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Pulmonary Clinical Case Study Three

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You have been assigned clinical case study three. For case description visit this update in the Pulmonary Physiology Community. A follow up email reiterating instructions will be sent shortly.

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Case 3

1.  Given the pt’s history and physical exam list your differential diagnosis including at least 5 possible diagnoses. (Remember the differential diagnosis should be broad and really just include causes that could account for the relevant symptoms) Essentially what could account for acute onset dyspnea, chest pain, and tachypnea.

Pulmonary Embolism

Myocardial Infarction

Pneumonia

Asthma attack

Anxiety attack

2. Now given the clinical presentation, physical exam and labs What is your top diagnosis? (Use your differential and think through what data lead you to believe your top diagnosis is correct and go against the others)

Pulmonary Embolism.

   The only abnormal presentation on the ECG was sinus tachycardia.  If a Myocardial Infarction was taking place, one would expect to find additional signs on the patient’s besides sinus tachycardia. The cardiac physical examination was also normal (disregarding the tachycardia), so this in combination with the ECG, would suggest another condition besides a myocardial infarction.  The WBC appears to be elevated, so it is possible that the patient could have bacterial pneumonia.  However, the X-ray of the patient was normal and one would expect to find white spots called infiltrates on an X-ray of someone with pneumonia.  It is possible that the patient could be experiencing an asthma attack, since has a history of asthma.  However, she should have experienced some relief when using her inhaler.  Based on her symptoms, the patient could also have been experiencing an anxiety attack.  There was no information presented, however, that would suggest the patient was experiencing anxiety.  When considering all of the information given, however, pulmonary embolism seems to be the most probable situation. The patient sat without moving for a 14 hour flight, so she probably did not have good blood flow in her legs.  The patient also recalled having swelling in her leg and had a previous incident of Deep Vein Thrombosis (DVT).  Additionally, the patient is taking oral contraceptive pills which can increase the risk of DVT.  On top of these factors, the d-dimer test results were above the normal range (normal 250ng/ml or less, patient=2000ng/ml).  The d-dimer test measures the breakdown products of a blood clot.  If this test is normal, then the likelihood of a pulmonary embolism is low.  If the test result comes back abnormal, however, it is not specific for blood clots in the lung.  It is thus only good for ruling out the possibility of a pulmonary embolism. Since the results could not rule out a pulmonary embolism, it further supports the possibility of the patient having one. A variety of conditions can give an abnormal test result. Taking all of these factors into consideration, the patient likely had another DVT incident, which resulted in a pulmonary embolism.  The pulmonary embolism would also not shown up on the X-ray. 

3. Given your top diagnosis what specific tests do you need to run in order to confirm it?

Clinical signs and symptoms for pulmonary embolism are nonspecific; therefore, patients suspected of having pulmonary embolism—because of unexplained dyspnea, tachypnea, or chest pain or the presence of risk factors for pulmonary embolism—must undergo diagnostic tests until the diagnosis is ascertained or eliminated or an alternative diagnosis is confirmed. 

It is recommended that clinical prediction rules be used to estimate the probability of a pulmonary embolism before proceeding with testing.  Currently, the use of the Wells prediction rule is used for this purpose.  If the Wells prediction rule and d-dimer test results come back normal, then it is believed that no tests are needed to determine if a pulmonary embolism is present.

If the probability prediction rules do not indicate a low probability, one can assess the ischemia-modified albumin (IMA) level.  This test provides a higher positive predictive value than the d-dimer test, however, it should not be used alone.  Troponin tests may also be used in order to support a diagnosis of pulmonary embolism.  Serum troponin levels can be elevated in up to 50% of patients with a moderate to large pulmonary embolism, presumptively due to acute right ventricular myocardial stretch. Although troponin assessment is not currently recommended as part of the diagnostic workup, studies have shown that elevated troponin levels in the setting of pulmonary embolism correlate with increased mortality.  Although these tests are helpful for supporting the diagnoses of a pulmonary embolism, Angiography, CT scans, and Ventilation-Perfusion Scanning provide much more information for the diagnoses. Ventilation-Perfusion Scanning is often used first to determine the location to focus on in pulmonary angiography.  If results are inconclusive from the Ventilation-Perfusion scanning, a CT scan may be used instead.  When pulmonary angiography has been performed carefully and completely, a positive result provides virtually a 100% certainty that an obstruction to pulmonary arterial blood flow exists. A negative pulmonary angiogram provides a greater than 90% certainty for the exclusion of pulmonary embolism.

4.  Results of a VQ Scan are shown below. Before interpreting the results below please elaborate on the following:

A. What is the ventilation perfusion ratio (V/Q ratio)? (Include a short discussion on hypoxic vasoconstriction)

The ventilation-perfusion ratio is the ratio between the amount of air getting to the alveoli (the alveolar ventilation, V, in ml/min) and the amount of blood being sent to the lungs (the cardiac output or Q - also in ml/min).

