Ranna25.com is a medical educational website addressed primarily for medical students and junior doctors studying in our country Sudan, yet the scope Of this website extends to encompass all medical personnel, inside and outside the country. The website is dedicated to the soul of Dr.Ranna Saad Osman Bashier (1979-2005) - May God Bless Her and his  Mercy Be upon Her - .

 

 

 

Copyright © 2006.
www.ranna25.Com
All rights reserved

 

     
 

Clinical Science: Medicine - Cardiology

 

 

Home Page      -     Back To Clinical Science Page   -      Back To Medicine Page

 

Acute Cor Pulmonale (Pulmonary Embolism)
 

Author: Musab T. Ejami, MBBS, Faculty Of medicine, University Of Al-Zaiem Al-Azhari

 
Two words best characterize the mortality and morbidity of due to venous thromboembolism: substantial and unacceptable.                                                    

                                                                      K.M. Mosers. Am. Rev. Resp. Dis. 1990

Introduction:

The term “Cor Pulmonale” means right heart failure arising secondary to pulmonary hypertension. However the term is unsatisfactory in that it is not a distinct disease, but represents very different disease process, so it should be remembered that is actually a final common pathway for the courses of these diseases not a distinct one. Pure right heart failure is uncommon, though it may occur following:
* Right ventricular myocardial infraction.
* Isolated right-sided valvular disease.
As said the causes of cor-pulmonale are numerous, but in clinical practice, one disorder of each type predominates:
* Pulmonary embolism as a cause for acute cor-pulmonale.
* COPD for chronic cor-pulmonale.

PE: Background:

Pulmonary embolism (PE) is a common and potentially lethal disease; unfortunately, the diagnosis is often missed because PE presents with nonspecific signs and symptoms. If left untreated, approximately one third of patients who survive an initial PE subsequently die from a future embolic episode. Most patients succumb to PE within the first few hours of the event. In patients who do survive, recurrent embolism and death can be prevented with prompt diagnosis and therapy.

Epidemiology:

* Unexpected death from a massive PE is second only to the sudden cardiac death. Autopsy studies of hospitalized patients have shown approximately 80% of these patients died from massive PE.
* Approximately 10% of patients who develop PE die within the first hour, and 30% die subsequently from recurrent embolism. Anticoagulant treatment decreases the mortality rate to less than 5%.
* The diagnosis of PE is missed in approximately 400,000 patients in the United States per year; approximately 100,000 deaths could be prevented with proper diagnosis and treatment.


Pathophysiology:
 

Sources of Emboli:
Veins of lower limb, ileo-femoral veins and calf veins may be the source, rarely emboli originating from the right atrium in atrial fibrillation. The risk factors are the same for those of DVT.
Respiratory consequences
Acute respiratory consequences of PE include increased alveolar dead space, pneumoconstriction, hypoxemia, and hyperventilation. Later, 2 additional consequences may occur: regional loss of surfactant and pulmonary infarction. Arterial hypoxemia is a frequent but not universal finding in patients with acute embolism. The mechanisms of hypoxemia include ventilation-perfusion mismatch, intrapulmonary shunts, reduced cardiac output, and intracardiac shunt via patent foramen ovale. Pulmonary infarction is an uncommon consequence because of the bronchial arterial collateral circulation.
Hemodynamic consequences
PE reduces the cross-sectional area of the pulmonary vascular bed, resulting in an increment in pulmonary vascular resistance, which, in turn, increases the right ventricular afterload. If the afterload is increased severely, right ventricular failure may ensue. In addition, the humoral and reflex mechanisms contribute to the pulmonary arterial constriction. Prior poor cardiopulmonary status of the patient is an important factor leading to hemodynamic collapse.

Clinical Presentation:

Many pulmonary embolisms occur silently, yet there are three typical clinical presentations, which are:
* Small/medium pulmonary embolism
* Massive pulmonary embolism
* Multiple recurrent pulmonary emboli.

1- Small/Medium Pulmonary Embolism:
In this case the embolus has impacted in the terminal pulmonary vessel. Symptoms are:
* Pluritic chest pain.
* Breathlessness.
* Haemoptysis. (30% of cases, 3 -5 days after the initial event).

Physical examination may reveal a pyrecxial/ tachypnic patient with the following:
* Pleural rub.
* Coarse crackles.
* Pleural effusion.

Differential diagnosis:

2- Massive Pulmonary Embolism:
It occurs due to sudden obstruction of the right ventricular outflow tract. The patient has the following symptoms:
* Severe central chest pain (due to cardiac ischemia).
* Syncope and collapse.

