Pulmonary Vascula Disorders Flashcards
1
Q
Pulmonary HTN
- pathophysiology
- what pressure is considered pulmonary HTN?
A
Pathophys:
- increased pulmonary arterial pressure from increased pulmonary vascular resistance.
- may be caused by a number of factors, all of which force the right side of the hear to work harder to pump blood to the lungs.
-any mean pulmonary arterial pressure greater than 20mmHg, Pulmonary artery systolic pressure greater than 30mmHg
2
Q
Pulm HTN etiology
A
- pulmonary arterial HTN
- Pulmonary HTN 2ndry left heart disease
- Pulm HTN 2ndry to lung disease/chronic hypoxia (breaking down lung tissue and destroying capillaries and arterioles)
- CHronic pulmonary thromboembolic disease
- Pulmonary htn with unclear multifactorial mechanisms
3
Q
pulmonary HTN may be genetic, what are some of the markers?
A
- BMPR2
- Endoglin
- SMAD9
- CAV1
- KCNK3
4
Q
Sx of Pulm HTN?
Signs??
A
Sx:
- dypnea on exertion (may be at rest)
- fatigue
- Chest pain (anginal)
- syncope with exertion
- nonproductive cough
Signs:
- Narrow splitting of S2 w/ loud pulm component
- Right ventricular hypertrophy
- Right atrial enlargement
- Enlarged central pulmonary arteries on CXR
- JVD
- RIght sided Heart failure sx (hepatomegaly, LE edema)
5
Q
Pulmonary HTN Work Up
A
- CXR
- CT chest
- PFTs
- Echocardiography w/ doppler flow (to help determine which side of the heart is involved.
- Right sided cardiac catheterization with vasodilator challenge
- V/Q Scanning (if suspect disease is from chronic thromboembolic dz)
- Exclude HIV and collagen vascular dz
6
Q
Tx of pulm HTN
A
- treat underlying cause
- Vasodilators:
- -oral ca2+ channel blockers (1st line)
- -oral phosphodiasterase inhibitors (sildenafil, tadalafil)
- -Oral endothelin receptor agonists (ambrisentan, bosentan)
- -Continuous infusion of prostacyclin agents (epoprostenol, treprostinil)
- Supplemental oxygen if hypoxemia present
- May require chronic anticoagulation
7
Q
Cor Pulmonale
- what is this?
- etiologies
A
What is this-
- right ventricular systolic and diastolic failure 2ndry to pulmonary vascular dz or pulm dz
- enlargement of the right side of the heart d/t high blood pressure in thepulmonary vessels.
etiologies:
- pulm HTN
- COPD
- Idiopathic pulmonary fibrosis
8
Q
Signs and Sx of Cor Pulmonale
A
Sx:
- chronic productive cough*
- exertional dyspnea
- wheezing
- easy fatigability
- weakness
- RUQ* pain (capsule of the liver becomes distended d/t increased backflow of blood from RA.)
- Dependent edema (increased hydrostatic pressure back up in the legs leading to edema)
Signs:
- cyanosis
- clubbing
- distended neck veins
- Right ventricle heave or gallup
- prominent lower sternal or epigastric pulsations
- hepatomegaly
- dependent edema
- ascities
- sever lung disease
9
Q
Work up of Cor Pulmonale
A
- EKG; may show RAD, peaked P waves, Deep S waves in V6, may see Q waves in inferior leads b/c of vertically placed heart.
- PFTs (confirm underlying lung disease, this will tell you if its obstructive vs restrictive)
-Polycythemia secondary to
chronic hypoxemia
- SaO2 of less than 85%
- echo (should show normal LV size and function, RV and RA dilation and RV systolic dysfunction w/ tricuspid regurgitation)
- CT or VQ scannign to rule out chronic thromboembolic dz
- serum BNP may be chronically elevated from RV dysfunction
10
Q
Tx Cor Pulmonale
A
- treat chronic resp failure
- supplemental O2 (help decrease RV after load by reducing the pulmonary vascular resistance)
- manage right heart failure sx w/ fluid and salt restriction and diuretics
11
Q
Pulmonary Embolism
-etiologies
A
Etiologies:
- air
- amniotic fluid during active labor (getting into the venous system)
- fat (long bone fx)
- foreign bodies (Talc in IV drug users)
- parasite eggs (schistomoniasis)
- septic emboli
- tumor cells
- venous thrombosis*
12
Q
Where do clots come from before they enter the lungs?
A
- 50-70% of patients with PE have lower extremity DVT
- -calf veins
- -popliteal and ileofemoral veins
13
Q
Risk factors for DVT & PE
A
- Virchows Triad:
- -venous stasis
- -injury to the vessel wall
- -hypercoagulability
14
Q
Factors the promote venous stasis
A
- immobility
- postoperative state
- obesity
- hyperviscosity (polycythemia)
- Increased ventral venous pressure (low cardiac output and pregnancy)
15
Q
Vessel Damage may come from?
A
- prior episodes of thrombosis (1st thrombus damages veins and valves)
- orthopedic surgery
- trauma