V/Q = alveolar ventilation/cardiac output

V/Q = (4 l/min)/(5 l/min)  - (average values for V and Q)

V/Q = 0.8

The V/Q ratio is important because the ratio between the ventilation and the perfusion is one of the major factors affecting the alveolar (and therefore arterial) levels of oxygen and carbon dioxide.

-------------Decreased V/Q ratio: A decrease in the V/Q ratio is produced by either decreasing ventilation or increasing blood flow (without altering the other variable). These will both have the same effect - the alveolar (and therefore arterial) levels of oxygen will decrease and the CO2 will increase.

Reasons for observed gas changes-

-A decrease in ventilation (without a compensatory change in perfusion) means we are not bringing in enough oxygen to meet our metabolic need for oxygen (the oxygen consumption) as well as not blowing enough CO2 to get rid of the CO2 we produced. It is easy for us to figure out why the alveolar and arterial blood gases change the way they do with a decrease in ventilation.

-An increase in perfusion will have the same effect on the blood gases because an increase in perfusion (without a compensatory change in ventilation) means more blood cells are coming to remove oxygen from the alveolus as they deliver more CO2 than will be exhaled.

--------------Increased ventilation-perfusion ratio

To produce an increase in the ventilation-perfusion ratio, one can do one of two things:

-Increase ventilation (bring in more oxygen to the alveoli, blow off more CO2 from the lungs)

-Decrease the perfusion (so the blood takes away less oxygen, delivers less CO2)

Effect of increased ratio:

This will lead to an increase in the PAO2 (and therefore PaO2) and a decrease in PACO2 and PaCO2

Summary

1. Low V-Q ratio

-Ventilation is not keeping pace with perfusion.

-The alveolar oxygen levels will decrease, which will lead to a decrease in arterial oxygen levels (PaO2)

-The alveolar CO2 levels will increase (we're not getting rid of it as fast), also leading to an increase in arterial CO2

2. Increased ventilation-perfusion ratio (increasing the V/Q ratio does exactly the opposite of a decrease)

-This will lead to an increase in the alveolar oxygen levels and therefore arterial oxygen levels as well (and therefore PaO2)

-A decrease in alveolar CO2 levels and arterial CO2 levels

 The body has a couple of mechanisms that tend to normalize the V/Q ratio.  One mechanism is hypoxic vasoconstriction.  When the V/Q ratio is low (a lot of perfusion or too little ventiliation) hypoxic vasoconstriction can occur, which will decrease the perfusion of the hypoxic region resulting in the V/Q ratio increasing and bringing the arterial blood values closer to a normal value. Another mechanism is Bronchoconstriction. In cases of high V/Q ratio, the bronchi will constrict slightly to increase the resistance and decrease the amount of ventilation coming into an area that is not well perfused (although it won't shut it down entirely). This limits the amount of alveoalr dead space that occurs and minimizes the 'wasted' work that occurs with alveolar dead space.

A defect which occurs in the lungs whereby ventilation (the exchange of air between the lungs and the environment) and perfusion (the passage of blood through the lungs) are not evenly matched

B. What is a V/Q defect? Does a regional V/Q mismatch normally exist in the lungs? What does it tell you? What do you expect for this situation? (Include short discussion of west zones)

A V/Q is a defect which occurs in the lungs whereby ventilation (the exchange of air between the lungs and the environment) and perfusion (the passage of blood through the lungs) are not evenly matched. Everytime you stand up, the blood flow to the different parts of the lung (apex vs. base) changes due to gravity. More blood flows to the base of the lung than goes to the apex. This creates areas of the lung with different V/Q ratios and changes the blood gas values of the arterialized blood leaving each region of the lungs. These different regions are reffered to as west zones.

            When standing up, ventilation and perfusion is higher at the base of the lung and lower at the apex of the lung.  At the base of the lung, blood flow is greater than ventilation, so there is a low V/Q ratio.  Blood flow is more effected by gravity than ventilation, so as you go to the apex of the lung, the blood flow actually decreases to levels below that of ventilation.  Both ventilation and perfusion decrease as you move towards the apex of the lung, however, perfusion decreases more quickly than ventilation resulting in a greater level of ventilation compared to blood flow.  A higher amount of ventilation compared to perfusion results in a high V/Q ratio at the apex of the lung. The middle of the lungs have a good match of blood to ventilation - the arterial blood leaving this area of the lungs is generally thought of to have our standard blood gas values: PaO2 = 100 mm Hg and PaCO2 of 40 mm Hg. These regional differences occur in normal individuals.

