Acute coronary syndrome Flashcards
what is Acute coronary syndrome
clinical manifestation of myocardial infarct and commonly the default working diagnosis in patients with new onset chest pain suspected to be of cardiac ischaemic origin
divided into unstable angina, NSTEMI and STEMI
define unstable angina
acute myocardial ischemia that is not severe enough to cause detectable quantities of myocardial injury biomarkers or ST segment elevations on ECG
define NSTEMI
acute myocardial ischaemia that is severe enough to cause detectable quantities of myocardial injury biomarkers without ST segment elevations on ECG
define STEMI
acute myocardial ischaemia that is severe enoiugh to cause ST segment elevations
cardinal sympotms of MI
diaphoresis
sense of impending doom
nausea and vomiting
dyspnoea
restrosternal pain radiating to the left side of the body (arm, shoulder, neck and epigastrium)
non specific signs of MI esp. in women
dizziness
lightheadedness, syncope
fatigue, exhaustion
jaw, neck, upper back pain
palpitations
epigastric discomfort or pressure
clinical presentation of angina type pain
occuring at rest with minimal exertion, not relieved by rest or nitroglycerin
new onset
severe, persistant, worsening (crescendo angina)
autonomic symptoms
diaphoresis, syncope, palpitations, nausea and/or vomiting
pathophysiology of unstable angina
partial occlusion of coronary vessel
decreased blood supply
ischaemic symptoms without infarction
pathophysiology of NSTEMI
classicially due to partial occlusion of a coronary artery
affects the inner layer of the heart (subendocardial infarction)
pathophysiology of STEMI
classically due to complete occlusion of coronary artery
affects the full thickness of the myocardium (transmural infarction)
cardaic troponins
elevated in NSTEMI and STEMI within 1-6 hours
may initially be undetectable in patients who present early after symptom onset, especially if conventional rather than high sensitivity troponin assays are used
ECG findings for unstable angina and NSTEMI
no ST elevations
normal or non-specific eg. ST depression, loss of R wave, T wave inversion
ECG findings for STEMI
ST elevations in two contiguous leads or new LBBB with strong clinical suspicion of myocardial ischaemia
ST elevations can be masked by LBBB. however the presence of a new of presumably new LBBB in a patient with ACS is not always an ndication for PCI
initial management for the patient presenting with acute coronary syndrome
direct to resus
monitor ECG and O2
take obs (bilateral BP if dissectionn is being considered)
takes bloods - FBC, UEC, BSL, trops (senior doctor may add d-dimer if indicated)
CXR
aspirin unless already given or contrindicated
oxygen only if hypoxic <93%
take ECG for urgent review by senior
GTN (SL and then IV if required)
other analgesia eg. titrated morphine
Management for unstable angina and NSTEMI
invasive management depends on risk stratification
aspirin 300mg and tiicagrelor load 180mg plus 90mg bd
statins
beta blockers
ACEIs
pain management (opoiods, nitrates, titratd morphine)
do an EDACS score
Management for STEMI
immidiate revascularisation
adjunctive therapy similar to NSTEMI
can subtypes of ACS be differentaited based on clinical presentation
no
the type of MI is determined based on
ECG findings
unstable angina is differentiated from MI by
positive troponins
clinical triad for right ventricular infarction
hypotension
elevated JVP
clear lung feilds
initial triage based on ECG findings
ST elevations present: start management of STEMI with immediate revascularisation therapy, preferably PCI
transthoracic echocardography
generally not necessary
should not delay reperfusion therapy
may be helpful study in patients with atypical symptoms or if the diagnosis is unclear
findings in transthoracic echcardioraphy
wall motion abnormalities
decreased LV function
signs of different conditions that cause chest pain
reperfusion therapy
PCI or thrombinolysis
STEMI treatment of choice
PCI vs. fibrinolysis
aim for PCI within 90 minutes of first medical contact
consider IV fibrinolytics if:
- PCI cant be performed within 120 minutes
- there are no contraindications to fibrinolytics for STEMI
ECG changes in STEMI
significant ST elevation in two contiguous leads
findings may change over time
hyperacute T waves can present without ST elevations in the very early stages of ischaemia
If inferior MI is suspected, investigate for signs of right ventricular involvement
when are Q waves pathological
duration >0.04 seconds
amplitude >1/4 of the R waves
any Q wave in leads V1-3
ECG changes in chronic stage
permanent scarring
persistent, broad deep Q waves
