cor pulmonale

Question 1

etiology

Answer 1

1. pulmonary vascular disorder
   - acute pulmonary thromboembolism
   - primary pulmonary HT
   - multiple pulmonary stenosis
   - recurrent pulmonary embolism
2. disease lung and parenchyma
   - COPD
   - Asthma
   - Bronchiectasis
   - Pulmonary fibrosis
   - Lung resection
3. musculoskeletal disorder (causing chronic underventilation)
   - kyposcoliosis
   - poliomyelitis
   - myasthenia gravis
4. disturbance of respiratory control
   - cerevascular disorder
   - obstructive sleep apnoe
5. left heart disorder
   - mitral stenosis
   - Left atrium myxoma
   - LVF

Question 2

pathogenesis

Answer 2

Alveolar hypoxia causes releasing of biogenic amines (histamines, serotonin) which attended by edema of capillary endometrium. This leads to narrowing of pulmonary vessel, hence increases the pressure in pulmonary artery. Subsequently, pulmonary hypertension develops which in turn causes hypertrophy in the right heart chamber: 1st RV then RA. When RV failure develops, decompensated cor pulmonale established.

Question 3

stages -

Answer 3

1. Acute – stage of pulmonary embolism
   - sign in heart, cyanosis upper part of body, distension jugular vein, liver enlargement
   - thrombus in systemic veins.
   - Clots formed, local injury or compression of the vein and hypercoagulable state.
2. Subacute
3. Chronic
   - in chronic obstructive pulmonary disease
   - enlargement of the right ventricle because of increase in afterload due to disease of the thorax, lung and pulmonary circulation.

Divided in to compensated and decompensated. Decompensated cor pulmonale
- central cyanosis
- peripheral edema
- neck vein distension
- +ve jugular +ve jugular pulse
- Enlargement of liver,+ve plesh sign (hepatojugular reflex)
- Ascitis
- Hydrothorax
- Hydropericardium

Question 4

clinical picture

Answer 4

• Pallor, sweating, hypotension, rapid pulse of small amplitude
• Pleuritic chest pain
• Exertional dyspnea
• Syncope, fatique
• The neck veins are distended, swelling and prominent v waves
• The liver pulsatile, distended, and tender. enlarged, painful to palpate
• systolic murmur of tricuspid regurgitation accompanied by gallop sound.
• Arterial blood gas shows reduced PaO2 and low Pa CO2
• epigastric pulsation, ascites, shifting of R atrium, pulm-trunk, P-pulmonale, deep S in V4-V6, complete/ incomplete RB block
• Sudden onset
• Respiration rate increase but expiration not elongate
• Haemoptysis (present only when infarction has occurred)
• Do not respond to bronchodilation preparation
• work capacity decreases, drowsiness and headache
• general cyanosis, Acrocyanosis
• Fingers and hand became cold to touch
• Shins became puffy and entire lower extremities are edematous
• Permanent tachycardia

Question 5

investigation

Answer 5

1. Chest X-ray
   - diaphragm well rounded
   - cardiac silhoute enlarged
   - pulmonary arteries more prominent
   - linear atelectasis /blunting of costophrenic angle
   - translucency of an underperfused distal zone is seen
   - RV enlargement and right artrial dilatation
   - Pulmonary trunk and hilar vessels enlarged, descending right pulmonary artery embolism
2. ECG
   - Increase P wave in 3rd and AVF leads ( p – pulmonale)
   - Increase R wave in V1-2
   - Increase S in V5-6
   - Right limb block in Hiss bundle in V1
   - T wave inversion in right precordial lead
3. Echocardiography
   - Shows vigorously contracting LV and a clot in RV outflow tract
   - Hypertrophy and dilation of RV
   - Tricuspid regurgitation
4. Spiral CT scan - IV contrast show good sensitivity & specificity for medium sized pulmonary emboli
5. Ultrasound - increase size in RV
6. Pulmonary angiography, MRI
7. Blood test
   - if infraction occurred polymorphonuclear leucocytosis
   - Elevated ESR
   - Increase lactate dehydrogenase level in serum
8. Blood gases - Shows hypoxia and hypocapnia
9. Ophthalmologic examination – papilloedema

Question 6

treatment

Answer 6

1. For acute management
   - high –flow oxygen (60-100%)
   - Diuretics for RV failure
   - bed rest and analgesics
   - Severe cases IV fluid and inotropic agents to improve pumping of right heart

• Prevention of further emboli
  a. IV 10000 units of unfractionated heparin
  b. Oral anticoagulants
  c. Insertion filter in the inferior vena cavae right above level of renal vein
• Dissolution of thrombus – fibrinolytic therapy (streptokinase IV)
• Surgery – embolectomy
• Management – treat underlying causes eg: COPD and pulmonary infection
• Treat resp failure

2. chronic management
   - determined by condition underlying pulmonary HT, used Diuretic
   - hypoxia use oxygen therapy