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What is the thickness of the A/C membrane?
- The A/C membrane is a fusion of the alvolar wall and the capillary wall.
- 0.5 to 1 um thick
What is the function of type 1-3 alveolar cells in the lung?
Type I: flat, thin cells that make up about 95% of the gas exchange area.
Type II: Thick cells that produce surfactant
Type III: Free-floating macrophage-like cells
Normal circulatory pressure values that lead to the gradient needed for gas movement:
- a) 35-45 mmHg
- b) 80-100 mmHg
- c) 40 mmHg
- d) 46 mmHg
What is the pressure gradient for carbon dioxide in the lungs?
- PvCO2-PaCO2= 6 mmHg
- Enough to drive CO2 from the capillaries to the alveoli (for removal)
What impact will extreme hyperventilation or hypoventilation have on arterial gas pressures?
- Hyperventilaiton: alkalosis.
- - O2 and CO2 near ammbient values (150 and 10 mmHg respectivley)
- Hypoventilation: acidosis
- - O2 < 50 mmHg and CO2 > 50 mmHg
What is the solubility coefficient of oxygen?
0.003 mL/dL plasma/mmHg at 37'C
What is cytochrome P450?
Most notably known for its anti-toxic role in the liver
- A hemoprotein enzyme attatched to the endoplasmic reticulum in A/C membrance cells.
- - Facillitates the diffusion of O2 accross the membrance (approx 10-15%)
How does body position affect pulmonary diffusion capacity?
Can be increased up to 20%
when in a recumbent position due to gravity
- - when lying, blood supply is more evenly distributed accross lung fields (improved V/Q matching)
- - pulmonary blood volume increases as well
What is the pulmonary diffusion capacity?
A measurement of the volume of a specific gas that can be transferred per unit time accross the A/C membrane (efficiency)
Normally 30 mL/O2/min/mmHg gradient
What factors affect the variabilty of diffusion capacity?
- 1. prop. to the pressure gradient accross the mem.
- 2. prop. to the solubility of the gas in the mem
- 3. prop. to the rxn rate of O2 with Hb
- 4. prop. to the volume of blood in the capillary bed
- 5. inverse to membrane thickness
- 6. inverse to the molecular weight of the gas
What patient factors affect diffusion capacity?
- 1. Body Position:
- - inc with lying
- 2. Body size:
- - refers to natural size, not obesity
- - inc size = inc A/C size (inc V/Q interface)
- 3. Exercise:
- - inc (35%) during exercise
- 4. Disease:
- - emphysema: destroys alveolar and capillary tissue
- - pneumonia: consolidates gas exchange regions
- - pulmonary embolism: capillary blood flow obstruction
- - V/Q mismatch: when majority of blood flow is not in the same region as the majority of gas (usually due to the above)
Explain the pressure gradients that lead to ventilation:
- The gradient is formed by the difference in the partial pressures of O2 and CO2 between alveolar and capillary gas.
- Venous blood returning from the body is relativley low in PO2 and high in PCO2, which creates an ideal condition under which CO2 can exit the body and O2 can enter.
- The volume and rate of gas exchange is directly related the gas pressure gradient
How does the wall size of the pulmonary arteries compare to the aorta?
The wall of each pulmonary artery is about 30% or 1/3 the size of the aorta
The pulmonary arteries and arterioles have relativley large diameters and thin walls= this allows for high compliance.
How does the right ventricle differ from the left in terms of thickness and why?
The Right ventricle is approximatley 30% or 1/3 the thickness of the Left ventricle.
This is a result of the pressure difference between the 2 systems (due to their requirements). The systolic pressure of the Right ventricle (pulmonary) is 25 mmHg compared to the 120 mmHg pressure of the Left (systemic) side.
What is the approximate stroke volume of the Right ventricle? What is the relationship to compliance and pressure in the pulmonary circuit?
The stroke volume
output is approximatley 70mL
and the compliance
of the vasculature is about 2mL/mmHg.
- This means that with a normal systolic pressure of 25 mmHg, 50mL out of the 70mL's pumped out/beat can be accommodated by the vessels.
- This aids in keeping the circuit pressure relatively low (decreased force required).
What percent of the cardiac output supplies the the bronchial vessels? How does it drain?
and nutrients for the lung-supporting tissues
- Once this supply passes through the tissues, it empties back into the pulmonary veins (not venous circ'n). = enters the Left atrium and mixes with oxygenated blood = anatomic shunt
- -note that this is one reason for the increased C/O of the Left ventricle
What is the term "safety factor" in regards to when dealing with pulmonary edema?
