• Increasing surfaced area by opening capillaries not normally involved in oxygen exchange. (upper lungs)

• More efficient utilization of total time spent in the capillary (which is reduced due to an increase in cardiac output.)

During strenuous exercise, the human body's oxygen requirements may increase as much as 20x.  The increase in cardiac output during exercise cuts the time that the blood remains in the pulmonary capillary substantially (blood is traveling through faster).  So how is the increase in demand met?

1) Increase in the surface area for diffusion:  the capillaries that do not normally participate in oxygen exchange open perfusing more areas of the lungs.  This often occurs in the upper areas of the lungs.  Therefore the entire lung ventilation to perfusion ratios improve. 

2) The blood in resting conditions stays in the pulmonary capillary about 3x longer than is needed to diffuse oxygen.  On the previous slide, note that the partial pressure of oxygen has reached equilibrium with the alveolar partial pressure of oxygen with the first 1/3 of the total time in the capillary.  During exercise, although this time is shortened, there is still ample time for oxygen to meet equilibrium. 

What is Shunt Blood.  Describe this concept.

98% of the blood that enters the left atrium has passed through the alveolar capillaries.  Where is the other 2%?

•  98% of the blood that enters the left atrium has passed through the alveolar capillaries
• Blood that bypasses the alveolar capillary system is called "shunt blood"  This is the other 2% and is called the venous admixture

Blood that bypassses the alveolar capillaries and is not oxygenated is called "shunt blood" because it has shunted past this system.  The unoxygenated blood has a PO2 of 40mmHg.  When added to the oxygenated blood in the left atria (a condition called venous add-mixing), the PO2 of the LA lowers to 95 mmHg.

1) Does supply and demand effect the interstitial fluid PO2?

2) Does Demand impact tissue oxygen?

1)  The answer is yes.

If the blood flow to a tissue is increased, greater quantities of oxygen are transported into the tissue and tissue O2 becomes greater.  Also not that as the blood flow increased (represented by % on the graph slide #8), the amt of oxygen in the interstitial fluid increases.  In this example, blood flow increases from 100-400%.  The amt of oxygen in the tissue increases from 40 to roughly 65 mmHg.  Notice there is a leveling off of the amt that can enter the tissue.  This occurs because the diffusion gradient is narrowing.  The  maximum oxygen would be the the amt that is in the blood (or 95mmHg) as has been described earlier.  This explains in part why vasoconstriction can lead to hypoxic tissue. 

2) Again Yes

If the demand for oxygen by the cells increases, the amt of interstitial oxygen is decreased.  This INCREASES the gradient between the interstitial oxygen and capillary oxygen.  Diffusion of oxygen from the capillary to the interstitial fluid is more pronounced.  Thus, the venous capillary oxygen is reduced.  This is seen with SVO2 catheters.  I could also determine this by drawing an arterial blood gas and venous blood gas and subtracting the two.

• Intracellular PO2 range: 5-40 mmHg
• 1-3 mmHg of PO2 is required to support intracellular function.
• This provides a large safety factor

Some cells lie closer to capillaries and others do not. Because of this distance, there is a discrepancy in the intracellular PO2 range with a range of 5-40 mmHg.  Fortunately, only 1-3 mmHg is required to support intracellular function.  This is important because it provides the cell with a huge safety margin. 

• Carbon dioxide diffuses in the opposite direction of oxygen
• BIG DIFFERENCE:  Carbon dioxide can diffuse 20x faster than oxygen
• The pressure differences required to drive the diffusion are lower.

Oxygen use by the cell generates carbon dioxide.  The concentration or partial pressure of carbon dioxide builds in the cell and sets up the gradient by which carbon dioxide diffuses out of the cell into the capillary.  At the lung level, the high venous capillary carbon dioxide sets up the gradient where carbon dioxide diffuses into the alveoli. 

There is one MAJOR difference between diffusion and carbon dioxide diffusion:  Carbon dioxide can diffuse 20x faster than oxygen.

Diffusion of CO2 in the alveoli.

(See slide #12)

Notice, that as was true with the oxygen exchange in the alveoli, the CO2 has performed the entire exchange within the first 1/3 of the capillary.

The effect of tissue metabolism and tissue blood flow on interstitial PCO2 is exactly the opposite to their effect on tissue PO2.

_______ of oxygen is transported bound to hemoglobin

_______ of oxygen is dissolved in the plasma

1) 97%

2) 3%

Systemic blood saturation averages 97%.  Venous blood saturation is about 75%.  Based on the carrying capacity formula, the most oxygen hemoglobin can carry is

1.34 ml's x the hemoglobin.  This is typically about 20.1 ml/dl.  Factors that shift the oxyhemoglobin curve to the left:

1) Decreased CO2

2) Increase pH

3) Decrease blood temp

4) Decrease 2,3 DPG

Curve shifts to the right with all the opposite of above.

Describe the Bohr Effect

• The see-saw effect of the curve shifting to the right and to the left to optimize tissue oxygen delivery and unloading and optimize oxygen uptake at the lungs.

The shifting of the curve to the right in response to PaCO2 and the pH significantly enhances the release of oxygen at the tissue level.  This is called the Bohr effect.  As tissue produces CO2 which enters the capillary blood which increases the amt of hydrogen ions.  This shifts the curve to the right.  At the lung, the CO2 diffuses into the alveoli reducing the CO2 and decreases the hydrogen ion concentration thus shifting the curve to the left thus increasing the loading of oxygen. 

• Diphosphoglycerate.
• Keeps the curve shifted slightly to the right (in favor of unloading at the tissue)
• Increases considerably in hypoxic conditions that last more than a few seconds to hours
• Shifts the curve more to the right with hypoxia
• Protective mechanism
• Also seen as 2,3 DPG

Carbon Monoxide has how much more affinity for hemoglobin than oxygen?

Does the PaO2 change? Why or why not?

What is the treatment?

1) 250 x the affinity

2) No the PaO2 does not change because PaO2 measures dissolved O2 not O2 bound to hemoglobin

3) Treatment is high flow O2 in an attempt to massively increase the O2 gradient. "Mass Effect"

Describe the transport of Carbon Dioxide in the Blood

Describe what happens with a chloride shift.

