PULMONARY EMBOLISM

CLINICAL features & Diagnosis

.

• Life threatening causes of chest pain and shortness of breath “DYSPNOEA

• Pain sharp worse fro deep breathe “often called pleuritic pain”.

• They may present with HEMOPTYSIS

• The patient may have stable vital signs (blood pressure, heart rate, respiratory rate, and

oxygen saturation) but frequently presents with an elevated heart rate.

• A severe pulmonary embolus can present with shock or cardiac arrest, particularly when a

large clot blocks the outflow of blood from the right side of the heart to the lungs (saddle

embolus).

• Depending on the amount of blood clot (clot burden or clot load),

• oxygen saturation can be variably compromised as can the blood pressure and heart

rate. In a classic presentation,

•The heart rate and respiratory rate are elevated as the body tries to compensate.

INVESTIGATIONATERIAL BLOOD

• PaCO2 – Partial pressure of CO2 in the blood ,critical in regulating levels and maintaining body ph

• PaCO2 is maintained at 5.3 kPa (40 mmHg)

• D- dimer and other circulating markers.

• D-dimers is a specific degradation product released into the circulation when cross-linked fibrin undergoes endogenosis.

• An elevated D-dimer is limited value, as it occurs in a number of conditions including P.E

.

• Take note of the chest pain and breathlessness

• Physical examination will concentrate Heart and lungsSince the chest pain may

be presenting complains of heart attackPneumonia,

pneumothorax ( collapsed lung)And dissection of an

aortic aneurysm

• The physical exam will also include looking for signs of a D.V.T in an extremely

warmth swelling

redness , andtenderness.

• NB note that the signs associated with deep vein thrombosis may be completely absent even in the PRESENTS of a clot.

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• Full blood count • Electrolytes• BUN (blood urea nitrogen)• Creatinine blood test• Chest x-ray, and • Electrocardiogram• The chest x-ray is often normal in P.E• The EKG/ECG may be normal, but usually

demonstration a rapid heart rate• So called sinus tachycardia (heart > 100 bpm).• If there is significant blockage in a pulmonary

artery.• It acts like a dam and it harder for the heart to

push blood pas t the obstruction clot or clots.• This can result in the change in the electrical

signal passing through the heart by stretching the heart muscle, revealed on a EKG a so called right heart strain.

• Since the cost of missing the diagnosis of P.E can be death, the approach to diagnosis is to prove that no P.E exists.

PULMONARY Hypertension

Fatigue Hoarseness Difficulty breathing (dyspnoea) Dizziness Palpitations Fainting spells ( syncope ) Swelling of legs and ankles ( edema) Bluish Lips, skin ( cyanosis ) Chest pain

. A complete history and physical exam is done.

An electrocardiogram (ECG) may show a strain on the right side of your

heart.

Blood tests are done to indicate how much oxygen is in your blood, or to test

if you have a collagen vascular disease.

A chest x-ray may show a large pulmonary artery and right-sided heart. This

test may also show diseases of the lung such as

emphysema.

A lung scan is done to show the blood supply

in your lungs

A CT or CAT scan is a computerized x-ray

that can get a better view of the lungs and your

heart.

Echocardiogram uses sonar (sound waves) to

show the pumping function of your heart and how the valves work.

A pulmonary function test is done to measure the volume of air in your

lungs. Results are obtained by breathing into a mouth piece while exercising

on a treadmill or bicycle.

An exercise tolerance test will require you to walk on a treadmill as fast as

you can for 6 minutes to evaluate how much exercise you can do before you

have symptoms.

A right heart catheterization is the most accurate way to diagnose

pulmonary hypertension. A small tube or catheter is put into a vein in your

neck and then guided into the right side of your heart and pulmonary artery to

measure pressures.

Clinical features Pulmonary edema

Cardiogenic pulmonary edema◦ ischemia with or without myocardial infarction

◦ exacerbation of chronic systolic or diastolic heart failure, and dysfunction of the mitral or aortic valve

◦ paroxysmal nocturnal dyspnea or orthopnea

Noncardiogenic pulmonary edema ◦ pneumonia

◦ sepsis

◦ aspiration of gastric contents

◦ major trauma associated with the administration of multiple blood-product transfusions

Laboratory Testing

Electrocardiography Elevated troponinlevels

Measurement of electrolytes, the serum osmolarity, and a toxicology screen

Serum amylase and lipase

Laboratory Testing

BNP level below 100 pg per milliliter indicates that heart failure is unlikely (negative predictive value, >90 percent)

BNP level greater than 500 pg per milliliter indicates that heart failure is likely (positive predictive value, >90 percent)

BNP is secreted predominantly by the cardiac ventricles in response to wall stretch or increased intracardiac pressures

Laboratory Testing

BNP levels between 100 and 500 pg per milliliter provide inadequate diagnostic discrimination

BNP can also be secreted by the right ventricle, and moderate elevations have been reported in patients with acute pulmonary embolism, cor pulmonale, and pulmonary hypertension

Echocardiography

The first approach to assessing left ventricular and valvular function in patients in whom the history, physical and laboratory examinations, and the chest radiograph do not establish the cause of pulmonary edema

Less sensitive in identifying diastolic dysfunction

Does not rule out cardiogenic pulmonary edema

Pulmonary-Artery Catheterization

Assess the pulmonary-artery occlusion pressure

Is considered the gold standard for determining the cause of acute pulmonary edema

Monitoring of cardiac filling pressures, cardiac output, and systemic vascular resistance

Common complications included hematoma at the insertion site, arterial puncture, bleeding, arrhythmias, and bloodstream infection

Clinical Presentation AV malformations

Present as:◦ Mass lesion◦ Birthmarks◦ Atypical varicosities◦ Limb enlargement

Most are evident at birth, except AVM which present at early childhood or adolescence.

Staging of AVMs

Stage Manifestation

Stag IQuiescence

Cutaneous blush or warmth

Stage IIExpansion

Bruit, thrill or other signs of expansion

Stage IIIDestruction

Pain, bleeding, ulceration or infection

Stage IVDecompensati

onCardiac Failure

Diagnosis

Essentially by Imaging studies:

US (initial evaluation)

CT scan, CT Angiography

MRI, MRA (leading imaging modality)

Conventional Angiography

1. Diagnosis

2. Determine the extent of the lesion

3. Search for associated abnormalities