Acute Coronary Syndrome (ACS) i.e Type 1 Myocardial Infarction

Question 1

Definition of a Type 1 Myocardial Infarction

Answer 1

1. 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:
   
   1. Symptoms of Acute Myocardial Ischemia (Central Crushing Chest Pain for Several Minutes)
   2. New Ischemic ECG Changes
   3. Development of Pathological Q waves
   4. Imaging evidence of New Loss of Viable Myocardium or New Regional Wall Motion Abnormality
   5. Identification of a Coronary Thrombus by Angiography or Autopsy
2. 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
   
   1. New ST Elevation at the J-Point in TWO Contiguous leads with the Cut-Off Points →
      
      1. >/1mm in all other leads except V2-V3 where the following cut-off points apply
      2. >/2mm in Men >/40years
      3. >/2.5 in Men <40years
      4. or >/ 1.5mm in Women regardless of age
   2. ST Depression and T-wave changes are defined as
      
      1. New Horizontal or Down-Sloping ST Depression >/0.5mm in Two Contiguous Leads
      2. and/or T-Wave inversion >1mm in Two Contiguous Leads with Prominent R Wave or R/S Ratio >1

Question 2

Categories

Answer 2

Question 3

Epidemiology

Answer 3

1. The Relative Incidence of STEMI is Decreasing, whilst the incidence of NSTEMI is increasing
2. The Inpatient Mortality rate is higher with STEMI Varying between 4-12%
3. Ischemic Heart Disease develops on average 7-10 years later in women in comparison to men
4. 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

Question 4

Pathophysiology/Aetiology (5): Type 1

Answer 4

Type 1 MI is an acute event caused by Atherosclerotic Plaque Disruption

Question 5

Pathophysiology/Aetiology (5): Type 2 MI

Answer 5

1. Type 2 MI is an elevated Troponin
2. with Evidence of an IMBALANCE between Myocardial Oxygen Supply and Demand, which is unrelated to Coronary AtheroThrombosis
3. Examples include Severe Anemia, Hypotension and Respiratory Failure

Question 6

Pathophysiology/Aetiology (5): Type 3 MI

Answer 6

1. Type 3 MI is diagnosed on Autopsy when patents have Sudden Cardiac Death
2. with Symptoms suggestive of Myocardial Ischemia
3. with associated ECG Changes
4. who die before blood samples could

Question 7

Pathophysiology/Aetiology (5): Type 4 MI

Answer 7

1. Is related to PCI
2. where there is a Significant Tropnin Rise (x5 ULN) Secondary to the Procedure
3. with associated evidence of MI

Question 8

Pathophysiology/Aetiology (5): Type 5 MI

Answer 8

1. Type 5 MI is related to CABG
2. where there is a Significant Troponin Rise (x10 ULN)
3. with associated Evidence of MI

Question 9

Type 1 Pathophysiology

Answer 9

1. Type 1 is the “Classical” MI → Caused by Athero-Thrombotic Coronary Artery Disease and usually Precipitated by Atherosclerotic Plaque Disruption
2. 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
3. Plaque Rupture may not only be complicated by Intraluminal Thrombosis but also by Hemorrhage into the Plaque through the Disrupted Surface, exacerbated the Thrombosis
4. 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

Question 10

Symptoms

Answer 10

1. Chest Pain
   
   1. SOCRATES: Ask about Onset, generally Acute Central Crushing Chest Pain that lasts several minutes.
   2. May radiate to the Jaw, Neck, or Left Arm
   3. This is more classically for Men rather than Women
   4. Atypical Presentations should always be considered
   5. It is important to ask associated Sx as well
2. Feelings of Heart Racing/Increased Awareness of Heart Beating → Ask about onset and duration. Ask about Rhythm. Ask about previous Stroke or TIA
3. Feeling Weak/Dizzy → Syncope or Pre-Syncope
4. Nausea and Diaphoresis → Generally only Nausea not Vomiting but be sure to ask
5. SOB →
   
