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Flashcards in ACS Deck (10):
1

What is acute coronary syndrome, and what is the difference between stable angina and ACS?

Acute coronary syndrome is the general term given to a STEMI, NSTEMI or unstable angina when there has not yet been a diagnosis of the cause of anginal chest pain at rest. In all forms of ACS, atheromatous plaques rupture, causing thrombosis and platelet aggregation, which causes further acute obstruction of the vessel. In a STEMI/NSTEMI this causes muscle infarction whereas in Unstable angina his only causes ischaemia.

2

What are the causes of ACS/MI

Most common - Atherosclerotic plaque rupture

Others: Emboli, Coronary Spasm, Vasculitis

3

What will you ask/find out in a history taking of ACS/MI?

Symptoms:
Chest Pain
Systemic (Due to sympathetic response) - Sweating, Pallor, Nausea, Collapse, SOB, Anxiety
Diabetic/Elderly/Hypertensive/Post-operative patients can have a "silent MI" where they feel no or less pain and only the systemic symptoms. This is due to loss of sympathetic nerve supply to heart due to neuropathy

Risk Factors:
Cardiovascular risk factors
History of angina
Cocaine Use

Specific questions to ask in a history taking:
Ask about contraindications to Thrombolysis - Recent haemorrhagic stroke, Head trauma, Bleeding disorder, Recent Internal bleeding, previous streptokinase use
Recent Stress levels - May precipitate the MI
Assess start times etc as this can affect management

Differentials:
Stable Angina - Relieved by GTN or rest, there will be no ECG changes and no rise in troponin
Pericarditis – Pain dependant on position (Worse lying flat better on leaning forward), global ST elevation on ECG
Aortic Dissection - Immediate onset of pain (Not over a few minutes), Radiates to back, Tearing type pain
PE - SOB, Risk factors for PE e.g. Cancer, Recent long-haul flight
Reflux - Associated with food, relieved by antacids, pain less severe
Pneumothorax - SOB, absent chest sounds on one side, pain is pleuritic
MSK pain - Pain very well localised, history of trauma, often costochondritis on the left side, worsened by movements
Pancreatitis - Epigastric Pain that radiates to back, no ECG changes and history of alcohol use or gallstones


4

What will you look for/find out in an examination of a patient with ACS/MI?

End of the Bed:
Patient will look acutely unwell
Sweating, Shock, Pale, Confused
Hands:
Tachycardia –Part of the sympathetic response
Arrhythmias – Tachycardia/Bradycardia can result from AV node ischemia
Blood Pressure - Hypertension (Part of the sympathetic response) or Hypotension (Cardiogenic Shocks caused by ischemia to heart muscle)
Unequal Pulses – Think aortic dissection
Poor Peripheral Pulses – Shock
Chest:
S3/S4 Heart Sound- Poor cardiac muscle compliance of the infarcted muscle
Scars from previous cardiac surgery
Valve Lesions -Commonly Mitral regurgitation (Post MI due to papillary muscle tear)
Legs:
Poor Peripheral Pulses - Shock

5

What investigations are used for an MI?

Bedside:
ECG – Looking for ST changes or Arrhythmias
Capillary Glucose – To assess cardiovascular risk and can get hyperglycaemia as the result of an MI

Bloods:
Troponin, on arrival and at 3 hours – Only rising in myocardial infarction so differentiates UA and NSTEMI (A rise > 30 ng/ml after 3 hours is significant)
FBC - Assess for any precipitating anaemia or infection
U&E - Will give many nephrotoxic drugs and contrast used in angiogram
LFT - Assess before use of a statin
Lipids - Assess cardiovascular risk
Clotting - Patient will likely need a stent
Creatinine Kinase at admission and 12 hours- To work out grace score
Amylase – Rules out pancreatitis

Imaging:
CXR - Used to exclude differential e.g. Pneumothorax/Aortic Dissection and assess current cardiac function e.g. Heart Failure
Coronary Angiogram - Diagnostic imaging test
Echo - Regional wall motion abnormality seen on areas of infarcted tissue

6

What ECG changes are seen on an MI and what are the some differentials for ST elevation?

