Physiology Flashcards
parietal pleural membrane
outer membrane of the lung that is against the inner surface of the thoracic cavity
visceral pleural membrane
membrane that covers the surface of each lung
pleural cavity
space between the parietal and visceral membranes
What is the order of branching in the respiratory tree from largest to smallest?
- trachea
- main bronchus
- lobar bronchus
- segmental bronchus
- conducting bronchiole
- terminal bronchiole
- respiratory bronchiole
- alveolar duct
- alveolar sac
- alveolus
Conducting zone vs. respiratory zone
conducting zone:
-trachea to terminal bronchiole
respiratory zone:
- respiratory bronchiole
- alveolar duct and sac
- alveolus
What functions are greatly decreased in the respiratory zone?
- smooth muscle
- ability to constrict passages
respiratory epithelium in the nasal cavity
mucous cells and mucus escalator
respiratory epithelium in the pharynx
stratified squamous for protection from abrasion and chemical attack
respiratory epithelium in the conducting portion of respiratory tract
typical respiratory mucosa
respiratory epithelium in the bronchioles
becomes cuboidal
respiratory epithelium in the gas exchange surfaces
delicate simple squamous epithelium
pneymocytes (3)
- Type I alveolar cells
- Type II alveolar cells
- Alveolar macrophages
type I alveolar cells
form the alveolar wall
type II alveolar cells
- secrete surfactant
- allows membranes to separate
- continuously released by exocytosis
- aqueous protein-containing hypophase and overlying phospholipid film composed primaryily of dipalmitoyl phosphatidylcholine
purpose of surfactant
lower surface tension
alveolar macrophages
phagocytize foreign material such as bacteria
pulmonary circulation of low oxygen blood
- returned from systemic circulation to RA
- RV to pulmonary artery
- to capillaries in lungs
pulmonary circulation of oxygenated blood
- from lungs to pulmonary veins to LA
- LV to aorta to systemic circ
atmospheric pressure at sea level
760 mmHg
intrapulmonary pressure
- where
- how does it change
- within alveoli
- changes w/ volumes
intrapleural pressure
- where
- relation w/ atmospheric pressure
- within pleural cavity
- about -4 from atmospheric pressure
What are the 3 factors that hold the lungs to the thorax?
- surface tension of pleural fluid
-holds membranes together - positive pressure in lungs
-always higher than
intrapleural
-net outward pressure - atmospheric pressure
-exterior force
-higher than subatm. P of intrapleural space
What are the 2 factors that pull lungs from thorax?
- recoil tendency
- elastic nature of lungs
- always seek smallest size - alveolar surface tension
- draws the alveolus in
- maintaining air in this space prevents collapses
- also fluid from type II cells
What is the most important factor in holding the lungs to the thorax?
negative pressure of the intraplueral space (positive pressure in lungs)
atelectasis
collapse/closure of the lung
Boyle’s Law
pressure of a gas varies inversely with its volume
effects of increasing thoracic volume in all direction
- lowers pressure interiorly
- air rushes in through trachea down its pressure gradient
- results in inspiration
effects of relaxation of the thorax
- compresses air inside
- air flows out from this area of increased pressure
- results in expiration
Sequence of events in inspiration (5)
- inspiratory muscles contract
- thoracic cavity volume increases
- lungs are stretched; intrapulmonary volume increases
- intrapulmonary pressure drops
- air flows into lungs down pressure gradient until intrapulmonary pressure is 0 (equal to atmospheric)
Sequence of events in expiration (5)
- inspiratory muscles relax
- thoracic cavity volume decreases
- elastic lungs recoil passively; intrapulmonary volume decreases
- intrapulmonary pressure rises
- air flows out of lungs down pressure gradient until intrapulmonary pressure is 0
Resistance
the opposition to airflow
resistance depends on what?
