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Dead space to Tidal Volume Ratio.VD/VT
Diffusion ratesCO2= 20 times faster than O2.
How long does alveolar-capillary membrane diffusion take?.25 seconds
In a healthy lung how much CO2 is in the blood before and after the alveolar-capilary gas exchange?46mmHg before, 40mmHg after.
What is carbon monoxides affinity for hemoglobin?210
What are the two ways O2 is carried in the blood?Dissolved in plasma (3%) and by hemoglobin (97%).
What is CaO2?Oxygen content of arterial blood.
CaO2 equation(Hgb x 1.34 x SaO2) + (PaO2 x 0.003)
What is CVO2?Oxygen content of mixed venous blood.
CVO2 equation(Hgb x 1.34 x SVO2) + (PVO2 x 0.003)
What is CC02?Oxygen content of pulmonary capillary blood.
CCO2 equation(Hg x 1.34)* + (PaO2 x 0.003) *it is assumed that the hemoglobin saturation with oxygen in the pulmonary capillary blood (SCO2) is 100%.
What is PAO2?Alveolar oxygen tension.
PAO2 equation(PB - PH2O) x FIO2 - (PaCO2 x 1.25)
Alveolar-Capillary Membrane1. Pulmonary Surfactant 2. Alveolar Epithelium, 3. Basement Membrane 4 tight space 5. capillary basement membrane 6 capillary endothelium 7 plasma 8 eukariotic cell membrane 9 intracellular fluid
Alveoli-Capillary Transit Time.75 seconds * blood travelling from pulmonary arteole -capillary-venule
Alveoli-Capillary PressuresArteoli (mixed venous) PVO2-40, PVCO2-46 Capillary (gas exchange) PAO2-100, PACO2-40 Venule (arteriole) PaO2-100-PaCO2
a - v Difference(arterial-venous O2 content differences) A-V Difference = CaO2 - CVO2 ie. 20 Vol%-15 Vol%=5 Vol% (normal)
Anatomic Shunt(true shunt) Blood from the right heart moves to the left heart without contact with Alveoli. - Congenital (unclosed foreman oval - Interpulmonary fistule (a-v grow together - trauma) - Vascular lung tumor
C(a-v)O2 FactorsIncrease: less cardiac output, more O2 consumption, exercise, seizers, shivering, hypothermia. Decrease: more cardiac output, skeletal muscle relax (drugs), shunting - sepsis - trauma. Poisons and hypothermia
Bohr EffectThe effect of PCO2 and PH on the ODC - most active in capillaries of working muscles especially the myocardium. Can cause Right or Left shift in curve.
Capillary Shunt(true shunt) - caused by the alv collapse (atelectasis) - alv fluid accumulation - alv consolidation (pudding in alv) lung infection
CO(carbon monoxide) - 210 x the affinity for Hgb than O2 - Odorless and colorless
Content of arterial O2CaO2 = (Hgb x 1.34)SaO2+(PaO2 x .003) Normal = 20 Vol%
Content of Mixed Venous O2CVO2 = (Hgb x 1.34)SVO2 + (PVO2 x .003) normal = 15 Vol%
Coximermachine used to detect hemoglobin type: oxyhemoglobin, carbohemoglobin, carbominohemaglobin, methhemogoblin,
deoxyhemoglobinno O2 attached
2,3 DPG- RBC Enzyme - helps kick O2 off Hgb
Hemoglobin (NORMALS)Male: 14-16 grams/100 ml of blood Female: 12-15 grams/100 ml of blood WEIGHT= 1.34 ml O2 per gram i.e. 1.34 ml O2 x 15 g Hgb = 20.1 Vol% 20.1 Vol % x .97%(SaO2) = 19.5 Vol% O2
Hypoxemiadecreased arterial O2
Hypoxic Hypoxia(abnormally low PaO2 & CaO2) (tissue hypoxia) Hypoxemia= low PAO2 & PaO2 Diffusion: Impairment=alv - cap membrane problem i.e, fibrous, consolidation, edema Ventilation perfusion mismatch: flow faster the ventilation - causes shunt-like effect.