The primary cause of PE is elevated pulmonary capillary pressure (from cardiac failure).
For edema to occur, capillary bp must rise 2-3 mmHg above colloid osmotic pressure.
Because normally capillary P is 8 mmHg while colloid osmostic is 28 mmHg, there existst a 23 mmHg buffer before edema will occur.
This buffer region not only means capillary P has to climb a long way, but because it would take longer to rise above the buffer, the lymphatic system has more to compensate (by inc flow)
How does hypoxia affect pulmonary vascular smooth muscle tone?
(also hyperoxia and hyoercapnia)
Hypoxia = vasoconstriction
Hyperoxia = vasodilation
Vascular pressures must increase as vascular caliber decreases. Resistance to blood flow increases with vasoconstriction and reduced with dilation.
List 5 factors that will result in increased vasular smooth muscle tone
- Sympathetic stimulation
- Pulmonary embolism
- alpha agonists...
What is pulmonary artery wedge pressure?
- Pressure measure distal to the balloon catheter (once inflated) , through the capillary bed. Represents Left ventricular preload or Left ventricular end diastolic pressure (normally 5-12 mmHg)
What do the "zones" of the lung relate to?
- The zones are a model for describing variations in pulmonary perfusion (uneven distribution) due to gravity.
- When a person is standing, Bp can differ by 90 mmHg at the feet vs the heart and by 23 mmHg between the base and the apex of the lung (8 below, 15 above due to heart placement)
Describe zones 1-3 in the lung
- Zone 1: Area of no blood flow (deadspace)
- - a result of pulmonary Bp < alveolar pressure = compression of the capillary around the vessel (closing it off)
- - usually only occurs during mech ventilation or reduced C/O
- Zone 2: Area of pulsatile blood flow
- - pulmonary arteriole pressure is great enough to overcome alveolar pressure during systole only
- - extends from 8cm above the heart level to the apex
- Zone 3: Area of continuous blood flow
- - from 8cm above the heart to the base.
- - both systolic and diastolic pressures overcome alveolar
What is normal central venous pressure?
What is the surface area of the blood-gas interface in the lung?
The A/C membrane is approx 75-100 m2
What is the approx volume of blood that interfaces with gas in the lung?
70-100 mL of blood interfaces with about 2L of gas (functional residual capacity)
Fluid accumulation in the alveolar interstitium may result from
a) increased capillary hydrostatic pressure (pulmonary HTN)
b) obstructed lymphatic flow
c) reduced blood osmotic pressure
d) membrane trauma
e) membrane fibrosing
g) all of the above
g) all of the above
Three primary factors that contribute to the maintenance of the alveolar/capillary gas pressure gradient
1. Alveolar ventilation: Ventilatory pattern must match the body's metabolic demands (recall hyper or hypoventilation)
2. Pulmonary capillary blood flow: As venous blood moves through a ventilated alveolus, gas exchange occurs rapidly and tapers off as the gradient decreases. When the demand for exchange is increased (i.e. exercise) a greater gradient is produced and the diffusion rate increases (as long as ventilation corresponds)
3. Chemical reactions: Gas carried by the blood is dependent on the erythrocyte and Hb
Carbon dioxide is approximatley __ times more soluble than oxygen in plasma?
- O2 = .003 mL/dL blood/mmHg @ 37'C
- CO2= 0.067 mL/dL blood/mmHg @ 37'C
is approx 20x
Lymphatic flow from the lung is approx ___ mL/hr/100g tissue
5-6 mL/hr/100g tissue
-Lymph vessels arise from tissues around vascular and bronchial spaces
- -They flow into the hilium of the lung and empty into the Right lymphatic duct
- -Helps remove debris, particulate matter and fluids
- -Anything that increases interstitial fluid P or lymphatic pump activity will inc lymph flow out.
