Pulm Circulation II Flashcards

1
Q

Define pulm hypertension

A

pathologic incr in pulm arterial pressure

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2
Q

what is normal pulm arterial pressure

A

25/10

mean = 15 mmHg

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3
Q

what is # criterion for pulm HTN

A

> 25 mmHg

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4
Q

what is pulm arterial pressure equation

A
PPA = CO x PVR + PLA
PPA = mean pulmonary artery pressure
PLA = left atrial pressure
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5
Q

based on equation for pulm arterial pressure, what can pulm HTN be caused by (3)

A

incr CO (less common b/c compensatory vessel dilation and recruitment)

incr pulm vascular resistance
incr LA pressure

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6
Q

what does pulm arterial HTN involve?

A

pre-capillary circulation

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7
Q

does pulm arterial HTN lead to edema? why?

A

NO because PAH does not incr pressure in microcirculation

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8
Q

3 types of pre-capillary HTN

1) primary vascular disorders

effect on pulm vascular resistance, DLCO, lung function

A

1) Primary vascular disorders –> incr pulm vascular resistance (no pulm edema, not affect lung parenchyma)

low DLCO

normal lung function

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9
Q

subtype of primary vascular disorder
idiopathic pulm arterial HTN

who does it mainly affect?
genetic or not?

A

affects young women

genetic = BMPR2 gene

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10
Q

3 types of pre-capillary HTN

2) pleural-pulm disease

what is it caused by?

effect on DLCO, FEV1 and FVC

A

impaired ventilation
destruction of lung

decr DLCO, decr FEV1, decr FVC

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11
Q

3 types of pre-capillary HTN

3) chronic alveolar hypoventilation

caused by?

A

chronic elev of PCO2 without parenchymal lung disease

–> causes vascular remodeling –> HTN

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12
Q

Define pulm venous hypertension

A

post-capillary hypertension due to obstruction between pulm venous system and LA

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13
Q

symptoms of pulm venous hypertension

A

1) edema
2) Kerley B lines
3) vascular redistribution

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14
Q

Dana point classification of pulm HTN

A

1) Pulm arterial hypertension
2) Pulmonary HTN due to left heart disease
3) Pulmonary HTN assoc with lung disease and/or hypoxemia
4) thromboembolic pulmonary hypertension
5) pulmonary hypertension with unclear multifactorial mechanisms

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15
Q

subtypes of pulmonary arterial hypertension

A
  1. 1) Idiopathic (Primary)
  2. 2) Heritable
  3. 3) Diet or drugs (weight loss medications = fen-phen = pulmonary arterial HTN, cocaine, meth)
  4. 5) HIV
  5. 6) Connective tissue disease = scleroderma = vessels thickened and narrowed
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16
Q

subtypes of pulmonary arterial hypertension

A
  1. 1) Idiopathic (Primary)
  2. 2) Heritable
  3. 3) Diet or drugs (weight loss medications = fen-phen = pulmonary arterial HTN, cocaine, meth)
  4. 5) HIV
  5. 6) Connective tissue disease = scleroderma = vessels thickened and narrowed
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17
Q

Causes of acute pulm HTN

A

1) pneumonia (hypoxic vasoconstriction)
affecting entire lung

2) thromboembolic disease (incr PVR)
3) hypoxia (high altitude)

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18
Q

Risk factors for DVT

A

1) Trauma
2) stasis
3) hypercoagulability

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19
Q

Effects of pulmonary emolism

A

1) RV strain (submassive, use collaterals) or RV failure (massive low blood pressure, can’t get blood thru lungs)
2) incr myocardial O2 demand (oxygenated blood can’t enter coronaries to feed RV to sustain RV pushing against obstruction)
3) decr myocardial O2 delivery
4) death

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20
Q

Idiopathic pulmonary arterial HTN

A

paradigm of WHO group 1 disease

affects young women in 30’s and 40’s

median survival without treatment = 2.8 yrs

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21
Q

a

A

a

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22
Q

a

A

a

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23
Q

4 classes of approved medications for PAH

A

1) endothelin receptor antagonists
2) PDE-5 inhibitors
3) prostacyclins
4) calcium channel blockers

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24
Q

names and mechanism of endothelin receptor antagonists

A

names = bosentan
ambrisentan

block receptors to cause vasodilation

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25
Q

names and mechanism of PDE-5 inhibitors

A

sildenafil
tadalafil

promote accum of cGMP to enhance NO-mediated vasodilation

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26
Q

names and mechanism of prostacyclins

A

epoprostenol
iloprost
trepostinil

  • upregulate cAMP to cause vadoilation and decr RV afterload
  • antithrombotic
  • continuous IV
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27
Q

mechanism of calcium channel blockers

A

block Ca2+ channel –> vasodilation

work in subtype of IPAH (have acute response to admin of an iNO or IV prostacyclin during right heart cath