- diameter of tube
- type of flow: turbinate; laminar
- viscosity of gas (humidity)
airflow equation
V = deltaP / R
airflow = pressure gradient / resistance
physical factors influencing ventilation through airway resistance
- obstruction
- bronchoconstriction: smooth muscle contraction, parasympathetic control, irritants, RAD
- bronchodilation: smooth muscle relaxation, sympathetic control
lung compliance
- ease w/ which lungs can be distended or stretched
- a measure of the change in lung volume that occurs w/ a change in the intrapulmonary pressure
compliance equation
C = delta V / delta P
hysteresis
gap between input and output
where is airway resistance the highest?
the medium sized bronchi of the conducting zone
lung compliance is dependent on what?
elasticity of tissues
lung compliance decreases with what? (4)
- decreased lung elasticity such as fibrosis
- obstruction
- alveolar film changes
- impaired thoracic cage flexibility
factors influencing ventilation through lung elasticity
- ability of tissues to recoil
- essential to expiration
- COPD reduces recoil d/t deterioration of alveolar walls
surface tension
- occurs at fluid-air interface
- liquid molecules are more attracted to each other
- creates tension across liquid surface
- water has high surface tension
surfactant
- alveolar film
- secreted from type II alveolar cells
- lipoprotein
- disrupts cohesiveness of water molecules
- decreases surface tension
- prevents alveolar collapse
- reduces energy required to overcome surface tension
infant respiratory distress syndrome
- insufficient surfactant in neonate
- incidence decreases w/ increasing gestational age
- 50% in babies born at 26-28 wks; 25% at 30-31 wks
- high HR, RR, cyanosis
- tx: surfactant spray and positive pressure ventilation
spirometry
- measuring of breath
- most common PFT
- measures lung function
- specifically the amount (vol.) and/or speed (flow) of air that can be inhaled and exhaled
tidal volume (TV)
quiet eupnea
inspiratory reserve volume (IRV)
air forced in above TV
expiratory reserve volume (ERV)
forced out after exp
residual volume (RV)
- remains after forced expiration
- maintains alveolar patency and prevents lung collapse
inspiratory capacity (IC)
- total amount that can be inhaled after tidal expiration
- TV + IRV
Have a general understanding of the amount of air in each pulmonary capacity
- IRV: 3100 ml
- TV: 500 ml
- ERV: 1200 ml
- RV: 1200
- IC: 3600
- FRC: 2400
- VC: 4800
- TLC: 6000
functional reserve capacity (FRC)
- amount of air remaining in lungs after tidal expiration
- ERV + RV
vital capacity (VC)
- total amount of exchangeable air
- TV + IRV + ERV
total lung capacity (TLC
sum of all
dead space
air which enters the pulmonary space but cannot be used
anatomical dead space
- conducting zone
- 150 ml of tidal volume
physiological dead space
- nonfunctioning alveolus
- d/t mucus or blood flow
pulmonary function tests (PFT)
measurement of pulmonary function, dysfunction and efficacy of medication
minute respiratory volume (MRV)
- total vol. moved in 1 minute
- TV x breaths per min
- 500 ml x 12 breaths per min. = 6000 ml/min
- rate and depth increases w/ activity
forced vital capacity (FVC)
-deep breath and rapid forced exhalation
forced exiratory volume (FEV)
- FVC measurements at specific intervals:
- FEV1: volume in first second
- FEV1 FVC ratio (normal is 80%)
FEV1 in obstructive diesase
- low and slow
- ratio = 40%
FEV1 in restrictive disease
- low and fast
- ratio = 88%
alveolar ventilation rate
- better index of effective ventilation than MRV
- subtracts dead space volume
What are processes other than breathing that move air?
