pfts work shop-lauren

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PFTs Work Shop (1/11) Patient 1 History o A 29 year old white female economist, who is a non-smoker, with no history of atopy, presents to her physician complaining of attacks of shortness of breath of sudden onset. These attacks are not accompanied by cough or sputum production and the patient has heard no wheezing in her chest. She feels quite anxious during the attacks. They have always resolved spontaneously within several minutes after their onset. She has not had one of these attacks at night. She has recently moved to Washington to begin a new job with the Federal Reserve. o Physical examination : within normal limits. o Chest roentgenogram : within normal limits. Notes about this patient’s history o Young person with SOB the most common thing you think of is asthma o Atopy allergic rhinitis, eczema, asthma but she is not atopic o Can also happen post bad respiratory tract infection where they continue to cough after the infection has resolved o She does have a lot of symptoms that indicate it might be asthma: Asthma symptoms tend to be episodic depending on triggers Underlying problem is that the airways are inflamed eoisnophilic Inflammation leads to damage to airways smooth muscle becomes “twitchier” (hyper-reactive) causes airway constriction when it normally wouldn’t constrict Flow-volume loop o Inspiration: below the X axis

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Page 1: Pfts Work Shop-lauren

Question #1: What type of problem does the flow-volume loop suggest?

o Poor patient efforto Obstructive ventilatory defecto Restrictive ventilatory defect

Hallmark of restriction means the TLC is down

FVC must be <80% predictive Probably not because she has a good

FVC o Normal expiratory airflow

3.5 L = forced vital capacity (width of loop) this is normal

o None of the above

Question#2: How do you interpret her PFT data?1. Obstructive ventilatory defect2. Restrictive ventilatory defect3. Normal airflow

o Ratio FEV1/FVC = 87% Younger person is = greater percent of air they should be able to get

out in one second She should be able to get out 85% based on her age

o VC could be down to 80% predictive and still be within normal limits for this individual a lot of variation for what constitutes normal lung function

PFTs Work Shop (1/11)

Patient 1 History

o A 29 year old white female economist, who is a non-smoker, with no history of atopy, presents to her physician complaining of attacks of shortness of breath of sudden onset. These attacks are not accompanied by cough or sputum production and the patient has heard no wheezing in her chest. She feels quite anxious during the attacks. They have always resolved spontaneously within several minutes after their onset. She has not had one of these attacks at night. She has recently moved to Washington to begin a new job with the Federal Reserve.

o Physical examination : within normal limits.o Chest roentgenogram : within normal limits.

Notes about this patient’s history o Young person with SOB the most common thing you think of is asthma o Atopy allergic rhinitis, eczema, asthma but she is not atopic o Can also happen post bad respiratory tract infection where they continue to cough after the

infection has resolved o She does have a lot of symptoms that indicate it might be asthma:

Asthma symptoms tend to be episodic depending on triggers Underlying problem is that the airways are inflamed eoisnophilic Inflammation leads to damage to airways smooth muscle becomes “twitchier”

(hyper-reactive) causes airway constriction when it normally wouldn’t constrict Flow-volume loop

o Inspiration: below the X axis Person didn’t fill the lung back up

completely on inspiration line doesn’t go all the way to TLC

Conclusion o She has normal airway flow o Not enough evidence to do further asthma studies:

Methacholine challenge: methacholine is a parasympathetic transmitter that can cause airway constriction

Aerosol of methylcholine chloride is given at increasing doses check PFTs with each dose

Page 2: Pfts Work Shop-lauren

Question #1: What type of problem does the flow volume loop suggest?

o Poor patient efforto Mild obstructive ventilatory defect o Emphysema because of very low

expiratory flow as the lung deflateso Restrictive ventilatory defect

Probably not because TLC is 3.5 L o Combined obstructive and restrictive

ventilatory defect

Question #2: How do you interpret the PFT data?

o Obstructive ventilatory defect with

When muscle is more reactive then normal we expect narrowing of airway and decreased airflow at an earlier point than normal airways

Patient 2 History

o He is 56-year-old white male, who had smoked 2-3 ppd of cigarettes for many years. He stopped smoking about 6 years ago when he became concerned about the shortness of breath he was experiencing on exercise. Despite cessation of smoking, the dyspnea has become progressively worse; he is now SOB while at rest. He denies productive cough. There is no history of asthma or industrial exposure to dusts or fumes.

o He is currently using an ipratropium bromide metered-dose inhaler three or four times per day, claiming to feel better for a short time following these inhalations.