O2 consumptionAmount of O2 extracted by peripheral tissues during one minute. VO2 = QT(C(a-v)O2 x 10)) (250 mil O2/minute is normal)
Vol %The amount of O2 (ml's) in 100 ml's of blood Vol% = mlO2/100ml of blood
Minute Alveolar VentilationVA=(VT-VD)x bpm (tidal volume less dead space x breaths per minute)
O2 content of arterial blood (CaO2)CaO2 = (Hbg x 1.34 x SaO2) + (PaO2 x .003)
O2 content of mixed venous bloodCVO2 = (Hgb x 1.34 x SVO2) + (PVO2 x .003)
O2 content of Pulmonary Cap bloodCcO2 = (Hgb x 1.34) + (PaO2 x .003)
Venous AdmixtureMixing shunted (non-reoxygenat) with reoxygenated blood distal to the alveoli
ScO2Hemoglobin Saturation with oxygen in the pulmonary capillary membrane Normal = 100%
SaO2O2 saturation in arterial hemoglobin Normal is 97% (3% shunted)
PO2Dissolved O2 that is moving freely in blood plasma Approx .3 Vol% normal (or .003 mil per 100 mil of blood
P50 Point- Point in ODC where Hgb is 50% saturated with O2 (27 mmHg is normal
Shunt-like EffectPulmonary capillarity perfusion in excess of alveolar ventilation. - Hypoventilation-uneven distribution ventilation- A-C diffusion defects
Shunt EquationMeasures the amount of intrapulmonary shunting QS/QT=CcO2 - CaO2/CcO2 - CVO2
Refractory to O2- No O2 exchange taking place, cannot be treated with simple increase in O2 levels - - O2 levels are not changing - happens to true shunt patients
Pulmonary shunts1. True Shunt = cardiac output that enters the left side of the heart without gas exchange. 2. Shunt Like = Blood that exchanges gases but does not obtain PO2 up to normal.
ODC flatline- PO2 can fall from 100 to 60 and Hgb will still be 90% saturated. (PO2 at 60 = 90% saturation) - shows safety zone that Hgb has for loading O2 into the lungs
Total O2 Delivery- Total amount of O2 delivered to tissue. - Dependent on O2 in blood, Hgb and cardiac output. DO2 = QT x (CaO2 x 10) QT = cardiac output (5L = norm) CaO2 = O2 of arterial blood (20 Vol% = norm)
True shunt1=Anatomic shunts: flows from the right to left but no alveoli contact (Heart disease, Intrapulmonary fistula, Vascular lung tumor) 2=Capillary shunt: collapsed alveoli
ODC Right Shift(Right) Hgb has less affinity for O2- Causes Hgb to dump more O2 in tissue Acidosis Temp increases PCO2 increases 2,3 DPG increases
ODC Left Shift(Left)Hgb has more affinity for O2-Causes Hgb to hold onto O2 Alkalosis - PH increases CO2 Decreases Temperature Increases 2,3 DP6 Decreases
O2 Extraction RatioO2ER = CaO2 - CVO2/CaO2 (.25 = Normal) i.e., 1 min = 250 ml's O2 are metabolized by tissue and 750 ml returned to lungs (of 1,000 ml's)
ODC(Oxygen Dissociation Curve) Left illustrates the %Hgb that is bound to O2 at each pressure Right illustrates O2 content carried by Hgb at each pressure P-50 = PO2 where Hgb is 50% saturation with O2 (27 mmHg normal)
Pulmonary Shunt Significances10% shunting = normal 10 - 20% shunting = Abnormal, potential life threatening 20 - 30% SHUNTING = significant decrease, life threatening
SVO2(mixed Venous O2 saturation) Used to detect changes in C(a-v)O2,VO2+O2er(Normal = 75%)Factors ↑(indicates VO2 and O2er going up)=CO ↑, skeletal muscles relax, shunting etc. Factors ↓ (indicates VO2 and O2er going down), CO ↓ , O2 consump ↑ exerciser, etc.
