Week 5 - Case One Flashcards
1
Q
what is acute coronary syndrome
A
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
2
Q
what is a STEMI
A
ST elevation MI
3
Q
how is a STEMI diagnosed
A
diagnosable on the basis of classical ECG changes
4
Q
what is an NSTEMI
A
non-ST elevation MI
5
Q
how is an NSTEMI diagnosed
A
usually diagnosed on the basis of a suggestive history, with positive biochemical markers e.g positive troponin
6
Q
what is unstable angina
A
ischaemia, without infarction
7
Q
how is unstable angina diagnosed
A
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.
8
Q
why are these three conditions grouped together
A
because they all have a common mechanism, rupture or erosion of the fibrous cap of a coronary artery plaque
9
Q
what is the textbook presentation of ACS
A
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
10
Q
what percentage of patients present without pain
A
30%
11
Q
what is the most common cause of death in the UK
A
coronary heart disease
12
Q
what is the epidemiology of MI
A
50% of deaths occur within 2 hours of onset of symptoms
15% of cases of MI are fatal
13
Q
what is the incidence of CHD
A
300,000 cases per year
14
Q
what is the non-modifiable aetiology
A
age
gender (male)
FD of IHD (only significant if symptoms presented before the age of 55 in relative)
15
Q
what are the modifiable risk factors for CHD
A
Smoking
Hypertension
Diabetes
Hyperlipidaemia
Obesity
Sedentary lifestyle
16
Q
how does cocaine use cause MI
A
acutely can cause coronary vasospasm which can cause MI
chronically increases the risk of MI from a traditional atherosclerotic disease process
17
Q
describe the character of the chest pain seen in CHD
A
- 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
18
Q
when is chest pain more predictive of an MI
A
if it radiates to both arms or the right arm
19
Q
what type of pain is it typically described as
A
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
20
Q
what are the 5 other symptoms associated with ACS, MI
A
diaphoresis
breathlessness
syncope
tachycardia
vomiting and sinus bradycardia
distress
21
Q
what does syncope occur as a result of
A
occurs aș a result of severe arrhythmia or severe hypotension
22
Q
why may vomiting and sinus bradycardia occur
A
as a result of excessive vagal stimulation, which is most common in inferior MI
23
Q
what does sudden death usually occur from
A
ventricular fibrillation or systole.
24
Q
why do most MI’s and strokes occur in the morning
A
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
25
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
26
what features suggest non-ACS chest pain
reproducible chest pain (tender chest wall or positional pain)
pleuritic chest pain
27
what features are not useful to predict the likelihood of ACS
severity of pain
response to GTN
response to ant-acids / PPI's
28
in what percentage of cases does MI present without pain
30%
29
what is this particularly important in
women
diabetics
the elderly
30
what are the symptoms associated with a silent MI
syncope
pulmonary oedema
epigastric pain
vomiting
acute confusional state
stroke
diabetic hyperglycaemia
31
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
32
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
33
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
34
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
35
when should patients call an ambulance
if they experience angina type pain, which after using a GTN spray does not subside within 15 minutes
36
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
37
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
38
what is a transmural MI
this is an infarct that causes necrosis of tissue through the full thickness of the myocardium
39
what is a non-transmural MI
this is an MI that does not cause necrosis through the full thickness of the myocardium
40
what are the early ECG changes
peaked T wave (very tall T wave)
raised ST segment
41
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
42
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.
43
what are the other patterns of ECG change
ST-depression
reciprocal change
44
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
45
what does ST depression show
ischaemia - the damage is reversible with the right treatment
46
what does ST elevation show
infarction - damage is irreversible
47
what are the ECG readings and troponin levels in a STEMI
ECG:
- ST elevation
or
- new LBBB
troponin:
- elevated
- dont wait for the result
48
what are the ECG readings and troponin levels in an NSTEMI
ECG:
- may be normal, or may include
1. non-specific changes
2. T wave inversion
3. hyper-acute T waves
4. ST depression
Troponin:
- raised serial troponin
49
what are the ECG readings and troponin levels in unstable angina
ECG:
- often normal however may include
1. non-specific changes
2. T wave inversion
3. hyper-acute T waves
4. ST depression
Troponin:
- normal serial troponin
50
when is ST elevation signifiant in STEMI
ST elevation >1mm in 2 contiguous (consecutive) leads except V2 or V3
ST elevation >2mm in V2 or V3 in men >45
ST elevation >2.5mm in V2 or V3 in men <45
ST elevation >1.5mm in V2 or V3 in women of any age
51
what is the Sgarbosa criteria used for
used to asses patients with previously known LBBB for ST elevation - as it can be difficult to discern ST elevation in the presence of LBBB.