   1. Usually Acute and a/w Severe Chest Pain.
   2. Ask if it is Brought on by Exercise and Relieved by Rest.
   3. Quantify level of Exercise
   4. Severe Disease may manifest as SOB at Rest
6. Exercise Related Chest Pain → Ask about Exercise Related Angina as it may be a feature int eh Proceeding Weeks/Months
7. Swelling of the Legs and Difficulty in Lying Flat/Increased Breathlessness
   
   1. Sx of HF should be explored during the Hx as they are indicators of more Severe Disease
   2. Ask about Orthopnoea and PND
   3. Generally more common in those with known CV hx

Question 11

Signs: General Inspection

Answer 11

1. Ashen Colour
2. Diaphoretic
3. Dyspnoeic
4. = Those with MI particularly STEMI will appear Unwell from the end of the bed. Those who are suffering from NSTEMI are generally more well
5. Levine’s Sign Positive

Question 12

Signs: Hands

Answer 12

Peripheral Cyanosis → Evidence of CCF

Question 13

Signs: Wrist and Pulse

Answer 13

1. Tachycardia → Comment on rate, Rhythm, Character and Volume
2. Hypotension → Evidence of Hemodynamic Instability

Question 14

Signs: Neck

Answer 14

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)

Question 15

Signs: Closer Inspection and Palpation

Answer 15

1. Look for Scars and Subcutaenous Devices → May be evidence of Previous CABG or stunting or ICD which may inform you about possible etiology
2. Palpate for Heave → Evidence of RH Strain/Failure
3. The Classic Presentation of Myocardial Ischemia is Chest Pain that is Non-Tender, Nonpositional, and Nonpleuritic
4. 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

Question 16

Signs: Auscultation

Answer 16

1. MR Murmur may be heard -→ Mitral Valve Disease may be a sequela of MI
2. Gallop Rhythm may be heard → S3 is a.w Rapid Ventricular Filling
3. Pulmonary Oedema may be heard at the Bases of the Lungs → Should be Screened for if patent is severely SOB

Question 17

Signs: Sacrum and Ankles

Answer 17

1. PO → Sign of RHF and Fluid Overload

Question 18

DDX: Pericarditis

Answer 18

1. Often there is a Viral Prodrome with a More Gradual Onset
2. Younger Population
3. No Radiation
4. Aggravated by LYING FLAT, Relived by Sitting Forward
5. Global ST Elevation Characteristic (SADDLE ST CHANGES) and PR Dpression
6. Elevated WCC, cRP
7. Normal or Mildly Elevated Troponin
8. ECHO can occasionally show a Small Pericardial Effusion

Question 19

DDX: Myocarditis

Answer 19

1. Often there is a Viral Prodrome with a More Gradual Onset
2. Younger Population
3. No Radiation
4. Prexic
5. Non-Specific ECG Changes
6. Elevated ECG Changes
7. Elevated WCC, CRP
8. Elevated Troponin
9. ECHO may show Regional Wall Motion Abnormalities of the LV
10. Cardiac MRI shows Myocardial Oedema

Question 20

DDX: PE

Answer 20

1. Acute Onset Dyspnoea with associated Chest Pain
2. Can present with Syncope or Presyncope
3. a.w Malignancy, OCP, Immobilization
4. Unilateral Lower Limb Oedema
5. 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
6. Wells Score → Can help calculate probability
7. CTPA is the diagnostic Test of Choice if High Index of Suspicion

Question 21

DDX: Aortic Dissection

Answer 21

1. Acute Onset
2. Described as TEARING Sensation
3. Radiates to the BACK → Intrascapular
4. Radio-Radial Delay
5. L-R Arm BP Difference 9>20 mmhm)
6. ECG can occasionally demonstrate ST Elevation if the Cusp of the CA is involved, causing a Simultaneous STEMI
7. Elevated Troponin
8. Elevated D-Dimer
9. CT Aortogram is the Diagnostic cTest of Choice

Question 22

DDX: Musculoskeletal Pain

Answer 22

1. Aggravated by Movement
2. Often preceded by Prior Physical Exertion
3. Reproducible on Physical examination
4. CXR may show Rib Fracture

