ACS Flashcards
Define ACS
Constellation of disease occurring as a result of myocardial infarction.
Range from unstable angina to AMI both NSTEMI and STEMI
Define stable angina
Transient episodic chest discomfort resulting from myocardial ischaemia. Typically predictable and reproducible with frequency of attacks stable over time.
Define unstable angina ( history and pathophys)
Angina that is new onset or occurring at rest with minimal exertion.
Worsening from a previously stable patient of pain occurrence in terms of frequency or duration, resistance to previously effective medications or provocation with decreased levels of exertion or stress.
pathophys: plaque rupture accompanied by thrombus formation and vasospasm. Freqeuntly characterisedby an ECG abnormality including T-wave and ST segment changes.
Define prizmental angina
Caused by coronary artery vasospasm at rest with minimal coronary artery lesions - it may be relieved with exercise or NTG. ECG can reveal ST segment elevation that is impossible to dicern from STEMI.
Define AMI
Either of the following
1: Typicall rise and gradual fall of TNI with at least one value above the 99th percentile with at least one of the following clinical parameters
- Ischaemic symptoms
- ECG changes
- Development of pathological Q
- Imaging evidence of presumably new finding such as a loss of viable myocardium or RWMA
- identification of intracoronary thrombus by angiography or autopsy
Discuss types of MI
Type 1: Spont Mi related to ischamia resulting from a primary coronary event - plaque rupture, erosion, fissuring or dissection
Type 2: Mi secondary to myocardial ischaemia caused by increased O2 demand or decrease supply - coronary artery spasm, coronary embolism, severe anaemia or systemic hypotension
Type 3: sudden unexpected cardiac death with symptoms suggestive of MI
Type 4 Mi associated with coronary instrumentation
Type 5 MI associated with CABG
List causes for ST elevation
MI Pericarditis LBBB BER Ventricular paced rhythm normal variant PE Left ventricular aneurysm Osborn wave of hypothermia Brugada's syndrome Acute cerebral haemorrhage Postelectrical cardioversion
Discuss the pathophysiology of ACS
The underlying pathophysiology of ACS is myocardial ischaemia resulting from inadequate perfusion to meet o2 demands.
Myocardial o2 demands depend on HR, after load, contractility, and wall tension.
Occlusion of more than 95% is usually required for angina at rest. With exertion or increase in o2 demand can be present at 60%
Composition of plaques can vary greatly from fibrous stable plaques to unstable fibrolipid plaques which are likley to rupture and lead to thrombosis and platelet aggregation and lead to occlusion and tissue necrosis
Angiography shows that often the initial atherosclerotic plaques is only 50% the diameter of the lumen and that the most important factors in MI are the acute events of rupture and platelet activation.
Another important factor in development of infarction is local vasospams. After a significant coronary vessel occlusion local mediators and vasoactive substances are released. Sympathetic response and release of adrenaline can lead to vasopspam and increase platelet aggregation worsening occlusion
Further damage occurs at a cellular level as inflammatory thombotic and other debris fromt he occlusive plaque lesion is released and embolisez inot the destal vessels leading to microvasculature obstruction and hypoperfusion/ischaemia. With PCI and thrombolysis CA2 o2 and cellular elements are released which can causea reperfusion injury and lead to myocardial stunning or reperfusion arrythmias
Describe the GRACE risk model (bonus what is killip class)
GRACE model uses 8 factors to predict mortality at 6 months from admission
Criteria include
- AGE
- SYstolic blood pressure
- Creatinine
- Arrest at arrival
- HR
- Killip class
- abnormal cardiac enzymes
- ECG ST elevation
Killip class system used in MI taking into account the development of heart failure to risk stratify mortality
- Killip class I includes individuals with no clinical signs of heart failure.
- Killip class II includes individuals with rales or crackles in the lungs, an S3, and elevated jugular venous pressure.
- Killip class III describes individuals with frank acute pulmonary edema.
- Killip class IV describes individuals in cardiogenic shock or hypotension (measured as systolic blood pressure lower than 90 mmHg), and evidence of peripheral vasoconstriction (oliguria, cyanosis or sweating).
Discuss TIMI risk socre for STEMI
The TIMI score was developed from the inTIME2 trial of 15000 STEMI patient and looked at 30 day mortality all cause. Thrombolytic trial and did not look at PCI-
Also used new LBBB as a STEMI equivilant which it is no longer considered especially with scarbossi criteria
Uses 8 crieteria
1) Age >65, 65-75, >75
2) systolic BP <100
3) HR> 100
4) diabetes, HTN or angina
5) anterior ST elevation
6) Killip class 2-4
7) weight less than 67kg
8) time to treatment > 4
Discuss TIMI risk score for UA/NSTEMI
Uses 7 criteria to predict composite all-cause mortality, myocardial infarction, or urgent revascularization up to 14 days
Criteria include
1) age >65
2) 3 or greater CAD risk factors
3) known CAD >50%
4) ASA use in the past 7 days
5) severe angina (2 episodes in the past 24 hours)
6) ECG changes
7) Postive TNI
Describe the classic history of ACS
Classic angina pectoris is described a discomfort with squeezing pressure tightness fulness heaviness or burning sensation.