Ipratropium anticholinergic drug dilates airways

o Physical examination He is a thin, emaciated male, appearing much older than his stated age. He

complains of being out of breath, RR – 16/ min Thorax: barrel-shaped Lungs: hyperresonant percussion note (= more air in chest); diaphragms percuss at

the 10th intercostal space posteriorly, with limited movement; breath sounds are distant, with a prolonged expiratory phase; no wheezes or crackles are heard.

Heart: heart sounds are barely audible below the left costal margin

Ext: no cyanosis or clubbing

Flow-volume curve o Lack of full inspiratory loop didn’t fill

lung up properly o TLC = 3.5 L o 2.5 L of which there is very limited flow o Very concave a lot of airflow

obstruction

o o Airways are not well supported

and something caused them to collapse early on

PFT data

Page 3: Pfts Work Shop-lauren

Question #2: How do you interpret the PFT data?

o Obstructive ventilatory defect with

Question #1: What type of problem does the flow volume loop suggest?

o Obstructiveo Restrictive o Normalo Combined obstructive and restrictive

Question #2: How do you interpret his PFT data?o Severe obstructive ventilatory defect o Severe restrictive ventilatory defecto Combined obstructive and restrictive

defects

o Look at TLC to detect hyperinflation of the lung TLC is 120% predictive signifies hyperinflation

o FEV1/FVC = 43 Only getting 43% of air out of the lungs in 1 second signifies airflow obstruction

o FEF25-75 = 25 Only 13% of predictive

o FVC showed ~15-20% improvement after bronchodilator administered somewhat significant acute bronchodilator response but in general, patients with COPD don’t usually respond as vigorously to bronchodilators as asthmatics

But we are seeing more patients with some acute bronchodilator response than in the past

o RV/TLC ratio shows what percent of total lung capacity is trapped air Supposed to be about 30% for his age His ratio is 65 which means over half his lungs are trapped air

o DLCO indicative of a membrane problem His diffusion capacity is only 56% of predicted Emphysema causes a broken down surface of alveolar membrane which would

decrease the DLCOPatient 3 History

o He is a 62-year-old white male, who had smoked two ppd of cigarettes for 10 years. He stopped smoking 10 years ago, and has not smoked since. Two years ago, he noted the onset of shortness of breath while climbing a flight of stairs. This dyspnea has progressively limited his exertion, but he is quite comfortable at rest. He has noted increasing dry cough without sputum production. He denies productive cough while he was smoking. There is a history of asthma. He has worked as a retail store clerk and denies exposure to industrial dusts. His hobby is stamp collecting.

o Physical examination The positive findings are limited to the lungs and extremities RR – 18 and unlabored at rest Lungs: late inspiratory crackles are present at the bases of both lungs posteriorly.

These crackles are no longer heard over the left lung when the patient is examined in the right lateral decubitus position. There are no wheezes. The diaphragms percuss at the 8th posterior intercostal space, but move normally.

