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