Topic I Pulmonary Embolism
Pulmonary embolism is a highly questioned topic on USMLE Step 2 and Step 3. Many students have questions and concerns regarding :
1. Stable vs. Unstable PE. Diagnosis/ clinical scenarios
2. Acute management of stable vs. unstable Pulmonary embolism
3. Indications for IVC filter ( Greenfield filter)
4. Duration of anticoagulation
5. Hypercoagulability work-up
We will discuss these here in three parts and self assessment questions will follow after the discussion.
Chapter I – Clinical scenarios – Acute PE.
1. Pulmonary embolism can manifest in several ways. You need to familiarize yourself with various clinical scenarios associated with PE that can be often tested on the exam. Commonest symptoms would be chestpain and/ or shortness of breath. But other scenarios that can be tested are : ( You should consider and rule out the possibility of PE in the following scenarios)
a) Acute onset atrial fibrillation in an immobilized hospitalized patient.
b) Shock with no other obvious causes in a patient with risk factors for PE
( Obstructive shock – understand that the embolus can be massive and occlude the right ventricular outlet i.e; pulmonary artery there by preventing filling of the left heart leading to shock)
c) Persistent tachycardia in a patient with risk factors for PE.
d) Hypoxemic respiratory failure with increased A-a ( alveolar-arterial gradient)
e) Sudden right ventricular strain pattern on the EKG ( Typical S1Q3T3 pattern on EKG -sudden onset).
f) Pumonary Hypertension ( If chronic and no other etiology, suspect and rule out chronic thromboembolism in patients with risk factors for PE)
There are several other scenarios a PE can present in a hospitalized patient. However, the above scenarios are commonly asked on the exam. In the self-assessment questions at the end of the section, we will give you sample questions for some of these scenarios.
a) In an inpatient with acute onset atrial fibrillation – you need to control the rate with drugs like beta blocker or diltiazem but you must also consider the differential diagnosis regarding the etiology of afib such as hypoxia, electrolyte abnormalities, acute MI, valvular diseases, accelerated hypertension, hyperthyroidism and congestive heart failure. It is important to know the etiology so that you can treat the underlying issue that led to afib. Controlling the rate alone in afib is not enough , you must also address the reversible etiology so as to prevent recurrence of afib.
When you consider hypoxia as the cause, the evidence can be obtained by pulse oximetry which shows Sao2 usually less than 90 – now, you need to consider the etiology of hypoxia – is it a hypoventilation as in COPD or is it a deadspace such as in pulmonary embolism or is it shunting as in collapse, pneumonia or ARDS? Such information can be obtained by ordering initial tests such as arterial blood gases and chest x-ray. Calculate the A-a gradient from the blood gases. ABGs give important clues – presence of hypercapnia usually indicates COPD/ opiod overdose etc as the causes of hypoxia. Presence of hypocapnia with low po2 and increased A-a gradient goes more in favor of pulmonary embolism.
If chest x-ray is normal but A-a gradient is increased on the ABGs, you should question yourself on what could be possibly causing the gradient with out any evidence of obvious disease on the CXR. This most likely indicates underlying pulmonary embolism in which case you need to pursue further tests to diagnose it such as V/Q scan or Spiral CT scan. Such an analytical approach will allow you to choose the correct diagnosis.
b) Shock – shock is mainly of four types such as Hypovolemic, cardiogenic. distributive and obstructive. Understanding this simple basic pathophysiology behind shock can help you diagnose the etiology of shock and there by, institute life saving therapy.
