ACS Flashcards

1
Q

What is ACS?

A

unstable angina and myocardial infarction

unstable angina
considered to be present in patients with ischaemic symptoms suggestive of an ACS and no elevation in troponins, with or without electrocardiogram changes indicative of ischaemia
however, as a rise in troponins may take some hours it may be indistinguishable for NSTEMI initially and is therefore treated the same until the troponin result is known

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2
Q

When to suspect ACS

A

-Pain in the chest or other areas (for example the arms, back, or jaw) lasts longer than 15 minutes.
-Chest pain is:
=Dull, central, and/or crushing.
=Associated with nausea and vomiting, sweating or breathlessness, or a combination of these.
=Associated with haemodynamic instability (for example the person has a systolic blood pressure less than 90 mmHg).
=Of a new-onset, or is the result of an abrupt deterioration of stable angina; with pain occurring frequently with little or no exertion, and often lasting longer than 15 minutes.
-Do not use the person’s response to glyceryl trinitrate to confirm or exclude a diagnosis of acute coronary syndrome.

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3
Q

Diagnosis of ACS

A

-Most people require referral, or admission to hospital to confirm the diagnosis of acute coronary syndrome (ACS).
-People suspected of having ACS should be offered a resting 12-lead ECG (electrocardiogram) and a blood sample taken for high-sensitivity troponin I or T measurement to confirm the diagnosis.
=Do not use high-sensitivity troponin tests for people in whom ACS is not suspected.

-If the person’s pain was more than 72 hours ago and they have no complications, consider diagnosing ACS in primary care. Arrange:
=An ECG — ECG changes that may indicate ischaemia or previous myocardial infarction include:
==Pathological Q waves (in particular).
==Left bundle branch block (LBBB).
==ST-segment and T-wave abnormalities (for example T-wave flattening or elevation, or T-wave inversion).
==A normal ECG does not confirm or exclude a diagnosis of ACS.

=A high-sensitivity blood test for serum troponin — cardiac troponin I and T are used to differentiate unstable angina from myocardial infarction.
==A detectable troponin level indicates damage to the myocardium (for example myocardial infarction).
==Serum troponin is normally detectable using high-sensitivity testing within 3–6 hours following a myocardial infarction, and remains elevated for a variable time (usually several days, but it can be up to 2 weeks).
==Other conditions that directly or indirectly damage heart muscle (such as arrhythmias, pericarditis, pulmonary emboli, and myocarditis) can also cause an increase in serum troponin.

-When interpreting high-sensitivity troponin measurements, take into account the:
=Clinical presentation.
=Time from onset of symptoms.
=Resting 12-lead ECG findings.
=Pre-test probability of non-ST-segment-elevation myocardial infarction (NSTEMI).
=Length of time since the suspected ACS.
=Probability of chronically elevated troponin levels in some people.
=Fact that 99th percentile thresholds for troponin I and T may differ between males and females.

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4
Q

Unmodifiable risk factors

A

Increasing age
Male gender
Family history

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5
Q

Modifiable risk factors

A

Smoking
Diabetes mellitus
Hypertension
Hypercholesterolaemia
Obesity

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6
Q

Symptoms and signs of ACS

A

The classic and most common feature of ACS is chest pain.
typically central/left-sided
may radiate to the jaw or the left arm
often described as ‘heavy’ or constricting, ‘like an elephant on my chest’
it should be noted however in real clinical practice patients present with a wide variety of types of chest pain and patients/doctors may confuse ischaemic pain for other causes such as dyspepsia
certain patients e.g. diabetics/elderly may not experience any chest pain

Other symptoms in ACS include
dyspnoea
sweating
nausea and vomiting

Patients presenting with ACS often have very few physical signs to ellicit:
pulse, blood pressure, temperature and oxygen saturations are often normal or only mildly altered e.g. tachycardia
if complications of the ACS have developed e.g. cardiac failure then clearly there may a number of findings
the patient may appear pale and clammy

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7
Q

Management of ACS

A

Once a diagnosis of ACS has been made there are a number of elements to treatment:
prevent worsening of presentation (i.e. further occlusion of coronary vessel)
revascularise (i.e. ‘unblock’) the vessel if occluded (patients presenting with a STEMI)
treat pain

A commonly taught mnemonic for the treatment of ACS is MONA:
Morphine (severe pain)
Oxygen (<94%)
Nitrates (sublingual/IV, caution if hypotensive)
Aspirin 300mg

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8
Q

Secondary prevention of ACS

A

Patients who’ve had an ACS require lifelong drug therapy to help reduce the risk of a further event. Standard therapy comprises the following as a minimum:
aspirin
a second antiplatelet if appropriate (e.g. clopidogrel)
a beta-blocker
an ACE inhibitor
a statin

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9
Q

Poor prognostic factors in ACS

A

Poor prognostic factors
age
development (or history) of heart failure
peripheral vascular disease
reduced systolic blood pressure
Killip class* (No clinical signs HF, lung crackles/S3, frank pulmonary oedema, cardiogenic shock 1-4)
initial serum creatinine concentration
elevated initial cardiac markers
cardiac arrest on admission
ST segment deviation

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