Dr Yaser Mufti resident Faisalabad institute of Cardiology faisalabad, pakistan

1.  Case presentation
Dr. Yaser Mufti
MD Cardiology Trainee
1/1
7/18/2012

2. CASE STUDY
 A 25 years old young female presented to emergency
complaining of Severe shortness of breath that
began abruptly when went for toilet.
 Associated symptoms included diaphoresis,
palpitation
 One weak back, prior to this event, Patient had
NVD at Home. After 3 days of NVD she has mild
SOB, unnoticed.
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3. Past history
She has no significant past medical history except NVD at home
wk back
Treatment history
No specific medication usage history
Family history
No family history could be elicited regarding DVT or phelbitits
Personal history
No history of any addiction /drug allergy
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4. General examination
 Her BP at was 80/60mmHg , temp N
 HR 147 BPM
 RR 40 PM ,oxygen saturation of 90 %
 She was pale , diaphoretic, and unable to speak full
sentence
 Her JVP was not recorded
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5. Systemic examination
 Cardiac exam shows tachy cardia, a fixed wide split of
the second heart sound
 Pulmonary exam non specific, NBVB
 Abd: soft, no liver or spleen palpable
 Her extremities were cold with Weak peripheral
pulses.
 Rest of examination normal
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6. Differential Diagnosis
 Pulmonary Embolism
 Congestive heart failure Post Partum
Cardiomyopathy
 Myocarditis
 ATN due to PPH
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7.  sinus tachycardia at a rate of 147 BPM,
ECG  Right Axis deviation 90+
 ST , T wave changes
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8.  Her ABG’s
Ph: 7.2, PCO: 30 , PO2 : 171 , K : 3.3 , BE: -13
 Her CBC , Hb 8.9 g/dl, ESR , 56mm/hr, TLC 10200, and
platelet count 208000, other is in normal range
 D dimer report is send but not collected
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9. 7/18/2012 9

10. Echo Findings
 Emergency Short Echo: (images not available)
 Dilated RV(49 MM) with moderately severe Systolic
dysfunction with good kinesis at RV apex
 Normal LV function
 TR ++, TVPG 14mmHg
 Normal Mitral and AV.
 IAS appears intact
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11. Management
 Oxygen
 Heparin 5000 iu bolus iv, 1000 iu /hr
 Inotropic suppor (Dobutamine/Dopamine)
 Plan.
Ct angio /V/Q scan / Lityic therarpy/ Doppler
 Outcomes
Unluckily she couldn’t survive and died after few hours
of admissions
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12. Short comings and Analysis
•We don’t have above mentioned tests availabilities to
make confirm diagnosis
•Can we use Lytic therapy in this patient, without
confirming PE is debatable.
• She should be managed in Full ICU facilities, rather to
mange in only emergency ward.
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13. 7/18/2012 13

