| Question | Answer |
| Dead space to Tidal Volume Ratio. | VD/VT |
| Diffusion rates | CO2= 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 Membrane | 1. 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 Pressures | Arteoli (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 Factors | Increase: 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 Effect | The 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 O2 | CaO2 = (Hgb x 1.34)SaO2+(PaO2 x .003)
Normal = 20 Vol% |
| Content of Mixed Venous O2 | CVO2 = (Hgb x 1.34)SVO2 + (PVO2 x .003) normal = 15 Vol% |
| Coximer | machine used to detect hemoglobin type:
oxyhemoglobin,
carbohemoglobin,
carbominohemaglobin,
methhemogoblin, |
| deoxyhemoglobin | no 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 |
| Hypoxemia | decreased 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 consumption | Amount 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 Ventilation | VA=(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 blood | CVO2 = (Hgb x 1.34 x SVO2) + (PVO2 x .003) |
| O2 content of Pulmonary Cap blood | CcO2 = (Hgb x 1.34) + (PaO2 x .003) |
| Venous Admixture | Mixing shunted (non-reoxygenat) with reoxygenated blood distal to the alveoli |
| ScO2 | Hemoglobin Saturation with oxygen in the pulmonary capillary membrane
Normal = 100% |
| SaO2 | O2 saturation in arterial hemoglobin Normal is 97% (3% shunted) |
| PO2 | Dissolved 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 Effect | Pulmonary capillarity perfusion in excess of alveolar ventilation.
- Hypoventilation-uneven distribution ventilation- A-C diffusion defects |
| Shunt Equation | Measures 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 shunts | 1. 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 shunt | 1=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 Ratio | O2ER = 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 Significances | 10% 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 Factors | Factors 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 Equation | PAO2=(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 Respiration | short periods of rapid, uniform and deep inspiration fallowed by 10-30 seconds of apnea (caused by meningitis) |
| Cheyne-Stokes Respiration | 10-30 seconds apnea, gradual increase in volume and frequency, then gradual decrease, then apnea again for 10-30 seconds (caused by cerebral disorders) |
| Hemoglobin Saturation | PaO2 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% |
| Hyperventilation | increased alveolar ventilation (↓ PACO2 & PaCO2) |
| Hypoventilation | Decreased 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 Center | located 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 Reflexes | Aortic and Carotid sinus reflexes that measure blood pressure= BP decreases cause HR and RR to increase etc. |
| Blood Brain Barrier | Barrier that separates blood from the CSF. very permeable to CO2 |
| Cerebral cortex | conscious control of breathing...speech, pain, emotion. messages sent to diaphragm and accessory muscles as needed. |
| C-Fibers | Extensive 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 Drive | Increased CO2 (hypoventilation) in arterial blood leads to CO2 crossing into Blood B. B.- CO2 becomes H+ & HCO3, increase in H+ activates central receptors. |
| DLCO Test | Diffusion 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 nerve | located 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 Reflex | stretch 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 Controls | excitement, temperature, sudden cold |
| Irritant Reflex | subepithelial receptor in trachea bronchi and bronchiole, triggered causes vent to increase, coughing, bronchi constriction...toxins, wrong pipe etc. |
| J-receptors | specific C-fibers located near the alv-cap that when stimulated trigger the juxtapulmunary reflex. |
| Juxtapulmonary Reflex | stimulated by alv inflammation, pulm-cap congestion, humeral agents, lung infections and emboli, causes a reflex of rapid shallow breathing |
| Medulla Oblongata | controls the DRG and VRG, primarily influenced by high H+ in CSF |
| Medulla Oblongata conditions | edema, acute poliomyelitis and cns drugs can effect the medullas ability to control breathing |
| Medulla monitoring system | 2 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 Factors | because 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 Reflex | located in muscles, tendons joins etc. send signal to medulla when tissues need more O2 |
| Phrenic Nerve | DRG 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 Center | part of the Pons, has 2 functions. 1. receives impulses from hering-breuer and stretch receptors via vagus nerve 2. inhibitor of apneustic center |
| vagus nerve | sends impulse from aortic arch to medulla when activated by low PaO2, also hering-beuer reflex signals |
| Ventilation Reflexes | Hering-Breur, irritant, justapulmonary, peripheral proprioceptor,, hypothalamic controls, aortic and coratid baroreceptors and peripheral chemoreceptors |
| VRG | ventral respiratory group-usually dormant) inspiratory and expiratory, used during exercise and stress etc |
| arterial blood gas partial pressures | PaO2=95, PaCO2=40, PaH2O=47, PaN2=573 Total arterial PP=755 |
| Alveolar Gas Partial Pressures | PAO2=100, PACO2= 40, PAH2O=47, PAN2=573, total 760 |
| Atmospheric Gas Percentages | N2=78%, O2=21%, Ar=.93%, CO2=.03% ***gas concentration does not change with altitude only barometric pressure |
| Daltons Law | in 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 |
| Diffusion | passive movement of gas molecules from an area of high pressure to a low pressure until both are equal |
| CO2 Diffusion Rate | 20 to 1 over O2 |
| Diffusion Limited Gas Flow | the 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 diffusion | gas 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 |
| Kelvin | Temperatures 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 Flow | the 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 Coefficient | the 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 Press | PVO2=40, PVCO2=46, PVH2O=47, PVN2=573 |