Pulmonary Vascular Disease Flashcards
pHTN and Cor Pulmonale
Defined as a mean pulmonary arterial pressure greater than 25 (normal is 15). Five classification categories:
1) Arterial pulmonary HTN
2) Increased pulmonary venous pressure from L sided heart disease
3) Hypoxic vasoconstriction secondary to chronic lung disease
4) Chronic thromboembolic disease
5) Pulmonary HTN with an unclear, multifactorial etiology
History and physical for pHTN/Cor Pulmonale
1) Presents with DOE, fatigue, lethargy, syncope with exertion, chest pain, and symptoms of R-CHF (edema, abdominal distention, JVD)
2) Inquire about a history of COPD, interstitial lung disease, heart disease, sickle cell anemia, emphysema, and pulm emboli
3) Exam reveals a loud, palpable S2 (often split), a flow murmur, and S4 or a parasternal heave
Dx of pHTN or Cor Pulmonale
1) CXR shows enlargement of central pulmonary arteries
2) ECG demonstrates RVH
3) Echo and R H cath may show signs of RV overload and may aid in dx of the underlying cause
Tx of pHTN or Cor Pulmonale
Supplemental O2, anticoagulation, vasodilators, and diuretics if symptoms of R-CHF are present.
Treat underlying causes of secondary pHTN
Pulmonary thromboembolism
An occlusion of the pulmonary vasculature by a blood clot. 95% of emboli originate from DVTs in deep leg veins. Often leads to pulmonary infarction, R H failure and hypoxemia
What are some other etiologies of embolic disease?
1) Postpartum status (amniotic fluid emboli)
2) Fracture (fat emboli)
3) Cardiac surgery (air emboli)
History and physical for pulm embolism
1) Factors predisposing to thromboembolism are summarized by Virchow’s triad (Vascular trauma, Increased coagulability and Reduced blood flow)
2) Presents with sudden-onset dyspnea, pleuritic chest pain, low grade fever, cough, tachycardia, tachypnea, and rarely hemoptysis
3) Hypoxia and hypocarbia are seen with resulting respiratory alkalosis
4) Exam may reveal a loud P2 and prominent jugular A waves with R HF
Dx of pulm embolism
1) ABG - Respiratory alkalosis (secondary hyperventilation) with a PO2 less than 80
2) CXR - usually normal, but may show atelectasis, pleural effusion, HAMPTONS HUMPS (wedge shaped infarct) or WESTERMARKS SIGN (oligemia in the affected lung zone)
3) ECG - Not diagnostic. Most commonly reveals sinus tachycardia. The classic triad of S1Q3T3 - acute right heart strain with an S wave in lead 1, a Q wave in lead 3 and an inverted T wave in lead 3 is rare
4) CT pulmonary angio with IV contrast (spiral CT) - sensitive for pulmonary embolism
5) V/Q scan - may reveal segmental areas of mismatch. Reported as low, indeterminate or high probability of PE
6) D-dimer - sensitive but not specific in patients at risk for DVT or PE. Most useful to rule out in patients with low clinical suspicion
7) Lower extremity venous US - can detect a clot that may have given off a PE
Risk factors for venous thrombosis
1) Venous Stasis - CHF, immobility, obesity, increased central venous pressure
2) Endothelial injury - trauma, surgery, recent fracture, previous DVT
3) Hypercoagulability - Pregnancy, postpartum, OCP use, Coagulation disorders (protein C def, Protein S def, factor V Leiden), malignancy, severe burns
Treatment of pulm embolus
1) Anticoagulation
Acute: Bolus followed by weight-based heparin infusion or LMWH SQ
Chronic: Warfarin or LMWH for at least 6m following event or as long as predisposition exists. Goal INR 2-3
2) IVC filter. Indicated in patients with a documented lower extremity DVT if anticoagulation is contraindicated or if patients experience recurrent emboli while anticoagulated
3) Thrombolysis: Indicated only in cases of massive DVT rr PE causing R-HF and hemodynamic instability
4) DVT ppx: Treat all immobile patients. Give SQH or LMWH, intermittent pneumatic compression of lower extremities (less effective) and early ambulation (most effective)
