Respiratory VI (P. Hypertension; PE Flashcards

1
Q
A
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2
Q

Define what is meant by pulmonary hypertension [1]

A

Pulmonary hypertension is defined as a mean pulmonary arterial pressure of more than 25  mmHg at rest when assessed with right heart catheterization

Pulmonary hypertension is an umbrella term for many different diseases which lead to increased pressure in the pulmonary arteries

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3
Q

Describe the general pathophysiology of pulmonary hypertension

A

In general, pulmonary hypertension occurs when the pulmonary arteries become narrowed due to hypoxic pulmonary vasoconstriction or thrombosis, thickened or damaged causing increased pressure in the vessels.

This causes strain on the right side of the heart. And can causes right ventricular hypertrophy

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4
Q

The causes of pulmonary hypertension can be classified into five groups.

What are they? [5]

A

Group 1 Idiopathic pulmonary hypertension or connective tissue disease (e.g., systemic lupus erythematous)

Group 2 – Left heart failure, usually due to myocardial infarction or systemic hypertension

Group 3 – Chronic lung disease (e.g., COPD or pulmonary fibrosis)

Group 4 – Pulmonary vascular disease (e.g., pulmonary embolism)

Group 5 – Miscellaneous causes such as sarcoidosis, glycogen storage disease and haematological disorder

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5
Q

What ECG changes would you expect to see of someone with pulmonary hypertension? [4]

A

All indicate right sided heart strain:

P pulmonale: peaked P waves

Right ventricular hypertrophy (tall R waves in V1 and V2 and deep S waves in V5 and V6)

Right axis deviation

Right bundle branch block

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6
Q

What blood test might indicate pulmonary hypertension? [1]

A

Raised NT‑proBNP blood test result indicates right ventricular failure

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7
Q

What imaging would you use to investigate pulmonary artery pressure? [1]

A

Echocardiogram can be used to estimate the pulmonary artery pressure

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8
Q

Name and state the drug classes used to treat idiopathic pulmonary hypertension [4]

A

Idiopathic pulmonary hypertension may be treated with:

Calcium channel blockers
Intravenous prostaglandins e.g., epoprostenol
Endothelin receptor antagonists e.g., macitentan
Phosphodiesterase-5 inhibitors e.g., sildenafil

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9
Q

Which inherited disorders increase the risk of PE? [5]

A

Factor V Leiden mutation:
- Normally used for blood clotting: helps enzyme reaction to form fibrin in blood clot
- Once the coagulation process is turned on in people with factor V Leiden, it turns off more slowly than in people with normal factor V

Antithrombin deficiency
- Normally anti-thrombin acts as the inhibitory component to thrombin formation

Prothrombin deficiency

Protein C & S deficiencies

Antiphospholiipid syndrome

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10
Q

Which type of hormone therapy increases the risk of PE? [1]

A

Hormone therapy with oestrogen (e.g., combined oral contraceptive pill or hormone replacement therapy)

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11
Q

What is important to note about symptoms of dysopnea in PE? [1]

A

Symptoms of PE usually come on acutely rather than gradually.

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12
Q

Explain what is meant by the PERC rule

A

The pulmonary embolism rule-out criteria (PERC) are recommended by the NICE guidelines (2020) when the clinician estimates less than a 15% probability of a pulmonary embolism to decide whether further investigations for a PE are needed. If all the criteria are met, further investigations for a PE are not required.

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13
Q

Describe the investigations you would conduct for a ptx suspected with PE

A

computed tomographic pulmonary angiography (CTPA)
- preferred investigation for definitive confirmation of PE

echocardiography:
- presence of any signs of right ventricular (RV) dysfunction is sufficiently suggestive of PE to confirm the diagnosis and justify urgent reperfusion treatment
- used if CTPA not immediately available / contraindicated

D-dimer:
- Elevated
- Used if Wells Score < 4.

ECG:
- An ECG is not diagnostic of PE but can be useful to support the diagnosis of PE or rule out other causes.
- S1Q3T3 pattern

urea and electrolytes:
- guides CTPA use

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14
Q

Why might a CTPA be contraindicated for PE investigation? [2]

A

The contrast dye used in CTPA for the evaluation of PE may cause nephropathy.

Radiation from CT is considered to be a risk factor for certain cancers.

