acute coronary syndrome Flashcards
ACS is an umbrella term used to refer to patients in whom there is a suspicion or confirmation of—- or — .
It includes three main conditions:
- —-elevation myocardial infarction( —-)
- —- elevationMI(— )
- — angina
acute myocardial ishcemia or infraction
NonST ( NSTEMI )
ST ( STEMI)
unstable
( so basically Myocardial infraction can be stable angina or ACS which can be either STEMI or non ST which has unstable angina or NSTEMI)
- Stable Angina is — caused by – where there is insufficient — to meet myocardial demand, it typically develops during — , lasts— minutes or less and is — with rest.
- Unstable Angina can occur at — , lasts – , and symptoms may be more –
- Chest pain at rest or ongoing chest pain is suspicious for —
chest pain
ishcemia
perfusion
physical activity
5 minutes
relieved
rest
loger
severe
ACS
how to distinguish between ACS subtypes: STEMI, NSTEMI, UA:
ACS diagnosis requires — out of 3 categories below to be positive;
- Presence of cardiac — (history),
- – changes
- Abnormal — (— )
1- STEMI has — and ecg of ST is — or new bundle branch — and the cardiac marker is —
2- NSTEMI has — and the ecg changes of ST is – and/or TWI and the cardiac biomarker is —
3- UA has —- the ecg shows — or — changes and the cardiac biomarker is —
2
chest pain
ECG
cardiac biomarker ( troponin )
chest pain
elevation
block
elevated
chest pain
depression
elevated
chest pain
normal or non specific
normal
PLS look at slide 7 for ECG pic
ECG in ACS:
STEMI:
- New ST — in two contiguous leads ≥ – mm
- Except in — where the following — points apply:
≥2mm in men – years;
≥ 2.5mm in men— years
≥1.5mm in — regardless of age
Or new Left bundle branch –
NSTEMI
New — or—-sloping ST — ≥ — mm in — contiguous leads and/or
– Wave inversion > – mm in two contiguous leads
Unstable Angina — or — changes
elevation
1
V2-V3
cut offs
> or = to 40
<40
women
block
horizontal or down
depression
0.5
2
t wave
1
normal or non specific
PLS check slide 8 so important for pics
cardio biomarkers:
Damage to — cells from ischaemia/infarction causes a release of — , these are known as — and are measured in — tests.
Commonly used biomarkers are — and —
— is the most used and is often normal in — presentations and should be repeated in approximately — hours
Typically, the value between the first and second reading must – to be suggestive of an acute myocardial infarction.
myocardial cells
cardiac enzymes
cardiac biomarkers
blood test
troponin I and CK-MB
troponin I
early
6 hours
double
typical stable angina NOT ACS:
Site - Central chest. Epigastrium to jaw, teeth, neck.
Onset – Can come on sudden or gradually with exertion
Character: Tightness, pressure, heaviness, strangling, constricting, burning
Radiation -May radiate to arms, scapula or underarms
Associated symptoms: Shortness of breath (It may be the sole symptom, particularly in women), nausea, fatigue
1- Timing:
- – – Usually only a few — , nearly always < —
-Prolonged pain (>— min) unlikely to be — angina -> consider ACS
- Very brief pain (— in duration) unlikely to be angina
2- Exacerbating / relieving factors
Worse with exercise, relieved with – or — .
Worse after large meal, worse first thing in the morning
Cold, physical and emotional distress can trigger angina
Severity – variable between patients, however stable in the individual, if worsening -> consider unstable angina
brief usually few minutes
<10 min
>20
stable
seconds
rest or nitrates
ACS presentation:
Classic Cardiac Chest pain
S: Central, retrosternal, intense
O: Acute, often at rest
C: Constricting, crushing, dull, vice-like, squeezing
R: Arm, shoulder, jaw, epigastrium
A: SOB, Nausea/Vomiting, Diaphoresis, Anxiety, sense of doom
T: Unremitting (typically >—min), peak incidence in—
E: Exacerbated by exertion or stress, alleviated by GTN
S: Severe pain, may collapse/arrest
In some cases, the patient cannot qualify the nature of the discomfort but places his or her clenched fist in the centre of the chest - “—sign”
Atypical ACS presentation:
These are patients presenting with e.g: Stabbing, sharp chest pain
No or minimal chest pain
Autonomic symptoms (e.g.,diaphoresis, nausea, vomiting,syncope, palpations)
Dyspnoea
Epigastric / GI discomfort
Common: affect both genders with a higher— preponderance accounting for up to 25% female presentations of ACS, high degree of – required
Who: — , — patients, — and — patients may have silent infarcts or atypical symptoms
other ACS symptoms:
Other cardiac symptoms, these can arise from the— complications of—:
Presyncope, syncope, palpitations, fatigue, distress, dyspnea, paroxysmal nocturnal dyspnea, orthopnea
Change from patient’s baseline effort/exercise tolerance
> 10 min
mornings
levine
females
suspicion
diabetics, older , female , post op patients
acute complication of myocardial infraction
features suggestive of non cardiac chest pain :
- — pain - worse with — and —
-Pain in the – or — – region
-Any discomfort localised with — finger
-Any discomfort reproduced by movement or palpation
-Constant pain lasting for –
- — pains lasting for a few seconds or less
- Pain radiating into the – extremities or above the mandible
pleuritic
movement and inspiration
mid or lower abdominal
one
days
fletting
lower
clinical signs of ACS:
Physical findings can range from normal to any of the following:
General inspection:ashencolour, diaphoretic,dyspneic, clutching at chest (Levine’s sign),altered level of consciousness
Vitals: Hypo/hypertension, tachycardia, hypoxia, tachypnoea
Hands: peripheral cyanosis, prolonged capillaryrefill.
