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206 Cards in this Set
- Front
- Back
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functions of the pulmonary system:
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ventilation
gas exchange gas transport regulation metabolism filtering blood reservoir |
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muscles of inspiration
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diaphragm
external intercostals constantly working |
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diaphragm
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flat when contracted
parachute shaped when relaxed increases size of thoracic cavity by lengthening it during contraction |
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increased abdominal cavity size
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inhibits diaphragm action,
e.g. pregnant woman has a baby in her abdominal cavity, the diaphragm cannot dilate to increase the size of the thoracic cavity because the baby is in the way |
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external intercostals
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allows rotation of ribs which pivot on the backbone to raise the sternum up and out
increases the size of the thoracic cavity by widening it |
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muscles of exhalation
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abdominal muscles
internal intercostals only work when body is under stress and needs more gas exchange, normally elastic recoil causes exhalation |
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abdominal muscles
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contract to bring chest in and force diaphragm up
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internal intercostals
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pull ribs in, decreasing vol. of the thoracic cavity
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pulmonary pressures
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pleural
alveolar transpulmonary |
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pleural pressure
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pressure between lung and chest wall (visceral pleura)
"potential space" is normally only a few mL in vol. but can fill with air or fluid under abnormal conditions negative pressure of ~-5cmH2O to ~-7.5cmH2O |
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alveolar pressure
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pressure inside of air sacs
when the glottis is open and there is no air flow pressure is 0cmH2O during inspiration, muscle contract to cause pressure to become negative (-1cmH2O) air flows into lung via pressure gradient during expiration, muscles recoil decreasing lung volume and expelling air to increase pressure (+1cmH2O) |
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transpulmonary pressure
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difference between pleural and alveolar pressures
measures elastic forces of the lung the pressure keeping smaller bronchioles/airways open |
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sources of negative pleural pressure
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tendency for the lungs to collapse
tendency for the thoracic cavity to expand removal of fluid via lymphatics |
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tendency for the lungs to collapse
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due to elastic recoil of tissue: structure of lung tissue causes recoil out of the stretched position
surface tension: polar fluid layers in lungs will attempt to pull the walls together surfactants prevent this |
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tendency for thoracic cavity to expand
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ribcage naturally expands, if internal forces were removed the cavity would get larger (increased volume leads to decreased pressure)
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removal of fluid by lymphatics
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arterial flow is greater than venous flow due to pressure differences, so fluid is constantly leaking into the pleural cavity; this fluid is removed by draining it into the lymphatic system via pores in the parietal pleura and diaphragm
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compliance
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change in volume over change in pressure, inverse of elasticity
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high compliance
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ability to stretch and accommodate a large volume with little change in pressure
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low compliance
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little ability to stretch without changes in pressure
more energy is required to expand something with low compliance |
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sources of compliance
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lung tissue
surfactants |
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lung tissue as a source of compliance
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matrix composed of elastin and collagen, which are somewhat stretchy structural tissues
1/3 total compliance due to stretch |
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surfactants as a source of compliance
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surfactants break up polar bonds, which prevents the lungs from collapsing due to surface tension
allows them to stretch and stay open 2/3 total compliance due to surfactant |
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inspiratory work
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lung must be expanded against the lung and chest forces
-work to push tissues open resistance of air -movement of the air itself takes energy -disease state can make it difficult to move air in/out of lungs, usu. 3-5% of bodies energy is used, some states will increase energy expended to breathe |
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expiratory work
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at rest no work is needed to exhale due to elasticity of lungs
with exercise the body must exchange more gas due to increased metabolism, so your muscles kick in in some disease states active exhalation is necessary and increases work |
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airway resistance
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most resistance to air movement is in the medium sized bronchioles
depends on flow type |
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laminar flow
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low resistance, singular direction flow is smooth and ordered
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turbulent flow
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high resistance, flow is chaotic and choppy, net flow is in one direction
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spirometry
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measurement of lung capacity
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Vt
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tidal volume = 500ml