- cough: forced expulsion of air from lower respiratory tract
- sneeze: forced expulsion of air from upper airways
- hiccup: diaphragm spasms
- crying/laughing: emotionally induced, release of air in short expirations
- yawns: deep inspiration w/ jaw open; ventilates all alveoli
Dalton’s Law
-total pressure exerted by a mixture of gases is the sum of the pressures of each gas
Henry’s Law
- the solubility of a gas in a liquid is directly proportional to the pressure of that gas above the surface of the solution
- i.e: dissolves in proportion to its pp
- depends also on the solubility of the gas in liquid
- CO2 is very soluble
hyperbaric chamber
- makes use of henry’s law
- increase atmospheric pressure
- increases partial pressure of O2
- increasing diffusion into blood
- use in CO poisoning, gas gangene, would healing, decompression sickness
properties of gases
atmospheric p. at sea level = 760 mmHg
- N2 (78.6%) - 597
- O2 (20.9%) - 159
- CO2 (0.04%) - 0.3
- H2O (0.46%) - 3.7
properties of alveolar gases
- N2 (74.9%) - 569
- O2 (13.7%) - 104
- CO2 (5.2%) - 40
- H2O (6.2%) - 47
What is the difference in amount of gases between air and alveolar gas due to?
- gas exchange
- humidification
- mixture of new and residual air
diffusing capacity
- diffusing capacity of the lung for a gas is indirectly proportional to the surface area of the alveolar-capillary membrane
- it is inversely proportional to its thickness
diffusing capacity equation
DLCO = V / P
DLCO (diffusing capacity of lung to CO2)
- a measure of how well oxygen and CO2 are transferred (diffused) b/w the lung and the blood
- CO2 is generally the test gas used to measure
When is DLCO reduced?
in diseases that:
- thicken the membrane (fibrosis)
- reduce the surface area of membrane (emphysema, cancer)
external respiration
- where
- based on what
- occurs at alveolus-capillary junction
- based on pressure gradients and solubility
what is the surface area for diffusion in the lung?
- 300 million alveoli
- 145m (size of tennis court)
ventilation
(V) = air reaching alveolus
perfusion
(Q) = gas reaching pulmonary capillaries
ventilation perfusion coupling
- V/Q
- ideally matched
VQ scan
- imaging
- inhaled radiolabeled isotope
- gold standard for PE
in pulmonary gas exchange, what happens when alveolar O2 is inadequate?
pulmonary vasoconstriction occurs to send blood to more ventilated areas
in pulmonary gas exchange, what happens when alveolar CO2 is high?
vasodilation occurs to allow for greater CO2 diffusion from blood
internal respiration occurs between ?
between blood and tissues
What solves the poor solubility of O2?
hemoglobin
At what partial pressure is Hgb saturated?
70 mmHg
purpose of the venous reserve
- it can deliver O2 rapidly to tissues in need w/o changing RR or HR
- about 20-25% O2 is unloaded in 1 venous circuit
What effect does temp have on hgb affinity for O2?
- as temp increases, affinity for O2 decreases (not linear)
- decreasing affinity relates to O2 unloading which is desirable in areas of high metabolic activity
Bohr effect
- As [H+] increases, pH decreases
- low pH decreases affinity for O2
- metabolically active tissues release more CO2 and H+
- so O2 unloading occurs at active tissues needing it
DPG
- diphosphoglycerate
- intermediate of glycolysis in RBCs
- binds Hgb and decreases its affinity for O2
as DPG increases, what is the result?
more O2 is available to the tissues
hormones that increase RBC activity
- thyroxine
- testosterone
- growth hormone
- catecholamines (epi norepi)
what does a left shift indicate in the O2 dissociation curve?
high O2 affinity
what does a right shift indicate in the O2 dissociation curve?
lower O2 affinity
oxygen saturation
- SaO2
- pulse ox measures peripheral O2 sat as an estimate of percentage of O2 bound to Hgb
- healthy: 96-99%
- <90% is hypoxemia
partial pressure oxygen
- PaO2
- low oxygen pressure Hgb tends to be unsaturated
- in cells= 40mmHg
- in blood = 75-100mmHg
PaO2 in the oxygen dissociation curve
- at low PaO2, Hgb becomes rapidly saturated w/ O2
- levels off w/ increasing partial pressures of O2
Hgb binding to CO
-Hgb binds CO 200-250 times more radily than with O2
-Hgb completely dissociates the oxygen molecules for the more favorable CO, yeilding HbCO
= hypoxia (w/o cyanosis), HA, confusion, respiratory distress, coma, death
Hgb CO reaction equation
HbO2 + CO HbCO + O2
what is the source of carbon dioxide?
