Physio Flashcards
Aa gradient
normal difference of 4mmHg between alveoli and artery
absorption curve for CO2 in the blood
with increased PCO2, total CO2 increases, pH decreases because Hb is buffering with imidazole group
airflow is dependent on….
resistance and pressure gradient (Palv-Patm)
amount of dissolved O2
18 ml/min of O2 to tissues, inadequate to meet needs (250-300 ml/min)
alveolar dead space
increased Aa gradient with hypoxemia; decreased alveolar ventilation, use O2 therapy to increase blood O2
amount of O2 bound to Hb
15 g/100 ml Hb, 1.34 ml O2 bound/Hb→1200ml/min
anemic hypoxia
ex. Fe deficiency anemia or congenital hemolytic anemias (e.g., sickle cell)
* normal PaO2 but low CaO2 with normal extraction→low PvO2
ATPS
ambient temperature and pressure, saturated (25ºC, 760mmHg, 24mmHg)
factors that induce bronchoconstriction
- histamine via H1 receptors (also causes profound vaso/venodilation, broncho and laryngeal spasm)
- parasymp via vagus on cholinergic muscarinic receptors
- **ß2 antagonists **on lung smooth muscle
- **reflex constriction: **noxious fumes, extreme cold, smoke particles
body plethysmography
closed system that measures total air in the lung at FRC
bohr effect
deoxyHb is a weaker acid than oxyHb (binds to H+ tighter) so at any given PO2, O2 sat. decreases as PCO2 increases because H+ binding to Hb causes 3D conformation change reducing affinity for O2
BTPS
body temperature and pressure, saturated
(37°C, 760mmHg, 47mmHg)
describe the control of breathing by the brainstem
-
mainly occurs in the medulla (CPG), modulated by the pons (PRG)
- when cut between pons and medulla: rhythmic breathing but series of gasping
- medulla: CPG; nuclei work together to generate respiratory rhythm
- DRG: inspiration
- VRG: expiration, some inspiration
- botzinger complex: mostly expiratory
describe the pathophysiology of exercise induced hypoxemia in patients with impaired diffusion capacity
cardiac output is increased, transit time in pulmonary capillaries is reduced (normal indviduals can equilibrate; leads to hypoxemia in individuals with diffusion problem)
diffusion problem
increased Aa gradient with hypoxemia; O2 therapy (even though you can’t fix diffusion problem you can drive up A PO2 enough to compensate)
dynamic compression
forced expiration; partially collapses airways causing equal pressure point to move closer to alveoli with greater expiratory efforts
- patients with elevated compliance (emphysema) experience greater dynamic compressure during expiration
emphysema
- neutrophils accumulate in lung to remove inhaled smoke particles→release proteases→lung CT digested by proteases→ elevated lung compliance
- smoke inhibits a1-antitrypsin (normally inhibits proteases and protects lung)
- *elevated compliance→greater dynamic compression during expiration (epp becomes closer to alveoli); *inspiration is easy but exhalation causes airways to collapse on themselves
eupnea
normal quiet breathing; inspiration is active and expiration is passive
- negative pressure pump because diaphragm contraction→expansive force on intrapleural space→decreases pressure→lungs inflate
factors that induce bronchodilation
- ß2 agonists: (ex. symp→ epi, albuterol) on lung smooth muscle
factors that influence DLCO
- anything that changes area or thickness
- greater when lying down (more blood to lung, distends capillaries and increases area)
- increased cardiac output→blood to the lung
- lung diseases and dysfunction
- loss of lung tissue
- ventiliation-perfusion mismatch
- fibrosis and edema increases diffusion distance (decreases DLCO)
fibrotic lung disease
- caused by inhalation of toxic mineral particles→granulomatous and fibrous tissue (collagen and elastin deposition)→decrease complaince (stiffer lung)
- inspiration is difficult
functional residual capacity
lung volume equilibrium; outward recoil of chest=inward recoil of lungs
- occurs on graph where P-V curve crosses 0 line
fick’s law for diffusion of gases
- governs diffusion through physical boundary
- flow of gas across membrane is directly proportional to membrane area and difference in PPgas in alveoli and capillarie; inversely proportional to membrane thickness
- V=(A/T)D(PA-PC)
- greater the PP graient the greater flow; single most important factor that governs new flow of as across the membrane
- DL=DA/T
gradients of intrapleural pressure
at top: V/Q ratio >1
- less Q because of gravity; high compliance because of small lung volume
at middle ratio=1
at base: ratio
- more Q because of gravity; lower compliance because of larger lung volume
haldane effect
*minimizes acidication of venous blood; *deoxyHb is a weaker acid than oxyHb (binds to H+ tighter) so CO2 absorption curve shifts upwards when you deoxygenate the blood, at any given PCO2, total CO2 content in blood is higher than in oxygenated blood
helium dilution
measures exchangeable air (FRC) because helium doesn’t get absorbed in alveoli
- blebs: trapped air that doesn’t communicate with bronchial tree; He underestimates FRC if blebs exist
henderson-hasselbalch equation
pH=6.1 + log [HCO3-]/0.03PCO2
- titration curve for bicarbonate seems like it is not a good buffer for arterial blood because little changes in acid form lead to big changes in pH BUT ventilatory response maintains blood pH (excess CO2 is exhaled; maintains PCO2 at 40mmhg)
henry’s law of gas solubility
[cg]=aPi
- Pi of gas in solution refers only to dissolved gas (NOT gas on Hb)
- Pi of a gas in solution equals Pi of gas with which the solution has equilibrated
- Dissolved gases don’t contribute to blood volume or BP
hering-breuer reflex
negative feedback during deep inspirations
- lung inflation→slowly adapting stretch receptors (in smooth muscle of tracheobronchial tree) causes L shift of dissociation curve and inhibits further inflation via vagal afferents and phrenic efferents
- important when TV increases during periodic deep breaths, exercise, and COPD when patients breathe at high FRC due to increased compliance
historesis
P-V relationship during inhalation is different than during exhalation; physiologically advantageous
- inspiration: slope initially steep but compliance goes down at high lung volumes because lung is more stretched out
- if you lose water-air interface, you lose historesis
histotoxic hypoxia
ex. poisoning of tissue metabolism (e.g., heavy metals, cyanide, toxins)
* normal PaO2 and CaO2 with reduced extraction→elevated PvO2
how are shunts and alveolar dead space exaggerations of physiological conditions?
- shunt: exaggeration of what happens at base of lung→small V/Q ratio, hypoxemia without much hypercapnia
- alveolar dead space: exaggeration of what happens at top of lung→ventilation without prfusion (e.g., PE) very high V/Q ratio
how do changes in frequency of nerve APs modulate breathing?
- eupnea: some APs generated in abs/internal intercostals but movements are mostly passive due to elastic recoil
- hyperpnea: phrenic and external intercostal APs intensify, abs/internal intercostal APs increase
how do pH, PCO2, temperature and 2,3 DPG affect the O2 dissociation curve?
RIGHT SHIFT when:
- pH: more acidic
- PCO2: higher
- temperature: higher
- 2,3 DPG: higher
how do peripheral chemoreceptors sense and influence minut rate of ventilation?
located in carotid and aortic bodies and activated by low blood PO2, high PCO2 and high [H+]
- glomus cell: changes to O2, CO2, H+ concentrations→inhibition of K+ channels→reduce ration of K+:Na+ permeability→depolarizes resting membrane potential→opens voltage-sensitive Ca2+ channels→Ca2+ in→NTs released (dopa)→activates CNIX→afferent signal to medulla