Heart: within normal limits Ext: fingers and toes reveal soft nail beds. They are thought to be “clubbed”

by one observer Flow-volume loop

PFT data

Page 4: Pfts Work Shop-lauren

Question #1: What type of problem does the flow-volume loop suggest if any?

o Poor patient effort o Mild obstructive ventilatory defecto Mild restrictive ventialtory defecto Normal expiratory airflowo None of the above

Question #2: how do you interpret his PFT data?

o Obstructive ventilatory defecto Restrictive ventilatory defecto Normal airflow

o Look at ratio first! He had 74% which is normal

o Not everyone who smokes goes on to have COPD some genetics involvedo More you smoke then more likely you are to get lung cancer association is linear o TLC = 48% of predictive

Indicative of restrictive disease since this is <80% of predictiveo DLCO is decreased shows that there is lung parenchyma stiffness o Restriction can result from a change in lung compliance OR a change in chest wall

compliance (and lung is normal) Restriction with normal DLCO = chest wall problem (usually in morbidly obese

patients) Restriction with decreased DLCO = lung compliance problem

Patient 4 History

o He is a 43-year-old man with a history of asthma since childhood. He relates allergies to multiple substances including pollens and dusts. He experiences frequent hay fever with nasal congestion and rhinorrhea. His mother and sister have had similar respiratory problems. He has been hospitalized on several occasions for treatment of acute exacerbations of his asthma. On one admission, he required intubation and mechanical ventilatory support when his PaCO2 rose to 70 (normal is 40), his pH falling to 7.22. He currently is feeling well. His medications include inhaled Advair® 100/50, one inhalation bid, montelukast (leukotriene antagonist to block inflammation), 10 mgm qd, and an albuterol (short acting beta agonist) MDI prn.

o Physical examination Within normal limits. His lungs are completely clear on auscultation.

o Questions to measure control of asthma you should ask: Are you waking up at night and how often? How often do you have to use your rescue

medication? Flow-volume loop

o Flow is reduced a little below what it should be at a given lung volume due to the concavity of the

expiratory loop PFT data

o FEV1/FVC ratio is decreased 71% o FEF25-75 129 which is only 55% of

predicted value Significant improvement post administration of bronchodilator to 175 (30%

improvement)o Doesn’t have restriction because his TLC is 94% predictedo Does have reversible airflow obstruction despite the fact that he feels fine

Page 5: Pfts Work Shop-lauren

From lecture on previous day titled “Clinical Assessment of Lung Function”

Alveolar gas equation o PAO2 = FiO2 (PB- PH2O) - PACO2/RQo Amount of O2 in inspired gas mixture is first determinanto How much breathing person is doing (reflected in CO2) is second determinant o If we are breathing room air at sea level the first term is going to become ~150

.21 (760-47) = 150o Normal level of breathing the PCO2 will be 40 divided by RQ (0.8) second term becomes

50o Alveolar pressure becomes about 100 torr

.21(760-47) – 40/.8 150-50 = 100 torr Considerably less than what the pressure was in the atmosphere

A-a gradient = different between alveolar (A) and arterial (a) pressure o There is not a perfect match between ventilation and perfusion…why?

Gravity is a big determinant Blood becomes shunted

About 4% of CO is shunted Mixing of deoxy blood and oxy blood causes gradient

Varies with age Take about ¼ of patients age 100 year old will have a gradient of 25 torr so their PaO2 should be 75 20 year old will have a gradient of 5 torr so their PaO2 should be 95

Arterial blood gas analysiso After a pulse is found a blood sample is taken from a superficial artery (usually the radial

artery)o Measure O2 pressure, CO2 pressure and pH

Causes of hypoxemia (lower than normal PaO2)o Decreased alveolar oxygen tension

Decreased PO2 in inspired gas (i.e. increased altitude) Hypoventilation V/Q mismatch low V/Q ratios give rise to problems with O2 transfer

o Shunts Increase amount of blood being shunted from RL side of circulation without

oxygen being added to it o Impaired diffusion

V/Q and gas exchangeo Lower ratio have more of an effect on gas exchange

No fresh air coming in will cause the gas pressures in the arteries to look just like the pressures in the veins returning from the circulation

