Ischaemic heart disease (angina pectoris, ACS, MI) Flashcards
Define stable angina.
Chest pain resulting from myocardial ischaemia that is precipitated by exertion and relieved by rest.
What are the causes of stable angina? (include different types)
- Atherosclerotic disease (most common)
- Rare types of angina:
- Decubitus angina - symptoms occur when lying down
- Prinzmetal angina - symptoms caused by coronary vasospasm
- Coronary syndrome X - symptoms of angina but normal exercise tolerance and normal coronary angiograms
What is the conservative and medical management of stable angina?
Conservative:
- Stop smoking
- Lose weight
- Exercise
- Cardioprotective diet
- Limit alcohol
Medical:
- Short acting nitrate - GTN spray - use before exercise or during pain, repeat as needed in 5mins. SE: flushing, headache, lightheadedness
- 2nd line: long acting nitrate e.g. isosorbide mononitrate, nicorandril, ivabradine
- BB/CCB - reduces symptoms
- Antiplatelet - aspirin 75mg OD (2nd line clopidogrel)
- ACEi - risk reduction if hypertensive, with HF, LV dysfunction, CKD, DM.
- Statin - if appropriate
When should you not start ivabradine?
If HR <70 bpm
Define acute coronary syndrome and name the 3 types.
ACS - a constellation of symptoms caused by sudden reduced blood flow to the heart muscle
3 types:
- Unstable angina pectoris
- NSTEMI
- STEMI
Define unstable angina pectoris.
Chest pain at rest due to ischaemia without cardiac injury
What are the signs and symptoms of ACS?
ACS all present the same.
Signs and symptoms:
- Acute onset
- Central, crushing chest pain
- Radiates to arms/neck/jaw
- Pallor
- Sweating
- NB: can be SILENT in elderly, diabetics, women
What investigations would you do for ACS?
- ECG
- Troponins
Other:
- FBC - low Hb could precipitate angina
- lipid profile - normal or increased total cholesterol and LDL
- CXR - patients with HF show pulmonary oedema; excludes alternative diagnosis or triggers of chest pain (aortic dissection-wide mediastinum; hyper-lucent area-PE; wedge shaped infarct-pulmonary infarction; consolidation-pneumonia; collapsed lung-pneumothorax; air under diaphragm-perforated viscus)
- ECHO (rest/stress) - wall motion abnormalities
- CT chest/MRI - exclude PE and aortic dissection
- coronary angiography - stenosis of coronary artery (allows concurrent treatment with angioplasty and stenting)
What are the ECG and troponin results in the 3 types of ACS?
ECG:
- STEMI - ST elevation, hyperacute T waves, new-onset LBBB
- NSTEMI and unstable angina - ST depression, T wave inversion
- Heart block =AV node involved; old infarcts = pathological Q waves.
Troponins:
- STEMI + NSTEMI - elevated troponins showing myocardial injury
- unstable angina - IS DEFINED by absence of biochemical evidence of myocardial damage
How does an old infarct present on ECG?
Pathological Q waves
What are the coronary arteries supplying the heart?
Important:
- LAD = ANTERIOR infarct
- LC = LATERAL infarct
- RCA = INFERIOR infarct
- PD = POSTERIOR infarct
Which leads will show ST elevation when the occluded artery is:
- right coronary
- left anterior descending
- left circumflex
- posterior descending (not ST elevation)
RCA = inferior = II, III, avF
LAD = anterior = V1-V4
LC = lateral = I, aVL, V5/6
PD = tall R wave, ST depression in V1-V3
What is the GENERAL management of ACS?
MONABAS(H)
- Morphine
- Oxygen
- Nitrates
- Antiplatelets (aspirin and clopidogrel)
- Beta-blockers
- ACE inhibitors
- Statins
Not heparin unless PCI
After general management, how do you manage STEMI?
Refer to cardiology
Arrange for PCI
Aspirin 300mg ASAP (check if ambulance given)
Oxygen - if <94%
Ticagrelol 180mg loading (or P2Y12 inhibitor)
Morphine IV with metoclopramide IV
Get patient to PCI quickly
Contact ITU/anaesthetic in case of needing bed
If delay in PCI consider thrombolysis
For discharge:
- Beta blocker
- ACEi
- High dose statin
- Dual antiplatelet e.g. aspirin and clopidogrel
-
4 pillars of HF with LF dysfunction following MI:
- ARNI (sacubitril/valsartan) OR ACEi
- BBI
- Aldosterone antagonist e.g. spironolactone or eplerenone
- SGLT2 inhibitor e.g. dapagliflozin
Patient cannot drive for 4 weeks after PCI
What medication should you send the patient home with?
- Clopidogrel 75mg O
- Atenolol 50mg OD
- Ramipril 10mg OD
- Aspirin 75mg OD
- Simvastatin 40-80mg OD
The NICE guidelines for the secondary prevention of MI recommend that all patients should be offered an ACEi, dual antiplatelet therapy, a beta-blocker and a statin.
How do you manage NSTEMI?
Anti-anginal
- GTN infusion if SBP>110mmHg
- Beta blockers e.g. bisoprolol
- DHP CCB e.g. amlodipine
+/- Oxygen
Morphine + metoclopramide
Aspirin 300mg
P2Y12 inhibitor (e.g. clopidogrel, ticagrelor)
Anticoagulation e.g. Fondaparinux (Xai) and/or LMWH. NB: they will need to have the LMWH in addition if undergoing PCI.