   Various pathologies can also change the V/Q ratios. In the case of a pulmonary embolism (patient’s condition) a V/Q mismatch is observed but for different regions.  In a pulmonary embolism, one route of blow flow is blocked, such that little to no blood flow is able to proceed through the occluded vessel.  In the blood vessel with the clot, there is a higher V/Q ratio because there is very little blood flow (Q) with normal ventilation.  The blood traveling through this vessel will then be highly saturated with oxygen.  Other vessels will experience a greater blood flow due to the blood that normally flows through the occluded vessel being directed to other areas.  In these vessels with increased blood flow, there will be a lower V/Q ratio (due to higher Q).  These vessels will be less saturated with O2 due to a smaller V/Q ratio.  The occluded vessel(s) and non-occluded vessel(s) eventually rejoin and the blood volumes with different O2 saturations combine.  You do not take an average between the two volumes to come up with a new percent oxygen saturation.  Since the vessels that were not occluded contribute more blood, the oxygen saturation is weighted more towards the un-occluded vessels. The overall result is blood with a lower than normal percent oxygen saturation resulting in hypoxemia. V/Q mismatches are the most common cause of hypoxemia and can be caused by a pulmonary embolism, asthma, pneumonia, and many other conditions.

C. What is a V/Q scan? How is it performed?

Ventilation-Perfusion Scan (VQ Scan) –

 A VQ lung scan may be a useful test to determine whether a person has experienced PE. This test evaluates both air flow (V = ventilation) and blood flow (Q = perfusion) in the lungs. About one hour before the test, a slightly radioactive version of the mineral technetium mixed with liquid protein is administered through a vein to identify areas of the lung that may have reduced blood flow. Multiple images are taken from different angles, using a special camera that detects radioactivity. For half of the images, the person breathes from a tube that contains a mixture of air, oxygen, and a slightly radioactive version of the gas xenon, which reveals air flow in different parts of the lung. For the other half of the images, the camera tracks the technetium, which reveals blood flow in different parts of the lung. PE is suspected in areas of the lung that have significant “mismatches”—that is, good air flow but poor blood flow. Except for the minor discomfort from having an intravenous catheter placed, a VQ lung scan is painless and usually takes less than an hour. The exposure to radioactivity from the test is very minor and results in no side effects or complications. A radiologist interprets the images from the VQ lung scan and decides whether the probability of a PE is high, low, or intermediate. If the probability is high, the diagnosis is made. If the probability is low or intermediate (that is, nondiagnostic), or if the VQ scan cannot be interpreted clearly, other testing must be considered. Even when PE is ultimately proven to be present, the VQ scan may be nondiagnostic. If clinical suspicion is low and the VQ scan reveals a low probability of PE, generally no further testing is needed. A normal VQ scan means PE is not present.

D.How would O2 help this patient and how would it change the V/Q ratio?

Administering 100% saturated O2 to the patient would help by increasing the percent oxygen saturation in the vessels that were below normal.  By increasing the V/Q ratio in these vessels, it would help bring up the overall percent oxygen saturation of the blood.

E. What is the interpretation of the scan below (Fig 1)? Match this up with the clinical findings.

The top​​ portion of the scan corresponds to the ventiliation part of the procedure (vent) and the bottom portion of the scan corresponds to the blood flow part of the procedure (perf). As you can see by looking at the posterior view of the scan, there is a significant difference between the ventilation and perfussion results. There is a significant amount of radioactive dye that did not show up in the perfussion results for the left lung. This indicates that there was a blockage somewhere in the left lung because the dye is in the blood and certain areas are not showing up on the scan. When looking at the perfussion results on the left anterior oblique view (LAO), it is very diffuse and not concentrated/dark as in other pictures. This indicates that not much dye is being concentrated (blood circulating) in that area. In the clinical findings, there was also diffuse wheezing in the left lung which supports the blockage being in that area.

 

5. Given the positive diagnosis and confirmation of your suspicions what additional tests might be indicated in this patient. Why is that important (Hint: Where did the embolus come from? There was a clinical finding and a major criteria of well’s score that would indicate further testing

An ultrasound could be performed on the calf in order to look for the presence of deep vein thrombosis. If a blood clot in the leg was originally responsible for the pulmonary embolism, it will be important to make sure that there are no further clots that would put the patient at risk for another occurence.

6. What do we do now that we have the diagnosis? What is the mainstay treatment for a PE? Does this actually remove the clot? There are newer treatment modalities available what is the evidence for these? (Hint: Einstein PE trial)

            According to American College of Chest Physicians (ACCP) guidelines, immediate therapeutic anticoagulation should be initiated for patients in whom DVT or pulmonary embolism (PE) is suspected.  Patients usually given warfarin (oral anticoagulant) and enoxaparin.  Enoxaparin is a low molecular weight heparin (LMWH) that works by blocking the formation of blood clots.  Xarelto (rivaroxaban) had recently been explored as a new treatment option.  Xarelto is an anticoagulant (blood thinner) that prevents the formation of blood clots. In the Einstein PE trial, the efficacy and safety of Xarelto was compared to the standard treatment of warfarin and enoxaparin.  Xarelto was shown to be just as effective as the standard treatment and potentially safer.  In the Einstein trial, it was shown that there were more incidents of major bleeding in patients given the standard treatment compared to those that were given Xarelto. These findings suggest that Xarelto may have an improved benefit-risk profile compared to the standard treatment of warfarin and enoxaparin.