• Dissolved State
• As Carbonic acid which dissociates
  • Bicarbonate Ions
  • Chloride Shift
• Carbaminohemoglobin

On average, 4ml of CO2 is transported from tissue per dl.  The body makes about 200 ml of CO2 per minute.  CO2 can be transported a number of ways:

1) A small portion is dissolved in the blood 7%

2) The carbon dioxide combines with water to form carbonic acid in the presence of carbonic anhydrase.  The dissociated hydrogen ions combine with hemoglobin (remember hgb is a huge buffer).

But what happens to HCO3- ?  It is transported out of the RBC in exchange for chloride ions by a powerful bicard-chloride carrier protein.  This is called the chloride shift.  This is the PRIMARY way CO2 is carried in the blood.   (Hamburg Effect)

3) Carbaminohemoglobin: reacts with amino radicals of hemoglobin and plasma proteins forming loose bonds (23%)

What is the Haldane Effect?

Is it a good thing or bad thing?

• Oxygen + hemoglobin = acidic hemoglobin
• Less binding to amino radicals = more carbon dioxide in the plasma and release of hydrogen ions in the plasma
• Oxygen levels drop at tissue= increase in CO2 uptake
• Oxygen levels increase at lungs = less CO2 attachement = better elimination

We stated that the Bohr effect changed the hemoglobin affinity for oxygen.  The Haldane effect is the displacement of carbon dioxide from the hemoglobin for oxygen.  It directly impacts the transport of carbon dioxide.  Oxygen combining with hemoglobin causes the hemoglobin to become a stronger acid.  This in turn prevents carbon dioxide from combining to the amino radicals pushing the carbon dioxide into the plasma and the acidity of the hemoglobin causes it to release hydrogen ions which combines with bicarbonate in the plasma, dissociates at the lungs. 

This sounds like a bad thing but in fact it is great!  At the tissue, the oxygen levels drop.  Based on the Haldane effect, the hemoglobin becomes less acidic allowing for more carbon dioxide pick up.  At the lungs the oxygen loads create an acidic hemoglobin which in turn causes the carbon dioxide to move out of the hemoglobin. 

This is a more important effect than the Bohr effect.

The respiratory center is made up of several groups of neurons located bilaterally in the medulla oblongata and pons of the brain stem.  It is divided into 3 major groups of neurons:

1) the dorsal respiratory group (DRG) which mainly deals with inspiration

2) The ventral respiratory group (VRG) which mainly deals with expiration

3) Pneumotaxic center (Located in the pons) which controls rate and depth of respiration.

• Peripheral chemoreceptors
• Baroreceptors
• Other lung receptors
• Ramping up
• Shutting down

The dorsal respiratory group extends the length of the medulla.  Most of its neurons are located in the nucleus of the tractus solitarius.  This area is the location where the sensory termination of both the vagus and the glossopharyngeal nerves transmit signals into the respiratory center from the peripheral chemoreceptors, baroreceptors and other lung receptors. 

The DRG controls the rhythmicity of respiration.  This works not by turning on a signal but by ramping up over a period of a couple seconds and then shutting down.  This allows for diaphragmatic stimulation and then allows time for elastic passive lung recoil.  The ramp up time can be shortened during heavy breathing or exercise and the expiratory phase is also shortened.

Hering-Breuer Iflation Reflex: receptors in the muscle portions of the bronchi and bronchioles which are stretch receptors.  Overstretch results in vagal stimulation which transmits to the DRG switching off the "ramp up" phase.  Protects against excessive lung inflation and barotrauma.  

****This reflex is extremely strong in children.

Decribe the pneumatic center.

Where is it located?

What does it do?

• Located in the upper pons
• Controls the switch-off point of the DRG

The pneumatic center is located in the pons.  Its primary function is to control the switch off point of the inspiratory ramp.  If the signal from the pneumatic center is strong, the inspiration lasts for a shorter period of time.  If the signal is weak, inspiration lasts for a longer period of time.  The pneumatic center then through this mechanism can control rate and increase the RR to 30-40 BPM or as little as 3-5 BPM. 

Describe the Ventral Respiratory group.

Where is it located?

What does it do?

• Location
• Inspiratory and expiratory mechanisms
• Contributory to the DRG system
• Abdominal Muscles
• Not utilized during quiet breathing

Located in the medulla in the nucleus ambiguous.  The VRG is located near the DRG.  This group of neurons do not fire during normal quiet breathing.  When the respiratory drive increases, then the signals spill over into the VRG area and the VRG acts as a contributory to the DRG.  Stimulation may lead to either inspiration or expiration.   Of honorable mention, these neurons provide a powerful signal to the abdominal muscles to help with exhalation during heavy breathing. 

Describe the Chemical Control of Respiration.

What is the goal of respiration

The ultimate goal of respiration is homeostasis of oxygen, carbon dioxide, and hydrogen ions (pH).  The respiratory center is very sensitive to changes in the chemical concentrations.  Excessive carbon dioxide can affect the central respiratory center and increase inspiration and expiration mechanisms.  (see slides for details 7,8)

Oxygen does not directly impact the respiratory center but acts on the peripheral chemoreceptors located in the carotid and aortic bodies.

They think that carbon dioxide can't directly stimulate the DRG, VRG or pneumatic center.  Instead, there are chemosensitive neurons located near these centers.  This area is very sensitive to changes in PaCO2 and hydrogen ions.  This area is located within the blood brain barrier.  Although is is most sensitive to hydrogen ions, hydrogen ions do not readily cross the BBB.  Carbon dioxide does not directly stimulate the chemosensitive area but quickly crosses membranes.  Here is combines with water to form carbonic acid which then dissociates into bicarbonate and and H+ ions  This is how the hydrogen stimulates the chemoreceptors.  So, changes in the blood carbon dioxide have a huge impact on the respiratory system. 

This carbon dioxide driven stimulation of the central chemoreceptors only lasts for a couple of days.   As the levels of Bicarbonate ions build, they then recombine with hydrogen ions AND the kidneys react to lower the pH by RETAINING bicarbonate.  For this reason, an elevation in carbon dioxide is a strong stimulus for a couple of days and the the effect disappers.  (ie: COPD- because they have blown out central receptors)

Stimulation of central chemoreceptors leads to an increase in minute ventilation.

Explain the significance of the steep part of the oxyhemoglobin dissociation curve. 

