deck_862050 Flashcards

(42 cards)

1
Q

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

A

Lungs and pleura GI systemChest 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

PneumoniaPulmonary EmbolismPneumothorax

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4
Q

What conditions of the GI system cause chest pain?

A

Oesophagus – RefluxPeptic ulcer diseaseGall Bladder – Biliary colic, cholecystitis

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5
Q

What conditions of the chest wall cause chest pain?

A

Ribs – fractures, bone metastasesMusclesSkin (herpes zoster) Costo-chondral joints

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6
Q

What conditions of the CVS cause chest pain?

A

Myocardium – Angina, MIPericardium – PericarditisAorta – Aortic dissection

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7
Q

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

A

ModifiableNon-modifiable

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8
Q

Give three non-modifiable risk factors for coronary artheroma

A

Increasing AgeMale gender (females catch up after menopause)Family history

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9
Q

Give seven modifiable risk factors for coronary atheroma

A

HyperlipidaemiaSmoking HypertensionDiabetes mellitus – Doubles IHD riskExerciseObesityStress

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10
Q

What are the four main risk factors for coronary artheroma?

A

HyperlipidaemiaSmokingHypertensionDiabetes 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 circulationO2 uptake already maximum!

20
Q

What increases myocardial demand?

A

Heart rateWall tension - preload, afterloadContractility

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
What is MONA?
o Morphine (2.5 – 10mg + antiemetic)o Oxygeno Nitrates (GTN spray 2 puffs sublingually) o Aspirin (300mg chewed)
26
What are three investigations you should do in STEMI?
- Bloods o FBC, U&E, LFTs, glucose, lipids, CK, Troponin I - Portable CXR - ECG
27
What are two main treatments in STEMI?
Thrombolysis or PCI
28
When is PCI used?
 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
What are the ECG changes which indicate thrombolysis or PCI?
• ST elevation >1mm in 2+consecutive leads• ST elevation >2mm in 2+consecutive leads• New onset LBBB
30
Give four contraindication for thrombolysis
• Haemorrhagic sroke or ischaemic stroke
31
What do you give along with PCI or thrombolysis?
B blockerACE inhibitor Clopidogrel
32
What complications can you develop as a result of a STEMI?
SPREADS – Sudden DeathP – Pump failure/pericarditisR – Rupture papillary muscle or septumE – EmbolismA – 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
What do you prescribe on discharge post-MI
Aspirin, clopidogrel, ACE inhibitor, B blocker, Statin, Risk factor modification, 1 month off work.
34
What are the two main ECG changes in an NSTEMI?
1) T wave inversion 2) ST depression
35
How do you differentiate between STEMI and NSTEMI?
NSTEMI will have a positive troponin I and unstable angina will be negative.
36
What are the management steps for an NSTEMI/
1) Analgesia a. Morphine2) Anti-ischaemica. Nitrates b. ACE inhibitor c. B blockersd. Calcium channel antagonistse. Statins3) Anti-platelets a. Aspirinb. Clopidogrel 4) Anti-thrombotic a. LMWH
37
When is PCI considered in an NSTEMI?
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
What is the SA Node suppliedby?
RCA
39
What is the AV node supplied by?
RCA
40
What is the bundle of HIS supplied by?
LAD
41
WHAT is the RBBB supplied by?
Proximal portion by LADDistal Portion by RCA
42
What is the LBBB suppied by?
LADLAD and PDA