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CRP 2: KCP1: Breathlessness, Cough & Haemoptysis > 1.3 Pulmonary Ventilation & Pulmonary Circulation - Physiology - Lecture > Flashcards

1.3 Pulmonary Ventilation & Pulmonary Circulation - Physiology - Lecture Flashcards

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1
Q

What are the 2 circulations IN the lungs

A
  1. Pulmonary Circulation: Carry non-oxygenated blood to respiratory zone
  2. Bronchial Circulation: Carry oxygenated blood to tracheobronchial tree
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2
Q

Give the major differences between Bronchial & pulmonary circulation, in terms of:
1. Origin
2. type of blood carried
3. % of cardiac output
4. Pressure system
5. Structures supplied
6. Drainage
7. Unique role (main function)

A
  1. Origin
    * P: Right ventricle
    * B: Aorta (systemic circulation)
  2. Blood Carried
    * P: Deoxygenated → to alveoli for gas exchange
    * B: Oxygenated → to bronchi & lung tissues
  3. % Cardiac Output
    * P: 100% (entire CO)
    * B: ~1–2% of left ventricular output
  4. Pressure System
    * P: Low-pressure, high-flow
    * B: High-pressure, low-flow
  5. Vessels Supplied
    * P:Respiratory bronchioles → alveolar ducts → alveoli
    * B: Bronchi and connective tissue (tracheobronchial tree)
  6. Drainage
    * P: Pulmonary veins → left atrium
    B: Partially drains into pulmonary veins → physiologic shunt
  7. Unique Role
    P: Site of gas exchange
    B: Nutrient supply to lung structure
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3
Q

List the 5 main functions of the pulmonary circulation

A
  1. Gas Exchange
  2. Supplies Nutrients to Alveolar Ducts & Alveoli
  3. Filter: Trap Thrombi and Other Sources of Emboli
  4. Fluid Exchange – Pressure in the Capillaries and Alveoli Cause Negligible Amount of Tissue Fluid Formation
  5. Angiotensin Converting Enzyme – Converts Angiotensin I to Angiotensin II
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3
Q

What is the cause and result of the physiological shunt

A

Cause:
- bronchopulmonary Anastomosis; mixing of bronchial venous blood (deoxygenated) with pulmonary venous blood (oxygenated)
- some blood bypasses the alveoli completely (non-ventilated areas)

Result:
So there is a decrease of 1-2% in Pulmonary Venous Oxygen Saturation

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4
Q

List the differences between Pulmonary & Systemic circulation based on the following:
1. Pressure
2. Driving Pressure
3. Resistance
4. Flow

A

Pulmonary VS Systemic (respectively)

Pressure
* Low pressure system (~15 mmHg mean)
* High pressure system (~95 mmHg mean)

Driving Pressure
* 15 (PA) – 8 (LA) = 7 mmHg
* 95 (Aorta) – 2 (RA) = 93 mmHg

Resistance
* Low (shorter vessels, large lumen)
* High (longer path, muscular arterioles)

Flow
* Entire cardiac output (100%)
* Divided among organs based on metabolic need

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5
Q

List the differences between Pulmonary & Systemic circulation based on the vessels and oxygenation in terms of:
1. Arteries
2. Veins
3. Capillary diameter
4. Vessel wall thickness

A

Pulmonary VS Systemic

Arteries
* Carry deoxygenated blood
* Carry oxygenated blood

Veins
* Carry oxygenated blood
* Carry deoxygenated blood

Capillary Diameter
* Larger (low resistance)
* Small (higher resistance)

Vessel Wall Thickness
* Thin (for gas exchange)
* Thick (withstand high pressure)

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6
Q

List the differences between Pulmonary & Systemic circulation based on the Structural & Functional differences in terms of:
1. True arterioles
2. Smooth muscles in vessels
3. Tissue fluid formation
4. Regulation
5. Gravity impact

A

Pulmonary Circulation VS Systemic Circulation:

True Arterioles
* Absent
* Present

Smooth Muscle in Vessels
* Less developed
* More developed

Tissue Fluid Formation
* No (low pressure, low filtration)
* Yes (due to capillary hydrostatic pressure)

Regulation
* Gravity + Hypoxia
* Neural & humoral

Gravity Impact
* Significant (affects flow by region)
* Negligible at arterial side