Pulse: weak, irregular
Chest:
Palpation: heave
Auscultate: new murmur e.g mitral regurgitation
Gallop Rhythm
Auscultation: crackles suggesting pulmonary oedema
Abdomen: pulsatile tender/enlarged liver
Lower limbs: pedal oedema and assess for absent pulses
Many of these signs are caused by complications of ACS which we explore later in the lecture
Main aims of physical examination: evaluate — status, exclude other — of chest pain, identify precipitating causes/complications, evaluate for —
hameodynamic
cayses
comorbidies
pathology of ACS:
The underlying pathophysiology in ACS is — blood flow to part of heart musculature; which is usually — to — disease with subsequent plaque – and formation of—.
–> This can result in — or — .
Sometimes ACS can be – to — with or without underlying — . E.g. due to – use
decreases
2ndary
atherscolerotic
rupture or thrombus
ischemia or infraction
2ndary to vasospasm
athersocoelris
cocain
( info: athersoclosis –> stable angina , intermittent claduication )
Atherosclerosis is a – , — disease caused by the deposition of fats, cholesterol, calcium, and other substances in the – layer of – of the – and —-sized arteries.
This creates a – , which over time becomes progressively larger causing a—/—in blood flow. This plague may suddenly rupture resulting in the formation of a clot (—) at the site.
This thrombus may fully or partially occlude the lumen of the blood vessel resulting in —/—
chronic
vascular
innermost
endothelium
large and medium
plaque
stenosis/limitation
thrombus
ishcemia/infraction
chest pain and referred pain :
-In ACS there is a disruption in — delivery to the myocardium which results in a — to — metabolism in the myocardial cells.
-This is followed by a stimulation of the— nerves that innervate the heart.
-These stimuli are carried in — pathways to the — and converge with individual spinothalamic tract neurons. At these neurons there is also innervation from — nerves, which for example supply the dermatomes in the arm.
-Referred pain occurs when activation of — in the — results in a perception of – that is — to the body surface.
-The brain interprets the information coming from — receptors as having arisen from receptors on the body surface, since this is where nociceptive stimuli originate more frequently
02
shift
anaerobic
sympathetic
afferent
spinal cords
somatic
nociceptors
viscera
pain
localised
visceral receptors
sympathetic signs:
-The sympathetic nervous system (SNS) – regulates our body’s “fight or flight” system.
-In ACS the SNS is activated as a compensatory mechanism to improve or maintain — and systemic — during episodes of impaired — function.
Activation of SNS causes the symptoms of – and — in ACS.
-SNS also causes peripheral — as blood is diverted to central organs which along with acute heart failure/ “—-” caused by ACS can contribute to a pale/ ashen appearance.
cardiac output
blood pressure
ventricular function
sweating and anxiety
vasoconstriction
pump failure
pump failure:
-Ischaemia/infarction of the myocardium can lead to the heart not working as an effective— – — cardiac output.
-Reduced cardiac output can result in — , where cardiac output is unable to meet — demands
-This presents with symptoms of fatigue, dyspnoea, pedal oedema and reduced exercise tolerance.
-Reduced cerebral — due to reduced cardiac output can cause syncope/collapse/feeling light-headed
dysponea:
- The pathophysiology of dyspnea(also called — of breath) is – , e.g it may be related to — , — or — conditions.
