Applied Physiology: Lecture 8 - Resp Phys 3

Question 1

CLOSING CAPACITY

Answer 1

What is Closing Capacity? (KNOW CLOSING CAPACITY!!!)

Remember that all “capacities” are the summation of other volumes
Closing Capacity = Closing Volume + Residual Volume

Closing Volume = the volume of air in the lungs at which the airways in the dependent portion (lowesetportion of lung most influenced by gravity) of the lung begin to close / collapse.

Residual Volume = the volume of air in the lungs following a maximum exhalation.

Question 2

CLOSING CAPACITY (WHAT IT LOOKS LIKE)

Answer 2

Question 3

CLOSING CAPACITY (WHAT IT LOOKS LIKE)

Answer 3

This is purely a “graphical
representation”
The line at which airway closure
begins may occur at volumes less than FRC (as seen here) or…

Question 4

CLOSING CAPACITY (WHAT IT LOOKS LIKE)

Answer 4

This is purely a “graphical
representation”
The line at which airway closure begins
may occur at volumes less than FRC (as seen here) or …
Closure might occur at higher volumes
(like in the diseased lung)
Less than Ideal when closing capacity is
greater than FRC… airways close before you even fill up your lungs

Question 5

CLOSING CAPACITY (HOW WE MEASURE IT)

Answer 5

Single Breath (Nitrogen) N
2washout method.
Patient is breathing room air (approx. 79%
N2)
Then we have the patient take a vital
capacity breath of 100% O2.
We then measure the N2 concentration at the lips on the subsequent exhalation
The concentration of the N2 is measured and recognized in 4 phases.

Question 6

CLOSING CAPACITY (HOW WE MEASURE IT)

Answer 6

Phase 1
Pure dead space

Phase 2
Mixture of dead space & alveolar gas

Phase 3
Pure alveolar gas

Phase 4
Occurs at near the end of expiration. It is signified by a sharp increase in N2 concentration.

Why?
Who can explain to the class why we see a sharp increase in N2at the end of expiration?

Question 7

CLOSING CAPACITY (HOW WE MEASURE IT) PHASE 4

Answer 7

Phase 4 explanation can be thinking about the
portion of the lungs that are best ventilated during a vital capacity.

The apex of the lungs are almost certainly
always “open” or expanded, so during a vital capacity they won’t expand much. Therefore they don’t take in much of the 100% O2 and they contain a lot of N2 from previous breaths.

The late N2 rise is due to collapse (closure) of the dependent regions of the lung and now exhalation is occurring primarily from the apex of the lungs.

This sharp increase in the N2 marks the point where we can calculate the closing volume.

Question 8

CLOSING CAPACITY (WHY DOES IT MATTER?)

Answer 8

A young person will have a closing volume
that is approx. 10% of their vital capacity.

As we age, our closing volume increases
(hence, so will our closing capacity)

At age 65yrs, our closing capacity is
approximately the same as our FRC.

Question 9

CLOSING CAPACITY (DISEASE STATES)

Answer 9

Certain Diseases Increase Closing Capacity
COPD
Asthma
Pulmonary Edema

Obesity?
Actually does NOT increase the closing capacity, but it does decrease the patient’s FRC.

So closing capacity will approach FRC earlier in life.

Question 10

DISEASED LUNGS PATHOPHYSIOLOGY

Answer 10

Obstructive Lung Diseases
(Can’t Exhale)
Reduced elasticity or premature
closure of small airways and decreased ventilation. Such as…
COPD
Emphysema
Chronic Bronchitis

Asthma
Usually a temporary obstruction that is reversible due to inflammation of airways.

Restrictive Lung Disease
(Can’t Inhale)
Reduced lung volumes due to
damage to the lung tissue itself or structural change/weakness of the thorax. Classified broadly as…
Intrinsic –pathology with the lung parenchyma (ex. Pulmonary fibrosis)
Extrinsic –chest wall or pleura dysfunction (ex. Severe scoliosis AS)

Cystic Fibrosis is obstructive (WHAT IS THE OTHER ONE???)

