CVPR Week 6: Pulmonary Circulation Flashcards
(115 cards)
1
Q
Objectives
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2
Q
In what way are the pulmonary and systemic circulations connected?
A
In series
3
Q
How much of the cardiac output does the pulmonary circulation receive?
A
The entire cardiac output for the purpose of gas exchange
4
Q
Explain the flow of air and blood in the cardiovascular and respiratory systems
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Q
A
6
Q
What is this?
A
7
Q
What is this?
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8
Q
Explain the difference
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9
Q
Explain the structure of pulmonary arteries
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10
Q
Identify
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11
Q
How are pulmonary capillaries arranged?
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12
Q
What is this?
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13
Q
Identify
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14
Q
Large pulmonic veins contain?
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Cardiac muscle and can produce ectopic beats which can initiate atrial fibrilation
15
Q
Pulmonary arteries structure
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pulmonary arteries are not highly muscular
16
Q
pulmonary capillaries are arranged in?
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dense networks ideal for gas exchange
17
Q
Pulmonary veins transport?
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oxygenated blood from the lungs to the LV
18
Q
Pulmonary veins caveat
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larger veins have a layer of cardiac muscle and can produce ectopic beats initiating atrial fibrillation which can be ablated and completely cure the atrial fibrillation
19
Q
Pulmonic pressure vs systemic pressures
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pulmonary circulation has very little if any tone at all
for the most part there is very low tone
and only 10 mmHg pressure gradient driving the flow through here
changing diameter of the alveoli changing resistance
20
Q
Alveolar and extra-alveolar vessel diameters are influenced by?
A
- an increase in alveolar pressure causes reduced radius of the capillary if the pressure was high enough = ↓ radius and ↑ resistance to flow
- When alveolar volume ↑ this will ↓ radius of capillary and ↑ resistance to flow
- both of things lead to ↑ resistance to flow and can increase pulmonary arterial pressure and over the long term can decrease CO and lead to right heart failure
- Setting ventilator right to minimize lung damage to infants
- the extra-alveolar vessels are physically attached to the lung tissue so when lung volume increases these vessels are pulled open which actually reduces resistance to flow
*
21
Q
Alveolar and extra-alveolar vessel diameters are influenced by?
A
Alveolar Pressure
Alveolar volume
Lung volume
22
Q
How does lung volume affect capillary pressure?
A
since the extra-alveolar vessels are physically attached to the lung, when the lung expands the vessels dilate.
Increase in lung volume = decrease in alveolar capillary pressure
23
Q
Pulmonary circulation site of greatest vascular resistance
A
capillaries - 60%
Arteries 20%
Veins - 20%
24
Q
What is the relative diameter of pulmonary capillaries?
A
a little bit smaller than a RBC’s diameter so they have to squeeze through creating more resistance and serving as the site of highest resistance in the pulmonary circulation
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How does alveolar volume affect perfusion
increased alveolar volume can impede upon and squish alveolar-capillaries leasing to a reduced capillary diameter and increased alveolar-capillary pressure
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Ventilation of infants or premies
a ventilator pressure that is too high may cause increased alveolar pressure leading to reduced alveolar-capillary radius and increase alveolar-capillary pressures and can damage the infants lungs
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What is the relative pressure of the pulmonary circulation?
low pressure and low resistance circuit
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How are the capillaries' diameter affected in the lungs?
alveolar pressure and alveolar volume and lung volume can affect the diameter of the capillaries
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What is the site of greatest vascular resistance in the pulmonary circulation?
the capillaries due to their smaller diameter than an average RBC
but the site of highest resistance can change in pulmonary hypertension
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Passive effects of increasing pulmonary arterial pressure
**leads to a passive reflex dropping in pulmonary vascular resistance by 2 mechanisms**
* recruitment of collapsed capillaries (parallel resistances add as reciprocals
* distension of capillaries (this is not vasodilation which would be muscular an active process, this is a passive increase in diameter, an increased radius of vessels will decrease resistance)
**These passive responses improve ventilation to perfusion matching (V/Q matching)**
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V/Q matching
Ventilation/perfusion
of alveoli
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Pulmonary vascular resistance as a function of pulmonary arterial pressure
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Pulmonary pressure vs time
resting pressure until flow is increased
get an increase in pressure
when pressure gets high enough more vessels are recruited and vessels are distended decreasing the pressure
This is important in protecting the lungs from high pressures
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Racehorses and pulmonary pressure
their CO is so high that distention and additional vessel recruitment still doesn't protect them
Pulmonary arterial pressures are so high that the pulmonary microvasculature is damaged and this is called stress failure of the pulmonary capillaries
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pulmonary vascular resistance as a function of lung volume
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Residual volume
volume left at the end of maximal forced expiration
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functional residual capacity
residual volume + forced expiratory volume
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Positive pressure ventilation effects
* you are increasing alveolar pressure (PA)
this increases
* ↑ PVR (pulmonary vascular resistance)
which leads to
* ↑PAP (pulmonary arterial pressure)
which leads to
* ↓CO (cardiac output)
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Factors affecting PVR
Hematocrit (viscosity and/or dehydration)
Lung volume
Alveolar pressure
Recruitment and distention
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Hematocrit and PVR
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Effects of hypoxia on pulmonary vs systemic vascular tone
* in systemic vasculature, as oxygen levels fall, causes relaxation so more blood (increased metabolic activity or other situations)
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Effects of hypoxia on pulmonary vascular tone
In pulmonary, reduced O2 results in constriction for increased ventilation-perfusion matching (V/Q matching)
so the hypoxic alveoli capillaries constrict and increase the resistance. So, the blood goes to areas of lower resistance so the blood is shunted to more ventilated alveolar capillaries
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When is Hypoxic Pulmonary Vasoconstriction
becomes more important in critical conditions like:
* pneumonia
* collapsed lung
* chronic lung diseases (have heterogeneity in lung ventilation)
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HPV AKA
Hypoxic Pulmonary Vasoconstriction
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When is Hypoxic Pulmonary Vasoconstriction dangerous
with global lung hypoxia
then all vessels constrict and lead to pulmonary hypertension and can lead to right heart failure
if there is an increase in pressure then it is a result of increased resistance because in this case flow is constant
changing the composition of the air changes the vascular tone in the lung
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What is the mechanism of Hypoxic Pulmonary Vasoconstriction?
