PULMONARY

EMBOLISM
 What is Pulmonary Embolism?
IT IS A BLOOD CLOT THAT LODGE IN THE LUNG ARTERIES.
THE BLOOD CLOT FORMS IN THE LEG, PELVIC, OR ARM
VEIN, THEN BREAKS OFF FROM THE VEIN WALL AND
TRAVELS THROUGH THE HEART INTO THE LUNG
ARTERIES.
IT FIRST GROW TO A LARGE SIZE BEFORE DETACHING
AND TRAVELING.
PULMONARY EMBOLISM CAN CAUSE DEATH OR CHRONIC
SHORTNESS OF BREATH FROM HIGH LUNG ARTERY
PRESSURE.
 Etiology

Deep Vein Thrombosis

-It is the formation of blood clots(thrombi) in the deep
veins. Thrombi can occur either in the deep leg veins,causing
deep vein thrombosis or in the superficial leg veins .Deep vein
thrombosis causes a little inflammation. The less inflammation
in the thrombus the less tightly the thrombus adheres in the to
the vein wall and more likely it will break loose(becoming an
embolus),travel through the bloodstream,and lodge in the artery
downstream,blocking blood flow.
 Other causes:

Another type of embolus may form from fat

and amniotic fluid
-It can escape into the blood from the bone marrow when a
bone is fractured. An embolus may also form from amniotic fluid
being forced into the pelvic veins during childbirth. However fat and
amniotic fluid emboli are rare. If they form, they usually lodge in the
small vessels such as arterioles and capillaries of the lung, where they
generally cause less damage than blood clots. However if many of
these smaller vessels become obstructed acute respiratory syndrome
(ARDS) and Pulmonary hypertension may develop. Both of these
conditions can lead to respiratory failure, heart failure and shock.
Cancerous Tumor
- Cancerous tumor fragment may break free into the
circulation to form emboli,which, if they are numerous, can
cause pulmonary hypertension as the cancer spreads
throughout the lungs.

Air bubbles
-It may form an emboli and cause pulmonary
embolism after a vein has been exposed to large amounts of
air, as may occur during intravenous infusion of drugs,
nutrients,or fluids.
 Risk Factors

The classical triad of risk factors for the occurrence of

thromboembolic disease proposed by Virchow in 1856local
injury to the vascular wall, increased coagulability, and
circulatory stasis can explain most cases of deep vein thrombosis
and pulmonary embolism.
VIRCHOW'S TRIAD
-Named after the prominent physician Rudolf Virchow. This
is the three main influences increase the chance of a thrombus
formation in a patient.
Alteration in the flow of the blood that may cause due to the lack
of movement after an immediate surgery,injury or conditions such
as pregnancy obesity or cancer.
Factors in the vessel walls that may arise dues to surgery dues to
catheterization known as endothelial injury.
Factors that affect blood coagulation properties such as
procoagcoagulant state.
Signs and Symptoms
Symptoms depends on the extent that the pulmonary aetery is
blocked and on the person's overall health. However, PE can be diffcult
to diagnose and has been called the Great Masquerader. It can mimic
pneumonia, congestive heart failure, and a viral illness known as
pleurisy.

In some peolpe the the first symptoms of PE Includes:

-light- headedness

-fainting

-seizures
 Next Steps of Action
Shortness of breath

Chest pain, often worse when taking a breath

A feeling of apprehension

Sudden collapse

Coughing

Sweating

Bloody phlegm (coughing up blood)

 Epidemiology
Pulmonary Embolism is the third greatest cause
of mortality.
It has been calculated that the incidence of
Pulmonary Embolism is 1 per 1000 anually.
PATHOPHYSIOLOGY

Blood clot

Ventilation-Perfusion Mismatch

Impaired Gas Exchange

Lung Infarction
 Prognosis
A bout half pf the people with untreated PE will have another
embolismwill have another embolism.As many of these recurrences may
be fatal.Anticoagulant treatment can reduce the rate of reocurrence to
about 1 in 20 people;only about 1 in 5 of these people will die of
pulmonary embolism.
 Diagnosis
Diagnosis

