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04/11/2023
Case presentation
Dr. Yaser Mufti MD Cardiology Trainee
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CASE STUDYA 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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Family historyNo family history could be elicited regarding DVT or
phelbitits
Personal historyNo history of any addiction /drug allergy
Past history She has no significant past medical history except NVD at home wk backTreatment historyNo specific medication usage history
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Her BP at was 80/60mmHg , temp N HR 147 BPMRR 40 PM ,oxygen saturation of 90 %She was pale , diaphoretic, and unable to
speak full sentenceHer JVP was not recorded
General examination
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Systemic examinationCardiac exam shows tachy cardia, a fixed
wide split of the second heart soundPulmonary exam non specific, NBVBAbd: soft, no liver or spleen palpableHer extremities were cold with Weak
peripheral pulses. Rest of examination normal
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Differential DiagnosisPulmonary EmbolismCongestive heart failure Post Partum
Cardiomyopathy MyocarditisATN due to PPH
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ECG sinus tachycardia at a rate of
147 BPM, Right Axis deviation 90+ST , T wave changes
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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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Echo FindingsEmergency Short Echo: (images not
available)Dilated RV(49 MM) with moderately severe
Systolic dysfunction with good kinesis at RV apex
Normal LV functionTR ++, TVPG 14mmHgNormal Mitral and AV. IAS appears intact
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ManagementOxygen 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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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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Pulmonary Embolism
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Virchow triadIntimal vessel injuryStasishypercoagulability
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PE: A Clinical ChallengeCommon: 250,000 cases/yearMimics many other illnessesPotentially fatal (15%)Treatment potentially dangerousNo single reliable diagnostic testUnder- and over-diagnosed
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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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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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Pathyphysiology
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Clinical Classification of PE Massive PE
Submassive PE
Small to moderate PE
Systolic BP< 90 mmHg,or poor tissue Perfusion Or Mulitsystem organ failure
Plus, Rt.or Lt main Pulmonary Art. Thrombus or high clot burden
Hemodyn. Stable,but mod. To severe RV dysfunction or enlargement
Normal hemodyn
And normal RV Size and function
Thrombolysis Or embolectomy Or IVC filter Plus anticoagulant
Addition of Thrombolysis
Emblectomy or filters remiain controversial
Anticoagulation
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Pulmonary Infarction Often characterized by pleuritic chest pain
and hemoptysisThe 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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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 DICIVDU 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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Clinical PresentationThe 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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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%
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Differential Diagnosis of Pulmonary Embolism
Anxiety, pleurisy, costochondritisPneumonia, bronchitisMyocardial infarctionPericarditisCongestive heart failureIdiopathic pulmonary hypertension
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INVESTIGATIONS
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WELL’s SCORING /GENEVA SCORING
•ECG•CHEST RADIOGRAPH•ECHOCARDIOGRAPHY•V/Q SCANNING•CT ANGIOGRAPHY
•CBC, •ABG’S,•D-DIMER•TROPONIN •BNP
INVESTIGATIONS
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Clinical probability of Risk A Determine probability of PE
LowModerateHigh
Overall clinical impressionModels/scoring systems
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Blood testsTroponin levels
Correlation with ECG and EchoIncrease mortality if positive with Acute P.E
BNPIn Absence of Renal function Marker of RV dystfunction , Predictor of adverse outcome
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ABG;sPE significant HypoxemiaPIOPED, only 26 % of proven PE had
Pao>80mmhgTherefore normal PaO2 can not rule out PEHowever Hypoxia in absence of
cardiopulmonary disease should raise suspicion of PE
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D-DimersIt is a fibrin degradation fragment Occurs
Through fibrinolysisValuable screening test
High sensitivity; low specificity Helpful only if Negative Strong Negative Predictive Value-- Rules out PE
when low probabilitySafe, noninvasiveRapid, inexpensive
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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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Chest Radiography Useful to R/o other causesNon specific findings; pleural Effusion,
atelectasis, consolidationClassic 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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V/Q Lung Scan2nd line investigation methodBeneficial if having normal xrayWho are dye allergic in CTRenal failurePregnancy Normal V/Q Sensitivity 99%
Rules out PEHigh Prob V/Q Specificity 96%
Rules in PEBut, >60% nondiagnosticTakes >2 hr to performNot available at all times
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Ultrasound and PEUS +DVT in 30-50% with PEPositive US—confirms PENegative ultrasound
PE less likely, but not excludedSequential 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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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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CT Angiogram
BenefitsAvailableDirect imageAlternative DxPelvic/leg veins
LimitationsIV contrastExpensivePatient
cooperationUncertain
sens/spec
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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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Pulmonary Angiography
Gold standard but these days not in practice due to availability of CT
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MRI/MRANo radiation or contrast exposureExpensiveNot uniformly availableLimited dataRole not established
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Thrombophilia evaluation
Hypercoagulable states
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Thrombophilia evaluationWhy test for hypercoagulability?
May affect intensity/duration of treatmentFamily counseling about risksIdentify need for prophylaxis in higher risk
situations
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Thrombophilia evaluationTests performed acutely
Leiden Factor V (APC resistance)Prothrombin G20210A mutationIncreased homocysteineAnti-cardiolipin antibodies
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Thrombophilia evaluationConsider testing later
Lupus anticoagulantDecreased Proteins C & SDecreased Anti-thrombin IIIIncreased Factor VIII
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SummaryHave index of suspicion for PEDevelop clinical probabilityInterpret all tests in context of pre-test
probabilitySelectively for thrombophiliaChoose therapy based on clinical status
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TREATMENT
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TREATMENT OF SYMPTOMS:
Bedrest Analgesics Supplemental O2
Therapy
Pulmonary Embolism
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MEDICAL MANAGEMENT:
Anticoagulant Therapy Thrombolytic TherapySurgical Embolectomy
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Duration of anticoagulationIdentified precipitant 3 mosFirst idiopathic episode 6 mosProlonged/indefinite:
2 thrombotic episodes 1 spont. life-threatening episode Anti-phospholipid antibody syndrome, ATIII
deficiency
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Un fractionated Heparin
Continue 4-5d and therapeutic on Warfarin for 2d (INR>2.0)
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ThrombolysisMassive PE
Acute pulmonary hypertensionRV dysfunctionSystemic hypotension
All age groups benefitAddition to Heparin therapyVarious agents appear equivalent
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ThrombectomySurgical or transvenous (catheter)When thrombolytic unsuccessful or
contraindicated, orMassive PE
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Vena Cava FiltersIndications:
Contraindication to anticoagulationRecurrent PE on anticoagulationComplications from anticoagulationMassive PE with poor reserve
Problems with filter thrombosis
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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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Take home messagePe common but overlookHigh suspicion to make diagnosisABG, d-dimer, CT imp diagnostic toolsPrevention is much more important than
treatmentTake home message: for DVT Diagnosis Combine clinical probability, d-dimer, and
ultrasonographyTake home message: for PE diagnosis
Combine clinical score, d-dimer, and CT pulmonary angiography
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Thanks