14. 7/18/2012 14

15. Virchow triad
 Intimal vessel injury
 Stasis
 hypercoagulability
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16. PE: A Clinical Challenge
 Common: 250,000 cases/year
 Mimics many other illnesses
 Potentially fatal (15%)
 Treatment potentially dangerous
 No single reliable diagnostic test
 Under- and over-diagnosed
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17. Acquired Risk Factors
 Advancing age
 Arterial disease, including carotid and coronary disease
 Personal or family history of VTE
 Recent surgery, trauma, or immobility, including stroke
 CCF/COPD
 Acute infection
 Long- air travel
 Pregnancy, OCP, HRT
 Pacemaker, implantable cardiac defibrillator leads, or
indwelling central venous catheter thromboembolism
 Obesity, Metabolic syndrome
 Cigarette smoking
 Hypertension, Abnormal lipid profile
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18. INHERITED RISK FACTORS
 Hypercoagulable states Factor V Leiden resulting in
activated protein C resistance
 Prothrombin gene mutation 20210
 Antithrombin III deficiency
 Protein C deficiency
 Protein S deficiency
 Antiphospholipid antibody syndrome(Acquired)
 Hyperhomocystenimia
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19. 
Pathyphysiology
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20. Clinical Classification of PE
 Massive PE Systolic BP< 90 mmHg,or  Thrombolysis
poor tissue Perfusion Or  Or embolectomy
Mulitsystem organ failure  Or IVC filter
Plus, Rt.or Lt main  Plus anticoagulant
Pulmonary Art.
Thrombus or high clot
burden
Hemodyn. Stable,but mod.  Addition of Thrombolysis
 Submassive PE To severe RV dysfunction  Emblectomy or filters
or enlargement remiain controversial
 Small to moderate PE Normal hemodyn  Anticoagulation
And normal RV Size and
function
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21. Pulmonary Infarction
 Often characterized by pleuritic chest pain and
hemoptysis
 The embolus usually lodges in the peripheral
pulmonary arterial tree, near the pleura.
 Tissue infarction usually occurs 3 to 7 days after
embolism.
 Sysmptom often includes fever, leukocytosis, elevated
erythrocyte sedimentation rate, and radiologic
evidence of infarction.
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22. Nonthrombotic PE
 They include fat, tumor, air, and amniotic fluid
 Fat embolism ,Usually after bone fractures.
 Air embolus during CV catheter central venous catheter.
 Amniotic fluid embolism , is characterized by
respiratory failure, cardiogenic shock, and DIC
 IVDU sometimes self-inject hair, talc, and cotton that
contaminate the drug they have acquired. These patients
also have susceptibility to septic PE, which can cause
endocarditis of the TV or PV.
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23. Clinical Presentation
The PIOPED study reported the following
incidence of common symptoms of pulmonary
embolism[30] :
• Dyspnea (73%)
• Pleuritic chest pain (66%)
• Cough (37%)
• Hemoptysis (13%) Symptoms
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24. Clinical Signs
• Tachypnea (respiratory rate >16/min) - 96%
• Rales - 58%
• Accentuated second heart sound - 53%
• Tachycardia (heart rate >100/min) - 44%
• Fever (temperature >37.8°C) - 43%
• Diaphoresis - 36%
• S3 or S4 gallop - 34%
• Clinical signs and symptoms suggesting
thrombophlebitis - 32%
• Lower extremity edema - 24%
• Cardiac murmur - 23%
• Cyanosis - 19%
7/18/2012 24

25. Differential Diagnosis of Pulmonary Embolism
 Anxiety, pleurisy, costochondritis
 Pneumonia, bronchitis
 Myocardial infarction
 Pericarditis
 Congestive heart failure
 Idiopathic pulmonary hypertension
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26. 7/18/2012 26

27. INVESTIGATIONS
WELL’s SCORING /GENEVA SCORING
•CBC,
•ABG’S,
•D-DIMER
•TROPONIN
•ECG
•BNP
•CHEST RADIOGRAPH
•ECHOCARDIOGRAPHY
•V/Q SCANNING
•CT ANGIOGRAPHY
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29. Clinical probability of Risk A
 Determine probability of PE
 Low
 Moderate
 High
 Overall clinical impression
 Models/scoring systems
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31. Blood tests
 Troponin levels
Correlation with ECG and Echo
Increase mortality if positive with Acute P.E
 BNP
In Absence of Renal function Marker of RV
dystfunction , Predictor of adverse outcome
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32. ABG;s
 PE significant Hypoxemia
 PIOPED, only 26 % of proven PE had Pao>80mmhg
 Therefore normal PaO2 can not rule out PE
 However Hypoxia in absence of cardiopulmonary
disease should raise suspicion of PE
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33. D-Dimers
It is a fibrin degradation fragment Occurs
Through fibrinolysis
Valuable screening test
 High sensitivity; low specificity
 Helpful only if Negative
 Strong Negative Predictive Value-- Rules out PE
when low probability
 Safe, noninvasive
 Rapid, inexpensive
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34. Electrocardiographic Signs of PE
 Sinus tachycardia
 Incomplete or complete right bundle branch block
 Right-axis deviation
 S wave >1.5 mm in I and aVL
 T wave inversions in leads III and aVF or in leads V1-V4
 S wave in lead I and a Q wave and T wave inversion in
lead III (S1Q3T3)
 QRS axis greater than 90 degrees or an indeterminate axis
 Atrial fibrillation or atrial flutter
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35. Chest Radiography
 Useful to R/o other causes
 Non specific findings; pleural Effusion, atelectasis,
consolidation
Classic sign
 Focal oligemia (Westermark sign) indicates massive
central embolic occlusion.
 A peripheral wedge-shaped density above the diaphragm
(Hampton hump) usually indicates pulmonary
infarction.
 Subtle abnormalities suggestive of PE include
enlargement of the descending right pulmonary artery.
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36. 7/18/2012 36

