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CR > ACS/MI > Flashcards

ACS/MI Flashcards

1
Q

The heart is supplied by the cardiac plexus of nerves which lies anterior to the bifurcation of the trachea and posterior to the arch of the aorta.
Describe the parasympathetic innervation.

A

Slows heart rate. Pathway via medullary reticular formation (cardioinhibitory centre) via vagus nerve to SA and AV nodes.

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2
Q

Describe the sympathetic innervation.

A

From sympathetic trunk – increases heart rate and force of contraction.
Pathway via cardioacceleratory centre in medullary reticular formation.
Pre-ganglionic sympathetic neurons in thoracic spinal cord and post-ganglionic sympathetic neurons to SA and AV node and to coronary VSM.

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3
Q

Describe the visceral general afferents.

A

Fibres extend from the plexus to the coronary vasculature and to components of the conducting system of the heart (especially SA node).

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4
Q

Lateral leads of ECG

A

I, avL, V5, V6

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5
Q

Anterior leads of ECG

A

V3, V4

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6
Q

Septal leads of ECG

A

V1, V2

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7
Q

Inferior leads of ECG

A

II, III, aVF

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8
Q

Leads II, III, aVF have ST elevation. Where is the infarct?

A

RCA or LCx

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9
Q

Leads V1-V4 have ST elevation. Where is the infarct?

A

LAD

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10
Q

Leads I, avL, V5, V6 have ST elevation. Where is the infarct?

A

LCx or diagonal branch of LAD

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11
Q

ECG changes in STEMI

A 
In STEMI:
•	Persistent (≥20 minutes) ECG features in ≥2 contiguous leads
•	ST elevation
-	≥2mm in leads V2-3
-	≥1mm in other leads 
•	New left bundle branch block
•	Peaked T waves 
•	Gradual loss of R wave
•	Development of pathological Q wave and T wave inversion
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12
Q

ECG changes in NSTEMI

A

May show ST depression or transient ST segment elevation

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13
Q

Explain changes in cardiac enzymes + timings etc.

A

Troponin begins to rise within 4-6 hours and peaks at 24 hours, continuing to be elevated for 7-10 days.
CK begins to rise within 4-8 hours and peaks at 16-24 hours, but returns to normal within 2-3 days so is useful to look for reinfarcts.

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14
Q

Complications of MI

A 
Cardiac arrest + death
Cardiogenic shock
Tachyarrhythmias (e.g. VT or VF)
Bradyarrhythmias (e.g. AV block)
Left ventricular free wall rupture (within 1-2 weeks)
VSD (within first week)
Pericarditis e.g. in first 48 hours, or Dressler's syndrome (2-6 weeks after).
Acute OR chronic heart failure
Left ventricular aneurysm
Acute mitral regurgitation
Stroke
Depression + anxiety
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15
Q

How might complications differ between anterior and inferior MI?

A

AV block more common with inferior infarcts

Acute MR more common with infero-posterior infarcts

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16
Q

Cardiogenic shock pathophys/explanation

A

Ventricular myocardium damaged –> ejection fraction decreases –> cardiogenic shock.

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17
Q

Chronic heart failure signs + symptoms

A 
dyspnoea
cough + pink/frothy sputum
orthopnoea + PND
wheeze ('cardiac wheeze')
weight loss 
bibasal crackles 
Right sided = raised JVP ankle oedema, hepatomegaly
18
Q

Pericarditis signs + symptoms

A

Pain, worse on lying flat, pericardial rub, pericardial effusion on echo

19
Q

Dressler’s - what is it? Signs and symptoms? Treatment?

A

autoimmune reaction against antigenic proteins formed as the myocardium recovers
Fever, pleuritic pain, pericardial effusion, raised ESR
NSAIDs

20
Q

Left ventricular aneurysm pathophys, features

A

Ischaemic damage –> weakened myocardium –> aneurysm formation

Persistent ST elevation and left ventricular failure

21
Q

Left ventricular free wall rupture features

A

acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds)

22
Q

Acute mitral regurgitation - cause? Features.

A

Due to ischaemia or rupture of the papillary muscle

Acute hypotension and pulmonary oedema may occur. An early-to-mid systolic murmur is typically heard.

