Respiratory Physiology Flashcards
what does the respiratory system do?
- oxygen into the blood to create ATP in mitocondria (electron transport chain)
- removes carbon dioxide from blood
- regulates blood pH
- speech
- microbial defense
- chemical messenger concentrations
- traps and dissolves small blood clots
conducting zone
trachea
primary bronchi
smaller bronchi
terminal bronchioles
functions:
cilia move mucus coordinatedly out of the lung toward the mouth
respiratory zone
alveolus is wrapped by capillaries
blood gas barrier between alveolus and capillary is 2 cells thick and very thin
type 1 cells, very thin
type 2 cells, produces surfactant
alveolar macrophage, immune cells, move around and picks up foreign particles
alveolar ventilation
pulmonary ventilation (VE) = volume of one breath (tidal volume VT) x breaths per min (respiratory rate RR)
conducting zone (amount of air that doesn’t participate in gas exchange anatomical dead zone VD) - every pound ~ 1 mL x RR
alveolar ventilation (VA)
VA = VE - VD
= (VT x RR) - (bodyweight x RR)
slower and deeper breaths - more air in alveoli
faster and shallow breaths - less air in alveoli
lung anatomy
right lung - 3 lobes
left lung - 2 lobes
lungs sit in thoracic cavity
ribs go around lungs and intercostal muscles between rib bones
parietal pleura membrane underneath ribcage
visceral pleura membrane surround lung and underneath parietal pleura
intrapleural space inbetween parietal and visceral pleura membranes
intrapulmonary pressure in lungs
intrapleural pressure inbetween pleura membranes
how does the thoratic volume change?
inhalation - ribs move up and out, diaphragm moves down
exhalation - ribs and diaphragm move back
atmosphere pressure - 760 mmHg
muscles of inhalation
external intercostals: muscles between ribs contract
diaphragm: dome-shaped skeletal muscle contract
breathing when exercising and at rest
passive exhalation - relax diaphragm and external intercostals
voluntary exhalation - contract obliques and rectus abdominus to force exhalation, which is faster
+ relaxation diaphragm and external intercostals
lung pressures
atmosphere pressure - 760 mmHg
intrapulmonary pressure - 760 mmHg
intrapleural pressure - 757 mmHg
transpulmonary pressure = intrapulmonary pressure - intrapleural pressure
= 3 mmHg
the intrapleural pressure must be lower than the intrapulmontary pressure to keep lungs from collapsing
inhaling and air is moving in, what happens to the intrapleural pressure?
the intrapleural pressure decreases to match the pressure difference between the 2 regions
lung compliance
“stretchability” of the lung
1 L of air in both A and B
Compliance = change in lung volume / change in lung pressure
A = 1 L / 1 mmHg
B = 1 L / 4 mmHg
the higher the compliance number the easier to stretch the lung
what influences compliance?
1) Elastic tissue (Elastin) of lungs (1/3 contribution)
considered recoil or “collapse” forces on the lungs
more elastin = harder to stretch (lower compliance)
2) Surface tension (2/3 contribution)
air-liquid interface (layer of water)
underneath the water layer is epithelium cells (type 1 & 2)
why don’t our alveoli collapse?
