LEARN MORE...

Pulmonary Vascular Disorders Notes

Content type

User Generated

Subject

Health & Medical

Type

Other

Uploaded By

whymzhecul95

Pages

Showing Page:

1/6

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

Showing Page:

2/6

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!

Showing Page:

3/6

End of Preview - Want to read all 6 pages?

Access Now

Unformatted Attachment Preview

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 • • • ? ...
Purchase document to see full attachment

Tags: pulmonary system ulmonary Vascular Disorders Elevated pulm pressure pulm vascular bed RV enlargement