University

ofGalway.ie
Our Case
• A 71 year old man presents to the emergency department in UCHG with a 1 hour history of
‘squeezing’ chest pain. His symptoms started 1 hour ago while he was out walking his dog.
He had experienced previous minor episodes of chest discomfort after pushing himself
physically that would usually go away after about 5 minutes of rest, but this mornings episode
was much more intense and didn’t go away.

•He is seen by the triage nurse at 09:30am who recognises that he is unwell and transfers him
straight into the resuscitation room where you are called to review the patient.

•You obtain a brief history from the patient while the nurse attaches him to the monitor.
 71 year old male

Past medical history Family history Medications (NKDA) Social history

§Type 2 diabetes (dx 1 year §Father RIP MI aged 60 § Metformin 1g BD PO §Retired
ago) § Drinks 6-8 pints at
§ Amlodipine 10mg OD PO
the weekend.
§Hypertension Overweight
§ Ex smoker with a 20
pack year history -
gave up 10 years ago
 On examination General inspection à Patient diaphoretic and appears to
be in pain. You note an increased body habitus.

• RR 24
• SpO2 98% RA
• BP 120/64
• HR 90
• T 37.2
S1 + S2 with no Good air entry SNT
murmurs
•Estimated weight
bilaterally BS+
110kg

Peripheral: No evidence of pitting oedema, no calf pain/swelling

Questions

1. Starting with the most likely diagnosis, provide 8

differential diagnosis for chest pain/tightness.

1(a). Give a key symptom and a sign that you might

expect to find for each potential diagnosis
Differentials for chest pain/tightness
Long list of differentials
Long list of
differentials
GI causes:
1. Oesophageal spasm
2. Boerhaave syndrome à Hamman’s
sign, “crunching” sound on
auscultation of heart
3. Pancreatitis à Epigastric pain,
Cullens/Turners sign
4. PUD/Gastritis à epigastric
tenderness & made better/worse
by food (GU vs DU)
Long list of
differentials
MSK causes:
1. Rib fracture à Hx of trauma, pain
on movement
2. Costochondritis à focal tenderness
on palpation
3. Shingles (Herpes Zoster) à may be
a rash in a dermatomal distribution
à look closely as could just be a
single vesicle or no rash at all.

Other:
1. Panic attack à only a diagnosis of
exclusion
How to tell them apart?
Questions

The resus nurse takes an ECG and hands it to you…

Subendocardial
ischaemia on ECG
o Usually widespread – for
whatever reason ST depression
does not usually localize
o If localized the could be a
reciprocal change youre seeing so
look elsewhere for ST elevation
 Suspected ACS

ECG

No persistent ST
ST elevation
elevation

STEMI Troponins

Immediate
Elevated Normal
revascularisation

NSTEMI Unstable angina

Inpatient Stress test/

revascularisation Echo

What is your diagnostic impression?

Questions

1. Describe what is meant by Acute Coronary

Syndrome? (ACS)
Acute Coronary
Syndrome (ACS)
• ACS refers to a spectrum of
conditions that are compatible
with acute myocardial ischemia
and/or infarction that are usually
due to an abrupt decrease in
coronary blood flow

• ACS can be divided into STE-

ACS and NSTE-ACS (NSTEMI
and UA)
• A 12 lead ECG should be performed
within 10 mins of suspected ACS
 Suspected NSTE-ACS
(NSTEMI or UA)

Other High troponin level (≥ 52ng/L)

Very low level (<5ng/L) AND
OR
chest pain onset >3 hours ago
Significant change at 1 hour
at the time of blood draw
(trop of ≥5ngl/L)
OR
Heterogenous group.
Low level (<12ng/L) AND no
May need a repeat trop at 3
significant change at 1 hour
hours and an echo
(<3ng/L)

Rule out Observe Rule in

The negative predictive value is The positive predictive value is

>99% 2020 NSTEMI ESC Guidelines
approx. 70-75%
https://doi.org/10.1093/eurheartj/ehaa575
o ALL of the below are on the
assumption that chest pain onset >
3hours
o If high or 1 hour increase – rule in
NSTE - ACS
o If very low/low and rising in 1
hour – rule out NSTE – ACS

o Exact number are assay specific

The patient responds well to your initial management and his pain improves. The lab
phones with an updated troponin result:

