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Year 1: Respiratory > PE and pulmonary hypertension > Flashcards

PE and pulmonary hypertension Flashcards

1
Q

define PE

A

blockage of a pulmonary artery by a blood clot, fat, tumour, or air

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2
Q

pulmonary infarction

A

if blood flow and oxygen to the lung tissues is compromised the lung tissue may die

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3
Q

DVTs in ileo-femoral vein (proximal) are more likely to embolise and more likely to lead to chronic venous insufficiency and venous leg ulcers than popliteal vein DVTs (distal). True/ False?

A

True

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4
Q

clinical presentation of DVT

A

swollen, red, hot, tender, whole leg/ calf

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5
Q

Differential diagnosis of DVT

A

could be:

  • popliteal synovial rupture (Baker’s cyst) - benign swelling of the semi-membranous or other synovial bursa found behind the knee joint
  • superficial thrombophlebitis (inflammation of the walls of a vein with associated thrombosis, often occurring in the legs during pregnancy)
  • calf cellulitis (bacterial infection involving the inner layers of the skin, especially the dermis and subcutaneous fat).
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6
Q

investigation of DVT

A 
ultrasound Doppler (non-invasive, excludes popliteal cyst or pelvic mass)
CT scan (ileo-femoral veins, IVC, and pelvis)
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7
Q

clinical presentations of large, medium and small pulmonary emboli

A

large: CVS shock, low BP, central cyanosis, sudden death
medium: pleuritic pain, haemoptysis, breathless
small recurrent: progressive dyspnoea, pulmonary hypertension, right heart failure

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8
Q

saddle PE

A

a form of large pulmonary thrombo-embolism that straddles the main pulmonary arterial trunk at its bifurcation. Its incidence amongst patients diagnosed with PE is 2.6^

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9
Q

Name some risk factors for DVT and PE

A
  • thrombophilia
  • contraceptive pill (particularly if also a smoker)
  • on hormone replacement therapy
  • pregnancy
  • pelvic obstruction e.g. uterus/ ovary/ lymph nodes
  • trauma e.g. RTA
  • surgery e.g. pelvic, hip, knee
  • malignancy
  • pulmonary hypertension/ vasculitis
  • obesity
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10
Q

thrombophilia

A

condition in which the blood has an increased tendency to form clots

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11
Q

vasculitis

A

group of disorders that destroy blood vessels by inflammation. Affects both arteries and veins. Primarily caused by leukocyte migration and resultant damage

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12
Q

lymphanagitis (a type of vasculitis)

A

inflammation/ infection of the lymphatic channels

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13
Q

HPC

A
  • SOB
  • chest pain (pleuritic)
  • haemoptysis
  • leg pain/ swelling
  • collapse/ sudden death
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14
Q

clinical features of PE

A

tachycardia, tachypnoea, cyanosis, fever, low BP, crackles, rub, pleural effusion
arterial blood gases: PaO2 decrease, SaO2 decrease
Type 1 respiratory failure
CXR: normal early on before infarction, then basal atelectasis and consolidation, then pleural effusion

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15
Q

what do crackles sound like?

A

clicking, rattling, crackling noises that may be made by one or both lungs during inhalation. Crackles are caused by popping open of small airways and alveoli collapsed by fluid, exudate, or lack of aeriation during expiration

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16
Q

What does the ECG shoe in PE?

A

right heart strain pattern

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17
Q

what happens to the d-dimers in PE?

A

raised

18
Q

V/Q scan (isotope lung scan)?

A

this is sensitive for small peripheral emboli
there is perfusion defect before infarction
perfusion and ventilation matched defect after infarction

19
Q

what use is CT pulmonary angiogram in PE diagnosis?

A

CTPA images pulmonary artery filling defects - picking up clots in proximal vessels

20
Q

what use are leg and pelvic ultrasounds in PE diagnosis?

A

they can detect silent DVTs

21
Q

what use is echocardiogram in diagnosis of PE?

A

echocardiogram measures pulmonary artery pressure and RV size. Acute dilation of RV is in keeping with acute PE

22
Q

Investigations of underlying cause of PE (cancer, autoantibodies, thrombophilia screen)

A

if there is no obvious cause of PE, consider:

  • cancer: clinical exam, CXR, other scans
  • autoantibodies (SLE)
  • thrombophilia screen
23
Q

prevention of DVT

A

early post-op mobilisation, compression stockings, calf muscle exercises, subcutaneous low dose low molecular weight heparin (blood thinner) perioperatively
Noverl Oral Anticoagulant (NOAC) medication

24
Q

Novel Oral anticoagulant medication (NOAC)

A

Diabigatran - a direct thrombin inhibitor

Rivaroxaban/ Apixaban - direct inhibitor of activated factor Xa

25
Q

use of thrombolysis in the treatment of DVT/ PE?

