covers outer surface of lungs; no sensory nerves
lines inner surface of chest & diaphragm
innervation - intercostal nerves
potential space w/ little fluid (~15mL in adults)
intrapleural pressure is subatmospheric
violation of pleural space, collapsed lung
normally an active process
- diaphragm (major muscle), innervated by phrenic nerve, spinal roots C3,4 & 5
- external intercostals - ↑ intrathoracic volume
-accessory muscles (seen in Dz): sternocleidomastoid & scalenes
usually a passive process
muscles involved (note: only in forced expiration)
- rectus abdominus
- internal intercostals
↑ compliance (stretchability) causes?
lung Dz's that cause obstruction
↓ complaince (stretchability) causes?
lung Dz's that cause scarring & fibrosis
ex: Pulmonary fibrosis
obstructive lung Dz
↑ compliance lung Dz - ex: emphysema
- tissue loss (↓ recoil forces) causes easily compressed airways
- produces ↓ air flow rates & ↑ airway resistance
- pts work hard to overcome airway resistance on expiration
restrictive lung Dz
↓ compliance lung dz - ex: pulmonary fibrosis
- fibrosis causes ↑ elastic recoil
- ↑ radial traction→ airway dilation
- produces → ↑ air flow rates & ↓ airway resistance
- pts work hard to overcome ↑ elastic recoil during inspiration
what is the cause if a pt has to work hard to overcome airway resistance on expiration?
obstructive lung Dz
what is the cause if a pt has to work hard to overcome increase elastic recoil during inspiration?
restrictive lung Dz
ability to retract or recoil from tissue & surface tension forces
generated by molecules of elastin & collagen
surface tension forces
generated primarily by water
reduced by surfactant
- synthesized by type II alveolar cells & coats lining of alveolous
- ↓ intermolecular forces between water molecules
- usually present by 35 weeks gestation
any impediment to flow of air throughout respiratory tree
what is airway resistance determined by?
- Major factor: airway diameter
-- note: if radius ↓ then resistance to airflow ↑
- rate of gas flow
major site of airway resistance = medium sized bronchi
Adrenergic stimulation causes what in airways?
name 2 β2-selective adrenergic agents
- β2-receptor stumlation = smooth muscle relaxation
β2-selective adrenergic agents:
- albuterol (short acting)
- salmetrol (long acting)
beta blockers causes what in airways? who is this bad for?
bad for asthmatics, people w/ obstructive Dz
cholinergic stimulation in airways causes? what agent would you administer?
bronchoconstriction & ↑ mucus production
administer anticholinergic agents for bronchodilation
nonadrenergic, noncholinergic activity for control of airway resistance
neuropeptides that contol airway smooth muscle
eg. vasoactive intestinal peptide (VIP), nitric oxide (NO)
note: no clinically available therapeutic agents for these substances yet
what inflammatory mediator controls airway resistance & what are its effects? what agent would you administer?
Leukotrienes (LT) - potent bronchoconstrictor
LT inhibitors (modifiers) for bronchodilation
LT inhibitors - Zafirlukast, Montelukast
air inspired or expired w/ each breath ~ 500mL (adult)
inspiratory reserve volume
additional air inspired above tidal volume (3L)
expiratory reserve volume
air that is forcefully expired after normal expiration (1.3L)
gas that remains in lungs after a maximal expieration (1.2L)
total lung capacity
volume in lungs after maximal inspiration (6L)
volume that can be expired after maximal inspiration
maximal volume that can be inspired after normal expiration
functional residual capacity
air that remains in lungs after normal expiration
volume of conducting airways ~ 150mL
forced vital capacity (FVC)
evaluated resistance properties of airways
forced expiratory volume in 1 sec (FEV1)
screening test for airway Dz
indicated volume of FVC expired in 1st second - shows flow resistance properties of airways
% of VC expired in 1 second (FEV1/FVC)
normally FEV1% > 75-80% FVC
peak flow meter
measures peak expiratory flow rate (PEFR) ~ FEV1
normally ~ 500 L/min
Barometric pressure of air
760mmHg & air is 21% of O2
Partial pressure of O2 (PO2) in air
what does pulse oximetry (pulse-ox) measure? what is is dependent on?
- using a red light emitting diode, pulse-ox indirectly measures O2 saturation (SaO2)
- measurement dependent upon adequate tissue perfusion
what does arterial blood gas (ABG) measure?
directly measures O2 & other parameters
what is the normal value for PO2 (or PaO2)?
what is the normal value for PCO2 (or PaCO2)?
~ 35-45 mmHg
what is the normal value for pH?
what is the pH range compatible with life?
what is the normal value for SaO2?
what is the normal value for [HCO3-]
explain oxygen transport in the lungs
- O2 diffuses across alveolus
- dissolves in plasma of pulmmonary capillaries
- diffuses into RBC & binds w/ Fe w/in Hb molecule
- deoxyhemoglobin → oxyhemoglobin (normal Hb=12-15 g/dL blood)
explain oxygen transport in the tissues
- PO2 is low secondary to metabolism
- O2 dissociates from Hb
- moves across RBC membrane
- dissolves in plasma
- diffuses across capillary wall
- finally enters interstitial tissue
An arterial O2 tension of ~ 85-100mmHg results in Hb saturation of?
- Hb + carbon monoxide (CO)
- gives skin a cherry color
- binding affinity of CO: 200x > O2
- binding is IRREVERSIBLE → TOXIC
Fe+2 → Fe+3 state → unable to bind O2
- gives skin "bluish" cyanotic color
- caused by drugs/foods (nitrates, fava beans) esp in pts w/ G6PD deficiency
explain carbon dioxide transport w/in the RBC
- 90% of CO2 enters RBC & is returned to lungs
- CO2 + H2O + carbonic anhydrase → H2CO3 → HCO3- + H+
- HCO3 - then diffuses out of RBC into plasma
how is most of CO2 carried in blood?
carried in blood as HCO3-
explain carbon dioxide transport in the lungs
HCO3- in blood enters RBC + H+ → H2CO3 → H2O + CO2
CO2 exists cell into alveolous
pulmonary blood flow
what is the normal V/Q ratio
list factors that affect V&Q?
- alveolar hypoxia, hypercapnia (↑ [CO2]) & acidosis → pulmonary vasoconstriction
- generalized alveolar hypoxia → ↑ total pulmonary vascular resistance