DVT, Pulmonary EmbolismDVT, Pulmonary Embolism

Rabih R. Azar, MD, MSc, FACCRabih R. Azar, MD, MSc, FACC

Director of Cardiovascular ResearchDirector of Cardiovascular Research

Hotel Dieu de France HospitalHotel Dieu de France Hospital

Associate Professor of MedicineAssociate Professor of Medicine

Saint Joseph University School of MedicineSaint Joseph University School of Medicine

Hypercoagulable States Associated with DVT

Symptoms, Signs and Diagnosis of DVT

- Leg pain

- Most commonly:

- mild discomfort on palpation of the lower calf

- palpation of a venous cord

- increase in the temperature of the calf

- presence of non pitting edema

- Homan’s sign

- Blood tests:

- Increased d-dimers

- Imaging modalities:

- Doppler of lower extremities

Pathophysiology of Pulmonary Embolism (1)

• Obstruction of pulmonary vessel

• Increase in pulmonary artery pressure

• Release of vasoconstricting compounds (serotonin)

• Reflex pulmonary vasoconstriction

• Hypoxemia

• Further increase in pulmonary vascular resistance and pulmonary hypertension

• Dilatation of right ventricle

• Vascular obstruction of pulmonary artery

• Ventilation without perfusion = increase alveolar dead space = shunt = hypoxemia

• Bronchoconstriction and increase airway resistance (due to secretion of vaso and broncho active substances such as serotonin)

• Alveolar hyperventilation due to reflex stimulation of irritant receptors = hypocapnia

Pathophysiology of PE (2)

Hemodynamic Consequences of PE

Nonimaging Diagnostic Methods in PE

• Plasma D-Dimers ELISA

– Fibrin clot break-down

– Sensitive but not specific

– Sensitivity 96.4%, neg. predictive value 99.6%

– Levels are increased: post op (1 week), MI, sepsis, cancer, any systemic illness

• BNP

– Increases in severe PE; not diagnostic

• Troponin

– Increases in severe PE; not diagnostic

• Arterial blood gases– Usually hypoxemia hypocapnia

– However, not sensitive and not specific

– In the PIOPED study: no difference between the average Pa02 among those with and those without PE (70 and 72 mm Hg)

– In the subset of angiographically proven PE but no prior cardiopulmonary disease, 26% had a Pa02 > 80 mm Hg

• Electrocardiogram– Sinus tachycardia, minor ST and T waves abnormalities or normal = most frequent

senario

– Less common but useful findings: negative T waves V1-V4 (RV ischemia), S1Q3T3 complex, incomplete or complet RBBB

– Help exclude other conditions such as acute MI

Other Nonimaging Tests in PE

• Chest X-Ray

– Normal = most common

– Focal oligemia = massive central embolic obstruction

– Peripheral wedge-shaped density above the diaphragme

– Distension of one of the pulmonary arteries

• Multiplanar Chest CT

– Most sensitive exam. Is now the standard for diagnosis of PE

– Include scanning of the venous system from the popliteal veins to the subsegmental pulmonary arteries

• Lung Scan

– Second choice imaging test, reserved for patients with renal insufficiency, contrast allergy or pregnancy

– Normal ventilation perfusion study; ventilation perfusion mismatch = high probability for PE

• Pulmonary Angiography

– Reserved for patients in who intervention is planned, such as suction catheter, embolectomy, mechanical clot fragmentation or catheter-directed thrombolysis

Imaging Methods in the Diagnosis of PE

Diagnostic Strategy

• Evidence of DVT or predisposing factors for DVT

• Evidence of acute right sided heart failure:

– Distended neck veins

– S3 gallop

– Right ventricular heave

– Clear lungs

• Echocardiographic finding of right ventricular dilatation or hypokinesis

• ECG evidence of acute cor pulmonale manifested by a new S1Q3T3 pattern, new RBBB or right ventricular ischemia

Characteristics Associated With Cardiogenic Shock Secondary to Massive PE

Indications for Inferior Vena Cava Interruption

• Major hemorrhage that precludes anti-coagulation

• Recurrent PE despite well-documented anti-coagulation

– Duration of anti-coagulation after DVT/PE

– DVT or PE in the presence of major transient risk factor without a thrombophilia risk: 3-6 months of anti-coagulation

– DVT or PE related to thrombophilia or a persistent underlying thrombotic risk (ie: cancer…) should receive long-term therapy (at least 1 year and likely indefinitely).

– Prevention of DVT/PE

– LMHW

– Low dose coumadin

– Subcutaneous unfractionated heparin

– Direct thrombine inhibitors

– Devices that perform intermittent pneumatic compression of the lower extremities

COR PULMONALE

DILATATION/HYPERTROPHY OR RIGHT VENTRICLE SECONDARY TO LUNG DISEASE (PARENCHYMAL OR

VASCULAR)

MAIN FEATURE: THE PRESENCE OF PULMONARY HYPERTENSION

Etiology of Chronic Cor PulmonaleDiseases Leading to Hypoxic Vasoconstriction 

Chronic bronchitis Chronic obstructive pulmonary disease Cystic fibrosis Chronic hypoventilation   Obesity   Neuromuscular disease   Chest wall dysfunction Living at

high altitudes

Diseases That Cause Occlusion of the Pulmonary Vascular Bed  Recurrent pulmonary thromboembolism Primary pulmonary hypertension Venocclusive disease Collagen vascular disease Drug induced lung disease

Diseases That Lead to Parenchymal Disease  Chronic bronchitis Chronic obstructive pulmonary disease Bronchiectasis Cystic fibrosis Pneumoconiosis Sarcoid Idiopathic pulmonary fibrosis

Pathophysiology

1- Pulmonary hypertension

2- Dilation of RV

3- Decrease in cardiac output

4- Na and water retention

Signs

o Lungs: signs of the underlying disease.

oHeart: dilated RV: parasternal lift, Harzer sign, pulmonary systolic click, increase in intensity of TR murmur with inspiration (Carvallo’s sign)

o Jugular venous distension, hepatomegaly, oedema

Diagnosis of Cor Pulmonale

• ECG: p pulmonale, RVH, right axis deviation

• Echo: RV dilation, pulmonary hypertension, normal LV

• Chest CT scan: underlying pulmonary disease