often incomplete recovery of R waves
permanent T-wave inversion is possible
the EDACS score
risk assessment for patients presenting to the ED with chest pain
procedure for PCI
coronary angiography with PCI ie. baloon dilatation with stent implantation
Fibrinolytic therapy is indicated if
PCI cannot be performed within 120 minutes of FMC
no contraindications to fibrinolysis are present
regimens for fibrinolysis
Tenecteplase
Alteplase
Reteplase
Streptokinase
absolute contraindications for fibrinolysis in STEMI
weigh risks and benefits carefully in individual patients
active bleeding (not including menses)
bleeding diathesis/known coagulopathy
any prior intracranial bleeding
intracranial or intraspinal surgery within the past 2 months
serious head trauma within the past 3 months
severe hypertension unresponsive to emergency therapy
intracranial conditions increasing risk of bleeding eg. AV malformation
suspected aortic dissection
intracranial malignancy
for streptokinase: previous exposure within the last 6 months (highly antigenic)
streptokinase is contraindicated when
there has been previous exposure to streptokinase within the last 6 months
antiplatelet therapy and anticoagulation in STEMI if undergoing PCI
DAPT: Aspirin and
ADP receptor inhibitor (Prasugral or ticagrelor is preferred, otherwise clopidogrel)
anticoagulation: unfractionated heparin, bivalirudin
consider adjunctive use of glycoprotein inhibitor
antiplatelet therapy and anticoagulation in STEMI if NOT undergoing PCI
aspirin and clopidogrel (DAPT)
one of: unfractionated heparin, enoxaparin, fondaparinux (anticogulant)
glycoprotein not routinely recommended
for patients presenting more than 12 hours after symptom onset
myocardial infarction may already be complete, but still consider PCI/thrombolytic therapy if
- ongoing ischaema (persistant pain, dynamic changes on ECG)
- viable myocaardium (preservation of R waves)
- major complications ( cardiogenic shock, heart failure, malignant arrythmia)
when is PCI preferred over thrombolytic therapy
PCI is mor beneficial over thrombolytic therapy in reducing mortality, recurrent MI and stoke.
the benefit of PCI over thrombinolysis increases aas time between symptom onset and patient presentation increases
if thrombolytic therapy fails
if the patient is at a centre where PCI is not available and thrombolytic therapy is either contraindicated or has failed, promptly transfer the patient to a centre where PCI is availble
how do you know if thrombolytic therapy has failed
50% or less ST resolution after 60 to 90 minutes
or
continued haemodynamic instability
what to do if thrombolytic therapy succeeds
arrange transfer to a centre where percutaneous coronary intervention is available with a plan for coronary angiography within 24 hours
long term medication for STEMI
antiplatelet
statin
ACEI/ARB
beta blocker
are fibrinolytics indicated in NSTEMI
no
how to risk stratify NSTEMIs
use EDACS score / GRACE score
ECG changes?
ongoing ischaemic-like chest pain
syncope, systolic BP<90 not due to GTN, haemodynamic instability, signs and symptoms of heart failure, signs and symptoms of heart failure/pulomnnary oedema, recent PCI pr prior CABG, sustainedarrythmia
invasive strategy for NSTEMI for very high to intermediate risk patients
within 2 hours for very high risk
within 24 hours for high risk
ischaemia guided strategy for NSTEMI
for stable, low risk patients
non invasive cardiac stress testing eg. exercise ECG, stress echo) to evaluate need for coronary angiography
antiplatelet therapy and anticoagulation for NSTEMI
DAPT: aspirin and either Ticagralor or clopidogrel (ADP receptor inhibitors)
anticoagulation: enoxaparin, unfractionated heparin, fondaparinux or bilivardin only in invasive strategy
consider glyoprotein inhibitor for intermediate/high risk patients with early invasive strategy
monitoring during ACS
continuous cardiac monitoring
serial 12 lead ECG every 15-30 minutes
serial serum troponin measurement every 1-6 hours
adjunct medical therapy in ACS
nitrates
beta blockers
opioids
ACE inhibitors/ARBs
aldosterone agonists
high intensity statin
acronym for MI management
MONA BASH
Morphine
Oxygen
Nitroglycerin
Antiplatelets (aspirin + ADP receptor inhibitor)
beta blockers
ACE inhibitors
Statins
Heparin
oxygen therapy should be used for patients with
cyanosis
severe dyspnoea
SpO2 <93%
fluid management
IV fluids: consider for inferior MI causing RV dysfunction, because increasing preload optimises left and right ventricular filling and reduces haemodynamic instaability
loop diuretic eg. furosemide: consider for patients with pulmonary oedema, acute heart failure