Classically substernal or precordial in location and radiates to the neck, jaw, shoulders or arms
Symptoms assoiated include dyspnoea, nausea and vomting, diaphoresis weakness, dizziness, excessive fatique and anxiety
ACS can masquarde as GIT abnormalities
Describe population that commonly present with atypical symptoms of ACS
Women, the elderly, diabetics, dementia patients
Patient with nil prior history of MI or risk factors
List DDX for chest pain (more than 20)
Cardiac
-MI, Unstable angina, stable angina, pericarditi, myocardial or pulmonary contusion, prizmetal’s angina
Resp:
-Pneumonia, PE, pneumothorax, pulmonary htn, pleurisy
GIT:
-GORD, mallory weiss syndrome, Boerhaavés syndrom, PUD, oesophageal spasm, gastritis , cholecysitis, panceatitis
Vascular
- disection,
Infectious
- VZV
MSK
Trauma
Discuss complications of MI
1) Arrythmias
- Bradydysrhythmia and AV block occur in 25-30% of patient with AMI - sinus brady is usualy seen
- Symptomatic bradycardias in the first few hours after MI tend to be atropine responisve
- Conduction block associated with anterior stemi has poor prognosis and respnds poorly to treatment
- Tachyarrhythmias are common and can be atrial or ventricular in origin
2) Cardiogenic shock
- seen with patient with alrge infarcts, prior MI, older age and DM
3) LV free wall rupture is uncommon - 1/3 of cases occur in the first 24 hours and the remainder 3-5 days later
- Clinically associated with sudden death
4) Interventricular septal rupture
- massive deterioation and a new harsh murmur heard best at the left sternal edge should prompt this diagnosis
-ECHO can show
-Vasopressor, inotropic support and intraortic balloon
pulsation are important measure to temporise until cardiac surgery
5) pericarditis ( MI related and post (Dressler’s syndrome)
Dresslers syndrome unlike infarct related pericarditi does not requir transmural involvement
-uncommon late complication occuring 1 week to several months post MI
6) Stroke both thrombotic and haemorrhagic
7) valvular complications
8) procedural complictation
- arterial injury with haemorrhage related to percutaneous interventions - pseudoaneyrsms
Discuss LVH as a mimic of ACS
LVH features prominent left sided forces manifesting as large rS or QS complexes in the right precoridal leads. THese changes rarely extend beyond V1-2
COnsistent with the rule of appropriate discordance (ST segment should be oppoisite the majority of the QRS) the leads with this paitten may feature ST elevation
The ST elevation is generally concave in LVH
The left precordial eads may show evidence of repolarization abnormality (strain pattern) with ST segment depression and asymmetrically inverted t-waves
Discuss Takotsubo cardiomyopathy
Left apical ballooning
Typically occurs in the setting of severe emotional distress
Patient have normal coronary arteries
Mimic STEMI and can have +ve TNI
Diagnosis
-New ecg changes (STE or TWI) or moderate TNI rise
-Transient akinesis/ dyskinesis of left ventricle with RWMA
Typicall it occurs in post menopausal women expierincing sudden emotional stress associated with a cathecolamine surge
Typically recovery wall motion within a month
Discuss the limitations of ECG in ACS
Single ECG is 60% sensitivity and 90% specific for AMI. Serial ECGs in the setting of continued or recurrent pain increases diagnostic value
Discuss the utility of a CXR in ACS
Exclude or confirm other DDX
Able to gather information conerning apllication of other therapies – ie. widened mediastinum and the use pf thrombolytics
SIgns of congestion can suggest Killip class of heart failure which can be used as a prognosticator on GRACE and TIMI
Discuss non ACS cardiac conditions in which there is a rise in TNI level
Can be seen in patient with myocarditis, pericarditis, CHF, LVH and non presnetrating cardiac trauma
Although the presence of TNI in these condition may be considered a false positive for ACS the source of these levels is likley underlying myocyte damage and have a significant prognostic effect
Discuss non cardiac condition that can lead to a rise in TNI
Massive and sub massive PE – right heart strain leads to right ventricular dysfunction and TNI rise – is a poor prognostic sign
Can also be seen in sepsis, extreme physical exertion, renal failure and essential hypertension
again a rise in troponin in any of these condition is associted with poorer outcome
Aortic dissection
Acute CNS pathology
Burns <30%
HCOM
Discuss elevated TNI in renal failure
These patient are at high risk for ACS
should not be ascribed to renal failure and poor clearance unless trend to show the same