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28
Q

a

A

a

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29
Q

a

A

a

30
Q

a

A

a

31
Q

a

A

a

32
Q

how to work up patient with PE

A

1) H&P with Wells score
2) D-dimer breakdown product of thrombin
3) ECG
4) CXR
5) V/Q san
6) CT angiogram
7) angiogram
8) echo

33
Q

Clinical presentation of pulmonary embolism

A

1) dypsnea
2) chest pain
3) hypoxemia
4) hemoptysis

34
Q

CXR of pulm embolism

A

1) normal or areas of atelectasis, effusions, or wedge shaped infarcts

Hampton’s Hump = lung not getting sufficient blood flow = and filling with fluid = infarcted lung

Westermark’s Sign = hypoperfusion = region of lung underperfused due to blood clot

35
Q

EKG of pulm embolism

A
RV strain (inverted T wave
Sinus Tachy

S1 QIII TIII

36
Q

is D-dimer sensitive for pulm embolsm

A

sensitive but NOT SPECIFIC

sepsis
pregnancy could also raise D-dimer

37
Q

what is gold standard of pulm embolism

A

pulm angiography but invasive

The catheter is placed through the vein and carefully moved up into and through the right-sided heart chambers and into the pulmonary artery, which leads to the lungs

38
Q

what is most widely used modality for pulm embolism diagnosis

A

CT pulm angiography

39
Q

how does pulm embolism appear in nuclear ventilation/perfusion studies

A

decr perfusion and normal ventilation

40
Q

Blood gas measurement of pulm embolsm

A

increased A-a gradient

41
Q

is D-dimer sensitive for pulm embolsm

A

sensitive but NOT SPECIFIC

sepsis
pregnancy could also raise D-dimer

42
Q

what is gold standard of pulm embolism

A

pulm angiography but invasive

The catheter is placed through the vein and carefully moved up into and through the right-sided heart chambers and into the pulmonary artery, which leads to the lungs

43
Q

what is most widely used modality for pulm embolism diagnosis

A

CT pulm angiography

44
Q

how does pulm embolism appear in nuclear ventilation/perfusion studies

A

decr perfusion and normal ventilation

45
Q

how do you assess severity of cardiac injury due to PE

A

echo

46
Q

how do you prevent pulm embolism

A

1) avoid stasis
2) take prophylactic anticoagulants
3) devices to incr blood flow

47
Q

how do you treat DVT cause of PE

A

heparin then warfarin for at least 6 months

48
Q

how do you treat PE itself

A

1) heparin + warfarin
2) thrombolytic therapy (maybe)
3) IVC filter for high risk patients
4) acute surgical thromboectomy in extreme

49
Q
A patient with possible pulmonary hypertension undergoes right heart catheterization and the following measurements are made: 
mPAP = 45 mmHg 
PCWP = 20 mmHg 
CO = 5 L/min 
PVR = 5 WU 
What does this patient have?

A. WHO Group 1 Pulmonary Arterial Hypertension

B. WHO Group 2 PH Due to Left Heart Disease

C. WHO Group 3 PH Due to Lung Diseases and/or Hypoxia

D. WHO Group 4 Thromboembolic Pulmonary Hypertension

A

B = WHO group 2 PH due to Left heart disase

PVR incr but more importantly, PCWP incr

For PCWP > 15 so pulm venous hypertension

50
Q

V/Q scan

A

preferred for pregnancy

1) patient inhale radioactive Xenon
see where gas goes in lung
find regions ventilated

2) use macroaggregated albumin IV not getting thru capillaries
uniformly diffuse throughout lung

with PE, get wedge defects in lung

51
Q

CT angiography

A

inject bolus of dye into antecubital vessels
time the CT scan as bolus going through lung

look for where dye not able to go

52
Q

if submassive stable PE, how do you treat

A

Parenteral Anticoagulation
Heparin: Unfractionated or low molecular weight

Oral Anticoagulation - warfarin

53
Q

if unstable hypotensive, RV failure = massive, how do you treat

A

1) Heparin
2) Consider thrombolysis (tPA) (contraindicated if brain tumor due to poor blood vessels or GI bleeding if small ulcer)
3) Consider IVC Filter (noncompressibility of vessel due to clot so put iVC filter to prevent blood clot from leg into lung)
4) Consider surgical thrombectomy

54
Q

A patient presents 1 week after left hip surgery with a swollen left leg and acute onset of shortness of breath and pleuritic chest pain. What would be an UNEXPECTED finding in this patient?