Troponin 195 0-14ng/L

Based on the information provided, what is the

most accurate diagnosis? Justify you answer
 Suspected ACS

ECG

No persistent ST
ST elevation
elevation

STEMI Troponins

Immediate
Elevated Normal
revascularisation

NSTEMI Unstable angina

Inpatient Stress test/

revascularisation Echo
 NSTEMI management

• ABCDEFG Overall approach and investigations

• Specific therapies:
• DAPT* Medications
• Parenteral anticoagulant
• Analgesia

• The goal is reperfusion Revascularisation

• PCI (timing will depend)
DAPT?
o DAPT is still indicated in all patients
o More emphasis on weighing the bleeding risks vs the ischemic risk when deciding on start time
and length of therapy
o Pre-treatment with DAPT in patients who are going for an early invasive strategy (ie.,
angiogram within 24 hours), where the coronary artery anatomy is not known, has been
associated with an increased bleeding risk with no ischemic benefit
o Recommended: Aspirin at time of diagnosis, and then second antiplatelet at time of angiogram
o Prasugrel is the preferred second antiplatelet in most patients*
o DAPT for 1 year (unless compelling reason not to such as pt is a high bleeding risk)
Other therapies in NSTEMI

• Oxygen – same rules as for STEMI

• Parenteral anticoagulation is indicated (UFH, enoxaparin,
fondaparinux)
• Sublingual or IV nitrates in patients with ongoing ischemic
pain
• Early beta blockers
• ACEI/ARB in those with HFrEF, diabetes or CKD
• MRAs are recommended in patients with heart failure
with reduced EF

Collet et al "2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: The Task Force for
the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation of the European Society of Cardiology (ESC)." European
Heart Journal.
What definitive management does this patient require? When should he have
this?
GRACE Score
 Figure 9 Selection of
non-ST-segment
elevation acute
coronary syndrome
treatment strategy and
timing according to
initial
risk stratification

©ESC
2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without
www.escardio.org/guidelines
persistent ST-segment elevation (European Heart Journal 2020 - doi/10.1093/eurheartj/ehaa575)
Revision….how would the diagnosis and management of this case change if there
was ST elevation as opposed to ST depression?
 Criteria to diagnose a STEMI

In the correct clinical context

‘Classic’ STEMI STEMI Equivalents

ST elevation at the J point in 2 contiguous leads • Posterior STEMI

of • New LBBB/RBBB
• In V2-V3 the ST elevation must be: • Paced rhythm
• ≥2mm in men ≥40 • Left main coronary occlusion
• ≥2.5mm in men <40 • DeWinters T waves**
• ≥1.5mm in women • Wellen’s syndrome**
• In posterior leads an elevation of >0.5mm is
enough
• ≥1mm in all other leads
This is in the absence of LBBB or LVH
2017 ESC STEMI Guidelines https://doi.org/10.1093/eurheartj/ehx393
ECG Localisation
Investigations
As said before… ECG! If normal? Repeat!
FBC – Hb, also platelets as will be starting anti platelet therapy
Venous blood gas – PH, lactate, glucose and quick turnaround for K and Na
Renal profile – Need contrast in angiogram. You will need to know renal function for meds such as ACE-I. Also K abnormalities can precipitate
arrhythmias.
Liver function tests – high dose statin will be started
High sensitivity cardiac troponins
BNP (or NT – pro BNP) – if suspect or known heart failure
Coag screen – again as patient will be anticoagulated
CXR – should not delay any treatment measures, especially reperfusion. Could see cardiomegaly, evidence of heart failure
Full risk factor screening panel at some point during admission – Hba1c, fasting lipids (LDL, HDL, total chol), iron, b12, folate
Echo – Not required for diagnosis of ACS but may be considered on an urgent basis in selected cases (e.g. diagnostic uncertainty ?RWMA, in
cases of cardiogenic shock, or if looking for complications of MI ? cardiac tamponade or valvular disruption
Coronary Angiography - This is the definitive investigation for any patient with a STEMI who is to undergo a PCI
Management
Management
Airway
o If patient presenting in cardiac arrest --> anaesthetic
involvement +/- intubation
Breathing
o Often tachypnoeic - ?anxiety vs pain
o Oxygen
o Both ESC and AHA recommend
o Oxygen only if saturations <90% due to theoretical risk of generation of
free radicals
o Different delivery systems of 02
o 2-4L, 24-36% via nasal prongs
o 15L, 100% via non-rebreather
o 10L, 40% via venturi

o May have evidence of acute heart failure (e.g. crepitations)

o If BP ok – can give IV diuretics (e.g., frusemide)
o If hypotensive – patients need vasopressors (e.g., NA) before diuretic à
This needs senior input!
ESC guidelines
Circulation
o Get IV access
o HR
o BP - if hypotensive à give IV Fluids
o Continuous cardiac monitoring
o Cap refill time >2sec
o Elevated JVP (acute heart failure/tamponade)
o Heart sounds - ?Murmur
o Acute mitral regurgitation
o Aortic regurgitation
o Muffled heart sounds in combination with hypotension –
?cardiac tamponade
Medications - DAPT
ASPIRIN 300mg PO