A

thrombolysis - only for large and life threatening PE (low BP and sever hypoxaemia due to main pulmonary artery occlusion)

26
Q

over-anticoagulation

A

address underlying cause e.g drug interaction, CHF, liver disease
If bleeding: stop anticoagulant and reverse effect
Low MW Heparin has long half life
Warfarin has long half life
May need prothrombin complex concentrate or fresh frozen plasma
reverse warfarin with vitamin K1 (especially if chronic liver disease)
reverse heparin with protamine
no reversible agent available for NOACs

27
Q

use of LMWH in the treatment of DVT/ PE?

A

therapeutic dose of low molecular weight heparin - once daily injection
ALSO: start warfarin at the same time as heparin (must have combination)
OR instead: use oral thrombin inhibitor or factor X inhibitor on its own from the start - less hassle and in most cases just as effective as heparin/ warfarin
oral warfarin takes 3 days to antagonise
after 3-5 days stop heparin: when INR>2
or use NOACs without LMWH
continue warfarin for 3-6 months
monitor warfarin with INR-target range 2.5-3.5
(beware of interactions: alcohol, antibiotics, aspirin, grapefruit…)

28
Q

use of IVC filter in DVT/ PE treatment?

A

IVC filter to prevent embolization (however, this itself is a risk factor for clot)

29
Q

use of thrombo-embolectomy in DVT/ PE treatment?

A

thrombo-embolectomy - rarely indicated

this is surgical removal of the clot and is highly specialised

30
Q

low molecular weight heparin and warfarin both have short/ long half lives?

A

long

31
Q

what can reverse the effects of warfarin?

A

vitamin K1 (especially in chronic liver disease)

32
Q

what can reverse the effects of heparin?

A

protamine

33
Q

what can reverse the effects of NOACS (Novel Oral Anticoagulants)?

A

Nothing

34
Q

pulmonary circulation is normally a high flow system with high/ low pressure?

A

low

normal mean pulmonary arterial pressure (mPAP) is 12-20mmHg

35
Q

If someone has mPAP> 25mmHg, they have _____ ________

A

pulmonary hypertension

36
Q

causes of pulmonary venous hypertension

A

CAUSED BY LEFT HEART DISEASE:

  • LVSD (LV systolic dysfunction - LV ejection fraction of <40% on echocardiography
  • mitral regurgitation (abnormal reversal of blood flow from LV to LA, caused by disruption in any part of mitral valve apparatus)
  • aortic stenosis (narrowing of aortic valve, restricting blood flow through the valve. Heart then needs to contract harder to pump blood in the aorta)
  • cardiomyopathy e.g. alcohol, viral (diseases of the heart muscle - heart muscle becomes enlarged, thick, or rigid, or even replaced with scar tissue)
37
Q

causes of pulmonary arterial hypertension

A

CAUSED BY RIGHT HEART DISEASE:

  • hypoxic (COPD, pulmonary fibrosis, OSA (obstructive sleep apnoea))
  • multiple PE (CTEPH: chronic thromboembolic pulmonary hypertension - caused by blockages in blood vessels to the lungs due to scar tissue, which are a result of clots in body which were not cleared properly)
  • vasculitis (SLE, PAN (polyarteritis nodosa), systemic sclerosis)
  • drugs (appetite suppressants e.g. fenfluramine)
  • HIV
  • cardia left to right shunt (Atrial septal defect, ventricular septal defect)
  • primary pulmonary hypertension
38
Q

cor pulmonarle

A

this is an alteration in the structure and function of the right ventricle of the heart, caused by a primary disorder of the respiratory system. Pulmonary hypertension is often the common link between lung dysfunction and the heart in Cor pulmonale
there is fluid retention due to hypoxia (and possibly right heart failure)
e.g. cor pulmonale can be secondary to COPD

39
Q

clinical signs of pulmonary hypertension and right heart failure

A
  • central cyanosis if hypoxic
  • dependent oedema
  • raised JVP with V waves (due to secondary tricuspid regurg)
  • RV heave at left parasternal edge
  • murmur of tricuspid regurgitation
  • loud P2
  • enlarged liver (pulsatile)
40
Q

investigation of pulmonary hypertension

A

-ECG
-CXR
-SaO2 and ABGs
-pulmonary function including DLCO
-echocardiogram (to estimate RV systolic pressure)
-cardiac catheterisation (measures mPAP)
-D-dimers and V/Q scan is suspected PE
-CT pulmonary angiogram
cardiac MRI
-autoantibodies if vasculitis suspected

41
Q

primary pulmonary hypertension

A

diagnosis by exclusion of other secondary causes

  • progressive SOBOE and signs of R heart failure
  • poor prognosis (3 years) without treatment
  • treatment (prophylactic warfarin, O2 if hypoxic, pulmonary vasodilators (see slide), lung transplant)
42
Q

chronic thromboembolic pulmonary hypertension (CTEPH) treatment

A

Riociguat - a pulmonary arterial vasodilator
pulmonary endarterectomy - blood vessels of lungs are cleared of clots and scar tissue
balloon angioplasty - widening narrowed lumen
no other effective targeted pulmonary vasodilator therapy for secondary pulmonary hypertension e.g. COPD associated pulmonary hypertension

Year 1: Respiratory (25 decks)

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