lobes of lungs
3 on right
2 on left
started out with 3 on both sides but 2 on left due to heart
remnant of 3rd left lobe
lingular lobe
location of apex of lungs at max inhalation
base
4cm above 1st rib
base to bottom of rib cage
hilar surface
area where vessels go in and out
lung pleura
visceral: next to lung
parietal: adheres to throacic cage
fluid in between pleura
pneumothorax
loss of vacuum between pleura
blood from aorta to lung via ____
blood from lung tissue to azygos and pulmonary veins ___
bronchial artery
bronchial vein
only artery in body that caries deoxygenated blood
pulmonary artery
what nerve constricts bronchioles, and is sensory to lungs
parasympathetic CNX
area defined by the heart
mediastinum (heart and pericardium) is middle mediastinum
area behind heart with esophagus, descending aorta, azygos veins, thoracic duct, sympathetic trunk
posterior mediastinum
what is in the anterior medastinum?
thymus gland
surface landmarks of resp system
- at mcl, where is lung?
- at axillary line
- costal angle
pleura = inhalation
- 6th rib, pleura to 8th
- 8th rib, pleura to 10th
- 10th rib, pleura to 12th
what is order of draining in sinuses?
sphenoid ethmoid
ethmoid and frontal to maxillary
maxillary to nasal cavity
tidal volume
inspiration and expiration that is just enough so you don’t pass out. Normal breathing
what is vital capacity
inspiratory capacity, tidal volume, expiratory capacity
inspiratory capacity
sum of tidal volume and IRV
FEV1 is what % of forced vital capacity?
80% and based on first second
Ventral Resp Group (VRG)
active respiration in Medulla - expiration
What stimulates inspiration?
what inhibits inspiration?
apneustic center in lower pons
pneumotaxic center in upper pons
during metabolic acidosis (decreased HCO3)
respond by decreasing CO2
- always respond with other chemical
how would body respond to respiratory acidosis (increased CO2)
by increasing HCO3
how would body respond to respiratory alkalosis (decreased CO2)?
by decreasing HCO3
at a PO2 of 100mm Hg what is hemoglobin saturation?
at 40 mm Hg
at 25 mm Hg
100% saturated
O2 bound to all four heme groups on all hemoglobin molecules
75% saturation (3 of 4 heme groups on each hemoglobin molecule have O2 bound)
50% saturation (2 of 4)
where does % saturation max out with carbon monoxide poisoning
50% (need more than that to stay alive)
- either die or have headaches
what does HCO3 leave RBCs in exchange for?
Cl- (chloride shift)
what inhibits smooth muscle in lungs?
sympathetic beta 2 autonomic nerve fibers
epiglottitis
epiglotis swells and then airways swell
- after H influenza or beta hemolytic strep
- steeple sign
- head bent over and drooling (only way air can still move through)
- stridor
what causes pulmonary edema?
left sided heart failure
- fluid overload/renal failure, decreased albumin, lymph obstruction
where do pulmonary emboli originate from?
originate in deep veins of legs and pelvis
sudden onset cyanosis and dyspnea
pulmonary HTN due to
left sided heart failure, mitral stenosis, increased pulmonary vascular resistance, emboli, scleroderma
Atelectasis
collapse or incomplete expansion of acini
tumors, FB, mucus blockage, surfactant deficiency
causes of pulmonary edema
left heart disease
pneumonia, toxic gas inhalation
decreased compliance due to
fibrosis
lack of surfactant
high pulmonary venous pressure
increased compliance due to
emphysema
obstructive lung disease
inability to move air out of lungs
interstitial/restrictive lung disease
scarring and tightening of lungs so they are unable to expand
chronic obstructive disease: emphysema
"pink puffers" normal pCO2 because compensating high RBCs/high hematocrit permanent dilation barrel chest
chronic bronchitis
blue bloaters increased pCO2 can cause cor pulmonale can become cyanotic persistant cough with sputum
lobar pneumonia
strep pneumonia
gm +
rusty brown sputum
starts at bottom and works its way up
(klebsiella gm - in alcoholics = red hepatization)
broncho pnemonia/lobular
patchy opportunistic infection
atypical pneumonia
see diffuse patchy feathery infiltrates
walking pneumonia
TB
delayed hypersensitivity type IV
caseating granulomas
apices of lungs/high O2
asthma
IgE type I hypersensitivity
cardiac asthma from left sided heart failure
pneumoconiosis
inhalation of dust
upper lobes
silicosis, asbestosis
type I hypersensitivity IgE
Goodpasture’s syndrome
antibodies against basement membrane of lung and kidneys
type II immune injury
hypersensitivity pneumonitis
farmers lung
pigeon breeders lung
non-caseating
pneumothorax
air/gas in pleural cavity
small/oat cell undifferentiated carcinoma
pancoast tumors, rapid death
ability to produce hormones
