VENOUS

THROMBOEMBOLISM AND
PULMONARY
HYPERTENSION
ADEVA, Anton Faisad MENGUITA, Kristia Katrina
ALI, Allayzah Ashley NEMENO, Jezaryka Xea Kristah
ESCOLANO, Abegail NOGOY, Michelle
JAPUZ, Garneth RACMAN, Haifa
SANGGACALA, Sonaya
GUIDE
QUESTIONS
 01
Epidemiology of Venous
Thromboembolism
Definition and Epidemiology
 What is Venous Thromboembolism?

Venous thromboembolism (VTE) encompasses deep-venous thrombosis

(DVT) and pulmonary embolism (PE) and causes cardiovascular death,
chronic disability, and emotional distress.

In the United States there are an estimated 100,000–180,000 deaths

attributed annually to PE.
 03
Clinical risk factors for
VTE/PE and other
inflammation linked
conditions that can
trigger DVT or PE
 Clinical Risk Factors
Common comorbidities include cancer, obesity, cigarette smoking, systemic
arterial hypertension, chronic obstructive pulmonary disease, chronic kidney
disease, long-haul air travel, air pollution, estrogen-containing
contraceptives, pregnancy, postmenopausal hormone replacement, surgery,
and trauma. Sedentary lifestyle is increasingly prevalent. A Japanese study
found that each 2 h per day increment of television watching is associated
with a 40% increased likelihood of fatal PE.
 04
Pathogenesis of
Thrombosis in COVID
19 patient
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 05
What are the pathophysiologic abnormalities of
VTE
MC: arterial hypoxemia and increased alveolar-arterial O2
tension gradient = Inefficient oxygen transfer

Increased pulmonary vascular resistance

Impaired gas exchange
Alveolar hyperventilation
Increased airway resistance
Decreased pulmonary compliance
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Classification: Pulmonary embolism and Deep vein
thrombosis
 CLASSIFICATION OF PULMONARY
EMBOLISM
MASSIVE SUBMASSIVE LOW RISK
(High Risk) (Intermediate Risk)
5-10% 20-25% 65-75%
Extensive thrombosis of at least RV dysfunction Excellent prognosis
half of pulmonary vasculature Normal systemic arterial
Systemic hypotension pressure
Extensive thrombosis Right heart failure
★ Cardiac markers
Hallmarks: ○ Troponin
★ Dyspnea
★ Syncope
★ Hypotension
★ Cyanosis

Cardiogenic shock
Multiorgan failure
 Lower Extremity DVT Upper Extremity DVT Superficial venous thrombosis

Begins in the calf Pacemakers Erythema

➔ Proximally Cardiac defibrillators Tenderness
◆ Popliteal Indwelling central venous Palpable cord
◆ Femoral catheter
◆ Iliac veins