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7
Q

What is the difference in response to hypoxia in pulmonary & systemic circulation

A

Response to Hypoxia

PULMONARY:
Vasoconstriction → to divert blood to well-ventilated alveoli (Hypoxic Pulmonary Vasoconstriction)

SYSTEMIC:
Vasodilation → to improve oxygen delivery to hypoxic tissue

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8
Q

What is the consequence of global hypoxia such as in cases of high altitude

A
  • Global hypoxia leads to generalised lung vasoconstriction (of the whole lung)
  • Which causes pulmonary hypertension
  • The increased pressure in pulmonary capillaries results in fluid from leaking out
  • Resulting in pulmonary oedema
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9
Q

The lungs are divided into 3 functional zones based on the relationship between what 3 pressures

A
  1. PA: Alveolar pressure
  2. Pa: Pulmonary artery pressure
  3. Pv: Pulmonary venous pressure
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10
Q

What are the 3 functional zones of the Lungs and how does the pressures compare in these zones

A
  1. Zone 1: PA > Pa > Pv
  2. Zone 2: Pa > PA > Pv
  3. Zone 3: Pa > Pv > PA
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11
Q

Describe the locations in the Lungs of the 3 perfusion zones

A
  1. Zone 1: does not exist under normal conditions
  2. Zone 2: At the apices of lungs
  3. Zone 3: At the bases of the lungs
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12
Q

Why is there no blood flow in Zone 1 under normal conditions

A

Because the capillaries collapse due to the high alveolar pressure

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13
Q

Why is Zone 1 referred to as a physiological dead space

A

because they are ventilated but not perfused as the capillaries are closed, hence why it is wasted ventilation

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14
Q

What are 2 conditions that cause zone 1 to appear

A
  1. Haemorrhagic shock / hypovolemia (decreased Pa)
  2. PEEP: Positive Pressure Ventilation
    (increased PA)
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15
Q

In which stage of the cardiac cycle does Zone 2 exist

A

only during the systole, there is any blood flow as the Pa momentarily increases more than PA

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16
Q

Why is referred to as the waterfall effect in Zone 2

A
  • because the driving pressure is Pa-PA in zone 2
  • so once the PA exceeds Pa again, the flow stops
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17
Q

Why is Zone 3 flow referred to as continous blood flow

A

because the capillaries are open through out the cardiac cycle as the pressure in the arteries are higher than both Alveolar and venous pressures

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18
Q

In which conditions does zone 2 changes into zone 3

A
  • during exercise or in cases of increased cardiac output,
  • the Pa rises more than the PA significantly
  • which keeps the capillaries open and there is a continues blood flow
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19
Q

What is the difference in responses to hypoxia in systemic and pulmonary circulation

A

Pulmonary circulation:
- Hypoxic Pulmonary Vasoconstriction (HPV)
- to shunt the blood away from poorly ventilated/oxygenated alveoli

Systemic circulation:
- Vasodilation
- to increase the oxygen delivery to the ischemic tissues

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20
Q

What is the possible mechanism behind HPV

A
  • mechanism not fully understood
  • but possibly due to chemicals from alveoli: such as
    • increased Leukotrienes (Vasoconstrictors)
    • Decreased NO & Prostaglandins (Vasodilators)
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21
Q

At what PaO2 does the HPV kicks in?

A
  • when it falls below 60mmHg
  • if it falls below severely the blood flow completely stop
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22
Q

What is the functional significance of HPV:

A
  • prevents WASTED perfusion of poorly ventilated areas (to prevent V/Q mismatch)
  • Helps to optimize the V/Q ratio
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23
Q

