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1

ANATOMY of bronchial circulation

Supplies conducting airways

Systemic in origin (aorta, intercostal arteries)

2

Function of bronchial circulation

1) protects lung from infarct (PE, pneumonia)

2) grow into diseased areas (intercostals)

3

Consequence of bronchial circulation dysfunction

1) source of hemoptysis (cough up blood)

2) arterial flow drains into LA = shunt

4

Equation for pulm artery pressure

PAP – LAP = CO * PVR

PAP: Pulmonary artery pressure
LAP: Left atrial pressure
CO: Cardiac output
PVR: Pulmonary vascular resistance

5

Units for
CO
Pressures
PVR

Cardiac output = Liters/minute Pressures = mmHg
PVR = “Wood Units” (WU)

6

Normal Woods unit is ___

7

The following measurements are made in a patient:
Mean PA pressure = 25 mmHg
Left atrial pressure = 10 mmHg
Cardiac output = 5 L/min
What’s the pulmonary vascular resistance?

A. 1 Wood Unit
B. 2 Wood Units
C. 3 Wood Units
D. Cannot be determined

Answer = C (3 woods units)

25-10 = 5 x PVR

8

Steps in pUlm circulation

1) arteries = carry deoxy blood
- large elastic arteries
- muscular pulm arteries
- pulm arterioles

2) capillary network

3) veins (run with lymphatics in interlobular septae)

9

Distinguish pulm vs. systemic vasculature

PUlm
1) low resistance
2) Low elastance/high compliance
3) low pressure

CO = 5L/min
same as systemic

10

How do you measure PA pressure
Non-invasive echocardiography

why?

equation?

errors?

Looking at tricuspid valve regurgitation

RV becomes dilated so you get jet of blood backwards
in normal person you can't measure

Simplified Bernoulli equation
P = 4 x V^2
= 4 x (3 m/s)^2
= 36 mm Hg (systolic) + RA pressure

Errors = +/- 10 mmHg common (greater)

11

How do you measure PA pressure
Pulm artery catheterization with Swan-Ganz Catheter

Method?

What do you measure?

1) Place catheter into body
2) catheter drift thru body into RV and then exists pulm valve into vasculature
3) obstruct a small pulm artery

Make a static water column, because no movement distal to balloon (Q = 0, dP = 0)

= Pulm capillary wedge pressure

12

what is pulm capillary wedge pressure can be equal to?

~ LA pressure
~ LV EDP

13

Modern PA catheter used to measure what? (5 things)

1) RA pressure

2) PA pressure

3) PCP

4) CO via thermodilution or laser doppler

5) central venous O2 saturation (light absorption)

14

Normal hemodynamics pressure values

RA
RV
PA
PCWP
CO
PVR

RA = 0-5 mmHg
RV = 25/0 mmHg
PA = 25/10 mmHg; PA mean = 15-20

PCWP = 5-8 mmHg
CO = 5L/min
PVR = 1-2 WU

15

Hemodynamics curve of Swan Ganz Cath

1) RA = low systolic, baseline diastolic
2-5

2) RV = peak systolic, same baseline diastolic
25/2

3) PA = peak systolic, peak diastolic
25/10

4) PA output = lower systolic, peak diastolic
10-12

16

Swan Ganz catheter is floated in a patient and the following tracing is seen. What does this patient have?

A. The pulmonary vascular resistance is increased.
B. Tricuspid valve regurgitation.
C. Pulmonic valve stenosis.
D. Low cardiac output.

Answer = C = pulm valve stenosis

RA = normal
RV = pressure incr stays low on the bottom
PA = bottom number should incr because one way valve behind you but top number should stay high

in this patient, there is a pressure gradient from RV into pulm artery (because pulm

PRESSURE DROPS FROM RV into PA

IF ANSWER WERE A, YOU WOULD SEE
if pulm vascular resistance there were a drop in diastolic pressure from pulm artery into wedge pressure

PA diastolic pressure should be same as PCWP diastolic pressure

17

Why does pressure not continuously incr linearly with incr CO?

