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COR PULMONALE
Definition:
Alteration in the structure and function of the right ventricle
caused by a primary disorder of the respiratory system.

Lung Dysfunction

Pulmonary
Hypertension

Cor Pulmonale

Pathophysiology:
Pulmonary vasoconstriction:
Alveolar hypoxia, blood acidaemia.

Anatomic compromise of the pulmonary vascular

bed secondary to lung disorder:
Emphysema, pulmonary thromboembolism, interstetial lung
disease all cause smooth muscle hypertrophy of
pulmonary vessels pulmonary HTN.

Increased vascular viscosity secondary to blood

disorders:
1) Polycythemia vera
2) sickle cell disease (the only anemia that cause
hyperviscosity)
3) macroglobulinaemia

Idiopathic primary pulmonary hypertension.

More in female in the 2nd and 3rd decade of life; especially
during pregnancy.
These patients should not have pregnancy; otherwise
therapeutic abortion is highly indicated.

Classifications:
Acute cor pulmonale:
Example: in massive pulmonary embolism (PE) acute right
ventricular dilatation (RVD) cuz there is no time for
exercising the ventricular muscles.

Chronic cor pulmonale:

Example: in chronic pulmonary artery HTN chronic right
ventricular hypertrophy (RVH) cuz there is time for exercising
the ventricular muscles.
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ACUTE COR PULMONALE

The most important cause is PE due to deep venous
thrombosis (DVT).

Deep venous thrombosis:

It could be triggered by:
1) Venostasis
2) Vessel wall inflammation and trauma
3) Hypercoagulability state.

Risk factors of DVT:

1) Age > 50 yrs.
2) Hypercoagulability state
- Pregnancy especially in peri and post partum stage.
- Protein C, protein S and anti-thrombin III deficiencies
- High fibrinogen level
- Cancers like bronchogenic Ca., pancreatic Ca., prostatic Ca.
3) Prior Hx of PE or DVT
4) Contraceptive pills estrogen coagulability
5) CHF venostasis
6) Post-operative state
7) Trauma and immobilization
8) Varicose veins (example multiparity, obesity, traffic
police)

Pathophysiology

pulmonary artery

Acute PE

Release of serotonin

pressure

Hypoxia and reflux VC

RV afterload

RV ischemia / infarction

RV wall tension

RV O2 demand

RV dilitation / dysfunction

Clinical Assessment
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o History:
Chest pain, S.O.B., Syncope, Haemoptysis.

o Physical:
Massive PE cause ACUTE COR PULMONALE
TACHYPNEA
TACHYCARDIA
HYPOTENSION due to low cardiac out put
Acc. S2 in pulmonary area.
Rales (crepitation and rhonchi)

o Investigation:
1) ABG: hypoxia and hypocabnia
2) ECG: S1 + QT III + rSR in V1 V2
(i.e. deep S-wave in lead I + presence of Q-wave and T-wave
inversion in lead III + right bundle branch block in lead V1 V2)

ECG has specificity of 95% but sensitivity of 25% (i.e. if the

these ECG changes are present definitely PE, but if not
possible PE)
3) CBC
4) Coagulation studies: anti-thrombin III, protein C & S,
PT, fibrinogen level should be done before anticoagulant and thrombolytic therapy.

o Imaging Studies:
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1) Chest X-ray: very insensitive. Occasionally absence

of vascular shadow in the lung is seen.

2) Ventilation-perfusion scanning of the lung(V/Q).

We ask the patient to inspirate Xenon radio active gas
to measure ventilation and then give Thalium injection
to see lung vessels perfusion. If there is mismatch
between ventilation and perfusion scans PE. So, it is
very sensitive (85%) but not golden stander test.