A. An incompressible deep vein in the leg on ultrasound.

B. A large infiltrate on chest x-ray.

C. An elevated plasma d-dimer.

D. An intraluminal filling defect on CT chest with contrast.

A

Answer = B. A large infiltrate on chest x-ray.

Has risk factors for DVT
now SOB due to blood clot embolize to lungs
get irritation of pleura –> pleuritic chest pain

exception = Hampton’s hump

55
Q

PAH Hemodynamic and Clinical Course

A

NYHA class 1
CO
PAP incr
PVR incr

NYHA II
decr CO
PAP incr
PVR incr 
symptomatic b/c cardiac output decr, SOB, and dizzy when walk (not enough blood flow to brain because blood flow to legs and not go to brain)
NYHA III
decr CO
BNP (out of RV not LV)
incr PAP
incr PVR

Class IV
Fall of of PAP because heart not able to push blood thru lungs
CO drops

56
Q

CXR over time

A

RV becoming more dilated over time

57
Q

PAH physical exam

A

distended neck vein

normal lung auscultation (NO RALES)

loud P2, murmur of tricuspid regurg

edema in extremities

58
Q

A 25 year old female presents with 6 months of progressive dyspnea. She has edema and a loud P2. An echocardiogram suggests a dilated right ventricle and a right ventricular systolic pressure of 80mmHg. What should you do next?

A. Start unfractionated heparin drip.

B. Start calcium channel blockers.

C. Start sildenafil.

D. Obtain a right heart catheterization.

A

Answer = D
Obtain a right heart catheterization

no suggestion of blood clot, no swollen leg

no Calcium channel blockers

haven’t confirmed diagnosis, you have suggestion so don’t start sildenafil

Right heart cath is definitive test to determine pulm vascular resistance and can’t calculate based on echo

59
Q

The right heart catheterization shows the following: mPAP = 45 mmHg
PCWP = 10 mmHg
CO = 5 L/min
PVR = 7 WU
There is no response to inhaled nitric oxide. A V/Q scan is negative. What should you do next?

A. Start unfractionated heparin drip.

B. Start calcium channel blockers.

C. Start sildenafil.

D. Surgical lung biopsy.

A

Answer = C start Sildenafil

elev MPAP
low PCWP

meet criteria for WHO class 1
no blood clot b/c V/Q is negative

during right heart cath, inhale NO vasodilator, acute drop in blood pressure –> candidate for calcium channel blocker (best prognosis)

60
Q

She does well for 2 years, but then the shortness of breath returns plus she has fainting spells. A repeat right heart catheterization finds:
mPAP = 43 mmHg
PCWP = 10 mmHg
CO = 3 L/min
PVR = 11 WU
A V/Q scan is negative. What should you do next?

A. Start unfractionated heparin drip.

B. Start calcium channel blockers.

C. Change sildenafil to tadalafil.

D. Add intravenous epoprostenol.

A

Answer = D
aDD IV epoprostenol

no blood clot because V/Q scan negative
not vasodilator responsive so calcium channel blocker not sensitive–> need to have positive NO vasodilator response to have effect

tadalafil longer acting sildenafil

use epoporostenol open up –> most potent vasodilator

contemplate lung transplatn

61
Q
A 55 year old man with a history of severe mitral regurgitation presents with shortness of breath. Right heart catheterization reveals: mPAP = 26 mmHg 
PCWP = 20 mmHg 
CO = 3 L/min 
PVR = 2 WU
What should you do next?

A. Start a beta blocker.

B. Start diuretics.

C. Start sildenafil.

D. Start salt tablets.

A

Answer = B
start diuretics

beta blockers = slow HR, disadvantage for patient with HF –> make them worse

Diuretics = pee out fluid
wedge pressure elev –> cardiogenic pulm edema
lower wedge pressure

sildenafil = don't start PAH 
salt = cause more fluid retention
62
Q
A patient with possible pulmonary hypertension undergoes right heart catheterization and the following measurements are made: 
mPAP = 45 mmHg 
PCWP = 20 mmHg 
CO = 5 L/min 
PVR = 5 WU 
What does this patient have?

