In this article we will discuss the Physical and Systemic Signs of Cor Pulmonale. So, let’s get started.
- Patient is orthopnoic, sits with elbows supported on a table and legs dangling by the side of the bed.
- Purse-lip breathing and cyanosis (lips, tongue, and buccal cavity) will be present in patients with COPD with acute exacerbation.
- Periorbital edema
- Neck veins: Distended with raised JVP and ‘VY’ collapse due to tricuspid regurgitation.
- Peripheral edema
- 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 (Grahm-steel) murmur and pansystolic or holosystolic murmur of tricuspid regurgitation (Carvallo’s sign) may be present.
- Abdominal examination: Abdomen may be distended with tender hepatomegaly. Hepatojugular reflex may be present. Ascites may also be present.
In this article, we will discuss the Clinical Risk Factors that predispose to DVT and Pulmonary Embolism. So, let’s get started.
Clinical Risk Factors
1. Surgery, trauma (in-plaster injuries or fracture of lower limb bones)
2. Prolonged immobilzation (stroke, or intensive care unit patients)
3. Oral contraceptives, hormonal replacement therapy, pregnancy, postpartum
4. Cancer and cancer chemotherapy
5. Varicosity of the veins
6. Chronic kidney disease, arterial hypertension, blood transfusions
7. Congestive heart failure (stasis of blood), COPD with cor pulmonale
8. Physical inactivity, e.g. obesity and smoking
9. Hypercoagulability (deficiency of protein C and S, antithrombin) prothrombin gene mutation, antiphospholipid antibodies, polycythemia
10. Inherited gene defect (resistance to activated protein C, and factor V Leiden mutation)
11. Long-hour air travel, air pollution
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.
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)
Jugular venous distention (raised JVP) and ‘VY’ (wave) collapse due to tricuspid regurgitation
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.
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.