change in lung volume during normal inspiration |
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IRV
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inspiratory reserve = 3000ml
allows for greater inspiration (deep breath) |
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ERV
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expiratory reserve = 1100ml
depletes when you push as much air out as you possibly can |
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RV
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residual volume, 1200ml
air that is constantly in your lungs |
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total lung volume
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5000-6000ml
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IC
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inspiratory capacity = 3500ml
VT + IRV |
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FRC
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functional residual capacity = 2300ml
ERV + RV |
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VC
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vital capacity = 4600ml
IRV + VT + ERV |
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TLC
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total lung capacity = 5800ml
VC + RV |
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dead air space
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parts of the airway that serve purely as a tube of air and do not function in exchange of gases
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anatomical dead air space
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actual structure of the airway will not allow gas exchange
e.g. the first 15 divisions of the bronchi |
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physiological dead air space
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something is disrupting the airway's ability to exchange gas
e.g. blockage won't allow air to enter the alveolus |
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measuring dead air space
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avg = 150ml
breath in pure O2, exhale expiration will yield pure O2 from all of the conducting airways, and only when N is present are we receiving air that has undergone exchange. |
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alveolar ventilation
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VA = RR (VT-VD)
increasing dead air space will have a great effect on alveolar ventilation (more so than changing tidal volume) |
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filtration by airway
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"cleans" air
filters out particulate matter before it can cause damage to the alveoli filters via moisture, conchae, hair |
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hydration of air in airway
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air needs to be moisturized before it reaches the lungs or osmosis will occur (cells of the lung will lose their water to the dry air)
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temperature regulation in airway
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warming the air prevents the lung tissue from freezing in extreme cold
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types of airways
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conducting
exchange |
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conducting airways
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begin at the trachea, (pharynx to non respiratory bronchioles)
lined with pseudostratified ciliated epithelium to help with filtration/removal of particles conduct air, do not exchange gas cartilage rings hold open the airways against negative pressure |
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exchange airways
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respiratory bronchioles (<1.5mm), alveoli, alveolar ducts
function in gas exchange held open by transpulmonary pressure, changes will change size of the airways air moves mostly by diffusion |
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airway wall structure
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pseudostratified epithelium
highly muscular: -conducting have a lot of smooth muscle, exchange do not under control by NS -sympathetic, airways respond to catecholamines which cause bronchodilation -parasympathetic, airways respond to acetylcholine which causes bronchoconstriction -local control, airways respond to histamine which causes bronchoconstriction |
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pulmonary blood vessels
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short, large diameter, distensible (high compliance)
can take in a lot of fluid without increasing pressure problem: when the left side of the heart fails and cant remove blood from the pulmonary circuit fast enough, blood will back up and causing edema in lungs |
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bronchiole vessels
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branches of the arteriole systemic tree (small arteries in the systemic circulation)
flow in these vessels is~1-2% cardiac output provide oxygenated blood to the conducting airways/lungs and then back to the heart to be pumped systemically |
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lymphatic vessels
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in all support structures in the lungs
remove interstitial fluid that has leaked from the arteriole side by draining it into the right lymphatic duct maintain pleural pressure |
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pulmonary blood pressures
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pulmonary artery:
systolic ~25 diastolic ~8 pulmonary capillaries: -steadier flow pressure ~7 LA: pressure~2 anything that increases LA pressure will back up flow in the pulmonary circuit pulmonary BP is much lower than systemic BP due to higher compliance of pulmonary vessels |
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pulmonary blood volume
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blood flowing through the pulmonary circuit is ~450ml
(9% of total blood vol.) only about 70ml in the capillary bed, spread thinly over a huge SA pulmonary circuit can act as a blood reservoir due to high compliance |
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pulmonary circuit as a blood reservoir
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we use high compliance to our advantage, pulmonary circuit can take in lots of blood when the right heart output is high and act as a buffer, slowly releasing it into the left side of the heart so that there are no large fluctuations in the function of the left heart
conversely, if there is low pressure in the left side of the heart due to blood loss or increased heart rate form exercise, the pulmonary circuit can help to fill the void temporarily |
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distribution of pulmonary blood flow
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controlled by alveolar O2
when PaO2 is less than 70% of normal value, blood vessels will constrict to decrease flow to the defunct area; this is a protective mechanism, so blood isn't being wastefully sent to an alveolus that can't oxygenate it |
