Respiration Quizlet by katie Flashcards
Ventilation
Movement of gas from environment to gas exchange space (i.e. lung)
How does gas move?
Driving force = pressure gradient
Goal of ventilation
Provide oxygen and remove carbon dioxide
Measuring ventilation
Breathing frequency * tidal volume
Law of Partial Pressures
P(total) = P1 + P2 + P3 +…… P(n)
Henry’s Law (dissolved gas)
C(x) = k*P(x) where k is the solubility constant and C = volume
Dalton’s Law
P(x) = P(tot) * F(x)
Respiratory chamber
The thorax (rib cage and diaphragm)
Diaphragm
Dome shaped, pushed up into the thorax when relaxed and flattens when contracted. Also expands lower rib cage by lifting up on ribs by its attachment to costal arch.
Intercostal muscles
External are oriented to lift the ribs
Internal are oriented to depress the ribs
Abdominal muscles
Respiratory muscles of expiration, contraction pushes the diaphragm into the thorax, decreasing thoracic volume
Drive to respiratory pump muscles
Network of brainstem neurons
Spinal motorneurons from cervical region to diaphragm via phrenic nerve
Thoracic spinal region to intercostal muscles via intercostal nerves
Lumbar spinal region to abdominal muscles via lumbar nerves
Respiratory muscle activation
Periodic and related to breath phase (inspiratory or expiratory)
Tidal volume (V(T))
Volume of air moved by a breath
Minute ventilation
V’(E) = V(T) * f
where f is frequency (1/(Ti + Te))
Interaction of pump and lung
Thorax lined with parietal pleura, outer surface of lung covered with visceral pleura, lung fills thorax and two pleural membranes separated by pleural fluid (hydraulic condition), movement of thorax also moves lung, increased thoracic volume expands lung
Pneumothorax
Hole in the chest leads to lung collapse (to resting volume) and chest expansion
Force of pleural fluid that held them together is compromised
Pleural pressure - P(PL)
Pressure caused by forces trying to separate parietal and visceral pleural membranes, allows pump to change lung volume.
Approximately -5 cm H2O at rest
Alveolar pressure - P(A)
Pressure difference between the atmosphere (P(B)) and the alveoli, equal to atmospheric at rest.
Expansion/inhalation makes P(A) negative
Expiration makes P(A) positive.
Air follows pressure gradient.
Transpulmonary pressure - P(TP)
Difference between P(A) and P(PL)
Pressure across the airways
Airflow
Rate at which gas moves. Zero at beginning of breath and when inspiration is complete. Magnitude can vary dramatically.
What is the reason for airflow?
Thoracic volume increases making P(PL) more negative which creates negative P(A), makes a pressure gradient and a driving force for air to move into the expanded lung.
Rate at which air moves is due to driving force and forces that resist air movement.
Relationship between compliance, volume, and pressure
C = dV/dP (mL/cm H2O)
2 major collapsing forces
Surface tension and lung elastic recoil
Surface tension
Force that acts at a gas-liquid interface which tends to reduce the surface area of the interface. Like molecules attract each other so they pull inward away from air (rain drops)
Laplace Law
Pressure required to keep bubble (aleveolus) open
P = 2T/r where Tau = surface tension and r is radius
Smaller bubble, greater tendency to collapse
Surfactant
Substance that works to reduce the air-liquid interface surface tension, produced by type II alveolar cells, phospholipid structure, layer thins and surface tension increases when lung expands (increased collapsing force), produced late in development, helps keep lung dry
Consequences of surfactant insufficiency
Lung cannot expand as easily and muscles work harder to inflate lung, small alveoli will collapse into larger alveoli, transudation of fluid into alveoli, flooded with fluid coming in from capillaries
Lung elastic recoil
Lung has connective tissue network composed of elastic fibers, stretch from rest position will create a retracting force that acts when stretching force stops, elastic tissue springs back to resting position when stretching force stops
Pressure volume curve of lung
Lung expands in volume increments and transpulmonary pressure measured at each. Initial volume increase (10-20%) requires and increase in pressure, greater compliance over middle range, curve flattens out at high lung volumes
Effect of lung stiffening on compliance and forces required to move lung
Stiffening decreases compliance and increases forces required to expand lung. Fibrosis decreases compliance. Emphysema increases compliance.