- cellular respiration
- 200 mL produced per min
3 forms of CO2 transport
- dissolved in plasma (7-10%)
- carbaminohemoglobin (20-30%)
- bicarbonate ion (60-70%)
carbaminohemoglobin
- hgb can bind to 4 CO2 molecules
- in absence of O2, unbound hgb molecules have greater chance of becoming carbaminohemoglobin
- distinctive blue color contributes to dark red color of low O2 in venous blood
bicarbonate ion forms d/t what?
enzymatic activity of carbonic anhydrase
equation yielding bicarb
CO2 + H2O H2CO3 HCO3- + H+
carbon dioxide + water carbonic acid bicarb + hydrogen
Bohr efffect
generation of H+ enhances O2 unloading
Haldane effect
- deoxygenation of Hgb increases its ability to bind CO2
- Hgb uptakes protons
- buffering pH in the RBC
pH blood values
- normal: 7.35-7.45
- acidosis: <7.35
- alkalosis: >7.45
acid base disorders are changes in what? (3)
- blood pH
- arterial pCO2
- blood HCO3
actual changes in pH depend on what?
the degree of physiologic compensation
respiratory causes of acid-base balance disorders
- inadequacy of respiratory function
- usually pCO2 imbalance
metabolic cause of acid-base balance disorders
any abnormalities resulting in pH changes except those caused by pCO2 imbalance
compensation mechanisms
- respiratory changes
- buffering systems in blood and tissues
- kidney absorption and secretion
metabolic acidosis can be d/t: (4)
- increased acid production
- acid ingestion
- decreased renal acid secretion
- GI or renal HCO3 loss
metabolic alkalosis causes: (2)
- acid loss
- HCO3 retention
respiratory acidosis
- blood pH <7.35
- pCO2 > 45mmHg (hypercapnia)
- CO2 accumulated in blood d/t hypoventilation
- pneumonia, CF, emphysema, overdose, brainstem dysfunction
compensation of respiratory acidosis (respiration and renal)
- respiration: increases to allow CO2 ventilation
- kidney:
- renal tubule cells have carbonic anhydrase
- retain bicarb
- eliminate H+
respiratory alkalosis
- blood pH >7.45
- pCO2 <35 (hypocapnia)
- CO2 decreased in blood d/t hyperventilation
- pneumonia, reactive airway dz, high altitude, anxiety, brain stem injury
compensation of respiratory alkalosis (respiration and renal)
- respiration: decreases to allow CO2 accumulation
- kidney:
- retain H+
- eliminate bicarb
hypoxia
oxygen deficit at tissue level
most common types of hypoxia
- hypoxemia: low arterial O2; pneumonia, high altitude;
- anemic hypoxia: adequate O2, low Hbg
- ischemic hypoxia: slowed circulation, heart failure, shock
- histotoxic hypoxia: poisoning i.e cyanide
hypoxemia S/S
- SOB, dyspnea
- HA
- fatigue/lethargy
- severe mood changes or irritability
- cyanosis
- digital clubbing (chronic)
causes of hypoxemia (decreased arterial pO2)
- ARDS
- asthma
- CO poisoning
- congenital heart disease
- COPD
- high altitude
- interstitial lung disease
- meds
- pneumonia
- pneumothorax
- pulmonary edema
- PE
- pulmonary fibrosis
- sleep apnea
high altitude causing hypoxemia
- composition of gases is unchanged by atm pressure but partial pressures are decreased
- as pO2 falls, ventilation increases, pCO2 falls and respiratory alkalosis can occur
altitude sickness
- irritability
- mental status change
- N/V
- HA
- LOC
- coma
- death
acclimatization to high altitude
- DPG increases resulting in O2 unloading
- ventilatory response decreases after about 4 d
- EPO secretion increases RBC
hypoxemia d/t venous to arterial shunts
- cardiovascular abnormalities
- ie. interseptal defect
- large amount of low O2 blood shunts from RV to LV bypassing pulmonary oxygenation
- chronic hypoxemia and cyanosis
- O2 administration has little effect
what is the most common cause of hypoxemia?