What is the O2 Saturation % when the PaO2 is:

90 mmHg?

60 mmHg?

30 mmHg?

27 mmHg?

Notice that on the oxygen hemoglobin dissociation curve, the steep part is between 20-60 mmHg PaO2.  This means that the hemoglobin is unloading the oxygen very quickly.

When the Saturation is 100% the PaO2 is 90 mmHg.

90% is 60 mmHg

60% is 30 mmHg

50% is 27 mmHg

What are the 4 types (causes) of tissue hypoxia?

Describe them.

• Hypoxic
• Anemic
• Circulatory
• Histoxic

There are several reasons why tissue becomes hypoxic.

1) Hypoxic tissue hypoxia is a result of low alveolar oxygen.  This may include:  Hypoventilation, high altitudes, delivering a gas mixture less than 21%, alveolar edema, fibrosis or pneumonia.

2) Anemic hypoxia means there is a problem with the carrier.  On a gas, the PaO2 may be OK but the carrier (hemoglobin bound portion) is not.  This may include anemia, carbon monoxide poisoning and methemoglobinemia.

3) Circulatory: (also called stagnant) is a delivery problem.  This may be a problem with the heart and cardiac output or can be a problem with the vessels or a problem with the capillary beds producing a stagnant capillary flow.  In these cases, the PaCO2 and the PaO2 may be normal but the tissue is hypoxic. 

4) Histoxic occurs when the cells can not utilize oxygen.  The PaO2 and PaCO2 may be normal and the delivery mechanism may be normal but the cells can not utilize the oxygen.  Examples of this type of hypoxia is ETOH intoxication and cyanide poisoning.

• Cyanosis may occur peripherilly with a decrease in perfusion
• Cyanosis may occur centrally with hypoxia or a reduction of oxygenated hemoglobin (unoxygenated hemoglobin is > 5 gm/dl of blood)
• May normally be seen in newborns- Acrocyanosis
• Usually a bad sign.

Cyanosis is the bluish color found around the lips (acrocyanosis), tongue, finger tips, and toes.  Cyanosis is divided into the peripheral and central categories.  Peripheral cyanosis is often due to a reduction in perfusion.  It is commonly seen in children with poor perfusion states.  Central cyanosis refers to the reduction of oxygen rich hemoglobin.  When the unoxygenated hemoglobin levels exceed 5 gm/ 100 ml of blood, cyanosis occurs.

Cyanosis is commonly seen in the newborn but is usually a bad sign.  The bluish tint around the lips is called acrocyanosis.

Comparison of PaO2 and Saturation

What saturation is predicted with the following PaO2s?

100

60

30

27

100= 97%

60= 90%

30= 60%

27=50%

Who would develop central cyanosis first?

A person who had a hemoglobin of 15 gm or the person who was anemic with a hemoglobin of 9 gm?

Person with Hgb of 15

(I don't know why- need to find out.)

1) What are the 3 goals of Pulmonary Functions tests?

2) PFT's are wonderful.  But what do we need to remember about them?

• Identify patients at risk for increased morbidity and mortality post op.
• Identify pt. who will need short or long term ventilatory support.
• Evaluate the benefit of reversing airway obstructions with bronchodilators.

• 2) PFT's do not act alone
• they act only to support or exclude a diagnosis
• A combination of a thorough history and physical exam, as well as supporting laboratory data and imaging will help establish a diagnosis.

Measurements Obtained from the forced vital capacity (FVC) Curve:

What is FEV₁?

What is FEF 25-75%?

What is FEV₁/FVC?

• FEV₁- the volume exhaled during the first second of the forced vital capacity (FVC) maneuver.
• FEF 25-75%- The mean expiratory flow during the middle half of the FVC maneuver; reflects flow through the small (<2 mm in diameter) airways
• FEV₁/FVC- The ratio of FEV₁ to FVC x 100 (expressed as a percent); an important value because a reduction of this ratio from expected values is specific for obstructive rather than restrictive diseases.

Pulmonary Function Tests

Describe the following:

• Forced Vital Capacity (FVC)
• total expiratory time (TET)
• Forced expiratory time (t)
• Peak Expiratory Flow (PEF or Peak Flow)
• MMEF or FEF 25-75%

The FVC is the maximum amount of air that can be exhaled forcefully and as rapidly as possible AFTER a maximal inspiration.  In the normal individual, the total expiratory time to completely exhale the FVC is 4-6 seconds.  In an obstructive lung disease (such as COPD), this time increases.  In obstructive pattern diseases, the FVC is usually also decreased due to air trapping.

The FEV_t is the forced expired volume in a given amt of time.  Various time frames are usually used in PFT's.  This measurement is reported as a % because it compares the amount of forced vital capacity that can be exhaled over the specified period of time.  The most commonly reported time frame is 1 second (FEV₁₎.

The FEV₁ is decreased in both obstructive and restrictive patterns of disease.  (Obstructive is obvious,  restrictive patterns have a reduction in volume or vital capacity).  The FEV₁ decreases with age.  The normal FEV₁ is 80%.

MMEF or FEF 25-75%:  Maximal mid expiratory flow or forced expiratory flow at the mid point between 25- 75%.  This is the average flow speed of air coming out during the mid portion of the expiration.  The FEF or MMEF 25-75% is the BEST test for assessing SMALL AIRWAY DISEASE. 

Peak expiratory flow or peak flow: is the speed of air moving out of the lungs at the beginning of the exhalation (liters/ sec)

Describe the 2 categories of Lung Pathology.

• Obstructive classification
  • Flow problem
  • Most frequent cause of pulmonary dysfunction
• Restrictive Classification
  • volume problem

Sprirometry Interpretation:  Obstructive vs. Restrictive Defects

Compare/ Contrast obstructive vs Restrictive Defects

• Obstructive Disorders
  • Characterized by a limitation of expiratory airflow so that airways cannot empty as rapidly compared to normal (such as through narrowed airways from bronchospasm, inflammation, etc.)
  • Examples
    • Asthma
    • Emphysema
    • Cystic Fibrosis

• Restrictive Disorders
  • Characterized by reduced lung volumes/ decreased lung compliance
  • Examples:
    • Interstitial Fibrosis
    • Scoliosis
    • Obesity
    • Lung resection
    • Neuromuscular diseases
    • Cystic Fibrosis

• Obstructive if:

1. Both FEV1 and FVC are low AND
2. FEV1/FVC < 0.7

Normal FVC = 5 Liters

Normal FEV1 is approx.  4 Liters

• Restrictive Disease if:

1. Both FEV1 and FVC are low AND
2. FEV1/ FVC is equal to or greater than 0.7

****Note: You can not tell with PFT's if a patient has both a restrictive and obstructive profile. ******

If FEV1 < 2 Liters and FEV1/FVC <50%,  More sophisticated split lung function tests should be done before proceeding with a case that will impact the lung.