Pulmonary embolism can cause obstructive shock i.e; hemodynamically unstable PE. This is also referred to as Acute corpulmonale ( Acute right ventricular failure). Diagnosing PE as the cause of shock is very important because immediate thrombolysis can lyse the thrombus that is obstructing the right ventricular outlet there by, restoring left ventricular filling and the blood pressure. Hence, it is a life saving decision to give thrombolytics in a hemodynamically unstable PE.
c) In any patient with persistent tachycardia with out obvious causes, one should consider if this patient is at risk for PE. If the patient has risk factors for PE, then a v/q scan or spiral CT must be obtained to rule out PE.
d) As mentioned above, hypoxemic respiratory failure in the presence of normal chest x-ray and increased A-a gradient on the ABGs strongly suggests PE as a possiblity.
e) Acute right ventricular strain can be presented to you in the form of an EKG with a typical S1Q3T3 pattern on the EKG or ST elevation in I or t-inversions in lead III. Always, it is important to rule our right ventricular MI or ischemia in these cases because such an MI can also cause similar changes. Obtaining cardiac enzymes is helpful to consider acute MI when there is elevated troponin but it should be remembered that a massive PE can also cause some elevation in troponin. So, best test in such a scenario where there is acute right ventricular strain pattern on the EKG would be a 2D-Echocardiogram. 2D-Echo will help you see wall motion abnormalities – if only some or single segment of the right ventricle wall are hypokinetic, it favors right ventricular MI. If the entire right ventricle is hypokinetic, it goes more in favor of Pulmonary embolism ( imagine a massive clot obstructing the right ventricle outlet, obviously, the entire right ventricle will not move – seen as global hypokinesis of RV on the 2D ECHO)
The above mentioned are some unique confusing scenarios in pulmonary embolism presentation. In the next chapter, we will discuss the diagnosis and management of stable vs. unstable PE
Self Assessment Questions:
1) A 75 year-old man with history of hypertension presents to the emergency room with complaints of shortness of breath and palpitations. His vital reveal a heart rate 142/min, blood pressure 130/86, temperature 98.6 and oxygen saturation of 89% on room air. On auscultation, there are no rhonchii or crepitations, the heart rate was irregular and rapid with out any murmurs. The patient is placed on oxygen by nasal cannula. An urgent EKG is obtained which reveals rapid atrial fibrillation with no evidence of significant ST-T changes. The patient is started on diltiazem. Chest x-ray is normal and a brain natriuretic peptide is 80ng/L. Electrolytes, TSH and complete blood count are with in normal limits. Cardiac enzymes are drawn. Arterial blood gases reveal a pH of 7.48, po2 of 58, pco2 of 20 on room air ( Fio2 of 21%). The next step in establishing the etiology of his atrial fibrillation :
A) Cardiac catheterization
B) Spiral CT scan of the chest
C) Venos doppler of lower extremities
D) 2D Echocardiogram
2) What is the most likely etiology of atrial fibrillation in Case 1?
A) Acute ST elevation MI
B) Acute pulmonary embolism
D) COPD exacerbation
E) Congestive heart failure
3) A 65 year-old man with history of recently diagnosed metastatic colon cancer being treated with chemotherapy is admitted to the hospital with constipation and vomiting. His colon cancer was diagnosed by colonoscopy 2 months ago when he presented with massive GI bleeding. At this admission, patient is diagnosed with bowel obstruction secondary to descending colon cancer and underwent a palliative left hemicolectomy to provide symptomatic relief. He has no occult or gross GI bleeding at this time. On the sixth post-operative day, you are called by the nurse because the patient’s blood pressure is 80/40. His heart rate is 82, respiratory rate 24 and temperature of 100.6. The patient is given Normal saline bolus. A CXR is normal. EKG reveals a prominent S wave in lead I, a Q wave and inverted T wave in lead III. Of note, a pre-operative EKG was completely normal. First set of cardiac enzymes are negative. A bedside 2D echo reveals global hypokinesis of the right ventricle. A repeat blood pressure obtained after normal saline bolus is still low at 70/40. The most likely etiology of the shock in this patient is :
B) Septic shock
C) Acute myocardial infarction leading to cardiogenic shock
D) Acute pulmonary embolism
E) Tension Pneumothorax
4) Most important next step in treating this patient’s shock?
