Acute coronary syndrome and acute myocardial infarction Flashcards
What is the pathology of an acute coronary syndrome
Spontaneous plaque rupture
Local thrombosis
Occlusion
What are the four types of acute coronary syndrome
Unstable angina
NSTEMI
STEMI
Sudden cardiac death
Why do plaques rupture?
Inflammation and stress
Important differentiation between angina and acute coronary syndromes
Symptoms at rest in ACS
Characteristics of pain
Site: retrosternal
Character: tight band, pressure, heaviness
Radiation to neck, jaw, down arms
Aggravation with exertion, emotional stress
GTN or physical rest DOES NOT relieve
Non-modifiable risk factors
Age, gender, creed, family history, genetics
Previous angina, cardiac events or interventions
Modifiable risk factors
Smoking Diabetes mellitus Hyperlipidaemia Hypertension Lifestyle - exercise and diet
What is unstable angina pectoris (UAP)
Angina on effort, but of progressive increasing frequency and severity, often provoked by less exertion and/or then at rest
What is NSTEMI
Non ST elevated myocardial infarction
often starting with myocardial ischaemic symptoms at rest
Findings in examination for UAP or NSTEMI
Patient may look very unwell or completely fine
Often no specific features
What would an ECG show for UAP and NSTEMI
Commonly ST-segment depression
T-wave inversion
Transient ST elevation
Why are serial ECGs essential in UAP and NSTEMI
To detect delayed changes
Who may present atypically or have a silent ACS due to reduced pain sensation
The elderly, diabetics or women
Typical symptoms of UAP and NSTEMI
breathlessness (may have signs of heart failure)
Nausea and vomiting
Epigastric pain
What cardiac biomarker is helpful in diagnosis and suggests high risk of adverse events
Cardiac troponin
After ABCDE when UAP/NSTEMI patient initially comes in, what is the next approach in terms of treatment (MONA)
Morphine
Oxygen
Nitroglycerine (GTN spray or tablet)
Aspirin 300mg orally
What anti-platelet therapy should the UAP/NSTEMI patient now receive?
Both aspirin and a ADP receptor blocker
Give 2 examples of an ADP receptor blocker (anti-platelet)
Clopidogrel
Ticagrelor
Prasugrel
What dosage of Clopidogrel
Bolus 300mg and 75mg daily
How long should patient be on dual anti-platelet therapy following ACS event
1 year
What anti-thrombotic therapy for UAP/NSTEMI patient to try and thrombolyse the clot
Low weight molecular heparin
What other medical therapy may you consider for patient as prevention measures
Beta blockers
Statins
ACE inhibitors
If you can’t control the unstable angina or NSTEMI with medication or high risk patient, what further treatment would you consider
Coronary angiography and revascularisation by PCI
CABG
What is STEMI
ST elevated myocardial infarction caused by complete/more complete thrombotic occlusion of coronary lumen
Proximal occlusion causes greater damage, however what significant problems can arise due to occlusion of distal or branch vessel to critical structures?
Rupture of papillary muscle
Acute mitral regurgitation
Occlusion of AV nodal artery
What are the two methods of opening the infarct related artery?
Primary percutaneous coronary intervention
Fibrinolysis
When is primary PCI best?
If door to balloon time is under 90 minutes If greater than 3 hour symptom onset Cardiogenic shock, HF High bleeding risk Diagnosis uncertain
When is thrombolysis best?
Door to balloon time is more than 90 minutes
Less than 3 hour symptom onset
Is primary PCI or thrombolysis better?
Primary PCI as reduced mortality, recued risk of recurrent MI or stroke
What secondary prevention can be done to reduce risk of recurrent STEMI?
General measures - stop smoking, diet, exercise Control co-morbidities Aspirin and clopidogrel (1 year only) Beta blockers Statins ACE inhibitors
If someone has had a STEMI, what in-patient investigation should be done?
Echo
What is sudden cardiac death?
When the atherothrombotic event causes acute myocardial ischaemia and subsequent sufficient electrical disturbance to cause ventricular arrhythmia
Treatment of sudden cardiac death (ventricular fibrillation)
Defibrillation
What are the two main groups of immediately life threatening complications of acute MI
Mechanical complications
Ventricular arrhythmic complications
What are the three main mechanical complications from an MI
Free wall rupture
Papillary muscle rupture
Rupture of IVS
What can be a later complication, which is less threatening but still needs treatment
Left ventricular thrombus
Which MI (STEMI or NSTEMI) or more likely to have complications
STEMI
Where abouts in the coronary arteries is a free wall rupture most likely to happen?
Left anterior descending
What does a free wall rupture lead to?
Haemopericardium
Acute tamponade
How may a free wall rupture be contained if it doesn’t result in death?
Adhesions
False aneurysm
What patients are more likely to have a free wall rupture?
Elderly
Females
Hypertension
Anterior MI
Management of free wall rupture
Urgent echo
Pericardiocentesis - fluid aspirated from pericardium
Drainage with pigtail catheter
Immediate surgery - if survives first episode
What do most patients who have a septal wall rupture have?
Multi-vessel coronary artery disease
What percentage of people survive a papillary muscle rupture
6%
Symptoms of papillary muscle rupture and VSD
Sudden severe breathlessness Sweating Nausea Vomiting Chest pain
Signs of papillary muscle rupture and VSD
Shock Tachycardia Pulmonary oedema New harsh systolic murmur Right parasternal heave Palpable thrill Elevated JVP
Investigation for papillary muscle rupture
Echo
Cath lab:
Right heart cath - oxygen sats with VSD, confirm defect
Left heart cath - establish coronary anatomy
Management of papillary muscle rupture (although generally only temporary as most die)
IV nitrates if systolic blood pressure > 90mmHg
Inotropes if SBP < 90mmHg
IABP (balloon pump)
Cardiac surgeons - mitral valve replaced, VSD repair, coronary artery bypass if needed
When does ventricular tachycardia occur
Any time following MI
What else can cause acute coronary syndromes (other than atherosclerosis)
Superimposed platelet aggregation and thrombosis
Vasospasm and vasoconstriction
What is the time frame for doing percutaneous intervention for a STEMI
within 2 hours ideally
How do thrombolytics work
They convert plasminogen into the natural fibrinolytic agent, plasmin.
Plasmin lyses clot by breaking down fibrinogen and fibrin, contained within it.
What are serine proteases
thrombolysis agents
What two categories are thrombolytic agents divided into
- Fibrin-specific agents (plasminogen to plasmin)
2. Non-fibrin-specific agents (catalyse systemic fibrinolysis)
Examples of fibrin-specific thrombolytic agents
Alteplase
Reteplase
Tenecteplase
Example of non-fibrin-specific agent
streptokinase
What can streptokinase cause
Anaphalaxis
When should you not use thrombolytics
If patient has had recent bleeding as they could die
Other contraindications for thrombolytics
Prior intracranial haemorrhage
Known structural cerebral vascular lesions
Known malignant intracranial neoplasm
Ischaemic stroke within 3 months
Suspected aortic dissection
Active bleeding or bleeding diathesis
Significant closed-head trauma or facial trauma within 3 months
In no evidence of STEMI, then ACS medical treatment protocol, which is:
Aspirin Ticagrelor/Clopidogrel Fondaparinux/ LMW heparin Intravenous nitrate Analgesia Beta blockers
Why is ticagrelor slightly more effective than clopidogrel
Clopidogrel is a prodrug so does not metabolise as easily as ticagrelor
What analgesia would be appropriate
Morphine / opiates
