- abnormal cardiac rhythms - increased risk of sudden death - cell necrosis

ACS Flashcards by Sarah Ramsbottom

What do all ACS result from?

an acute plaque rupture in wall of epicardial coronary artery

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3 clinical subtypes of CAD

UA
NSTEMI
STEMI

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NSTEMI (stand for)

non-ST segment elevation myocardial infarction

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STEMI

ST segment elevation myocardial infarction

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Which types are incomplete/transient?

NSTEMI

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Which types are complete/sustained?

STEMI

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What is the difference between UA and NSTEMI?

difference in duration and severity of ischaemia and symptoms

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What type is more severe?

STEMI

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characteristics of UA

acceleration in severity/frequency of chest pain
new anginal pain
pain at rest

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Necrosis in UA?

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Necrosis in NSTEMI?

yes

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Features of STEMI

abnormal cardiac rhythms
increased risk of sudden death
cell necrosis

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When does necrosis occur in STEMI and NSTEMI?

within 20-40mins

significant death after 2-3hrs

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2 phases in STEMI/NSTEMI

ischaemia

2. infarction

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What 3 changes can be seen on ECG?

ST changes
T wave inversion
pathological Q wave development

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What causes an inverted T wave?

altered repolarisation

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What is ST elevation a sign of?

myocardial injury

What do abnormal Q waves result from?

absence of depolarisation current from dead tissue and presence of opposing currents from other areas in heart

ECG changes in STEMI

ST elevation

pathological Q wave development

ECG changes in UA/NSTEMI

ST depression
T wave inversion
(persistent in NSTEMI and transient in UA)

4th diagnosis for ACS?

elevated troponin levels

What is given for immediate management of ACS?

aspirin 300mg
additional O2
GTN
diamorphine/morphine
beta blocker 4

clinical management for STEMI

coronary revascularisation/reperfusion

Open artery theroy

prompt and complete restoration of flow in occluded artery decreases infarct size, preserves LV function and improves survival rates

2 types of coronary revascularisation

- mechanical (PCI) | - pharmacological (thrombolytic/fibrinolytic therapy)

2 treatments for UA and NSTEMI

- initial conservative strategy | - early invasive strategy

What is the initial conservative strategy?

antiplatelet and anticoagulant therapy (low risk patients)

What is the early invasive strategy?

mechanical or surgical reperfusion (PCI/CABG)

What are the 2 pathways for antithrombotic therapy?

prothrombotic and antithrombotic pathways

What happens in the prothrombotic system?

blood clot formed

What happens in the antithrombotic systam?

blood clot dissolved

2 thrombolytic agents

- streptokinase (SK) | - tissue type plasminogen activators (t-PAs)

When is thrombolytic therapy used?

if PCI not possible within 120mins of STEMI diagnosis

Side effects of thrombolytic therapy

- haemorrhage - allergic reaction (SK) - hypotension - reperfusion induced arrhythmias

antiplatelet agents

cyclooxygenase inhibitors (aspirin) ADP receptor antagonists GP2b/3a receptor antagonists

What is factor IIa?

thrombin

What does anticoagulant therapy inactivate?

IIa and/or Xa and 9a

Drugs used in anticoagulant therapy?

- unfractionated heparin (UFH) - LMW heparins - synthetic pentasaccharides - direct thrombin inhibitors

What are the 2 classes of anticoagulants?

1. indirect thrombin inhibitors | 2. direct thrombin inhibitors

3 types of indirect thrombin inhibitors

- UF heparin - LMW heparins - fondaparinux

1 direct thrombin inhibitor

bivalirudin