Lowest V/Q ratios = PO2 40; PCO2 45 Lower ratio = lower PO2 and higher PCO2

o Higher ratio not as much effect on gas exchange because there is not enough blood flow Shunt equation

o Part of CO is not seeing oxygen (i.e. there is perfusion but decreased ventilation) low V/Q ratios

o Etiology: Pulmonary arterial/venous malformation that bypasses the lung Hole in heart so that flow goes from R L Non-functional alveoli in setting of pneumonia (for example) – blood is going

through the lung but not getting in contact with O2

Page 6: Pfts Work Shop-lauren

Oxygen-hemoglobin dissociation curve o Relationship between PO2 and Hb saturation o Looks at the PaO2 which is the dissolved oxygen pressure

Pulse oximetryo Measurement of O2 saturation (SpO2) o Non-invasive but nail polish/fake nails is a problem o Shine light through the nail bed and the waves reflect back Measure the color of

hemoglobino Hemoglobin color changes depending on whether it is oxygenated or not (oxy = red, deoxy =

blue) The different colors will absorb different wavelengths of light

o SpO2 tells you nothing about the CO2 or the ventilation Causes of hypercapnia (increase in PaCO2)

o Signifies a reduction in effective alveolar ventilation (VA)o VE = VD + VA

Minute ventilation (VE) is composed of 2 things. Some of the air is actually reaching down to the alveolus and ventilate the alveolus (VA) and part of every breath is simply moving through the dead space of the conducting airways, so that’s dead space ventilation (VD)

o High V/Q ratios = dead space ventilation Units don’t have adequate blood flow for the amount of ventilation that’s going to

them Ventilation

o Relationship between alveolar ventilation and alveolar PCO2

o CO2 production picks up then must pick up the minute ventilation to maintain normal PCO2 at 40

Example: exercise Dead space

o Measure dead space by changes in expired CO2

oo Decreased expired CO2 increased dead space/tidal volume ratio

Causes of hypercapniao Reduction in minute ventilation (VE)

Depression of respiratory center drive (with opiates, for example) Loss of neuromuscular coupling

Impaired neuromuscular coupling (someone with impaired transmission between the brainstem and spinal cord)

Excessive respiratory load respirator muscle fatigueo Increased dead space ventilation (Vd) with a normal or increased Ve

Alveoli with high V/Q ratios

Patient 5 History

o A 25 year old woman, who has smoked one pack-per-day of cigarettes for 6 years, presents to the emergency room complaining of intermittent episodes of shortness of breath unrelated to exertion. Physical examination is within normal limits.

o pH - 7.51o PaO2 - 110o PaCO2 - 27

Page 7: Pfts Work Shop-lauren

o HCO3- - 23

Question: assess the patient’s oxygenation o Normal or abnormal? it is normal on the surface but must to alveolar gas equationo Must look at alveolar gas equation there will be a problem on the exam where you will

have to calculate an A-a gradient!! PAO2 = FiO2 (PB- PH2O) - PACO2/RQ = 150 – 27/.8 =115 Gradient is 5 torr (115 – PaO2 of 110)

Does the patient have an abnormal A-a gradient?o Yes vs. no? No, her gradient is normal o Age 25 divided by 4 gradient should be about 6o She has a gradient of 5 so this is normal o A normal gradient is telling us that there is no disease in the lungs her lungs are

transferring O2 normally Describe the patient’s ventilation:

o Normal vs. hypoventilation vs. hyperventilation hyperventilation b/c the patient’s CO2 is lower than normal (27 vs. the normal 40)

o Hyperventilation causes the PAO2 to be higher than normal as you blow CO2 off you raise the O2 pressure in the alveolar reservoir

What is the patient’s acid-base status? o Acute respiratory alkalosis o We know she is hyperventilation and the HCO3- is just below normal range (normal = 24-28)

so her kidneys have not been doing anything to affect HCO3-o Looks like it’s only the lung that is affecting the acid-base status