A) Continued fluid boluses
B) Antibiotics and pressor support with dopamine
C) Intra-aortic balloon counter-pulsation followed by urgent cardiac catheterization.
D) Anticoagulation with heparin
E) Tissue plasminogen activator ( tpA)
G) Chest tube placement.
H) Inferior vena cava filter
5) The patient was appropriately treated. The discharge recommendations should include :
A) Inferior venacava filter
B) Life-long low-molecular weight heparin
C) Life-long coumadin
D) Hypercoagulability testing
E) Compression stockings
Q1) Ans. D
– 2D echocardiogram in this case will help to evaluate for different etiologies of atrial fibrillation such as acute MI, acute PE and valvular heart disease. From the question, we understand that hypoxia could have possibly initiated the atrial fibrillation. A normal CXR rules out gross lung pathologies such as emphysema, pneumothorax, ARDS, pulmonary edema and pneumonia which could be various etiologies of hypoxia. However, pulmonary embolism and acute MI can not be readily eliminated from a normal Chest X-ray. Hence, a quick bed side echo should be considered. If the Echo reveals segmental hypokinesis of right ventricle, this favors the diagnosis of Acute MI where as if it revealed a global hypokinesis of the right ventricle, it would more favor a diagnosis of acute pulmonary embolism.
– Spiral CT scan is a close distractor here since one may choose this considering the strong diagnosis of pulmonary embolism in the above case. However, spiral CT scan will help you to confirm or rule out PE but it does not help you to evaluate for other possible etiologies of atrial fibrillation at the same time. Hence, 2D echo is a superior initial test in the above case.
– Urgent cardiac catheterization should be performed in the presence of ST elevation MI. There is no evidence of ST elevation in the above case.
– Venos doppler of lower extremities should be considered once we are more certain that PE is the most likely etiology and hence, is not an initial test.
– D-Dimer can be used as a screening test for PE when the pre-test probability is low. A low D-dimer combined with a low pre-test probability of PE can be used to rule out PE. While a low D-dimer < 500 may exclude PE, a higher d-dimer is non-specific and does not differentiate between other causes of thromosis such as DIC, presence of arterial thrombi, PE and DVT.
The presence of Hypoxia, hypocapnia and increased A-a gradient (about 70) with a normal CXR findings in the above question indicates that an Acute Pulmonary Embolus is the most likely diagnosis.
Choice A – is not the answer because the EKG did not reveal any ST elevations.
Choice C – is not the answer since the physical exam revealed normal breath sounds and CXR was normal.
Choice D – is not the answer since the ABGs in the above patient reveal Hypocapnia and increased A-a gradient. Hypercapnia secondary to acute CO2 retention is often a feature of COPD exacerbation. The A-a gradient is usually normal in COPD except in emphysema.
Choice E – a normal CXR, absence of significant CHF physical findings and a BNP ( brain natriuretic peptide) less than 100 virtually rules out Congestive Heart Failure.
Pulmonary embolism is a common complication that can occur in post-surgical patients, usually after post-operative day 5.
The patient has a very high risk profile for pulmonary embolism. The clinical probability of the PE from his history is extremely high – age > 60 years, cancer, immobilization and surgery with in last few days are well known risk factors for pumonary embolism which this patient clearly possess. Also, sudden appearance of right ventricular strain pattern (S1Q3T3) and a classic acute corpulmonale findings on 2D Echo suggests that PE is the most underlying etiology for this patient’s shock. ( Obstructive type shock)
Although. all the other choices are potential causes for shock in the above patient, their probability can be reduced by considering and analyzing important clues in the question.
– Choice A not correct – Failure to respond to normal saline indicates that this is not hypovolemia. Also, hypovolemic shock should not produce acute right ventricular strain on the EKG or hypokinesis on the 2D Echo.
– Choice B not correct – Fever may suggest sepsis but it needs to be remembered that fever can also be seen with PE. Also, septic shock should not produce acute right ventricular strain on the EKG or acute right ventricular hypokinesis alone on the 2D Echo.
