Acute Coronary Syndromes Flashcards
acute coronary syndrome (ACS)
an umbrella term covering a number of acute presentations of ischaemic heart disease
STEMI (ST-elevation myocardial infarction):
- ST-segment elevation
- elevated biomarkers of myocardial damage
NSTEMI (non ST-elevation myocardial infarction)
- ECG changes but no ST-segment elevation
- elevated biomarkers of myocardial damage
unstable angina
Ischaemic heart disease is a term synonymous with coronary heart disease and coronary artery disease.
True
acute coronary syndrome pathophysiology
gradual narrowing, resulting in less blood and therefore oxygen reaching the myocardium at times of increased demand. This results in angina, i.e. chest pain due to insufficient oxygen reaching the myocardium during exertion
2. The risk of sudden plaque rupture. The fatty plaques which have built up in the endothelium may rupture leading to sudden occlusion of the artery. This can result in no blood/oxygen reaching the area of myocardium.
What are Unmodifiable risk factors?
Increasing age
Male gender
Family history
What are modifiable risk factors?
Smoking Diabetes mellitus Hypertension Hypercholesterolaemia Obesity
Poor prognostic factors?
age development (or history) of heart failure peripheral vascular disease reduced systolic blood pressure Killip class* initial serum creatinine concentration elevated initial cardiac markers cardiac arrest on admission ST segment deviation
What is Killip Class?
system used to stratify risk post myocardial infarction
Describe Killip Classes
I No clinical signs heart failure, 6% 30 day mortality
II Lung crackles, S3 17% 30 day mortality
III Frank pulmonary oedema 38% 30 day mortality
IV Cardiogenic shock 81% 30 day mortality
initial endothelial dysfunction in IHD is triggered by a number of factors such as
smoking, hypertension and hyperglycaemia
initial endothelial dysfunction results in a number of changes such as?
pro-inflammatory, pro-oxidant, proliferative and reduced nitric oxide bioavailability
What type of lipoproteins infiltrate the subendothelial space in IHD?
by low-density lipoprotein (LDL) particles
How do foam cells form?
monocytes migrate from the blood and differentiate into macrophages. These macrophages then phagocytose oxidized LDL, slowly turning into large ‘foam cells’. As these macrophages die the result can further propagate the inflammatory process.
smooth muscle proliferation and migration from the tunica media into the intima results in formation of a fibrous capsule covering the fatty plaque.
What are the complications of atherosclerosis?
the plaque forms a physical blockage in the lumen of the coronary artery. This may cause reduced blood flow and hence oxygen to the myocardium, particularly at times of increased demand, resulting clinically in angina
the plaque may rupture, potentially causing a complete occlusion of the coronary artery. This may result in a myocardial infarction
What is the classic and most common feature of ACS?
chest pain.
What are the symptoms of ACS?
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
dyspnoea
sweating
nausea and vomiting
Patients presenting with ACS often have very few physical signs to ellicit
true
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
What are the two most important investigations when assessing a patient with chest pain?
ECG
cardiac markers e.g. troponin
Which cardiac marker is first to rise?
myoglobin is the first to rise
Which marker is useful to look at for re-infarctation?
CK-MB is useful to look for reinfarction as it returns to normal after 2-3 days
How long does troponin T remain elevated?
10 days
What are the cardiac enzymes and protein markers?
Myoglobin CK-MB CK Trop T AST LDH
Interpretation of the various cardiac enzymes has now largely been superceded by the introduction of troponin T and I. Questions still however commonly appear in exams.
true
Describe the orrelation between ECG changes and coronary territories
Anterior V1-V4 usually Left anterior descending artery
Inferior II, III, aVF usually Right coronary artery
Lateral I, V5-6 usually Left circumflex artery
What are the aims of ACS 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 intial treatment of ACS is MONA, what does it stand for?
morphine should only be given for patients with severe pain
previously IV morphine was given routinely
evidence, however, suggests that this may be associated with adverse outcomes
oxygen should only be given if the patient has oxygen saturations < 94%
nitrates
can be given either sublingually or intravenously
useful if the patient has ongoing chest or hypertension
should be used in caution if patient hypotensive
aspirin 300mg
After pharmacological treatment (MONA) what is the next step?
determine whether they meet the ECG criteria for STEMI
What is STEMI criteria?
clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of:
2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years
1.5 mm ST elevation in V2-3 in women
1 mm ST elevation in other leads
new LBBB (LBBB should be considered new unless there is evidence otherwise)
In management of a STEMI all patients should be given?
aspirin
a second antiplatelet drug should be given in addition to aspirin. P2Y12-receptor antagonist (ticagrelor is often favoured or prasugrel if the patient is going to have a PCI)
unfractionated heparin is usually given for patients who’re are going to have a PCI
In STEMI management what should you do in terms of oxygen therapy?
do not routinely administer oxygen, but monitor oxygen saturation using pulse oximetry as soon as possible, ideally before hospital admission. Only offer supplemental oxygen to:
people with oxygen saturation (SpO2) of less than 94% who are not at risk of hypercapnic respiratory failure, aiming for SpO2 of 94-98%
people with chronic obstructive pulmonary disease who are at risk of hypercapnic respiratory failure, to achieve a target SpO2 of 88-92% until blood gas analysis is available.