• Obstructive Disorders
  • FVC normal or decreased
  • FEV1 decreased
  • FEF 25-75% Decreased
  • FEV1/ FVC decreased
  • TLC normal or increased
• Restrictive Disorders
  • FVC decreased
  • FEV1 Decreased
  • FEF 25-75% normal to decreased
  • FEV1/FVC normal to increased
  • TLC decreased

• PFTs are usually performed before AND after bronchodilator therapy.
• a 15% improvement in PFT's are considered a positive response to bronchodilator therapy
• The therapy should be initiated post operatively
• Look at improvement in FVC, FEV1 and FEF 25-75%

Generally speaking, obstructive patterns are more amenable to treatment versus restrictive lung patterns.

What are the effects of Surgery on Lung Volumes?

Specifically:

• Total lung capacity
• Vital Capacity
• Forced Vital Capacity
• Reserve Volume
• Tidal Volume
• Functional residual capacity
• Expiratory reserve volume
• Compliance

• the total lung capacity decreases after abdominal surgery but not after surgery on the extremities
• the VITAL CAPACITY IS DECREASED BY 25-50% WITHIN 1-2 DAYS AFTER GENERAL ANESTHETIC SURGERY AND RETURNS TO NORMAL AFTER 1-2 WEEKS!  YOUR VITAL CAPACITY CORRELATES WITH YOUR ABILITY TO COUGH AND DEEP BREATH!
• Forced vital capacity is largely dependent on a pt's effort and cooperation. 
• There is a 60% reduction in vital capacity after abdominal and thoracic surgery which returns to normal after 7-10 days.  The reason for this is due to the reflex diaphragmatic dysfunction due to surgical incision or the presence of intraperitoneal or intrathoracic air versus post operative pain.
• A forced vital capacity <15 ml/ kg is associated with an increase in post operative pulmonary complications.
• The reserve volume increases by 13%.  The expiratory reserve volume decreases by 25% after abdominal surgery.
• The tidal volume decreases by 20% within 24 hours and returns to normal after 2 weeks.  Pulmonary compliance decreases by 22% with a similar reduction in FRC due to small airway closures.
• Ideally the FRC is > than the closing capacity.  if the FRC is less than the closing capacity, airways close and you now have an increase in shunting.  Upper abdominal surgeries reduce FRC by 40-50% and are associated with the HIGHEST incidence of post operative lung complications.  FRC recovers after 3-7 days however, if CPAP by mask is used, the FRC can recover in 72 hours!!  Lower abdominal and thoracic operations decrease the FRC by 30%.

• % of oxygen delivered (FiO2) x 5 = estimated PaO2
• Example: FiO2 is 21%
  • 21 x 5 = PaO2 of 105 torr
• Example: FiO2 of 50%
  • 50 x 5 = PaO2 of 250 torr

• % of oxygen delivered (FiO2) x 6
• Example: FiO2 of 50%
  • 50 x 6 = 300 torr
• Example: FiO2 of 21%
  • 21 x 6 = 126 torr

Discuss Gradients. (For O2)

What is the normal gradient between PAO2 and PaO2?

• If ventilation and perfusion were perfectly matched, there would be NO difference between the alveolar O2 (PAO2) or the blood O2 (PaO2).  Or, I could say the gradient would be ZERO. 
• This is not the case, even healthy people have some mismatching. 
• The normal gradient between PAO2 and PaO2 is 5-15 mmHg.

Discuss Gradients (for CO2)

• The normal PACO2 to PaCO2 gradient is 2-10 mmHG
• The PaCO2 - PACO2 gradient is NOT impacted by the FiO2
• The ETCO2 can be substituted for PACO2

• If a patient hypoventilates, the gradients should remain the same or within normal limits.
• If the patient has a V:Q mismatching, these gradients will change
• If the gradient is normal and the patient is hypoxic, you have a ventilation problem
• if the gradient is increased and the pt. is hypoxic, you have a V:Q problem.

• We know the normal gradients
• The normal gradient ON ROOM AIR FOR OXYGEN is 5-15  torr.
• The normal gradient on 100 % O2 is > 100 torr
• The CO2 gradient is unaffected by oxygen concentration
• THE GREATER THE ABNORMAL GRADIENT THE GREATER THE V/Q ABNORMALITY.

Sample problems to distinguish hypoventilation from V:Q mismatch

• 1. PaCO2 = 60;  ETCO2 = 45
• 2. PAO2 = 55 torr;  PaO2 = 45 torr
• 3. A pt. is being mechanically ventilated and has a PaO2 of 200 torr on 100% FiO2.  Is there a problem?

1.  The gradient is 60-45 = 15 mmHg (normal is 2-10) thus the pt. has a V:Q problem
2. The gradient is 55-45 = 10 mmHg.  The normal gradient is 5-15.  Thus the gradient is normal.  The pt. is obviously hypoxic (PaO2 of 45 torr) which is due to a ventilation or oxygen delivery problem.
3. The pt. has a PaO2 of 200 torr on 100% FiO2.  However the predicted PaO2 should be 500 torr.  The predicted PAO2 on 100% would be 600 torr  producing a normal gradient of 100 torr.  In this case, the PAO2 is 600 torr and the PaO2 is 200 torr thus there is a gradient on 100% of oxygen of 400 torr.  Thus we do have a V:Q problem.  Is the pt hypoxic?  No- not by textbook but certainly the patient does not have wonderful lungs. 