What is the consequences of Chronic Hypoxia

Study These Flashcards
A
  • Increased pulmonary artery pressure due to increase in resistance upon vasoconstriction
  • leads to pulmonary hypertension
  • leads to right ventricular overload (cor pulmonale)
  • Due to the high capillary hydrostatic pressure, fluid leaks out and thus leads to pulmonary oedema
24
In standing position, what is the pressure at lung base and apex compared to the heart level
Apex: 15mmHg lower Level of heart: 25mmHg Base: 8mmHg higher
25
Describe the blood flow is affected based on posture, standing (upright) and lying (supine)
Upright: * Linear increase from apex to the base * Base gets more blood flow Supine: - Apices and base is perfused equally - posterior side gets more perfusion
26
What is the effect on perfusion during exercise
* Perfusion increases through out * the increase is mos signifcantly noticed at the base
27
What is the potential risk of increased cardiac output on pulmonary blood flow
* Increased cardiac output * more blood is pumped out of the heart, and more enters into the pulmonary circulation * so the pulmonary arterial pressure increases * if the lungs cant accomodate it, it will raise the capillary hydrostatic pressure * results in fluid leakage * pulmonary oedema
28
What are the 2 major protective adaptations of lungs that ensure a low pulmonary vasvular resistance when blood flow increases dramatically
Capillary recruitment: - previously underperfused capillaries are opened - to accomodate the extra blood flow Capillary distension - the existing capillaries increase in diameter - increases the flow without raising the pressure much
29
What are the 5 key regulatory factors of pulmonary blood flow
1. Sympathetic Stimulation (a1 receptors) - Vasoconstriction - Reduces Blood Flow By 30% 2. Hypoxia (low O2) &Hypercapnia (high CO2) - both triggers Vasoconstriction - Reduced blood flow 3. Cardiac Output - increases blood flow - Pulmonary Blood Flow is Directly Proportional 4. Vascular Resistance - decreases blood flow - blood flow is inversely proportional to resistance 5. Inspiration (negative intrathoracic pressure) - increased venous return (RA) - increased blood flow (RV)
30
What are some of the vasoconstrictors that regulate pulmonary blood flow
CAPE THAt lungs 1. Catecholamines 2. Angiotensin II 3. Endothelin 4. Prostaglandin F2a 5. Thromboxane 6. Histamine 7. Alveolar hypoxia
31
What are some of the vasodilators that regulate pulmonary blood flow
BAN BP 1. Bradykinin 2. Acetylcholine 3. Nitrix oxide 4. Beta adrenergic agonists 5. Prostacyclin (PGI2)
32
Define alveolar ventilation
the volume of new air enters into the respiratory passages and undergo gas exchange each minute; this is equal to VA= (Vt - DS) x RR Normal values: VA= (500-150) x 12 = 4200 mL/min
33
Describe the regional difference in alveolar ventilation in terms of intrapleural pressure
Mechanism: * In a standing position, gravity pulls the lungs downward. * This results in intrapleural pressure (IPP) being more negative at the apex than at the base. ○ IPP at apex: -10 cm H₂O ○ IPP at base: -2.5 cm H₂O Consequences: * At end expiration, the apex of the lung is more expanded than the base. * However, during inspiration, more air is drawn to the base because: ○ The base is less expanded and hence more compliant. It receives a greater change in volume → hence, better ventilation.
34
Describe the V/Q gradient from apex to the base of the lungs
Base: - High perfusion due to gravity - Lower ventilation relative to the perfusion - lower V/Q ratio: 0.3 Apex: - Low perfusion - relatively better ventilation - higher V/Q ratio: 2.1 - contributes to physiological dead space: ventilation with no perfusion
34
What is meant by Ventilation perfusion ratio and what is a normal value of it
Ratio of air reaching alveoli (ventilation) to the blood reaching alveoli via capillaries (perfusion). * Normal VA ~4000 mL/min * Normal Q:~5000 mL/min V/Q≈40005000=0.8 Significance: * Ideal ratio = efficient gas exchange * Mismatch = impaired oxygenation or CO₂ clearance
35
Give 2 causes of V/Q mismatch
1. Lower V/Q: - due to airway obstruction or hypoventilation (Lower ventilation) 2. Higher V/Q: - due to pulmonary embolism or vascular obstruction (Lower perfusion)
36
Mismatch 2: High V/Q What is the result of low perfusion in cases such as pulmonary embolism
- leads to wasted air in alveoli (as these are not in contact with blood) - CO2 removal therefore becomes less efficient - potentially lead to hypercapnia
