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Last updated 12:18 PM on 9/22/26
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286 Terms

1
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What is a pulmonary embolism (PE)?

A critical medical condition caused by a blockage in one or more pulmonary arteries.

2
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What is the most common cause of a pulmonary embolism?

A thrombus (blood clot) that has traveled from another part of the body.

3
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Where do most clots causing PE originate?

The legs, most commonly from a deep vein thrombosis (DVT).

4
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What happens when a clot obstructs a pulmonary artery?

Blood flow to the lung tissue supplied by that artery is obstructed.

5
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Why can't the affected lung tissue adequately oxygenate blood during a PE?

Blood cannot reach the affected alveoli to pick up oxygen.

6
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What can happen to lung tissue if a PE is sufficiently large?

The affected lung tissue can infarct and die.

7
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What is a thrombus?

A blood clot that forms within a blood vessel.

8
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What is an embolus?

Material that travels through the bloodstream and becomes lodged in a blood vessel.

9
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What is the most common type of embolus causing PE?

A blood clot.

10
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What are non-thrombotic emboli?

Emboli made of materials other than blood clots.

11
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What can cause a fat embolus?

Fractures of large bones, such as the femur or pelvis.

12
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What can cause an air embolus?

Improper removal of central venous lines or accidental injection of air through an IV.

13
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What is a tumor embolus?

A fragment of a cancerous tumor that travels through the bloodstream.

14
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What is an amniotic fluid embolism?

A rare complication of childbirth in which amniotic fluid enters the maternal circulation.

15
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What happens first in the pathophysiology of a PE?

A clot lodges in a pulmonary arterial vessel.

16
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What happens to pulmonary vascular resistance when a clot lodges in a pulmonary artery?

Pulmonary vascular resistance immediately increases.

17
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How does increased pulmonary vascular resistance affect the right ventricle?

The right ventricle must pump against much higher pressure.

18
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What happens to the right ventricle when it must pump against massive pressure?

It dilates, works harder, and can eventually fail.

19
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What can result from right ventricular failure during a massive PE?

Shock.

20
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What happens when the clot interacts with vessel linings and platelets?

It triggers the release of chemical mediators.

21
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Which chemical mediators are released during PE-related vascular reactions?

Serotonin and thromboxane A2.

22
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What effect do serotonin and thromboxane A2 have on blood vessels?

They cause widespread vasoconstriction.

23
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What respiratory imbalance does a PE create?

Alveolar dead space.

24
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What is alveolar dead space?

Ventilation without adequate perfusion.

25
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Why does a PE create alveolar dead space?

Air can enter the alveoli, but blood cannot flow past them because the pulmonary artery is blocked.

26
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What happens to oxygen levels because of the V/Q mismatch in PE?

Hypoxemia develops.

27
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How can PE cause atelectasis?

Loss of blood flow can stop surfactant production, contributing to alveolar collapse.

28
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Is PE primarily a ventilation problem or a perfusion problem?

A perfusion problem.

29
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Why is PE considered a perfusion problem?

Air can still enter the alveoli, but blood cannot adequately flow past them for gas exchange.

30
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What happens to ventilation during PE?

Air can still enter the affected alveoli.

31
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What happens to perfusion during PE?

Blood flow to affected alveoli is reduced or blocked.

32
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What type of V/Q mismatch occurs with PE?

Ventilation exceeds perfusion.

33
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What is the result when ventilation exceeds perfusion?

Alveolar dead space.

34
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What happens to the pulmonary vessel lining during PE?

The clot damages the endothelium and triggers inflammation.

35
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What is the endothelium?

The inner lining of a blood vessel.

36
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What happens to the airways during the inflammatory response to PE?

Bronchoconstriction can occur.

37
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What causes bronchoconstriction during PE?

Inflammatory mediators released in response to endothelial injury.

38
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How does bronchoconstriction affect the alveoli?

It further limits airflow into the alveoli.

39
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What is hypoxemia?

Low oxygen levels in the blood.

40
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Why does hypoxemia occur with PE?

Blocked pulmonary blood flow and bronchoconstriction interfere with effective gas exchange.

41
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What part of the heart is most affected by a large PE?

The right side of the heart, especially the right ventricle.

42
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What does the right ventricle normally do?

It pumps deoxygenated blood into the pulmonary arteries.

43
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How does a large PE affect right-ventricular workload?

It dramatically increases the pressure against which the right ventricle must pump.

44
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Why is the right ventricle vulnerable during a large PE?

It is highly sensitive to sudden pressure changes.

45
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What happens to blood when the right ventricle struggles against the increased pulmonary resistance?

Blood backs up, causing right-ventricular volume overload.

46
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What happens to the right ventricle during severe volume overload?

It dilates and can rapidly begin to fail.

47
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What happens to blood flow to the left side of the heart when the right ventricle fails?

Less blood reaches the left ventricle.

