Oxygenation Flashcards
physiology of pulmonary gas exchange
inspiration & delivery of O2 from environment -> alveoli, diffusion across alveolar-capillary membrane -> attaches to Hgb, dissolves in blood -> left heart
ventilation
movement of gases from atmosphere to alveoli (and vice versa)
diffusion
mechanism by which O2 moves across the alveoli and into pulmonary capillary
perfusion
O2 leaves alveoli to combine with Hgb (HbO2) or dissolve in blood (PaO2) to be carried to left side of heart
ventilation is dependent ong
conducting airways/airway diameter
ventilatory muscles (diaphragm, intercostals)
thorax/flexibility of rib cage
elasticity of the lungs (compliance)
nervous system/regulators
conducting airways
trachea
segmental bronchi
bronchioles
alveolar ducts
regulation of ventilation is done by …
Controller: CNS (brainstem, cerebral cortex, neurons in spinal cord)
group of effectors (muscles that work in coordinated fashion)
what chemoreceptors are used as sensors in regulation of ventilation
central chemoreceptors in the medulla
peripheral chemoreceptors in the aortic arch, carotids
how does the body respond to increase in hydrogen ions (acid)
increase ventilation
how does the body respond to decrease in PaO2
increase ventilation
how does the body respond to increase in PaCO2
increase ventilation
characteristics of inadequate ventilation
minimal/absent chest wall motion
use of accessory muscles (WOB)
wheezes
decreased/absent breath sounds
paradoxical chest wall motion
respiratory distress: PaCO2 >= 50, PaO2 <= 60, Ph <= 7.3
diffusion
movement of molecules from HIGH concentration to LOW concentration
mechanism by which O2 moves across alveoli and into bloodstream
type 1 alveolar epithelial cells
90% of total alveolar surface within lungs
highly susceptible to injury and inflammation
type 2 alveolar epithelial cells
produce, store, secrete pulmonary surfactant
surfactant in alveoli
phospholipid that lowers surface tension of the lungs
stabilizes alveoli, increases pulmonary compliance, eases WOB
in disease, disruption of synthesis/storage of surfactant = collapse of alveoli, impairment of pulmonary gas exchange
macrophages in alveoli
monocytes -> macrophages in alveoli -> phagocytic role
move from alveoli -> alveoli keeping them clean and sterile
release enzymes (H2Ow) when killing microorganisms
what are the 3 factors that affect diffusion of gas across alveolar-capillary membrane
pressure gradient (driving pressure)
surface area
thickness
PaO2 gradient
driving pressure- difference in pressure concentration concentrations (gradient)
an increase in surface area causes
increases amount of gas that can diffuse
interventions to increase surface area
incentive spirometer
turn cough, cough breath
sighs/yawn
positive end expiratory pressure (PEEP)
increased thickness of alveolar capillary membrane results in
slower rate of diffusion
conditions that increase alveolar capillary membrane thickness
ARDS
pulmonary edema
pulmonary fibrosis
what are the 2 ways O2 is transported in the blood
oxyhemoglobin (HbO2)
dissolved in blood (PaO2)
respiratory acidosis
excessive retention of CO2 due to hypoventilation leading to a decrease in pH below 7.35
respiratory acidosis causes
COPD
pneumonia
atelectasis
neuromuscular disease
post-op recovery
narcotics
metabolic acidosis
decreased HCO3 and decrease in pH below 7.35
metabolic acidosis causes
diabetic acidosis
starvation
impending shock
ASA OD
diarrhea
respiratory alkalosis
low PCO2 due to hyperventilation (excess amount of CO2 exhaled)
resulting in pH above 7.45
respiratory alkalosis causes
hysteria
fear
anxiety
head injury
pain
fever
ventilator
metabolic alkalosis
increased HCO3 and an increase in pH above 7.45
metabolic alkalosis causes
diuretics
prolonged NG suction without electrolyte replacement
excessive vomiting
overuse of antacids
shift to the left
Hgb increases its affinity
easier for the Hgb to pick up O2, but harder to release O2 into the tissues
more O2 stays on Hgb and returns to lungs
result in tissue hypoxia even though there is sufficient O2 in blood
effects of shift to the left
low CO2
low body temp
high CO
high pH