Lyphatic flow through the lungs is a result of:
- 1. Valves
- 2. Smooth muscle tone
- 3. Vessel compression
Name 3 causes of pulmonary edema
- 1- Left ventricular failure
- 2- leaky capillary membrane
- 3- decreased plasma osmotic pressure (colloid)
- 4- fluid overload
- 5- increased pulmonary Bp/vascular resistance
List 3 factors that contribute to pulmonary artery Bp
- 1- cardiac output
- 2- pulmonary vascular resistance
- 3- pulmonary vascular compliance
(recall that RV C/O is 70mL and vasculature is thin with about 2mL/mmHg of compliance)
The 3 most important factors regarding gas exchange
* if V/Q matching is offset, the majority of blood flow is not in line with the majority of gas flow and diffusion capacity is severely hindered.
- 1- Alveolar ventilation (V)
- 2- Pulmonary ventilation (Q)
- 3- Matching of the two (V/Q)
What is the V/Q relationship for :
a) true shunting
b) deadspace ventilation
c) Shunt effect
d) deadspace effect
- a) 1:0
- b) 1:0
- c) 1:2
- d) 1: .05
What is the normal value for anatomical deadspace?
1 mL/lb ideal body weight. (or 2mL/kg)
How is alveolar deadspace calculated?
- = physiological VD - anatomical VD
- PaCO2- PETCO2 / PaCO2
What affect does hyperventilation have on V/Q?
- it increases V/Q
- V is in excess of Q
What is the difference between the respiratory exchange ratio and the respiratory quotient?
They both describe the relationship between CO2 production and O2 absorbtion
The respiratory exchange ratio deals with the rlsp in the lungs while the respiratory quotient deals with it at the cellular level.
List the structures responsible for anatomical shunting past the lungs
Anatomical shunt: routes venous blood directly into arterial blood (=-venous admixture)
1- Thebesian veins: Drain a portion of coronary blood directly into the L ventricle = admixture. (coronary blood is supposed to empty into the R ventricle but a portion empties into the pulmonary veins where it mixes with oxygenated blood)
2- Bronchial circulation: 1-2% of arterial blood is used to supply lung tissue. Once it has been used it drains into the L atrium/ventricle = admixture.
3- Pleural circulation: System that supplies the visceral pleura with blood also drains into the L atrium/ventricle= admixture.
How is the ideal oxygen content in the blood (CIO2) calculated?
CIO2= (PAO2 x 0.003) + (1.34 x Hb)
PAO2 = PP of alveolar oxygen
Calculate the physiological shunt using the following values:
= combined total of all shunts (capillary and anatomical)
- = QS/QT= _______(CIO2- CaO2)_______
- _________(CIO2 - CaO2) + (CaO2 - CvO2)
- QS= Shunted cardiac output
- QT = total cardiac output
Ex: (21-20)/(21-20)+(20-15)= 16.6
What are normal values of:
a) mixed venous oxygen content
b) actual content of oxygen in the blood
c) physiological shunt
- a) 15 mL/dL
- b) 20 mL/dL
- c) .05 or 5%
How is CvO2 calculated?
= (1.34 x Hg x Satv) + (0.003 x PvO2
- The blood sample for analysis is best taken from the pulmonary artery.
- Satv= saturation of venous blood (sat of Hb)
How long is blood in the pulmonary capillary bed?
It takes 0.75 seconds for an RBC to pass through the pulmonary capillary bed.
May be reduced by 1/3 when cardiac output is significantly increased (i.e. exercise).
Alveolar deadspace results from:
Due to absence of perfusion in the alveoli which does not normally exist in a healthy lung:
- Decreased cardiac output
- Pulmonary hypotension
- Pulmonary embolus
How does a pulmoanry embolus effect perfusion and the End-tidal CO2 / PaCO2 relationship?
- The embolus would obstruct flow to pulmonary vasculature= decreased perfusion
- - would cause expired air to not take part in gas exchange
As the embolus increases in size, End-tidal CO2 decreases
(= increasing the difference between end-tidal and PaCO2
What is the deadspace effect?
An area of hyperventilation (ventilation in excess of perfusion) with an increased V/Q
- Ideal, both blood flow and ventilation are matched with each other:
- = a balance or equilibriation between blood and gas in the alveoli.