Question 11

DISEASED LUNGS (LIST YOU NEED TO KNOW)

Answer 11

Obstructive Lung Diseases
(Can’t Exhale)
COPD
Chronic Bronchitis –aka the blue bloater
Emphysema –aka the pink puffer
Asthma
Bronchiectasis
Cystic Fibrosis

Restrictive Lung Disease
(Can’t Inhale)
Obesity
Pulmonary Fibrosis (stiff lungs)
Scoliosis (severe)
Neuromuscular disease
ALS (aka Lou Gehrig’s disease)
Muscular dystrophy
Myasthenia Gravis
Sarcoidosis
Auto-immune diseases

Question 12

Blue Bloater vs Pink Puffer

Answer 12

Question 13

DISEASED LUNGS (DIFFERENTIATING THE TWO WITH PFT RESULTS)

Answer 13

Obstructive Lung Diseases
(Can’t Exhale)

Restrictive Lung Disease
(Can’t Inhale)

Question 14

DISEASED LUNGS (DIFFERENTIATING THE TWO)

Answer 14

Obstructive Lung Diseases
(Can’t Exhale)
Restrictive Lung Disease
(Can’t Inhale)

DLCO (Perfusion capacity of carbon monoxide)
One must remember that DLCO is really a function of how well a gas transitions from the alveoli to the blood stream. If you have less alveolar surface area (like in severe emphysema) less CO can be taken up by the blood. Therefore the DLCO in emphysema would be low.

Low DLCO
Conditions that decrease effective alveolar surface area.
COPD / Emphysema (less alveolar surface area), Restrictive lung diseases (less lung volume/area), decreased effective blood supply to lungs (CHF and anemia), drug pulmonary toxicity (bleomycin, amiodarone)

Normal to High DLCO
Asthma, Polycythemia (increased Hgb), L→R intra-cardiac shunt, alveolar hemorrhage.

Question 15

DISEASED LUNGS (DIFFERENTIATING THE TWO)
DLCO Changes –More Complete list

Answer 15

Question 16

DISEASED LUNGS (PERI-OP MANAGEMENT / OPTIMIZATION)

Answer 16

Obstructive Lung Diseases
(Can’t Exhale)
Preoperative Bronchodilator
Albuterol
Preoperative Steroids
Solu-Medrol
Anti-cholinergic
Ipratroprium
Warm & Humidify Air
(HME)
Increase the I:E ratio
(provide longer for exhalation)
Avoid Hyperventilation
Allow some permissive hypercapnia

Restrictive Lung Disease
(Can’t Inhale)
Avoid “elective procedures” in settings of acute respiratory events. (Don’t do a face lift just after the patient aspirates)

If smoker – get them to stop (even 24hrs and reducing carboxyhemoglobin will help these patients)

Decreased compliance – may require increased PEEP, increased RR & increased FiO2 to oxygenate.

May require post-op ventilation

Treat their pain – obviously don’t oversedate, but they need their pain treated to prevent splinting.

Question 17

WHAT IS ASTHMA?

Answer 17

Asthma is a chronic inflammatory disease characterized by obstruction of the airways that is partially or completely reversible with treatment or spontaneously.

Bronchoconstriction is precipitated by irritants….

Wheezing is a common symptom in asthmatics but is not specific for this disease. Patients with chronic obstructive pulmonary disease (COPD), gastroesophageal reflux disease, vocal cord dysfunction, tracheal or bronchial stenosis, cystic fibrosis, allergic bronchopulmonary aspergillosis, and heart failure may wheeze.

Spirometry is the preferred diagnostic test, but a normal result does not exclude asthma

PFTs have no perioperative predictive value but in rare instances may be useful to gauge the severity of disease or the adequacy of therapy

Typical findings on PFTs are reduced forced expiratory volume in 1 second (FEV1)

Question 18

WHAT IS COPD

Answer 18

COPD includes chronic bronchitis and emphysema and is characterized by obstruction to airflow that is not fully reversible (main cause: increased resistance)

Caused by environment, a1-antitrypsin deficiency, chronic infections, and long-standing asthma

Dyspnea, coughing, wheezing, and sputum production are common features

A barrel chest and pursed-lip breathing suggest advanced disease.

