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1ST YEAR SYSTEMS: Cardiovascular > Acute coronary syndromes: presentation, management and treatment > Flashcards

Acute coronary syndromes: presentation, management and treatment Flashcards

1
Q

what is the 2nd most common cause of death in Scotland?

A

Heart disease

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2
Q

What is an Acute Coronary Syndrome?

A

Any sudden event suspected or proven to be related to a problem with the coronary arteries. ie Spontaneous plaque rupture & local thrombosis, with degrees of occlusion Problems arise due to myocardial ischaemia (reduction in the blood supply to the heart muscle) ie unstable angina, NSTEMI and STEMI

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3
Q

what is cardiac arrest? (4)

A

Abnormal heart rhythm not compatible with life - Ventricular fibrillation or tachycardia - Asystole Can occur during the acute phase of an MI Can occur late after an MI Can be unrelated to an MI

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4
Q

example of a chronic ischaemic heart disease

A

stable angina

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5
Q

examples of acute coronary syndromes? (2)

A

unstable angina myocardial infarction - STEMI (full thickness damage of heart muscle - transmural, more serious) or Non STEMI (subendocardial - partial thickness)

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6
Q

complete coronary occlusion causes what changes on an ECG initially and at 3 days?

A

ST elevation Q waves

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7
Q

partial coronary occlusion causes what changes on an ECG initially and at 3 days?

A

no ST elevation no Q waves

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8
Q

what is a transmural MI

A

a myocardial infarction that involves the full thickness of the myocardium STEMI

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9
Q

diagnosis of myocardial infarction

A

Detection of cardiac cell death/injury: +ve cardiac biomarkers AND one of: - symptoms of ischaemia - new ECG changes - evidence of coronary problem on coronary angiogram or autopsy - evidence of new cardiac damage on another test

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10
Q

what are cardiac biomarkers

A

Cardiac biomarkers are substances that are released into the blood when the heart is damaged or stressed. Measurements of these biomarkers are used to help diagnose acute coronary syndrome (ACS) and cardiac ischemia, conditions associated with insufficient blood flow to the heart.

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11
Q

Name some cardiac biomarkers

A

cardiac troponin - 2 types, 1 in STEMI 1 in NSTEMI myoglobin CK-MB

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12
Q

non-coronary causes of a troponin rise? (6)

A

Pulmonary embolism Cardiac contusion Anaemia Sepsis Renal failure Sub-arachnoid haemorrhage - burst blood vessel in the brain

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13
Q

types of MI

A

Type 1,2,3,4a,4b and 5 1 - spontaneous MI 2- imbalance of O2 supply/demand 3- sudden cardiac death 4a- MI associated with percutaneous coronary intervention 4b- associated with verified stent thrombosis via angiography or autopsy 5- MI associated with CABG

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14
Q

spontaneous MI can be due to what types of things?

A

atherosclerosis (but not always) Coronary vasospasm - cocaine, triptans (anti-migraine medication), 5-FU (chemotherapy) Coronary dissection - often younger, healthy females Embolism of material down coronary artery - thrombus or a tumour Inflammation of coronary arteries (vasculitis) Previous radiotherapy to chest causing fibrosis and stenosis of coronary arteries

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15
Q

MI typical history

A

Chest pain - may radiate to neck/arm - often they deny it is a “pain”, more a “discomfort” - Severe, but not “agony” - May be associated with nausea, sweating, breathlessness

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16
Q

cardiac risk factors (8)

A

Male Age Known heart disease Known high blood pressure High cholesterol Diabetes Smoker Family history of premature heart disease

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17
Q

Examination for ACS

A

May look very unwell or completely fine Often no specific features to find Ensure that you check: HR, BP Listen for murmurs, crackles in chest

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18
Q

key investigations for ACS

A

ECG bloods FBC - U&E, Glucose, lipids, cardiac enzymes CXR - cardiomegaly ECHO - regional wall abnormalities

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19
Q

what are hyperacute T waves

A

seen in transmural ischaemia (complete occlusion) are broad-based and symmetrical (normally asymmetric- sharper decline) usually with increased amplitude often associated with a depressed ST take off Almost always seen in conjunction with ST segment elevation

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20
Q

what are the T waves like in partial coronary occlusion

A

T wave inversion or may be normal ST depression

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21
Q

Problems in L anterior descending coronary artery causes what type of MI?

A

anterior MI

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22
Q

Problems in circumflex coronary artery causes what type of MI?

