03: Respiratory Physiology Flashcards
FIO2
Fractional concentration of oxygen in inspired gas (21%).
Hypercapnia
Too much CO2 in blood; increases cerebral blood flow/intracranial pressure; causes tremor, confusion, coma; causes acidemia (low blood pH)
Calculation of a partial pressure.
Pgas = Fgas x Ptotal
Use to calculate partial pressure of oxygen in air at sea level.
Caution: Must also accont for water vapor pressure!
PiO2 = (Patm - PH2O) x FiO2
Where PH2O = 47 mmHg
Muscles of inspiration
Diaphragm, external intercostals, accessory muscles (scalenes & SCMs)
Muscles of expiration
Passive during quiet breathing, but active during exercise or times of stress (abdominal wall musculature, internal intercostals)
Transpulmonary pressure
The pressure expanding the lung.
Ptp = Palv - Pip
Where Ptp is transpulmonary pressure, Palv is alveolar pressure, and Pip is intrapleural pressure.
At rest, Ptp = +5cm H2O
Pleural pressure
Pressure within the pleural cavity.
Normally -5 cm H2O, due to chest wall elastic recoil (outward) = lung elastic recoil (inward).
RR
Respiratory rate.
10-16 per minute.
VT
Tidal volume
Gas inspired in a single breath.
~0.5 liters.
Composed of gas delivered to dead space and to alveolar space: VT = VD + VA (500mL = 150mL + 350 mL).
Use to determine V.A (alveolar ventilation):
VT x RR = (VD x RR) + (VA x RR)
V.E = V.D + V.A
(6 L/min = 1.8 L/min + 4.2 L/min)
VE
Minute ventilation
Volume of gas expired per minute.
~6-7 liters/minute.
VE = RR x VT
Hyperpnea
Increased tidal volume
Dead space
Anatomic dead space: conducting zone; does not participate in gas exchange; normal; 1ml per lb of body weight.
Physiologic dead space: ADS + diseased areas of lung; areas not participating in gas exchange.
Alveolar ventilation
- Eliminates CO2 from alveoli (too much = hypercapnia); hypercapnia causes:
- ↑cerebral blood flow, intracranial pressure
- tremor, confusion, coma
- acidemia
- Delivers O2 to alveoli (not enough = hypoxemia); hypoxemia causes:
- tissue hypoxia
- inhibition of cellular aerobic respiration
- death
What factors control breathing?
-
Peripheral chemoreceptors (O2, CO2, H+ [via CN IX, X])
- Located in carotid and aortic bodies
-
Central chemoreceptors (H+)
- Indirect response to CO2 stimulation
- CO2 readily passes through BBB, joins with H2O to form H+ and HCO3-
- Strongest influence on minute-to-minute control of breathing!
- Note: If arterial PCO2 > 100 mmHg, can actually cause decrease in respiratory drive (especially if acute); due to metabolic depression of all CNS functions: CO2 narcosis
-
Inspiratory inhibition reflex (Hering-Breuer reflex)
- Mechanoreceptors in airway smooth muscle
- Deep inspiration (distension stimulus) triggers decreased breathing rate
-
Irritant receptors
- Inhaled irritants stimulate receptors in airway epithelium
- Causes tachypnea, bronchoconstriction
-
J (juxtacapillary) receptors
- Located in alveolar walls
- Pulmonary edema, other long processes activate receptors
- Cause ↑ respiratory drive
-
Joint & muscle receptors
- ↑ respiratory drive in anticipation of exercise
All activate the inspiratory center, which stimulates the phrenic nerve (which controls the diaphragm).
V.CO2
Rate of transfer of CO2from pulmonary circulation to alveolus.
CO2 diffuses freely between blood and alveolus; highly soluble in tissues and not limited by properties of lung.
V.CO2 dependent on amount of CO2 delivered to alveolus (alveolar perfusion); depends on CO2 production and cardiac output (both constant at rest).
PACO2
Alveolar PCO2
Determined by 1) CO2 transer from blood to alveolus (V.CO2) and 2) CO2 elimination via expiration (V.A).
Can rearrange equation to measure alveolar ventilation.
Since CO2 diffuses freely between blood and alveolus, PACO2 = PaCO2.
Clinical assessment of alveolar ventilation.
- Normal PaCO2 = 37-42mmHg
- PaCO2 < 37mmHg
- Hypocapnia
- 2/2 alveloar hyperventilation
- PaCO2 > 42mmHg
- Hypercapnia
- 2/2 alveolar hypoventilation
Causes of alveolar hyperventilation
Due to increased respiratory drive
- Hypoxemia
- Acidemia
- Stimulation of lung receptors
- Drugs (ASA, progestins)
- Pain
- Anxiety
- Fever
- Pregnancy
- Exercise
- Hypercapnia
Causes of alveolar hypoventilation
Decreased respiratory drive and/or effort
- Drugs (benzodiazepines)
- Brain injury (trauma, stroke, ↑intracranial pressure)
- CO2 narcosis: PCO2 >100mmHg causes metabolic depression
- Sleep
- Breath-holding
Neuromuscular problem
- Failed NM transmission (spinal cord, peripheral nerve)
- Muscle weakness
Muscle fatigue due to increased load
- Abnormal mechanics
- ↑dead space
Work of breathing
- Energy expended during ventilation
- Causes of ↑WOB
- ↑respiratory drive
- abn. respiratory system mechanics
- ↑dead space
- Signs of ↑WOB
- accessory muscle use
- tachypnea
- nasal flaring
- paradoxical breathing
- Consequences of ↑WOB
- respiratory muscle fatigue
- cannot continue indefinitely
- fatigue –> alveolar hypoventilation
Dead space
- Ventilated space that does not participate in gas exchange
- Sources
- External conducting airways (e.g., snorkel, ventilator tubing)
- Created from alveolar space
- ↑dead space, ↓alveolar space
- Results in ↑minute ventilation –> ↑WOB –> fatigue
Factors ↑ventilatory load
- ↑respiratory drive
- dead space
- tight airways
- stiff lungs
Factors ↓ventilatory capacity
- Muscular fatigue
- Neuromuscular disease
- CNS depression
Acute vs. chronic alveolar hypoventilation
- Acute: minutes to hours
- Renal compensation limited
- pH < 7.3
- Acute hypercapneic respiratory failure
-
Chronic: days or longer
- Renal compensation nearly complete
- pH nears 7.4