What is gold standard treatment for STEMI?
Primary percutaneous coronary intervention (PCI)
In this procedure the blocked arteries are opened up using a balloon (angioplasty) following which a stent may be deployed to prevent the artery occluding again in the future. This is done via a catheter inserted into either the radial or femoral artery
radial access is preferred to femoral access in PCI
When should PCI be offered?
should be offered if the presentation is within 12 hours of onset of symptoms AND PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given (i.e. consider fibrinolysis if there is a significant delay in being able to provide PCI)
if patients present after 12 hours and still have evidence of ongoing ischaemia then PCI should still be considered
When should fibrinolysis be offered?
should be offered within 12 hours of onset of symptoms if primary PCI cannot be delivered within 120 minutes of the time when fibrinolysis could have been given
Which drugs are used in fibrinolysis?
tissue plasminogen activator (tPA) has been shown to offer clear mortality benefits over streptokinase
tenecteplase is easier to administer and has been shown to have non-inferior efficacy to alteplase with a similar adverse effect profile
Patients undergoing fibrinolysis should also be given an antithrombin drug.
What test should be performed after fibrinolysis?
An ECG should be performed 90 minutes following thrombolysis to assess whether there has been a greater than 50% resolution in the ST elevation
if there has not been adequate resolution then rescue PCI is superior to repeat thrombolysis
for patients successfully treated with thrombolysis PCI has been shown to be beneficial. The optimal timing of this is still under investigation
What is the guidance on the management of hyperglycaemia in acute coronary syndromes for diabetic patients?
it recommends using a dose-adjusted insulin infusion with regular monitoring of blood glucose levels to glucose below 11.0 mmol/l
intensive insulin therapy (an intravenous infusion of insulin and glucose with or without potassium, sometimes referred to as ‘DIGAMI’) regimes are not recommended routinely
NICE produced guidelines on the management of patients following a myocardial infarction (MI) in 2013. Some key points are?
All patients should be offered the following drugs:
dual antiplatelet therapy (aspirin plus a second antiplatelet agent)
ACE inhibitor
beta-blocker
statin
What are the lifestyle points post MI?
diet: advise a Mediterranean style diet, switch butter and cheese for plant oil based products. Do not recommend omega-3 supplements or eating oily fish
exercise: advise 20-30 mins a day until patients are ‘slightly breathless’
sexual activity may resume 4 weeks after an uncomplicated MI. Reassure patients that sex does not increase their likelihood of a further MI. PDE5 inhibitors (e.g, sildenafil) may be used 6 months after a MI. They should however be avoided in patient prescribed either nitrates or nicorandil
What are the widely used drugs for dual antiplatelet therapy (DAPT)?
ticagrelor and prasugrel (ADP-receptor inhibitors)
What DAPT does NICE reccomend post acute coronary syndrome (medically managed)?
add ticagrelor to aspirin, stop ticagrelor after 12 months
this 12 month period may be altered for people at a high-risk of bleeding or those who at high-risk of further ischaemic events
What DAPT does NICE reccomend post percutaneous coronary intervention?
add prasugrel or ticagrelor to aspirin, stop the second antiplatelet after 12 months
this 12 month period may be altered for people at a high-risk of bleeding or those who at high-risk of further ischaemic events
When are Aldosterone antagonists indicated post acute MI?
who have symptoms and/or signs of heart failure and left ventricular systolic dysfunction
aldosterone antagonist licensed for post-MI treatment (e.g. eplerenone) should be initiated within 3-14 days of the MI, preferably after ACE inhibitor therapy
What complications can you get post-MI?
Cardiac arrest Cardiogenic shock Chronic heart failure Tachyarrhythmias Bradyarrhythmias Pericarditis Left ventricular aneurysm Left ventricular free wall rupture Ventricular septal defect Acute mitral regurgitation
Cardiac arrest most commonly occurs due to patients developing ventricular fibrillation
true
is the most common cause of death following a MI. Patients are managed as per the ALS protocol with defibrillation
How does cardiogenic shock occur post MI?
If a large part of the ventricular myocardium is damaged in the infarction the ejection fraction of the heart may decrease to the point that the patient develops cardiogenic shock.
Other causes of cardiogenic shock include the ‘mechanical’ complications such as left ventricular free wall rupture
Patients may require inotropic support and/or an intra-aortic balloon pump.
How does Chronic heart failure occur post MI?
if the patient survives the acute phase their ventricular myocardium may be dysfunctional resulting in chronic heart failure
Both ACE-inhibitors and beta-blockers have been shown to improve the long-term prognosis of patients with chronic heart failure.
true
Loop diuretics such as furosemide will decrease fluid overload
Atrioventricular block is more common following what type of MI?
inferior myocardial infarctions.