Typically, FEV1 is reduced because of obstructed airflow, but FVC is increased because of reduced airflow, loss of elasticity, and overexpansion

Diffusing capacity (DLCO) is typically decreased

PFTs have not been shown to predict perioperative outcome

ECG may demonstrate right axis deviation, RBBB, or peaked P waves, which suggest pulmonary hypertension and possibly right ventricular changes in response to the chronic lung disease

Chronic hypoxia leads to polycythemia and respiratory acidosis

Question 19

COPD- CLOSING CAPACITY

Answer 19

Airway closure occurs at higher lung volumes in patients with obstructive lung disease, asthma and lung edema edema

Any process that increases the CC by increasing the functional residual capacity (FRC) can increase an individual’s risk of hypoxemia, as the small airways may collapse during exhalation, leading to air trapping and atelectasis.

Airways collapse during normal breathing

Question 20

COPD

Answer 20

Normal physiological drive to breathe is related to CO2 levels in the blood

COPD patients are accustomed to elevated CO2 levels.

COPD patients ventilate in response to Hypoxia.

What do you think will happen to a COPD patient receiving 1OL O2 Satting 99% in PACU? Could depress their respiratory drive to CO2, they are no driven by O2

You may want to maintain O2 sats in the low 90s vs higher.

Question 21

COPD-BULLAE

Answer 21

Many patients with moderate or
severe COPD will develop cystic air spaces in the lung parenchyma known as bullae.

Remember:
Volumetrauma associated with increased incidence of pneumothorax in normal lung

COPD: Barotrauma associated with
increased incidence of pneumothorax

Keep Plateau pressured under 35mmHG

Volume = cause of pneuos in normal, healthy
Baro = cause of pneuos in COPDers… thus the keep pressure under 35 mmHg

(What is the TRANSPULMONARY PRESSURE???? LOOK UP!!!)

Question 22

COPD POINTS

Answer 22

Severe COPD patients are often “flow limited” even during tidal volume expiration at rest

Flow limitation occurs particularly in emphysematous patients, who primarily have a problem with loss of lung elastic recoil and have marked dyspnea on exertion.

Severely flow-limited patients are at risk for hemodynamic collapse with the application of positive-pressure ventilation owing to dynamic hyperinflation of the lungs.

Auto-PEEP has been found to develop in most COPD patients during one-lung anesthesia

Pulmonary complications are decreased in thoracic surgical patients who cease smoking for
more than 4 weeks before surgery.
Carboxyhemoglobin concentrations decrease if smoking is stopped more than 12 hours.

Cessation of smoking, ABX for purulent sputum, Chest physiotherapy, Nebulizers all decrease morbidity in the Periop period

8 weeks or more of smoking cessation was associated with a 66% reduction in
postoperative pulmonary complications

Incentive spirometry and deep breathing before abdominal surgery had more than a
50% lower incidence of clinical complications

Question 23

Bronchectasis

Answer 23

Chronic lung issue where lung tissue is scarred, and persistant buildup of mucus

Non curable

Focus on treatment modalities

Recurrent lung/bronchial infections is the primary culprit and cause

Treatment included: ABX, chest physiotherapy, inhlaers

Question 24

DISEASED LUNGS (SPECIAL CASE – CUTTING OUT SOME LUNG & DETERMINING WHO WILL TOLERATE IT AND WHO WON’T)

Answer 24

Calculating the post-operative pulmonary function in a patient undergoing thoracotomy and lung resection is important.

Three (3) cardiopulmonary function tests are important.

1. The predicted post-operative FEV1 (ppoFEV1) assesses pulmonary mechanics.
2. ppoDLCO assesses lung parenchymal function
3. Preoperative VO2max assess interaction between cardiac and pulmonary function.

