Pulmonary HTN - pathophysiology - what pressure is considered pulmonary HTN?

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

- 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

- 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

- 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

Pulmonary Vascula Disorders Flashcards by Angela Roden

Pulmonary HTN

pathophysiology
what pressure is considered pulmonary HTN?

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

How well did you know this?

Not at all

Perfectly

Pulm HTN etiology

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

How well did you know this?

Not at all

Perfectly

pulmonary HTN may be genetic, what are some of the markers?

BMPR2
Endoglin
SMAD9
CAV1
KCNK3

How well did you know this?

Not at all

Perfectly

Sx of Pulm HTN?

Signs??

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)

How well did you know this?

Not at all

Perfectly

Pulmonary HTN Work Up

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

How well did you know this?

Not at all

Perfectly

Tx of pulm HTN

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

How well did you know this?

Not at all

Perfectly

Cor Pulmonale

what is this?
etiologies

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

How well did you know this?

Not at all

Perfectly

Signs and Sx of Cor Pulmonale

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

How well did you know this?

Not at all

Perfectly

Work up of Cor Pulmonale

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

How well did you know this?

Not at all

Perfectly

Tx Cor Pulmonale

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

How well did you know this?

Not at all

Perfectly

Pulmonary Embolism

-etiologies

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*

How well did you know this?

Not at all

Perfectly

Where do clots come from before they enter the lungs?

50-70% of patients with PE have lower extremity DVT
-calf veins
-popliteal and ileofemoral veins

How well did you know this?

Not at all

Perfectly

Risk factors for DVT & PE

Virchows Triad:
-venous stasis
-injury to the vessel wall
-hypercoagulability

How well did you know this?

Not at all

Perfectly

Factors the promote venous stasis

immobility
postoperative state
obesity
hyperviscosity (polycythemia)
Increased ventral venous pressure (low cardiac output and pregnancy)

How well did you know this?

Not at all

Perfectly

Vessel Damage may come from?

prior episodes of thrombosis (1st thrombus damages veins and valves)
orthopedic surgery
trauma

How well did you know this?

Not at all

Perfectly

Factors associated w/ hypercoagulability

surgery
meds (hormones)
Disease (malignancy)
Genetic factors
-Factor V leiden (most common)
-Dysfunction of Protein C, S, and ANtithrombin III, prothrombin gene mutation, antiphospholipid bodies)

Physiologic Changes w/ PE

reflex bronchoconstriction and vasoconstriction from neurohormonal responses
right ventricular failure (if massive thrombus)
Pulmonary Vascular Obstruction (increased pulmonary vascular resistance, causes physiologic deadspace…ventilation without perfusion leading to hypoxemia d/t R to L shunting of blood, decreased cardiac output, surfactant depletion causing atelectasis

Signs and Sx of PE

Sx:
pleuritic chest pain**
cough
leg pain
hemoptysis
palpitations
wheezing
anginal pain
Signs:
Tachypnea*
crackles
tachycardia
S4
S3
Accentuated S2 (only if chronic thromboembolic dz)
Low grade fever
Homans sign (dorsiflex the leg, if they have pain its +)
Pleural friction rub
cyanosis

PE Work Up/Diagnostic Studies

EKG
ABG’s (if ABGs dont go up after O2 think PE)
D-dimer
Troponin I or T
BNP
CXR
CT angiography
Ventilation Perfusion Scan
Venous ultrasound of the extremities
pulmonary angiograph***( gold standard)
MRI

PE EKG findings

-S1G3T3
S wave in lead 1
Q waves in lead III
T wave inversion in lead III

may have Right bundle branch block
Tachycardia

Are arterial blood gases specific for PE?

no, they are non-specific

- -may show hyperventilation

D-dimer for PE work up

when is this useful?
when would it be elevated?

useful if its negative meaning it is unlikely that there is clotting
*Sensitivity 95-97%
*Specificty 45%

-this will be elevated if there is a clot.

PE Cardiac testing

Troponin I, Troponin T and BNP may be elevated d/t?
are these test useful in dx PE?

R ventricular strain or acute RV failure

- no, they often confuse the mattter. :)

PE Dx studies

CXR
CT angiogram
V/Q scan
lower extremity venous ultrasound
pulmonary angiography
MRI

PE findings on CXR

- wedge shaped defect (hamptons hump) - atelectasis - parenchymal infiltrates - pleural effusion - prominent central pulmonary artery (Westermark Sign) - **A normal CXR is the most common finding, if normal in the setting of acute hypoxemia without prior hx of lung disease = highly suggestive of PE.

WHich test is most sensitive for detecting proximal PE in the larger pulmonary arteries?

-CT Pulmonary ANgiography

How does a V/Q scan work?

- radioactive compound inhaled into spaces of lung. | - radioactive compound injected into vein, travels to lung tissues in blood vessels

Wells Criteria - what is this used for? - Scoring - what is the next step if score is less than 4? greater than 4?

-used to claculate pretest probabilty of PE in non-pregnant patients. - unlikely score less than or equal to 4 - likely score greater than 4. Score less than 4; -get D-dimer, if less than 500ng/ml no further testing needed. Score greater than 4: - D-dimer greater than 500ng/ml proceed to CTA or VQ/scan - HOWEVER if high prob score (greater than 6) skip the d-dimer and go directly to CTA or V/Q scan

WHat is PERC? | -How do you apply this?

PERC is Pulmonary Embolism Rule Out Criteria - used only for patients with low probablity of PE - if all criteria are met no further testing needed - if not meeting all 8 criteria then further testing with D-dimer or imaging is needed.

Tx of PE

- hospitalization - supplemental O2 - Heparin (LMWH or UFH) - assess for fibrinolytics if significant hemodynamic compromise - outpatient anticoagulation for 3-6 mo depending on situation (usually for life) - inferior vena cava filter if large clot burden or unable to anticoagulate as outpatient.