52
what is the criteria of Sgarbosa
- concordent (gong in the same direction as the QRS spike) ST elevation >1mm in any lead
- ST depression >1mm in V1,V2,V3
- discordant (going in the opposite direction to QRS) ST elevation of >5mm in any lead
53
what is the basis that NSTEMI is used diagnosed on
- a suggestive history
- elevated troponin levels
- ECG changes
54
what are the ECG changes seen in an NSTEMI
- an ABSENCE of ST elevation
- ECG may be normal
- ST depression
- hyperacute T wave
- TWI (T wave inversion) - this is often a late sign and indicates previous MI
55
how is unstable angina distinguishable from NSTEMI
only through troponin results
56
what are the troponin and ECG results in unstable angina
negative troponin and same ECG changes as an NSTEMI
57
what are the two types of troponin that can be tested for
troponin I and troponin T
58
what is the traditional troponin test
is a positive or negative test. serial troponin tests are performed over several hours (6-8) and any detected troponin results in a 'positive test' and therefore a diagnosis of an NSTEMI
59
what is the usual pattern of troponin levels in ACS
troponin levels rise from 2-24 hours after onset of pain, and peak around 24-48 hours
return to baseline within 5-24 days
60
what is high sensitivity troponin testing
50% of the healthy population have an undetectable troponin
50% of the healthy population have a detectable level of troponin
The exact reference range will very from centre to centre. At my hospital, the “normal range” is quoted as <16ng/L
61
what is the recommended troponin test method
TWO troponin tests, 2 hours apart within 3 hours of the onset of chest pain
62
what is a single negative troponin test acceptable for
as a rule out (for ACS) if it is >3 hours since the onset of pain
63
what is a positive test defined as
as an increase in troponin between the two tests
the exact levels of increases which signifies an NSTEMI is hotly debated but a 20% increase is agreed.
64
what are the other 6 causes of raised troponin
Renal failure
Myocarditis
PE
Pericarditis
Heart failure
Arrhythmia
65
why would creatine kinase be taken
it is found in skeletal and myocardial muscle
raised after any sort of muscle trauma, also raised after MI
previously used in MI diagnosis but has now been superseeded by troponin testing
66
what are the changes seen on CXR
Cardiomegaly
Pulmonary oedema and other signs of treat failure
Widened mediastinum
67
what is the pre-hospital acute management for ACS/MI
call ambulance
aspirin 300mg orally
pain relief (5-10mg morphine + metoclopramide (anti-emetic)10mg IV – avoid IM injections as there is a risk of bleeding – and you just gave loads of aspirin!)
GTN spray
oxygen is stats are below 94%
68
when do you not give GTN spray
if patient is hypotensive
69
what is the acute management in hospital
ECG as soon as possible – it is also likely that this will have been done in the ambulance.
It is important to differentiate STEMI for other ACS / other causes of chest pain as soon as possible
Serial ECGs are a very important part of the emergency work-up of chest pain. Dynamic ECG changes refer to intermittent and changing ECG findings and are highly suggestive of ACS
Assess oxygen saturation – if sats are above 94% you do not need to give oxygen (in practice, people are often given oxygen regardless but this is not best practice). If sats are below 94% then give high-flow oxygen via a non-rebreather mask (i.e. with an inflated bag on)
In patients with known COPD, aim for sats between 88-92% – give oxygen via a 24% or 28% Venturi mask (colour coded) and get an ABG.
70
what bloods do you take for suspected ACS/MI
FBC, U+E, glucose, lipids, troponin, ABG
71
what are the usual medications given
Give 300mg aspirin if not already administered
Give 5-10mg morphine and metoclopramide 10mg IV if not already administered
72
what is not indicated for an NSTEMI
thrombolysis
73
what are the commonly used thrombolysis drugs
Streptokinase, recteplacse or tenecteplase are commonly used thrombolysis drugs
74
what is the MONA pneumonic for acute management of all ACS patients
Morphine
Oxygen
Nitrates
Aspirin
75
what is the MONAC pneumonic for high risk STEMI or NSTEMI
morphine
oxygen
nitrates
aspirin
clopidogrel
76
what is the management after acute event when stable
beta-blocker
ace-inhibitor
statin
77
how long should you avoid sex and travel for after MI
Sex – Should avoid for 1 month after MI
Travel – avoid air travel for 2 months
78
what is the COBRA-A pneumonic for secondary prevention in ACS
C – Clopidogrel – antiplatelets
O – Omacar – Omega 3
B – Bisoprolol – β-blocker
R – Ramipril – ACE-i
A – Aspirin
A – Atorvastatin – very potent statin!