Question 25

DISEASED LUNGS (SPECIAL CASE – CUTTING OUT SOME LUNG & DETERMINING WHO WILL TOLERATE IT AND WHO WON’T)

Answer 25

You need to know the patients pre-operative pulmonary function tests and cardiopulmonary functional status. Additionally you need to know a little bit about the pulmonary anatomy and how much of the lung the surgeons plan to resect. Humans have 42 total lung subsegments. If you remove a patients left upper lobe, you will be left with 32 total lung subsegments. (simply a ratio)

Question 26

DISEASED LUNGS (SPECIAL CASE – CUTTING OUT SOME LUNG & DETERMINING WHO WILL TOLERATE IT AND WHO WON’T)

Answer 26

The “3 Legged” Stool: 1. FEV1 If ppoFEV1 > 40% - low risk for perioperative resp. complications. ppoFEV1 < 30% - high risk 2. VO2max (Preoperative) >20ml/kg/min – low risk of resp. respiratory complic. < 15ml/kg/min – high risk (unacceptable) 3. DLCO ppoDLCO > 40% of predicted – low risk of periop complications. Not good predictor of long term survival 1.5 flights of stairs = VO2 max ~ 10mL/kg/min (might not be good to get a lung cut out)

Question 27

PULMONARY HTN

Answer 27

A bad actor Defined as a mean PAP greater than 25 mmHg 42% of patients with PH undergoing non cardiac surgery have some morbid event, and 7% had an early death You need to understand the different classifications of pulmonary hypertension When taking care of these patients you need to be VERY GENTLE

Question 28

PULMONARY HTN

Answer 28

Definition of precapillary pHTN? mPAP >25, wedge <15, Pulmonary VR > 240 (post capillary mPAP >25, PCWP >15, PVR <240) Mild mPAP 25-40 mmHg, PASP 25-49 Moderate mPAP 41-55 mmHg, PASP 50-69 Severe mPAP >55, PASP >70 Note portopulmonary (precapillary) hypertension has different criteria, with... Mild mPAP> 25 mmHg Moderate > 35 mmHg Severe > 45 mmHg. Precapillary pHTN vs Post capillary pHTN? Evaluate Tpg= PAPm-PCWP Greater than 12mmHg-15mmHg= Precapillary. Less than 12mmHg-15mmHg post capillary KNOW TWO DIFFERENT TYPES OF PULMONARY HYPERTENSION and TREATMENTS ARE DIFFERENT (LOOK UP WEDGE PRESSURE!!) (NEED TO LOOK UP MORE ABOUT THIS SLIDE!!!)

Question 29

PRE VS POST CAPILLARY HTN

Answer 29

PVR = mPAP- PCWP/CO X(80) to get into Dynes-sec/cm^5 Determining PVR can help you identify pre vs post capillary HTN Usually greater than 240: Pre capillary Less than 240 Post capillary Post capillary pHTN: left heart disease, MR, AR, LVH, diastolic function, low EF Precapillary pHTN: OSA, COPD, pulmonary emboli, autoimmune dz, HIV (NEED TO LOOK UP MORE ABOUT THIS SLIDE!!!)

Question 30

Patients with PH

Answer 30

Question 31

S1 QIII TIII

Answer 31

Classic PE Problem

Question 32

MONITORING

Answer 32

Arterial line pre induction Consider PA catheter Consider Central access because of flow problem through the right heart Consider TEE

Question 33

HD GOALS with those with Pulmonary Hypertension

Answer 33

Keeping them where they live is a good start Avoid hypoxemia, hypercarbia, hypotension, pain, acidosis, hypothermia, lung over-inflation, lung under-inflation Maintain SR Requires a lot of fine tuning & finesse Keep euvolemic No one anesthetic technique is better than any other, but most of us would avoid spinals. Sedation can be very difficult to manage optimally. Pressors can hurt you (some that are not used in pulmonary hypertension)

Question 34

Cardiogenic Shock Causes due to Pulmonary Hypertension

Answer 34

Vassopressors most indicated for precapillary hypertension = vasopressin?? (Not Neo because make it worse????) CHF causes post capillary = want to get fluid off

