Pulmonary Vascular Disease Flashcards
Pulmonary Embolism Causes
Venous thrombosis (lower extremities or pelvis),
fat, amniotic fluid, clumps of tumour cells or bone marrow
Pulmonary Embolism Risk factors
Stasis of blood flow (prolonged bed rest or
immobilisation), hypercoagulable states, use of oral
contraceptives
Saddle embolus
Large emboli → Major vessels
Clinical finding of Saddle embolus
Sudden increase in Pulmonary Artery pressure
Acute right ventricular strain → Sudden death
Clinical findings of Pulmonary infarction
Sudden onset of dyspnoea and tachypnoea
Pleuritic chest pain
Friction rub
Effusion
Expiratory wheezing
Laboratory Findings of pulmonary embolism
Respiratory alkalosis (arterial PCO2 <33 mmHg)
PaO2 <80 mmHg (90% of cases)
Increase in Alveolar - arterial gradient (100% of cases)
Increase in D-dimers
✓Positive D-dimers
Chest X-ray of pulmonary embolism
Elevation of ipsilateral hemi-diaphragm
Pleural effusion (haemorrhagic)
Westermark’s sign of peripheral oligaemia
Fleischner’s sign of “amputated” pulmonary artery
Hampton hump (wedge-shaped area of
consolidation)
Ventilation scan will be _______ in pulmonary embolism
Normal
Perfusion Radionuclide Scan
Abnormal
What is the Gold standard
confirmatory test of pulmonary embolism?
Pulmonary angiogram
Macro-/Microscopic finding in pulmonary embolism
Red-blue raised wedge-shaped area that extends to
the pleural surface
Majority are located in the lower lobes (Perfusion >
Ventilation)
Fibrinous exudate on pleural surface
Haemorrhagic pleural effusion
Mean pulmonary artery pressure >25mmHg
at rest (normal: 15 mmHg) >30mmHg
with exercise (normal: 20 mmHg)
Pulmonary Hypertension
Histologic picture of pulmonary hypertension
Characteristic plexiform lesions
Which form of pulmonary hypertension is more common?
Secondary pulmonary hypertension
Pathogenesis of 2nd pulmonary hypertension
Endothelial cell dysfunction ->Loss of vasodilators (e.g. NO) -> Increase in vasoconstrictors (e.g. Endothelin)
Hypoxaemia & Respiratory Acidosis → Pulmonary
arteries vasoconstriction → Smooth muscle
hyperplasia and hypertrophy
Causes of 2nd pulmonary hypertension
Chronic hypoxaemia (e.g. Chronic lung disease)
Chronic respiratory acidosis (e.g. Chronic bronchitis)
Loss of pulmonary vasculature → Workload for
remaining vessels (e.g. Emphysema, recurrent
pulmonary emboli)
Left-to-right cardiac shunts → Volume overloading
pulmonary vasculature
Left-sided valvular disease (e.g. Mitral stenosis) →
Backup of blood into pulmonary veins → Venous
hypertension
Histologic picture of 2nd pulmonary hypertension
Atherosclerotic changes of main pulmonary
arteries (Result of ↑ pressure to endothelium →
Endothelial injury)
Proliferation of myo-intimal and smooth muscle
cells
Intra-alveolar accumulation of fluid
Pulmonary Oedema
Pathogenesis of pulmonary oedema
Due to alterations in Starling forces (transudate)
Due to micro-vascular or alveolar injury (exudate)
Increased alveolar capillary permeability
Causes of Adult Respiratory Distress Syndrome
Shock, sepsis, trauma, uraemia, aspiration of
gastric contents, acute pancreatitis, inhalation of chemical irritants, oxygen toxicity, heroin, bleomycin
Pathogenesis of Adult Respiratory Distress Syndrome
Damage to alveolar capillary endothelium and alveolar epithelium (Diffuse alveolar
damage) → ↑ in alveolar capillary permeability →
Leakage of protein-rich fluid into alveoli
Pathogenic factors of Adult Respiratory Distress Syndrome
Neutrophils → Release of substances, toxic to
alveolar wall
Activation of coagulation cascade → Micro-emboli
Oxygen-derived free radicals → Oxygen toxicity
ARDS can be a manifestation of
Severe Acute Respiratory Syndrome
SARS Coronavirus destroys
type II pneumocytes and causes diffuse alveolar damage