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flow zones
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in the lung, weight of blood itself will contribute to pressure, creating three zones of blood flow (apex, middle, base of the lung)
realize if you lay down, there is no more weight from top to bottom and zones are dispersed PA = alveolar pressure |
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zone 1
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PA>Pa>Pv
no blood flow occurs during normal conditions because the low arterial pressure can't overcome the high alveolar pressure |
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zone 2
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Pa<>PA>Pv
intermittent flow, blood will flow during systole (high pressure) |
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zone 3
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Pa>Pv>PA
constant flow, arterial pressure is so high that blood will always be flowing, even during diastole |
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capillary fluid balance
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pressure differences cause fluid to flow (capillary pressure vs interstitial pressure)
+ is pushing out, - is pulling in |
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oncotic pressure
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subset of osmotic pressure, due to proteins acting as a solute
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edema formation
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results as an imbalance in pressure which would lead fluid to accumulate in the interstitium
e.g. capillaries become leaky due to bacterial toxin so proteins enter the interstitium, and the shift in solute concentration causes water to follow, thus changing oncotic pressure e.g. LV fails, pulmonary hydrostatic pressure increases because blood is not removed, fluid leaves capillaries into interstitium |
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pleural fluid balance
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normally pleural pressure ~7mmHg and there are onl a few mL in the cavity
pathology: -high pressure (SCUBA) can force blood into the pleural space -infection, bacterial metabolism produces gas/fluid in the pleural space increase in positivity of pleural pressure will cause lung collapse |
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gas exchange and partial pressures
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partial pressures are considered concentrations
all respiratory gases are highly lipid soluble so they can pass through membranes easily CO2 is 20x more diffusible than O2 liquid diffusion is the biggest barrier to diffusion of gases (i.e. gas diffusing through plasma) |
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air content comparison (gases)
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atmospheric: N2: 597 O2:158 CO2: .3 H2O: 3.7
humidified: N2: 563 O2:149 CO2: .3 H2O: 47 alveolar: N2: 569 O2:104 CO2:40 H2O: 47 expired: N2: 566 O2: 120 CO2: 27 H2O: 47 |
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atmospheric air
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the air you breathe in, normal air
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humidified air
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air that you have breathed in is humidified with H2O so it does not damage your lungs, adding H2O decreases other partial pressures
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alveolar air
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has a high CO2 content, as your body is releasing it into the alveolus, has low O2 content, as your body is taking it away from the alveolus
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expired air
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mixture of alveolar air and dead air, thus CO2 is decreased and O2 is increased as the alveolar air mixes with atmospheric air trapped in your conducting airways
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respiratory membrane
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the structures you must pass through to exchange gas between air and plasma:
1.alveolar air 2.surfactant/fluid layer 3.alveolar basement membrane 4.interstitium 5.capillary basement membrane 6.endothelium 7.plasma 8.RBC |
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factors in gas diffusion
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-thickness of membrane
-surface area of membrane -diffusion coefficient of the gas -partial pressure gradient note: the lung has a large SA and huge differences in alveolar pressure/venous pressure to maximize diffusion |
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pressure gradient in lungs
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venous blood partial pressures:
-O2 : 40 -CO2: 45 alveolar blood partial pressures: -O2 : 104 -CO2: 40 differences in pressures: O2:64 CO2: 5 note: the diff in CO2 is much less, as it is much more highly diffusible and does not need as great a pressure gradient |
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perfusion
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how much blood flow there is to the area to carry gas (or other molecules) away
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diffusion
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how much gas actually crosses the membrane into the blood
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perfusion limited
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gas exchange is limited by the amount of blood flowing to an area
i.e. the gas will all diffuse quickly and saturation will be reached, it is a matter of how much blood is there to pick up the gas ex: NO2, CO2, O2 |
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diffusion limited
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gas exchange is limited by the rate of diffusion of the gas
i.e. gas diffuses slowly, so depending on how long the blood is there we will have varying amounts of saturation ex: CO |
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O2 exchange
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perfusion limited:
takes about .25 seconds for full saturation, blood stays in the capillary for .8 seconds the .8 seconds is a protective mechanism, so if your diffusion/saturation is somehow impaired, there is extra time for it to fully saturate |
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CO2 exchange
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perfusion limited:
saturation is reached quickly, well before the .8seconds is up pathology: pulmonary edema can affect gas exchange, fluid in the alveoli means diffusion will occur more slowly (thicker membrane) |
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VA/Q
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Q = blood flow, rate of perfusion
VA = alveolar ventilation thus VA/Q = rate of alveolar ventilation vs. the rate of perfusion |
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blood flow:
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blood flow can be summarized as three major conditions:
venous blood normal alveolar air humidified air |
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"venous blood"