Clinical examination may reveal some or all of the following:
* Tachypnic and tachycardic with hypotension and peripheral shutdown.
* Raised JVP with prominent “a” wave.
* Positive left Parastenral heave.
* Gallop rhythm.
* Palpable 2nd heart sound.
* Wide splitting of the 2nd heart sound.
* Pansystolic murmur over the left sternal edge may be noted (due to tricuspid regurgitation).

Differential Diagnosis: myocardial infarction, septic shock and hypovolemia.

3- Multiple recurrent emboli:
This occurs due to multiple occlusions of the pulmonary vasculature by small emboli, thus these patients do not present acutely, but run a more chronic course with the gradual development of pulmonary hypertension, and symptoms are:
* Increasing breathlessness over weeks or months.
* Weakness and syncope on exertion.
* Occasional angina.

Physical examination may reveal Signs of pulmonary hypertension (palpable 2nd heart sound, loud 2nd heart sound, enhanced splitting, Raised JVP and left a left parasternal heave). Signs of established of right-sided heart failure may be present.

Differential diagnosis: CHF and asthma.

Index of Suspicion:

The symptoms of PE are nonspecific; therefore, a high index of suspicion is required, particularly when a patient has risk factors.

The most common symptoms of PE in the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) study were:
* Dyspnea (73%)
* Pleuritic chest pain (66%)
* Cough (37%)
* Hemoptysis (13%).

The most common physical signs in the PIOPED study were as follows:
* Tachypnea (70%)
* Rales (51%)
* Tachycardia (30%)
* Fourth heart sound (24%)
* Accentuated pulmonic component of the second heart sound (23%)
* Fever of less than 39°C may be present in 14% of patients; however, temperature higher than 39.5°C is not from PE.
* Chest wall tenderness upon palpation, without a history of trauma, may be the sole physical finding in rare cases


Investigations:

Clinical signs and symptoms are nonspecific; therefore, patients suspected to have PE must undergo diagnostic tests until the diagnosis is ascertained or eliminated or an alternative diagnosis is confirmed.

Blood Test:
If pulmonary infarction has occurred there will be a polymophonuclear leuckocytosis, elevated ERS and increased serum LDH.

Blood Gases:
May show hypoxia and hypocapnia in massive pulmonary embolism..

Plasma D-Dimer:
D-dimer, a degradation product produced by plasmin-mediated proteases of cross-linked fibrin is detected in over 90% of the cases, however false positive may be as high as 70%.

Chest X-ray:

Small/Medium:

Often normal, but the following features can be found:
- Linear atelectasis.
- Blunting of costophrenic angle.
- Raised hemidiaghram
-Wedge-shaped pulmonary infarct.
- Cut-off sign.

Massive:

- Oligaemia
- Dilatation of the pulmonary artery at the hilia
- Often no changes.

Recurrent:

May be normal, enlarged pulmonary arterioles with oligaemic zones usually indicate advanced disease.

Electrocardiogram (ECG):

Small/Medium Emboli:
The ECG is usually normal, except for signs tachycardia. But the following also may occur:
- Atrial fibrillation.
- Other forms of tachycardia.
- Evidence of right ventricular strain.

Massive Embolism (see Figure 3):

* incomplete/complete RBBB
* S wave in lead I and aVL > 1.5 mm (or r:s ratio < 1)
* clockwise rotation of the heart and a shift in the transitional zone to lead V5 or further
* Q waves in leads III and/or aVF
* frontal plane axis to the right of + 90 degrees (or an indeterminate axis)
* low voltage (< 5 mmm) QRS complexes in the limb leads
* T wave inversions in lead 3, aVF and/or leads V1 - 4
* elevated ST segments in leads aVR and V1 - 2
* prominent P waves in leads II, III and aVF
* S1,Q3, T3 pattern or S1,S2,S3 pattern
* ischemic appearing ST segment/T wave changes in the inferior + anteroseptal leads
* cardiac arrythmias (sinus tachycardia, atrial flutter, atrial fibrillation)

Multiple Recurrent emboli:
Normal or show signs of pulmonary hypertension:
- Right axis deviation.
- Dominant R waves in V1.
- Prolongation of QRS complex.
 

Previous Figure: ECG abnormalities include:
* Prominent P waves (P Pulmonale) in leads II, III and aVF suggesting right atrial enlargement/strain
* a prominent R wave in lead aVR
* Borderline ST elevation in lead aVR
* disproportionately large s waves in the limb leads with a r/s ratio < 1 in lead I and aVL
* RS complexes in the precordial leads which extend all the way to lead V5
* Small QRS complexes in the limb leads
* An indeterminate frontal plane axis.