REVEIW FLOW LOOPS

DO IT NOW

SLIDES 26, 27, 28

REVEIW FLOW LOOPS

DO IT NOW

SLIDES 26, 27, 28

• decreases ciliary function
• increases sputum production
• Therefore high volume of sputum but unable to clear it
• Airway reactivity occurs
• development of obstructive pattern disease occurs
• increase in proteolytic enzymes which destroy lung parynchema
• increases sysnthesis and release of elastolytic enzymes which directly damage lung tissue
• elastolytic enzymes are secreted from the macrophage
• further damage occurs due to the reactive metabolites of oxygen which are typically used by the macrophage to kill micro-organisms.
• The epithelium undergoes changes making the membrane more permeable and surfactant production is reduced.

Early Effects

• Mile V/Q mismatching
• Bronchitic disease
  • such as cough, URI's, bronchitis, and reactive airway symptoms.
  • remember that reactive airway disease is not synonymous with asthma.  RAD is due to environmental irritants. 
• Airway hyperreactivity

Late Effects

• Gas trapping
• flattening of diaphragm
• barrel chest formation
• increased lung compliance
• forced (versus passive) exhalation
• ineffective CO2 elimination
• Arterial hypoxemia
• Increased carboxyhemoglobin

Later effects of cigarrette smoking include an increasing V/Q mismatch due to gas trapping.  The trapped gas areas contribute to large areas of deadspace.  This increases the amount of venous admixture (unoxygenated blood).  Furthermore, CO2 elimination is reduced d/t the deadspace and leads to an increasing PaCO2.  the venous admixture results in arterial hypoxemia (low PaCO2).  Carbon monoxide levels increase due to the inspired smoke.  The normal carboxyhemoglobin levels in a nonsmoker is 1%.  It can increase to as high as 8-10% in chronic smokers.  CESSATION OF SMOKING 12-24 HOURS CAN DECREASE THE CARBOXYHEMOGLOBIN LEVEL TO NEAR NORMAL. 

• 2-6 x risk of post operative complications in COPD
• If no clinical pulmonary dx, risk is still 2x the norm
• must cease smoking at least 8 weeks to see a reduction in post operative complications
  • studies show that pts who stop smoking in a shorter time frame (ie: 4 weeks before surgery) actually have an INCREASE in post operative complications of 4x those who never stopped smoking. 
• Mucociliary function requires 2-3 weeks of abstinence
  • During this time, sputum production increases significantly as evidenced by their need to cough and clear the airways. 
• Reduction in smoking does NOT decrease risk for post operative pulmonary complications. 

• Post operative site (upper abdominal and thoracic surgery.
• History of dyspnea
• pre-existing pulmonary disease
• smoking
• obesity
• Age > 60 years
• Prolonged general anesthetic > 3 hours

The incidence of pulmonary post operative complications ranges between 6-60%.  This can include atelectasis, pneumonia, pulmonary embolism, or respiratory failure. 

1. Post operative site: upper abdominal incisions and thoracic incisions carry the highest pulmonary post operative complication rate. Incisions near the diaphragm often result in procedures that reduce the FRC by 60-70%.  This effect peaks during the first post operative day and lasts 7-10 days. 
2. Dyspnea:  Reported preoperative dyspnea is a big risk factor because it correlates to the degree of existing disease. 
3. Pre-existing pulmonary disease
4. Smoking:  The previous slides discuss this
5. obesity:  decreases functional residual capacity, increases the work of breathing and increases the risk for deep vein thrombosis. 
6. Aging (even without smoking) leads to a breakdown in the recoil capability of the lung and an increase in the closing capacity.
7. Prolinged general anesthetics:  Although it would logically make sense, this is the LEAST consistent factor. 

NOTE:  When discussing surgical site, laparascopic abdominal surgeries do NOT count.

1) Operative site

2) Reported Preoperative Dyspnea

• It would seem that utilizing a regional technique would decrease the incidence of post operative complications.  This has not been established!  Regional anesthesia above the T-6 levels should not be employed as this reduces the expiratory reserve volume and significantly reduces the ability of the pt. to cough and deep breath.
• Obviously smoking cessation would be of great benefit if the pt. would stop >8 weeks before surgery.  Other strategies would include choice of post operative anelgesia, epidurals for chest and upper abdominal operations reduces pain often without the effects of opioid induced hypoventilation.
• FRC does not recover for up to 7 days;  with the use of CPAP, FRC can recover within 72 hours.  Here is an interesting statistic:  Pts correctly us their incentive spriometry 10% of the  time unless therapy is supervised.
• Stir up regimens are more effective than spirometry and include coughing, deep breathing, fluid hydration and early ambulation. 
• Pt's who stop smoking for > 2 months and institute aggressive pulmonary toileting regimens have a complication rate nearly equal to the normal pt. 

Obstructive diseases in which air flow is the primary problem.

Restrictive disease in which volume is the primary problem. 

Not all diseases fit neatly into either category.  Many diseases can have both obstructive and restrictive components.

Obstructive Pulmonary Diseases.

Give Examples

Hallmark signs etc...

• Includes asthma, emphysema, chronic bronchitis, cystic fibrosis bronchiectasis, and bronchiolitis
• Hallmarks: Resistance to air flow (FEV1 and FEV1/FVC are less than 75% predicted.
• Early in the disease, the FEF 25-75% (or MMEF 25-75%) May be the only abnormality
• Increased work of breathing
• Air Trapping

Obstructive pulmonary diseases have 1 key commonality: THEY ALL LEAD TO A PROBLEM WITH AIR FLOW.  The hallmarks are a resistance to flow as evidenced by a reduction in the forced expiratory volume in 1 second and the FEV1/FVC ratio of less than 75% predicted.  (Normal is 80%)

Early in these diseases, the FEF or MMEF 25-75% is the most reliable indicator and only abnormality.

Each disease has its own etiology.  All lead to an increase in airway resistance which reduces the exhalation volume and leads to gas trapping.  This increases both the reserve volume and tidal volume.  Inspiratory wheezes may be heard due to turbulent flow.

See slide # 11

With no obstruction:  Complete exhalation takes place before the next breath

Obstruction: Exhalation just completed (with no pause) prior to next breath

More Severe Obstruction or increased rate with obstruction:  Incomplete exhalation prior to next breath with progressive Air trapping.  (Breaths get stacked)

If on the vent change the I:E ratio to assist with expiration.

Describe Asthma

Hallmark signs with asthma

3 Components of Ashtma

The hallmark of asthma is bronchiolar hyperactivity in response to stimuli which results in dyspnea, cough and wheezing.