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VA/Q = 0,
occurs when there is regular blood flow, but no ventilation in the alveoli blood gas content will remain at the venous concentration of the pulmonary veins as CO2 and O2 are not exchanged ventilation has been blocked, perhaps by bronchiole obstruction (there is no air for the blood to exchange with) |
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"normal alveolar air"
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VA/Q = normal
there is slightly more blood flow than ventilation, resulting in gas exchange and whatnot |
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"humidified air"
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VA/Q = infinity
there is no blood flow to the alveolus, so despite breathing the air in there is no gas exchange the air gets into the alveolus and gases come to equilibrium with inspired humidified air physiological dead air space, likely due to a clot blocking blood flow |
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uptake of O2 in pulmonary capillary
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as blood flow through the pulmonary capillary it becomes oxygenated
arterial end: PaO2 = 40 venous end: PaO2 = 104 |
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O2 in circulation
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after the pumonary capillary PaO2 = 104, this mixes with blood from the pulmonary shunt, dropping it to ~97 in the systemic arterial blood
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uptake of O2 in systemic tissues
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systemic arterial blood PaO2 = 97, flows to the systemic capillaries, at the arterial end ~97, diffuses into the interstitium which has a PaO2 of 40, then from there into the RBC where PaO2 is 23, at the venous end of the capillary the PaO2 in the blood will be 40, at eq with the interstitium and no net exchange will occur
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oxygen transport in blood
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oxygen is transported in the bloodstream in two forms
dissolved: .3mL O2/dL (1.5%) Hb bound: 19.7ml O2/dL (98.5%) |
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Hb bound O2
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hemoglobin bound
hemoglobin has great affinity to the O2 molecules at its heme (iron) molecules it has 4 heme units, one in each subunit (2alpha 2beta) |
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abnormal hemoglobin
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hemoglobin can have abnormal mutations (altered aa sequences) which may cause binding issues
babies have strong affinity hemoglobin, as they need to be able to steal nutrients from their mothers |
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Hb dissociation curve
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binding of O2 is not linear, but a sinusoidal curve
98% of available Hb sites are occupied by O2 -left shift means increased affinity (babies need increased binding) -right shift means decreased affinity |
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decreased Hb affinity via Bohr Affect
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increased acid via increased metabolism requires the tissues get more O2, so Hb affinity decreases and O2 leaves the RBC to get to the tissues more easily
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decreased Hb affinity via temperature
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increased in temperature will cause increased metabolism, so more O2 is required
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decreased Hb affinity via 2,3 BPG
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2,3 BPG increase means that glucose metabolism is increasing for energy consumption, more O2 is required to sustain this
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decreased Hb affinity via CO2
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increased CO2 will lead to decreased affinity, as CO2 has a greater affinity to Hb than O2, and will essentially kick it off
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uptake of CO2 from tissues
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in the cell, PaCO2 is 46
in the interstitium PaCO2 is 45 the 1mmHg pressure difference will allow diffusion across the gradient as CO2 is highly diffusible at the arterial end of the capillary PaCO2 is 40, thus CO2 will travel across the gradient into the blood until it reaches the venous end, where the PaCO2 of both the capillary and interstitium is 45 |
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CO2 transport
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CO2 is carried in three forms:
dissolved in solution: 7% bound to Hb: 23% as HCO3-: 70% |
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CO2 uptake at cells/release at lungs
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as HCO3-
CO2 enters the RBC and combines with H2O via carbonic anhydrase to form H2CO3, which then degrades to H+ and HCO3- HCO3- will leave the cell and enter the plasma where it will travel to lungs for exchange as HCO3- leaves, the charge must be balanced so Cl- enters the RBC to counter that loss (note: water will follow the Cl-, this is why venous RBC are larger than arterial RBC) |
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pulmonary regulation
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dependent on functioning nervous system, everything from the pons down must be intact (i.e. brainstem)
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pulmonary regulation: alveolar ventilation
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alveolar ventilation is constantly monitored and adjusted
-tidal volume and resp rate are adjusted to maintain VA/Q ratio (.8-1) -PaO2 and PaCO2 are kept relatively constant via safety mechanisms |
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factors determining PaO2
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inspired air is 20%O2 (150mmHg)
equilibration activity: increased metabolism leads to increased velocity of oxygen use which decreases PaO2 |
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factors determining PaCO2
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inspired air is 0%CO2, thus it will dilute CO2 in the alveolus
increased CO2 leads to increased Q leads to increased PaCO2 increased VA leads to increased outside air, leads to alveolar air dilution increased production of CO2 can occur via exercise, infection, hyperthyroidism |
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respiratory control
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respiratory muscles will change the respiratory rate, depth/tidal vol
if we dont move enough air, expiratory muscles will activate respiratory muscles are regulated by the CNS at respiratory centers |
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respiratory control centers in the CNS
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Pons and Medulla
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medulla
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located next to the control center for the cardiovascular system
DRG and VRG |
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DRG
