Vascular Lung Diseases Flashcards
pulmonary edema as a result of increased capillary hydrostatic pressure
(pulmonary edema: a condition caused by excess fluid in the lungs; this fluid collects in the numerous air sacs in the lungs, making it difficult to breathe
*precipitating events include: MI, mitral stenosis, fluid overload, pulmonary venoocclusive disease
*interstitial edema can progress to alveolar edema (excess fluid)
*results in decreases in O2 saturation
3 mechanisms that can increase pulmonary artery pressure
- increased pulmonary vascular resistance (pulmonary arterial abnormalities)
- increased left atrial pressure (left heart abnormalities or global volume overload)
- increased pulmonary blood flow (congenital heart disease, often with left to right shunting)
classification of pulmonary hypertension
*mean pulmonary artery (PA) pressure is > 20 mmHg
*pre-capillary pulmonary HTN if: left atrium/wedge pressure </= 15 mmHg
*post-capillary pulmonary HTN if: left atrium/wedge pressure > 15 mmHG
recall: formula for calculating pulmonary vascular resistance
pulmonary vascular resistance = (mean pulmonary artery pressure - pulmonary capillary wedge pressure) / cardiac output
= (MPAP - PWCP)/CO
note - normal PVR (pulmonary vascular resistance) is 1.9 to 3.1 Wood units
pulmonary hypertension: defined
*pulmonary hypertension (PH) is defined as mPAP > 20 mmHg
*precapillary PH is likely present at pulmonary vascular resistance > 3 Wood units (or PCWP < 15)
*postcapillary PH is likely present at PCWP > 15 mmHg
how to determine the cause of pulmonary hypertension
*EKG
*transthoracic echocardiogram
*CXR
*ventilation/perfusion scanning
*polysomnography
*additional tests for infectious, hematologic, autoimmune, endocrine, and metabolic disorders
pulmonary arterial hypertension - pathology
*common sequence of changes in blood vessel, from early to late:
1. intimal hyperplasia
2. medial hypertrophy
3. vessel occlusion
4. plexiform lesion
5. fibrinoid necrosis
plexiform lesions in pulmonary arterial hypertension
classes of treatments of pulmonary arterial hypertension
- endothelin-receptor antagonist (ERA)
- phosphodiesterase type 5 inhibitor (PDE5i)
- prostacyclin derivative (PG)
- guanylate cyclase stimulator (sGC)
- calcium channel blocker (CCB)
3 pathways of pulmonary arterial hypertension
- endothelin-1 pathway (promotes cell growth)
-treated using endothelin-receptor antagonists - prostacyclin (PGI2) pathway (increases vasodilation)
-treated using prostacyclin derivatives - nitric oxide pathway (increases vasodilation)
-treated using phosphodiesterase type 5 inhibitors and guanylate cyclase stimulators
treatment of pulmonary hypertension in all of the WHO groups
*LOOP DIURETICS
*supplemental oxygen (if SpO2 < 90%)
treatment of pulmonary hypertension group 1 (pulmonary arterial hypertension)
*loop diuretics & supplemental oxygen, plus pulmonary vasodilators
treatment of pulmonary hypertension group 2 (PH due to left heart disease)
*loop diuretics & supplemental oxygen, plus afterload reduction, ionotropic agents
treatment of pulmonary hypertension group 3 (PH due to lung disease)
*loop diuretics & supplemental oxygen, plus bronchodilators
treatment of pulmonary hypertension group 4 (PH due to arterial obstructions)
*loop diuretics & supplemental oxygen, plus pulmonary thromboendarterectomy, sGCis
treatment of pulmonary hypertension group 5 (PH due to multifactorial mechanisms)
*loop diuretics & supplemental oxygen, plus treatment of underlying cause
pulmonary arteriovenous malformations (AVMs) - overview
*abnormal connection between pulmonary arteries and veins
*bypass the alveolar capillary system, creating a “shunt”; results in lower systemic PaO2 and hypoxemia
*suspect in a patient with hypoxemia or cyanosis who has mucosal or facial telangiectasia (ex. Hereditary Hemorrhagic Telangiectasia)
pulmonary arteriovenous malformations (AVMs) - clinical presentation
*cyanosis
*telangiectasias
*rarely, stroke due to “paradoxical” embolism
venous thromboembolic disease - overview
*includes deep vein thrombosis (DVT) and pulmonary embolism (PE)
*a major and common preventable cause of death
*risk factors: cancer, hospitalization, surgery, pregnancy, smoking, estrogen-containing hormone therapy, immobility (long plane or car rides)
pathogenesis of venous thrombosis
*Virchow’s Triad: blood stasis, endothelial injury, and hypercoagulability
*often forms at the valve pockets of the veins, composed primarily of red cells and thrombin
clinical presentation of DVT
*history: recent surgery, hospitalization, or long trip (car/plane); pt may report any or none of:
-swelling, pain, cramping/soreness, purple coloration of the skin
*exam: any or none of:
-swelling in an extremity
-palpable superficial “cord” in a vein, +/- warmth
-Homen’s sign: calf pain when you dorsiflex the foot
-rare presentation: extreme purplish discoloration of a limb (“phlegmasia cerulea dolens”)
diagnosing DVT
- Wells Clinical Model helps assess probability of DVT using history & exam findings (very sensitive for DVT; low score helps rule out DVT)
- blood D-dimer levels (very sensitive; normal levels help rule out DVT)
- ultrasound of deep veins (very specific for presence of clot; positive findings rule in DVT)
treatment options for DVT
*anticoagulants for 3+ months (heparins, oral direct thrombin inhibitors, factor Xa inhibitors)
*thrombolysis
*if the above are too high risk: inferior vena cava filter (to delay/prevent embolism)
thromboembolism - defined
*pieces of a clot in a deep vein (most often from the femoral veins) break off and travel in the bloodstream until they are stopped by the pulmonary circulation