Question 23

DDX: Atypical Pneumonia/Pleurisy

Answer 23

1. Often a/w Infective Symptoms such as Cough/FEver/chils
2. Raised WCC?CRP
3. CXR may show consolidation

Question 24

DDX: Oesophageal Spasm/GORD

Answer 24

1. Chest/Epigastric (GTN Relieves Oesophageal Spasm, so can confuse Clinical Picture)
2. CXR to screen for Oesophegal Rupture

Question 25

Diagnostic IX/Screening for other Etiologies : Bloods

Answer 25

1. FBC
   
   1. H WCC → Infection/LRTI
   2. L Hemoglobin → Anemia driving Demand Ischemia
   3. L Platelets → C/I to Thrombolysis
2. Cardiac Biomarkers Troponin and CKMB. Serial data
   
   1. A Rise in Cardiac Biomarkers is a Sign Ischemia
   2. Elevation in Troponin is seen in many forms of Myocardial Injury
   3. Typically the Value between the First and Second reading must double to be suggest an Acute MI
3. Serum U&E
   
   1. Urea and Creatinine → If Renal Function is Impaired, need to use LOWEST possible dose of Contrast during Angiography
4. CRP → Can be Elevated in Myocarditis/Pericarditis
5. Fasting Lipids and HbA1C → Major Contributory risk factors in the development of MI
6. ABG → Assess for Type 1 Response Failure (Pulmonary Oedema) and Assess Lactate
7. D-Dimer → Is a non-specific Hematological investigation; however, it can be useful if negative, as it significantly reduces the probability of an Alternative Diagnosis such as PE, or an AD

Question 26

Diagnostic IX/Screening for other Etiologies: Imaging

Answer 26

1. CXR → Widened Mediastinum in AD/Consoldiation
2. ECHO
   
   1. TTE
      
      1. TTE is performed to evaluate Atrial and Ventricular Size and Function; to Detect Valvular Heart Disease, LVH, and Pericardial Disease, and to estimate RV Systolic Pressure
      2. TTE may also identify LA Thrombus, although the sensitivity is low
   2. TOE
      
      1. Much more sensitive for identifying Thrombi in the LA or LA Appendage and can be used to determine the need for Anticoagulation prior to any attempt to Pharmacological or Electrical Cardioversion

Question 27

Diagnostic IX/Screening for other Etiologies: Procedures

Answer 27

1. ECG
   
   1. ECG Findgings are a key component in diagnosing ACS
   2. They can provide full diagnostic Information
   3. However, an ECG is also just a snapshot in time
   4. ECG findings include:
      
      1. ST elevation in 2 Contigous leads with the cut-off points: >/1mm
      2. Evidence of ST Depression
      3. Evidence of Arrythmia
      4. New BBB

Question 28

Screening for Complications: Bloods

Answer 28

1. FBC
   
   1. H WCC and H CRP may be consistent with Infection/Dressler’s syndrome

Question 29

Screening for Complications: Imaging

Answer 29

1. CXR → Cardiomegaly/Pulmonary Oedema–HF

Question 30

Screening for Complications: Procedures

Answer 30

1. ECHO
   
   1. HF and Valvular HD are major complications o fMI
2. ECG
   
   1. Repeat ECG should be performed to evaluate for New Arrhythmias
   2. Heart Blocks secondary to Ischemia
   3. Broad Complex Tachycardia

Question 31

Management: Prevention

Answer 31

1. Lifestyle Management:
2. Increased Exercise
3. Reduce Salt Intake
4. Reduce Fatty Diet
5. Smoking Cessation
6. Tight Glycemic Control if Diabetic

Question 32

Management: Acute

Answer 32

1. Initial Assesmsnent → Airway, Breathing, Circulation and Assessment for Hypovolemic Shock, ECG
2. Key Factors from Hx: Timeline/Onset of Sx. Key RF (Hypertension, Previous Events, Smoking, Diabetes)
3. Actions in Parallel
   
   1. Obtain IV Access 2x, Wid eBore
   2. ALL BLOODS
   3. ECG STEMI/NSTEMI
   4. ACS Suspected → Load with Dual Antiplatelt Therapy (Aspirin 300mg + Ticagrelor 180mg OR Alternatively Clopidogrel 600mg if patient has high bleeding risk
4. ECG
   
