Q: What is the pulmonary circulation? Use? What is it not?
A: from blood leaving right ventricle to lungs to left atrium
Perfusion of the respiratory airways for gas exchange
bronchial circulation (blood to cells that constitute lung)
Q: What are the 3 main differences between pulmonary and systemic circulation?
A: arterial thickness
- systemic has thicker wall and less lumen
- pulm has thinner walls and more lumen
circuit length/distance
- systemic has to go much further eg finger tips
- pulm just has to go to lungs and back to heart
ventricular thickness
-thicker wall for left ventricle (more efficient pump- allows the left ventricle to generate HIGH PRESSURES)
pressure
- higher systemic circ pressure
- pulm circuit has lower pressure
Q: Compare the circuit pressures for the systemic and pulmonary circulation via the difference in pressure between the aorta and pulmonary artery. One other.
A: 120/80
25/8
RA of systemic circ has pressure of 1 while LA of pulm has 3mmHg
Q: What’s the pressure difference between the LV and aorta? why?
Aorta and systemic capillaries?
Systemic capillaries and vena cava?
Vena cava to RA?
RA and RV?
RV and pulmonary artery?
Pulmonary artery and pulmonary capillaries?
Pulmonary capillaries and pulmonary vein?
Pulmonary vein and LA
A: all are drops
due to structure of aorta and its recoil
massive drop
massive drop
RA pressure is 1 (not relying on blood pressure from vena cava to get blood back-> relying on skeletal muscle pump and pressure difference too)
increase (force of RV contraction)
drops..
returns back to left side of heart at higher pressure than blood did to right side
Q: Comparing systemic and pulmonary circulation. What is overall cardiac output? how much of total body blood? How does volume differ between the circuits?
Pressure gradient?
Resistance?
A: 5L (10%)
-4.5 is systemic and 0.5 is pulmonary
lower in pulmonary-> give lower flow rate
smaller in pulmonary
Q: What are the functions of the pulmonary circulation? (3)
A: 1. Gas exchange (oxygen delivery, carbon dioxide, CO and NO delivery too
- Metabolism of vasoactive substances
- Filtration of blood
Q: How much time is available for gas exchange? called?
Q: time available for gas exchange= pulmonary transit time- 0.75s
Q: What is the pulmonary circulations role in terms of metabolism? (2)
A: ACE is present on pulmonary endothelial cells
- turns ANG I to ANG II= potent vasoconstrictor (and waste)
- breaks down bradykinin (vasodilator)
both result in more vasoconstriction
Q: Define embolus. Embolism.
A: An embolus is a ‘mass’ within the circulation capable of causing obstruction
An embolism is an ‘event’ characterised by obstruction of a major artery
Q: What type of circuit is the pulmonary one? What can still happen? which side? How does this reflect the role of the pulmonary circulation?
A: Although the entire circulation is principally a closed circuit
sometimes things can get ‘caught’ in the blood (usually on venous side- slower flow)
the pulmonary circulation filters before systemic arteries
Q: Name 3 types of embolus? 2 types they can become? Result of both?
A: Venous thrombosis
Ruptured fatty plaques
Air bubbles
small-> eliminated in pulmonary microcirculation
large-> trapped in pulmonary microcirculation (pulmonary embolism) = local perfusion is obstructed-> can lead to death
Q: What is a pulmonary shunt? Name 3.
A: ‘…circumstances associated with bypassing the respiratory exchange surface…’
- Bronchial circulation
- Foetal circulation
- Congenital defect
Q: Describe the bronchial circulation.
A: -> technically a shunt because the blood that leaves the LV into the aortic arch and eventually perfuses some of bronchial tree (keeps it alive)-> instead of returning to right side of heart-> bronchial drainage
Q: Describe foetal circulation.
A: -> not using lungs
use foramen ovale (LA and RA) and ductus arteriosus (aorta and pulm artery) -> allow heart to beat normally
Q: How can a congenital defect lead to a shunt? (2)
A: -if your foramen ovale doesn’t close-> patent FO -> type of atrial septal defect
-ventral septal defect
Q: Pulmonary circuit resistance? capacity? when? What should happen when CO is increased? (4) What actually happens?