O2 Consumption FactorsFactors that Decrease=Skeletal muscle relaxation (drugs, Shunting (sepsis - trauma), Poisons and hypothermia. Factors that Increase=increased cardiac output, increased O2 consumption, anemia, decreased Arterial oxygenation.
Alveolar Gas EquationPAO2=(Pb-PH2O) x FIO2-(PaCO2 x 1.25)***Note that if patient is receiving O2 therapy, adjust FIO2 (accordingly) and drop the 1.25 multiplier).
Biot's Respirationshort periods of rapid, uniform and deep inspiration fallowed by 10-30 seconds of apnea (caused by meningitis)
Cheyne-Stokes Respiration10-30 seconds apnea, gradual increase in volume and frequency, then gradual decrease, then apnea again for 10-30 seconds (caused by cerebral disorders)
Hemoglobin SaturationPaO2 of 60mmHg= Hgb of 90% saturation. Hgb will only increase in very small increments up to 97% saturation. sooooo- PaO2 of 70 mmHg is approx 93% and PaO2 of 80 is Hgb of approx 95%
Hyperventilationincreased alveolar ventilation (↓ PACO2 & PaCO2)
HypoventilationDecreased Alveolar ventilation (under ventilating) (causes ↑ PaCO2)
Hypoxia(Low O2 for cellular metabolism) 1. Hypoxic Hypoxia 2. Anemic Hypoxia 3. Circulatory Hypoxia 4. Histotoxic Hypoxia
Apneustic Centerlocated in lower Pons, sends continuous impulses to DRG & VRG, causes apneustic (gasping) breathing, inhibitory signals from pneumotaxic center keep it as a back up center unless needed. keeps person alive but only when necessary
Baroreceptor ReflexesAortic and Carotid sinus reflexes that measure blood pressure= BP decreases cause HR and RR to increase etc.
Blood Brain BarrierBarrier that separates blood from the CSF. very permeable to CO2
Cerebral cortexconscious control of breathing...speech, pain, emotion. messages sent to diaphragm and accessory muscles as needed.
C-FibersExtensive network of free nerve endings found in the small conducting airways, blood vessels, interstitial tissues and pulmonary capillaries
Central Chemoreceptors(aka CO2 drive) Located in medulla, it is stimulated by the H+ in CSF, very sensitive- and very quick to react.works to keep normal quiet breathing CO2 at 40 mmHg
CO2 DriveIncreased CO2 (hypoventilation) in arterial blood leads to CO2 crossing into Blood B. B.- CO2 becomes H+ & HCO3, increase in H+ activates central receptors.
DLCO TestDiffusion capacity of CO test=measures CO that has moved across the alv-cap membrane. ie=measures physiological effectiveness of membrane (25 ml/min mmHg normal)
DLCO Factors(factors that can change diffusion capacity) age, lung volume, body size, body position, exercise, PAO2, Hgb, carbohgb
DRG(dorsal resp group) Inspiratory center, responsible for quiet breathing, prioritizes signals from central chemo, periphial chemo, stretch etc. sends action to diaphragm via L&R Phrenic nerves.
Glassopharyngeal nervelocated in carotid body, sends impulse to Medulla when activated by low PaO2
H+most powerful stimulus known to influence DRG and VRG, when found in excess amounts in CSF
Hering-Breuer Reflexstretch receptor in Bronchi and bronchiole get excited when over inflation occurring. Vagus nerve carries message to medulla, medulla stops inspiration before damage to alveoli
Hypothalamic Controlsexcitement, temperature, sudden cold
Irritant Reflexsubepithelial receptor in trachea bronchi and bronchiole, triggered causes vent to increase, coughing, bronchi constriction...toxins, wrong pipe etc.