79
what is a mural thrombus
this is a thrombus attached to the wall of the endocardium in a damaged area, or sometimes it is attached to the aortic wall over an intimal lesion. MI leads to akinetic areas of ventricular wall.
this stasis allows the formation of a thrombus on the wall. the larger the infarct, the greater the risk of thrombus. parts of the thrombus can easily break off and embolise
80
when does a ventricular wall rupture happen and why
this occurs about 5-10 days after the initial infarct.
at this time, the myocardium is particular soft. blood can then come out of the rupture, and enter the pericardial sack, causing haemopericardium
81
what does haemopericardium usually lead to
cardiac tamponade
82
how does cardiac tamponade classical present
with electromechanical dissociation - a perfectly normal ECG, but no cardiac output and no pulse
83
what almost always results in death
PEA - pulseless electrical activity as it is a non-shockable rhythm
84
what is a ventricular aneurysm
Ventricular aneurysm – this is a late complication of a transmural MI. the infracted muscle will be replaced by a thin layer of collagenous scar tissue, that will gradually stretch as intraventricular pressure rises during systole. The aneurysm itself has complications of left ventricular failure, arrhythmias, mural thrombus. Rupture of the aneurysm is rare.
85
what is mitral valve incompetence commonly caused by
ommonly caused by ischaemic damage to the papillary muscles, especially in posterior infarcts. Post ischaemic fibrosing and shortening of the papillary muscles can also cause incompetence. In some patients, the papillary muscles can be completely destroyed by the infarct, resulting in instant and complete torrential mitral valve incompetence.
86
what is Dressler's syndrome
An autoimmune pericarditis, provoked by MI. Occurs in 5-10% of cases of MI. Onset 1-3 weeks post MI. Localised pericarditis. Causes fever, pericardial effusions, anaemia, raised ESR, enlarged heart on CXR, pericardial rub (on auscultation). may be similar to PE – another post-MI complication.
It is often self-limiting, and symptoms last a few days.
87
what is Dressler's syndrome usually treated with
NSAID's, and in more serious cases, steroids
88
what are the ECG leads and heart area associated with the left coronary artery
Anterolateral
I, aVL, V3-6
89
what are the ECG leads and heart area associated with the left anterior descending artery
Anterior
V1-4
90
what are the ECG leads and heart area associated with circumflex artery
Lateral
I, aVL, V5-6
91
what are the ECG leads and heart area associated with the right coronary artery
Inferior
II, III, aVF
92
what is the pneumonic used in patients presenting with symptoms of ACS for initial management
C – Call an ambulance
P – Perform an ECG
A – Aspirin 300mg
I – Intravenous morphine for pain if required (with an antiemetic, e.g., metoclopramide)
N – Nitrate (GTN)
93
what is the management of a STEMI presenting within 12 hours of onset
Percutaneous coronary intervention (PCI) (if available within 2 hours of presenting)
Thrombolysis (if PCI is not available within 2 hours)
94
what is PCI
Percutaneous coronary intervention (PCI) involves putting a catheter into the patient’s radial or femoral artery (radial is preferred), feeding it up to the coronary arteries under x-ray guidance and injecting contrast to identify the area of blockage (angiography). Blockages can be treated using balloons to widen the lumen (angioplasty) or devices to remove or aspirate the blockage. Usually, a stent is inserted to keep the artery open.
95
what is thrombolysis
Thrombolysis involves injecting a fibrinolytic agent. Fibrinolytic agents work by breaking down fibrin in blood clots. There is a significant risk of bleeding, which can make thrombolysis dangerous. Some examples of thrombolytic agents are streptokinase, alteplase and tenecteplase.