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dorsal respiratory group
inspiratory center controls regular pattern of breathing composed of a group of loosely bound neurons has a right and left section receives sensory input, relays output to motor cells |
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VRG
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ventral respiratory group
"overdrive" center activated only when forced expiration is required |
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pons
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pneumotaxic center
stretch receptors turn respiration on and off primary function is to limit respiration strong pneumotaxic signal increases resp rate |
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peripheral chemoreceptors
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located in aortic arch and carotid artery
monitor blood that passes through sensitive to PaO2, also detects H+ and PaCO2 (but is 7x less responsive) |
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central chemoreceptors
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in pons
sensitive to PaCO2 and H+, PaO2 has no effects CO2 has direct and indirect effects, can directly travel across BBB to CNS where it will increase resp rate acid cant directly cross BBB to the CNS, so it crosses as CO2, then is converted to HCO3- and H+ in the CSF CSF has a low buffer capacity, (not much proteins) so these effects are felt much more strongly than in the blood |
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factors affecting respiration
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voluntary factors
stretch receptors irritant receptors j-receptors brain swelling anesthesia/drugs |
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voluntary factors
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higher brain centers can override resp control for short periods of time
once blood chemistry begins to change, however, involuntary will take control |
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stretch receptors
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"herring breur" reflex, as the lungs fill with air, airways stretch and once they are at a threshold value (3x normal tidal vol) they will set off receptors that respond by inhibiting the DRG (reducing resp rate)
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irritant receptors
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part of the pseudostratified layer between epithelial cells
receptors will respond to particulate or noxious materials and gases cause bronchoconstriction to reduces the amount of irritant coming in cause increased respiratory rate, with decrease in tidal vol, so that the same amount of air is exchanged, but only a small part of the lung does it (prevents further damage/exposure to danger) |
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J receptor
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juxtaalveolar receptor
responds to engorgement of capillary beds on alveoli, stimulates rapid shallow breathing e.g. left heart fails, large BV in pulmonary circuit |
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brain swelling
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above the brainstem are higher brain centers, swelling in the cranium can cause these centers to be pushed down on the brainstem reducing respiration
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anesthesia/drugs
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e.g. morphine causes respiratory depression by inhibiting brainstem
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cheyne stokes breathing
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last effort of the body to keep things going
pattern of hyperventilation and then apnea eventually the length of each phase will increase to the point where you arent breathing overall the dramatic flux in CO2 levels that are reaching the brain slower than normal due to a disease state leads to a pattern of irregular breathing resulting in death |
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cheynes stokes breathing: hypervent
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during hyperventilation
rapid breathing results in the blood in the lungs having no CO2 so the brain involuntarily shuts down breathing because of the time it takes for the brain to respond, breathing is so slow that you are in need of O2 |
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cheynes stokes breathing:
apnea |
now that the breathing is so incredibly slow, the brain will speed it up because there is not enough O2, resulting in hyperventilation
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FEV1/FVC ratio
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calculated ratio
normal is 80% FVC = forced vital capacity FEV1 = forced expiratory volume ratio may change in certain disease sates, differentiates between: obstructive (ratio decreases) restrictive (ratio stays same) |
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obstructive lung disease
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it is difficult to get air out of the lungs
caused by increased air resist, decreased compliance results in decreased airflow decreased VC increased TLC, RV, FRC |
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asthma
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chronic airway inflammation resulting in narrowing or obstruction of the airway
associated with decreased compliance peak expiratory flow decreases as airway diameter is compromised |
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causes of asthma
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usually sensitive to environmental airborne triggers
intrinsic: not triggered by allergens extrinsic: triggered by allergens |
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pathophysio of asthma
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hypersens to environment is IgE ab mediated
B cells react to stimuli, release IL4, produce IgE ab eosinophils recruited by allergen, inhibit ciliary action consequences of airway inflammation: affect nerve stimulation (irritant receptor involved) vasodilation, bronchoconstriction major increase in mucus secretion fibrosis |
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fibrosis
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scar tissue formation
compromises elasticity of lung, thickening of basement membrane, inhibits movement of gas across membranes, fibrosis around the bronchioles will decrease compliance |
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treatment of asthma
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short term: reduce obstruction
break up mucus and dilate bronchioles via B2 agonists or anticholinergic agents long term: control inflammation use steroids or NSAIDS |
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COPD
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chronic obstructive pulmonary disorder
describes anything from emphysema to bronchitiis problem expelling air clinical presentation: cough, mucus, shortness of breath increased work of breathing V/Q mismatching cor pulmonale |
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cor pulmonale
