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PULMONARY EMBOLISM PowerPoint

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PULMONARY EMBOLISM

Cause --- Consequences --- Diagnosis --- Treatment


• Pulmonary embolism (PE) is the sudden occlusion of a pulmonary artery or
any of its branches by an embolus (most often a thrombus that had originated
elsewhere, typically in the large veins of the legs or pelvis = deep vein
thrombosis)
• Note: PE can also arise from non-thrombotic sources (e.g., embolism of air,
amniotic fluid, fat, infected material, foreign body, tumor).

• PE is a potentially life-threatening condition


• Why “potentially” ???
• Oftentimes, its small thrombi that embolize into the lungs – occlude some
small vessels in one area – then they quickly lyse – and one doesn’t even
realize anything has happened
• Because lungs have a dual blood supply (pulmonary arteries and
bronchial arteries), even if a few pulmonary arteries become occluded by
small emboli, lung tissue does not undergo any immediate infarction since
the bronchial arteries are supplying O2

• Must have relatively large embolus to begin seeing lung infarction


• In fact, it is only when over 50% of pulmonary arteries are occluded that we
begin to witness signs of RV failure (When a large embolus acutely
occludes major pulmonary arteries or when many smaller emboli begin to
combine)
• Could lead to RV failure to due to immense increase in RV pressure 
obstructive shock  decreased cardiac output and death.

• Massive PE without cardiac arrest – 30% mortality rate


• Massive PE with cardiac arrest - mortality may be as high as 95%
• Pulmonary embolism is a recognized reversible cause of cardiac
arrest and must be actively excluded in the collapsed pulseless
patient.
RISK FACTORS for DVT
Pathophysiology
 Effect on heart Pulmonary vascular resistance

“Series effect” “Parallel effect”

Decreases outflow
from LV

Note: Hypokinesia
= Decreased ventricular
range of motion
Poor gas exchange in lungs
 V/Q mismatch  decreased
perfusion (Q)  V/Q to infinity
 less O2 diffusion into pulmonary
veins beyond the embolus =
decreased PaO2 = hypoxemia
 dyspnea (difficulty breathing)
 tachypnea (increased breathing
rate)
Massive pulmonary emboli may manifest with hypotension,
tachycardia, light headedness/presyncope, syncope, or cardiac
arrest.

The most common signs of pulmonary embolism are


• Tachycardia (reflex increase in HR)
• Tachypnea (reflex increase in breathing rate)

• Hypotension (decreased systemic CO)


• Could see JVD (decreased venous return due to RV dilation
and increased RV pressure)
• Cold extremities (hands and feet) – due to reflexive
vasoconstriction

• Pleuritic chest pain


How do we diagnose a suspected pulmonary embolism ?
1) Determine clinical probability (of a PE) based on Wells criteria
Suspected PE in a patient (pre-test probabilities)  Negative D-DIMER RULES OUT PE

 + D-dimer test does not fully rule in PE


 proceed with more specific tests  CTPA

Fibrin breakdown
product
• Grey area within pulmonary arteries = embolus
• Black = air (can even see L and R primary
bronchi here)
Alternate diagnosis pathway

If patient had
high probability
for DVT
“DOPPLER
ULTRASOUND”
Highly
specific

*If: morbidly obese,


allergic to iodine, or Gold standard
with renal failure

– takes longer
- less specific
Treatment of PE

• Dissolve! [Fibrinolysis]
> Anticoagulants (tPA, urokinase,
heparin IV)
> Surgically remove –
embolectomy

• In patients with hypoxemia, oxygen


should be given.

• In patients with hypotension due to


massive PE (hemodynamic
instability), 0.9% saline can be
cautiously given IV; overloading
the right ventricle can result in
deterioration

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