Net compliance of lung
Combination of lung elastic recoil and surface tension
Lung hysteresis
Inflation and deflation curves follow different paths, shown via in vivo measurements of lung pressure and volume
Minimal volume
Small lung volume that lung collapses to due to natural collapsing force of the lung
Pressure-volume curve of chest wall
Measured similar to lung. Non-linear curve. Lowest chest volume associated with very negative pressure. Lower compliance at low volumes. Natural resting point of chest at high volumes. Expanding force up to ~80% max volume
Pressure-volume curve of total respiratory system
Airway pressure is negative at low lung volumes, positive P(aw) at high lung volumes. Slope of the curve is the total system compliance. Airway pressure is 0 at FRC. Curve is linear over middle 1/3 (most breathing)
Total respiratory system compliance
Balance of lung and chest wall compliance
Functional residual capacity (FRC)
Resting lung volume. Point where collapsing forces of lung and expanding forces of chest wall are exactly balanced
Main effect of compliance
On magnitude of lung stretch and pressure required to produce that stretch, major factor in tidal volume and associated P(PL), change will change the force required to change lung volume while breathing.
Inspiration and Expiration: active or passive?
Inspiration is active due to net deflating force present when lung volume is above FRC.
Expiration is a passive return to FRC
Tidal volume
Normal breath above FRC
Vital capacity
Amount of air expired after inspiration to max capacity and expiration to lowest volume possible.
Residual volume
Volume of air left in lung after expiring as much as possible.
Total lung capacity
Vital capacity + residual volume
Activity of muscles at, above, and below FRC
No muscle force at FRC.
Abdominal force required below FRC.
Diaphragm active above FRC
Two types of resistance to airflow
- Elastic resistance due to moving lung tissue (related to compliance and tendency of lung to collapse above FRC)
- Airway resistance due to properties of tubes that oppose movement through them
Five factors on which airway resistance depends
- Rate of airflow
- Driving pressure
- Tube diameter
- Tube length
- Gas density or viscosity
Poiseuille’s law
V' = (pi(P1-P2)(r^4))/8nl R = (P1-P2)/V' = 8nl/(pi*(r^4))
What do Poiseuille’s Law relationships predict?
Airflow is high if there is low resistance or high pressure difference.
Airflow decreases as radius decreases.
Increased area decreases the resistance.
Why is the airflow and resistance lower in distal airways?
Even though the radius of each airway is smaller, the total cross sectional area is larger, major resistance is in proximal, large airways.
Is resistance of airways constant or varied?
Varied because the radius of the tubes changes with lung volume
Turbulence
Disruption of smooth flow profile at high airflows and tube branch points. Opposes airflow.
How does airflow change inspiration P(PL) and P(A)?
P(PL): More negative, greatest difference when airflow is maximum
P(A): negative only with inspiratory airflow
Resistive pressure
Difference between elastic recoil pressure and total P(PL)
How can you determine total resistance (airways plus tissue)?
Measure P(PL) and flow rate during a breath and subtract elastic component of P(PL)
Airway resistance (R(aw))
R(aw) = ΔP(A) / ΔV’
Can be changed by bronchial smooth muscle, increased contraction increases resistance (occurs with asthma and allergic reactions).
Has major effect on flow rate and P(A)
Flow limitation
Linear slope beyond which, flow can’t be increased no matter how much expiratory force
Reason for effort independent flow limitation
Relationship between resistance, compliance, and expiratory driving pressure during expiration
Equal pressure point
P(PL) = P(aw)
Beyond this point (toward mouth), airway has a collapsing force acting on it.
Point normally occurs in cartilaginous airways, preventing total collapse. Increased expiratory effort move EPP further back.
EPP and emphysema
Increased compliance moves EPP into collapsible airways, patient can’t expire
Alveolar ventilation
How pumping actions affect P(O2) and P(CO2) in the alveolus
Two major divisions of the lung
- Gas exchange area
- Gas conducting zone
Both are ventilated
What affects the concentrations of O2 and CO2 in the gas exchange zone?
Absorption of O2 by the blood and release of CO2 into the alveoli. Gas must be periodically refreshed by ventilation to adjust blood gases.
