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Semester 2 - CVS > Session 10 - Ischaemic Heart Disease and Chest Pain (1) > Flashcards

Session 10 - Ischaemic Heart Disease and Chest Pain (1) Flashcards

1
Q

Name three organs/systems other CVS which can cause chest pain

A

Lungs and pleura
GI system
Chest wall

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2
Q

What can be used to distinguish between different types of pain?

A

Character and type of pain, other special symptoms.

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3
Q

What conditions of lungs and pleura cause chest pain? (3)

A

Pneumonia
Pulmonary Embolism
Pneumothorax

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4
Q

What conditions of the GI system cause chest pain?

A

Oesophagus – Reflux
Peptic ulcer disease
Gall Bladder – Biliary colic, cholecystitis

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5
Q

What conditions of the chest wall cause chest pain?

A

Ribs – fractures, bone metastases
Muscles
Skin (herpes zoster)
Costo-chondral joints

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6
Q

What conditions of the CVS cause chest pain?

A

Myocardium – Angina, MI
Pericardium – Pericarditis
Aorta – Aortic dissection

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7
Q

What are the two types of risk factors for coronary atheroma?

A

Modifiable

Non-modifiable

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8
Q

Give three non-modifiable risk factors for coronary artheroma

A

Increasing Age
Male gender (females catch up after menopause)
Family history

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9
Q

Give seven modifiable risk factors for coronary atheroma

A 
Hyperlipidaemia
Smoking		            
Hypertension
Diabetes mellitus – Doubles IHD risk
Exercise
Obesity
Stress
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10
Q

What are the four main risk factors for coronary artheroma?

A

Hyperlipidaemia
Smoking
Hypertension
Diabetes mellitus (doubles IHD)

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11
Q

What type of pain can IHD cause?

A

Central, retrosternal or left sided

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12
Q

Describe the course of the pain from IHD

A

Pain my radiate to shoulder and arms, with left side more common that the right
- May radiate along the neck, jaw, epigastrium and back.

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13
Q

Describe the character of the pain from IHD

A

Crushing, occasionally described as burning epigastric pain (inferior MI)

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14
Q

How does pain from IHD vary?

A

In intensity, duration, onset and precipitation.

Aggravating and relieving factors and associated symptoms

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15
Q

How does pain from IHD get worse?

A

Stable angina –> Unstable angina –> MI

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16
Q

Describe the structure of atheromas in stable angina

A

Atheromatous plaques with a necrotic centre and fibrous cap

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17
Q

What is the effect of atheroma in IHD?

A

Occlude more and more of the lumen as they build up in coronary vessels. This leaves less space for passage of blood and ischaemia in myocardium

18
Q

What area is most at risk of ischaemia?

A

Subendocardial surface, myocardial wall pressure greatest

19
Q

How does coronary arteries increase O2 uptake?

A

Increase flow, via vasodilator metabolites (adenosine, K+, H+)
Collateral circulation

O2 uptake already maximum!

20
Q

What increases myocardial demand?

A

Heart rate
Wall tension - preload, afterload
Contractility

21
Q

What does myocardial O2 supply depend on?

A

Coronary blood flow

  • perfusion pressure
  • coronary artery resistance

O2 carrying capacity

22
Q

What is the usual presentation of a STEMI?

A
  • Chest pain not relieved by GTN
  • N&V
  • May be painless +/- atypical
  • Acute pulmonary oedema, SOB, syncope, cardiogenic shock
23
Q

What are four ECG findings you will see in STEMI?

A
  • ST elevation (see above)
  • New LBBB
  • +/- T wave inersion
  • Pathological Q waves
24
Q

Give 4 steps in initial management of STEMI

A
  • Airway, Breathing, Circulation
  • IV access
  • 12-lead ECG
  • MONA
25
Q

What is MONA?

A 
o	Morphine (2.5 – 10mg + antiemetic)
o	Oxygen
o	Nitrates (GTN spray 2 puffs sublingually) 
o	Aspirin (300mg chewed)
26
Q

What are three investigations you should do in STEMI?

A
  • Bloods
    o FBC, U&E, LFTs, glucose, lipids, CK, Troponin I
  • Portable CXR
  • ECG
27
Q

What are two main treatments in STEMI?

A

Thrombolysis or PCI

28
Q

When is PCI used?

A

 PCI is the gold standard for acute coronary syndrome and should only be used if primary PCI programme available within 120 minutes of first medical contact
 Indications are the same as thrombolysis

29
Q

What are the ECG changes which indicate thrombolysis or PCI?

A
  • ST elevation >1mm in 2+consecutive leads
  • ST elevation >2mm in 2+consecutive leads
  • New onset LBBB
30
Q

Give four contraindication for thrombolysis

A

• Haemorrhagic sroke or ischaemic stroke

31
Q

What do you give along with PCI or thrombolysis?

A

B blocker
ACE inhibitor
Clopidogrel

32
Q

What complications can you develop as a result of a STEMI?

A 
SPREAD
S – Sudden Death
P – Pump failure/pericarditis
R – Rupture papillary muscle or septum
E – Embolism
A – Aneurysm/arrhytmias 
D – Dresslers syndrome ( pleuritic chest pain, pericarditis and low grade fever which develops post-MI and is thought to be immune mediated.
33
Q

What do you prescribe on discharge post-MI

A

Aspirin, clopidogrel, ACE inhibitor, B blocker, Statin, Risk factor modification, 1 month off work.

34
Q

What are the two main ECG changes in an NSTEMI?

A

1) T wave inversion

2) ST depression

35
Q

How do you differentiate between STEMI and NSTEMI?

A

NSTEMI will have a positive troponin I and unstable angina will be negative.

36
Q

What are the management steps for an NSTEMI/

A

1) Analgesia
a. Morphine
2) Anti-ischaemic
a. Nitrates
b. ACE inhibitor
c. B blockers
d. Calcium channel antagonists
e. Statins
3) Anti-platelets
a. Aspirin
b. Clopidogrel
4) Anti-thrombotic
a. LMWH

37
Q

When is PCI considered in an NSTEMI?

A

PCI can be considered if Troponin is persistently raised, the angina persists despite best medical therapy or there are features of

  • Heart failure
  • Poor LV function
  • Haemodynamic instability
  • PCI
38
Q

What is the SA Node suppliedby?

39
Q

What is the AV node supplied by?

40
Q

What is the bundle of HIS supplied by?

41
Q

WHAT is the RBBB supplied by?

A

Proximal portion by LAD

Distal Portion by RCA

42
Q

What is the LBBB suppied by?

A

LAD

LAD and PDA

Semester 2 - CVS (15 decks)

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