Are you ready to learn about Pulmonary Vascular Disease? If so then you’re in the right place, because that is what this study guide is all about.

The practice questions listed below correlate well with Egan’s Chapter 28, so you can use this information to prepare for your exams.

Let’s go ahead and dive right in!

What is Pulmonary Vascular Disease?

Basically, it is any condition that affects the blood vessels is the route between the lungs and the heart.

In its normal flow, blood travels from the heart to the lungs, and then back to the heart. This process is extremely important because the lungs are continually loading blood with oxygen. All the while, they are getting rid of carbon dioxide.

So if there is a disease that interferes with this flow, it goes without saying that this is a very serious problem for the patient.

What are the Causes of Pulmonary Vascular Disease?

The causes of Pulmonary Vascular Disease include the following:

  • Pulmonary Arterial Hypertension
  • Pulmonary Venous Hypertension
  • Pulmonary Embolism
  • Chronic Thromboembolic Disease

What are the Tests for Pulmonary Vascular Disease?

The tests for Pulmonary Vascular Disease include the following:

  • Computed tomography (CT scan)
  • Ventilation/perfusion scan (V/Q scan)
  • Echocardiography (echocardiogram)
  • Right heart catheterization
  • Chest X-ray film
  • Pulmonary angiography (angiogram)

So now that you have a better understanding of Pulmonary Vascular Disease, so go ahead and go through some practice questions on this topic. This will really help you reinforce the information into your brain. Are you ready?

If your RT program is like mine, then you probably use the Egan’s Workbook. Don’t get me wrong, it’s a great workbook that can be helpful at times. The problem is, it takes way too long to look up all the answers.

To help with that, we looked up all the answers for you so that you don’t have to waste any more of your valuable time. Get instant access inside of our Workbook Helper. 🙂

Pulmonary Vascular Disease Practice Questions:

1. What is VTE?
It stands for Venous Thromboembolic Disease. It’s a diseases category that specifically refers to deep venous thrombosis (DVT) and pulmonary embolism (PE).

2. What is deep venous thrombosis?
A thrombus that originates in the deep veins of the lower extremities.

3. What is a pulmonary embolism?
A blockage of a pulmonary artery by foreign matter. The obstruction may be fat, air, tumor tissue, or a thrombus that usually arises from a peripheral vein, most frequently
arising from a DVT.

4. VTE is an important cause of morbidity and mortality among who?
Hospitalized patients.

5. Why is early recognition and treatment essential and can be lifesaving?
Because one-third of the deaths caused by PE occur within 1 hour of the symptom onset. The mortality rate in the group of patients with PE that goes undiagnosed is 30%; if the venous thrombosis is recognized and managed, the mortality rate is less than 8%.

6. Where is the point of origin of a pulmonary embolism?
It occurs from a DVT of the lower extremities or pelvis in 86% of cases.

7. Most of the time, the clinical presentation of PE and DVT is what?
It is nonspecific. A high index of suspicion is important to make the diagnosis in patients at risk.

8. Can you reduce the risk for a VTE?
Yes, prophylactic therapy reduces the risk for VTE in patients at risk, but, unfortunately, prophylactic therapy is underused.

9. Pharmacologic choices for prophylaxis include what?
Low-dose subcutaneous heparin, warfarin, LMWH, and dextran.

10. What are the mechanical ways to prevent a VTE?
Mechanical measures include early ambulation, wearing elastic stockings, pneumatic calf compression, and electric stimulation of calf muscles.

11. Management of VTE includes what?
Anticoagulation therapy (heparin and warfarin).

12. What is IPAH?
It stands for idiopathic pulmonary arterial hypertension. It is a rare disease that mainly affects young adults. In IPAH, damage to the endothelium of the pulmonary artery alters the balance between vasoconstrictors and vasodilators, favoring vasoconstriction. Thrombosis and cellular proliferation are contributors to PH.

13. The management of IPAH includes what?
Anticoagulation and the administration of vasodilators (calcium channel blockers, prostanoids, endothelin receptor antagonists, PDE5 inhibitors, and soluble guanylate cyclase stimulators). Lung transplantation is an option for refractory cases.

14. What is a Deep Vein Thrombosis?
Blood clot forming in the deep veins, usually in the legs.

15. How can you detect a Pulmonary Embolism in patients?
Pulmonary embolism is detected by chest x-ray, pulmonary angiography, and radio scanning of the lung fields.

16. IPAH is a rare disease but it normally affects what group of people?
Young Adults.

17. Name some pharmacologic choices for prophylaxis of venous thromboembolism?
Low-dose subcutaneous heparin, Warfarin, low-molecular-weight heparin (enoxaparin) and dextran. These would be considered anticoagulation drug therapy.

18. What are the 5 categories Pulmonary Hypertension is classified as?
(1) Pulmonary Artery Hypertension (PAH), (2) Pulmonary Hypertension owing to left heart disease, (3) Pulmonary hypertension owing to lung diseases or hypoxia or both, (4) Chronic thromboembolic pulmonary hypertension, and (5) Pulmonary hypertension with unclear multifactorial mechanism.

19. What is Pulmonary Hypertension?
Condition characterized by abnormally high pulmonary artery pressures. (i.e., mean pulmonary artery pressure greater than 25mm Hg at rest).

20. What do hospitalized patients who are immobile need for the prevention of thromboembolism?
Prophylaxis

21. What is Pulmonary Hypertension called in patients with no underlying etiology that can be identified?
Idiopathic Pulmonary Artery Hypertension (IPAH).

22. Why is early recognition and treatment of DVT and PE essential?
Because 1/3rd of deaths occur within 1 hour of symptom onset. Mortality rates in patients with PE undiagnosed is 30%; if venous thrombosis is recognized and managed, the mortality rate is less than 8%.

