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Spr2015_Week5 > PULM CIRCULATION FINAL > Flashcards

PULM CIRCULATION FINAL Flashcards

1
Q

ANATOMY of bronchial circulation

A

Supplies conducting airways

Systemic in origin (aorta, intercostal arteries)

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2
Q

Function of bronchial circulation

A

1) protects lung from infarct (PE, pneumonia)

2) grow into diseased areas (intercostals)

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3
Q

Consequence of bronchial circulation dysfunction

A

1) source of hemoptysis (cough up blood)

2) arterial flow drains into LA = shunt

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4
Q

Equation for pulm artery pressure

A

PAP – LAP = CO * PVR

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

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5
Q

Units for
CO
Pressures
PVR

A

Cardiac output = Liters/minute Pressures = mmHg

PVR = “Wood Units” (WU)

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6
Q

Normal Woods unit is ___

A
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7
Q

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

A

Answer = C (3 woods units)

25-10 = 5 x PVR

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8
Q

Steps in pUlm circulation

A

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

2) capillary network
3) veins (run with lymphatics in interlobular septae)

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9
Q

Distinguish pulm vs. systemic vasculature

A

PUlm

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

CO = 5L/min
same as systemic

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10
Q

How do you measure PA pressure
Non-invasive echocardiography

why?

equation?

errors?

A

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)

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11
Q

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

Method?

What do you measure?

A

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

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12
Q

what is pulm capillary wedge pressure can be equal to?

A

~ LA pressure

~ LV EDP

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13
Q

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

A

1) RA pressure
2) PA pressure
3) PCP
4) CO via thermodilution or laser doppler
5) central venous O2 saturation (light absorption)

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14
Q

Normal hemodynamics pressure values

RA 
RV 
PA
PCWP
CO
PVR
A 
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
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15
Q

Hemodynamics curve of Swan Ganz Cath

A

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

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16
Q

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.

A

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

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17
Q

Why does pressure not continuously incr linearly with incr CO?

A
  1. High capacitance
    – More distensible vessels than systemic
    arteries
  2. Recruitment of unperfused vessels
    West zones
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18
Q

what are the “west zones” of the lung

A

3 vertical regions organized by

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

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19
Q

how do

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

vary in west zones of lung

A

alveolar pressure = constant

arterial and venous pressure vary due to gravity

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20
Q

the zones are ___ not anatomic so …

A

physiologic

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

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21
Q

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

A

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

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22
Q

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

A

Parterial > PAlveolar > Pvenous

since Pa > PA, greater flow than zone 1

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23
Q

what is determinant of driving force for flow in zone 2

A

difference btwn arterial and alveolar pressure

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24
Q

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

A

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)

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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 ```

Spr2015_Week5 (19 decks)

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