Angina and myocardial infarctions Flashcards
What is stable angina often referred to?
‘Exercise-induced’ angina
What are the clinical presentations of stable angina?
Ischaemic chest pain caused by atherosclerotic plaques that cause narrowing of the lumen diameter of the arteries and reducing blood supply to the heart muscles. Meaning the oxygen demand can’t be met during periods of increased demand:
The chest pain becomes critical at a point of certain oxygen demand from the heart so usually presents itself when:
- Exercising
- Stressed
- After heavy meals
- In the presence of extreme temperatures
This chest pain is relieved by periods of rest, as the demand from the heart is decreased again
Also by use of sublingual glyceryl trinitrate (in tablet or spray form)
How can the chest pain caused by stable angina be reduced?
- Periods of rest- reducing the oxygen demand by the heart
- Sublingual GTN
What are the symptoms of stable angina?
Central, crushing chest pain
Pain may radiate to jaw, neck back or arms
is relieved by rest or GTN
What are the treatment guidelines/management options for stable angina?
FOR ACUTE ATTACKS:
- All patients should be given sublingual (under the tongue) Glyceryl trinitrate in the form of tablets or a spray
FIRST LINE TREATMENT:
- Anti-anginals- used to prevent attacks in the first place
1st line = Beta blockers or Calcium channel blockers
Add-on= long-acting nitrates e.g. Isosorbide mononitrate, Ivabradine, Ranolazine or Nicorandil
Secondary prevention- Prevent worsening of symptoms or cardiac events
Lifestyle changes;
smoking cessation
weight loss
diet
exercise
- Anti-platelet- Aspirin 75mg OD
- Statins- Atorvastatin 20-80mg OD
What conditions are covered in the umbrella term of Acute coronary syndrome?
Myocardial infarctions
- ST elevated (STEMI)
- Non-ST elevated (NSTEMI)
AND
- Unstable angina
Which three factors are used to differential diagnose between the three components of Acute coronary syndrome and other conditions?
- History of ischaemic chest pain- check is not gastro-related pain e.g. indigestion
- ECG changes
- Increased release in cardiac enzymes in blood tests results
What is the typical ECG abnormality in a patient who has had a STEMI?
- An elevation in the ST segment of the ECG trace
this is not seen in an NSTEMI or unstable angina!
What is the relevance of cardiac enzyme levels in differential diagnoses of ACS?
Troponin I (the more common isomer of the two) and Troponin T are enzymes that are released in the presence of cardiac muscle damage.
After a myocardial infarction, these enzymes after 2-4 hours, they will peak at 12 hours and can persist for up to 7 days ( beneficial for non-immediate diagnoses)
Levels will be measured on admission to hospital AND 3 hours later
If the increase in Troponin levels have increased to more than the 99th Percentile, they are indicative of a STEMI or NSTEMI
In unstable angina, there may be slight changes in levels, but nowhere near this 99 percentile increase criteria
other enzymes are also increased in the presence of a STEMI/NSTEMI but are not used for diagnosis due to lack of specificity
- Creatine kinase
- Aspartate transaminase (AST)
- lactate dehydrogenase (LDH)
Note that troponin levels can also be increased in other conditions e.g.:
pulmonary embolism
heart failure
chronic kidney disease
myocarditis
sepsis
What is the difference between a STEMI and a NSTEMI? (look for more detail online!!!!)
STEMI- the damage to the full thickness of cardiac muscle ( the whole depth= WORSE)
NSTEMI- Damage to partial thickness of cardiac muscle
Clinical features/ symptoms of NSTEMI/STEMI?
- Severe chest pain- sudden, constant, even at rest
- Not received by rest or sublingual GTN
- Sweating
- Breathlessness
- N+V
- Restlessness
- Pale/grey appearance
What are the symptoms and clinical manifestations of unstable angina?
- Sudden deterioration in anginal symptoms
- Chest pain- not relieved by rest or S/L GTN
- No ECG changes or changes in troponin levels
What are the immediate treatment steps for a STEMI?
- Oxygen- only if indicated- an oxygen saturation below 90%
- Diamorphine- used for pain relief (opioid).
However, also has other beneficial effects:
Anxiolytic effects- patients after MI are likely to be anxious
Vasodilatory- increased blood flow - Anti-emetic (anti-sickness), as opioid analgesics often cause N+V e.g. Cyclizine, Metoclopramide
- Aspirin- STAT dose of 300mg (may have already been administered prior to admission e.g. by paramedic or GP)
- A second anti-platelet
e.g. 300mg STAT clopidogrel
180mg STAT Ticagrelor
60mg STAT Prasugrel
AND primary percutaneous coronary intervention (PPCI)- This is the first line of management for a STEMI as has better outcomes and fewer contraindications than thrombolysis:
- Have an angiogram to assess where the blockage is, the causative clot is then removed by sucking it out with a radio-peque tube. Then a stent or angioplasty will be continued.
OR Thrombolysis:
- Breaks down the clot and reperfuses the area to minimise damage- Activates plasminogen to be concerted to the active form of plasmin. Plasmin then breaks down the fibrin network in the clot.
e.g. Alteplase, Recteplase, Tenecteplase
- need to give heparin for first 48 hours after thrombolysis- to prevent further clot formation
both thrombolysis and PPCI need to be done URGENTLY
What is the treatment for secondary prevention following a STEMI (+ their durations)?
NEED FIVE DRUGS!
1+2: DUAL-ANTIPLATELET THERAPY
1. Aspirin
2. Clopidogrel or Ticagrelor or Prasugrel
dual-therapy for 12 months and then stop clopidogrel/ticagrelor/prasugrel
Aspirin continued for life
3: BETA-BLOCKER- review after 12 months, it may be stopped ( if have heart failure will definitely be continued)
4: ACE-INHIBITOR- for life
5: STATIN- Atorvastatin 80mg OD
AND lifestyle changes:
- Smoking cessation
- Weight loss
- Improve diet to be more balanced and healthy
- Increased exercise and physical activity
What are the immediate treatment steps for a NSTEMI or presentation of unstable angina?
THESE STEPS ARE THE SAME AS THAT OF A STEMI (+ Fondaparinux) and (- thrombolysis or ppci):
- Oxygen- only if indicated- an oxygen saturation below 90%
- Diamorphine- used for pain relief (opioid).
However, also has other beneficial effects:
Anxiolytic effects- patients after MI are likely to be anxious
Vasodilatory- increased blood flow - Anti-emetic (anti-sickness), as opioid analgesics often cause N+V e.g. Cyclizine, Metoclopramide
- Aspirin- STAT dose of 300mg (may have already been administered prior to admission e.g. by paramedic or GP)
- A second anti-platelet
e.g. 300mg STAT clopidogrel
180mg STAT Ticagrelor
60mg STAT Prasugrel
AND give Fondaparinux- A factor Xa inhibitor that prevents the formation of any new blood clots
Given via an injection until stable
NO thrombolysis or PPCI