A: Pulmonary circulation is a low resistance high capacity circuit at a resting CO of 5 L/min
- increase MAP
- increased fluid leakage into tissue
- increased pulmonary oedema
- decreased pulmonary function
- because walls are thin, you get increased pulmonary artery distension (relatively complient vessels)
AND you increase perfusion of underperfused capillary beds
so 1234 of prev don’t happen
Q: Why doesn’t pulmonary function decrease with increased CO?
A: at rest of 5L/min (with the 3 zone model) the lower part of the lung is more perfused that top (top 2 have more capacity)
at 25L/min the 3 sections have equal perfusion
Q: What’s the effect of inspiration and expiration on alveolar vessels? Show this on a lung volume resistance graph.
A: Inspiration compresses alveolar vessels, and expiration compresses extra-alveolar vessels
u shape
- ResidVol has high resistance-> expiration= compresses extra-alveolar vessels
- FRC has low resistance
- TotLC has high resistance-> inspiration= compresses alveolar vessels
Q: How does hypoxia affect the systemic and pulmonary circuit? Cause? (2)
A: Systemic vascular response to hypoxia is vasodilation
Pulmonary response to hypoxia is vasoconstriction
- low O2 environment
- hypo-ventilated alveolus (under vent)
Q: When is the pulmonary response to hypoxia beneficial? Explain (3).
A: During foetal development
- Blood follows the path of least resistance
- High-resistance pulmonary circuit means increased flow through shunts
- First breath increases alveolar PO2 and dilates pulmonary vessels
Q: When is the pulmonary response to hypoxia detrimental? Explain (5).
A: Chronic obstructive lung disease
- Reduced alveolar ventilation and air trapping
- Increased resistance in pulmonary circuit
- Pulmonary hypertension (Cor pulmonale)
- Right ventricular hypertrophy
- Congestive heart failure
Q: What do blood vessels carry on the way to interpulmonary circulation? What do they provide?
Explain normal fluid balance. (4) Result? What happens if final part is not controlled?
A: plasma RBC etc-> content provides pushing or pulling force
- plasma hydrostatic pressure = pushing force out of blood vessel -> more prevalent at arterial than venous end
- interstitial hydrostatic pressure (from outside blood vessels) = pushing force into blood vessel = but effectively 0
- plasma oncotic pressure from blood vessel = pulling force = quite high due to high protein content
- interstitial oncotic pressure is doing the opposite
(9-0-25+17) = 1mmHg roughly out of vessel in total
->Steady fluid accumulation is easily controlled by the lymphatic system
If production exceeds maximum rate of clearance, or lymphatic system fails, then fluid will accumulate
OEDEMA
Q: How can mitral valve stenosis affect fluid balance? (4)
A: Increased plasma hydrostatic pressure
More fluid forced into interstitium
Lymph clearance exceeded (50-0-25+17= 42mmHg)
OEDEMA
Q: How can hypoproteinaemia affect fluid balance? (5)
A: Plasma oncotic pressure reduced
Less fluid drawn into capillary
Fluid accumulates in interstitium
Lymph clearance exceeded (9-0-5+17=21mmHg)
Oedema
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3 Ventiliation58
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6 Lung Cell Biology44
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11 Control of Breathing- Asleep52
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18 Lung Mechanics37
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4 Gas Transport62
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5 Structure and Function of the Airways40
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7 Respiratory Pathology: Lung Cancer47
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8 Breathlessness and Control of Breathing in the Awake State49
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10 Lung Infection: Viral and Bacterial Pneumonias34
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14 Lung Immunology and Allergic Disease Airway38
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12 Acid Base Disturbance23
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15 Hypoxia27
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16 Lung Development30
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17 Pulmonary Circulation26
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1 Why is Studying Lung Disease Important?14