V’(O2) and V’(CO2)
Rate at which O2 is removed from the alveolus and rate CO2 is released, respectively
Concentration is O2 and CO2 in gas conducting zone
Zone doesn’t participate in gas exchange so concentrations are whatever was last moving through the region. Gas levels remain equal to air mixed with water vapor during inspiration, higher CO2 during expiration
Dead space volume
Volume of air in the conducting zone, wasted as far as alveoli are concerned, portion of tidal volume
Alveolar volume (V(A))
Tidal volume minus dead space volume
Alveolar ventilation
Portion of minute ventilation involved directly in refreshing the alveolar gas
V’(A) = V(A) * f
Directly related to concentrations of O2 and CO2 in the blood
Negative interrelationship w/ V(D) (increased V(D) with constant V(t) decreases V’(A))
How do you increase alveolar ventilation?
Most effective to increase Vt since V(D) is constant and increased Vt has a larger volume used to refresh alveolar gas
Alveolar gas equation for CO2
P(A,CO2) = (V’(CO2)/V’(A))*k
Need to match V’(CO2) and V’(A)
Ex: increased V’(CO2) = hypoventilation
Rate at which CO2 is removed from the lung is a function of?
V’(A) and V’(CO2) (source from blood)
Alveolar gas equation for O2
P(A,O2) = P(I,O2) - [(V’(O2)/V’(A))*k]
Ex: Metabolism increases, cells take more O2, so V’(O2) increases and P(A,O2) decreases
Effect of increasing alveolar ventilation
Increased net inflow of oxygen -> P(A,O2) increases
Carbon dioxide not allowed to accumulate -> P(A,CO2) decreases
How to control arterial gas levels?
Appropriately adjust V’(A)
P(O2) and P(CO2) are nearly equal in alveolus and arterial blood
How to measure alveolar gas levels?
Measure P(O2) and P(CO2) in last gas to leave the mouth at the end of an expiration
Respiratory work
Energy expended during breathing that is not recovered
W = int(P*dV)
Area under the volume vs. pressure curve during breathing
Elastic work
Overcome by increased respiratory muscle effort to increase tidal volume, volume related
Resistive work
Overcome by increased respiratory muscle effort to increase frequency, flow related and affected by changes in frequency
Total work relationship and minimum point
Combination of elastic and resistive work. Has a minimal point with a Vt and f where breathing work is at a minimum. Almost all animals optimize Vt and f to minimize work
How are adjustments of V’(A) affected by work?
Greatest increase with increased Vt.
Increasing Vt requires more work than increasing f.
Increasing f requires less work but produces less V’(A) increases
Horse breathing strategy
Breathe around FRC
Vt split above and below
Gait synchronized breathing
Striking of forelimb causes a forward thrust of abdominal viscera which pushes diaphragm forward (expiratory), inspiration more difficult.
Relevant in quadruped animals.
Newborn breathing strategy
Flexible chest wall, expiratory braking mechanisms help maintain FRC
Concentration of O2 in alveoli
P(A,O2) = (Pb - 47) * F(O2)
P(H2O) = 47 mmHg
Maintained close to 100 mmHg
Concentration of Co2 in alveoli
Returned by venous blood ~ 45 mmHg
Will reach equilibrium with arterial blood when it leaves lung -> 40 mmHg (maintenance level)
Hyperventilation effect on P(O2) and P(CO2)
Decrease P(CO2) and increase P(O2) CO2 removed from alveoli faster than it is delivered by venous blood
Hypoventilation effect on P(O2) and P(CO2)
Increased P(CO2) and decreased P(O2)
Concentration gradient for O2
Alveolus in equilibrium with arterial blood, concentration gradient forms between alveolus and venous blood (100 -> 40), O2 diffuses into blood
Concentration gradient for CO2
Produced by tissue, higher concentration in venous blood than arterial (arterial in equilibrium with alveolus), CO2 diffuses from venous blood to alveoli
Fick’s Law of Diffusion for Gas
J = DAα(ΔP/x)
V’(g) = DAα(ΔP(g)/x)
Where g is the gas being measured
Diffusing capacity: D(L)
A, D, α, and x are usually constant for the lung so coming inked into this term.
V’(g) = D(L) * ΔP(g)
Hard to measure so usually determined by measuring O2 uptake and knowing P(O2)
Determining D(L) for diagnosis
Many diseases affect membrane thickness and area, changing diffusion. Determining D(L) is useful to diagnose diffusion impairment (low arterial O2, and high CO2)
Regional distribution of ventilation
P(PL) is more negative at the base, making more negative P(TP), more positive P(PL) at apex means greater distending forces at apex.