Question 35

Pulmonary Vasodilators

Answer 35

Know milrinone!!! If patient is on milrinone, that means it is bad Two choices for anestheisa: wide awake, fully asleep

Question 36

PHTN SUMMARY

Answer 36

Be shared Keep them where they live Be gentle Have a plan & a back up plan Avoid hypotension, hypoxia, hypercarbia, pain, hypothermia, elevated airway pressures Maintain SR If GA, have a perfect ventilation strategy☺

Question 37

DIFFUSION CAPACITY

Answer 37

Volume of gas that will diffuse through the membrane each minute for a partial pressure difference of 1 mmHg

Question 38

LAW OF DIFFUSION: FICK

Answer 38

Vgas≈ A/T x D x (p1-p2) Vgas= volume of gas transferred A= surface area T= membrane thickness D= diffusion constant for said gas P1-p2 is pressure gradient driving gas flow. Between pulmonary capillary and alveolus (typically for us it is O2) Diffusion is inversely proportional to membrane thickness

Question 39

RESPIRATORY MEMBRANE

Answer 39

Layers: 1) A layer of fluid lining the alveolus and containing surfactant. 2) The alveolar epithelium 3) An epithelial basement membrane 4) A thin interstitial space btn alveolar epithelium and capillary membrane 5) A capillary basement membrane 6) The capillary endothelial membrane

Question 40

CARBON MONOXIDE

Answer 40

CO from alveolus moves rapidly across the membrane and binds to RBC intracellularly A lot of CO can bind with the cell so the partial pressure of the gas won’t increase as the RBC moves through the capillary So, amount of CO in the blood is limited by the diffusion properties of the b/g barrier not the amount of blood available CO is diffusion limited This is why we use CO to test diffusion capacity of the lung

Question 41

DIFFUSION CAPACITY CO

Answer 41

Question 42

OXYGEN

Answer 42

O2 combines with Hb, but not as well as CO Under normal conditions O2 is perfusion limited When diffusion properties of the lung are impaired ( eg thickening), there is some diffusion limitation as well

Question 43

A-a GRADIENT

Answer 43

Useful for detecting presence of v/q mismatch Ideal minus real Normal less than 10 on RA

Question 44

ALVEOLAR GAS

Answer 44

Oxygenation... Alveolar Gas Equation: (WHAT DOES THIS MEAN???) PA = FiO2(PB-PH2O) – (PaCO2/R) PA = Alveolar oxygen partial press. FiO2 = inspired O2 partial press. PaCO2 = partial pressure CO2 in blood. R= Respiratory quotient (0.8) PH20=47mmHg PB= atmospheric pressure 760 at sea level 630 in Denver

Question 45

FIVE CAUSES OF HYPOXEMIA

Answer 45

Hypoventilation Diffusion Abnormality Shunt VQ mismatch (#1 Cause of Hypoxemia on all tests if it is an option) Low Inspired air pressure

Question 46

HYPOVENTILATION

Answer 46

As CO2 goes up, your PaO2 goes down unless.. You increase your FiO2 Increasing your FiO2 easily reverses hypoxia

Question 47

SHUNT

Answer 47

Defined as blood that enters the arterial system but does not go through ventilated area of the lung…perfusion without ventilation There is an equation to determine shunt fraction. We wont cover that (LOOK THIS UP and KNOW IT AND WHAT CAUSES IT TO MOVE ONE WAY OR ANOTHER!!!) Where does it come from? ASD, Pulmonary AVMS, Bronchial Vein to Pulmonary vein blood flow (WHAT IS AVMS??? LOOK UP)

Question 48

OXYGEN TRANSPORT

Answer 48

Once O2 has diffused from alveoli, it is transported to the peripheral tissue capillaries almost entirely in combination with Hemoglobin. 2 ways in which O2 is carried: Attached to hemoglobin Dissolved Oxygen Carrying Capacity [CaO2]= (1.39 x Hb x Sat/100) + (0.003 x PaO2) (WHAT IS THE Sat/100???)