Coronary angiography/revascularisation + GRACE score -
- Consider immediate PCI if intermediate or high risk scores (score of >109 or >140 GRACE >3%) or haemodynamic instability or other complications.
- Consider non-invasive testing (imaging) if low risk before invasive evaluation
How much aspirin is given in acute MI?
300mg stat
What scoring system is used to predict mortality from ACS?
GRACE score - risk stratification for intervention and 6-month mortality calculator for ACS
What are the complications of ACS?
DARTH VADER
- Death
- Arrhythmia
- Rupture
- Tamponade
- Heart Failure
- Valve disease
- Aneurysm
- Dressler’s syndrome
- Embolism
- Reinfarction
What is Dressler’s syndrome?
Dressler’s syndrome is a type of pericarditis — inflammation of the sac surrounding the heart (pericardium). Dressler’s syndrome is believed to be an immune system response after damage to heart tissue or to the pericardium, from events such as a heart attack, surgery or traumatic injury
When should you use anticoagulants vs antiplatelets?
Can you use warfarin in ACS?
No because initially it is pro-thrombotic - it blocks protein C and protein S.
Therefore heparin must be co-administrated with warfarin to begin with, until the INR stabilises (between 2-3)
Explain the findings of this ECG.
There is ST elevation most pronounced in V2-V5, but also to a lesser extent in the lateral leads I and aVL.
Note that there is ‘reciprocal’ ST depression in leads III and aVF.
In the context of acute chest pain, the ECG findings are unequivocal and diagnostic of acute anterolateral myocardial infarction.
What is shown?
Acute pulmonary oedema secondary to myocardial infarction.
- Bibasal pleural effusions
- Heart is enlarged
Is this….
- anteroseptal MI
- anterolateral MI
- S1, Q3, T3 of PE
Anterolateral - ECG findings:
- ST segment elevation leads V2, V3 and leads I and aVL,
- pathological Q wave V2,
- reciprocal ST segment depression I leads, II, III and aVF.
Diagnosis: acute anterior myocardial infarction with lateral extension (acute anterolateral MI).
Which 5 treatments should you give first to a person with acute MI?
- IV opiates- morphine 10mg (titrate up as necessary)
- High flow oxygen (only if sats are below expected range)
- Sublingual GTN
- Oral aspirin 300mg
- IV metoclopramide 10mg (antiemetic)
What is shown on this ECG?
- Sinus rhythms
- Normal axis
- Ventricular ectopics
- Anterior MI
- First degree heart block
What could a new onset LBBB indicate?
New LBBB could indicate a new full thickness MI and hide the MI below it. High probability if chest pain also present.
NB:
RBBB – look at V1 – if wide and upgoing complexes = RBBB
LBBB = wide and predominantly downgoing V1 complexes
Complications of MI with time.
What is SALI?
Views of the heart on the ECG
What is the normal cardiac axis?
-30 to +90
What is the benefit gained from statins in terms of increase in life expectancy?
7% of people on statin will gain 7 years (99months)
93% of people will not benefit at all
What % of men in the UK will undergo a cardiovascular event (angina, myocardial infarction, stroke) during their life?
33% of men (1 in 3)
25% of women (1 in 4)
Per mmol/L reduction in LDL in those on lipid lowering drugs, what is the relative reduction in cardiovascular events?
10% per 1mmol/L of LDL reduction
What are the main side effects of beta blockers?
Fatigue/lethargy
Insomnia and nightmares
Worsening claudication or asthma
Impotence and erectile dysfunction
Which medication is best for vasospastic angina?
CCB - verapamil and diltiazem
NB: BB could worsen symptoms by increasing coronary vasomotor tone.
Why is the combination of BB and CCB mutually beneficial?
CCB would cause a reflex tachycardia due to peripheral vasodilation
BB prevent the tachycardia
NB: diltiazem and verapamil also slow HR so should not be used with BB (unless prescribed by expert)
What are the side effects of CCB?
Hypotension
Peripheral oedema e.g. ankle swelling in amlodipine
Cardiac decompensation
Constipation
Headache
Flushing
Dizziness
What are the C/I to CCB use?
Decompensated heart failure
Diltiazem/verapamil should not be used in bradycardias, AV block or sick sinus syndrome
What is the issue with nitrate use chronically?
Nitrate tolerance - must have a 8-12hr nitrate free period daily
What are the side effects of nitrates?
Headache
Hypotension
Presyncope/syncope
C/I in outflow tract obstruction.
Simply, what are the complications of left vs right MI?
Right MI will cause rhythm disturbances
Left MI will cause heart failure because the left coronary artery supplies so much of the anterior heart
What long-term complication of MI is shown?
LV aneurysm - causes persistent ST elevation
What is a type 2 MI? How does it present?
Subendocardial MI
No Q waves and hypotension
Anterior STEMI
Does this patient need a pacemaker?
No
There is no arrhythmic problem
LMS + multi-vessel disease
LMS + multi-vessel disease - ST depression in II, III, aVF and in V4-6. Some ST elevation in AVR.
Anterolateral NSTEMI because extending V3-6
AF
Does this patient need a pacemaker?
Pacemakers usually not used for tachycardias but bradycardias.
What is Wellen’s syndrome?
ECG finding of deeply inverted or biphasic waves in V2-3 in a person with the previous history of angina= Wellen’s syndrome.
This is highly specific for a critical stenosis of the left anterior descending artery