STEMI – ST elevation, Tall T waves, New LBBB, T wave inversion or pathological Q waves after a few hours
NSTEMI - ST Depression, T wave inversion, Pathological Q waves, can be normal or show nonspecific changes

Regions of the heart: An MI will affect one or more territories of the heart, if the change do not then consider another cause for the changes
V1, V2 - Septal View (LAD supply - Branch of left coronary)
V3, V4 - Anterior View (LAD supply - Branch of left coronary)
V5, V6, 1, AVL - Lateral View (Circumflex Artery - Branch of left coronary)
V1-V6, 1, AVL – Extensive Anterior (Left Coronary Artery)
2, 3, AVF (+/- Tall R in V1) - Inferior View (Right Coronary Artery)

Differentials of ST elevation on an ECG:
Old infarction
Pericarditis
Physiological
Bundle branch block
Hyperkalaemia

7

What is the Emergency management of ACS

Resuscitation:
A-E approach
Get IV Access/Give O2 to maintain saturations of 94+ /Attach 12 lead ECG
Assessment with AMPLE history and brief examination
Get help - Cardiovascular Registrar
Frequent Observations – Constant monitoring
Patient may be in cardiogenic shock – Treat with fluid challenge or inotropic support Dobutamine IV

Medical:
MONAV – Morphine, Oxygen, Nitrate, Aspirin, VTE prophylaxis
Morphine + Metoclopramide
Controlled Oxygen Therapy
GTN and Nitrates
Aspirin and Clopidogrel
VTE prophylaxis -Use unfractionated heparin as better in patients who are going to undergo PCI (Can use LMWH if not doing PCI)
Hyperglycaemia is common - Check blood glucose and keep <11mmol/L. This may require insulin sliding scale

Specific Treatment for STEMI:
PCI (re-vascularisation of blocked vessel (seen on angiography) with an expandable metal stent through femoral artery) if available within 2 hours of medical contact (No more than 2 hours since thrombolysis could have been given) and within 12 hours of the start if the MI
Thrombolysis (e.g. Alteplase) if not available within 2 hours, likely followed by PCI a few days later.
If PCI fails, then do a CABG.

Specific Treatment for NSTEMI:
Assess the grace score – Used to assess risk
High risk (>3%) – Glycoprotein 2b/3a inhibitor + coronary angiography with cardiologist review to assess for PCI
Low risk – Start chronic management

Specific Treatment for Unstable Angina:
Reduce CVS risk factors – Start chronic management
Unstable angina is a good indicator of impending MI - May be treated with PCI

8

What is the chronic management of ACS?

Lifestyle:
Education on the red flag symptoms for another MI and when to seek medical help
Reduce cardiovascular risk factors
Cardiac rehab programme referral – Exercise and lifestyle management
Notify DVLA that unable to drive for 4 weeks. HGV drivers need an exercise stress test and a consulatnat review to ascertain suitability to return to work

Medication:
BAASH – Betablockers, Ace inhibitors, Anti Platelet, Statin, Heparin (Until the patient is ambulatory again)
B-Blocker - titrated up to highest max dose tolerable
Ace inhibitor - titrated up to highest max dose bearable
Anti-platelet therapy- Aspirin lifelong and Clopidogrel (For 12 months) with a PPI for the aspirin
Atorvastatin - Highest dose tolerated
LMWH + NOAC (Abciximab) till discharge
PRN GTN for pain control if PCI was not done

9

What scoring system is used for ACS?

Grace score - Estimates admission/6-month mortality for patients with acute coronary syndrome
Age
Pulse
BP
Creatinine Kinase
Cardiac Arrest on admission
ST segment deviation
Abnormal cardiac enzymes
Heart failure symptoms

10

What are the main complications on an MI?

The commonest cause of early death in acute myocardial infarction is an electrical dysrhythmia - typically ventricular tachycardia or ventricular fibrillation.
Aneurysm
Rupture of the papillary muscles or wall
Heart failure
Dressler’s Syndrome (Pericarditis)