– Choice C not correct – Acute MI is a possiblity but it usually produces segmental hypokinesis rather than global hypokinesis on 2D Echo. The cardiac enzymes are also negative.
– Choice E not correct since CXR was normal.
Pulmonary embolectomy is the correct choice. In scenarios where thrombolysis is contraindicated, embolectomy is used for patients with PE who are hypotensive despite supportive measures (persistent systolic BP ≤ 90 mm Hg after fluid therapy and O2) i.e; hemodynamically unstable PE.
The patient has obstructive shock and obstruction should be removed urgently to restore the blood pressure. Clot can be lysed by thrombolysis or mechanically with embolectomy. The patient had GI bleeding in last 6 months which is an absolute contraindication to thrombolysis and also, surgery 6 days ago which is a relative contraindication for tpa. Hence, embolectomy is the choice.
Choice A – not correct – this is the treatment of hypovolemic shock. Hypovolemic shock is unlikely because of the above mentioned reasons in this patient.
Choice B – not correct – this is the treatment of septic shock. Septic shock is unlikely because of the above mentioned reasons in this patient.
Choice C – not correct – this is the treatment of cardiogenic shock. Cardiogenic shock is unlikely because of the above mentioned reasons in this patient.
Choice D – not correct – this is the treatment of stable pulmonary embolism. In unstable pulmonary embolism, clot obstruction must be relieved rapidly with thrombolysis or embolectomy. If tpa is planned, Heparin should only be started 24 hours after thrombolytics. Heparin will help in preventing further clot extension or further embolism but will not help in immediately treating the obstructive shock.
Choice E – not correct – The patient has contraindications for tpa ( thrombolytics). Absolute contraindications to thrombolytics include prior hemorrhagic stroke, ischemic stroke within 1 yr, active external or internal bleeding from any source, intracranial injury or surgery within 2 mo, intracranial tumor, GI bleeding within 6 mo, and CPR.
Relative contraindications include recent surgery (≤ 10 days), hemorrhagic diathesis (as in hepatic insufficiency), pregnancy, current use of anticoagulants and an INR > 2, punctures of large noncompressible veins (eg, subclavian or internal jugular veins), recent femoral artery catheterization (eg, ≤ 10 days), peptic ulcer disease or other conditions that increase the risk of bleeding, and severe hypertension (systolic BP > 180 or diastolic BP > 110 mm Hg).
Choice G – not correct – This is the treatment for tension pneumothorax. Tension pneumothorax is an important cause of obstructive shock but a normak CXR rules it out.
Choice H – not correct – this is the treatment for pulmonary embolism or DVT in the presence of contraindications to anticoagulation with heparin or warfarin or in cases of warfarin failure.
Indications for IVC filters:
– Contraindications to anticoagulation
– Recurrent DVT (or pulmonary emboli) despite adequate anticoagulation ( i.e; warfarin failure)
– In patients with low cardio-pulmonary function and extensive DVT ( extending in to inferior venacava) – where any additional small pulmonary emboli may compromise their cardio-pulmonary status further.
LMWH is superior to warfarin in preventic venos thromboembolism in cancer patients. Cancer is a hypercoagulable condition and this patient hence, requires life-long anticoagulation.
Choice A is incorrect. IVC filter is indicated for thromboembolism prophylaxis in the presence of absolute contraindication to anticoagulation. The patient has no active bleeding. Also, IVC filter can only protect against PE but not against DVT .
Choice C is incorrect because LMWH is superior to warfarin in cancer patients.
Choice D is incorrect – the patient already has a known hypercoagulable state which is a cancer and requires life long anticoagulation with LMWH. This is not a idiopathic PE where full hypercoagulability work-up would be warranted.
Choice E is incorrect – compression stockings are more effective for preventing calf than proximal DVT and thus, provides inadequate prevention. Also, they are contraindicated in patients with active DVT or those with possible occult DVT as compression can dislodge the clots and lead to PE in those with active DVT.