A. WHO Group 1 Pulmonary Arterial Hypertension

B. WHO Group 2 PH Due to Left Heart Disease

C. WHO Group 3 PH Due to Lung Diseases and/or Hypoxia

D. WHO Group 4 Thromboembolic Pulmonary Hypertension

A

B = WHO group 2 PH due to Left heart disase

PVR incr but more importantly, PCWP incr

For PCWP > 15 so pulm venous hypertension

63
Q

V/Q scan

A

preferred for pregnancy

1) patient inhale radioactive Xenon
see where gas goes in lung
find regions ventilated

2) use macroaggregated albumin IV not getting thru capillaries
uniformly diffuse throughout lung

with PE, get wedge defects in lung

64
Q

CT angiography

A

inject bolus of dye into antecubital vessels
time the CT scan as bolus going through lung

look for where dye not able to go

65
Q

if submassive stable PE, how do you treat

A

Parenteral Anticoagulation
Heparin: Unfractionated or low molecular weight

Oral Anticoagulation - warfarin

66
Q

A patient presents 1 week after left hip surgery with a swollen left leg and acute onset of shortness of breath and pleuritic chest pain. What would be an UNEXPECTED finding in this patient?

A. An incompressible deep vein in the leg on ultrasound.

B. A large infiltrate on chest x-ray.

C. An elevated plasma d-dimer.

D. An intraluminal filling defect on CT chest with contrast.

A

Answer = B. A large infiltrate on chest x-ray.

Has risk factors for DVT
now SOB due to blood clot embolize to lungs
get irritation of pleura –> pleuritic chest pain

exception = Hampton’s hump

67
Q

PAH Hemodynamic and Clinical Course

A

NYHA class 1
CO
PAP incr
PVR incr

NYHA II
decr CO
PAP incr
PVR incr 
symptomatic b/c cardiac output decr, SOB, and dizzy when walk (not enough blood flow to brain because blood flow to legs and not go to brain)
NYHA III
decr CO
BNP (out of RV not LV)
incr PAP
incr PVR

Class IV
Fall of of PAP because heart not able to push blood thru lungs
CO drops

68
Q

CXR over time

A

RV becoming more dilated over time

69
Q

A 25 year old female presents with 6 months of progressive dyspnea. She has edema and a loud P2. An echocardiogram suggests a dilated right ventricle and a right ventricular systolic pressure of 80mmHg. What should you do next?

A. Start unfractionated heparin drip.

B. Start calcium channel blockers.

C. Start sildenafil.

D. Obtain a right heart catheterization.

A

Answer = D
Obtain a right heart catheterization

no suggestion of blood clot, no swollen leg

no Calcium channel blockers

haven’t confirmed diagnosis, you have suggestion so don’t start sildenafil

Right heart cath is definitive test to determine pulm vascular resistance and can’t calculate based on echo

70
Q

The right heart catheterization shows the following: mPAP = 45 mmHg
PCWP = 10 mmHg
CO = 5 L/min
PVR = 7 WU
There is no response to inhaled nitric oxide. A V/Q scan is negative. What should you do next?

A. Start unfractionated heparin drip.

B. Start calcium channel blockers.

C. Start sildenafil.

D. Surgical lung biopsy.

A

Answer = C start Sildenafil

elev MPAP
low PCWP

meet criteria for WHO class 1
no blood clot b/c V/Q is negative

during right heart cath, inhale NO vasodilator, acute drop in blood pressure –> candidate for calcium channel blocker (best prognosis)

71
Q

She does well for 2 years, but then the shortness of breath returns plus she has fainting spells. A repeat right heart catheterization finds:
mPAP = 43 mmHg
PCWP = 10 mmHg
CO = 3 L/min
PVR = 11 WU
A V/Q scan is negative. What should you do next?

A. Start unfractionated heparin drip.

B. Start calcium channel blockers.

C. Change sildenafil to tadalafil.

D. Add intravenous epoprostenol.

A

Answer = D
aDD IV epoprostenol

no blood clot because V/Q scan negative
not vasodilator responsive so calcium channel blocker not sensitive–> need to have positive NO vasodilator response to have effect

tadalafil longer acting sildenafil

use epoporostenol open up –> most potent vasodilator

contemplate lung transplatn

72
Q
A 55 year old man with a history of severe mitral regurgitation presents with shortness of breath. Right heart catheterization reveals: mPAP = 26 mmHg 
PCWP = 20 mmHg 
CO = 3 L/min 
PVR = 2 WU
What should you do next?

A. Start a beta blocker.

B. Start diuretics.

C. Start sildenafil.

D. Start salt tablets.

A

Answer = B
start diuretics

beta blockers = slow HR, disadvantage for patient with HF –> make them worse

Diuretics = pee out fluid
wedge pressure elev –> cardiogenic pulm edema
lower wedge pressure

sildenafil = don't start PAH 
salt = cause more fluid retention