The bronchiolar obstruction has 3 components:

1) Smooth muscle constriction

2) Bronchiolar edema

3) An increase in secretions

The pathology is as follows:

1.  It begins with exposure to a causitive condition or agent which either causes release of chemical mediators or an over activity of the parasympathetic nervous system.

2.  Bronchial mast cells degranulate after the antigens bind to IgE

3. Histamine is released as is bradykinin, seratonin, leukotrienes, platelet activating factor, prostaglandins and neutrophil and eosinophil chemotactic factors. 

4. Vagal afferent fibers in the bronchi are sensitive to histamine and noxious stimuli (cold air, inhaled irritants, intubation).  This produces a reflexive vagal activation which leads to..........

5. Bronchoconstriction which is mediated by increasing intracellular cyclic guanosine monophosphate.

•  FEV-1 < 50% predicted = moderate to severe disease
• FEV-1 < 25% = Impending doom
• CXR = air trapping, flattened diaphragm

There are many things that can trigger an asthmatic attack. (pollen, mold, dust mites, pet danger, exercise, temperature, infection, occupational, exposure)

It is important that you assess the following in the preoperative area:

1.  What is the pts triggers?

2. When is the last time the pt had an asthmatic attack?

3. What do they do to treat their asthma?

4. Do they take medication daily?

5. Did they take their medication the day of surgery?

6. Have they ever been hospitalized for asthma? If so when?  Were they placed on a ventilator?

7.  What do they sound like?  If the pt. has audible wheezes prior to surgery, they should receive an aerosol treatment.  If they continue to wheeze, the ELECTIVE surgery should be cancelled and the pt should see their doctor for further tweaking. 

8.  Give the pts a couple of albuterol puffs prior to induction.  Make sure the pt performs good technique.

• 8-20 % of adult asthmatics
• 15 min- 4 hour onset after ingesting small amts of aspirin
• blocks the cyclo- oxygenase
• Draw leukotriene pathway
• If allergic to aspirin don't give NSAIDS.

Inflammatory mediators promote the release of arachadonic acid from the cell membrane.  Arachadonic acid is then converted to endoperoxides and leukotrienes. 

• Increased TCL, RV, FRC
• Increased work of breathing
• Poor V/Q = hypoxemia
• Tachypnea = hypocapnea
• A normal or high PaCO2 is a BAD sign

• Beta 2 agonists
  • Activate adenyl cyclase which increases cyclic AMP.  Cyclic AMP in the bronchial smooth muscle promotes relaxation which results in bronchodilation.
  • Terbutaline is a longer active beta 2 agonist.  By using selective Beta 2 agonists, we can avoid many of the beta 1 side effects.  However, in large doses, these side effects are often times seen. 
  • Use of Beta Blockers in Asthmatics is not good.  Promotes bronchoconstriction
• Methylxanthines
  • inhibit phosphodiesterase (enzyme that breaks down cyclic AMP)
  • Promotes bronchodilation AND DIRECTLY stimulates the diaphragm
  • Theophylline is a long acting oral methylxanthine
  • Aminophylline is the IV form:  5 mg/kg over 20 minutes load then 0.5 mg/kg/hour.
  • Narrow therapeutic index (10-20)
• Glucocorticoids
  • Anti-inflammatory membrane stabilization
  • Beclomethasone
  • Triamcinolone
• Advair = steroid + Beta 2
• Anticholinergics
  • Atropine or robinul
  • ipratropium
• Cromolyn
  • Inhibits inflammation by inhibiting the release of chemical mediators from mast cells (membrane stabilization?).  Cromolyn is NOT effective once bronchospasm starts.  It must be used several days before.
• Leukotriene inhibitors
  • are effective in pts with mild to moderate asthma. 

• Preoperative sedation
  • Preoperative sedation can be extremely useful in pts with emotional asthmatic components
• H2 blockers should not be used
  • theoretically detrimental becase H2 blockers block the h2 receptor which when stimulated actually promotes bronchodilation.  This also leaves the H1 receptors unopposed thus the combo can produce or exacerbate bronchospasm.
• Theophylline Levels
  • people using theo should have levels drawn
  • assures that pt is therapeutic and has optimal dilation
  • No toxicity
  • Guides treatment should aminophylline be required.  Normal range: 10-20 mg/l
• Critical times for bronchospasm
  • most likely to occur in a lighter anesthetic plane and during airway manipulation and instrumentation.
• Histamine releasing drugs
  • should be avoided or give slowly (pentothal, atracurium, succs, morphine, demerol)
  • Ketamine has sympathomimetic properties and promotes bronchodilation.  Note of caution:  Theophylline can promote seizure activity and ketamine lowers the seizure threshold. 
  • Desflurane is an airway irritant and must be increased slowly to blunt bronchospasm

Describe proper inhaler use.

Describe how much of the Beta 2 agonist gets to the lungs with different techniques.

• With proper technique, 12% of the drug is delivered to the lungs.
• If ETT is in place, this is reduced 50-70%
  • therefore dose must be increased 6- 10x
  • 12 puffs with hand ventilation

• ETT obstruction (kink, secretions, over inflation of ETT cuff)
• inadequate anesthetic depth
• Endobronchial intubation
• Pulmonary aspiration
• Pulmonary edema
• Pulmonary emboli
• Pneumothorax

Describe/ Discuss COPD. 

Prevalence

Pulmonary Function Results

• The most commoon pulmonary disorder encountered in anesthesia
• Prevalence increases with age and smoking
• Early changes usually respond to bronchodilation therapy
• FEV1 is decreased FEV1/FVC is Decreased and  MMEF 25-75% is decreased.
• Pts. are classified as either: Chronic bronchitis or emphysemic
• Most have features of both.

What are the mechanisms that lead to airflow obstruction in COPD?

(See slide 27 for pictures)

1) Secretion in airway lumen

2) Thickening of airway walls

3) Loss of tethering by parynchema

How is the diagnosis of Chronic Bronchitis made?

• Productive cough on most days for > 3 consecutive months for at least 2 consecutive years
  • Causitive factors for chronic bronchitis can be due to cigarette smoking, pollutants, pulmonary infection or familial factors.