Inspiration causes larger Vt % to go to base, increased V’(A) to basal regions
Gravity effect differences in P(CO2) and P(O2)
Apical O2: 132, Basal: 89
Apical CO2: 28, Basal: 42
Not a great factor in animals with horizontally oriented lungs
Ratio of ventilation to perfusion (V’(A)/Q)
Provides an estimate of the match between blood perfusion of a pulmonary capillary around an alveolus and the ventilation of the alveolus.
High ratio means good ventilation, poor perfusion.
Low ratio means good perfusion, poor ventilation.
Both result in inadequate gas exchange.
Other functions of pulmonary vasculature beside gas exchange
Epithelium regulates vasoactive substances, enzyme rich sites exposed to blood may inactivate substances such as prostaglandins, serotonin, NE, and histamine. May also activate substances such as enzyme that converts angiotensin I to II.
Bronchial circulation
Part of systemic circulation (in lung), provides oxygenated systemic blood to bronchi, doesn’t normally get into gas exchange areas
Physiological dead space
Areas (e.g. lung apex) where alveoli are ventilated but pulmonary capillaries don’t have blood flowing adjacent to space (no perfusion). In addition to anatomical dead space, makes up total dead space.
2 methods for transporting O2 in blood
- Dissolved in fluid
2. Bound to protein in RBC, hemoglobin
Oxygen Solubility
Oxygen solubility = (0.003 mLO2/dL/mmHgO2) * P(O2)
P(a,O2) = 100mmHg, P(v,O2) = 40 mmHg
P(O2) and Hemoglobin
Higher pressure -> greater drive for Oxygen to attach to Hemoglobin
Lower pressure -> oxygen moves off Hb to plasma (moves as dissolved fraction)
Structure of hemoglobin
4 O2 molecules per Hb. Reversible binding of O2 to Fe and H+ to histidine. Binding of O2 changes molecule conformation and bumps off H+. Important in acid/base buffering function of blood.
Hemoglobin bound oxygen content
1 g Hb binds 1.39 mLO2/dL blood
Normal blood [Hb] = 15 g/dL
C(O2) = 1.39 * [Hb] = 20.85 mLO2/dL blood (fully saturated all molecules)
Percent saturation of Hb
(HbO2 bound/HbO2 capacity) * 100 = % saturation
P(50)
P(O2) at 50% saturation
About 26 mmHg in normal blood at 37 C
Oxygen dissociation curve
Steep at 60 mmHg -> highest affinity of Hb for O2
Curve flattens at > 60 mmHg and 97% saturated at arterial P(O2)
75% saturation at P(v,O2) (~40mmHg, higher than P50)
O2 affinity
Right shifted curve: Less O2 bound for given P(O2), higher P50, decreased affinity
Left shifted curve: More O2 bound for given P(O2), smaller P50, increased affinity
What causes shifts in dissociation curve?
pH: decrease causes right shift (decreased affinity, acidosis)
P(CO2): increase causes right shift
Temp: increase causes right shift
2,3-DPG: increase causes right shift
Normal changes in pH, temp, CO2, and metabolites in tissue vs. lung
Act to promote O2 release where needed for metabolism in tissues.
Effect on dissociation curve is reversed in lung where effect is to promote O2 loading
Oxygen content: C(O2)
Volume of O2 in the blood, both dissolved and bound
How does Hb-bound O2 affect C(O2)?
Decreased [Hb] decreases content.
Competition for binding sites by other molecules will decrease content (CO has 250x greater affinity for Hb)
Arterial blood content: C(a,O2)
Blood equilibration with alveolar gas -> blood P(O2) -> Hb saturation w/ O2 + Hb concentration —> arterial O2 content
Oxygen extraction
Amount of oxygen removed by tissues from arterial blood by blood passing through capillaries.
C(a,O2) - C(v,O2)
CO2 transport
Greater solubility in water than O2, also transported bound to Hb
Haldane effect
CO2 bound to Hb (carbamino) weaken affinity for O2 in tissues and aid O2 unloading, elevated P(O2) in lung aids unloading of CO2.
Bicarbonate (HCO3)
Major storage form of CO2 in blood, important for buffering capacity. CO2 in water dissociates to bicarbonate and hydrogen ions via action of carbonic anhydrase.