ventilation/perfusion imbalance
ventilation/perfusion imbalance causing hypoxemia
- defects in ventilation (low V/Q ratio): chronic bronchitis, RAD, acute pulmonary edema, hepatopulmonary syndrome of liver failure
- defects in perfusion (high V/Q ratio): PE, emphysema
anemic hypoxia
- decreased Hg
- compensated by increased DPG production
- shifts dissociation curve to right
CO poisoning hypoxia
- decreases O2 sat
- fatal is >70% COHgb
ischemic hypoxia
- slowed circulation therefore poor delivery
- shock
- heart failure
- ARDS
histotoxic hypoxia
- decrease in oxidative processes
- i.e: toxin like cyanide
- treat w/ methylene blue
- binds Hgb then cyanide to form cyanomethemoglobin which is non toxic
decompression sickness
- result of increases pressure esp when diving
- inert gases (N2) will dissolve in plasma
- forms gas bubbles on ascent
- decompress on ascent to allow gases to be unloaded by lungs
Henry’s law
-increased pressure increases partial pressures (think decompression sickness)
onset of decompression sickness symptoms
- w/i 1 hr: 42%
- w/i 3 hrs: 60%
- w/i 8 hrs: 83%
- w/i 24 hrs: 98%
although onset of DCS can occur rapidly, in more than 1/2 cases they don’t occur for at least an hour
top 3 most common symptoms of decompression sickness?
- local joint pain
- arm symptoms
- leg symptoms
others: dizziness, paralysis, SOB, extreme fatigue, collapse/unconsciousness
hyperoxia
- oxygen toxicity
- O2 at pressures above normal
3 settings for hyperoxia
- underwater diving
- hyperbaric O2 therapy
- provision of supplemental O2 (particularly to premature infants)
effects of hyperoxia
- CNS: convulsions followed by LOC
- Pulmonary: SOB, dyspnea
- Ocular: myopia, retinal detachment, damage
hypercapnia
- retention of CO2
- usually d/t hypoventilation
- stimulates respiration to blow off CO2
- respiratory acidosis
S/S and causes of hypercapnia
S/S: confusion, decreased sensory acuity, respiratory depression and coma
causes: heart failure, sleep apnea, LOC
hypocapnia
- depletion of CO2
- secondary to hyperventilation
- respiratory alkalosis
S/S and causes of hypocapnia
- S/S:
- cerebral vasoconstriction leads to ligh headedness, numbness and tingling
- tetany
- Cvostek sign d/t increases plasma Ca2+
- Causes: hyperventilating; brainstem dysfunction
What controls the regulation of respiration?
-two separate neural control centers; voluntary and involuntary
voluntary system control center
cerebral cortex to respiratory motor nerves via the corticospinal tracts
involuntary system control center
- medulla and pons of brain stem
- sets pace
- appropriating responses to sensory info from chemoreceptors and mechanoreceptors
what is found within the medullary center?
- VRG
- DRG
ventral respiratory group (VRG)
- contains both inspiratory and expiratory neurons
- secondarily responsible for initiation of inspiratory activity after the DRG
- pre-botzinger complex
- expiratory respiratory group
pre-botzinger complex
- in VRG of medulla
- pacemaker of breathing
- neurons send rythmic signals
- results in expansion of rib cage, air enters
- cycles 12-18 times per min
- inspiration 2 sec
- expiration 3 sec
neuron signals from the pre-botzinger complex (3)
- phrenic nerve: contraction of diaphragm
- intercostal nerve: external intercostals
- hypoglossal nerve: tongue
expiratory respiratory group
- located in the VRG of medulla
- maintains tone
- increases contraction of inner intercostals and abs for forced exhalation
dorsal respiratory group (DRG)
- primarily responsible for the generation of inspiration
- stimulated via the apneustic center in the lower pons and is also a part of the solitary tract (responsible for appropriating responses to sensory info from chemo and mechanoreceptors)
DRG is inhibited by ?
pneumotaxic center
pontine control centers
- appear to modulate medullary centers
- if medullary-pontine connection is transected, breathing is rhythmic by occurring in gasps
- responsible for transition b/w inhalation and exhalation
What are the 2 pontine control centers?
