilation or severe V/Q mismatch
symptoms: acidosis
treatment: mechanical support to improve ventilation
how to distinguish between cardiac and respiratory pain?
taking a deep breath doesn’t increase cardiac pain, but does increase respiratory pain
types of pleura
visceral pleura: covers lung
parietal pleura: lines chest cavity
pleural space inbetween - fluid
is there normally negative pressure in the lung system?
yes
pleuritis
inflammation of the pleura (localized) - acute pain
worse with deep breathing/coughing
may need analgesics, NSAIDS
pleural effusion
abnormal collection of fluid in the pleural cavity
causes of pleural effusion
negative intrapleural pressure (atelectasis)
high capillary pressure (HF)
high capillary permeability (infection)
low lymph drainage (mediastinal cancer)
symptoms of pleural effusion, diagnosis, treatment
symptoms: dyspnea, low breath sounds, hypoxia
Dx: chest x-ray, CT scan
treatment: thoracentesis
what is transudate
serous fluid - HF
what is exudate
fluid with protein or LDH
inflammatory process
what is empyema
pus in the pleural cavity
rupture of an abscess
what is chylothorax
lymph in the pleural cavity
trauma, inflammation, malignancy
what is hemothorax
blood in the pleural cavity
trauma, aneurysm, malignancy
pneumothorax
air in the pleural cavity causing partial or complete lung collapse
spontaneous or traumatic
spontaneous pneumothorax is caused by what, and types (primary/secondary)
caused by the rupture of a bleb
primary: no known cause (common in tall men + smokers)
secondary: asthma, TB, CF, lung cancer
spontaneous pneumothorax leak
lung collapse can seal the leak
otherwise, the leak continues until a negative intrapleural pressure is abolished
traumatic pneumothorax
caused by a rib fracture or penetrating external wound
may be accompanied by other traumatic injuries like a hemothorax
tension pneumothorax (life-threatening)
opening from pleural space covered by flap valve
air enters during inspiration but can’t leave
pleural pressure > atmospheric
mediastinum shifty and other lung and great vessels compromised
type of traumatic pneumothorax
symptoms of pneumothorax
depends on size
respiratory distress and hypoxemia
asymmetry of the chest
tension pneumo can cause cardiovascular collapse
diagnosis of pneumothorax
chest x-ray
CT
ABG
pulse oximetry
treatment of pneumothorax
a small spontaneous one may resolve itself
needle aspiration or chest tube and closed drainage
tension pneumo - emergency chest tube
cover sucking chest wounds with an airtight dressing
on a CXR what does a collapsed lung look like
an empty, dark space
what is atelectasis and what are the types
incomplete expansion of part of the lung
caused by a blockage of airway, compression, or lack of surfactant
primary or acquired
primary atelectasis
infant’s lung fails to expand at birth
seen in premature and high risk infants
acquired atelectasis
caused by bronchial obstruction or external compression (tumor, pleural effusion, mucus plug)
once bronchus becomes obstructed, air is absorbed from alveoli leading to the atelectasis
seen post op: pain, anesthesia, immobilization –> retention of secretions
symptoms of atelectasis
tachypnea
tachycardia
dyspnea
cyanosis
low breath sounds
fever
diagnosis and treatment of atelectasis
Dx: CXR, CT
Rx: mobilization and cough/deep breath for post op patients (produces neg pressure)
may require bronchoscopy
what is obstructive airway disease
caused by an obstruction that limits expiration
reversible (asthma), or not (COPD)
bronchial smooth muscle plays a role
SNS dilates and PNS constricts bronchi
bronchial asthma
bronchospasm and activation of inflammatory cells
always hyper-responsive
wheezing, cough, SOB
asthma acute phase (10-20 min) response
immediate bronchoconstriction (SMC activation) to antigen or irritant
sensitized mast cells release histamine
mucus membranes are permeable to cells/antigen
increased vascular permeability causes mucosal edema
what reverses the acute phase of asthma
beta2-agonists
dilators
asthma late phase (4-8hrs) response
sensitized mast cells release histamine
strong inflammatory response
multiple types of leukocytes recruited
cholinergic nerves activated
are early childhood infections preventative of asthma?
can be
extrinsic causes of asthma
airborne allergens
familial pattern
intrinsic causes of asthma
respiratory infection
inhaled irritants
NSAIDS, beta-blockers
emotional trigger
GE reflux
exercise
VE
minute ventilation
VE = Vt x RR
FRC
fractional residual capacity
FVC
forced vital capacity
Vt - Vd
dead space
VE =
VT x f (500ml/breath x 12 breaths/min) = 6L/min
symptoms of asthma
wheezing, chest tightness
prolonged expiration, air trapping (high RV, low FVC)
alveolar ventilation less effective –> V/Q mismatch (shunt) –> hypoxia
symptoms of mild asthma attacks
chest tightness
wheezing
cough
symptoms of severe asthma attacks
distant breath sounds
loud wheezing
inaudible breath sounds and wheezing signals onset of respiratory failure
FEV1
forced expiratory volume in 1 second
how much was breathed out in 1 second?