   1. STEMI Diagnosed → Time is Muscle
      
      1. Discuss with cardiology
      2. Urgent Revascularization (PCI or Thrombolysis)
      3. PCI if <120 minutes since onset of Sx and Thrombolysis if >120mins (discuss with Cardiology/Helicopter Transfer
      4. If >120mins consider Thrombolysis
   2. NSTMEI Diagnosed
      
      1. Discuss with Cardiology
      2. ECGs if developing ongoing Pain
      3. Serial data (ECG and Troponin) @6hours post first sample
      4. If patient has ongoing pain, despite Analgesia, this suggests ongoing Myocardial Ischemia, consider Urgent Revascularization–discuss with cardiology
   3. Anticoagulate (UFH/MWH)→ Discuss preference with Cardiology
   4. Analgesia → 2.5 mg Cylcopmorph IV and/or IV Paracetamol
   5. Consider Rate Cotnrol/Anti-Arrythmic may be considered → BB/Amiodarone
   6. Maintain Sats >90. Hypoxia → Oxygen only if SaO2 <90%, routine oxygen is not recommended in those with SaO2 >90%
   7. Consider Antiarrythmic
   8. Nitrates → Consider GTN Spray Sublingual/Patch or via IV Infusion if SBP is >90 mmHG
   9. Place Defribillator Pads on patient
   10. CXR
       
       1. If evidence of Pulmonary Oedema, or Desaturation, tx with IV Diuretics. Check BP is not low (<100 mmhg( as this may worsen the condition
       2. Consider CPAP if patient continuing to desaturate
   11. Transfer patient to a specialized setting (Resus/CATHLAB CCU/HDU) Whislt awaiting transfer
   12. Observe for evidence of Ventricular Failure
       
       1. Inferior MI infracting the RV → Avoid Nitrates, Ensure Adequate IV Fluid Support, can develop HB/Brady Arrhythmias
       2. anterior/Lateral MI Infracting the LV → Avoid BB/CCB. If Acute LV Decompensation, treat with IV Diuresis/Nitrates/CPAP
       3. Manage BP if Hypotensive. If severe, may benefit from Inotropes/Intra-aortic Balloon Pump, LV Assist Device

Question 33

Management: Long Term

Answer 33

1. MDT Approach Cardiac Rehabilitation including input from:
   
   1. Physiotherapy with regard to increasing exercise
   2. Specialized Cardiac Nurses discuss Recogniton of Sx and Care
   3. Dietition for Advice around Healthy Eating with a View to Tighter Glycemic Control if Diabetic and Lowering Lipids if Hypercholestrolemic
   4. Social Work and Occupational Therapy
2. Pharmacological
   
   1. Continue Antiplatelt Therapy for at least 12 months following PCO
   2. Rhythm Control e.g. BB
   3. Antihypertensive e.g. ACEi
   4. Consider Lipid Lowering Agent e.g. Statin
   5. Review with endocrinology if Diabetic
   6. Diuretic if Evidence of HF

Question 34

Complications

Answer 34

1. NSTMEI may convert to STEMI
2. Broad Complex Tachycardias → Ventricular Tachycardia which if not treated quickly can degenerate to V Fib
3. HB cna occur if Ischemia affects Conductive Tissues
4. Cardiac Arrest/Death → Arrhythmogenic or Systole or Pump Failure
5. Decompensated Ventricular Function:
6. Ventricular Aneurysm/Ventricular Septal Defect
7. Dressler’s Syndrome (Pericarditis Post MI)

Question 35

Prognosis

Answer 35

1. Ischemic Heart disease is the number one cause of Death in Adults worldwide, although the Rate of Mortality is Decreasing
2. Thrombolysis In Myocardial Infarction (TIMI) Score predicts outcomes.
   
   1. It is best used for those who have UA/NSTEMI to predict likelihood of further Thrombotic Events
   2. Takes into account Age, RF (i..e Hypercholestrol and Diabetes, eCG Changes, Angina Events and Cardiac Biomarkers
3. Outcomes: Short-Term NSTEMI > STEMI, Long-Term NSTEMI = STEMI