~42 mL CO2/dL at P(a,CO2) = 40 mmHg (2x total O2 content, 90% total blood CO2 content)
CO2 dissociation curve
Curvilinear relationship over range of P(CO2) between arterial and venous blood (40-45mmHg).
Haldane effect facilitates offloading of CO2, creates steeper curve than for arterial or venous blood alone.
Effect of steep slope of CO2 dissociation curve
Effect is that small PCO2 difference results in same CO2 release into alveolus as same amount of O2 absorbed from alveolus with large difference in PO2 .
Hypoxemia
Low blood oxygen, results from mismatch between ventilation and perfusion rates
Hypoxic hypoxemia
Decreased inspired P(O2), causes low P(A,O2), low P(a,O2), and low P(a,CO2)
Alveolar hyperventilation
Decreased ventilation, not enough fresh air to refresh alveolar gas and maintain P(A,O2), causes low P(a,O2) and high P(a,CO2)
Diffusion limitation
Increased difficulty for O2 to diffuse from alveoli to blood (pulmonary edema), decreased P(a,O2) and normal P(a,CO2)
Shunted blood flow from R to L heart
Bypasses gas exchange area, occurs with blood flowing past unventilated regions, low P(a,O2) and slightly high P(a,CO2)
V’(A)/Q mismatch
Most common reason for hypoxemia, rate of ventilation and perfusion mismatched, low P(a,O2) and high P(a,CO2)
Respiratory quotient
Needed to assess V’(A)/Q inequality, ratio of CO2 excreted to O2 consumed (V’(CO2)/V’(O2))
How to assess V’(A) inequality
Determine respiratory quotient, calculate expected P(A,O2) with alveolar gas equation, measure P(a,O2).
P(A,O2) - P(a,O2) > 10 mmHg means there’s a ratio inequality.
May also be indicated by measuring physiological dead space.
Normal inequality of ~5 mmHg due to non-uniformity of lung
Basic acid-base priniciples
H+ concentration critical for cell function
Acids release H+, bases accept
Strong acids/bases rapidly release/accept H+ ions
Weak acids/bases have reduced tendency to release/accept H+
Henderson Hasselbach equation
pH = pK + log [A-]/[HA]
pK = -log(K)
Small K -> weak acid
Large K -> strong acid
Principles of buffer action
System most resistant to [H+] concentration changes when pH = pK, still has buffering ability one pH unit on either side of pK, strength directly related to concentration of buffer pair components
Phosphate buffer system
HPO4(2-): base, H2PO4(-): acid
Weak system in plasma since buffer power is low, stronger in kidney where environment is more acidic and [PO4(3-)] is higher
Protein buffer system
Large fraction of all chemical buffering power, Hb most important blood protein buffer, histidine buffers H+, pK of imidazole groups on histidines vary from 5.3 to 8.3, many within physiological range
Bicarbonate buffer system
CO2: acid, HCO3(-): base, free proton sets pH
Open system linked to lungs (CO2) and kidneys (H+)
Continuously removed at rates exactly matching production, may build up pathologically (resp or metabolic acidosis)
Most important H+ buffer in body?
