In this article, we will discuss in brief the Management of Cor Pulmonale. So, let’s get started.


  • The patient is rested in a supine comfortable position.
  • Treatment of the basic cause.
  • The patient is advised to avoid smoking.
  • O2 therapy: O2 therapy to be given intermittently.
  • Salt restriction and diuretics: Salt restriction is advised to avoid fluid retention and RV volume overload. Intravenous diuretics such as furosemide, etc are given to relieve fluid overload.
  • Bronchodilators: They are given intravenously to relieve bronchospasm (due to acute exacerbation) and to improve oxygenation.
  • Carbonic-anhydrase inhibitor, e.g. acetazolamide to be given in order to relieve hypercapnia.
  • Antibiotics are given to treat superadded infection causing acute exacerbation.
  • Reduction of afterload by angiotensin-converting enzyme inhibitor (ACE inhibitors) in patients with left heart failure causing right heart failure.

In this article, we will discuss the Clinical Features of Cor Pulmonale. So, let’s get started.

Clinical Features

Productive cough


Chest discomfort


Abdominal pain

Lower extremity swelling


Physical Signs include:


The patient sits with elbows supported on a table and legs dangling by the side of the chest

Pursed lip breathing and cyanosis (presents in patients with COPD with acute exacerbation)

Periorbital edema

Jugular venous distention (raised JVP) and ‘VY’ (wave) collapse due to tricuspid regurgitation

Peripheral edema

Systemic Signs

Respiratory system may show signs of COPD (barrel-shaped chest, restricted chest movements and expansion, hyper-resonant note and vesicular breathing with prolonged expiration, muffled breath sounds)

Signs of RV hypertrophy or failure e.g. parasternal heave, loud P2, midsystolic and early diastolic (Graham-steel) murmur and pansystolic or holosystolic murmur of tricuspid regurgitation (Carvallo’s sign) may be present.

Abdominal distention may be present along with tender hepatomegaly. Hepatojugular reflex may be present.

In this article, we will discuss the Pathology and Clinical Features of Acute Empyema Thoracis. So, let’s get started.


In acute empyema, there is accumulation of large amount of pleural fluid with many polymorphs, bacteria, and cellular debris. Fibrin gets deposited on both layers of pleura (visceral and parietal) and there is a tendency towards loculation. Later, as the disease progresses (empyema becomes chronic), fibroblasts grow from both the layers into the exudate resulting in adhesions of both the surfaces of pleura and form an inelastic membrane called thickened pleura or pleural peel.

Clinical Features

Patients with aerobic infection (parapneumonic pleural effusion) present with acute onset of fever with chills, productive cough with mucopurulent expectoration (bronchopleural fistula), dyspnea and chest discomfort.

Patients with anaerobic infection present with subacute illness with non-specific signs and symptoms such as weight loss, leucocytosis, mild anemia and history of predisposing factor for aspiration from the oral cavity. Tubercular empyema presents with long-standing (for weeks and months) low-grade fever along with weakness and cough.

In acute phase, there are signs of toxemia such as fever, tachypnea, tachycardia, and pleural effusion. Presence of tenderness on percussion with some edema of the chest wall. Clubbing of fingers and toes are usually seen. Rarely there is a sign of empyema necessitans (empyema may track into the subcutaneous tissue of chest wall and presents as a localized swelling with positive cough impulse, and is mostly seen with actinomycotic infections).

Chronic cases present with pleural thickening and loculation of pus will show significant deformity with retraction of chest on the same side of empyema and even scoliosis. The signs will be dull percussion note with diminished breath sounds. extensive pleural calcification may occur. Tubercular empyema is often chronic and present with thickened pleura.

In this article, we will discuss the Pathophysiology of Chronic Obstructive Pulmonary (COPD). So, let’s get started.


Airflow obstruction (both large and small airways), hyperinflation due to air-trapping resulting in large voluminous lungs and inadequate gas exchange leading to hypoxemia and hypercapnia which are the most frequently encountered changes that constitute the clinical picture of COPD. A persistent reduction in the expiratory flow rate is the hallmark of COPD. An increase in residual volume, ratio of residual volume to total lung capacity, uneven ventilation, and ventilation-perfusion mismatch occur in COPD. Changes in the large airways (bronchitis) produce cough and sputum while changes in the small airways and alveoli are responsible for hypoxemia and hypercapnia. In most cases both bronchitis and emphysema are present but their relative contribution to obstruction varies from person to person.

In this article, we will discuss various Causes of Asphyxia. So, let’s get started

Asphyxia refers to an airway obstruction leading to less or non-delivery of atmospheric oxygen to the lungs resulting in carbon-di-oxide retention. Asphyxia can be caused due to mechanical or non-mechanical obstructions.


Mechanical causes

Covering of face (e.g. plastic bag)

Gag or pad smothering (closing of the external respiratory orifice by hand or by other means)


Food or foreign body obstruction (choking)

Throttling (compression of the neck manually)

Hanging or strangulation


Traumatic asphyxia

Non-mechanical causes

Diseases such as Diptheria, infectious mononucleosis, H.influenzae

Rupture of aortic aneurysm in air passages

Hemoptysis in pulmonary tuberculosis

Erosion of bronchus by a tubercular gland

Laryngeal edema because of steam inhalation, ingestion of irritant substances, drug allergies, and poisons

Retropharyngeal edema

Laryngeal or bronchial outgrowths

Non-penetrating injury to the front of the neck