48
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What happens to cardiac output when less blood reaches the left ventricle?

Cardiac output decreases.

49
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What type of shock can result from severe PE?

Obstructive shock.

50
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What is obstructive shock?

A life-threatening condition in which an obstruction prevents adequate blood flow to the body's tissues.

51
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Why can PE cause obstructive shock?

Right-ventricular failure decreases forward blood flow to the left side of the heart and the systemic circulation.

52
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Why is PE with cardiac dysfunction a medical emergency?

Immediate intervention may be necessary to prevent death.

53
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What is Virchow's triad?

Three major factors that contribute to DVT formation: venous stasis, hypercoagulability, and vascular endothelial damage.

54
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Why is Virchow's triad important when assessing PE?

DVT is the most common source of a PE.

55
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What are the three components of Virchow's triad?

Venous stasis, hypercoagulability, and vascular endothelial damage.

56
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What is venous stasis?

Slow or pooled blood flow within the veins.

57
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How can prolonged immobility cause venous stasis?

Remaining still for long periods slows venous blood flow.

58
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What situations can cause prolonged immobility?

Bed rest, long-distance travel, and casting.

59
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Why are long-distance travelers at risk for DVT?

Prolonged sitting can cause venous stasis.

60
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Why are long-haul truck drivers at risk for DVT and PE?

Long periods of sitting contribute to venous stasis.

61
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How can heart failure contribute to venous stasis?

An inefficient cardiac pump can cause blood to pool.

62
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How can varicose veins contribute to venous stasis?

Damaged venous valves allow blood to pool.

63
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What is hypercoagulability?

An increased tendency of the blood to clot.

64
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What types of events can cause hypercoagulability?

Trauma and major surgery.

65
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How can cancer increase DVT risk?

Cancer can create a hypercoagulable state.

66
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How does pregnancy increase DVT risk?

Pregnancy is associated with increased blood-clotting tendency.

67
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How can estrogen-containing contraceptives affect DVT risk?

They can contribute to hypercoagulability.

68
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How can hormone replacement therapy affect DVT risk?

It can contribute to hypercoagulability.

69
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What genetic disorder listed in the notes increases clotting risk?

Factor V Leiden mutation.

70
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What is vascular endothelial damage?

Injury to the inner lining of a vein.

71
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What can cause vascular endothelial damage?

Trauma and surgery.

72
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How can atherosclerosis contribute to endothelial damage?

It can damage the inner lining of blood vessels.

73
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What indwelling devices can contribute to endothelial damage?

Central venous catheters and cardiac catheterization sheaths.

74
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Where does a DVT typically form?

In large veins of the leg.

75
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What is a proximal DVT?

A DVT located in an upper-leg vein.

76
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Which veins are examples of proximal DVT locations?

External iliac, deep femoral, great saphenous, and popliteal veins.

77
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Why are proximal DVTs more dangerous?

They are more unstable and more likely to dislodge and travel to the lungs.

78
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Why can proximal DVTs form larger emboli?

Larger veins can hold larger clots.

79
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What is a distal DVT?

A DVT located in the lower-leg veins.

80
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Which veins are examples of distal DVT locations?

Anterior and posterior tibial veins.

81
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How do distal DVTs compare with proximal DVTs?

They are generally more stable and less likely to dislodge.

82
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Can a distal DVT become more dangerous?

Yes. The clot can propagate upward and become proximal.

83
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What is clot propagation?

Growth or extension of a clot into larger or more proximal veins.

84
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What is the most classic subjective respiratory symptom of PE?

Sudden-onset dyspnea.

85
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How might a patient describe dyspnea from PE?

“I feel like I can't catch my breath.”

86
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What is pleuritic chest pain?

Sharp chest pain that worsens with breathing.

87
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How might a patient describe pleuritic chest pain?

“It's a sharp pain in my chest when I breathe in.”

88
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What psychological sensation can occur with PE?

A sense of impending doom.

89
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How might a patient describe a sense of impending doom?

“I feel like something terrible is about to happen” or “I feel like I might die.”

90
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What emotional symptoms can occur with PE?

Anxiety and restlessness.

91
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What respiratory-rate change commonly occurs with PE?

Tachypnea.

92
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What is tachypnea?

Rapid breathing.

93
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What heart-rate change commonly occurs with PE?

Tachycardia.

94
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What temperature finding can occur with PE?

Low-grade fever.

95
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What blood-pressure change can occur with severe PE?

Hypotension.

96
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What cough finding can occur with PE?

Cough, sometimes with hemoptysis.

97
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What is hemoptysis?

Coughing up blood.

98
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What is a pleural friction rub?

A harsh, grating sound heard during respiratory assessment.

99
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What heart sounds may occur with PE?

Extra heart sounds such as S3 or S4.

100
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Where may S3 or S4 be particularly notable in PE?

On the right side of the chest.