A

lateral MI - easily missed as may be little ECG change

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23
Q

posterior MI

A

easily missed because no ECG leads on chest usually the posterior wall is supplied b ythe RCA - see some inferior ST elevation left circumflex may supply posterior wall - may not see any ST elevation

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24
Q

posterior ECG leads

A

posterior myocardium is not directly visualised by the standard 12-lead ECG take the 6 anterior leads off and replace with V7, V8, V9

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25
Q

inferior ST depression on ECG (dip in ST) could be caused by what?

A

NSTEMI or unstable angina

26
Q

reperfusion therapy options (2)

A

mechanical - in cath lab - PCI (Angioplasty, also called percutaneous coronary intervention) pharmacological

27
Q

thrombolysis bolus is called

A

tenecteplase

28
Q

risks of thrombolysis (3)

A

used in more severe cases - if you can’t get to a cath lab Bleeding Don’t give if recent stroke, ever had a previous intracranial bleed Caution if recent surgery, on warfarin, severe hypertension

29
Q

if you’re having a STEMI and can get to a cath lab in 2 hours then what should you do?

A

transfer to cath lab for primary PCI

30
Q

if you’re having a STEMI and can’t get to a cath lab in 2 hours then what should you do?

A

Thrombolysis and then transfer

31
Q

Describe typical patient with NSTEMI

A

Compared to STEMI, patients tend to be: older more likely to have previous MI/CABG/PCI more likely to have other medical problems May not be such a clear, obvious “coronary” presentation Could be type 2 MI (imbalance of O2 s+d) in a 85 year old with anaemia and pneumonia

32
Q

troponin will NOT be elevated in which condition

A

unstable angina

33
Q

describe unstable angina

A

Convincing anginal symptoms Rapidly worsening (crescendo history) Occurring at rest ECG may be normal or abnormal NO cell death so troponins will NOT be raised

34
Q

general management of suspected ACS

A

Admit to hospital Cardiac monitor Give O2 only if levels low

35
Q

Investigations carried out for ACS (2)

A

ECGs Repeat if not sure about changes Consider doing posterior leads Blood tests Check troponin Now can do immediate “Point of Care” test Also check Hb, kidney function, cholesterol

36
Q

Treatment for ACS:

A

To manage chest pain:

  • Glycerol trinitrate (GTN) - Vasodilator - opens up coronary arteries - Can give sub-lingual or as intravenous infusion - no releif if STEMI
  • Opiates (eg morphine) - Helps relieve anxiety. Also venodilator

Optimise cardioprotective treatments:

  • Antiplatelets - aspirin, clopidogrel
  • Anticoagulate
  • B blockers - reduce myocardial O2 demand
  • ACE inhibitors
  • High-dose statin - lower cholesterol

Revascularisation:

  • STEMI and high risk NSTEMI - angioplasty
  • If multi vessel damage - CABG instead
37
Q

anti-thrombotic drug options

A

anti platelet (usually dual):- Aspirin and an ADP receptor blocker: clopidogrel ticagrelor check that they’ve not been sick anti-coagulant:- subcutaneous heparin LMWH - Low-molecular-weight heparin Fondaparinux

38
Q

other drugs used to treat ACS

A

beta blockers - reduce work the heart has to do statin - cholesterol lowering drugs ACE inhibitors - help heart muscle recover

39
Q

coronary angiography after NSTEMI

A

Ideally do angio within 48 hours Can use a risk calculator to assess whether should have angio

40
Q

coronary artery bypass is used for which heart diseases

A

Three vessel disease Left main stem disease Disease not amenable to PCI

41
Q

management of ACS in hospital

A

Now often home within 3-4 days Keep attached to monitor for first 24-48 hours Get an echo - shows size of wall motion abnormality and whether hypokinetic or akinetic; overall contractility, degree of mitral regurgitation. Presence of mural thrombus - form in the heart or aorta. Also ocheck for LV function Listen for murmurs and signs of heart failure every day

42
Q

mechanical complications with following an MI

A

rupture of infarcted myocardium Acute Ventricular Septal Defect Mitral valve dysfunction due to papillary muscle rupture

43
Q

how can a stent cause thrombosis

A

Takes a period of time for a stent to become endotheliesed ie “embedded” into coronary artery wall During that time, the blood is exposed to the metal stent and could thrombose, blocking off the stent unless on anti-platelet drugs Need anything from 1 month to 12 months of dual anti-platelet therapy (DAPT) Premature discontinuation of DAPT may be fatal

44
Q

ST elevation suggests what

A

a blocked coronary artery and ongoing myocardial cell death need to open a coronary artery ASAP

45
Q

how do ACS symptoms contrast with stable angina?

A

ACS symptoms will almost always be at rest SA are only on exertion

46
Q

history of stable angina vs NSTEMI

A

Unstable Angina-angina on effort, but of progressive, increasing frequency and severity, often provoked by less exertion and/or then at rest. NSTEMI will much more often start with myocardial ischaemic symptoms occurring at rest.