pulmonary surfactant is made by type 2 cells in the alveoli, made of phospholipids lying over the air-liquid interface
the fatty-acid tails are not attracted to the water, and the hydrophobic head attracts to the water
this balances the water layer and prevents a water droplet from forming and collapsing
pulmonary surfactant function
1) reduces surface tension *prevents alveolar collapse
2) microbial defense
Neonatal Respiratory Distress Syndrome (nRDS)
- occurs in premature infants
- poor lung function, alveolar collapse, hypoxemia (low blood oxygen)
- lack mature surfactant system
Treatment = administer surfactant (put surfactant inside lungs)
surfactant taken from cows
breathing amounts
tidal volume - normal breaths
inspiratory reserve volume - max amount of air you can breath in after a tidal inhalation
expiratory reserve volume - max amount of air you can exhale after tidal exhalation
residual volume - minimum air left in lungs
total lung capacity = residual + expiratory reserve volume + tital volume + inspiratory reserve volume
vital capacity - the amount of air that can be moved (total lung cap - residual)
lung function test
FVC (forced vital capacity) = 5 L (after max air inhaled, the total air that can be exhaled)
FEV1 = 5 - 1 L = 4 L (amount of air in lungs after 1 second of exhaling from max inhalation)
FEV1/FVC = 4 L/ 5 L = 0.8 = 80%
lung function test in obstructive lung disease
FVC (force vital capacity) = 5 L (normal amount)
FEV1 = 2.5 L at 1 second compared to 4 L at 1 second (normal amount)
FEV1/ FVC = 50%
<80%
asthma
asthma: airway spasms in smooth muscle
airway inflammation + airways hyperresponsive
result: airway narrows
induced by allergens, pollution, exercise, cold air
emphysema
smoking is a major cause
- destruction of alveolar walls
- loss of elastin
- reduces elastic recoil
lung function test with restrictive lung diseases
FVC = 4 L (lower FVC than normal)
FEV1 = 3.5 L
FEV1/ FVC = 3.5 L / 4 L
= 88%
>80%
pulmonary fibrosis
pulmonary fibrosis: less compliant due to scar tissue
causes: chronic inhalation of asbestos, coal dust, pollution. sometimes unknown
- scar tissue is less elastic and hard to expand to inhale more air
partial pressure of air
oxygen - 21%
nitrogen - 78%
carbon dioxide - 0.03%
partial pressure oxygen = 21/100 x 760 mmHg = 160 mmHg
partical pressure carbon dioxide = 0.03/100 x 760 mmHg = 0.3 mmHg
gas exchange in alveoli
simple diffusion
blood-gas barrier
type 1 cell wall in alveolar (squamous)
endothelial cell under type 1 cell
then capillary
oxygen and carbon dioxide are small and hydrophobic and can diffuse through cell wall
Fick’s law = surface area x gradient / thickness
oxygen pathway
- O2 enters capillaries from alveoli
- O2 rich blood circulates (some CO2)
- O2 leaves capillaries into body tissues
- CO2 enters capillaries from body tissues
- CO2 rich blood circulates (some O2)
- CO2 enters alveoli from capillaries
how does oxygen go into blood from lungs and body to blood?
atmospheric PO2 = 160 mmHg
“stale air” alveolar PO2 = 100 mmHg
pulmonary vein PO2 = 100 mmHg
systemic arteries PO2 = 100 mmHg (no capillaries yet)
body tissue at rest PO2 <= 40 mmHg
systemic veins PO2 = 40 mmHg (same as body tissues)
pulmonary artery PO2 = 40 mmHg (no capillaries)
blood composition
plasma - 55% (water, proteins, ions, gases, vitamins, glucose, other nutrients, wastes)
white blood cells and platelets - <1% (leukocytes and cell fragments)
red blood cells - 45% (erythrocytes)
transport of oxygen
oxygen is carried in blood in two ways
1) dissolved in plasma (1.5%)
2) bound to hemo in hemoglobin: inside erythrocytes (98.5%)
4 chains of globin
4 heme groups that contain iron that binds oxygen
oxyhemoglobin (HbO2) ⇔ O2 + Hb
oxyhemoglobin dissociation curve
resting cell PO2 = 40 mmHg
alveolar PO2 = 100 mmHg
hemoglobin saturation % is around 70% after delivering oxygen to resting cells
saturation goes down if not at rest
carbon monoxide (CO) poisoning
- CO from car exhaust & tobacco smoke
- binds to Hb heme group better than O2
- treat by administering higher % of O2
CO2 pathway
at body tissues PCO2 < 46 mmHg
venous PCO2 = 46 mmHg
pulmonary artery PCO2 = 46 mmHg
alveolar PCO2 = 40 mmHg
atmospheric PCO2 = 0.3 mmHg
pulmonary vein PCO2 = 40 mmHg
arterial PCO2 = 40 mmHg
carbon dioxide transport