10x more common Likelihood=Diameter Risk of extension

CLASSIFICATION OF DEEP VEIN THROMBOSIS

 07
Why is PE considered a “ Great Masquerader”?
 08
DISCUSS WELLS POINT SCORE
BASED ON CLINICAL FINDINGS
Escolano, Abegail A.
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 09
DISCUSS THE DIFFERENTIAL
DIAGNOSIS OF PE AND DVT
Escolano, Abegail A.
DIFFERENTIALS
● Sudden, severe calf discomfort suggests a ruptured Baker’s cyst.
● Fever and chills usually herald cellulitis rather than DVT. Physical findings, if
present, may consist only of mild palpation discomfort in the lower calf.
● Massive DVT often presents with marked thigh swelling, tenderness, and
erythema.
● Recurrent left thigh edema especially in young women raises the possibility
of May- Thurner syndrome, with right proximal iliac artery compression of
the left proximal iliac vein.
● If a leg is diffusely edematous, DVT is unlikely.
● More probable is an acute exacerbation of venous insufficiency due to
postthrombotic syndrome.
● Upper extremity venous thrombosis may present with asymmetry in the
supraclavicular fossa or in the circumference of the upper arms.
DIFFERENTIALS
● Pulmonary infarction usually indicates a small PE. This condition is
exquisitely painful because the thrombus lodges peripherally, near the
innervation of pleural nerves.
● Nonthrombotic PE etiologies include fat embolism after pelvic or long bone
fracture, tumor embolism, bone marrow, and air embolism.
● Cement embolism and bony fragment embolism can occur after total hip or
knee replacement.
● Amniotic fluid embolism occurs when fetal membranes leak or tear at the
placental margin.
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 10
WHAT ARE THE DIFFERENT NON
IMAGING MODALITIES IN THE
DIAGNOSIS OF DVT?
Escolano, Abegail A.
Non-imaging modalities in the diagnosis of DVT
Blood Tests
● Quantitative plasma d-dimer enzyme-linked immunosorbent assay
(ELISA)
❖ Increased
❖ Breakdown of fibrin by plasmin
❖ >80% for DVT and >95% for PE sensitivity.
❖ “rule out” test for PE
❖ Not specific
❖ Increase in patients with myocardial infarction, pneumonia, sepsis,
cancer, the postoperative state, and those in the second or third
trimester of pregnancy.
Non-imaging modalities in the diagnosis of DVT

Elevated cardiac biomarkers

● Serum troponin and plasma heart type fatty acid–binding protein levels
increase because of RV microinfarction. Myocardial stretch causes release
of brain natriuretic peptide or NT-pro-brain natriuretic peptide.

Electrocardiogram
● S1Q3T3 sign
● Specific but insensitive
● RV strain and ischemia, T-wave inversion in leads V1 to V4.
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What are the different Non-invasive
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and Invasive imaging diagnostic

modalities in VTE?
Non-invasive Imaging Modalities
VENOUS ULTRASONOGRAPHY
● relies on loss of vein compressibility as the primary diagnostic criterion for DVT
● thrombus is directly visualized
○ appears homogeneous and has low echogenicity
● vein appears mildly dilated, and collateral channels may be absent
Non-invasive Imaging Modalities
VENOUS ULTRASONOGRAPHY
● relies on loss of vein compressibility as the primary diagnostic criterion for DVT
● thrombus is directly visualized
○ appears homogeneous and has low echogenicity
● vein appears mildly dilated, and collateral channels may be absent

CHEST CT
● with contrast is the principal imaging test for the diagnosis of PE
● provides an excellent four-chamber view of the heart
Non-invasive Imaging Modalities
CHEST ROENTGENOGRAPHY
● normal or nearly normal chest x-ray results in PE
● if with abnormalities;
○ Westermark’s sign
■ focal oligemia
○ Hampton’s hump
■ peripheral wedge-shaped density usually located at the pleural base
○ Palla’s sign
■ enlarged right descending pulmonary artery
Non-invasive Imaging Modalities
LUNG SCANNING
● second-line diagnostic test for PE
● used mostly for patients who cannot tolerate intravenous contrast

MAGNETIC RESONANCE (MR) (CONTRAST-ENHANCED) IMAGING

● MR venography with gadolinium contrast is an excellent imaging modality to
diagnose DVT
● MR pulmonary angiography may detect large proximal PE but is not reliable for
smaller segmental and subsegmental PE
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 14
Discuss the different anticoagulants use in PE
JEZARYKA XEA KRISTAH N.
NEMENO
ANTICOAGULANTS
1. UNFRACTIONATED HEPARIN
➔ UFH binds to and accelerates the activity of antithrombin, thus preventing additional
thrombus formation.
➔ UFH is dosed to achieve a target activated partial thromboplastin time (aPTT) of 60–80 s.
➔ Use an initial bolus of 80 U/kg, followed by an initial infusion rate of 18 U/kg per h in
patients with normal liver function.
1. LOW MOLECULAR WEIGHT HEPARIN
➔ These fragments of UFH exhibit less binding to plasma proteins and endothelial cells
and consequently have greater bioavailability, a more predictable dose response, and a
longer half-life than UFH.
ANTICOAGULANTS
3. FONDAPARINUX
➔ An anti-Xa pentasaccharide, is essentially an ultra-low-molecular-weight heparin.
➔ It is administered as a weight-based once-daily subcutaneous injection in a prefilled syringe.