- Normal pressures:
- PAO2 = 100 mmHg
- PACO2 = 40 mmHg
- true, anatomical and physiological
- Shunt effect= a region of higher perfusion than ventilation, resulting in blood leaving the lung before gas exchange is complete
- (= hypoventilated blood; gas values are off and V/Q is decresaed to 1:2)
- True shunt: vascular communication that bypasses circulatory channels. (i.e. if blood went from the R-L ventricle without entering pulm circulation)
- Capillary shunt: Bypassing the alveolar capillaries
- Anatomical shunt: normal shut used to route venous blood directly into arterial (venous admixture)= appox 1-3% of cardiac output
- Physiological shunt: Combined anatomical and capillary shunts = approx 2-6% total cardiac output. Note that anatomical values don't change so any increase is due to capillary shunting in the lung
Find the arterial O2 concentration in normal blood (5% shunt) vs that with a 30% shunt
- with a 5% shunt, 95% of blood has actual O2 values of 20 mL/dL (CaO2) and 5% has mixed venous content of 15 mL/dL (CvO2):
- 95% x CaO2 (20 mL/dL)= 19 mL/dL
- 5% x CvO2 (15 mL/dL) = 0.75 mL/dL
- = 19.75 mL/dL of O2 in arterial blood
- With a 30% Shunt (i.e. due to obstruction)
- 70% CaO2= 14 mL/dL
- 30% CvO2= 4.5 mL/dL
- = 18.5 mL/dL (a difference of 1.25 mL or 14.5%)
What is the normal quantity of oxygen consumed and carbon dioxide produced by the body per minute?
- 250 mL of O2 consumed
- 200 mL of CO2 produced
The partial pressure at which Hb is 50% saturated with oxygen
List 4 factors which shift the oxyhemoglobin dissociation curve to the right
Shift to the right= Hb has decreased affinity for O2
- - increased Temp
- - increased PCO2
- - increased [H+] / decreased pH
- - increase in 2,3 DPG
the opposite is true for increasing affintity
List and describe 3 methods of carrying carbon dioxide in the blood
- 1- Dissolved in plasma: 5-10%
- 2- As carbaminohemoglobin: 20-30%, then carried by plasma proteins (25%) or by Hb (75%)
- 3- Bicarbonate: 60-70%
- a) Tissue: CO2 and H2O are coverted to H+ (which binds with Hb) and HCO3- (which diffuses into plasma).
- Cl- diffuses into the RBC to balance charges (chloride shift).
- b) Lungs: Cl- out and HCO3- switch back where CO2 and H2O is again formed and diffuse out of the cell for gas exchange
Describe the hemoglobin molecule
- A conjugated protein (attatched to an iron pigment)
- 2 major components:
- 1) Heme: Iron centered (Fe), made of 4 pyrrol groups (C4H4NH) linked via methene (CH2) bridges. There are 4 heme groups/hemoglobin molecule. Each heme can carry one O2 molecule.
- - 2 states of heme:
- a) Ferrous (reduced, Fe2+): normal state, available to accept oxygen
- b) Ferric (+ reduced Fe3+)= Methemoglobin, cannot accept oxygen
- 2) Globin: A protein with 4 polypeptide chains (2 alpha, 2 beta).
- Acts as a buffer (acid-base balance)
A term used to describe a deficiency in red blood cells
- 1) Hemorrhage or rapid blood loss.
- 2) Aplastic anemia: bone marrow disfunction= lack of RBC production
- 3) Megaloblastic anemia: deficiency in erythroblast production= slow production of oddly shaped cells in insufficiant quantities
- 4) Hemolytic anemia: disorder with fragile RBC's that rupture.
Factors producing abnormalities in gas transport (7)
- 1) Reduced blood flow: circulatory hypoxia
- 2) Anemia: decreased RBC's (4 types)
- 3) Hemoglobinopathies: Hb abnormalities
- a) Sickle cell anemia: abnormal substitution of an amino acid in the Hb molecule
- b) Thalassemia: defect if peptide production= smaller RBC's (microcytic) with low Hb content (hypochromic)
- 4) Cyanide poisoning: Blocks cytochrom oxidase= impeding the Krebs cycle
- 5) Carboxyhemoglobin: carbon monoxide poisoning (Hb has an affinity 200x greater for CO so any PCO > 0.7 mmHg is lethal)
- 6) Methemoglobin: reducing agents present in the blood state reduce Hb to its ferric state, where it can't accept O2. (methemoglobinemia: disorder where the body doesn't produce enzymes to counter this reduction)
- 7) Sulfhemoglobin: When Hb binds hydrogen sulfide= can't accept O2
The quantity of gas dissolved in a liquid at a given temp is directly proportional to the partial pressure of the gas to which the liquid is exposed. This is an example of ___ Law
Henry's Law of solubility
What are the normal arterial mean values for
- O2 content
- CO2 content
compare to mixed venous?