37. V/Q Lung Scan
 2nd line investigation method
 Beneficial if having normal xray
 Who are dye allergic in CT
 Renal failure
 Pregnancy
 Normal V/Q Sensitivity 99%
 Rules out PE
 High Prob V/Q Specificity 96%
 Rules in PE
 But, >60% nondiagnostic
 Takes >2 hr to perform
 Not available at all times
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38. Ultrasound and PE
 US +DVT in 30-50% with PE
 Positive US—confirms PE
 Negative ultrasound
 PE less likely, but not excluded
 Sequential ultrasound
 Persistently negative ultrasound at 1-2 wks
<2% DVT/PE at 6mos
Hull et al. J. Thromb 1996; 3:5-8.
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39. Echocardiographic Signs of P.E
 Right ventricular enlargement or hypokinesis, especially
free wall hypokinesis, with sparing of the apex (the
McConnell sign)
 Interventricular septal flattening and paradoxical
motion toward the left ventricle, resulting in a D-shaped
left ventricle in cross section
 Tricuspid regurgitation
 Pulmonary hypertension with a tricuspid regurgitant jet
velocity >2.6 m/sec
 Loss of respiratory-phasic collapse of the inferior vena
cava with inspiration
 Direct visualization of thrombus (more likely with
transesophageal echocardiography)
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40. CT Angiogram
 Benefits  Limitations
 Available  IV contrast
 Direct image  Expensive
 Alternative Dx  Patient
 Pelvic/leg veins cooperation
 Uncertain
sens/spec
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41. CT Angiogram
 “CT should not be used alone for
suspected PE, but combining tests
improves accuracy and reduces need for
angiography”
”
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44. Pulmonary Angiography
 Gold standard but these days not in practice due to
availability of CT
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45. MRI/MRA
 No radiation or contrast exposure
 Expensive
 Not uniformly available
 Limited data
 Role not established
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46. Hypercoagulable states
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47. Thrombophilia evaluation
Why test for hypercoagulability?
 May affect intensity/duration of treatment
 Family counseling about risks
 Identify need for prophylaxis in higher risk
situations
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48. Thrombophilia evaluation
Tests performed acutely
 Leiden Factor V (APC resistance)
 Prothrombin G20210A mutation
 Increased homocysteine
 Anti-cardiolipin antibodies
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49. Thrombophilia evaluation
Consider testing later
 Lupus anticoagulant
 Decreased Proteins C & S
 Decreased Anti-thrombin III
 Increased Factor VIII
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50. Summary
 Have index of suspicion for PE
 Develop clinical probability
 Interpret all tests in context of pre-test
probability
 Selectively for thrombophilia
 Choose therapy based on clinical status
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53. Pulmonary Embolism
TREATMENT OF
SYMPTOMS:
 Bedrest
 Analgesics
 Supplemental O2 Therapy
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54. MEDICAL MANAGEMENT:
 Anticoagulant Therapy
 Thrombolytic Therapy
 Surgical Embolectomy
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56. Duration of anticoagulation
 Identified precipitant 3 mos
 First idiopathic episode 6 mos
 Prolonged/indefinite:
 2 thrombotic episodes
 1 spont. life-threatening episode
 Anti-phospholipid antibody syndrome, ATIII
deficiency
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57. Un fractionated Heparin
 Continue 4-5d and therapeutic on
Warfarin for 2d (INR>2.0)
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58. Thrombolysis
 Massive PE
 Acute pulmonary hypertension
 RV dysfunction
 Systemic hypotension
 All age groups benefit
 Addition to Heparin therapy
 Various agents appear equivalent
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60. Thrombectomy
 Surgical or transvenous (catheter)
 When thrombolytic unsuccessful or
contraindicated, or
 Massive PE
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61. Vena Cava Filters
 Indications:
 Contraindication to anticoagulation
 Recurrent PE on anticoagulation
 Complications from anticoagulation
 Massive PE with poor reserve
 Problems with filter thrombosis
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62. Predictors of Increased Mortality
 Hemodynamic instability
 Right ventricular hypokinesis on echocardiogram
 Right ventricular enlargement on echocardiogram or
chest CT scan
 Right ventricular strain on electrocardiogram
 Elevated cardiac biomarkers
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63. Take home message
 Pe common but overlook
 High suspicion to make diagnosis
 ABG, d-dimer, CT imp diagnostic tools
 Prevention is much more important than treatment
 Take home message: for DVT Diagnosis
Combine clinical probability, d-dimer, and
ultrasonography
 Take home message: for PE diagnosis
Combine clinical score, d-dimer, and CT
pulmonary angiography
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