Acute Coronary Syndrome (ACS) i.e Type 1 Myocardial Infarction Flashcards
Definition of a Type 1 Myocardial Infarction
- Detection of a RISE and/or FALL of Troponin with AT LEAST ONE Value above the 99th percentile Upper Reference Limit (URL) and with at LEAST ONE of the following:
- Symptoms of Acute Myocardial Ischemia (Central Crushing Chest Pain for Several Minutes)
- New Ischemic ECG Changes
- Development of Pathological Q waves
- Imaging evidence of New Loss of Viable Myocardium or New Regional Wall Motion Abnormality
- Identification of a Coronary Thrombus by Angiography or Autopsy
- ECG is a key investigation to determine the diagnosis and decide the Immediate Management of either STEMI or NSTEMI. ECG changes suggestive of Acute Myocardial Ischemia
- New ST Elevation at the J-Point in TWO Contiguous leads with the Cut-Off Points →
- >/1mm in all other leads except V2-V3 where the following cut-off points apply
- >/2mm in Men >/40years
- >/2.5 in Men <40years
- or >/ 1.5mm in Women regardless of age
- ST Depression and T-wave changes are defined as
- New Horizontal or Down-Sloping ST Depression >/0.5mm in Two Contiguous Leads
- and/or T-Wave inversion >1mm in Two Contiguous Leads with Prominent R Wave or R/S Ratio >1
- New ST Elevation at the J-Point in TWO Contiguous leads with the Cut-Off Points →
Categories
Epidemiology
- The Relative Incidence of STEMI is Decreasing, whilst the incidence of NSTEMI is increasing
- The Inpatient Mortality rate is higher with STEMI Varying between 4-12%
- Ischemic Heart Disease develops on average 7-10 years later in women in comparison to men
- ACS occurs 3-4 times more often in MEN than in Women LESS than 60 years, but AFTER the age of 75, Women represent the majority of patients with ACS
Pathophysiology/Aetiology (5): Type 1
Type 1 MI is an acute event caused by Atherosclerotic Plaque Disruption
Pathophysiology/Aetiology (5): Type 2 MI
- Type 2 MI is an elevated Troponin
- with Evidence of an IMBALANCE between Myocardial Oxygen Supply and Demand, which is unrelated to Coronary AtheroThrombosis
- Examples include Severe Anemia, Hypotension and Respiratory Failure
Pathophysiology/Aetiology (5): Type 3 MI
- Type 3 MI is diagnosed on Autopsy when patents have Sudden Cardiac Death
- with Symptoms suggestive of Myocardial Ischemia
- with associated ECG Changes
- who die before blood samples could
Pathophysiology/Aetiology (5): Type 4 MI
- Is related to PCI
- where there is a Significant Tropnin Rise (x5 ULN) Secondary to the Procedure
- with associated evidence of MI
Pathophysiology/Aetiology (5): Type 5 MI
- Type 5 MI is related to CABG
- where there is a Significant Troponin Rise (x10 ULN)
- with associated Evidence of MI
Type 1 Pathophysiology
- Type 1 is the “Classical” MI → Caused by Athero-Thrombotic Coronary Artery Disease and usually Precipitated by Atherosclerotic Plaque Disruption
- The Relative Burden of Atherosclerosis and Thrombosis is in the Culprit lesion varies greatly, and the Dynamic Thrombotic component leads to Distal Coronary Embolization resulting in Myocycte Necrosis
- Plaque Rupture may not only be complicated by Intraluminal Thrombosis but also by Hemorrhage into the Plaque through the Disrupted Surface, exacerbated the Thrombosis
- It is essential to Integrate the ECG Findings with the aim of classifying Type 1 MI into STEMI or NSTEMI in order to establish the Appropriate treatment
Symptoms
- Chest Pain
- SOCRATES: Ask about Onset, generally Acute Central Crushing Chest Pain that lasts several minutes.
- May radiate to the Jaw, Neck, or Left Arm
- This is more classically for Men rather than Women
- Atypical Presentations should always be considered
- It is important to ask associated Sx as well
- Feelings of Heart Racing/Increased Awareness of Heart Beating → Ask about onset and duration. Ask about Rhythm. Ask about previous Stroke or TIA
- Feeling Weak/Dizzy → Syncope or Pre-Syncope
- Nausea and Diaphoresis → Generally only Nausea not Vomiting but be sure to ask
- SOB →
- Usually Acute and a/w Severe Chest Pain.
- Ask if it is Brought on by Exercise and Relieved by Rest.
