CBL 5: A Patient with Breathlessness Flashcards

1
Q

What are the differential diagnoses you may consider based on the given
history alone?

A

Pneumonia
Hypertension
Pleuritis
ACS

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2
Q

How does a PE present?

A

Haemoptysis
Dyspnoea — this is the most common feature and is present in 50% of people with PE
Pleuritic chest pain — present in 39% of people with PE; Pain is normally localised to one side.
Cough — present in approximately 23% of people with PE.
Syncope or pre-syncope
Tachypnoea — present in 21-39% of people with PE.
Features of deep vein thrombosis (DVT)
Retrosternal chest pain (due to right ventricular ischaemia).

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3
Q

Describe the heart sound often occurs in PE [1]

A

Gallop rhythm, a wide split-second heart sound, tricuspid regurgitant murmur.

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4
Q

How does ACS present differently in females? [1]

A

Present atypically:
- epigastric or back pain or pain that is described as burning, stabbing, or characteristic of indigestion

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5
Q

Which populations present atypically with ACS? [2]

A

Women
Diabetes patients

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6
Q

Q4. Identify the terms you would like to learn about and to discuss.
Q5. What is your interpretation of the given signs?
Q6. What are the main priorities of management now?

A

ABCDE
A:
- Given she’s talking, her airways are fine

B:
- She has high resp. rate
- Give 15L oxygen
- Examine the chest for breath sounds: see if equal chest expansion, percuss and listen to breath sounds

C:
- PC: Tachycardia, central cyanosis, hypotensive
- Give 500ml 0.9% NaCl STAT (less than 15mins)
- (Stop amlodopine anti-hypertensives for acute attack)

D:
- Leg swollen - check for pitting oedema
- Check GCS
- Check blood glucose (i.e. for DKA - probably not for this case, but need to consider)
- Temperature

E
- Leg swollen, squeeze calf - see it patient complains [? why]
- Check pulses

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7
Q
A
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8
Q

What type of shock is the patient potentially in?

A

Obstructive shock

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9
Q

This patient is haemodynamically unstable. What does this mean? [1]

A

SBP < 90 mmHg

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10
Q

Q8. Which specific investigations are indicated and useful?

A

CXR:
- Want to exclude pneumothorax and other pathologies

CTPA

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11
Q

What is the management plan if you suspect a PE but the Wells Score < 4? [2]

A

Offer a D-dimer test with the result available within 4 hours

If the D-dimer test is positive:
arrange admission to hospital for an immediate CTPA and, where necessary, other investigations

If the D-dimer test is negative
- Stop interim therapeutic anticoagulation (if appropriate).
- Advise the person that it is not likely that they have a PE, but discuss the signs and symptoms, and when they should seek further medical help.
- Consider an alternative diagnosis.

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12
Q

Q7. What specific medication(s) you may administer before the investigations
being done?

A

Administer:
- IV Alteplase: anti-fibrinolytic. Preferred because shes haemodynamically unstable

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13
Q

Name 4 other pathologies that can cause raised D Dimer? [5]

A

Pneumonia
Malignancy
Heart failure
Surgery
Pregnancy

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14
Q

What do you do if want a CTPA because you suspect a PE, but it takes ages to occur? [1]

A

Start treatment

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15
Q

There are three imaging options for establishing a diagnosis of a pulmonary embolism [3]

A

There are three imaging options for establishing a diagnosis of a pulmonary embolism:

CT pulmonary angiogram (the usual first-line)

Ventilation-perfusion single photon emission computed tomography (V/Q SPECT) scan:
- Ventilation-perfusion (VQ) scan involves using radioactive isotopes and a gamma camera to compare ventilation with the perfusion of the lungs.
- First, the isotopes are inhaled to fill the lungs, and a picture is taken to demonstrate ventilation
- Next, a contrast containing isotopes is injected, and a picture is taken to illustrate perfusion
- The two images are compared.
- With a pulmonary embolism, there will be a deficit in perfusion as the thrombus blocks blood flow to the lung tissue. The lung tissue will be ventilated but not perfused

Planar ventilation–perfusion (VQ) scan

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16
Q

How long does a DOAC take to work? [1]

A

Few days

17
Q

How long does warfarin take to work? [1]

A

5 days

18
Q

Which differential diagnoses are you trying to rule out on CXR with PE? [3]

A

Pneumothorax
Pleural effusions
Pneumonia

19
Q
A

Sinus tachycardia

20
Q

What is the rate in this ECG? [1]
Why is this calculation important? [1]

A

300/2.5 = 120

Because sinus: rules out afib

21
Q

Why do you get sinus tachycardia in PE?