• Inspired irritants result in inflammation of the airways with infiltration of neutrophils, macrophages, and lymphocytes into the bronchial wall. 
• Causes bronchial edema and increases size and number of mucous glands and goblet cells.
• Mucous is thick and tenacious, and can't be cleared because of impaired ciliary function. 
• Increases susceptibility to infection and injury.
• Initially affects only larger bronchi, but eventually all airways are involved.
• Airways collapse in early expiration, blocked by mucous, and air is trapped in distal portion of the tract.
• Leads to ventilation/perfusion mismatch
• hypoxemia occurs
• Air trapping prevents respiratory muscles from functioning efficiently (barrel chest), and pts get hypoventilation and hypercapnia.

1. The hypoxemia results in intrapulmonary shunting (remember hypoxic pulmonary vasocontriction?)
2. The chronic hypoxemia and carbon dioxide tension increases lead to pulmonary vasoconstriction, an increase in pulmonary pressures and eventually Cor Pulmonale (right ventricular failure.)
3. Pts gradually lose their normal carbon dioxide (central chemoreceptors)  ventilatory drive and become increasingly dependent on the peripheral chemoreceptors and "hypoxic" drive.  For this reason, by alleviating the hypoxia, we can theoretically decrease a pt's drive to breath by delivering high concentrations of oxygen. 
4. Chronic hypoxia triggers RBC production.

• Best treatment is prevention because changes are not reversible
• Cessation of smoking halts progression of the disease
• Bronchodilators, expectorants, and chest physical therapy are used as needed.
• Acute attacks may require antibiotics, steroids, and possibly mechanical ventilation.
• Chronic oral steroids as a last resort
• Home oxygen therapy.

• Characterized by irreversible enlargement of the airways distal to terminal bronchioles and destruction of alveolar septa.

The diagnosis of emphysema is often made by CT.  Mild emphysemic changes in the apex of the lung are commonly seen with aging.  Emphysema is almost always associated with cigarrette smoking.  Less commonly, emphysema occurs at an early age and is associated with a homozygous deficiency of alpha-1 antitrypsin which is a protease inhibitor that prevents excessive activity of elastase.  This enzyme is typically produced by the macrophages in response to infection or pollutants.  It is thought that smoking also reduces the protease inhibitors.  Both conditions result in elastic recoil  Recall that elastic recoil often tugs at the adjacent structures keeping them open or providing support.  A loss of this support results in collapse of the small airways during exhalation.  Patients typically have an increase in Residual Volume, FRC, and TLC.

The capillaries are also destroyed leading to pulmonary hypertension.

It becomes apparent that an increase in deadspace is a prominent feature of emphysema.  Arterial oxygen and carbon dioxide levels are typically normal early in the disease (but progress to hypoxemia and carbon dioxide retentinon)

• Dyspnea
• Barrel Chest
• Miniman Wheezing
• Prolonged expiration
  • Pursed lip breathing "pink puffers"
• Hypoventilation and polycythemia late in the progression of the disease

Emphysemic patients who are dyspneic will often purse their lips to delay closure of the small airways.  They are called Pink Puffers.

In order for air to move, a driving force is needed.  Think trans-airway pressure.  If the positive pressure in the lung can be maintained over a longer period of time, more air can move out of the alveoli.  Remember that they have lost a lot of recoil capability.  By keeping the airways open longer:

1.  More air can be moved out of the lung (trapped air can be released)
2. Exhalation is prolonged
3. More fresh gas can now be exhaled
4. The compensatory resp. rate can be reduced
5. Work of breathing improves.

1. Smoking cessation
2. Bronchodilators (for those who showed improvement or a reversible component)
3. Oxygen therapy
   1. Oxygen therapy targets a PaO2 of >60 torr.  Oxygen therapy can dangerously elevate the PaCO2.  Why?  Increasing PaO2 decreases the hypoxic drive. 
4. Diuretics if a pt has cor pulmonale.

• Preoperative evaluation
• Preoperative intervention aimed at correcting hypoxemia
• Relieving bronchospasm
• Early mobilization
• reducing secretions
• treat infections
• Arterial PaCO2
• Extubation

Pts should be asked if there has been any recent changes in dyspnea, sputum and wheezing.

Pts with an FEV1 < 50% predicted usually have dyspnea on exertion.  FEV1< 25% predicted value have dyspnea with minimal or no exertion. 

We have discussed the benefits of smoking cessation.

We have discussed the pros and cons of regional vs. general anesthetic.

Use of bronchodilators improves only the REVERSIBLE component of the air flow obstruction.  Significant expiratory obstruction is still often present even under deep anesthesia.

Ventilation should be controlled with large tidal volumes and slow rates to prevent air trapping.  The I:E ratio (normally 1:2) should be adjusted to allow for an increase in expiratory time.

Nitrous should be avoided in pts with known blebs or bulla.  Nitrous can also increase pulmonary vascular vasoconstriction and therefore should not be used in pts with pulmonary hypertension. 

The PaCO2 and ETCO2 gradient is widened in patients with an increase in deadspace (obstructive diseases).  If you adjust your ventilation parameters to "normalize" the PaCO2, (in pts who are CO2 retainers), you will induce alkalosis.  It is better to adjust your ventilation parameters to pH.

A CVP line in a pt with cor pulmonale or pulmonary HTN will only reflect the right ventricular pressure vs. the intravascular volume.  Thus CVPs in patients with these conditions are inaccurate to use as a guide for fluid or intravascular volume.  They only reflect the PRESSURE in the right side. 

The use of an LMA is thought to decrease the incidence of bronchospasm in smokers or pts with reactive airways.  The reduction in intrumentation of the oral and posterior pharynx reduces the stimulation.  Deep extubation of smokers and pts with reactive airway components decreases the incidence of bronchospasm but also assumes that the pt has adequate pulmonary function.

Pts with FEV1 < 50% will most likely require a period of post operative ventilation especially with upper abdominal and thoracic procedures.

• Characterized by decreased lung compliance
• Lung volumes are typically reduced
• The expiratory flow rates are usually normal
• Both FEV1 and FVC are reduced so the FEV1/FVC is normal
• Reduced lung volume leads to an increase work of breathing (rapid and shallow)
• Gas exchange is normal till the disease becomes advanced. 

• Intrinsic or Extrinsic
• Intrinsic is further divided into acute and chronic intrinsic disease
• Extrinsic are not further subclassified.