Question 49

OXYGEN TRANSPORT (DISSOLVED O2)

Answer 49

Henry’s Law: The amount of a gas that is dissolved in the blood is proportional to the partial pressure of that gas. For O2: for each mm Hg of PO2, there is 0.003 mL O2/100mL of blood. Therefore, normal arterial blood with a PO2 of 100 mm Hg contains 0.3 mL O2/100 mL (very little) Obviously, just this method of gas transport is not enough to meet the needs of the body.

Question 50

OXYGEN TRANSPORT (HGB BOUND)

Answer 50

Hemoglobin – an iron-porphyrin compound attached to a protein globulin made up of two types of polypeptide chains. Polypeptide chain types: Hgb α Hgb β Normal Adult: Hgb = Hgb A Normal Fetal: Hgb = Hbg F Abnormal Hgb: S = Sickle Cell

Question 51

OXYGEN TRANSPORT

Answer 51

A few notes about hemoglobin: Hemoglobin F (fetal): part of Hb of newborn, gradually replaced over the first 6-8 mo of postnatal life. Higher affinity for O2 than Hb A. (Shifts it to the left) Hemoglobin S (sickle) has valine instead of glutamic acid in beta chains. Decreased O2 affinity and shift in Hb/O2 curve (which direction?) to the right Also, deoxygenated form is poorly soluble and crystallizes with red cell . . .

Question 52

OXYGEN TRANSPORT

Answer 52

Oxygen Dissociation Curve O2 + Hgb → HgbO2 Hgb in the oxygenated state is said to be “Relaxed” or R state Hgb in the deoxygenated state is said to be “Tensed” or T state Oxygen rapidly binds to Hgb up to approx. PaO2 = 50mmHg but then the rate of binding slows. The maximum amount of O2 that can be bound is called the O2 Capacity O2 Saturation is the percentage of available O2 binding sites that have O2 attached is determined by the equation: Saturation = (O2 combined with Hgb / O2 capacity) x 100

Question 53

OXYGEN UPTAKE IN THE LUNGS

Answer 53

Question 54

O2/CO2 TRANSPORT: EXERCISE

Answer 54

During strenuous exercise, O2 requirements may increase by 20x normal. Shortened exposure time of blood to alveoli, but the blood can still become almost fully oxygenated (almost fully oxygenated when only 1/3 way through capillaries normally). And diffusing capacity for O2 increases almost threefold during exercise due to increased surface area of capillaries participating in diffusion (Due to what mechanism?) What primary mechanism allows your PVR to drop during exercise?

Question 55

OXYGEN TRANSPORT

Answer 55

Blood from lung will mix with blood that passed from aorta through bronchial circulation (shunt flow). Shunt blood =40 mm Hg, Pulm. Venous blood=104 mm Hg. Venous admixture: 95 mm Hg.

Question 56

OXYGEN TRANSPORT (OFF LOADING AT TISSUE)

Answer 56

Tissue PO2 is determined by a balance between: Rate of O2 transport to the tissues in the blood Rate at which the oxygen is used by the tissues

Question 57

OXYGEN DISSOCIATION CURVE

Answer 57

Right Shift O2 bound to Hgb with less affinity Increased H+ (Acidosis) Increased PCO2 (Bohr Effect) Increased Temperature Increased 2,3-diphosphoglycerate Left Shift O2 bound to Hgb more strongly Alkalosis Lowered PCO2 (redundant) Hypothermia Decreased 2,3-diphosphoglycerate Carbon monoxide

Question 58

Patient is 150kg... over 1 hour

Answer 58

Tension Pneuo (immediate, no go) Venous Air Embolism (not the position for this surgery, no go) Lab Problem (no go) PE (immediate change, no go) Mainstem Intubation (increases the peak inspiratory pressure and would be gradual)

Question 59

65 yo Patient, appendecatomy, ABGs... COPD, PaO2 + PaCO2 abnormal

Answer 59

Rule of 5 (FiO2 times 4/5 should be your PaO2, thus why normal is 80-100) Needs HgB for this answer