4. WARFARIN (Dosing Adjustment)

➔ The dose of warfarin is usually targeted to achieve a target international normalized ratio
(INR) of 2.5, with a range of 2.0–3.0.
➔ Centralized anticoagulation clinics have improved the efficacy and safety of warfarin
dosing.
ANTICOAGULANTS
ANTICOAGULANTS
3. NOVEL ORAL ANTICOAGULANTS
➔ Are administered in a fixed dose
➔ Establish effective anticoagulation within hours of ingestion,
➔ Require no laboratory coagulation monitoring and no restriction on eating green leafy
vegetables, and have few drug-drug interactions.
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Comp;ications of anticoagulants
JEZARYKA XEA KRISTAH N.
NEMENO
COMPLICATIONS
Excessive bleeding is the most common reaction. It can occur in a variety of ways, including:
○ Heavy periods
○ Bloody or discolored urine or feces
○ Nosebleeds
○ Bleeding gums
○ Prolonged bleeding from a cut
● The presence of blood thinners in your system can increase your risk of internal bleeding after
an injury.
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PAH development is influenced by:
● Vasoconstriction
● vascular proliferation
● Thrombosis
● inflammation
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STEPWISE
APPROACH TO
DIAGNOSING PH
RACMAN, Haifa H.
● Pulmonary Function and Lung imaging
● Sleep Studies
● Assessment of Pulmonary Arterial Thrombosis
● Serology
● Invasive cardiopulmonary hemodynamics
 PULMONARY FUNCTION & LUNG IMAGING

★ In PAH, isolated reduction in diffusing capacity of lungs for

carbon monoxide (DLCO) is a CLASSICAL FINDING
★ CT Scan - provides useful information, particularly enlargement of
the main pulmonary artery, right ventricle and atria, as well as
peripheral pruning of small vessels
 SLEEP STUDIES

Nocturnal desaturation is COMMON finding, even in the absence

of sleep-disordered breathing
 ASSESSMENT OF PULMONARY
ARTERIAL THROMBOSIS
★ Chronic thromboembolic pulmonary hypertension (CTEPH)
○ It is a specific PH subtype characterized by vascular fibrosis
and arterial microthrombus.
○ Ventilation-perfusion (V/Q) scanning - primary test to screen
and diagnose CTEPH
○ CT angiography - commonly used to stage anatomic
thromboembolic burden, which may be ultimately necessary to
determine operative candidacy.
○ Pulmonary angiography - definitive diagnostic procedure
 SEROLOGY

➔ HIV test
➔ Antinuclear antibodies
➔ Rheumatoid factor and anti-Scl-70 antibodies
➔ Liver function
➔ Brain natriuretic peptide (BNP) and the N-terminus of its pro-peptide
(NT-proBNP)
◆ Biomarker for assessing treatment response
INVASIVE CARDIOPULMONARY
HEMODYNAMICS
WHO PH Clinical Group:
Group 1: Pulmonary
Arterial Hypertension
Group 2: PH from left
heart disease
Group 3: PH from
primary lung disease
and sleep-disordered
breathing
Group 4: Chronic
thromboembolic
pulmonary hypertension
Group 5: Selected (rare
or miscellaneous)
causes of PH
➔ Right heart catheterization - gold standard to both establish the
diagnosis of PH
➔ Vasoreactivity testing
◆ Should be reserved mainly for patients with idiopathic or
hereditary PAH.
◆ Inhaled nitric oxide (NO), or inhaled epoprostenol are preferred
for testing
◆ (+) pulmonary vasodilator response
● Defined as a decreased in mPAP by ≥10 mmHg to an
absolute level ≤40 mmHg without a decrease in CO.
○ Calcium channel blockers as long-term treatment.
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Thank you.
 REFERENCES
● Harrison's Principles of Internal Medicine,
19th Edition