Acute Intrinsic

• Increased extravascular water
• Decreased compliance
• increased pulmonary capillary pressure
• Increased capillary permeability

Chronic Intrinsic

• Insidious onset
• chronic inflammation of alveolar walls
• pulmonary fibrosis
• decreased gas exhange
• confined or multiorgan
• VC impairment

Acute intrinsis disorders include pulmonary edema (including RDS), infectious pneumonia and aspiration pneumonitis.  Acute intrinsic disorders lead to an increase in extravascular water which decreases lung compliance.  The extravascular fluid may be due to an increase in pulmonary capillary wedge pressure or hydrostatic pressure or by increased capillary permeability. 

Chronic intrinsic pulmonary disorders (interstitial lung diseases) are characterized by an insidious onset, chronic inflammation and progresses to pulmonary fibrosis which results in a decrease in gas exchange and ventilatory function.  The inflammation may be confined to the lungs or part of a general multiorgan process.  Causes of chronic intrinsic diseases can be hypersensitive pneumonitis, drug toxicity (bleomycin), radiation pneumonitis, idopathic pneumonitis, sarcoidoisis, oxygen toxicity, and ARDS--- All which can lead to chronic fibrosis.

• Delay elective surgery
• Emergency surgery- well oxygenated
• Diuretics, vasodilators, inotropes
• PPV and PEEP
• Lower tidal volumes, higher rates
• Peak airway pressures < 40 cm H20
• May require a more sophisticated Ventilator

Pts with acute pulmonary disease are very ill.  Fluid overload should be treated with diuretics, vasodilators, and positive inotropes.  If emergency surgery is needed, maximal oxygenation conditions should be employed.  Positive pressure ventilation with increasing PEEP is needed to improve hypoxia.  These pts often have high peak airway pressures thus a lower tidal volume and higher rate may be needed to ventilate them.  Ventilatory pressures should be kept at < 40 cm H20.  High PEEP requires chest tubes.  If the institution where you work has older machines, using a more sophisticated ICU vent may be required.  Patients on high PEEP and high ventilatory pressures should be transported on the vent if possible.  Ambu bags can provide PEEP but the manual bagging is often not efficient. 

• Steroids
• Determine the degree of impairment
• Dyspnea history may require PFT's
• Oxygen toxicity
• How low can you go
• High peak pressures
• Lower TV, Higher rates

With chronic intrinsic disease, pts typically complain of varying degrees of dyspnea with exertion and a NON-PRODUCTIVE cough.  Cor Pulmonale/ RV failure can occur in more advanced states.  Fine crackles may be heard at the bases.  The CXR takes on a "ground glass" or honey comb appearance.  Blood gases show mild hypoxemia with normocarbia.  PFT's show a restrictive process.  Carbon dioxide diffusion slows as much as 50%. 

Treatment is steroids for the idiopathic conditions and autoimmune disorders (sarcoidosis).  If the pt reports a history of dyspnea with moderate to mild impairment, PFT's and ABG's should be considered.  A vital capacity of < 15 ml/kg is indicative of severe impairment. 

In the O.R., there is a decrease in FRC which leads to rapid desaturation after induction.  These pts are prone to oxygen toxicity. (High partial pressures of oxygen leads to superoxides and free radicals which further destroy lung tissue).  FiO2 is kept as low as possible to maintain a saturation of 90%.  These patients may also have high peak pressures (stiff lungs) and require smaller tidal volumes and higher rates.

• Interfere with normal lung expansion resulting in alterred gas exchange. 
• There are lists of extrinsic disorders
• Anesthetic intervention same as for intrinsic

Pleural effusions, pneumothorax, mediastinal masses, kyphoscoliosis, pectus excavatum, neuromuscular disorders, ascites, pregnancy, air in stomach. 

• Blood clot, air, fat, tumor cells, amniotic fluid, foreign material into the VENOUS system
• Clots from the lower extemity are most common cause.
• Pathology
• If pt. survives acute episode, clot will resolve in 1-2 weeks. 

An embolism can be many things.  Each has unique features.  All enter the venous system.   The most common source of embolisms is from blood clot formation in the deep veins of the lower extremities.  The pathology is as follows:

1. emboli lodges in pulmonary circulation
2. this increases dead space (ventilated but not perfused)
3. This leads to reflexive bronchoconstriction
4. The V/Q gets worse
5. Affected areas lose surfactant within hours and become atelectic within 24-48 hours.
6. Pulmonary infarction can occur if a larger vessel is occluded and collateral circulation is insufficient
7. The cross sectional area of the pulmonary capillaries is reduced which increases the overall vascular resistance. 
8. The injured tissue releases leukotrienes, histamine, (inflammatory substances) thus a small PE can lead to a whole lung problem. 

• sudden tachycardia, dyspnea, chest pain, tachypnea, hemoptysis, (implies infarction)
• Symptoms often absent or mild and non-specific unless massive embolism (> 50% of pulmonary circulation is affected)
• CXR/ Angiography
• hemodynamics

Symptoms are often absent or mild or non-specific.  CXR is usually normal or has signs of radiolucency.  Pulmonary angiography is the MOST ACCURATE means of diagnosing pulmonary embolism.  ABGs usually show mild hypoxemia with resp. alkalosis.

Hemodynamically, hypotension may develop with an elevated CVP and PAP.  A WEDGED SWAN CAN CAUSE embolic like symptoms. 

Large embolic events in the O.R. are characterized by a sudden unexplained drop in ETCO2 and accompanying hypotension, tachycardia, and cardiac collapse.

• Prevention
• Drugs
• ambulation and antiembolic stockings
• Umbrella filters
• embolectomy

Prevention is the best medicine.  Early ambulation, hydration, mini-dose heparins, coumadin, ASA, dextran, and embolic stockings should be utilized in pts at risk for emboli.  Thrombolytic therapy with TPA or streptokinase may be used.  Inferior vena cava umbrellas are placed and embolectomy is performed in those where thrombolytic therapy is contraindicated.

In the O.R. treatment is fluids, inotropes, and overall support.

• Prolonged bedrest
• post partum state
• Fx of lower extremity
• Surgery of lower extremity
• Carcinoma
• Heart failure
• obesity
• Surgery >30 minutes
• Hypercoagulability states
  • Antithrombin III deficiency
  • Protein C deficiency
  • Protein S deficiency
  • Plasmin Activator deficiency