When does Pericarditis typically occur?
first 48 hours following a transmural MI is common (c. 10% of patients).
How does Pericarditis typically occur?
pain is typical for pericarditis (worse on lying flat etc), a pericardial rub may be heard and a pericardial effusion may be demonstrated with an echocardiogram.
When does Dressler’s syndrome typically occur?
2-6 weeks following a MI
What is the pathophysiology of Dressler’s syndrome?
The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers
What are the characteristics of Dressler’s syndrome?
combination of fever, pleuritic pain, pericardial effusion and a raised ESR. It is treated with NSAIDs.
What is Left ventricular aneurysm typically associated with?
persistent ST elevation and left ventricular failure
ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation
What is a complciation of left ventricular aneurysm?
Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated.
When does Left ventricular free wall rupture typically occur?
1-2 weeks post MI afterwards
Left ventricular free wall rupture is seen in 3% of MIs
true
How does Left ventricular free wall rupture present?
acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds). Urgent pericardiocentesis and thoracotomy are required.
When does Ventricular septal defect occur?
Rupture of the interventricular septum usually occurs in the first week and is seen in around 1-2% of patients.
What are the features of Ventricular septal defect?
acute heart failure associated with a pan-systolic murmur. An echocardiogram is diagnostic
Urgent surgical correction is needed.
acute mitral regurgitation presents in a similar fashion to?
Ventricular septal defect
Excluded with echo
acute mitral regurgitation is more common with?
infero-posterior infarction and may be due to ischaemia or rupture of the papillary muscle.
How does Acute mitral regurgitation present?
Acute hypotension and pulmonary oedema may occur. An early-to-mid systolic murmur is typically heard. Patients are treated with vasodilator therapy but often require emergency surgical repair.
What Further antiplatelet prior to PCI is required?
‘dual antiplatelet therapy’, i.e. aspirin + another drug
if the patient is not taking an oral anticoagulant: prasugrel
if taking an oral anticoagulant: clopidogrel
What Drug therapy is required during PCI?
patients undergoing PCI with radial access:
unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI) - this is the action of using a GPI during the procedure when it was not intended from the outset, e.g. because of worsening or persistent thrombus
patients undergoing PCI with femoral access:
bivalirudin with bailout GPI
What other procedure may be considered during PCI?
thrombus aspiration, but not mechanical thrombus extraction, should be considered
complete revascularisation should be considered for patients with multivessel coronary artery disease without cardiogenic shock
The management of NSTEMI/unstable angina is complicated and depends on individual patient factors and a risk assessment.
true
What is the first step after NSTEMI/Unstable angina is identified?
Aspirin 300mg
Fondaparinaux if no immediated PCI planned
What is the 2nd step after NSTEMI/Unstable angina is identified?
Estimate 6 - month mortality such as using GRACE tool
The Global Registry of Acute Coronary Events (GRACE) is the most widely used tool for risk assessment. It can be calculated using online tools and takes into account the following factors?
age heart rate, blood pressure cardiac (Killip class) and renal function (serum creatinine) cardiac arrest on presentation ECG findings troponin levels
GRACE tool predicts 6 month mortality - what are the categories?
1.5% or below Lowest > 1.5% to 3.0% Low > 3.0% to 6.0% Intermediate > 6.0% to 9.0% High over 9.0% Highest
Which patients with NSTEMI/unstable angina should have a coronary angiography (with follow-on PCI if necessary)?
immediate: patient who are clinically unstable (e.g. hypotensive)
within 72 hours: patients with a GRACE score > 3% i.e. those at immediate, high or highest risk
coronary angiography should also be considered for patients is ischaemia is subsequently experienced after admission
In Primary coronary intervention for patients with NSTEMI/unstable angina what is the drug therapy?
- Prasugrel or Ticagrelor
- Unfractionated heparin
- Drug-eluting stents
Further drug therapy
unfractionated heparin should be given regardless of whether the patient has had fondaparinux or not
further antiplatelet (‘dual antiplatelet therapy’, i.e. aspirin + another drug) prior to PCI
if the patient is not taking an oral anticoagulant: prasugrel or ticagrelor
if taking an oral anticoagulant: clopidogrel
What is Conservative management for patients with NSTEMI/unstable angina?
further antiplatelet ('dual antiplatelet therapy', i.e. aspirin + another drug)
if the patient is not at a high risk of bleeding: ticagrelor
if the patient is at a high risk of bleeding: clopidogrelWhat ECG changes would you see in Acute MI?
hyperacute T waves are often the first sign of MI but often only persists for a few minutes
ST elevation may then develop
the T waves typically become inverted within the first 24 hours. The inversion of the T waves can last for days to months
pathological Q waves develop after several hours to days. This change usually persists indefinitely
A posterior MI causes ST depression not elevation on a 12-lead ECG.
true
