PULM CIRCULATION FINAL Flashcards
ANATOMY of bronchial circulation
Supplies conducting airways
Systemic in origin (aorta, intercostal arteries)
Function of bronchial circulation
1) protects lung from infarct (PE, pneumonia)
2) grow into diseased areas (intercostals)
Consequence of bronchial circulation dysfunction
1) source of hemoptysis (cough up blood)
2) arterial flow drains into LA = shunt
Equation for pulm artery pressure
PAP – LAP = CO * PVR
PAP: Pulmonary artery pressure
LAP: Left atrial pressure
CO: Cardiac output
PVR: Pulmonary vascular resistance
Units for
CO
Pressures
PVR
Cardiac output = Liters/minute Pressures = mmHg
PVR = “Wood Units” (WU)
Normal Woods unit is ___
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
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)
Distinguish pulm vs. systemic vasculature
PUlm
1) low resistance
2) Low elastance/high compliance
3) low pressure
CO = 5L/min
same as systemic
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)
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
what is pulm capillary wedge pressure can be equal to?
~ LA pressure
~ LV EDP
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)
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
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
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
Why does pressure not continuously incr linearly with incr CO?
- High capacitance
– More distensible vessels than systemic
arteries - Recruitment of unperfused vessels
West zones
what are the “west zones” of the lung
3 vertical regions organized by
1) pulm arterial pressure
2) pulm venous pressure
3) alveolar pressure
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
the zones are ___ not anatomic so …
physiologic
so change in position, change orientation with respect to apex and base
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
what is relationship of 3 pressures in zone 2 (middle)
Parterial > PAlveolar > Pvenous
since Pa > PA, greater flow than zone 1
what is determinant of driving force for flow in zone 2
difference btwn arterial and alveolar pressure
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)
Gravity affects ___ not air pressure
blood
so air pressure = 0 throughout entire lung but slightly change +/- 2 with breaths
Blood only flows when ___ > ___
Pa > PA
intermittent pulsatile pressure
systolic = spurt of blood
diastolic = no blood flow because below air pressure
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
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
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
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
how is hypoxic pulm vasoconstriction different from systemic circulation
systemic = hypoxic vasodilation
what are endogenous vasodilators and vasoconstrictors
1) NO
2) prostacyclin
3) endothelin
4) thromboxiane
2 functions of pulm circulation in lung
1) gas exchange
2) water-solute balance
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)
how can fluid accumulate in lungs?
1) originates in capillaries
2) little blood enters interstitium
3) blood then goes to lymphatics
what happens if lymphatics are filled with fluid?
fluid goes to alveoli = pulm edema
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
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
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
in normal vessels what is relationship between hydrostatic and oncotic pressure
Pmv»_space;> Pi
Πmv > Πi
Net fluid out of vessels
returned to circulation by lymphatics
NO FLUID INTO ALVEOLI
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
in noncardiogenic shock what happens
incr permeability/damaged vessels
Proteins leave vasculature
Πmv decr
Πi incr
Ø effectively goes down (proteins can cross easily)!
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
how does noncardiogenic pulm edema due to ARDS present as
1) bilateral alveolar infiltrate
2) PaO2/FiO2
Distinguish cardiac vs noncardiac pulm edema
clinical setting
CHF
pneumonia/ARDS
CHF = cardiogenic
pneumonia/ARDS = noncardiogenic
Distinguish cardiac vs noncardiac pulm edema
elevated PCWP (LA) pressure not elevated PCWP
Elevated = cardiogenic
Not elevated = noncardiogenic
Distinguish cardiac vs noncardiac pulm edema
Diuretics help
Diuretics don’t help
diuretics help = cafrdiogenic
diuretics don’t help = noncardiogenic
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
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
Definition of pulm HTN
what is normal mPAP
mean pulm artery pressure > 25 mmHg
normal mPAP = 15-18 mm Hg
incr PA pressure does ___ incr pulm vascular resistance
NOT
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!
if you have mPAP > 25 mmHg
and PCWP
pre-capillary
so pulm arterial hypertension (PAH)
if you have mPAP > 25 mmHg
and PCWP > 15 what do you have
post-capillary
pulm venous hypertension (PVH)
what is most often cause of PAH vs. PVH
PAH due to incr pulm vascular resistance thru lung
PVH due to incr LA pressure
hemodynamic definition of PAH
Mean PAP ≥25 mm Hg plus
PCWP/LVEDP ≤15 mm Hg plus
PVR > 3 Wood Units
Classification of pulm HTN (WHO groups)
- Pulmonary Arterial Hypertension
- PH Due to Left Heart Disease”
- PH Due to Lung Diseases and/or Hypoxia”
- Thromboembolic Pulmonary Hypertension”
- PH With Unclear/Multifactorial Mechanisms
Causes of PAH
Idiopathic (“Primary”) Heritable PAH Diet drugs Cirrhosis HIV Collagen vascular disease Congenital heart disease
Pulmonary Hypertension due to lung diseases and/or hypoxia
COPD
interstitial lung disease
obstructive sleep apnea
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
Causes of Acute pulmonary HTN
1) pneumonia = hypoxic vasoconstriction
2) thromboembolic disease
3) hypoxia (high altitude)
Causes of DVT
Virchow’s Triad
- trauma
- stasis
- hypercoagulability
Effects of pulmonary embolism
1) RV strain “submassive” / RV failure (massive)
2) incr myocardial O2 demand
3) decr myocardial O2 delivery
4) death
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
ECG of pulmonary embolism
S1 QIII TIIII
most common: sinus tachycardia
if you see S1 QIIII TIIII
or sinus tachycardia
what does it appear on ECG
pulmonary embolism
how does CXR of pulm embolism appear
1) Hampton’s Hump = infarcted lung
2) Westermark’s Sign = hypoperfusion
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
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
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
is D-dimer sensitive for pulm embolsm
sensitive but NOT SPECIFIC
sepsis
pregnancy could also raise D-dimer
Treatment of submassive stable PE
1) Parenteral Anticoag
= heparin = unfractionated or LMWH
2) oral anticoag
= warfarin
Treatment of unstable (hypotensive, RV failure = massive)
1) heparin
2) consider thrombolysis (tPA)
3) consider IVC filter
4) surgical thrombectomy
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
Major subtypes of pulmonary arterial hypertension
- 1) Idiopathic (Primary)
- 2) Heritable
- 3) Diet or drugs (weight loss medications = fen-phen = pulmonary arterial HTN, cocaine, meth)
- 5) HIV
- 6) Connective tissue disease = scleroderma = vessels thickened and narrowed
describe PAH
paradigm of which WHO group
Patient population?
WHO Group 1 disease
Affects young women in 30’s and 40’s
Clinical course and Hemodynamics of PAH
NYHA Class 1
CO high
incr PAP
incr PVR
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)
Clinical course and Hemodynamics of PAH
NYHA Class 3
decr CO
incr PAP
incr PVR
incr BNP (out of RV not LV)
Clinical course and Hemodynamics of PAH
NYHA Class 4
Fall of of PAP because heart not able to push blood thru lungs
CO drops
CXR over time
RV becoming more dilated over time
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
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
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!
Endothelin receptor antagonists
Bosentan
Ambrisentan
Macitentan
PDE 5 inhibitors
sildenafil
tadalafil
soluble guanylate cyclase stimulator
riociguat
prostacyclina nalogues
epoprostenol
treprostinil
prostacyclin analogues
mode of administration
effect
continuous IV pump
potent vasodilator
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
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)
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
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
WHAT DO YOU NOT USE IN TREATMENT OF PVH
DO NOT USE PAH SPECIFIC THERAPY
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
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