1. High capacitance
– More distensible vessels than systemic
arteries

2. Recruitment of unperfused vessels
West zones

18

what are the "west zones" of the lung

3 vertical regions organized by
1) pulm arterial pressure
2) pulm venous pressure
3) alveolar pressure

19

how do
1) pulm arterial pressure
2) pulm venous pressure
3) alveolar pressure

vary in west zones of lung

alveolar pressure = constant

arterial and venous pressure vary due to gravity

20

the zones are ___ not anatomic so ...

physiologic

so change in position, change orientation with respect to apex and base

21

what is relationship of 3 pressure in zone 1 (apex)

PAlveolar > Parterial > Pvenous

since PA > Pa, arterial microvasculature compressed, minimal blood flow

when pressure cross 0 = air pressure, capillaries close up b/c adjacent alveolus pressure is greater than indiv capillaries

22

what is relationship of 3 pressures in zone 2 (middle)

Parterial > PAlveolar > Pvenous

since Pa > PA, greater flow than zone 1

23

what is determinant of driving force for flow in zone 2

difference btwn arterial and alveolar pressure

24

what is relationship of 3 pressures in zone 3 (base)?

Parterial > Pvenous > PAlveolar

greatest flow
driving force = difference btwn arterial and venous pressure

continuous flow from arteries across alveoli into venous (blood vessels always distended)

25

Gravity affects ___ not air pressure

blood

so air pressure = 0 throughout entire lung but slightly change +/- 2 with breaths

26

Blood only flows when ___ > ___

Pa > PA

intermittent pulsatile pressure
systolic = spurt of blood
diastolic = no blood flow because below air pressure

27

when you give positive pressure (ventilator, auto-PEEP), incr alveolar pressure, creates zones __ and ___

zones 1 and 2 incr
because incr PA so less zone 3

28

patient with COPD or dehydration
what happens to zones

PA incr and then create physiologic zone 1
when CO incr, pressure in PA incr

so zone 2 that was intermittently perfused is now more often perfused —> capillaries between zone 2 and zone

29

A dehydrated patient receives an intravenous bolus of fluid. What will happen to the patient’s lung zones?

A. There will be an increase in Zone 1.
B. There will be a decrease in Zone 3.
C. Some Zone 2 lung will become Zone 3.
D. Some Zone 2 lung will become Zone 1

answer = C

dehydrated
so low pressure in pulm vsculature
augment pulm vasculature (incr little bit, incr CO)
some zone 3 that was intemrittently perfused will have continuous blood flow now and become zone 2

30

Describe hypoxic pulm vasoconstriction

why?

is it necessary in healthy lungs

vasoconstriction in areas with alveolar hypoxia

to preserve V/Q matching

not necessary in healthy lungs

31

how is hypoxic pulm vasoconstriction different from systemic circulation

systemic = hypoxic vasodilation

32

what are endogenous vasodilators and vasoconstrictors

1) NO

2) prostacyclin

3) endothelin

4) thromboxiane

33

2 functions of pulm circulation in lung

1) gas exchange

2) water-solute balance

34

what do disruptions to normal function of pulm circulation manifest as?

1) abnormal gas exchange (hypoxemia = low O2 or hypercapnea = high CO2)

2) abnormal incr in fluid (pulm edema can't exchange gas)

3) incr in pulm vasc resistance (pulm HTN with decr CO, heart failure)

35

how can fluid accumulate in lungs?

1) originates in capillaries

2) little blood enters interstitium

3) blood then goes to lymphatics

36

what happens if lymphatics are filled with fluid?

fluid goes to alveoli = pulm edema

37

how does gravity affect variation in blood pressure and blood flow in lung when standing

divides into 3 zones when standing

1) base of lung = greatest BP, constant flow

2) middle = middle BP, intermittent flow

3) apex = low BP, little to no flow

38

how does smooth muscle respond to alveolar hypoxia?

what is this caused?

what happens to blood?

smooth muscle contracts

called hypoxic pulm vasoconstriction (HPV)

diverts blood from hypoxic areas of lung

39

what is equation for net filtration

Qf = Kf [(Pmv-Pi) – σ(Πmv -Πi)]

Qf = fluid filtration rate

Kf = filtration coefficient, dependent on leakiness of vessel (higher=leakier)

Pmv/i = vascular and interstitial hydrostatic pressure

σ= osmotic reflection coefficient
(0=unrestricted passage of protein; 1=no passage of protein)

Πmv/I = vascular and interstitial oncotic pressure

40

in normal vessels what is relationship between hydrostatic and oncotic pressure

Pmv >>> Pi
Πmv > Πi

Net fluid out of vessels
returned to circulation by lymphatics
NO FLUID INTO ALVEOLI

41

In cardiogenic shock what happens to vascular pressure

incr pulm capillary wedge pressure

incr hydrostatic pressure (incr vascu pressure Pmv)

enlarges interlobular septa of lymphatics

acinus fills with fluid

42

in noncardiogenic shock what happens

incr permeability/damaged vessels

Proteins leave vasculature

Πmv decr
Πi incr
Ø effectively goes down (proteins can cross easily)!