- Quantify level of Exercise
- Severe Disease may manifest as SOB at Rest
- Exercise Related Chest Pain → Ask about Exercise Related Angina as it may be a feature int eh Proceeding Weeks/Months
- Swelling of the Legs and Difficulty in Lying Flat/Increased Breathlessness
- Sx of HF should be explored during the Hx as they are indicators of more Severe Disease
- Ask about Orthopnoea and PND
- Generally more common in those with known CV hx
Signs: General Inspection
- Ashen Colour
- Diaphoretic
- Dyspnoeic
- = Those with MI particularly STEMI will appear Unwell from the end of the bed. Those who are suffering from NSTEMI are generally more well
- Levine’s Sign Positive
Signs: Hands
Peripheral Cyanosis → Evidence of CCF
Signs: Wrist and Pulse
- Tachycardia → Comment on rate, Rhythm, Character and Volume
- Hypotension → Evidence of Hemodynamic Instability
Signs: Neck
Raised JVP → May be Elevated secondary to Right HF and Fluid Overload.
You may consider augmenting the JVP by using the Hepatojugular Reflex (pressing on the Liver)
Signs: Closer Inspection and Palpation
- Look for Scars and Subcutaenous Devices → May be evidence of Previous CABG or stunting or ICD which may inform you about possible etiology
- Palpate for Heave → Evidence of RH Strain/Failure
- The Classic Presentation of Myocardial Ischemia is Chest Pain that is Non-Tender, Nonpositional, and Nonpleuritic
- However, because Chest Pain is now no longer the only Anginal Equivalent, Pain that is Tender, Positional and Pleuritic only increases the probability of some other cause, WITHOUT REDUCING THE PROBABILITY OF CORONARY ISCHEMIA
Signs: Auscultation
- MR Murmur may be heard -→ Mitral Valve Disease may be a sequela of MI
- Gallop Rhythm may be heard → S3 is a.w Rapid Ventricular Filling
- Pulmonary Oedema may be heard at the Bases of the Lungs → Should be Screened for if patent is severely SOB
Signs: Sacrum and Ankles
- PO → Sign of RHF and Fluid Overload
DDX: Pericarditis
- Often there is a Viral Prodrome with a More Gradual Onset
- Younger Population
- No Radiation
- Aggravated by LYING FLAT, Relived by Sitting Forward
- Global ST Elevation Characteristic (SADDLE ST CHANGES) and PR Dpression
- Elevated WCC, cRP
- Normal or Mildly Elevated Troponin
- ECHO can occasionally show a Small Pericardial Effusion
DDX: Myocarditis
- Often there is a Viral Prodrome with a More Gradual Onset
- Younger Population
- No Radiation
- Prexic
- Non-Specific ECG Changes
- Elevated ECG Changes
- Elevated WCC, CRP
- Elevated Troponin
- ECHO may show Regional Wall Motion Abnormalities of the LV
- Cardiac MRI shows Myocardial Oedema
DDX: PE
- Acute Onset Dyspnoea with associated Chest Pain
- Can present with Syncope or Presyncope
- a.w Malignancy, OCP, Immobilization
- Unilateral Lower Limb Oedema
- ECG → Most common finding is Sinus Tachycardia, rarely S1Q3T3, suggestive of RH Strain → S1 Q3 T3 refers to the Pathological Signs and the leads in which they occur on ECG. This is rarely seen in PE, but is suggestive of RH Strain
- Wells Score → Can help calculate probability
- CTPA is the diagnostic Test of Choice if High Index of Suspicion
DDX: Aortic Dissection
- Acute Onset
- Described as TEARING Sensation
- Radiates to the BACK → Intrascapular
- Radio-Radial Delay
- L-R Arm BP Difference 9>20 mmhm)
- ECG can occasionally demonstrate ST Elevation if the Cusp of the CA is involved, causing a Simultaneous STEMI
- Elevated Troponin
- Elevated D-Dimer
- CT Aortogram is the Diagnostic cTest of Choice
DDX: Musculoskeletal Pain
- Aggravated by Movement
- Often preceded by Prior Physical Exertion
- Reproducible on Physical examination
- CXR may show Rib Fracture
DDX: Atypical Pneumonia/Pleurisy
- Often a/w Infective Symptoms such as Cough/FEver/chils
- Raised WCC?CRP
- CXR may show consolidation
DDX: Oesophageal Spasm/GORD
- Chest/Epigastric (GTN Relieves Oesophageal Spasm, so can confuse Clinical Picture)
- CXR to screen for Oesophegal Rupture