TICAGRELOR 180mg PO
PRASUGREL 60mg PO

CLOPIDOGREL 300mg PO
Anticoagulant
o Unfractionated heparin (Recommended by ESC) à 70-100mg/kg IV bolus
o Enoxaparin 0.5mg/kg IV bolus
Nitrates
o Can be given Intravenously or sublingually
o GTN spray – Glyceryltrinitrate
o 1-2 puffs sublingually (1 puff = 400mcg)
o NB - Large RV infarctions will significantly affect the RV contractility à Ultimately this can reduce LV
preload
o Be careful when giving drugs that reduce venous return e.g., nitrates and diuretics Patients with RV
infarction may require fluids/inotropes
o Avoid/use with caution (and senior direction) in hypotensive patients
o Also contraindicated in patients who have taken phosphodiesterase inhibitors such as Sildenafil,
Tadalafil or Vardenafil within the previous 24-48 hours
Analgaesia/anti
emetic
o Not just being nice à pain
increases sympathetic activation
à vasoconstriction
o Morphine à Titrated morphine
(start low and titrate up)

o Anti emetic à metoclopramide

IV if nausea/vomiting
Question - What is the definitive management for this
patient? Justify your answer
Remember. Two strategies (NOT equally weighted):
1. Primary Coronary Intervention (PCI)
2. Thrombolysis
What are the risks associated
with coronary angiography?
Invasive coronary angiography
Common: Rare (<1%)
o Bruising o In stent re-thrombosis
o Reaction to medications
o Discomfort o Contrast induced
o Bleeding at site nephropathy
o Significant bleeding
requiring transfusion
Uncommon(1-5%) o Infection
o Stroke (<0.1%)
o Arrhythmia – may require o MI (<0.1%)
a shock o Death (<0.1%)
o Aneurysm – may require
surgical input
What are the complications
post MI?
Back to our man, he has PCI to his LAD and has been rehabbing on the
ward for the past 3 days. He finds himself short of breath on minimal
exertion. He has his inpatient echo prior to discharge…
 Post MI à
Patients can
develop Atrial
Fibrillation any
time!

MI complications timeline
MI complications
Øcardiac failure
Øpost-infarction ischaemia
Øventricular free wall rupture
Øtherapy: pericardiocentesis and repair
Øventricular septal rupture
Øtherapy: IABP, inotropes, surgery
Øacute mitral regurgitation
Øtherapy: afterload reduction, IABP,
inotropes, surgery ASAP
Øright ventricular infarction
Øtherapy: IV fluids, inotropes, AV
synchrony, IABP, reperfusion
Øarrhythmias
Øtherapy: correct hypoxia, acidosis,
hypovolaemia, K+, Mg2+
Øcardiogenic shock
Øtherapy: must get revascularisation (PCI
or CABG) within 24 hours
Øthromboembolism
Øtherapy: mural thrombus -> anticoagulate
Øpericarditis and Dressler’s syndrome
Øcomplications of treatment, e.g.
haemorrhage, coronary artery
dissection, stent thrombosis, surgical
complications
Dressler’s syndrome
Secondary Pericarditis
o Present 1-6 weeks (sometimes longer) after the initial
damage to the pericardium
o Fever
o Malaise/generalised weakness
o Pleuritic chest pain
o Palpitations/tachycardia
o Dyspnoea
o Arthralgias
o High ESR
Echocardiogram
There is impaired left ventricular
systolic function with an estimated
ejection fraction of 30%. There is
extensive hypokinesia of the lateral
ventricular wall.

How do you classify heart failure,

what type of heart failure does this
patient have?

How would you describe these

findings?
Reduced EF (<40%), mildly reduced EF (41-49), preserved EF (>50%)
What are the four pillars of treatment for patients with this
condition?
Question – Risk factors for the development of CAD (modifiable and non
modifiable)
Cardiovascular risk factors
Secondary
prevention targets
o LDL <1.8 – or reduction of 50% from baseline
Lifestyle advice on discharge
o Smoking cessation – absolutely essential – Far more likely to quit using adjuncts such as patch/gum – GP
can help with this
o Blood pressure control
oDiet advice
o Decrease salt intake (<5g per day)
o Increase fruits and veg
o Increase fish
o Limit alcohol

o Weight control
oPhysical activity
o All patient should take part in specialized cardiac rehab
o The program should include exercise training, risk factor modification, education, stress management, psychological
support
o 30 mins moderate vigorous activity per day (3.5-7 hours approx.)
Discharge meds – 6/52
opd follow up to ensure
compliance/complications

1. DAPT – Two anti platelets for 12

months – then aspirin for life
2. PPI for gastric protection in those
with hx of GI bleeding/at high risk of
same
3. Beta blocker - e.g bisoprolol
4. ACE inhibitor – e.g ramipril
5. Statins/cholesterol lowering drugs – if
already on statin – increase dose.
6. If HFrEF à also ensure MRA
(spironolactone) & SGLT2 ihibitors
(dapagliflozin)
Thank you –
questions?