- - 20 mL/dL
- - 98%
- - 49 mL/dL
- - 7.4
- Mixed Venous:
- - 15 mL/dL
- - 75%
- - 53 mL/dL
- - 7.3
As blood saturates with O2, the decreasing affinity of Hb for CO2 is known as ___ law?
Haldane's Law/Haldane effect
Desaturation of Hb with O2 increases its affintity for CO2
What is the life span of an RBC?
Then destroyed in the spleen, liver and red mone marrow
When and why is O2 carried in plasma instead of with Hb?
It's the mechanisms of transport between lungs-RBC,s and Tissue-RBC's.
Accounts for only 3.6% of transport in the body (represents degree of use at the tissue level or gas exchange)
What are the normal levels of Hb in the blood?
- Men: 14-18 g/dL
- Women: 12-16 g/dL
Each gram of Hb can carry approx 1.34 mL
Describe Reversible Combination (affinity)
(shift L= increased O2
affinity, note the rlsp between affinity and PO2
-Mechanism for O2 transport as Hb must bind O2 in the lungs (inc affinity) yet release it in tissues (dec affinity).
- The oxyhemoglobin dissosiation curve
describes Hb's affinity for O2
under various physiological conditions: Due to the Bohr effect (inc [CO2] or [H+]= dec affinity for O2)
and the Haldane effect (dec O2 saturation= dec O2 affinity
) - and visa versa for both effects.
- -i.e. local conditions affect Hb's affinity in a way that facilitates transport:
- - tissues (due to aerobic metabolism)= inc CO2 and dec pH (inc H+)
- - lungs (after ventilation)= inc O2 and inc pH
If flow= 30 L/min, I:E = 1:5 and RR= 12 bpm, calculate tidal volume.
VT can be calculated from TI x flow
- TI= cycle time/I+E (total parts)
- cycle time = 60/RR= 60/12= 5
- TI= 5/6= .833
- VT= 0.833 seconds x 0.5 L/sec= .417 L or 417mL
Determine peak airway pressure when: Flow= 60 Lpm, I:E= 1:5, RR= 12bpm, compliance= 25mL/cmH2O, Resistance= 5 cmH2O/L/sec
PPeak= pressure from resistance (PTA) + pressure from compliance (PPlat)
- PTA= R x flow
- = 5 cmH2O/L/sec x 60 L/min (or 1L/sec)
- = 5 cmH20
- PPlat= VT/Compliace
- VT = TI x flow
- (TI= cycle time/I+E= 5/6)
- = .833 sec x 1 L/sec= 833 mL
- = 833 mL/25 mL/cmH2O= 33.32 cmH2O
Ppeak= 5 cmH2
O + 33.32 cmH2
What are at least 4 conditions that can increase
oxygen consumption in the patient who is not breathing (i.e. on mech ventilation)?
How can positioning a ventilated patient flat on the bed result in increased work of breathing?
- If the patient is morbidly obese, pregnant or has significant ascites, the abdominal organs or fluid can press against the diaphram when in a lying
- This may cause considerable resistance to inhalation and require increased work to achieve a desired tidal volume
What are the two settings used to enable the patient to initiate, or trigger, a breath from the ventilator?
Which method is generally considered to be more responsive to patient effort?
or pressure triggering
are two different breath initiation settings.
- Flow triggering is generally seen as requiring less patient effort to initiate
- a breath as it requires less negative flow
Does a patient who has asthma need longer or shorter time for exhalation?
What would be an I:E ratio that you would use for this type of patient?
- Asthma patients may need longer exhalation times (TE) to prevent worsening hyperinflation.
- An I:E ratio of 1:4 would be a recommended ratio to use
What are the primary dangers of using tidal volumes of 15 mL/kg (patient weight) to ventilate your patient?
VILI can alter capillary permeability and lead to alveolar flooding
- High tidal volumes can result in ventilator-induced
- lung injury (VILI) as a result of either barotrauma and/or vulutrauma.
How does PEEP improve oxygenation?
- PEEP helps to increase the volume of gas remaining in the lungs after exhalation.
- = This prevents the de-recruitment of diseased
- alveoli and maintains an even distribution of gas throughout the lungs, resulting in maximal oxygen uptake and preventing over-distension of healthy
- Also, helps with the redistribution of lung water.
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