47
Q

atypical ACS presentation is found often in whom?

A

women the elderly diabetics

48
Q

immediate treatment of unstable angina and NSTEMI

A

ABCDE approach then MONA morphine O2 nitroglycerin (GTN) aspirin

49
Q

Angiotensin converting enzyme inhibitors used if what is present?

A

L ventricular dysfunction

50
Q

options for opening infarct related artery?

A

primary PCI (better) fibrinolysis

51
Q

when is fibrinolytic therapy opted for

A

treatment of choice when PCI cannot be performed Pre-hospital fibrinolysis significantly reduces ‘call for help-to-needle’ compared with in-hospital administration

52
Q

fibrinolytic therapy and clear increased risk of bleeding & intra-cranial haemorrhage in some patients:

A

Age > 75 Female sex Previous stroke Low body weight (F<65 kg, M<70 kg) SBP > 160 mmHg INR > 4 Chronic kidney disease & elevated creatinine

53
Q

ACS secondary prevention

A

General measures: stop smoking, diet, exercise etc Co-morbidities: control BP, glycaemic control etc. Aspirin and clopidogrel (for one year only) beta-blockers (to heart rate <60bpm) Statins (to LDL-c <3.2mmol/l, Total-c 5 mmol/l) Angiotensin converting enzyme inhibitors (always if left ventricular dysfunction, probably if “normal” function) ramipril 5mg BiD or equivalent.

54
Q

sudden cardiac death often caused by what?

A

VT or VF As an ACS, the atherothrombotic event causes acute myocardial ischaemia and subsequent sufficient electrical disturbance to cause ventricular arrhythmia. Not all SCDs or aborted SCDs are ACS events.

55
Q

ventricular fibrillation

A

Defibrillation the only effective treatment for VF arrest. VF tends to rapidly deteriorate into asystole. Asystole more difficult to restore CO Rapid & effective team work in resuscitation efforts is essential to give optimal chance of success.

56
Q

2 main groups of immediately life threatening complications of acute MI?

A

Mechanical complications Ventricular arrhythmic complications both need urgent intervention

57
Q

free wall rupture

A

type of mechanical complication Occurs at the edge of the infarcted area. Leads to haemopericardium and acute tamponade

58
Q

ECG signs of VF

A

P-waves and QRS complexes are not present Heart rhythm is highly irregular The heart rate is not defined (without QRS complexes)

59
Q

STEMI: Signs, symptoms, diagnosis/investigation, management

A

Signs:

  • No GTN relief
  • Distress/anxiety
  • tachycardia
  • HF

Symptoms:

  • Severe chest pain >20 mins, left arm, neck or jaw
  • SOB
  • Fatigue
  • pre-syncope
  • syncope
  • nausea/sweating
  • palpitations

diagnosis/investigation:

  • ECG - tall T waves, ST elevation
  • CXR - cardiomegaly, pulmonary oedema
  • FBC
  • Cardiac biomarkers - raised troponin levels

management: - Emergency!

  • PCI or thrombolysis if they can’t get that
  • Aspirin and clopidogrel, Morphine, O2
  • Beta blockers
  • Consider CABG
  • opiates
60
Q

NSTEMI: Signs, symptoms, diagnosis/investigation, management

A

Signs:

  • ECG - no ST elevation

Symptoms:

  • Severe chest pain >20 mins, left arm, neck or jaw
  • SOB
  • Fatigue
  • pre-syncope
  • syncope
  • nausea/sweating
  • palpitations

diagnosis/investigation:

  • ECG - repeated
  • CXR - cardiomegaly, pulmonary oedema
  • FBC
  • Cardiac biomarkers - raised troponin levels
  • GTN trial

management:

  • Aspirin and clopidogrel
  • Beta blockers/ CCB
  • GTN
  • ACEI if hypertensive
  • LMW heparin
  • Coronary angiography
61
Q

Unstable angina: Risk factors. signs, symptoms, diagnosis/investigation, management

A

Risk factors:

  • Female
  • CAD
  • Smoking
  • Age
  • Diabetes
  • Hypertension

Signs:

  • ECG - ST depression or normal
  • 4th heart sound
  • Carotid bruits - murmur due to stenosis

Symptoms:

  • Chest pain - increased freq, severity and duration
  • Pain radiating to jaw/arm
  • SOB

Diagnosis/investigation:

  • ECG
  • Cardiac biomarkers - Troponin
  • CXR/CT/MRI

Management:

  • Aspirin/clopidogrel
  • Statin
  • B blocker
  • ACEI
  • cardiac rehab

1ST YEAR SYSTEMS: Cardiovascular (39 decks)

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