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15
Q

Explain a specific sign seen on echocardiogram that would indicate a PE [1]

A

60/60 sign :a combination of
- pulmonary acceleration time (PAT) less than 60 milliseconds
and
- tricuspid regurgitation (TR) jet gradient of less than 60 mmHg

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16
Q

What is the McConnell sign? [1]
What does it indicate? [1]

A

reduced contractility of the RV free wall compared with the RV apex

indicates PE

Typically this looks as if the apex of the RV is a trampoline bouncing up and down while the rest of the RV remains still

Ty

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17
Q

What ABG results would indicate PE? [1]

Explain your answer [1]

A

TOM TIP: Patients with a pulmonary embolism often have respiratory alkalosis on an ABG.

Hypoxia causes a raised respiratory rate.

Breathing fast means they “blow off” extra CO2.

A low CO2 means the blood becomes alkalotic.

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18
Q

What are the two causes of respiratory alkolosis in an ABG? [2]

How do you differentiate between them? [2]

A

PE
and
Hyperventilation syndrome.

Patients with PE will have a low pO2

Patients with hyperventilation syndrome will have a high pO2.

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19
Q

A V/Q scan is of limited use in patients with which co-morbidities? [3]

A

A V/Q scan is of limited use in patients with:
* significant underlying lung disease
* left ventricular failure
* congestive cardiac failure

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20
Q

What is the leading cause of death for patients with massive PE? [1]

A

The leading cause of death in patients with high-risk (massive) PE is acute right ventricular (RV) failure with resulting hypotension.[65]

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21
Q

Describe the treatment algorithm for patients who have PE confirmed and are haemodynamically unstable [4]

A

First line:
- heparin: 10,000 units intravenously as a loading dose initially, followed by 18 units/kg/hour intravenous infusion

PLUS: thrombolysis: (involves injecting a fibrinolytic (breaks down fibrin) medication that rapidly dissolves clot)
- Alteplase or
- Streptokinase or
- Urokinase

PLUS:
- anticoagulation with unfractionated heparin (UFH) for several hours after the end of thrombolysis before: switching to apixaban or rivaroxaban; low molecular weight heparin (LMWH) is an alternative if these are unsuitable - this is preferable

CONSIDER: vasoactive drug if SBP < 90 mmHG after thrombolysis
- noradrenaline or
- dobutamine

-

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22
Q

Describe the treatment algorithm for patients who have PE confirmed and are haemodynamically stable [4]

A

Stable, no renal impairment or co-morbidities: offer apixaban/rivaroxaban. If not-suitable, LWMH for 5 days then offer edoxaban/warfarin*

First line: anticoagulation:
- apixaban or
- rivaroxaban

OR

  • UFH / LMWH / Fondaparinux lead AND warfarin
  • Target INR 2-3 then stop heparin
23
Q

Describe the long term managment of PE for:

  • most people [4]
  • patients suffering from antiphospholipid syndrome [1]
  • pregnant people [1]
A

DOACs: most people
- apixaban
- rivaroxaban
- edoxaban
- dabigatran

Warfarin: for antiphospholipid syndrome patients

LMWH for pregnant people

24
Q

How long would you continue treatment for patients:
- with a reversible cause [1]
- unprovoked PE [1]
- with cancer p1[

A

Treatment time:
* 3 months with a reversible cause (then review)

  • Beyond 3 months with unprovoked PE, recurrent VTE or an irreversible underlying cause (e.g., thrombophilia)
  • 3-6 months in active cancer (then review)
25
Q

All patients of PE should have anticoagulation for at least [] months

A

All patients of PE should have anticoagulation for at least 3 months

26
Q

State 4 acute complications of PE

A

Right ventricular failure:

Cardiogenic shock:

Arrhythmias

Respiratory failure

27
Q

Describe the clinical consequence of PE causing right ventricular failure [2]

A

Large or multiple emboli can cause acute right ventricular (RV) dilata hypertrophy strain, leading to RV dysfunction and failure.

This may result in systemic hypotension, shock, and even sudden cardiac death.

28
Q

Describe how massive PE causes hemodyanmic collapse [7]

A
29
Q

Describe how PE can cause cardiogenic shock [2]

A

Cardiogenic shock
- Severe PE may lead to decreased cardiac output, causing systemic hypotension, impaired end-organ perfusion, and ultimately cardiogenic shock.

30
Q

Which arrythmias can PE lead to [3]

A

Arrhythmias: PE can provoke supraventricular and ventricular arrhythmias, such as:
- atrial fibrillation
- ventricular tachycardia
- ventricular fibrillation

which can further compromise hemodynamics.