diagnosis of asthma
H&P
spirometry FEV1/FVC low, PEF low
peak expiratory flow (PEF) meter
methacholine challenge to trigger attack
see if bronchodilators reverse
treatment of asthma
education and desensitization to allergens
short-term meds for asthma
beta-agonists (albuterol, terbutaline) by inhaler
anti-cholinergics by inhaler
systemic steroids
long-term meds for asthma
steroids
mast cell stabilizers
long-acting beta-agonists
SMC relaxers
leukotriene modifiers (block synthesis/receptors)
Xolair: monoclonal Ab against IgE
how is asthma classified
by severity
allows proper treatment and identification at those at risk for complications
severe asthma
virtually constant symptoms and requires frequent use of steroids
deterioration can be rapid - don’t delay treatment
chronic obstructive pulmonary disease: COPD
a group of diseases that produce chronic obstruction of air flow
4th leading cause of death in US
what causes COPD
smoking
alpha1-antitrypsin deficiency
when do you get symptoms of COPD?
when the disease is advanced
in COPD, the airway can be obstructed by… 3 things
fibrosis with hypertrophy of bronchial wall
inflammation with hyper-secretion of mucus
destruction of elastic fibers
progression of COPD
destruction of alveoli decreases gas exchange area
destruction of elastic fibers causes airway collapse
V/Q mismatch = wasted effort and hypoxia
low elastic recoil causes airway collapse and air trapping
2 types of COPD
emphysema - enlarged airspaces
chronic bronchitis - small airway obstructions
emphysema
loss of lung tissue (elastic, alveolar walls destroyed)
airspaces enlarged
lungs hyperinflated
high TLC
_______ is the leading cause of emphysema
smoking
smoking and emphysema
activates macrophages and neutrophils to release elastases
decreases antitrypsin activity (inhibits elastases)
elastin fibers destroyed
genetics of alpha1 antitrypsin deficiency
PI (protein inhibitor) genes produce alpha1 antitrypsin
PIZ mutation most severe 5% of population
homozygotes have 1/5 or less of normal enzyme activity
if emphysema in a person less than 40 YOA then cause is likely…
alpha1 antitrypsin deficiency
2 types of emphysema
centriacinar
paracinar
centriacinar emphysema
bronchioles in central lung affected 1st
alveoli initially normal
common in male smokers
paracinar emphysema
peripheral alveoli affected 1st
bronchioles initially normal
common in alpha1-antitrypsin deficiency
chronic bronchitis cause
caused by inflammation of airways (hyperplasia and a lot of mucus production)
middle aged males that smoke (multiple infections)
bacterial/viral infection
diagnosis of chronic bronchitis
cough for 3 months consecutively fo 2 years
progression of COPD
from cough to severe respiratory distress
older terminology for COPD
pink puffer: emphysema
blue bloater: chronic bronchitis
most people with COPD have some of both
emphysema causes loss of both _________ & _________
ventilation & perfusion
emphysema causes hypoxia when
late in disease
chronic bronchitis leads to _______ obstruction, and low V/Q areas lead to _______
airway, hypoxia
symptoms of emphysema
dyspnea with use of accessory muscles
seated position at night
barrel chest from air trapping
pursed lip breathing
symptoms of chronic bronchitis
dyspnea
exercise intolerance
hypoxia & hypercapnea
polycythemia –> HTN + Rt HF
death from COPD occurs from
exacerbation from infection
eventually respiratory failure
diagnosis of COPD
CXR - shower hyperinflation
PFT’s: FEV1 and FEV1/FVC are low
TLC & RV high
if FEV1/FVC less than 50% – severe disease
exercise tolerance test
blood gases
CXR of a COPD patient
hyperinflation seen as:
increased lung volume
low flat diaphragm
increased retrosternal air
treatment of COPD
stop smoking
prevent respiratory infection
increase physical/psychosocial function
O2 therapy when hypoxia present (PO2 to 60)
drugs for COPD
beta-agonists
anti-cholinergics
theophylline
steroids
bronchiectasis
uncommon, but serious type of COPD (airway obstruction)
2ndary to persistent infection/inflammation (TB)
symptoms of bronchiectasis
productive cough
purulent sputum
hemoptasis
anemia
weight loss
diagnosis/treatment of bronchiectasis
H&P, CXT, CT
postural drainage, chest PT, treat infection