- apneustic center
- pneumotaxic center
apneustic center
- excitatory to medullary inspiratory center (DRG)
- creates inspiratory drive
- prolongs inspiratory phase
- receives inhibitory signals from pneumotaxic center
pneumotaxic center
- location superior to apneustic
- inhibitory to apneustic center
- inhibitory to DRG medullary center
- prevents over inflation
factors influencing rate and depth of breathing
- irritant reflexes
- hering-breuer reflex (inflation and deflation)
- medullary chemoreceptors (central receptors)
- carotid and aortic bodies
irritant reflexes
- particles such as debris, dust, lint, fumes
- stimulate release of histamine by granulocytes in airway -stimulate irritant receptors
- vagus mediated response: sneeze, cough, bronchocontricition
Hering-Breuer reflex
- mechano or stretch receptors in vesceral pleura and airways
- inflation reflex
- deflation reflex
inflation hering-breuer reflex
- prevents over-inflation of lung
- receptors respond to excessive stretching of lung during large inspirations
- action potential through vagus n. to inspiratory area in the medulla
deflation hering-breuer reflex
- shorten exhalation when the lung is deflated
- by stimulation of stretch receptors or stimulation of proprioceptors activated by lung deflation
- impulses travel afferently via Vagus and pneumotaxic centers of pons
medullary chemoreceptors i.e central receptors
- located on ventral surface of medulla, bathed in CSF
- sensitive to pH
- CO2 diffuses into CSF, carbonic anhydrase releases H+ and HCO3
- hypercapnia
- hypocapnia
carotid and aortic bodies
- perpherial receptors
- sensitive to pO2 <60mmHg
- aortic impulses ascend afferent vagal nerves to medulla
- carotid impulses ascend afferent hypoglassal fibers
- result is medullary stimulated ventilation to increase O2
there is an increase in ventilation during exercise d/t:
- physic stimulation
- stimulation of cortical motor activation of skeletal muscle and respiratory centers
- proprioceptors in muscles, tendons, and joints send excitatory impulses to respiratory center
ventilation plateaus during exercise d/y:
- central stimulatory effects of rising body temp
- sympathetic nervous system stimulation
- decreased activity shuts down respiratory stimulation
skeletal muscle energy/oxygenation
- skeletal muscle has myoglobin (hold 1 O2)
- muscle cell energy needs to exceed ability to oxidatively phosphorylate ADP
- anaerobic respiration ensues
fatigue and exhaustion during exercise
- consumption of resources
- increased neural inputs to brain
- lactate increase
- temp increase
- dyspnea
- pain
breathing pattern imbalances
- Cheyne Stokes
- Kussmaul breathing
- sleep apnea
cheyne stokes
- rapid breathing d/t hypoxia followed by apnea d/y hypercapnia
- seen in CHF, uremia, bain dysfunction
Kussmaul breathing
- deep and labored breathing pattern
- often associated w/ severe metabolic acidosis, particularly DKA but also kidney failure
- form of hyperventilation
- in metabolic acidosis: first breathing is rapid and shallow, then gets deep and labored and gasping
sleep apnea
- obstructive most common, can be central
- pharyngeal muscles relax or genioglossus pulls tongue foward
- during REM, muscles are most tonic
- airway obstruction and reduced effort awaken pt
- fatigue, HA, snoring, reduced learning
- tx: CPAP
sleep apnea is associated with:
- HTN
- obesity
- ETOH/drug use