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right side heart failure due to pulmonary arteriole pressure increase
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V/Q mismatching
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decreased PaO2
increased PaCO2 leads to shunting CO2 is retained in the lung, buildup causes acidosis |
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bronchitis
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upper airway obstruction
-chronic: inflammation/mucus -asthmatic: asthma, but long time -chronic obstructive manifestation: productive chronic cough tachychardia pulmonary hypertension jugular venous distension increased lung volumes thickened bronchioles increased heart side increased RV, FRC (air is being trapped in the lungs) polycythemia |
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jugular venous distension
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engorgement of the jugular vein indicates right heart has failed, blood backs up
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polycythemia
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increase in hemocrit is a sign of chronic hypoxia
blood becomes viscous, low PaO2 results hypoxia is what gives "blue" color |
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emphysema
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walls between the alveoli break down, resulting in larger and fewer alveoli
decreased SA leads to decreased surface tension, increasing compliance lungs fill easily, but lack ability to recoil increases work of breathing, pursed lips increase pressure less SA is available for gas exchange in damaged ascites body must compensate for lack of O2 exchange, so you hyperventilate |
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COPD treatment
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stop smoking
relieve airway (B2 for obstruction, steroids for inflammation) treat infection if present give oxygen if hypoxic (PaO2<60) |
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restrictive lung disease
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difficult to get air into the lungs
usually lungs are scarred decreased compliance due to loss of elasticity from scarring muscles of inspiration work harder decreased VC and TLC result in a overall smaller lung |
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idiopathic pulmonary fibrosis
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usually airway resistance is unchanged (there is no problem with the airway itself)
issues with parenchymal tissue decrease compliance capacities reduced dry nonproductive cough, rapid shallow breathing leading to hypocapnia |
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idiopathic pulmonary fibrosis pathology
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scarring/inflammation causes decrease in surfactant production
less surfactant leads to decreased compliance increases in blood pressure due to destroyed capillary beds lead to pulmonary hypertension and cor pulmonale |
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idiopathic pulmonary fibrosis treatment
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corticosterods are ineffective
lung transplant at advanced stages survival rate after transplant: 2year 70% 5year 40% 10year 14% |
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cystic fibrosis
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chloride transporter issue, genetics
results in thick viscous sticky pulmonary secretions treat by managing airway inflammation, preventing infection, and reducing obstruction by breathing humid air and pounding on the back |
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pulmonary edema
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fluid fills alveolar space itself (not interstitium)
cardiogenic and noncardiogenic types clinical signs: dyspnea, productive cough, rales/crackles, increase in work of breathing, frothy sputum, hypoxemia treat via diuretic |
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cardiogenic pulmonary edema
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due to changes in vascular function (e.g. pulmonary hypertension)
increases transneural pressure leads to alterations in fluid balance |
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noncardiogenic pulmonary edema
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due to changes in lung tissue permeability (e.g. proteins into ISF leads to increased osmotic pressure)
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acute respiratory disorders
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e.g. damaged alveolar epithelium from bacterial toxins causing inflammation and damage
doesnt necessarily have to be bacteria, anything that compromises the alveolar wall will result in alveoli filling and virulent pus formation severe hypoxia will ensue followed by death in about 12hrs |
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diphtheria
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toxin prevents protein synthesis
upper resp tract infection tonsils/other lymph tissues are enlarged danger is that you can suffocate from blocked airway, arrhythmias and paralysis possible 50% fatal untreated, but generally responds to antibiotics |
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lower respiratory infections
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pertussis: whooping cough
paroxysms, lasts 2-4month most adults recover, babies die tuberculosis: highly infectious blood in sputum body will encapsulate the bacteria in cysts which will remain in the body causing issues |
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nonspecific lung defenses
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clearance: cough, cilia, sneeze
secretions: mucus, surfactant cellular defense: cells that react to invaders biochemical defense: cells lining airways have proteases that attack proteins nonspecifically |
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specific lung defenses
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antibody mediated
lymphatic system |
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respiratory failure
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two types:
-hypoxia with normal or low CO2 (PaO2<60) -hypoxia with high CO2 (PaO2>60, PaCO2>50) |
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cardiovascular system
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3 functional divisions
-blood -heart -peripheral vasculature |
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blood
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connective tissue with tons of interstitial space
transport medium: -nutrients, waste, etc. travel homeostatic: -circulating blood aids in keeping environment constant defensive: -protects vs foreign invaders via circulating WBC -prevents blood loss from wounds via clotting communication: -transports hormones from endocrine system -cytokines are released during infection to signal immune response |
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heart
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two pumps, left and right
right side pumps to longs -pulmonary circuit, low pressure high compliance left side pumps to systemic capillaries -systemic, high pressure low compliance generates blood pressure, but does not control it |
