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Year 3 > Week 5 - Case One > Flashcards

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

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2
Q

what is a STEMI

A

ST elevation MI

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3
Q

how is a STEMI diagnosed

A

diagnosable on the basis of classical ECG changes

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4
Q

what is an NSTEMI

A

non-ST elevation MI

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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

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6
Q

what is unstable angina

A

ischaemia, without infarction

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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.

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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

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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

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10
Q

what percentage of patients present without pain

A

30%

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11
Q

what is the most common cause of death in the UK

A

coronary heart disease

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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

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13
Q

what is the incidence of CHD

A

300,000 cases per year

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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)

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15
Q

what are the modifiable risk factors for CHD

A

Smoking
Hypertension
Diabetes
Hyperlipidaemia
Obesity
Sedentary lifestyle

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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

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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
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18
Q

when is chest pain more predictive of an MI

A

if it radiates to both arms or the right arm

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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

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20
Q

what are the 5 other symptoms associated with ACS, MI

A

diaphoresis
breathlessness
syncope
tachycardia
vomiting and sinus bradycardia
distress

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21
Q

what does syncope occur as a result of

A

occurs aș a result of severe arrhythmia or severe hypotension

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22
Q

why may vomiting and sinus bradycardia occur

A

as a result of excessive vagal stimulation, which is most common in inferior MI

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23
Q

what does sudden death usually occur from

A

ventricular fibrillation or systole.

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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

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25
Q

what factors are particularly signifiant for the likelihood of ACS compared to other causes of chest pain

A

Pain that radiates to the arms or jaw
Diaphoresis
Vomiting
Exertional chest pain

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26
Q

what features suggest non-ACS chest pain

A

reproducible chest pain (tender chest wall or positional pain)

pleuritic chest pain

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27
Q

what features are not useful to predict the likelihood of ACS

A

severity of pain
response to GTN
response to ant-acids / PPI’s

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28
Q

in what percentage of cases does MI present without pain

A

30%

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29
Q

what is this particularly important in

A

women
diabetics
the elderly

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30
Q

what are the symptoms associated with a silent MI

A

syncope
pulmonary oedema
epigastric pain
vomiting
acute confusional state
stroke
diabetic hyperglycaemia

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31
Q

what are the signs of impaired myocardial function

A

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

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32
Q

what are the signs of sympathetic activation

A

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

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33
Q

what are the differentials for MI/ACS/CHD

A

Angina
Pericarditis
Myocarditis
Aortic dissection
Pulmonary

PE
Pneumothorax
Anything that causes pleuritic chest pain
Oesophageal

Oesophageal reflux
Oesophageal spasm
Tumour
Oesophagitis

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34
Q

what is the pathology behind an MI

A

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

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35
Q

when should patients call an ambulance

A

if they experience angina type pain, which after using a GTN spray does not subside within 15 minutes

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36
Q

what are the two different mechanisms of an MI

A

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

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37
Q

what do the platelets release and what does this cause

A

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

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38
Q

what is a transmural MI

A

this is an infarct that causes necrosis of tissue through the full thickness of the myocardium

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39
Q

what is a non-transmural MI

A

this is an MI that does not cause necrosis through the full thickness of the myocardium

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40
Q

what are the early ECG changes

A

peaked T wave (very tall T wave)

raised ST segment

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41
Q

what are the ECG changes within 24 hours

A

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

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42
Q

what are the ECG changes within days

A

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.
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43
Q

what are the other patterns of ECG change

A

ST-depression

reciprocal change

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44
Q

what is reciprocal change

A

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

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45
Q

what does ST depression show

A

ischaemia - the damage is reversible with the right treatment

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46
Q

what does ST elevation show

A

infarction - damage is irreversible

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47
Q

what are the ECG readings and troponin levels in a STEMI

A

ECG:
- ST elevation
or
- new LBBB

troponin:
- elevated
- dont wait for the result

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48
Q

what are the ECG readings and troponin levels in an NSTEMI

A

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
Q

what are the ECG readings and troponin levels in unstable angina

A

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
Q

when is ST elevation signifiant in STEMI

A

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
Q

what is the Sgarbosa criteria used for

A

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
Q

what is the criteria of Sgarbosa

A
  • 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
Q

what is the basis that NSTEMI is used diagnosed on

A
  • a suggestive history
  • elevated troponin levels
  • ECG changes
54
Q

what are the ECG changes seen in an NSTEMI

A
  • 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
Q

how is unstable angina distinguishable from NSTEMI

A

only through troponin results

56
Q

what are the troponin and ECG results in unstable angina

A

negative troponin and same ECG changes as an NSTEMI

57
Q

what are the two types of troponin that can be tested for

A

troponin I and troponin T

58
Q

what is the traditional troponin test

A

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
Q

what is the usual pattern of troponin levels in ACS

A

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
Q

what is high sensitivity troponin testing

A

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
Q

what is the recommended troponin test method

A

TWO troponin tests, 2 hours apart within 3 hours of the onset of chest pain

62
Q

what is a single negative troponin test acceptable for

A

as a rule out (for ACS) if it is >3 hours since the onset of pain

63
Q

what is a positive test defined as

A

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
Q

what are the other 6 causes of raised troponin

A

Renal failure
Myocarditis
PE
Pericarditis
Heart failure
Arrhythmia

65
Q

why would creatine kinase be taken

A

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
Q

what are the changes seen on CXR

A

Cardiomegaly
Pulmonary oedema and other signs of treat failure
Widened mediastinum