23. What is Pulmonary Hypertension?
It is an increase in the pressure in the pulmonary arteries that could result from a large number of conditions that affect the lung vessels, lung parenchyma, and/or the heart.

24. What is a venous thrombosis?
A formation of blood clots caused by prolonged bed rest.

25. Where do most clots form?
In the deep veins of the lower legs.

26. What is a Pulmonary Infarction?
If a PE results in death of the lung tissue.

27. What is Pulmonale?
Chronic elevation of pulmonary blood pressure will eventually cause a form of right heart failure.

28. How many people develop thromboembolic disease each year in the US?
200,000 to 300,000 people.

29. How does a venous thrombosis form?
They form in deep veins or legs. 37% form in the right heart.

30. Which patient population or situations have the most risks of thrombosis?
Older or bedridden patients and trauma or heart failure are risky situations.

31. How does a pulmonary embolism affect the heart and lungs as they function together?
When blood vessels are blocked in the lung, the heart has to work much harder. If oxygenation is affected, the heart does not get the energy it needs, and cardiac output drops.

32. What are the primary hemodynamic consequences of a pulmonary embolism?
Increased right heart pressure, increased resistance, and poor cardiac output.

33. What are the most common symptoms of a pulmonary embolism?
Dyspnea and pleuritic pain (could mimic a heart attack).

34. What are the most frequent physical findings associated with a pulmonary embolism?
Tachypnea, tachycardia, and crackles heard in infected lung where edema is logged.

35. What are the most common ECG abnormalities associated with a pulmonary embolism?
Tachycardia and ST-segment depression.

36. How is a chest radiograph used in diagnosing a pulmonary embolism?
While the x-ray is frequently abnormal, it is not specific enough. It helps to rule out a pneumothorax and other causes. You could use contrast dye to inject in injured site it will show on a CT-scan.

37. How can you use an ABG to rule out a pulmonary embolism?
An ABG is not helpful in the diagnosis as associated abnormalities (hypoxemia and hypercarbia) are nonspecific. They are done to assess the patient’s pulmonary and acid status and to guide pulmonary management.

38. What is the gold standard for diagnosing a DVT?
Compression ultrasonography (check blood flow in the legs).

39. What tests are sensitive and reliable in confirming the diagnosis of a pulmonary embolism?
V/Q scans and spinal CT, and pulmonary angiography.

40. Will a chest x-ray and ultrasound show pulmonary embolism in the lungs?
No, no it will not.

41. What is the relationship between (V) ventilation and (Q) perfusion portions of scans in making a high-probability diagnosis of a pulmonary embolism?
A large segmental perfusion deflect without corresponding ventilation. The deflect is highly suggestive of a pulmonary embolism. When ventilation and perfusion deflects match in a lung segment, this equals a lower probability.

42. What is the pharmacologic prophylaxis for a pulmonary embolism?
Low-dose subcutaneous heparin (inject under skin), Warfarin (Coumadin), and low-molecular-weight heparin (heparinoids/dxtran).

43. What is the mechanical prophylaxis for a pulmonary embolism?
Early ambulation, elastic stockings, and pneumatic calf compression devices.

44. What is the standard pharmacologic therapy for an existing DVT or PE?
Drug: heparin; Action: inhibits coagulation; and Risks: bleeding (blood thinners) or thrombocytopenia.

45. What are the mechanical options available for the treatment of a massive pulmonary embolism?
Pulmonary embolectomy, catheter tip embolectomy, and catheter tip fragmentation.

46. When are vena cava filters indicated?
When a DVT is present and the patient has poor reserves. Filters may also be used with chronically immobilized patients and when anticoagulants are contraindicated.

47. What is the importance of providing oxygen to keep up the patient’s saturations with pulmonary hypertension?
Supplemental oxygen results in an increased alveolar partial pressure of oxygen, which causes pulmonary vasodilation and reducing PVR and possibly HTN.

48. What is the drug treatment for Pulmonary hypertension?
Iloprost and Treprostinil.

49. What is the role of alveolar hypoxia in the development of pulmonary hypertension?
It is multifactorial. Alveolar hypoxia (low PAO2) causes pulmonary vasoconstriction, which equals increased PVR and BP.

50. What are the factors seen in COPD that contribute to pulmonary hypertension?
Loss of pulmonary vascular bed, increased blood viscosity, and hyperinflation compresses pulmonary vasculature and this equals an increased PVR.

51. What is the only treatment that improves COPD and pulmonary hypertension patient survival?
Oxygen therapy, and if they are smoker, smoking cessation would also apply.

52. A patient on the mechanical ventilator shows increased VD/VT ratio. What disorder is most likely responsible?
Pulmonary Embolism.

53. What is the most appropriate test to confirm the presence of a suspected pulmonary embolism?
Pulmonary Angiography.

54. A V/Q scan reveals a defect in the right lower lobe without a corresponding decrease in ventilation. What is most likely the diagnosis?
Acute pulmonary embolus.

55. A patient presents to the ED with severe dyspnea and chest pain. Their respiratory rate is 24, minute volume is 14 L, and their ABG results are as follows: pH = 7.44, PaCO2 = 37, PaO2 = 100. What is most likely the cause of a normal CO2 when the patient has a large increase in minute ventilation?
The most likely cause is a pulmonary embolus.

Final Thoughts

And that officially wraps up our study guide on Pulmonary Vascular Disease. Thank you so much for reading all the way to the end. All of your hard work is going to pay off for you in a big way — I have no doubt about that.

Keep working and studying hard and as always, breathe easy my friend. 

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