 



Radionucleotide Ventilation Perfusion Scan (V/Q):

A very good and important diagnostic tool, 99mTc scintigram shows the unperfused area in the lung and if accompanied by a normal CXR or ventilation scan, then PE is highly suggested. The PIOPED classification scheme allows the interpretation of the V/Q scan more meaningfully:

Diagnostic pattern - Normal V/Q scan findings or findings indicating a high probability:
* Normal V/Q scan findings indicate an absence of any perfusion defects. Four percent of these patients still may have PE. Unless the patient has features indicating very high clinical suspicion, these findings may be considered negative for PE.
* High-probability scan findings are 2 or more segmental or 1 larger perfusion defect in the presence of normal chest radiography findings and ventilation scan findings. Approximately 87% of these patients were found to have PE. If accompanied by high pretest probability, the likelihood of pulmonary emboli increases to 95%.

Diagnostic pattern - Nondiagnostic scans interpreted as low or intermediate probability:
* Low-probability scan findings consist of small perfusion defects associated with corresponding abnormalities upon chest radiograph or ventilation scan. A single segmental perfusion defect with normal chest x-ray findings and nonsegmental perfusion defects are common nondiagnostic patterns. Twelve percent of the patients with this pattern have PE, unless the patient has a very low pretest probability or clinical suspicion. Further diagnostic studies must be carried out to confirm or exclude the diagnosis of PE.
* Intermediate probability is indicated by those patients with any V/Q abnormality that is not classified as high or low probability. Approximately 30% have PE; therefore, the finding of this scan pattern must be followed by further investigation to definitely exclude the diagnosis of PE.

Pulmonary Angiography:
The golden standard diagnostic investigation for PE, angiographic signs include cut-off sign due to intra-luminal defect and poor perfusion in supplied areas.

   

Echocardiography:
It is not specific, and of no diagnostic value, it shows vigoursly contracting left ventricle & occasionally a clot in the right ventricle outflow tract with strain compatible with pulmonary hypertension. Transesophageal echocardiography may identify central PE, and the sensitivity for central PE is reported to be 82%

Ultrasound:
Detection of clots in the pelvic or femoral veins.

Spiral CT-scan:
With intravenous contrast, show god sensitivity to medium pulmonary emboli, they do not exclude small emboli.

MR imaging:
Similar results to CT.


Management of Thromboembolism:

Management For established embolism:

1- Acute Management:
* Admit the Patient to ICU.
* Oxygen by mask 60-100% unless COPD.
* Analgesia.
* I.V. Fluids & intropic agents if haemodynamiclly collapsed.

2- Anticoagulants:
* Aim: prevention of further emboli.
* Unfractioned Heparin 5000U – 10,000 I.V. Bolus is given Followed by infusion at a rate of 1000 U/h for 24 hours.
* Warfarin is introduced on day 5 in a dose of 10mg/day for 2 days and later dosage adjusted to keep PT more than 1.5 – 2 times control for a period of 3 month.
* LMWH although more expensive are increasingly being used, that is because they simplify the treatment.
* Risk of Heparin: ineffectiveness due to in sufficient dose bleeding and thrombocytopenia.

3- Thrombolytic Therapy:
* Aim: Dissolution of emboli.
* Indications: Massive PE with hypotension, cardiopulmonary failure with shock, angiographic evidence of occlusion of 40% of the pulmonary circulation.
* 250,000 U streptokinase I.V. infusion over 30 min, followed by 100,000 untis I.V. hourly.
* Other agents include: Urokinase – loading dose 4400 U over 10 min, infusion 4400u/kg for next 12 hours. Or tPA: 100mg infused over 24 hours.

Prevention Of thrombo-embolism:

* An objective for critically ill in high risk group.
* Modify Modifiable Risk factors such as smoking, obesity, pregnancy, oral contraceptives.
* 5000 u 12hrly is effective, LMW heparin 3000us/e OD is a good prophylaxis.
* Caval filters, compression stockings and other means of preventing DVT should be undertaken.


References & Resources:


1. Parveen Kumar & Michael Clark: Clinical Medicine 4th edition.
2. Pulmonary embolism: Sat Sharma, MD, FRCPC, FCCP, DABSM, Program Director, Associate Professor, Department of Internal Medicine, Divisions of Pulmonary and Critical Care Medicine, University of Manitoba; Site Coordinator of Respiratory Medicine, St Boniface General Hospital (article at: www.emedicine.com)
3. Dr. Shyam Sunder, MD: Current Status in diagnosis, management and prophylaxis in pulmonary embolism.