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peripheral vasculature
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controls blood pressure by adjusting diameter of arterioles
in a sense, controls metabolism by controlling blood flow |
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organization of the CVS
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blood flow through tissues is locally controlled
heart provides the pressure for the flow local control can be overriden by CNS (symp/parasymp) |
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portal system
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capillaries on either side for a vein
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renal system
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has two control points, afferent and efferent
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normal blood pressures
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pulsitile flow
BP is slightly higher in large arteries because of the echo effect greatest change in pressure occurs in the arterioles, once you reach them, pulsitile flow becomes steady and diameter of the arteriole will determine overall BP pulmonary circuit has 5xless pressure than systemic circuit |
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echo effect
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blood bounces off of the walls of arteries and pressure is amplified
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three basic functional principles of CVS
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1. heart pumps what is returned to it
-cardiac output is controlled by the periphery (venous return) 2. blood flow is locally controlled unless overriden by parasympathetic/sympathetic 3. arteriole blood pressure is controlled independently of the control of local blood flow or cardiac output |
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blood flow through heart
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one way pump
valves prevent backflow RA>RV>pulmonary>LA>LV>systemic, loop |
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histology (heart)
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nodal cells:
-pacemaker (SA and AV) -SA has higher intrinsic firing rate, so it is generally the pacemaker -any cell given conditions can act as a pacemaker myocytes: -contracting muscles of the heart conductive cells: -modified myocytes that have lost ability to contract and instead function as neurons structural cells: -skeleton of heart -all valves are ensheathed in stiff cartilage and connective tissue |
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myocardial histology
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heart cells have similar properties to skeletal and smooth muscle as well as some unique properties:
-striated like skeletal muscle, organelles are similar -stimulation works like smooth muscle, if one is stimulated all respond -have unique structure: intercalated disc |
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intercalated disc
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connect myocytes end to end, gap junctions allow ions to pass from one cell to the next quickly for communication
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myocardial cellular arrangement
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allows action potentials pass on to the next cell very rapidly due to gap junctions
atria and ventricles are separated electrically, conduction will only pass at the AV node |
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gap junction
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connected by 6 protein globules that have a pore in the middle, action potential travels through the pore as if there is no plasma membrane
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ion currents and channels
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ion channels are places where ions can travel through a plasma membrane, the ions traveling through create a current
often drugs are grouped based on what ion channels they affect |
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ion distribution
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intracellular:
Na+ : 15 K+ : 150 Cl- : 5 Ca++:(10^-7) extracellular: Na+ : 145 K+ : 5 Cl- : 120 Ca++:(2um) note: the ratio for Ca++ is giant, this is because we only need a few meq/L Ca++ to bind to troponin |
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fast vs slow currents
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fast/slow refers to the rate at which electrical charges change
activation threshold: differentiates skeletal and cardiac muscle action potentials -fast channels -70 to -55 (like nerve cells) -slow channels -40 to -30 (adapted for heart function) about 1/10th the ions pass through a slow channel |
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Ltype slow channel
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L type:
-long lasting large conductance =open a long time, lots of ions pass -inactivation is slow -threshold is less negative -sensitive to dihydropyridine (CCB) |
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Ttype slow channel
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T type:
-transient, tiny conductance =open briefly, very few ions pass through -inactivation is fast -thresholds more negative -not sensitive to dihydropyridine (CCB) |
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neurotransmitters and ion channels
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generally more likely for a neurotransmitter to affect slow channels
sympathetic and parasympathetic |
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sympathetic system
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epinephrine/norepinephrine increase sympathetic activity when they bind to beta adrendergic or alpha adrenergic
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parasympathetic system
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acetylcholine increases parasympathetic activity when bound to muscarinic receptor in the heart (decreases heart rate)
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fast sodium channel
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electrochemical gradient draws ions in passively when it is open
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slow calcium channel
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there are two types of slow inward Ca++ channels
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potassium channel
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electrochemical gradient allows repolarization
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Na+/Ca++ exchanger
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action depends on ion concentration, it is not a transportation pump
foward puts Na+ in and Ca++ out reverse puts Ca++ in and Na+ out |
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Na+/K+ pump
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creates resting membrane potential
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Ca++ ATPase pump
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on the cell:
uses ATP to move Ca++ against the concentration gradient from the inside of the cell to the out side of the cell on the SR: uses ATP to move Ca++ against the gradient from cytosol into the SR |