1) dissolved in plasma (7%)
2) carbamino form: attached to blood proteins (23%)
“globin” subunits of hemoglobin (not heme)
3) bicarbonate ion (HCO3-)(70%)
- CO2 + H2O combine to form carbonic acid that dissociates into H+ and HCO3- ion
- by lots of enzyme Carbonic Anhydrase in the red blood cell
- H2CO3 unstable and → HCO3- + H+ bicarbonate builds up and will reverse the reaction
- to remove more CO2 from the body tissue, bicarbonate is exchanged for Cl- from the blood
CO2 + H2O → H2CO3 → HCO3- + H+
Bohr Effect
Borh effect: changes the structure of protein, to make hemoglobin less affinity to oxygen and release more oxygen into cells
increase temperature - temperature changes metabolic rate and protein structure and changes affinity for oxygen (more heat, more oxygen is released from hemoglobin to body cells)
increased pCO2 - oxygen affinity decreases (more oxygen is released from hemoglobin to body cells)
decrease pH (acidic) - H+ like lactic acid is created when exercising, more oxygen is needed and removes CO2 and H+
events at the tissue
→ high PO2 (100 mmHg), low PCO2 (40 mmHg) from arterioles into capillaries
low PO2 in cells - some dissolved O2 leaves plasma H100
- O2 leaves Hb from HbO2
high PCO2 in cells- some CO2 binds to Hb
CO2 + H2O ⇔CA H2CO3 ⇔ HCO3 + H+
some CO2 dissolves in plasma
→ low PO2 (40 mmHg), high PCO2 (46 mmHg) from venules to veins
events at alveoli
→ low PO2 (40 mmHg), high PCO2 (46 mmHg) from pulmonary arterioles into capillaries
some dissolved CO2 leaves plasma into alveoli
CO2 + H2O ⇔CA H2CO3 ⇔ HCO3 + H+ (drive to CO2 + H2O)
CO2 removed from Hb into alveoli
O2 binds to Hb → HbO2
some O2 dissolves in plasma
→ high PO2 (100 mmHg), low PCO2 (40 mmHg) into pulmonary venules then pulmonary veins
homeostasis of breathing
set point - PO2 = 100 mmHg, PCO2 = 40 mmHg, pH = 7.4
control center → medulla respiratory center
effector → diaphragm, intercostals (breathing muscles)
controlled variable → PO2 PCO2 pH
receptor → chemoreceptors (central and peripheral)
receptor ⇔ control center (⇔ action potentials)
chemoreceptors
1) peripheral chemoreceptors: in aortic arch, carotid body
2) central chemoreceptors: in medulla oblongata
peripheral chemoreceptors
sensitive to PO2, PCO2 and pH
if not normal, chemoreceptor detects this and sends APs to the respiratory center in medulla
respiratory center in medulla sends APs to respiratory muscles
central chemoreceptors
sensitive to pH (hydrogen ions)
CO2 + H2O ⇔CA H2CO3 ⇔ HCO3 + H+ (brain capillary near medulla)
blood brain barrier separates blood from cerebrospinal fluid
cerebrospinal fluid (interstitual fluid)
central chemreceptor in cerebrospinal fluid
CO2 can cross through the barrier and combines with water→ H2CO3 → HCO3- + H+
pH lots of H+ increase AP and increases alveolar ventilation (VA)
respiratory acidosis/alkalosis
respiratory acidosis: pH < 7.4 due to changes in pulmonary gas exchange
A intercalated cells (removes H+)
respiratory alkalosis: pH > 7.4
B intercalated cells (removes HCO3-)
metabolic acidosis/alkalosis
metabolic acidosis: pH < 7.4 due to changes in pH unrelated to CO2
- kidney disease, acetylsalicylic acid overdose, diarrhea
metabolic alkalosis: pH > 7.4 due to changes in pH unrelated to CO2
- prolonged vomiting
how is metabolic acidosis/alkalosis fixed?
metabolic acidosis is fixed by increasing the VA (alveolar ventilation)
metabolic alkalosis is fixed by decreasing the VA
blood composition and properties
hematocrit (blood cells)
properties: biconcave, no nucleus, no organelles
packed with hemoglobin
carbonic anhydrase: CO2 (bicarbonate)
anemia and polycythemia
anemia: depressed hemocrit % (red blood cells, erythrocytes)
- fatigue, muscle weakness, breathlessness, increased heart rate
polycythemia: elevated hemocrit %
- too many blood cells
causes of anemia
low production of erythrocytes
- bone marrow issues
- improper nutrition (eg. iron, Vit B12, folic acid)
- kidney failure
increased loss of erythrocytes
- bleeding
- hemolytic diseases (eg. sickle cell)
red blood cell hemostasis
red blood cell made from bone marrow
regulated by hormone erythropoietin (EPO)
erythropoietin
- peptide hormone
- acts on bone marrow
- released from kidney
- stimulus → low PO2
⇒ 1. anaemia
- circulatory issues
- lung disease
- altitude