23
Q

Ventricular septal defect features

A

acute heart failure associated with a pan-systolic murmur

- echo is diagnostic

24
Q

Most common cause of death following MI?

A

ventricular fibrillation

25
Q

Non-pharmacological secondary prevention for MI

A 
Cardio rehab
Smoking cessation
Cardioprotective diet - minimising refined sugars, low salt intake, wholegrain, 4-5 portions a week of unsalted nuts and seeds, eating 2 portions of fish per week, 5 fruit/veg a day, less animal-based fats, less fat/sat fat
Exercise 
Weight loss
Keep alcohol to 14 units a week max
26
Q

Medications after an MI

A 
ACE inhibitor
Dual antiplatelet therapy (75mg aspirin plus clopidogrel or ticagrelor)
Beta-blocker
Statin
\+ annual flu jab
27
Q

Driving post-MI

A

Does not need to inform the DVLA (unless bus, coach, lorry driver)

28
Q

Sexual intercourse post-MI

A

4 weeks

29
Q

Signs and symptoms of acute MI

A
  • chest pain, typically central/left-sided
  • may radiate to the jaw or the left arm
  • often described as ‘heavy’ or constricting
  • dyspnoea
  • sweating
  • nausea or vomiting
  • obs often normal, may have tachycardia
  • pale and clammy
30
Q

Criteria for diagnosis of MI

A 
Rise and/or fall of troponin with at least one value >99th percentile of the URL, plus at least one of the following: - Cardiac chest pain
ECG changes (new ST-T change or new LBBB)
31
Q

Emergency investigations to confirm diagnosis

A

ECG

Tropinin I and T

32
Q

STEMI management

A 
Morphine
Only give oxygen if sats <94%
Nitrates (GTN)
Aspirin 300mg
Ticagrelor (180mg) or prasugrel (60mg)

Primary percutaneous coronary intervention (PCI)
Thrombolysis if no access to PCI

In diabetes, keep glucose below 11 with dose-adjusted insulin infusion

33
Q

NSTEMI management

A 
Morphine
Oxygen if sats <94%
Nitrates
Aspirin 300mg
Ticagrelor or prasugrel 
Fondaparinux or unfractionated heparin 
Coronary angiography
34
Q

Diamorphine - mechanism, side effects

A

Mechanism = activation of the opioid receptors in the CNS that reduces neuronal excitability and pain transmission

Major side effects = respiratory depression, euphoria, nausea, vomiting, constipation, dependence

35
Q

GTN - mechanism, side effects

A

Mechanism of action - cause the release of nitric oxide in smooth muscle, increasing cGMP, which in turn leads to a fall in intracellular calcium levels
Dilate the coronary arteries and also reduce venous return which in turn reduces left ventricular work, reducing myocardial oxygen demand.

Side-effects
hypotension
tachycardia
headaches
flushing
36
Q

GP IIb/IIIa inhibitors - mechanism, side effects

A

Mechanism = prevents platelet aggregation by binding irreversibly to ADP receptors (P2Y12 subtype) on the surface of platelets

Role in therapy = 2ndary prevention, for 12 months

Major side effects = bleeding, dyspepsia, abdo pain, diarrhoea, thrombocytopenia

37
Q

Aspirin - mechanism, side effects

A

Mechanism = irreversibly inhibits COX to reduce production of thromboxane, reducing platelet aggregation and risk of arterial occlusion. Effects last for lifetime of platelets.

Role in therapy = life-long for 2ndary prevention

Major side effects = GI irritation and ulceration and haemorrhage, bronchospasm, tinnitus

38
Q

Mechanism of thrombolysis and examples of agents

A

Thrombolytic drugs activate plasminogen to form plasmin. This in turn degrades fibrin and help breaks up thrombi.

Examples
alteplase, tenecteplase, streptokinase

39
Q

Contraindications to thrombolysis

A 
active internal bleeding
recent haemorrhage, trauma or surgery
coagulation and bleeding disorders
intracranial neoplasm
stroke < 3 months
aortic dissection
recent head injury
pregnancy
severe hypertension
40
Q

Side-effects of thrombolysis

A

haemorrhage
hypotension - more common with streptokinase
allergic reactions may occur with streptokinase - can get anti-streptokinase antibodies if previous treatment

CR (19 decks)

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