43

what does cardiogenic pulm edema due to LV failure look like?

1) incr apical lung marking (cephalization)

2) fluid in alveoli (pulm edema)

3) Kerley B lines = perpendicular to pleural surface and related to enlarged interlobular septa

44

how does noncardiogenic pulm edema due to ARDS present as

1) bilateral alveolar infiltrate

2) PaO2/FiO2

45

Distinguish cardiac vs noncardiac pulm edema
clinical setting

CHF
pneumonia/ARDS

CHF = cardiogenic

pneumonia/ARDS = noncardiogenic

46

Distinguish cardiac vs noncardiac pulm edema

elevated PCWP (LA) pressure
not elevated PCWP

Elevated = cardiogenic

Not elevated = noncardiogenic

47

Distinguish cardiac vs noncardiac pulm edema

Diuretics help
Diuretics don't help

diuretics help = cafrdiogenic
diuretics don't help = noncardiogenic

48

A patient sustains a crush injury of the leg in a car accident, and then 6 hours later develops respiratory failure with this chest x-ray. What will help the patient?

A. Lung protective ventilation."
B. Antibiotics."
C. Diuretics."
D. Pulmonary vasodilators.

Answer = A

lung protective ventilation

pulm vessels not narrow
pulm vessels are leaky

49

A patient in respiratory failure has this chest x-ray. A Swan Ganz catheter is placed and the pulmonary capillary wedge pressure is 20mmHg. What will help this patient?

A. Lung protective ventilation.

B. Antibiotics.

C. Diuretics.

D. Pulmonary vasodilators.

Answer = C
Diuretics due to cardiogenic failure with incr PCWP

50

Definition of pulm HTN

what is normal mPAP

mean pulm artery pressure > 25 mmHg

normal mPAP = 15-18 mm Hg

51

incr PA pressure does ___ incr pulm vascular resistance

NOT

52

what are causes of incr PA pressure?

equation for PA pressure

PAP = CO x PVR + LAP

1) Increased pulmonary vascular resistance
2) Increased left atrial pressure!
3) Increased cardiac output– rarely by itself!

53

if you have mPAP > 25 mmHg
and PCWP

pre-capillary

so pulm arterial hypertension (PAH)

54

if you have mPAP > 25 mmHg
and PCWP > 15 what do you have

post-capillary

pulm venous hypertension (PVH)

55

what is most often cause of PAH vs. PVH

PAH due to incr pulm vascular resistance thru lung

PVH due to incr LA pressure

56

hemodynamic definition of PAH

Mean PAP ≥25 mm Hg plus
PCWP/LVEDP ≤15 mm Hg plus
PVR > 3 Wood Units

57

Classification of pulm HTN (WHO groups)

1. Pulmonary Arterial Hypertension


2. PH Due to Left Heart Disease"

3. PH Due to Lung Diseases and/or Hypoxia"

4. Thromboembolic Pulmonary Hypertension"

5. PH With Unclear/Multifactorial Mechanisms

58

Causes of PAH

Idiopathic (“Primary”)
Heritable PAH
Diet drugs
Cirrhosis
HIV
Collagen vascular disease
Congenital heart disease

59

Pulmonary Hypertension due to lung diseases and/or hypoxia

COPD
interstitial lung disease
obstructive sleep apnea

60

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

B = WHO group 2 PH due to Left heart disase

PVR incr but more importantly, PCWP incr

For PCWP > 15 so pulm venous hypertension

61

Causes of Acute pulmonary HTN

1) pneumonia = hypoxic vasoconstriction

2) thromboembolic disease

3) hypoxia (high altitude)

62

Causes of DVT

Virchow's Triad
- trauma
- stasis
- hypercoagulability

63

Effects of pulmonary embolism

1) RV strain "submassive" / RV failure (massive)

