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RESPIRATORY EXAM 1 > CLINICAL 2 > Flashcards

CLINICAL 2 Flashcards

1
Q

Most common presenting symptom of PHTN?

A

Dyspnea on exertion, maybe w/ palpitations and dizziness

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2
Q

What is different about the CXR of PHTN and CHF?

A

PHTN should not have infiltrates on CXR and CHF should

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3
Q

What murmurs may be heard with PHTN?

A

Systolic tricuspid regurgitation with a loud P2

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4
Q

Why isn’t PHTN picked up much as a Dx?

A

It is asymptomatic until the disease has progressed quite a ways

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5
Q

What causes the Sx of PHTN? i.e. why do they BECOME symptomatic?

A

The beginning of a decrease in cardiac output causes the beginning of the Sx

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6
Q

Why do Sx of PHTN get worse without increasing pulmonary arterial pressures?

A

Because the Sx fo PHTN are from a decrease in cardiac output; thus, as CO decreases less blood is pumped into the PA so the pressures will kind of plateau, even though pulmonary vascular resistance increases

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7
Q

By the time idiopathic PHTN is Dx’d the median survivial is:

A

2.8 years

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8
Q

Name the 4 high risk populations for pulmonary HTN

A

FMHx, Connective tissue Dz (SLE, scleroderma), Congenital heart disease, Hx of pulmonary embolism–scarring is part of dissolution process!

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9
Q

What is the least invasive diagnostic test for PHTN?

A

ECHOCARDIOGRAM

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10
Q

What will an echocardiogram show in PHTN?

A

Normal left ventricular function but severe RV dysfunction with an end systolic pressure GREATER THAN 90 mmHg in the RV, no shunt

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11
Q

What is the purpose of doing additional studies once the echo results are significant for PHTN?

A

To discover a primary cause, i.e. most PHTN is idiopathic but it may be secondary to something else!

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12
Q

What are the next steps as the doctor after discovering that a person has PHTN on echo (3)?

A

Do additional tests to figure out if primary or secondary, confirm with cardiac catheterization and then target Tx accordingly

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13
Q

What is the hemodynamic defintion of PAH?

A

mPAP >25 mmHg resting or >30 mmHg with exertion with a normal PCWP

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14
Q

If the pulmonary capillary wedge pressure is high can you Dx PHTN? Why or why not?

A

NO. If the PCWP is high, then the cause of their high PA pressures may be left heart failure, as the most common cause of RH failure is LH failure

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15
Q

What are the 4 approved classes of drugs for the Tx of PHTN?

A

Prostacycline, Endothelin receptor inhibitors, Phosphodiesterase inhibitors, and NO

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16
Q

What is the MOA of prostacyclines?

A

Vasodilation via a prostaglandin-analogue mechanism

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17
Q

What is the added benefit of prostacylines in Tx of PHTN? Name 2 drugs.

A

inhibition of platelet aggregation; epoprosterol, treprostinil

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18
Q

What is the major drawback of epoprosterol?

A

Good to Tx PHTN but is IV only and assoc with infections and rebound HTN that can kill the pt

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19
Q

What are 2 endothelin receptor antagonists?

A

Ambrisentan and Bosentan

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20
Q

Which drug for Tx of PAH is associated with high liver function tests?

A

Bosentan

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21
Q

What is the cause of Sx in acute PE vs. chronic PE?

A

Acute PE Sx are FROM the embolus itself, Chronic PE Sx are sort of from the PE but REALLY they are from the development of PHTN

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22
Q

What are some signs of a massive PE?

A

Hypotension with an increased central venous pressure

23
Q

What is the % mortality of an untreated PE? What is the most common cause of death in PE?

A

30% die if untreated, recurrent PE

24
Q

Name 5 prognostic indicators of PE:

A

Right ventricular dysfunction, Brain Natriuretic peptides, Serum troponins, presence of right ventricular thrombus, presence of DVT

25
Q

What do BNP’s and Troponins reveal about pulmonary emboli?

A

Both reflect right heart strain, troponins indicate a probable subendocardial MI

26
Q

Where do most pulmonary emboli originate?

A

Deep leg veins

27
Q

Where do most pulmonary emboli go in the lungs? What Sx will a small pulmonary embolus produce?