autonomic mechanisms are not involved because they aren't innervated
so this response is inherent to the vasculature in the pulmonary arterial smooth muscle cells
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Verapamil effect on Hypoxic Pulmonary Vasoconstriction
Verapamil reverses Hypoxic Pulmonary Vasoconstriction because it causes vasodilation
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What is the mechanism of Verapamil
Voltage-gated L-type Ca2+ channel inhibitor
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Actual mechanism of Hypoxic Pulmonary Vasoconstriction
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Actual mechanism of Hypoxic Pulmonary Vasoconstriction
Hypoxia inhibits vascular smooth muscle voltage-sensitive K+ channels
so they are inhibited and this causes decreased K+ efflux as increases depolarization causing contraction
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summary of hypoxic pulmonary vasoconstriction
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hypoxic pulmonary vasoconstriction matches?
local ventilation and perfusion
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Generalized hypoxia results in?
pulmonary hypertension
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hypoxia effect on pulmonary arterial smooth muscle
Involves a direct contractile effect on pulmonary arterial smooth muscle by inhibiting voltage-sensitive K+ channels
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Classifications of pulmonary hypertension
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Group I WHO classification of pulmonary hypertension
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Group II WHO classification of pulmonary hypertension
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Group III WHO classification of pulmonary hypertension
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Group IV WHO classification of pulmonary hypertension
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Group V WHO classification of pulmonary hypertension
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Group I WHO classification of pulmonary hypertension **AKA**
Pulmonary Arterial Hypertension
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Group II WHO classification of pulmonary hypertension **AKA**
Pulmonary venous hypertension
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Group III WHO classification of pulmonary hypertension **AKA**
Hypoxemia-associated pulmonary hypertension
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Group IV WHO classification of pulmonary hypertension **AKA**
Thromboembolic disease
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Group V WHO classification of pulmonary hypertension **AKA**
Miscellaneous
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Group I WHO classification of pulmonary hypertension description
caused by increased resistance to flow on the arterial side
pressures can reach or even exceed systemic arterial pressures
the right heart is not adapted to deal with these types of pressures
this is unvariably fatal
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Idiopathic pulmonary hypertension **AKA**
Primary pulmonary hypertension
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Types of Group I WHO classification of pulmonary hypertension
* idiopathic
* familial
* Persistant Pulmonary Hypertension of the newborn
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Idiopathic pulmonary hypertension most common in?
Women in 30-40s and invariably fatal
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The most common type of pulmonary hypertension
Pulmonary venous hypertension
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Pulmonary venous hypertension cause
Caused by left-sided heart or valvular disease
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Group II WHO classification of pulmonary hypertension description
* caused by left-sided heart or valvular disease resulting in an increase in pulmonary venous pressure which is transmitted up stream leading to the microvasculature and pulmonary arteries and eventually lead to right-sided heart failure
* most common form of pulmonary hypertension
*
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Group IV WHO classification of pulmonary hypertension description
results from blood disorders that form microthrombi and they often get caught in the lung and build up and can lead to pulmonary hypertension
can also from dislodged Deep vein thrombosis if it is small enough, if it is too large it will obstruct flow from pulmonary artery and cause death very quickly
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Group IV WHO classification of pulmonary hypertension causes
6 listed
* high-altitude
* COPD
* Sleep-disordered breathing
* Interstitial lung disease
* alveolar hypoventilation (obesity hypoventilation syndrome, when the mass of the chest wall impairs the ability to breath so they breath at low-lung volumes)
* developmental abnormalities
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COPD V/Q mismatch
mismatch of ventilation to perfusion from obstruction of airflow due to inflammation and excessive mucus secretion (can also have some vasoconstriction)
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Emphysema V/Q mismatching
* destruction of lung tissue and elastic lung tissue
* increased compliance but reduced recoil
* the airways also collapse as they try to exhale
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V/Q mismatching in COPD vs Emphysema
**COPD:** mismatch of ventilation to perfusion from obstruction of airflow due to inflammation and excessive mucus secretion (can also have some vasoconstriction)
**Emphysema:** the destruction of lung tissue and elastic lung tissue, increased compliance but reduced recoil, the airways also collapse as they try to exhale
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Sleep apnea and respiration
* leads to chronic intermittent hypoxia from stopping and starting breathing all night
* common risk factor for pulmonary hypertension, stroke, metabolic syndromes, etc.