J-receptorsspecific C-fibers located near the alv-cap that when stimulated trigger the juxtapulmunary reflex.
Juxtapulmonary Reflexstimulated by alv inflammation, pulm-cap congestion, humeral agents, lung infections and emboli, causes a reflex of rapid shallow breathing
Medulla Oblongatacontrols the DRG and VRG, primarily influenced by high H+ in CSF
Medulla Oblongata conditionsedema, acute poliomyelitis and cns drugs can effect the medullas ability to control breathing
Medulla monitoring system2 major are ...central and peripheral chemoreceptors, also in a lessor way by exercise and certain reflexes.
Peripheral Chemoreceptors(aka hypoxic drive) receptors found in carotid and aortic bodies, afferent signals from glosso and vagus, stimulated by O2 below 60 or low PH (lactic or keto acid), stops working below 30- O2, back up system, activation caused increased ventilation
Peripheral Chemoreceptor Factorsbecause it is only looking at PaO2, it can be easily mislead by anemia, CO poisoning etc. Granny with chronic high CO2-causes central chemo to shut down, and makes peripherals more sensitive to CO2-allowing it to take over ventilation.
Peripheral Proprioceptor Reflexlocated in muscles, tendons joins etc. send signal to medulla when tissues need more O2
Phrenic NerveDRG sends message to diaphragm via these nerves
Pons(mostly a back up system when medulla is damaged) Pneumotaxic center and apneustic center. Keeps patient alive with labored gasping breathing
Pneumotaxic Centerpart of the Pons, has 2 functions. 1. receives impulses from hering-breuer and stretch receptors via vagus nerve 2. inhibitor of apneustic center
vagus nervesends impulse from aortic arch to medulla when activated by low PaO2, also hering-beuer reflex signals
Ventilation ReflexesHering-Breur, irritant, justapulmonary, peripheral proprioceptor,, hypothalamic controls, aortic and coratid baroreceptors and peripheral chemoreceptors
VRGventral respiratory group-usually dormant) inspiratory and expiratory, used during exercise and stress etc
arterial blood gas partial pressuresPaO2=95, PaCO2=40, PaH2O=47, PaN2=573 Total arterial PP=755
Alveolar Gas Partial PressuresPAO2=100, PACO2= 40, PAH2O=47, PAN2=573, total 760
Atmospheric Gas PercentagesN2=78%, O2=21%, Ar=.93%, CO2=.03% ***gas concentration does not change with altitude only barometric pressure
Daltons Lawin a mixture of gas-the total pressure is equal to the sum of the partial pressures of each separate gas. example= since O2 is 21% of room air, then if the Bp is 760, O2 is 21% of 760 or 159
Diffusionpassive movement of gas molecules from an area of high pressure to a low pressure until both are equal
CO2 Diffusion Rate20 to 1 over O2
Diffusion Limited Gas Flowthe movement across the alv-cap membrane is a function of the membrane integrity. can be effected by atelectasis, emphysema, fibrosis, pneumonia, pulmonary or interstitial edema
Ficks law and diffusiongas exchange is proportional to the thickness of the tissue...thicker tissue, slower diffusion
Alv-cap gas exchange time.25 seconds
Alv-cap transit time.75 seconds, arteriole to venule
KelvinTemperatures in Gas calcs MUST be converted to Kelvin F to C = 5/9(F-32)=C, C to K = C + 273 = K
Mixed Venous(PV) venous blood from both the upper and lower body
Perfusion Limited Gas Flowthe transfer of gas across the alv-cap membrane is a function of the amount of blood that flows past the alveoli. blood flowing to fast limits the amount of gas exchange
Solubility Coefficientthe amount of gas that can be dissolved by 1 ml of a given liquid at standard press and a specific temperature
Venous Blood Gas Partial PressPVO2=40, PVCO2=46, PVH2O=47, PVN2=573