67
Q

what is the pre-hospital acute management for ACS/MI

A

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
Q

when do you not give GTN spray

A

if patient is hypotensive

69
Q

what is the acute management in hospital

A

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
Q

what bloods do you take for suspected ACS/MI

A

FBC, U+E, glucose, lipids, troponin, ABG

71
Q

what are the usual medications given

A

Give 300mg aspirin if not already administered
Give 5-10mg morphine and metoclopramide 10mg IV if not already administered

72
Q

what is not indicated for an NSTEMI

A

thrombolysis

73
Q

what are the commonly used thrombolysis drugs

A

Streptokinase, recteplacse or tenecteplase are commonly used thrombolysis drugs

74
Q

what is the MONA pneumonic for acute management of all ACS patients

A

Morphine
Oxygen
Nitrates
Aspirin

75
Q

what is the MONAC pneumonic for high risk STEMI or NSTEMI

A

morphine
oxygen
nitrates
aspirin
clopidogrel

76
Q

what is the management after acute event when stable

A

beta-blocker
ace-inhibitor
statin

77
Q

how long should you avoid sex and travel for after MI

A

Sex – Should avoid for 1 month after MI
Travel – avoid air travel for 2 months

78
Q

what is the COBRA-A pneumonic for secondary prevention in ACS

A

C – Clopidogrel – antiplatelets
O – Omacar – Omega 3
B – Bisoprolol – β-blocker
R – Ramipril – ACE-i
A – Aspirin

A – Atorvastatin – very potent statin!

79
Q

what is a mural thrombus

A

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
Q

when does a ventricular wall rupture happen and why

A

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
Q

what does haemopericardium usually lead to

A

cardiac tamponade

82
Q

how does cardiac tamponade classical present

A

with electromechanical dissociation - a perfectly normal ECG, but no cardiac output and no pulse

83
Q

what almost always results in death

A

PEA - pulseless electrical activity as it is a non-shockable rhythm

84
Q

what is a ventricular aneurysm

A

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
Q

what is mitral valve incompetence commonly caused by

A

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
Q

what is Dressler’s syndrome

A

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
Q

what is Dressler’s syndrome usually treated with

A

NSAID’s, and in more serious cases, steroids

88
Q

what are the ECG leads and heart area associated with the left coronary artery

A

Anterolateral
I, aVL, V3-6

89
Q

what are the ECG leads and heart area associated with the left anterior descending artery

A

Anterior
V1-4

90
Q

what are the ECG leads and heart area associated with circumflex artery

A

Lateral
I, aVL, V5-6

91
Q

what are the ECG leads and heart area associated with the right coronary artery

A

Inferior
II, III, aVF

92
Q

what is the pneumonic used in patients presenting with symptoms of ACS for initial management

A

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
Q

what is the management of a STEMI presenting within 12 hours of onset

A

Percutaneous coronary intervention (PCI) (if available within 2 hours of presenting)

Thrombolysis (if PCI is not available within 2 hours)

94
Q

what is PCI

A

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
Q

what is thrombolysis

A

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
Q

what is the pneumonic for the management of an NSTMEI

A

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
Q

what is the GRACE score

A

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
Q

what is the 6A’s pneumonic used for secondary management

A

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
Q

what are the 4 types of myocardial infarction

A

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
Q

when are Q waves considered pathological

A

a. > 40 ms (1 mm) wide
b. > 2 mm deep
c. > 25% of depth of QRS complex
e. Seen in leads V1-3

101
Q

what are the ECG characteristics of LBBB

A

a. Broad QRS (>3 small square/0.12sec) and
b. Deep S wave in V1 and
c. No Q wave in V5/V6

102
Q

what imaging diagnoses CHD

A

CTCA imaging

103
Q

how many deaths does CHD account for in the UK per year

A

64,000

104
Q

how many people out of 10 survive a heart attack

A

7 out of 10

105
Q

how does CHD develop

A

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
Q

what are the diagnosis features of angina chest pain

A

Constricting discomfort in front of chest, neck, shoulders, arms
Precipitated by physical exertion
Relieved by GTN or rest in about 5 minutes

107
Q

what are the 4 steps of the pathophysiology of CAD

A
  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

  1. the degree and duration of the occlusion will dictate the subtype of ACS.
108
Q

what will all patients with acute chest pain (lasting more than 15 minutes) need

A

an immediate 12 lead ECG to exclude ST elevation

109
Q

what is the name of the tool used in general practice to determine somebody’s cardiovascular risk

A

QRISK3 is an updated version that has replaced QRISK2 in general practice. The score establishes a patients 10 year risk of cardiovascular events.

110
Q

what components are required to calculate a QRISK3 score

A

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
Q

if somebody has been diagnosed with stable anigna, what may they be prescribed

A

He prescribes Aspirin 75mg orally once a day and gives him a glyceryl trinitrate spray (GTN) to use sublingual as needed (prn).

112
Q

what is the NICE guidelines on starting statins

A

NICE uses a threshold of QRISK3 score >10% for primary prevention of cardiovascular disease with lipid lowering medications such as statins

113
Q

can a normal ECG rule out ACS

A

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
Q

what is the further test required after ECG to exclude ACS

A

troponin

115
Q

what anti platelets are prescribed along with aspirin

A

An additional antiplatelet (potent P2Y12 inhibitors, e.g., ticagrelor or prasugrel) is prescribed alongside Aspirin as recommended by the PPCI pathway guidelines*.

116
Q

what is the dual antipatelet therapy offered for people with acute STEMI having primary PCI

A

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
Q

what are the drugs used in secondary prevention for people who have had MI treatment

A

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
Q
A

Year 3 (63 decks)

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