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int med 2024 > Acute coronary syndrome > Flashcards

Acute coronary syndrome Flashcards

1
Q

what is Acute coronary syndrome

A

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

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2
Q

define unstable angina

A

acute myocardial ischemia that is not severe enough to cause detectable quantities of myocardial injury biomarkers or ST segment elevations on ECG

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3
Q

define NSTEMI

A

acute myocardial ischaemia that is severe enough to cause detectable quantities of myocardial injury biomarkers without ST segment elevations on ECG

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4
Q

define STEMI

A

acute myocardial ischaemia that is severe enoiugh to cause ST segment elevations

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5
Q

cardinal sympotms of MI

A

diaphoresis
sense of impending doom
nausea and vomiting
dyspnoea
restrosternal pain radiating to the left side of the body (arm, shoulder, neck and epigastrium)

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6
Q

non specific signs of MI esp. in women

A

dizziness
lightheadedness, syncope
fatigue, exhaustion
jaw, neck, upper back pain
palpitations
epigastric discomfort or pressure

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7
Q

clinical presentation of angina type pain

A

occuring at rest with minimal exertion, not relieved by rest or nitroglycerin
new onset
severe, persistant, worsening (crescendo angina)

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8
Q

autonomic symptoms

A

diaphoresis, syncope, palpitations, nausea and/or vomiting

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9
Q

pathophysiology of unstable angina

A

partial occlusion of coronary vessel
decreased blood supply
ischaemic symptoms without infarction

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10
Q

pathophysiology of NSTEMI

A

classicially due to partial occlusion of a coronary artery
affects the inner layer of the heart (subendocardial infarction)

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11
Q

pathophysiology of STEMI

A

classically due to complete occlusion of coronary artery
affects the full thickness of the myocardium (transmural infarction)

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12
Q

cardaic troponins

A

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

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13
Q

ECG findings for unstable angina and NSTEMI

A

no ST elevations
normal or non-specific eg. ST depression, loss of R wave, T wave inversion

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14
Q

ECG findings for STEMI

A

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

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15
Q

initial management for the patient presenting with acute coronary syndrome

A

direct to resus
monitor ECG and O2
take obs
takes bloods - FBC, UEC, BSL, trops
CXR
aspirin
oxygen only is hypoxic
take ECG for urgent review by senior

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16
Q

Management for unstable angina and NSTEMI

A

invasive management depends on risk stratification
anticoagulants, antiplatelet therapy. eg. aspirin, ADP receptor inhibitors)
statins
beta blockers
ACEIs
pain management (opoiods, nitrates)

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17
Q

Management for STEMI

A

immidiate revascularisation
adjunctive therapy similar to NSTEMI

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18
Q

can subtypes of ACS be differentaited based on clinical presentation

A

no

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19
Q

the type of MI is determined based on

A

ECG findings

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20
Q

unstable angina is differentiated from MI by

A

positive troponins

21
Q

clinical triad for right ventricular infarction

A

hypotension
elevated JVP
clear lung feilds

22
Q

immediate management of ACS

A

obtain 12-lead ECG within 10 minutes of patient arrival
measure cardiac troponin as soon as possible.
initiate supplimental O2 for cyanosis, respirtaory distress, or SpO2<90%
give aspirin if there are no contraindications
consider adjunct medical therapy for ACS eg. sublingual nitroglycerin for chest pain relief

23
Q

initial triage based on ECG findings

A

ST elevations present: start management of STEMI with immediate revascularisation therapy, preferably PCI

24
Q

transthoracic echocardography

A

generally not necessary
should not delay reperfusion therapy
may be helpful study in patients with atypical symptoms or if the diagnosis is unclear

25
Q

findings in transthoracic echcardioraphy

A

wall motion abnormalities
decreased LV function
signs of different conditions that cause chest pain

26
Q

STEMI treatment of choice

A

PC vs. fibrinolysis
aim for PCI within 90 minutes of first medical contact
consider IV fibrinolytics if:
- PCI cant be performed within 90 minutes
- there are no contraindications to fibrinolytics for STEMI

27
Q

ECG changes in STEMI

A

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

28
Q

ECG changes in acute stage

A

myocardial damage ongoing
hyperacute T waves
ST elevations in two contiguous leads with reciprocal ST depressions

29
Q

ECG changes in intermeediate stage

A

myocardial necrosis present
absence of R wave
T wave inversions
pathological Q waves

30
Q

when are Q waves pathological

A

duration >0.04 seconds
amplitude >1/4 of the R waves
any Q wave in leads V1-3

31
Q

ECG changes in chronic stage

A

permanent scarring
persistent, broad deep Q waves
often incomplete recovery of R waves
permanent T-wave inversion is possible

32
Q

the HEART score

A

risk assessment for patients presenting to the ED with chest pain

33
Q

procedure for PCI

A

coronary angiography with PCI ie. baloon dilatation with stent implantation

34
Q

Fibrinolytic therapy is indicated if

A

PCI cannot be performed within 120 minutes of FMC
symptom onset <12 hours or 12-24 hours with clinical signs of ongoing ischaemia
no contraindications to fibrinolysis are present
PCI is still indictaed even after successful PCI

35
Q

regimens for fibrinolysis

A

Tenecteplase
Alteplase
Reteplase
Streptokinase

36
Q

absolute contraindications for fibrinolysis in STEMI

A

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)

37
Q

streptokinase is contraindicated when

A

there has been previous exposure to streptokinase within the last 6 months

38
Q

antiplatelet therapy and anticoagulation in STEMI

A

DAPT: Aspirin and
ADP receptor inhibitor (Prasugral, ticagralor or clopidogrel)
anticoagulation: unfractionated heparin, bivalirudin
glycoprotein inhibitor: consider adjunctive use of one of the following at time of primary PCI: abciximab, eptifiibatide, tirofiban

39
Q

antiplatelet therapy and anticoagulation in STEMI if not undergoing PCI

A

aspirin and clopidogrel
one of: unfractionated heparin, enoxaparin, fondaparinux
glycoprotein not routinely recommended

40
Q

are fibrinolytics indicated in NSTEMI

A

no

41
Q

invasive strategy for NSTEMI for very hgh to intermediate risk patients

A

coronary angiography within 2-72 hours

42
Q

ischaemia guided strategy for NSTEMI

A

for stable, low risk patients
non invasive cardiac stress testing eg. exercise ECG, stress echo) to evaluate need for coronary angiography

43
Q

antiplatelet therapy and anticoagulation for NSTEMI

A

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

44
Q

monitoring during ACS

A

continuous cardiac monitoring
serial 12 lead ECG every 15-30 minutes
serial serum troponin measurement every 1-6 hours

45
Q

adjunct medical therapy in ACS

A

nitrates
beta blockers
opioids
ACE inhibitors/ARBs
aldosterone agonists
high intensity statin

46
Q

acronym for MI management

A

MONA BASH

Morphine
Oxygen
Nitroglycerin
Antiplatelets (aspirin + ADP receptor inhibitor)
beta blockers
ACE inhibitors
Statins
Heparin

47
Q

oxygen therapy should be used for patients with

A

cyanosis
severe dyspnoea
SpO2 <90%

48
Q

fluid management

A

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

49
Q
A

int med 2024 (22 decks)

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