Pulmonary Circulation and Pulmonary Embolism Flashcards

1
Q

Describe blood supply to lungs

A
  • Bronchial: bronchial arteries from systemic circulation supply smooth muscle in airways, nerves and interstitial tissue, 2% of LH output, blood drains to LA via PV
  • Pulmonary circulation: PA comprising CO from RH, supplies dense capillary network around alveoli, returns blood to LA via PV
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2
Q

Describe bronchial circulation

A
  • Arises from aorta and supplies trachea and bronchi
  • Nourishes pulmonary vessels, interstitial, pleura
  • Drains into azygos vein and pulmonary veins
  • Also has a role in regulation of temp and humidity in airways
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3
Q

Describe pulmonary circulation

A
  • Right to left
  • Low pressure, low resistance circuclation
  • Contrasts with systemic circulation- high pressure, high resistance circulation
  • Considerable room for adaptation enabling large increases in CO accommodated without increasing pressure/ resistance within circulation
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4
Q

What is the equation for vascular resistance?

A

(P1-P2)/ blood flow

- Resistance 10x greater in systemic than pulmonary

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5
Q

What are the influences on pulmonary vascular resistance?

A
  • Mediator, e.g. serotonin (arterial vasoconstriction) and histamine (venoconstriction)
  • Intravascular pressures
  • Lung volumes
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6
Q

Describe intravascular pressure

A
  • Fall in pulmonary vascular resistance as pulmonary arterial or venous pressure rises
  • Two adaptations- recruitment and distension
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7
Q

What are the effects of recruitment and distension?

A
  • Recruitment- increase number of perfused capillaries in response to a stimulus
  • Distension- individual capillary segments get bigger
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8
Q

Describe pulmonary vascular resistance and lung volumes

A
  • Extra-alveolar vessels pulled open as lung expands- low resistance at lung volumes and vice versa
  • Capillaries- squashed as alveolar press. rises and resistance rises
  • Calibre reduced at large lung volumes due to stretching/thinning of alveolar walls- hence vascular resistance rises
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9
Q

How is blood flow distributed in the lung?

A
  • Unequal throughout lung
  • Blood flow decreases from bottom to apices
  • Explained by hydrostatic pressure differences within the blood vessels
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10
Q

How are ventilation and perfusion controlled locally?

A
  • Ventilation in alveoli matches perfusion through capillaries
  • If vent decreases in group of alveoli, PCO2 increases and PO2 decreases
    • blood flowing here not oxygenated
  • Decreased tissue PO2 around under-ventilated alveoli- constricts arteries and diverts blood to better ventilated alveoli
  • Ventilation perfusion mismatch
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11
Q

What are the non-respiratory functions of pulmonary circulation?

A
  • Filter: vital function in protecting systemic arterial circulation from emboli
  • Mediator metabolism: ACE involved in converting Ang I to Ang II
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12
Q

What is pulmonary hypertension?

A
  • mean pulmonary artery press >25mmHg at rest or >30mmHg on exercise
  • In health mean PA is 15mmHg
  • Associated with an increase in pulmonary vascular resistance
  • Ultimately may lead to RH failure
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13
Q

What are the causes of pulmonary hypertension?

A
  • Group 1- pulmonary arterial hypertension which includes familial and associated with conditions
  • Group 2- secondary to heart disease (huge group)
  • Group 3- secondary to lung conditions (big group)
  • Group 4- chronic thromboembolic PH (small group)
  • Group 5- mixed bag of rarities
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14
Q

Describe group 1 causes of pulmonary hypertension

A
  • Disease of small arteries per se, characterised by vascular proliferation and remodelling
  • Increased PVR due to vasoconstriction, remodelling of vessel wall and thrombosis in situ
  • Respond to new vasodilator
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15
Q

Describe group 2 and 3 causes of pulmonary hypertension

A
  • Cause PH secondary to underlying condition
  • Heart disease causes post-capillary disease
  • Lung conditions can cause pulmonary hypertension due to combination of hypoxia, vasoconstriction and destruction of vascular bed (E.g. emphysema)
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16
Q

Describe group 4 causes of pulmonary hypertension

A
  • CTEPH (chronic thromboembolic PH)
  • PH secondary to chronic changes- failure of resolution of pulmonary embolism
  • Curable if surgically accessible, i.e. clot needs to be proximal so surgeons can access it and dissect out
  • About 4% of patients post PE develop CTEPH
17
Q

What is a pulmonary embolism?

A
  • Common cardiovascular emergency
  • Occlusion of pulmonary arterial bed by thrombi commonly originating from leg/ pelvic veins
  • Acute life threatening but potentially reversible RH failure
  • Mortality higher in those presenting with PE of DVT
18
Q

Describe the pathophysiology of pulmonary embolism

A
  • Blockage of pulmonary arterial tree
  • Abrupt increase in pulmonary vascular resistance
  • Level of after-load generated that RV can’t match
  • Non-precondition thin-walled RV cannot generate a mean pressure >40mmHg
19
Q

Describe low risk PE

A
  • Haemodynamically stable
  • No clinical signs of HR impairment
  • Short term PE related mortality <1%
  • Suitable for early discharge
20
Q

Describe high risk PE

A
  • Haemodynamic instability
  • Shock and hypotension- principal markers of high risk of early death in acute PE
  • 90 day all cause mortality rate of 52.4% in patients with SBP <90mmHg
  • Short term mortality more than 15%
  • 5-10% cases high risk
21
Q

Describe intermediate risk PE

A
  • Heamodynamically stable, significant PE
  • RH injury
  • Tests to risk stratify include markers of myocardial injury (troponin, NT-proBNP) and echo
22
Q

What tests can be done to confirm PE?

A
  • Confirmatory test must be done
  • CPTA gold standard
  • Ventilation perfusion also considered, particularly if CTPA contraindicated or no cardiorespiratory background disease
23
Q

What immediate treatment options are available for PE?

A
  • Life-saving restoration of flow through occluded pulmonary arteries- thrombolysis
  • Prevention of potentially fatal early recurrences- heparins
  • Immediate treatment highly effective
24
Q

What treatment options are available for PE (long-term)?

A
  • Anticoagulation- prevents further thrombus deposition, allows stability + endogenous lysis- prevents propagation and embolisation
  • Reduces risk of recurrent thrombosis
  • Approx. 6 months or lifelong in those with unprovoked event/following life-threatening event
  • Investigate for provoking factors if non-evident