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Types of sleep apnea
2 listed
* central sleep apnea (impaired central control of breathing at night)
* Obstructive sleep apnea (1/4 adults has some degree of sleep apnea)
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Sleep apnea exacerbating pHTN
if this occurs with other comorbid conditions such as COPD and these patients can develop severe pHTN
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Interstitial lung diseases
causes thickening of the alveolar walls due to inflammation, scarring or edema
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What is this?
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What is this?
normal alveoli
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Interstitial lung diseases are a _______ lung disease.
Restrictive
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Interstitial lung diseases effect on compliance
reduces lung compliance
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Interstitial lung diseases lung volumes
because of the reduced compliance these patients tend to operate on low lung volumes
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Interstitial lung diseases cause of pHTN
diffusion impairment
V/Q mismatch
and hypoxemia
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Interstitial lung diseases causes
* idiopathic
* pathogens
* inhaled irritants
* drugs
* Autoimmune diseases
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Interstitial lung diseases and pHTN
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How does chronic hypoxia lead to pHTN?
6 listed
* Vasoconstriction
* hypertrophy
* hyperplasia
* fibrosis
* polycythemia
* right ventricular hypertrophy
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Arterial remodeling consists of?
hypertrophy and hyperplasia of the vascular smooth muscle cells that then encroaches upon the luminal radius
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Cows and high altitude
* don't respond well to high altitude because of high amounts of arterial remodeling
* brisket disease
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Fibrosis secondary effects for pHTN
leads to arterial remodeling, inflammation, edema, scarring that physically restrict blood flow
these patients can also be hypoxic which would be additive
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Polycythemia Mechanism in pHTN
hypoxia stimulates erythropoietin from the kidneys
more blood cells = ↑ hematocrit
↑ blood density
also ↑ likelihood of forming emboli or microemboli that can contribute to pHTN
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How does the heart respond to chronic pHTN
* adaptive right ventricle hypertrophy
* thought to contribute to right heart failure with chronic lung disease
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Endothelial dysfunction's role in hypoxia-associated pulmonary hypertension
* chronic and intermittent hypoxia leads to contraction of smooth muscle but also hypertrophy and hyperplasia
* But endothelial cells increased production of vasoconstrictors and mitogenic factors such as Reactive oxygen species and endothelin-1 (ET-1)
* Also, endothelial cells have reduced the production of vasodilators and anti-proliferative factors like Nitric Oxide and PGI 2
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Endothelin pathway
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Nitric oxide pathway
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Prostacyclin pathway
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Drugs to treat pHTN utilizing targets in the endothelin pathway
endothelin receptor antagonist
which prevent vasoconstriction and smooth muscle proliferation
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Drugs to treat pHTN utilizing targets in the nitric oxide pathway
* Inhaled NO
* PDE-5 inhibitors
* soluble guanylyl cyclase activators
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Drugs to treat pHTN utilizing targets in the prostacyclin pathway
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Nitric oxide pathway agent targets
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Nitric oxide pathway agents
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Endothelin pathway agent targets
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Prostacyclin pathway agents
prostacyclin analogs
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Prostacyclin pathway agent targets
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Summary of response to hypoxia
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What factors contribute to pHTN
Active vasoconstriction
vascular remodeling
polycythemia
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Endothelium's role in vasoconstriction and vascular remodeling
an imbalance in the production of endothelium-derived vasoactive and vasoproliferative factors
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drugs to treat hypoxemia-associated pHTN
* stuff to help control symptoms but the endothelin, nitric oxide, or prostacyclin drugs are approved to treat group III pHTN
* only therapies shown to prolong life are supplemental of oxygen and cessation of smoking
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In pulmonary hypertension what is the site of greatest resistance in the pulmonary circulation?
It can vary, for instance in LCHF the pulmonary veins may be of the highest pressure
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If pulmonary arterial pressure goes up what happens to resistance & flow?
P = R x Q
so
if ↑P
then ↓R
and
↑↑Q
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If pulmonary arterial pressure goes down what happens to resistance & flow?
P = R x Q
so
if ↓P
then ↑R
and
↓↓Q
