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TEP

consiste en la oclusion del lecho arterial pulmonar por un trombo (embolo) desprendido desde
alguna parte del territorio venoso

TEP: urgencia cardiovascular comun, que pone en riesgo la hemodinamia del paciente, porque
puede producir una insufic. VD aguda.

TEP-TVP: ETV

La tEP no puede entenderse como una enfermedad independiente de la TVP, sino como una
misma entidad. Por esta razon actualmente se prefiere emplear el termino enfermedad
tromboembolica para resaltar que se trata de manifestaciones de la misma enfermedad

90-95% el origen es una TVP de EEII, generalmente asintomatica.

10-20% de las TVP producen TEP

Dx precoz fundamental, ya que el tratamiento es altamente efectivo, restableciendo flujo de


arterias ocluidas, previniendo recurrencias precoces morales.

CLASIFICACION

A pesar de que es llamativo la clasificacion de TEP, en si no tiene incidencia absoluta como tal en
las comorbilidades del paciente y solo se centra en el Evento embolico en si, asi una TEP aguda NO
MASIVA podria estar asociado a un alto riesgo de complicaciones en un paciente con muchas
comorbilidades, como un EPOC o ICCongestiva.

CLASIFICACION

TEP MASIVO 20%: definicion mas anatomica, refiriendose a obstruccion mayor al 50% de vasos
pulmonares o de dos o mas arterias lobares o basarse en la fx CardioPulm del paciente.

AHA define:

TEP aguda con shock y/o hipotension

PA sistolica menor a 90 al menos 15 min, o que requiere apoyo inotropico, sin que la causa sea
arritmia, hipovolemia, sepsis o disfuncion VI, ausencia de ppulsos, bradicardia produnda (menor a
40 lpm con signos de shock)

- Mortalidad del 52%

- Implica terapia vasopresora


TEP GRAVE: combinacion, inestabilidad hemodinamica (desde hipotension- paro cardiaco)-
mortalidad 30%.

TEP submasivo: hipoquinesia VD por ecocardio sin hipotension ni shock. Mayor mortalidad

Epidemiologia

Tercera causa de muerte CV, luego de CardioP isque y ACV

Hombres>ujeres

Aumenta con edad

Mortalidad 11% primera hora

Difícil de determinar dado que un gran grupo permanece asintomático.

100-200/1000.000 habitantes

317.000 muertes de 454 mill de seis paiss de UE


-34% muere súbita

-59% muere por una EP sin diagnosticar durante la vida

-7% mueren post un correcto diagnostico previo.

>40 años riesgo

Niños 53-57/100.000 por año

Nomenclature — PE can be classified by the following: ●The temporal pattern of


presentation (acute, subacute, or chronic) –

Patients with PE can present acutely, subacutely, or chronically: •Acute –

Patients with acute PE typically develop symptoms and signs immediately after
obstruction of pulmonary vessels. •Subacute – Some patients with PE may also present
subacutely within days or weeks following the initial event. •Chronic – Patients with chronic
PE slowly develop symptoms of pulmonary hypertension over many years (ie, chronic
thromboembolic pulmonary hypertension; CTEPH). An overview of acute and subacute PE
is discussed in this review. The etiology, clinical manifestations, diagnosis, and treatment
of CTEPH are discussed separately. (See "Clinical manifestations and diagnosis of chronic
thromboembolic pulmonary hypertension" and "Overview of the treatment of chronic
thromboembolic pulmonary hypertension".) ●The presence or absence of hemodynamic
stability (hemodynamically unstable or stable) – Hemodynamically unstable and stable PE
(sometimes called massive or submassive, respectively) are defined as the following:
•Hemodynamically unstable PE is that which results in hypotension. Hypotension is
defined as a systolic blood pressure <90 mmHg for a period >15 minutes or that requiring
vasopressors or inotropic support and not explained by other causes including sepsis,
arrhythmia, left ventricular dysfunction from acute myocardial ischemia or infarction, or
hypovolemia. Although hemodynamically unstable PE is often caused by large (ie,
massive) PE, it can sometimes be due to small PE in patients with underlying
cardiopulmonary disease. Importantly, not all patients with massive PE develop
hypotension. (See 'Pathophysiologic response to PE' below.) •Hemodynamically stable PE
is defined as PE that does not meet the definition of hemodynamically unstable PE. There
is a spectrum of severity within this population ranging from patients who present with
small asymptomatic PE to those who present with mild or borderline hypotension that
stabilizes in response to fluid therapy, or those who present with right ventricle dysfunction
(also known as “intermediate” PE). (See "Fibrinolytic (thrombolytic) therapy in acute
pulmonary embolism and lower extremity deep vein thrombosis", section on
'Hemodynamically stable patients'.) The distinction between hemodynamically stable and
unstable PE is important because patients with hemodynamically unstable PE are more
likely to die from obstructive shock (ie, severe right ventricular failure). Importantly, death
from hemodynamically unstable PE often occurs within the first two hours, and the risk
remains elevated for up to 72 hours after presentation [1,2]. (See "Clinical presentation,
evaluation, and diagnosis of the adult with suspected acute pulmonary embolism", section
on 'Hemodynamically unstable patients' and "Fibrinolytic (thrombolytic) therapy in acute
pulmonary embolism and lower extremity deep vein thrombosis", section on
'Hemodynamically unstable patients' and "Overview of the treatment, prognosis, and
follow-up of acute pulmonary embolism in adults", section on 'Prognosis'.) ●The anatomic
location (saddle, lobar, segmental, subsegmental) – Saddle PE lodges at the bifurcation of
the main pulmonary artery, often extending into the right and left main pulmonary arteries.
Approximately 3 to 6 percent of patients with PE present with a saddle embolus [3,4].
Traditionally, saddle PE was thought to be associated with hemodynamic instability and
death. However, retrospective studies suggest that among those diagnosed with a saddle
embolus, only 22 percent are hemodynamically unstable, with an associated mortality of 5
percent [3,4]. Other smaller PE (and occasionally saddle emboli) will move beyond the
bifurcation of the main pulmonary artery to lodge distally in the main lobar, segmental, or
subsegmental branches of the pulmonary artery. Smaller thrombi that are located in the
peripheral segmental or subsegmental branches are more likely to cause pulmonary
infarction and pleuritis (image 1). (See 'Pathophysiologic response to PE' below.) ●The
presence or absence of symptoms (symptomatic or asymptomatic) – Symptomatic PE
refers to the presence of symptoms that usually leads to the radiologic confirmation of PE,
whereas asymptomatic PE refers to the incidental finding of PE on imaging in a patient
without symptoms (eg, contrast-enhanced computed tomography). (See "Clinical
presentation, evaluation, and diagnosis of the adult with suspected acute pulmonary
embolism", section on 'Diagnosis'.)