36
Mismatch 1: Low V/Q What is the result of low ventilation as in conditions such as airway obstruction and hypoventilation
alveolar O2 levels drop - less O2 diffuses into the blood - leads to arterial hypoxemia
37
37
State the Starlings Law of capillary equation
Q̇f = Kf[(Pc − Pis) − σ(πpl − πis)] - Q̇f: Net fluid movement - Pc: Capillary hydrostatic pressure - Pis: Interstitial fluid pressure (normally negative) - πpl: Plasma oncotic pressure - πis: Interstitial oncotic pressure - Kf: Filtration coefficient (capillary permeability) - σ: Reflection coefficient (permeability to proteins)
38
What are the outward and inward forces and their estimated values and what is the net fluid movement (Qf)
Outward forces 1. Pc: capillary hydrostatic pressure= +7mmHg 2. πis: insterstitial oncotic pressure= +14mmHg 3. Pis: (negative) interstitial pressure= -8mmHg TOTAL outward forces: +29mmHg Inward force: 1. πpl: Plasma oncotic pressure= -28mmHg Net fluid movement: Outward, by +1mmHg so slight fluid leak out occurs
39
What happens to the fluid that leaks out
It is drained by the lymphatics
40
Define pulmonary oedema
the extravascular accumulation of fluid in the lung. (interstitial space and alveoli)
41
What is the sequence of fluid build up/accumulation
Interstitial --> Alveolar flooding this leads to impaired gas exchange (especially O2 diffusion decreases)
42
Why is the lung lobules outlined in white in patients with pulmonary oedema
due to increased fluid in the lymphatics that run between lung lobules
42
43
List the clinical causes of increased capillary permeability (Kf, sigma)
1. ARDS 2. oxygen toxicity 3. Toxins (inhaled or circulating)
44
List the clinical causes of increased capillary hydrostatic pressure (Pc)
1. Left-sided heart failure 2. Mitral stenosis 3. Fluid overload (IV fluid overadministration)
45
List the clinical causes of decreased interstitial pressure (Pis)
1. Sudden pneumothorax evacuation 2. Upper airway obstruction
46
List the clinical causes of decreased plasma oncotic pressure
1. Hypoproteinemia (protein starvation) 2. Dilution of blood proteins (due to IV fluids) 3. Proteinuria
47
What are the factors in starling equation that predispose to pulmonary oedema
1. Increased filtration coefficient and reflection coefficient 2. Increased capillary hydrostatic pressure 3. Decreased plasma oncotic pressure 4. Decreased insterstitial pressure
48
What are the other etiologies that predispose to pulmonary oedema
1. decreased lymphatic drainage: - due to: - tumours - interstitial fibrosis 2. Unknown aetiology: such as: - high altitude - head trauma (neurogenic pulmonary oedema) - drug overdose
49
What are the 2 main pathophysiological types of pulmonary oedema:
1. Cardiogenic: (high pressure oedema) - due to increased Pc 2. Non-cardiogenic: (permeability oedema) - due to increased permeability (Kf & Sigma)
50
Describe the clinical findings of Cardiogenic oedema
- LV failure - Lung Weight Increased - Dark Bluish Red Lungs - Frothy Fluid Exuding From Airways - Dilated Lymphatic Channels - Interlobular Septa Widened
51
Describe the pathophysiology of Non-Cardiogenic oedema
- A R D S - Endothelial Cell Injury - Cell Lose the Integrity - No Longer Semi permeable - Cell Swelling, Intercellular Gaps and Necrosis - Normal Vascular Hydrostatic Pressure
52
What are the main/common causes cariogenic and non-cariogenic pulmonary oedema
1. Cardiogenic: - Left-sided heart failure - mitral stenosis both of these leads to increased pulmonary venous pressure and results in insterstitial and alveolar flooding 2. Non-cardiogenic: - capillary membrane damage - due to: pneumonia, or inhalation of toxic gases - results in leakage of proteins and fluid
53
What are the main 5 causes of pulmonary hypertension
1. increased pulmonary blood flow: - cardiac shunts such as in ASD and VSD 2. Pulmonary venous congestion - Mitral valve disease (stenosis) - Chronic left ventricular failure 3. Mechanical arterial Occlusion - multiple pulmonary thromboemboli - Foreign body emboli (drug addicts) 4. Alveolar hypoxia causing Pulmonary vasoconstriction (HPV) - high altitude - Chronic obstructive airway disease 5. Destruction of Lung capillary beds - emphysema - Interstitial fibrosis of lungs
53
What is the definition of Pulmonary hypertension
Increased pressure in the pulmonary arteries

CRP 2: KCP1: Breathlessness, Cough & Haemoptysis (6 decks)

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