Week 5 - Case One Flashcards
what is acute coronary syndrome
an umbrella term for a spectrum of disease caused by ischaemia (and sometimes infarction) of myocardium (loss of blood supply to heart muscle)
it is a medical emergency and requires immediate hospital admission
what is a STEMI
ST elevation MI
how is a STEMI diagnosed
diagnosable on the basis of classical ECG changes
what is an NSTEMI
non-ST elevation MI
how is an NSTEMI diagnosed
usually diagnosed on the basis of a suggestive history, with positive biochemical markers e.g positive troponin
what is unstable angina
ischaemia, without infarction
how is unstable angina diagnosed
no obviously evident ECG changes (there may be some transient changes) , negative troponin, often a history suggestive of ACS. Unstable angina is significant due to the high risk of an MI in the subsequent 30 days.
why are these three conditions grouped together
because they all have a common mechanism, rupture or erosion of the fibrous cap of a coronary artery plaque
what is the textbook presentation of ACS
acute onset central or left sided chest pain, which often comes at rest, in the morning, gradually increasing in intensity over a period of minutes, radiates down the left arm, associated with diaphoresis and pre-syncopal or syncopal symptoms
what percentage of patients present without pain
30%
what is the most common cause of death in the UK
coronary heart disease
what is the epidemiology of MI
50% of deaths occur within 2 hours of onset of symptoms
15% of cases of MI are fatal
what is the incidence of CHD
300,000 cases per year
what is the non-modifiable aetiology
age
gender (male)
FD of IHD (only significant if symptoms presented before the age of 55 in relative)
what are the modifiable risk factors for CHD
Smoking
Hypertension
Diabetes
Hyperlipidaemia
Obesity
Sedentary lifestyle
how does cocaine use cause MI
acutely can cause coronary vasospasm which can cause MI
chronically increases the risk of MI from a traditional atherosclerotic disease process
describe the character of the chest pain seen in CHD
- can radiate down the inside of the arm, and into the neck and jaw and can last up to a couple of hours. may also radiate to the epigastrium or back
when is chest pain more predictive of an MI
if it radiates to both arms or the right arm
what type of pain is it typically described as
a crescendo pain with increasing severity over a period of several minutes after onset
typically a mid range pain e.g 5-7 out of 10
what are the 5 other symptoms associated with ACS, MI
diaphoresis
breathlessness
syncope
tachycardia
vomiting and sinus bradycardia
distress
what does syncope occur as a result of
occurs aș a result of severe arrhythmia or severe hypotension
why may vomiting and sinus bradycardia occur
as a result of excessive vagal stimulation, which is most common in inferior MI
what does sudden death usually occur from
ventricular fibrillation or systole.
why do most MI’s and strokes occur in the morning
because BP lowers during the night, and then rises again in the morning when the person wakes up.
this higher BP may then dislodge any thrombus that has formed over night
what factors are particularly signifiant for the likelihood of ACS compared to other causes of chest pain
Pain that radiates to the arms or jaw
Diaphoresis
Vomiting
Exertional chest pain
what features suggest non-ACS chest pain
reproducible chest pain (tender chest wall or positional pain)
pleuritic chest pain
what features are not useful to predict the likelihood of ACS
severity of pain
response to GTN
response to ant-acids / PPI’s
in what percentage of cases does MI present without pain
30%
what is this particularly important in
women
diabetics
the elderly
what are the symptoms associated with a silent MI
syncope
pulmonary oedema
epigastric pain
vomiting
acute confusional state
stroke
diabetic hyperglycaemia
what are the signs of impaired myocardial function
3rd / 4th heart sounds
Pan systolic murmur
Pericardial rub
Pulmonary oedema – crepitations in the lungs
Hypotension
Quiet first heart sound
Narrow pulse pressure (difference of <40mmHg)
Raised JVP
what are the signs of sympathetic activation
pallor (looking pasty)
- this can be generalised or localised, but is only really clinically significant if generalised. most evident in the palms and on the face.
sweating
tachycardia
what are the differentials for MI/ACS/CHD
Angina
Pericarditis
Myocarditis
Aortic dissection
Pulmonary
PE
Pneumothorax
Anything that causes pleuritic chest pain
Oesophageal
Oesophageal reflux
Oesophageal spasm
Tumour
Oesophagitis
what is the pathology behind an MI
almost always due to occlusive thrombus formation at the site of rupture or erosion of an atheromatous plaque
the pain experienced is usually the same as angina, but lasts longer and is more severe
when should patients call an ambulance
if they experience angina type pain, which after using a GTN spray does not subside within 15 minutes
what are the two different mechanisms of an MI
the fibrous cap of the plaque itself gets a superficial injury, and a thrombus forms on it
or
in more advanced, unstable plaques, the fibrous cap completely ruptures, and not only can some of the contents escape, but the blood can also enter the plaques, forming a thrombus within the remaining cap of the plaque
what do the platelets release and what does this cause
platelets then release serotonin and thromboxane A2 and this causes vasoconstriction in the area, resulting in reduced blood flow to the myocardium, and resulting in ischaemic injury
what is a transmural MI
this is an infarct that causes necrosis of tissue through the full thickness of the myocardium
what is a non-transmural MI
this is an MI that does not cause necrosis through the full thickness of the myocardium
what are the early ECG changes
peaked T wave (very tall T wave)
raised ST segment
what are the ECG changes within 24 hours
inverted T waves, this may or may not persist
ST segment returns to normal. Raised ST segment may persist if a left ventricular aneurysm develops
what are the ECG changes within days
Pathological Q waves form – these may resolve in 10% of cases
- We say the Q wave is pathological if it is >25% of the height of the R wave, and/or it is greater than 0.04s width (1 small squares) and/or greater than 2mm height (2 small squares)
- Q waves are also a sign of a previous MI – the changes in Q waves are generally permanent. The changes in T waves may or may not revert. The ST segment can return to normal within hours.
- Non-q-wave infarcts are infarcts that occur without the changes seen in the Q waves, but still with the ST and T changes.
what are the other patterns of ECG change
ST-depression
reciprocal change
what is reciprocal change
sometimes seen in STEMI.
This refers to a phenomenon whereby there is ST depression in some leads, in the presence of ST elevation in others. this occurs as the ECG leads are viewing the heart from different angles. the ST depression will typically occur in leads viewing the heart at the opposite angle to those showing ST elevation. The presence of reciprocal change is thought to indicate an earlier presentation of MI but is not particularly associated with different outcomes
what does ST depression show
ischaemia - the damage is reversible with the right treatment
what does ST elevation show
infarction - damage is irreversible
what are the ECG readings and troponin levels in a STEMI
ECG:
- ST elevation
or
- new LBBB
troponin:
- elevated
- dont wait for the result