3) Pulmonary Angiography:
It is the golden stander test to diagnose
PE where we inject a contrast media
through femoral vein to stain the
pulmonary vessel during imaging but it
has high morbidity and mortality rate (12%) cuz when we inject the contrast we
increase the pulmonary vessels
pressure.
4) Spiral Computed Tomographic Angiography
scan.
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It is the best
modality,
since it is Fast
do. Inject a
contrast
media in the
antecubital
vein in very
low amounts,
it will not
Increase the
already increased pulmonary artery pressure.

to

so

Management:
1) Fibrinolytic therapy
It is indicated in:
i. Massive PE.
ii. Evidence of RV strain (by ECHO).
iii. Hemodynamic instability.
iv. Past H/O PE, DVT, proteins C, S, anti-thrombin III
deficiencies.
v. Any patient with DVT with no contraindication.
Examples
o Reteplase(r-PA): Two 10-unit IV boluses, given 30 min
apart.
o Alteplase(rt-PA): 100 mg IV infusion over 2 h.
o Urokinase:
- Loading dose: 2000 U/lb infused over 10 min.
- Maintenance dose: 2000 U/lb/h for 24 h.
o Streptokinase:
Loading dose: 250,000 U over 30 min.
Maintenance dose: 100,000 U/h for 12-72 h.
2) Anti-Coagulant:
To prevent further thrombus formation
We use Unfractionated heparin or LMWH for 1 week.
Warfarin is started at the 4th day of initiating Heparin
therapy, and is continued for 3 to 6 months and
sometimes all over the life.
3) Oxygen
4) Compression stocking
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To prevent showering of thrombi from lower limbs to

lungs.

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CHRONIC COR PULMONALE

Epidemiology:
6-7% of all adult heart disease in USA.
>50% of case the causative factor is COPD due to chronic
bronchitis or emphysema.
It correlates with prevalence of cigarette smoking or air
pollution.
Cor pulmonale has poor prognosis, patients with COPD who
developed cor pulmonale have a 30% chance of surviving 5
years.

Causes:
1) Chronic obstructive pulmonary disease (COPD).
2) Obstructive sleep apnea.
3) Central sleep apnea.
4) Chronic mountain sickness.
5) Cystic fibrosis.
6) Primary pulmonary hypertension.
7) Pneumoconiosis.
8) Kyphoscoliosis lung disease.
9) Diffuse interstitial pulmonary fibrosis.
10) Chronic thromboembolic pulmonary disease
(especially in those using contraceptive pills and have
hypercoagulability)

Symptoms:
-

Shortness of breath.
Symptoms of underlying disorder (cough, wheezing).
Swelling of the feet or ankles.
Exercise intolerance.
Chest discomfort.

SIGNS:
-

Central Cyanosis.
High JVP.
Pleural effusion.
Hepatomegaly, ascites.
Lower limb edema.
Cardiac examination: Left parasternal heave, TR
(pansystolic murmur), loud P2.

Investigation:
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Chest X-ray.
CBC, PT, PTT, protein S and C, anti-thrombin III, anticardiolipin antibodies, homocystin (hyperhomocysinemia
CAD).
Alpha-1 anti-trypsin.
ECG.
ABG hypoxia and hypercabnia.
ECHO TR, RVH.
Pulmonary function test.
CT scan chest.
V/Q lung scan.

Management:
o Medical:
-

Treat underlying illness.

Oxygen (either 1-2L/min through nasal canula or 28% O2
conc. as face mask).
Loop diuretic.
Diet (low salt diet).
Ca. channel blocker to dilate pulmonary artery but not
proven.
I.V. prostacyclin to dilate pulmonary artery but not
proven.
Oral bosentan (endothelin-1 receptor antagonist).

N.B: endothelin-1 is strong VC and if we antagonize it we will

cause VD

o Surgical:
-

Venesection, (withdrew of Venus blood).

Embolectomy in massive PE in hopeless patients; but it
is replaced by thrombolytic therapy.
Heart-Lung transplant.

Patient education:
-

Regular follow up.

Adherence to medication.
Importance of O2.
Danger of cigarette smoking

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