Acid-base disorderso Normal arterial blood pH = 7.40 +/- 0.02

Acidemia: pH < 7.38 Alkalemia: pH > 7.42

o Normal PaCO2 = 40o Normal serum HCO3- = 24 +/- 2o Changes in pH can result from both respiratory and metabolic disturbances

Respiratory alters the PaCo2 Metabolic alters the serum HCO3-

o Respiratory acidosis rise in PaCO2 Hypoventilation

o Respiratory alkalosis fall in PaCO2 Hyperventilation Can be from brainstem strokes, pregnancy (b/c it stimulates breathing)

Respitratory acid-base disturbances o Acute respiratory alkalosis

For each 10 torr fall in PaCO2, pH rises by 0.08-0.1 pH units Normal bicarb tells you it is a respiratory issue pH increase = 0.08 x (40-PaCO2) / 10

Patient 6 History

o A 25 year old woman complains of nocturnal episodes of shortness of breath and productive cough which awaken her from sleep. On physical examination scattered wheezes are heard over both lung bases.

o pH - 7.47o PaO2 - 84

Page 8: Pfts Work Shop-lauren

o PaCO2 - 34o HCO3

- - 23o Classical story for asthma

Assess the patient’s oxygenation o Normal vs. Abnormal abnormal because the PaO2 is below 100

Does the patient have an abnormal P(A-a)DO2?o PAO2 =150 – 34/.8o PAO2 = 107.5 o 107.5 – 84 = gradient of about 25o Patient is 25 so gradient should be about 6 but it is 4 times this o Yes vs. No? Yes, the patient has an abnormal gradient

What is the mechanism of her abnormal gradient?o Problem is that she has asthma and her airways are swollen so the air can’t get through

low levels of ventilation relative to the perfusiono Low V/Q ratios are the cause of her hypoxemia

Causes of hypoxemiao Decreased alveolar O2 tension

Decreased PO2 in inspired gas (i.e. altitude) Hypoventilation (i.e. obesity hypoventilation syndrome) V/Q mismatch most common mechanism of hypoxemia= low V/Q ratios

o Second most common is shunting occurs in pulmonary edema or when you have alveolar spaces that are packed full of inflammatory cells (like in pneumonia)

o Impaired diffusion Describe the patient’s ventilation:

o Normal vs. hypoventilation vs. hyperventilation hyperventilation b/c PaCO2 is less than 40

What is the patient’s acid-base status?o Acute respiratory alkalosis caused by hyperventilation o PaCO2 is down by about 5 torr so we would expect to see about a 0.5 increase in pH

Patient 7 History

o A 25 year old woman, in her third trimester of pregnancy, complains of feeling short of breath, worse when she lies in bed at night. Examination of her heart and lungs is normal.

o pH - 7.43o PaO2 - 108o PaCO2 - 30o HCO3- - 21

Assess the patient’s oxygenation o Normal vs. abnormal normal? (he didn’t ever say..)

Does the patient have an abnormal P(A-a)DO2?o =150 – 30/.8o =114 o 114-108 = 6o This is a normal gradient for a 25 year old (25/4 = ~6)o Yes vs. no no, the patient has a normal A-a gradient

Describe the patient’s ventilationo Normal vs. hypoventilation vs. hyperventilation She is hyperventilating b/c her PaCO2 is

below 40 What is the patient’s acid-base status?

o 10 torr decrease in PaCO2 should have a 0.1 increase in pH but we don’t see that this can’t be acute

Page 9: Pfts Work Shop-lauren

o Also, HCO3- is lower than we expected o The kidneys excrete more HCO3- (so you get a decrease in HCO3) to compensate and

maintain normal pH levels o Answer: Chronic Respiratory Alkalosis

Respiratory acid-base disturbanceso Chronic respiratory alkalosis reflects sustained PaCO2 fall AND renal-mediated HCO3-

shifts Develops in several hours, maximal 4 days Low PaCO2, accompanied by a smaller pH shift of only 0.03 units HCO3- decreases 2.5 mEq for each 10 torr decline in PaCO2 pH back toward normal, but not completely pH increase = 0.03 x (40-PaCO2)/10

