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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A
  • BMPR2
  • Endoglin
  • SMAD9
  • CAV1
  • KCNK3
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Risk factors for DVT & PE

A
  • Virchows Triad:
  • -venous stasis
  • -injury to the vessel wall
  • -hypercoagulability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Factors the promote venous stasis

A
  • immobility
  • postoperative state
  • obesity
  • hyperviscosity (polycythemia)
  • Increased ventral venous pressure (low cardiac output and pregnancy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Vessel Damage may come from?

A
  • prior episodes of thrombosis (1st thrombus damages veins and valves)
  • orthopedic surgery
  • trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Factors associated w/ hypercoagulability

A
  • 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)
17
Q

Physiologic Changes w/ PE

A
  • 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
18
Q

Signs and Sx of PE

A
  • 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
19
Q

PE Work Up/Diagnostic Studies

A
  • 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
20
Q

PE EKG findings

A

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

  • may have Right bundle branch block
  • Tachycardia
21
Q

Are arterial blood gases specific for PE?

A
  • no, they are non-specific

- -may show hyperventilation

22
Q

D-dimer for PE work up

  • when is this useful?
  • when would it be elevated?
A
  • 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.

23
Q

PE Cardiac testing

  • Troponin I, Troponin T and BNP may be elevated d/t?
  • are these test useful in dx PE?
A
  • R ventricular strain or acute RV failure

- no, they often confuse the mattter. :)

24
Q

PE Dx studies

A
  • CXR
  • CT angiogram
  • V/Q scan
  • lower extremity venous ultrasound
  • pulmonary angiography
  • MRI
25
Q

PE findings on CXR

A
  • 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.
26
Q

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

A

-CT Pulmonary ANgiography

27
Q

How does a V/Q scan work?

A
  • radioactive compound inhaled into spaces of lung.

- radioactive compound injected into vein, travels to lung tissues in blood vessels

28
Q

Wells Criteria

  • what is this used for?
  • Scoring
  • what is the next step if score is less than 4? greater than 4?
A

-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
29
Q

WHat is PERC?

-How do you apply this?

A

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.
30
Q

Tx of PE

A
  • 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.