96
what is the pneumonic for the management of an NSTMEI
B – Base the decision about angiography and PCI on the GRACE score
A – Aspirin 300mg stat dose
T – Ticagrelor 180mg stat dose (clopidogrel if high bleeding risk, or prasugrel if having angiography)
M – Morphine titrated to control pain
A – Antithrombin therapy with fondaparinux (unless high bleeding risk or immediate angiography)
N – Nitrate (GTN)
97
what is the GRACE score
score that gives a 6 month probability of death after having an NSTEMI
3% or less is considered low risk
above 3% Is considered medium to high risk
98
what is the 6A's pneumonic used for secondary management
Aspirin 75mg once daily indefinitely
Another Antiplatelet (e.g., ticagrelor or clopidogrel) for 12 months
Atorvastatin 80mg once daily
ACE inhibitors (e.g. ramipril) titrated as high as tolerated
Atenolol (or another beta blocker – usually bisoprolol) titrated as high as tolerated
Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)
99
what are the 4 types of myocardial infarction
Type 1: Traditional MI due to an acute coronary event
Type 2: Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension)
Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event
Type 4: MI associated with procedures such as PCI, coronary stenting and CABG
100
when are Q waves considered pathological
a. > 40 ms (1 mm) wide
b. > 2 mm deep
c. > 25% of depth of QRS complex
e. Seen in leads V1-3
101
what are the ECG characteristics of LBBB
a. Broad QRS (>3 small square/0.12sec) and
b. Deep S wave in V1 and
c. No Q wave in V5/V6
102
what imaging diagnoses CHD
CTCA imaging
103
how many deaths does CHD account for in the UK per year
64,000
104
how many people out of 10 survive a heart attack
7 out of 10
105
how does CHD develop
usually develops over many years due to the process of atherosclerosis which can give rise to the various clinical syndromes namely stable angina and ACS
106
what are the diagnosis features of angina chest pain
Constricting discomfort in front of chest, neck, shoulders, arms
Precipitated by physical exertion
Relieved by GTN or rest in about 5 minutes
107
what are the 4 steps of the pathophysiology of CAD
1. atherosclerosis and atheroma formation results in progressive narrowing of the lumen in a coronary artery
2. at rest, there is no chest pain but during exertion the myocardial demand rises, and the supply cannot meet the myocardial demand resulting in an external chest pain that is relieved by rest or GTN. this is called stable angina
3, an unstable plaque can rupture resulting in platelet aggregation and thrombus formation which causes sudden occlusion of the coronary artery. this results in acute chest pain and is called ACS
4. the degree and duration of the occlusion will dictate the subtype of ACS.
108
what will all patients with acute chest pain (lasting more than 15 minutes) need
an immediate 12 lead ECG to exclude ST elevation
109
what is the name of the tool used in general practice to determine somebody's cardiovascular risk
QRISK3 is an updated version that has replaced QRISK2 in general practice. The score establishes a patients 10 year risk of cardiovascular events.
110
what components are required to calculate a QRISK3 score
QRISK3 requires:
- Age
- Gender
- Smoking status
- History of diabetes, hypertension
- Family history of cardiovascular event
- Physical exercise
- Diet
- BMI
- Cholesterol
QRISK3 includes more factors than QRISK2 to help enable doctors to identify those at most risk of heart disease and stroke. These are:
- Chronic kidney disease, which now includes stage 3 CKD
- Migraine
- Corticosteroids
- Systemic lupus erythematosus (SLE)
- Atypical antipsychotics
- Severe mental illness
- Erectile dysfunction
- A measure of systolic blood pressure variability
111
if somebody has been diagnosed with stable anigna, what may they be prescribed
He prescribes Aspirin 75mg orally once a day and gives him a glyceryl trinitrate spray (GTN) to use sublingual as needed (prn).
112
what is the NICE guidelines on starting statins
NICE uses a threshold of QRISK3 score >10% for primary prevention of cardiovascular disease with lipid lowering medications such as statins
113
can a normal ECG rule out ACS
No.
if the ECG is performed at the time of acute chest pain in ACS here usually are ECG changes. in patients with NSTEMI or unstable angina there is often a normal ECG by the time it is perfumed the pain has already subsided.
114
what is the further test required after ECG to exclude ACS
troponin
115
what anti platelets are prescribed along with aspirin
An additional antiplatelet (potent P2Y12 inhibitors, e.g., ticagrelor or prasugrel) is prescribed alongside Aspirin as recommended by the PPCI pathway guidelines*.
116
what is the dual antipatelet therapy offered for people with acute STEMI having primary PCI
Prasugrel, as part of dual antiplatelet therapy with aspirin, if they are not already taking an oral anticoagulant (use the maintenance dose in the prasugrel summary of product characteristics; for people aged 75 and over, think about whether the person’s risk of bleeding with prasugrel outweighs its effectiveness, in which case offer ticagrelor or clopidogrel as alternatives)
Clopidogrel, as part of dual antiplatelet therapy with aspirin, if they are already taking an oral anticoagulant.
117
what are the drugs used in secondary prevention for people who have had MI treatment
angiotensin-converting enzyme (ACE) inhibitor
dual antiplatelet therapy (aspirin plus a second antiplatelet) unless they have a separate indication for anticoagulation (see the section on antiplatelet therapy for people with an ongoing separate indication for anticoagulation)
beta-blocker
statin
118