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cardiac action potentials
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two types:
myocyte (muscular) nodal (SA/AV node) |
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myocyte action potential
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resting membrane potential is -90mV, and is stable until the threshold is reached, at which point there is a rapid depolarization spike with a large amplitude (up from -90 to +20)
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nodal action potential
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resting membrane potential is around -50 to -40mV, and slowly depolarizes until it reaches the threshold where it will rapidly depolarize with a small amplitude (-50 to almost 0)
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myocyte AP phases
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five phases:
0 - rapid depol 1 - early repol 2 - plateau 3 - rapid repol 4 - resting |
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myocyte phase 0
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caused by fast Na+ channel only open a short amount of time, but lots of ions pass through which leads to rapid depolarization
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myocyte phase 1
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repolarization caused by influx of Cl- ions and partially by the Na+ gate closure
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myocyte phase 2
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Ca++ channel opens, followed by the K+ channel opening
takes several milliseconds Ca++ will influx, while K+ effluxes, they attempt to balance each other out creating a somewhat flat plateau |
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myocyte phase 3
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Ca++ channels close, but K+ channels remain open, thus K+ efflux is still occurring, repolarizing the cell
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absolute refractory period
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nothing can be done to reset action potential while ion channels are open, channels must reach a negative resting potential to fire
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effective refractory period
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begins at phase 3, action potential is still not possible
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relative refractory period
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second part of phase three, it is possible now to fire an action potential, however it will take a stronger signal and the potential will be weakend
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supranormal period
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at undershoot, where K+ efflux has exceeded normal resting potential due to the slow closing of the gate it is even easier for an action potential to fire
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nodal action potentials
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three phases:
phase 0 phase 3 phase 4 |
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nodal phase 0
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threshold of -40 is reached, Ca++ Ltype slow channels open, depolarization occurs
this causes us to skip phase 1 and 2, as the Ca++ is already used and will not be countering K+ to create a plateau |
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nodal phase 3
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K+ channels open and cause repolarization unopposed
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nodal phase 4
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slow depolarization (from -50 to -40) is caused by Na+ funny channels
Na+ funny channels slowly leak Na+ ions in causing depolarization phase 4 is ended by activation of transient Ca++ channels |
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nodal action potential adjustment
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changing funny channels will affect heart rate, decreased activity means that phase four will take longer, resulting in decreased heart rate
ACh binding to K+ channel will allow K+ efflux during phase 4 which would counter Na+ influx from funny channels, decreasing HR |
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impulse conduction pathway in the heart
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normal:
SA atrial muscle AV bundle of His bundle branches purkinje fibers |
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overdrive suppression
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any tissue can function as a pacemaker, if it is generating an impulse at a faster rate than the normal pace maker
ex: if your SA node fails, AV will take over, note that on the EKG there will be no P wave from the SA since it is not functioning appropriately |
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action potential and EKG
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an action potential is a single tissue reacting
EKG is the sum total of the electrical events that are occurring ventricles are so massive that their waves can mask others |
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acetylcholine on the heart
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increases K+ conductance
-hyperpolarizes and decreases phase 4 slope (decrease HR) decreases Ca++ current, affects phase 0 of nodal cells (leads to decreased contractile strength) -it is a negative inotrope as the concentration of ACh increases, we lose ability to reach the threshold potential for firing |
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epinephrine/norepinephrine on the heart
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activate beta receptors which increases HR
activates Ca++ channels (increasing contractile strength) increases contraction rate in muscles -this can be a problem, purkinjes may start to act as pacemakers leading to arrhythmias |
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core temperature on the heart
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increased temperature increases HR
increases spontaneous nodal firing increases slope of repolarization |
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hyperkalemia ([K+] > 5meq/L)
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hyperkalemia hypopolarizes, leading to slow repolarization in myocytes
the pwave will disappear when [K+] >9, longer PR interval, wider QRS, ST depression |
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hypokalemia ([K+] < 3.5meq/L)
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decreases rate and amplitude of phase 0 in nodal cells
slows conduction twaves may revert (flatten) wider PR occurs U waves occur |
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kalemias in general
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both slow HR
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hypercalcemia
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lengthens all phases, longer action potential but decreased amplitude, if Ca++ levels are too low the heart will stop
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