-In the context of acute coronary syndrome, it can occur due to a decrease in the output of the — ventricle. This has two effects which lead todyspnoea:
-Due to decreased peripheral tissue— with blood, the bodytries to compensate by — the respiratory ratein order to — oxygen saturation of blood
-With reduced — output, there is an increase in the—- pressure of the blood in the pulmonary capillary beds,leading to extravasation of fluid into theinterstitium, which leads topulmonaryoedema
pump
reducing
acute heart failure
metabolic demand
perfusion
shortness
multifactorial
anemia , respiratory , cardiac
left ventricle
perfusion
increasing
increase
left ventricular
hydrostatic
signs of heart failure - a complication of ACS:
Heart failure is divided into —,— and — heart failure.
1- In right heart failure the —- does not pump effectively causing back pressure into the — this can be seen clinically in the form of an — JVP, enlarged – and pedal—.
A raised JVP can be seen in — in a —-sided MI.
2- In left heart failure, the — does not pump efficiently and there is back pressure into the — resulting in —
left right and congestive
right ventricles
right atrium
elevated
liver
pedal oedema
acute ventricular dysfunction
right
left ventricles
lungs
pulmonary oedema
palpitation/arrythmia:
- —- of the myocardial wall due to — can interfere with normal heart — .
-Interference with normal — conduction is sometimes called ‘—-‘
-Pump failure/ heart failure / mitral regurgitation post ACS can lead to— of the — which can cause —, the patient may complain of —
-Activation of the SNS “fight or flight response” may induce a — acutely.
scarring
infraction
conduction
electrical
heart block
dilation
left atria
arterial fibrillation
palpitation
tachycardia
Murmur – mitral regurgitATION:
-Bloodflowingbackinto the — from the — due to — incompetence is calledMitral regurgitation (MR).
-MI causing rupture of the — may result in — . This is a potentially life threatening event, and may cause —/—
- Mitral regurgitation can be heard as a — murmur at the — beat
left atrium
left ventricle
mitral valve
papillary muscle
MR
acute pulmonary oedema/cardiogenic shock
systolic
apex
- differential diagnosis for cardiac chest pain - chest pain cardiac , respiratory , MK , GI miscellaneous
- Atypical ACS presentations:
Not rare:
20% — and 25% — presentations of ACS
Diabetics, elderly, post-op patients may have silent infarcts or very atypical symptoms
Older patients, diabetics and women are more likely to present with symptoms such as dyspnoea, weakness, nausea and vomiting, palpitations, and syncope
1- pericarditis:
symptoms:
Chest Pain
Central/anterior, sharp, usually non-radiating, exacerbated by lying down, alleviated by leaning forward
Dyspnoea
May have a viral illness prodrome
Fever, malaise, myalgia
signs:
Diaphoresis
Pulsus paradoxus
Paradoxical drop in BP of >10mmHg on inspiration
Kussmals sign
Paradoxical rise in JVP on inspiration
Pericardial friction rub
High pitch scratchy sound heard on auscultation of the heart
male
female
1- pulmonary embolism:
symptoms
Acute onset pleuritic chest pain
Sharp, catching chest pain, usually non-radiating, exacerbated by deep inspiration
Dyspnoea
May have had recent illness/immobility/surgery/long travel or previous clot
signs
Sinus tachycardia on ECG
Cough/haemoptysis
Tachypnoea
Hypoxia
Signs of DVT
2- gastroesophegeal reflux disease:
symptoms
Chest pain
Retrosternal burning pain (heartburn)
Worse lying flat and after certain meals
Dysphagia
Nausea
Regurgitation
Dry cough
signs: — more likely to occur in patients with raised — (raised intraabdominal pressure causing acid reflux)
GORD
BMI
MSK pain :
symptoms
Chest pain
Sharp or dull ache, localised and reproducible on palpation
Maybe worse on movement
Can affect anywhere eg arms, back, neck, chest
May have history of recent injury
signs :
Patient appears well
Pain likely to reproducible on examination (localised tenderness)
May have evidence of other joint involvement
aortic dissection: Chest pain
Sudden onset andseveretearing/rippingpain in anterior chest or back , may radiate to Interscapulararea, Neck, jaw.
May also present as abdominal or periumbilical, colickypain
Character: migratesas the dissected wall propagatescaudally
signs:
Hypertensionorhypotension
Asymmetricalblood pressureandpulsereadings between limbs
Widepulse pressure
Syncope,diaphoresis
summary:
ACS – is diagnosed if 2 of 3 criteria are fulfilled;
1. Abnormal ECG
2. Elevated cardiac biomarkers
3. History
Not all patients present with classical chest pain, so always keep an open mind for ACS
Atherosclerosis and plaque rupture are the main causes of ACS
When considering a differential consider each of the anatomic structures in the chest as a potential cause