HCO3(-)
H+ ion can be removed by both respiratory and renal systems
Respiratory acid-base regulation
Changing V’(A) changes P(a,CO2) which changes [H+]
Neural system senses P(CO2) and [H+] and changes V’(A) accordingly
Respiratory acidemia
Low pH, high [H+] Increased P(a,CO2), high [HCO3(-)]
Respiratory Alkalemia
High pH, low [H+] Decreased P(a,CO2), low [HCO3(-)]
Metabolic Acidemia
Low pH, high [H+] Decreased P(a,CO2), low [HCO3(-)]
Metabolic Alkalemia
High pH, low [H+] Increased P(a,CO2), high [HCO3(-)]
Causes of respiratory alkalosis
CNS mediated hyperventilation, peripherally stimulated hyperventilation (hypoxemia, heart failure), physical control of ventilation, drugs/hormones (thyroxine, progesterone, catecholamines), disease (liver cirrhosis, sepsis,np regnant, heat exposure)
Signs of respiratory alkalosis
Decreased cerebral blood flow, clouded consciousness, raised pain threshold, tetany, increased lactic acid and poor perfusion
Causes of respiratory acidosis
Insufficient ventilation, CNS defect, equipment failure (valve failure, incorrect ventilator use, inc apparatus dead space), chronic respiratory disease, chest wall weakness, obesity, drugs/toxins (relaxants, botulinum)
Signs of respiratory acidosis
CNS and skin vasodilated, hypokalemia, increased sympatho-adrenal tone (inc HR and BP)
Causes of metabolic acidosis
Adding or retaining a non-volatile acid (ketoacidosis, lactic acidosis, renal failure, ethylene glycol or salicylate intoxication, Addison’s, dehydration)
Loss of base (GI disorders, acid ingestion, carbonic anhydrase inhibitors, renal tubular acidosis)
Signs of metabolic acidosis
2-Hb binding reduced, impaired myocardial contractility, clouded sensorium, increased ventilation
Causes of metabolic alkalosis
Loss of non-volatile acid (GI, diuretic therapy), intake of base (cushings, hyperaldosteronism), unclassified (alkali admin, blood transfusion, glucose after starvation, large dose penicillin)
Signs of metabolic alkalosis
Decreased ventilation and cerbrovasodilation
How does the body compensate in cases of acidosis or alkalosis?
If origin is metabolic, the respiratory system changes V(A) to compensate.
pH range
7.35 - 7.45
Oxygen consumption
Rate at which the whole body consumes O2, V’(O2).
Measured by having an animal respire from a spirometer filled with 100% O2, slope of FRC line on meter is V’(O2) (corrected for STPD)
CO2 production
Rate at which CO2 is produced by tissues, V’(CO2). Linked to V’(O2) but not equal. Measured by collecting expired gas and determine rate at which CO2 is released from lung
Inequality between V’(O2) and V’(CO2)
Due to type of substrate available for metabolism, different foods produce different amounts of CO2
Ratio for V’(CO2)/V’(O2) on a mixed protein, fat, and carb diet
~ 0.85
R = 0.7 for fat
R = 1 for carbs
R = 0.8 for protein
Greatest source of H+
Metabolism, CO2 via oxidation of glucose and fatty acids
Origin of respiratory rhythm
Neural networks and interaction of inspiratory and expiratory neuron pools
Goal of respiratory control system
To provide appropriate blood gases for life
3 components of neural drive to breathing
Central neural activity, peripheral sensory neural feedback, chemical status of blood and CSF
Feedback control of breathing
Efferents cause action by effector, afferents monitor and transduce action, acts on efferent to regulate output (may be inhibitory or excitatory, -/+ feedback)
Basic respiratory neural oscillator location
Medulla, essential and sufficient for automatic rhythmic respiration, neural activity occurs near obex
Inspiratory neurons
Active during inflation phase of ventilators cycle, no overlap with activity of expiratory neurons
Expiratory neurons
Discharge in phase with the deflation phase, no overlap with activity of inspiratory neurons
Dorsal respiratory group
Subpopulation of medullary neurons, located in solitary nucleus, mostly inspiratory, rhythmic drive to contralateral phrenic motor neurons, project to VRg, afferent feedback from CN 9&10
Ventral respiratory group
Sub population of medullary neurons, located in nucleus ambiguous and retroambiguous, 2/3 are expiratory, vagal motor of ipsilateral auxiliary resp. muscles and larynx (NA), rhythmic drive to ext. and int. intercostal sand abdominals (NRA), projects to pons
Control circuit of basic respiratory rhythm generator
Interconnected inspiratory and expiratory neuronal pools, phase switching between in and out activity phases, CIA drives inspiratory muscles and feeds back to inhibit inspiration, CEA drives expiratory muscles and feeds back to inhibit expiration.
Two regions in pons that exert major influence on medullary oscillator
Apneustic center and pneumotaxic center
Apneustic center
Caudal pons near cerebral peduncles, produces prolonged sustained inspiration and tonic contraction of diaphragm and other muscles, keeps switch in inspiratory position
Pneumotaxic center
Dorsolateral rostral pons near inspiratory parabrachial nucleus, facilitates inspiratory off-switching, turns switch from inspiratory to expiratory but doesn’t work if apneusis isn’t terminated first
3 types of peripheral vagal afferents than modulate medullary oscillator
Slowly adapting pulmonary stretch receptors (PSR)
Rapidly adapting receptors (RAR)
Lung C fibers
Slowly adapting pulmonary stretch receptors (PSR)
Smooth muscle of airways, activity increases with inflation, sensitive only to airway CO2 increase (decreases activity), mediates Hering-Breuer reflex, inhibits inspiration, acts with other switch centers to make normal resp. rhythm.