decreased 2,3-DPG
shift to the right
Hgb loses its affinity
harder to bind, easier to release
shift to the right effects
high CO2
high temp
low CO
low pH
increased 2,3-DPG
normal V/Q
4:5
V/Q > 0.8
ventilation exceeds perfusion
V/Q < 0.8
poor ventilation
pulmonary perfusion
distribution of perfusion is gravity dependent
preferential blood flow to gravity dependent areas
causes of impaired perfusion
decreased Hgb: anemia, CO poisoning
decreased flow: hemorrhage, PE, pulmonary vasoconstriction
physiologic shunt: anatomic left to right cardiac shunt
alveolar dead space
occurs in diseased states when alveoli are ventilated but not perfused
only occurs with PE
ventilation with no perfusion
pulmonary absolute shunt
anatomic shunt + intrapulmonary shunt
pulmonary anatomic shunt
blood vessel skips alveoli, doesn’t get diffusion
blood that moves from the right heart into the left heart without coming into contact with alveoli
intrapulmonary shunt
perfusion but no ventilation
no diffusion
no surface area
aka right to left shunt
shunt-like effect
not a true shunt
excess of perfusion in relation to alveolar ventilation
alveolar ventilation is reduced
obstructive lung disease
difficulty exhaling all the air from the lungs
abnormally high amount of air still lingers in lungs (air trapping)
types of obstructive lung disease
COPD
asthma
bronchiectasis
cystic fibrosis
restrictive lung disease
cannot fully fill their lungs with air
lungs are restricted from fully expanding
from conditions causing stiffness in lungs
types of restrictive lung disease
interstitial lung disease (idiopathic pulmonary fibrosis)
sarcoidosis
obesity
scoliosis neuromuscular disease (Muscular dystrophy, ALS0
signs of impaired gas exchange
tachypnea
restlessness
anxiety
confusion
crackles
decreased PaO2, SaO2
increased PaCO2, pH
intrapulmonary shunt
infiltrates by CXR
acute respiratory distress syndrom
pathologic injury to the lung occurring from a wide diversity of causes and associated conditions
inflammatory syndrome marked by disruption of alveolar-capillary membrane
clinical definition of ARDS
acute onset
bilateral infiltrates on CXR
PAWP < 18 mmHg or no clinical evidence of left ventricular failure
hypoxemia refractory to O2 tx
direct causes of ARDS
aspiration of gastric contents or other substances
viral or bacterial pneumonia
chest trauma embolism: fat, air, amniotic fluid, thrombus
inhalation of toxic substance
near-drowning
O2 toxicity
radiation pneumonitis
indirect causes of ARDS
sepsis
severe massive trauma
acute pancreatitis
anaphylaxis
cardiopulmonary bypass
DIC
opioid drug overdose
severe head injury
shock states
transfusion-related
signs and symptoms of ARDS
severe shortness of breath
dyspnea
labored breathing
tachypnea
low O2 levels in blood
cough and fever
hypotension
confusion
extreme tiredness
pathophysiology of ARDS
increase in permeability of the alveolar-capillary barrier, leading to an influx into the alveoli
type 1 and type 2 epithelial cell destruction
initiation of inflammatory-immune response
activation of cytokines
release of mediators: what causes increase in capillary membrane permeability
alveolar flooding
damage to alveolar epithelial cells type 1 and 2
loss of surfactant
alveolar collapse or filling
release of mediators: change in small airway diameter
increased airway resistance
decreased lung compliance
release of mediators: injury to pulmonary vasculature
pulmonary vasoconstriction
microemboli formation (DIC)
pulmonary hypertension
alveolar dead space
increased PVR
decreased CO
effects of increased work of breathing
alveolar hypoventilation
V/Q mismatching
intrapulmonary shunting
causes hypoxemia refractory to oxygen therapy
tests and diagnostics for ARDS
imaging: CXR, CT, bronchoscopy
labs: ABG, BMP, CBC, blood/urine/sputum CX
heart tests: electrocardiogram, echocardiogram
collaborative management ARDS
treat underlying cause
promote pulmonary gas exchange
fluids: NS, LR
meds: abx, vasopressors, anti-clots, pain meds
ARDS complications
pulmonary fibrosis, barotrauma, PE, VAP
pneumothorax
cardiac dysfunctions
blood clots
acute renal failure
memory, cognitive, and emotional problems