2) incr myocardial O2 demand

3) decr myocardial O2 delivery

4) death

64

physical exam of pulm embolism

1) H&P - Wells Score
2) D-dimer (breakdown products of thrombin)
3) ECG
4) CXR
5) CT angiogram
6) Angiogram
7) Echo

65

ECG of pulmonary embolism

S1 QIII TIIII
most common: sinus tachycardia

66

if you see S1 QIIII TIIII
or sinus tachycardia
what does it appear on ECG

pulmonary embolism

67

how does CXR of pulm embolism appear

1) Hampton's Hump = infarcted lung

2) Westermark's Sign = hypoperfusion

68

V/Q scan for pulm embolism

What is it preferred in

procedure

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

69

CT angiography for pulm embolism

procedure/mechanism

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

look for where dye not able to go

70

gold standard for pulm embolism diagnosis

pulm angiogram

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

71

is D-dimer sensitive for pulm embolsm

sensitive but NOT SPECIFIC

sepsis
pregnancy could also raise D-dimer

72

Treatment of submassive stable PE

1) Parenteral Anticoag
= heparin = unfractionated or LMWH

2) oral anticoag
= warfarin

73

Treatment of unstable (hypotensive, RV failure = massive)

1) heparin

2) consider thrombolysis (tPA)

3) consider IVC filter

4) surgical thrombectomy

74

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.

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

75

Major subtypes of pulmonary arterial hypertension

1.1) Idiopathic (Primary)

1.2) Heritable

1.3) Diet or drugs (weight loss medications = fen-phen = pulmonary arterial HTN, cocaine, meth)

1.5) HIV

1.6) Connective tissue disease = scleroderma = vessels thickened and narrowed

76

describe PAH
paradigm of which WHO group

Patient population?

WHO Group 1 disease

Affects young women in 30's and 40's

77

Clinical course and Hemodynamics of PAH
NYHA Class 1

CO high
incr PAP
incr PVR

78

Clinical course and Hemodynamics of PAH
NYHA Class 2

decreasing CO
incr PAP
incr PVR

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)

79

Clinical course and Hemodynamics of PAH
NYHA Class 3

decr CO
incr PAP
incr PVR
incr BNP (out of RV not LV)

80

Clinical course and Hemodynamics of PAH
NYHA Class 4

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

81

CXR over time

RV becoming more dilated over time

82

PAH physical exam (4)

1) Neck veins: distended

2) Lung auscultation: normal (no rales)!

3) Cardiac exam; loud P2, murmur of TR!

4) Extremities: edema

83

Discuss WHO group 4 = chronic thromboemboli

which patient group
ideal treatment

blood clot scarred into lung and fibrotic --> late SOB after PE

patients with acute PE --> late CTEPH

treatment = surgical pulm endartectomy

84

Steps in treatment of PAH (WHO Group 1)

1) Treat underling cause!

2) Correct hypoxia!

3) Control intravascular volume status!
– Limit fluid intake!
– Limit sodium intake!
– Diuresis!
4) Anticoagulation(?)!

5) Pulmonary vasodilators!
– Calcium channel blockers, only in acute responders!

6) Lung transplantation!

85

Endothelin receptor antagonists

Bosentan
Ambrisentan
Macitentan

86

PDE 5 inhibitors

sildenafil
tadalafil

87

soluble guanylate cyclase stimulator

riociguat

88

prostacyclina nalogues

epoprostenol
treprostinil

89

prostacyclin analogues
mode of administration

effect

continuous IV pump

potent vasodilator

90

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.

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

91

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.

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)

92

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.

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

93

Treatment of post-capillary pulm venous hypertension

1) decr intravascular filling
- limit fluid intake
- limit sodium intake
- diuresis

2) improve LV contractility
- decr LV afterload (control systemic HTN) = move blood out of LA into systemic

3) correct causes of LV failure
- ischemia
- valvular

NO PAH SPECIFIC THERAPY

94

WHAT DO YOU NOT USE IN TREATMENT OF PVH

DO NOT USE PAH SPECIFIC THERAPY

95

why do you not use PAH specific therapy for PVH

1) with PVH you have incr pressure

2) if you use vasodilators,
incr vasodilation
incr pressure --> pulm edema

in pulm veins
more blood flow in
alveoli fill up with
edema

96

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.

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