Pulmonary vascular disease Flashcards

1
Q

Define hypertension.

A

Abnormally high BP.

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2
Q

What are the 2 main types of thromboembolic disease?

A

DVT and PE.

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3
Q

Where do most emboli originate?

A

Thromboses/clots in the leg veins. They travel upwards to the right side of the heart then the pulmonary arteries. Thrombi in bigger veins (ileofemoral and above) are more likely to embolise. Thrombi in smaller veins usually resolve on their own.

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4
Q

Where else can emboli originate?

A

Cardiac, septic (IDU’s), air embolus (post-trauma) and amniotic fluid embolus.

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5
Q

How does thromboembolic disease occur?

A

A thrombus is a blood clot that forms in a vein. An embolus is anything that travels through blood vessels until it reaches a vessel that is too small to let it pass - blood flow is then stopped by the embolus.

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6
Q

Describe Virchows triad.

A

3 catagories of factors that are throught to contribute to thrombosis. 1) Reduced blood flow: immobility, bed bound, travel, heart failure etc. 2) Abnormal vessels: post-MI, leg trauma, pelvic surgery. 3) Hypercoagulable stress: pregnancy, OCP, HRT, malignancy etc. Young person presents with DVT/PE? Check if they have an interited hypercoagulable state.

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7
Q

What are the signs and symptoms of DVT?

A

Leg swelling, tenderness, oedema and tight calves - not always present and can mimic other conditions.

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8
Q

Which investigations would be carried out if a DVT is suspected?

A

D-dimer blood test –> ultrasound –> venography.

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9
Q

Why is the D-dimer test helpful?

A

Looks for products of fibrin degradation which are break off products in clot formation. Non-specific and not helpful if positive, however if negative effectively excludes DVT/PE.

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10
Q

What is the gold standard for diagnosing venous thrombosis?

A

Venography - injecting a radiopaque liquid into a vein then radiography.

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11
Q

What is a PE?

A

When a blood clot (usually from deep veins of legs) lodges in the pulmonary arterial circulation. Usually multiple clots. 10% can cause pulmonary infarction. A large clot can cause a massive PE: hypoxia, hypotension, pain and collapse. Small clots usually lodge in lower lobes.

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12
Q

What are the symptoms of PE?

A

73% breathlessness, pleuritic chest pain in 66%, cough, haemoptysis and central cardiac chest pain if massive.

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13
Q

What are the signs of PE?

A

Unwell, cyanosed (blue), tachypnoea, tachycardia, fever, drop in BP due to circulatory collapse etc.

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14
Q

Which investigations can be used for PE?

A

ABG’s; raised troponin (poor indicator); D-dimer; ECG (abnormal in 70% but non-specific); CXR.

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15
Q

What is the first line test for chronic TED and how does it work?

A

V/Q scan. Inhalation of radioactive xenon then injection of technicium labelled albumin. Gamma camera compares - looking for an area that is ventilated but not perfused. Positive? Treat. Negative? Don’t treat. Intermediate? Further investigation required.

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16
Q

If V/Q scan is inconclusive, what further tests can be performed? Describe them briefly.

A

Doppler leg US; CTPA (contrast); echocardiogram (acute PE cannot cause > right heart pressures, chronic PE can; RV bigger than LV as it cannot get blood to lungs).

17
Q

What is the gold standard for diagnosis of acute PE?

A

Pulmonary angiography. Inject contrast into pulmonary artery branch after percutaneous cathetersation via femoral vein.

18
Q

What are the guidelines for investigating suspected PE?

A

Use Wells (NICE guidelines) or modified Geneva scoring, then D-dimer.

19
Q

How is PE managed?

A

Supportive care - prevention/resuscitation; respiratory support O2 ventilation; fluids; analgesia. Anti-coagulation reduces fatal occurence but does not treat an existing clot. Give for 3 months if provoked, 6 months if unprovoked or for life if clots are recurrent.

20
Q

What is a massive PE associated with?

A

Systolic BP 15 mins which cannot be explained by hypovolaemia, sepsis or a new arrhthymia. Can cause acute RHF.

21
Q

What are the symptoms of massive PE?

A

Clinical emergency: sudden chest pain, right heart ischaemia, SOB, loss of consciousness, low BP etc. ECG is useful in showing right heart strain and excludes dissecting aortic aneurysm.

22
Q

Describe treatment of massive PE.

A

Resuscitation, IV heparin, thrombolysis (only if no contraindications like recent surgery etc). If thrombolysis fails or is contraindicated –> embolectomy (surgery).

23
Q

Define pulmonary hypertension.

A

High pressure in the pulmonary arterial circulation. If mean PA pressure is >25 mmHg at rest and >30 mmHg on exercise this is PH. More common in women.

24
Q

What are the values for mild, moderate and severe PH?

A

Mild: 25-45 mmHg. Moderate: 45-65 mmHg, Severe: > 65 mmHg.

25
Q

Describe the 5 groups of PAH.

A

1) PAH: idiopathic, heritable, drug (appetite suppressants) and toxin (cocaine) induced, persistent PH of newborn; associated with connective tissue disease, portal disease, HIV, schistosomiasis etc.
2) PH due to left heart disease: systolic dysfunction, diastolic dysfunction or valvular disease.
3) PH due to lung diseases/hypoxia: COPD, interstitial lung disease, other restrictive/obstructive lung diseases, sleep-disordered breathing, alveolar hypoventilation disorders, chronic exposure to high altitude and developmental disorders.
4) Chronic thromboembolic PH.
5) PH with unclear, multifactorial mechanisms: systemic/metabolic disorders, hematologic disorders etc.

26
Q

What are the 2 main mechanisms of PAH?

A

Hypoxic vasoconstriction and cardiac disease.

27
Q

Describe the 2 main mechanisms of PAH.

A

HYPOXIC vasoconstriction: COPD, hypoventilation (sleep, neuromuscular, kyphoscoliosis), > altitude. CARDIAC disease: RV volume/pressure overload; volume overload ASD or VSD; pressure overload.

Resting PAP only increases when loss of pulmonary vessels is over 60%.

28
Q

Which patients have the worst prognosis in PAH?

A

Aged > 44, connective tissue diseases, poor functional status (breathless), evidence of heart strain and failure to respond to trial treatment of epoprostenol.

29
Q

What investigations are used to diagnose PH?

A

CXR, ECG, PFT’s, V/Q, Echo, HRCT chest (high resolution) and referral to specialist centre.

30
Q

Which surgical procedures are available for PAH?

A

Atrial septostomy (shunt that > CO and improves RVF); pulmonary endarterectomy; or transplantation if all other treatment options have failure (bilateral/heart and lung).