Hering-Breuer reflex
Hyperinflation of lung that induces apnea
Rapidly adapting receptors (RAR)
Airway epithelium and smooth muscle, discharge with inflation and deflation, rapidly dissipate with sustained inflations, some discharge with tidal ventilation, sensitive to histamines, unclear reflex response (may be inspiratory excitatory, augment inspiration, involved in cough)
Lung C fibers
Airway epithelium and interstitial spaces b/w alveolar membrane and capillary, may be pulmonary or bronchial fibers, no phasic respiratory activity, chemosensitive: pulmonary respond to histamine, PGs, pulmonary congestion (dec. HR and BP, apnea), bronchial respond to histamine and PGs (dec. HR, inc. BP, hypernea and cough)
Muscle afferent modulation of medullary oscillator
Alter I and E durations via dorsal roots to spinal cord, discharge behavior in relation to muscle force and length changes
Types of afferents
Found in diaphragm and intercostals: muscle spindles (length info) and tendon organs (tension info)
Found in costo-vertebral joint: joint receptors (rib joint motion)
Oxygen chemoreceptor locations
Peripheral
Carotid and Aortic bodies (nerve aggregations at respective sinuses)
Carotid and Aortic body connections and information relay
Aortic to brainstem via vagus nerve, carotid via glossopharyngeal nerve
Info to medullary respiratory centers (solitary and ambiguous nucleus)
Carotid bodies have very high metabolic rate (small a-v O2 diff)
Effect of P(O2) on receptors
Stimulated by decreased P(O2), no effect on O2 content or BP
Oxygen receptor output
Decreased P(O2) increases discharge, activity increases rapidly <100 mmHg, functional denervation possible with inhalation of 100% O2
Hypoxia ventilatory response
Weak until P(O2) < 60 mmHg
Hyperbolic increased in ventilation (if CO2 doesn’t change), increases respiratory frequency, increased ventilation = decreased P(CO2) = depressed ventilation to counteract hypoxia
Carbon dioxide chemoreceptor location
Peripheral (same as O2 receptors)
Central: in CNS, inside blood brain barrier
Physiological stimulus of peripheral CO2 receptors
Increased P(a,CO2) increases carotid body receptor activity, actual stimulus is H+ ion from dissociation, same afferents that are sensitive to O2
Physiological stimulus of central CO2 receptors
None found, BBB freely permeable to CO2, acid-base changes easily sensed in CSF due to poor buffering, CO2 dissociates after crossing BBB and H+ stimulates central chemoreceptors
Peripheral and central feedback
40% of CO2 ventilatory response due to peripheral receptors, major response is central and consists initially of increase in Vt with increasing CO2
Ventilatory response to CO2
Increased CO2 causes increased ventilation, sensitivity determined by slope of relationships b/w P(CO2), ventilation, and constant P(O2), usually 3 L/min/mmHg CO2
CO2 sensitivity modulators
Decreased steady state O2 increases sensitivity, decreases during sleep, affected by narcotics and other drugs, decreases with chronic lung disease and prolonged hypercapnia, also affected by age/sex/temperature/catecholamines etc.
High brain center modulation of medullary oscillator
Little known, most likely located on switch Sensorimotor cortex (timing, vagus and phrenic input), cerebellum (rate and depth of inspiration, phrenic and intercostal input), limbic influences (rate and depth, poorly understood)
Cardiovascular modulation of medullary oscillator
Significant interaction, increase in carotid baroreceptor activity inhibits respiration, afferents from great veins/heart and pulmonary circulation may cause initial apnea then rapid shallow breathing with increase in pulmonary arterial pressure
Pain and temperature modulation of medullary oscillator
Pain causes respiratory excitation, hyperthermia causes hypernea, reduced ventilation response with chronic hypothermia but transient hypothermia increases V(E)
Exercise modulation of medullary oscillator
Increases ventilation, increases O2 requirement, increases body temp and minute ventilation, ventilation not solely explained by metabolic chemicals, neurogenic component too, activation of skeletal muscle proprioceptors increases ventilation