A doctor suspects PE based on the person's symptoms and

perdisposing factors such as,a recent surgery or a prolonged period of
bed rest. A large PE may be relatively easy for a doctor to diagnose
,specially when there are obvious reconditions such as signs of blood
clot in the leg.
Procedures needed for diagnosis:

Arterial Blood Gas

Most patients with PE have hypoxemia and
hypercapnia but many patients (15 % to 25%) have PaO2 greater
than 80 mmHg. Although a widened alveolar-arterial O2 gradient
may occur in 20% of patients with angiographically documented PE.
Thus the ABG can never establish the diagnosis of PE.
 Chest x-ray
May reveal subtle changes in the blood vessel patterns after
embolism and signs of pulmonary infarction.However the results are
often normal,and even when they are abnormal,they rarely enable the
doctor to establish the diagnosis with certainty.

Electrocardiogram
May show abnormalities,but often the abnormalitiesare
transient and can only support the possibility of PE
Lung Perfusion scan
One of the best test to diagnose PE.A tiny amount of radioactive
substance is injected to a vein and travels to the lungs,where it outlines
the blood supply (perfusion)of the lung.

Pulmonary Angiography
Accurate means of diagnosing PE,but it poses some risk and is
more uncomfortable than the other tests.
 Treatment

The cornerstone of therapy for PE is the prevention of new

embolic episodes with anticoagulant treatment or a filter in the inferior
vena cava, since it has been found that the majority of patients do not die
from the embolism that leads to diagnosis, but to the con- tinuing
deterioration of their condition due to new emboli.However, when the
patient is in shock, or the haemodynamic condition is particularly poor, it
is necessary to attempt primary lysis of the thrombus/ embolus using
thrombolysis or some invasive em- bolectomy technique.
Supportive therapy
The patients often present with hypoxemia, which responds to
O2 administration, since the main pathophysiological mechanism is V/Q
disturbances. Bed rest appears to help via two mechanisms. First, the
restriction of movement reduces the likelihood of thrombus detachment
from its peripheral location; second, it reduces O2 consumption (VO2)
and therefore the need for increased cardiac output. In extreme cases of
patients in shock, it may be necessary to instigate pharmaceutical
muscle paralysis and mechanical ventilation in the ICU, in order to
reduce VO2 to the minimum.
Anticoagulant therapy
Heparin is the basic treatment for PE, preventing the formation
of new thrombi and giving time for the endogenous fibrinolysis to take
effect, dissolving older thrombi. Heparin administration should be started
immediately, even before the diagnosis of PE is established, provided
that anticoagulant therapy is not contraindicate
Thrombolysis

Thrombolysis should be performed immediately in patients with

circulatory shock, or obvious haemodynamic instability (massive PE).
The outcome in these patients is clearly better in comparison with
anticoagulant therapy alone.A recent meta-analysis found a significant
reduction in deaths and PE reoccurrence in studies that included
haemodynamically unstable patients (9.4% versus 19%).

In patients with stable blood pressure, but signs of right cardiac

dysfunction on echocardiography (submassive PE), there is no
consensus regarding the use of thrombolysis.
Embolectomy

In patients with hemodynamic instability, in whom thrombolysis has failed

or is contraindicated (intracranial haemorrhage, recent surgery or
trauma), transvenous catheter thromboectomy is performed. Various
devices have been developed for the aspiration or pulverisation of
thrombus in the pulmonary circulation. If such a device is not available,
or the procedure fails, surgical thrombus removal is indicated, with open
thoracotomy and extracorporeal circulation. Although emergency
embolectomy has found wide acceptance, the results are not satisfactory,
since the condition of patients who are referred for surgery is extremely
serious.