Patient 8 History

o A 50 year old man with a long and heavy cigarette smoking history is seen by his family physician because of complaints of chronic productive cough, which is yielding copious amounts of thick yellow sputum, and worsening shortness of breath on exertion.

o pH - 7.37o PaO2 - 55 o PaCO2 - 52o HCO3

- - 30 Assess the patient’s oxygenation

o Normal vs. abnormal? Abnormal b/c PaO2 is below the normal 100 Does the patient have an abnormal P(A-a)DO2?

o Yes or no? Yes! o =150 – 52/.8 o =85o 85-52 = gradient of about 35 o A 50 year old patient should have a gradient of ~12 (=50/4) so this is abnormal which tells

you this man has a disease of his lungs Describe the patient’s ventilation

o Normal vs. hypoventilation vs. hyperventilation hypoventilation b/c the PaCO2 is greater than 40

Causes of hypercapnia o Increase in PaCO2 signifies a reduction in effective alveolar ventilation (Va) o In this patient’s cause it’s probably the excessive respiratory load because he has COPD

which causes him to have very high airway resistance What is the patient’s acid-base status?

o Should be down to 7.32 but it’s not not an acute problemo Also see an increase in HCO3 o Kidneys hold on to HCO3 to compensate in an effort to maintain normal pH levels o Answer: Chronic respiratory acidosis

Respiratory acid-base disturbances o Chronic respiratory acidosis reflects sustained PaCO2 elevation AND renal mediated

HCO3- shifts Develops in several hours, maximal 4 days Elevated PaCO2, accompanied by a smaller pH shift of only 0.03 units HCO3- increases 4mEq for each 10 torr elevation of PaCO2 pH back towards normal, but not completely

Patient 8: Scenario 2 History

Page 10: Pfts Work Shop-lauren

o The above patient is started on oral bronchodilators and a broad spectrum antibiotic. Three days later he is brought to the emergency room by his wife because of worsening dyspnea and confusion.

pH - 7.30 (before = 7.37)PaO2 – 45 (before = 55)

PaCO2 – 60 (before = 52)HCO3

- - 32 (before = 30) Assess the patient’s oxygenation

o Normal vs. abnormal abnormal b/c it is below the normal 100 Does the patient have an abnormal P(A-a)DO2?

o =150 – 60/.8o =74o 74 -45 = gradient of 29o Since he is 50 years old his gradient should be about 12 (50/4 = ~12)o Yes or no? Yes, this patient has an abnormal gradient

Describe the patient’s ventilation o Normal vs. hyperventilation vs. hypoventilation hypoventilating more than he was

before What is the patient’s acid-base status

o PaCO2 is up 10 torr and pH has fallen from what we expected o His airways are more obstructed and he has increased airway resistance higher work of

breathing ventilation deteriorates pH falls acutely on top of his chronic problem o Answer: Acute on Chronic Respiratory Acidosis

Patient 9 History

o A 23 year old male is brought to the emergency room by the rescue squad after having been found unresponsive and unarousable by his roommate. An empty bottle of barbiturates was found beside the bed

o pH - 7.26o PaO2 - 71o PaCO2 - 60o HCO3

- - 25 Assess the patient’s oxygenation

o Abnormal vs. normal? abnormal b/c his O2 is <100 Does the patient have an abnormal P(A-a)DO2

o =150 – 60/.8o = 75o 75 – 71 = gradient of 4 o At age 23 you would expect him to have a gradient of about 5-6 so this is normal o Yes vs. no? No, he has a normal gradient

Describe the patient’s ventilation o Normal vs. hyperventilation vs. hypoventilation hypoventilation b/c his CO2 is up

What is the patient’s acid-base status? o Patient is acidotic, PaCO2 is high, and the HCO3- is normal o Answer: acute respiratory acidosis