A
22
Q

What ECGs indicate a patient is suffering from PE? [2]

A

Sinus tachycardia is a very common finding in PE

S1: deep S waves in S1
Q3: deep Q waves in lead 3
T3: T wave inversion in lead 3

23
Q

How do you acutely treat PE in a patient who is suspected to be suffering from PE and is haemodynamically stable? [3]

A

Acutely:
- 15 L oxygen
- Consider 500ml saline over 15-30mins (STAT) if SBP < 90 and JVP is elevated
- apixaban or rivaroxaban (DOAC)
- LMWH is alternative

24
Q

How do you acutely treat PE in a patient who is confirmed (on echocardiography or CTPA); haemodynamically unstable? [5]

A

Acutely:
- Thrombolysis: alteplase; streptokinase; urokinase
- Start on heparin
- apixaban or rivaroxaban
- 15 L oxygen
- Consider: noradrenaline or dobutamine: as a vasoactive drug if SBP remains < 90
- Consider: surgical embolectomy/percutaneous catheter-directed treatment if thrombolysis fails

25
Q

How do you long term treat PE? [3]

A

Give apixaban, rivaroxaban, edoxaban and dabigatran for 3 months

26
Q

Which patient populations would you give LMWH instead of a DOAC in a suspected PE? [1]

A

Use a weight-adjusted dose of LMWH in women who are (or may be) pregnant.

Active cancer patients

27
Q

Which groups of patients would you have longer (3-6 months) DOAC treatment for that 3months post PE? [1]

A

Active cancer: give 6 months of DOAC

28
Q

What drug choice is used for long term treatment of PE in pregnant population [1] and how long for? [1]

A

In pregnant patients, continue LMWH for the remainder of the pregnancy and for at least 6 weeks postnatally and until at least 3 months of treatment has been given in total

29
Q

WQ16. What is the underlying pathophysiology of this condition?

A

Virchow’s triad:

1.Vessel wall damage:
- endothelial cell damage promotes thrombus formation, usually at the venous valves
- Damage to the vessel wall can occur after a number of insults including trauma, previous DVT, surgery, venous harvest, and central venous catheterisation

  1. Venous stasis:
    - poor blood flow and stasis promote the formation of thrombi.
    - Venous stasis and congestion result in valvular damage, further promoting thrombus formation. Increased venous stasis
    s associated with age >40 years, immobility, general anaesthesia, paralysis, spinal cord injury, myocardial infarction, prior stroke, varicose veins, advanced congestive heart failure, and advanced COPD.
  2. Hypercoagulability:
    - Causes include cancer, high-oestrogen states (oral contraceptives, hormone replacement, obesity,
    pregnancy), inflammatory bowel disease, nephrotic syndrome, sepsis, blood transfusion, and inherited
    thrombophilia
    (factor V Leiden mutation, prothrombin gene mutation, protein C and S deficiency, antithrombin deficiency, and antiphospholipid antibody syndrome).
30
Q

Which medications increase the liklihood of PE?

A

Contraceptive pills
Hormone replacement therapy

31
Q

Why does the combined pill increase likilihood of blood clots? [1]

A

Increased oestrogen causes hypercoagulability

32
Q

Which patient populations are more at risk of PE? [5]

A

Suffer from DVT
Recent surgery
Significant immobility
Pregnant women
Active cancer
Recent MI
Antiphospholipid antibody syndrome
Recent trauma

33
Q

The leading cause of death in patients with high-risk (massive) PE is acute [1]

A

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

34
Q

Explain what ABG would present like for a PE patient? [3]

A

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.

35
Q

Name differential diagnosis to PE that would cause respiratory alkalosis [1]

How would you distinguish between the two? [1]

A

The other main cause of respiratory alkalosis is hyperventilation syndrome

  • Patients with PE will have a low pO2
  • Patients with hyperventilation syndrome will have a high pO2.
36
Q

Why does BP fall in PE ? [1]

A

Causes obstructive shock

37
Q

What is the MoA of warfarin? [1]

What is the INR targer for warfarin when treating DVTs and PEs? [1]

A

Warfarin is a vitamin K antagonist.

The target INR for warfarin is between 2 and 3 when treating DVTs and PEs.

38
Q

What pathology would contraindicate anti-embolic compression stockings for PE / VTE [1]

A

Anti-embolic compression stockings are also used unless contraindicated (e.g., peripheral arterial disease).

39
Q

Why would CTPA be contraindicated when investigating PE? [1]

A

Kidney damage; contrast toxicity