A

Most pulmonary emboli go to the lower lobes and small pulmonary emboli go more distally and produce PLEURITIC SX

28
Q

Why are people with pulmonary emboli hypotensive?

A

Because the increased pulmonary vascular resistance decreases the CO and decreases left ventricular preload = lower systemic stroke volume = hypotension

29
Q

How do you know that a person with PA pressures of 50-60 has a chronic problem?

A

Because if the problem were acute and caused pulmonary artery pressures that high, they would be dead (acute cor pulmonale)

30
Q

What is the most common presentation of pulmonary embolus? What peripheral signs might they have?

A

Dyspnea with rest or exertion; may have thigh or calf tenderness (DVT)

31
Q

What are the most common SIGNS of PE?

A

Tachypnea and tachycardia

32
Q

What is the utility of troponins for the diagnosis of PE?

A

They are not useful for diagnosis. However, if there is a known PE, then the troponins are useful for PROGNOSIS

33
Q

What is the most common EKG finding with PE?

A

NONSPECIFIC FINDINGS

34
Q

What is hypoxemia with a normal CXR until proven otherwise?

A

PULMONARY EMBOLISM

35
Q

What is the most common finding on CXR for PE?

A

If anything, cardiomegaly

36
Q

When is a V/Q scan useful for Dx of PE?

A

If there was a high clinical suspicion of PE being present already

37
Q

When would it be better to use a V/Q scan than contrast angiography?

A

Contrast allergies or renal impairment

38
Q

What is the gold standard for ACUTE PE Dx? What makes the Dx?

A

CT angiography; acute cutoff in the filling of a vessel indicates PE

39
Q

What is a major benefit of spiral CT (CT angiography)?

A

You can see other parenchymal disease, such as fibrosis

40
Q

What Tx is useful for hemodynamic and respiratory support of PE?

A

Hemodynamically: Tx the hypotension with fluids, if refractory, use vasopressors? Respiratory give supplemental O2 and if severe then mechanical ventilation

41
Q

Discuss the utility of anticoagulation and thrombolytics for PE.

A

Anticoagulants decrease risk of death bc decrease recurrent emboli (the most common cause OF death) but they don?t get rid of the embolus that is present; fibrinolytics breakdown the clot but don?t improve survival and increase risk of hemorrhage

42
Q

What are the 6 indications of THROMBOLYTICS?

A

1) Persistent Hypotension 2) RV dysfunction 3) free floating atrial/ventricular emboli 4) Large perfusion defects 5) severe hypoxemia and 6) patent foramen ovale (paradoxical emboli)

43
Q

What are 4 absolute contraindications to thrombolytic therapy?

A

1) History of hemorrhagic stroke 2) Active cranial neoplasm 3) Trauma or surgery in past 2 months (cranial) 4) internal bleeding in past 6 months

44
Q

5 relative C/I to thrombolytic therapy

A

1) Bleeding diathesis 2) Severe HTN 3) surgery in past 100 days 4) thrombocytopenia 5) NON hemorrhagic stroke in past 2 months

45
Q

What clinically defines ARDS? How is it diff from PE?

A

It is acute with bilateral hilar infiltrates and NO evidence of left atrial pressure increase? This is different from PE in that there is pulmonary edema

46
Q

Where are the infiltrates in ARDS?

A

BILATERAL

47
Q

What is the mnemonic for ARDS?

A

Acute process, Restrictive process, Diffuse infltrates, Shunt hypoxemia

48
Q

What is the prognosis of RV dysfunction in PE?

A

2/3 fold increase in mortality

49
Q

What is the prognostic value of a right atrial thrombus in a pt with a PE?

A

Worse 14 day mortality

50
Q

What are the most common Sx of PE? What are the most common SIGNS of PE?

A

Sx = dyspnea at rest or exertional; SIGNS = tachypnea and tachycardia

51
Q

Why would a patient with PE be tachycardic?

A

Because they are hypotensive, so there is reflex tachycardia from baroreceptors

52
Q

Can a D-Dimer rule out a PE?

A

NO

53
Q

What is the probability of a recurrent PE if the aPPT is not therapeutic within the first 24 hours of therapy for a PE?

A

25%

54
Q

If a person has persistent hypotension from a PE despite fluids and pressors should you anticoagulate or use fibrinolytics?

A

Fibrinolytics, that is the main indication for them

RESPIRATORY EXAM 1 (8 decks)

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