31
Q

Describe three subacute complications of PE

A

Infarction and lung necrosis
- PE can cause ischemic injury to the lung parenchyma, leading to pulmonary infarction, haemorrhage, or lung necrosis.

Pleural effusion:
- Inflammatory processes triggered by PE may cause pleural effusion, which may be exudative or hemorrhagic.

Pneumothorax:
- Rarely, PE-induced lung infarction may lead to pneumothorax due to the rupture of a bulla or necrotic lung tissue

32
Q

Describe a chronic complication of PE [1]

A

Chronic thromboembolic pulmonary hypertension (CTEPH):

  • CTEPH is a rare but serious complication characterized by unresolved thrombotic occlusions in the pulmonary arterial system, turning into fibrotic tissue leading to increased pulmonary vascular resistance, pulmonary hypertension, and eventually right heart failure.
33
Q

What is the most appropriate next step in the investigation of suspected pulmonary embolism if D-dimer negative?

A

Stop anticoagulation and consider an alternative diagnosis

34
Q

What is the most appropriate next step in the investigation of suspected pulmonary embolism if medium-high (> 15%) pre-test probability of PE? [1]

A

A 2-level PE Wells score should be performed:

Clinical probability simplified scores
PE likely - more than 4 points
PE unlikely - 4 points or less

35
Q

What is the most appropriate next step in the investigation of suspected pulmonary embolism if CTPA negative? [1]

A

Consider the possibility of DVT and arrange proximal leg vein ultrasound if suspected

36
Q

PE would cause change to axis deviation? [1]

A

Right axis deviation

37
Q

Describe if lung tissue becomes infarcted during a PE

A

May infarct if not perfused by PE. But oxygen continues to be supplied by the bronchial circulation and airways

38
Q

State 3 respiratory and 4 CVS differential diagnoses for PE

A

Respiratory:
- Pneumothorax
- Pneumonia
- Acute exaerbation of resp disease

CV:
- MI
- Pericarditis
- Aortic dissection
- Cardiac tampondade

39
Q

What ECG findings would a PE cause? [6]

A

Sinus tachycardia
New onset AF
Right axis deviation
RBBB
T wave inversion
P pulmonale
S1Q3T3

40
Q

Describe the S1Q3T3 ECG changes in PE [3]

A

deep S wave in lead I
Q wave in III
inverted T wave in III (20%)

41
Q

Which drug is contraindicated in pregnancy, but safe with breastfeeding? [1]

A

Warfarin

42
Q

State 4 invasive procedures used to treat PE if needed

A
  • Embolectomy
  • Mechanical fragmentation with R heart angiography
  • Pulmonary thombro-endarterectomy
  • IVC filter
43
Q

Which of the following is used to treat chronic PEs unresolved after 3 months

  • Embolectomy
  • Mechanical fragmentation with R heart angiography
  • Pulmonary thombro-endarterectomy
  • IVC filter
A

Pulmonary thombro-endarterectomy (PTE)

44
Q

Name a risk [1] and benefits [2] of using unfractionated heparin in treating PE [4]

A

Risks:
- Heparin induced thrombocytopenia (HIT)

Benefits:
- Rapid reversal possible
- More rapid anticoagulation

45
Q

What is an IVC filter? [1]

When is it used? [3]

A

Traps fragmented thrombemboli on the way to pulmonary circulation

Used if:
- patient is contraindicated to anticoagulation in proximal PE/DVT
- Recurrent VTE despite anticoagulation tx
- Only temporary

46
Q

What level of thrombophilia should make sure that you screen a patient? [2]

A

< 50 & recurrent unprovoked VTE or strong FHx

47
Q

What ECHO findings might you find in acute PE? [6]

A

 Direct visualization of
thromboemboli in the RT heart
and PA.
 RV dilatation.
 RV dysfunction.
 Normal or hyper dynamic LV.
 Septal flattening.
 PA dilatation

48
Q

Describe the different bridging times for LMWH if using:
- Warfarin
- Dabigatran or edoxaban
- Rivaroxaban or apixaban

A

Warfarin:
- Start LMWH and initiate warfarin at same time then after 5-10 days change to just warfarin

Dabigatran or edoxaban
- 5 days of LMWH with both then switch to doac same day

Rivaroxaban or apixaban
- No bridge - only use them

49
Q
A

a prolonged PR interval

50
Q
A

Hepatotoxicity

51
Q
A

Optic neuritis

52
Q
A

Gout

53
Q
A

Type IV

54
Q

Describe the diagnostic pathway for PEs

A