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Pulmonary Vascular Disorders Notes

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PULMONARY VASCULAR DISORDERS
PULMONARY SYSTEM
Lungs need to remain perfused to support all other organs
Rest of systemic circulation dilates response to hypoxia
Pulmonary vasoconstriction occurs LOCALLY in response to hypoxia
Resp failure SaO2 falls- pulm arterial pressure rises
Hypoxic pulmonary vasoconstriction pus or fluid fills alveoli- no reason to send blood there (no one at
the station to pick up, send less trains!)
-vessels there will contrict LOCALLY! Allow blood flow to the caps that are working well.
-A few? Not bad. A lot? more constricted vessels, higher blood pressure
PULMONARY HTN:
Can be primary ; idiopathic (not as common)
secondary ; result of other disease, often cardiac (CHF, decreased EF)
Elevated pulm pressure results from increase in pulm vascular resistance to blood flow through
small arteries, arterioles
Mean artery pressure is above 25mmHg at rest- 30mmhg while exercising w no cause.
50% of area of normal pulmonary bed can be compromised due to hypoxia before symptoms
occur
Reduced size of pulm vascular bed increased pressure w circulation of blood
Death due to right ventricular failure, pulm embolism, hemorrhage due to sudden death
-increased workload on heart, right side is not equipped to handle this and will fail
- S/S = JVD, edema, eventually fluid in the lungs
-lungs are resistant at first, but heart is still working harder
PRIMARY PULMONARY HTN: unknown etiology
Persistent elevated pressures
Cause deficient release of vasodilating mediators from pulm epithelium, could be genetic
More common in women, young! 36 average age-> symptoms prob show later; dyspnea,
weakness, reccurent syncope
Diagnostics;
-CXR big pulm artery, clear lungs, big heart, enlarge R side
-Chest CT initially decreased PaO2- normal or low PaO2
-ABG’s at first, decreased PaCO2- normal or low PaO2
- PFTs restrictive lung volumes pattern on PFT
ECG/ECHO- RV hypertrophy, other changes
Right sided cardiac catheterization
measure PAP, CO, LVFP

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PATHO MA
TREATMENT: (primary)
Early recognition! Prevent progression; NO cure, treat symptoms
OXYGEN given to treat hypoxemia- goal of >/= 90% sats, prevent pulm vasoconstriction
ANTICOAGS prevent thrombus, coumadin, INR 2-3
DIURETICS reduce dyspnea, peripheral edema, may reduce volume overload in R. failure
CALCIUM CHANNEL BLOCKERS vasodilate, reduce afterload, improve r sided failure, reduce
PAP Diltiazem, Nifedepine
PHOSPHODIESTERASE inhibitors watch orthostatic hypotension
VASODILATORS; (IV) Prostacyclin -promotes pulmonary vasodilation/reduces pulm vascular
resistance
-no effect on SVR, platelet aggregation inhibitor (6 min half life!)
-can see rapid deterioration in abrupt withdrawal
VASOLDILATOS (inhaled) Prostacyclin inhalant 6-9x a day
LUNG TRANSPLANT limited availability, may still re-occur 
SECONDARY;
Occurs when another disease causes it
Symptoms will reflect underlying disease causing it
-1)capillary loss (COPD)
-2) Stiffening of pulm vasculature (fibrosis!)
-3) Obstructed blood flow (PE)
Treatments; treat underlying cause!
-initiate PPH shit to manage symptoms
COR PULMONALE ; shitty lungs, poor r side function
RV enlargement
Condition of hypertrophy/dilation of RV results from disease process that affects
function/structure of lung
Acute cor pulmonale
-associated with pulm embolism- causes RV dilation (quick, high pressures, lung stress)
Chronic cor pulmonale
-associated w/caused by various disorders and characterized by RV hypertrophy
-DILATION/STRETCHING, HYPERTROPHY/OVERGROWTH of CELLS
RV doesn’t have good compensating ability (unlike LV) dilates -fails quick!
Complications of PE and Pulm infarct
Normally RV doesn’t work hard and has low pulm resistance – R. heart flow passes easily
usually. Weak lil bitch
RV failure leads to increased pressure- causing RV to bulge into septum
It will try to stretch and thicken but it needs TIME to do this!

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PULMONARY VASCULAR DISORDERS PULMONARY SYSTEM • • • • Lungs need to remain perfused to support all other organs Rest of systemic circulation dilates → response to hypoxia Pulmonary vasoconstriction occurs LOCALLY in response to hypoxia Resp failure → SaO2 falls- pulm arterial pressure rises Hypoxic pulmonary vasoconstriction → pus or fluid fills alveoli- no reason to send blood there (no one at the station to pick up, send less trains!) -vessels there will contrict LOCALLY! Allow blood flow to the caps that are working well. -A few? Not bad. A lot? → more constricted vessels, higher blood pressure PULMONARY HTN: Can be → primary ; idiopathic (not as common) → secondary ; result of other disease, often cardiac (CHF, decreased EF) • • • • • Elevated pulm pressure results from increase in pulm vascular resistance to blood flow through small arteries, arterioles Mean artery pressure is above 25mmHg at rest- 30mmhg while exercising w no cause. 50% of area of normal pulmonary bed can be compromised due to hypoxia before symptoms occur Reduced size of pulm vascular bed → increased pressure w circulation of blood Death due to right ventricular failure, pulm embolism, hemorrhage due to sudden death -increased workload on heart, right side is not equipped to handle this and will fail - S/S = JVD, edema, eventually fluid in the lungs -lungs are resistant at first, but heart is still working harder PRIMARY PULMONARY HTN: unknown etiology • • • ? ...
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