Week 4 Acute Coronary Syndromes Flashcards
Define ACS
ACS refers to any group of symptoms consistent with acute myocardial ischaemia. It includes Unstable angina, STEMI and NSTEMI. Associated with rupture of an atherosclerotic plaque that can lead to partial/ full occlusion of coronary vessel leading to ischaemia.
Describe the symptoms of ACS
- Central chest pain: crushing/ heavy/ chest tight
- Radiates to shoulder, neck, jaw, left arm
- Diaphoresis (excessive sweating) due to SNS activation
- Nausea and Vomiting due to parasympathetic NS
- Feeling of impending doom
Describe the difference between stable and unstable angina.
What are the exacerbating and relieving factors for stable angina?
Unstable angina- chest pain present even at rest
Stable angina- chest pain presents during exercise/ effort that increases the metabolic demands of the heart, CA narrowed leading to ischaemia with effort.
Exacerbating factors: exercise/ stress/ tachycardia/ effort
Relieving factors: Sublingual nitrates/ rest
What are some of the differential diagnoses for ACS?
1) Lungs:
- PE, pleuritic chest pain
- Costochondritis- pain reproducible and localised
2) Oesophageal and gastric:
- Oesophageal rupture
- Reflux oesophagitis - not effort related, nausea
- Gastritis - worse on eating, relieved antacids
3) Anxiety
4) Aortic Aneurysm
5) Pericardium:
- Pericarditis: pain better on leaning forward, pericardial rub heard on auscultation, ECG
- Pericardial effusion or cardiac tamponade
6) Infection :
- Endocarditis
- Myocarditis
- In both patient would have signs of infective illness, raised inflammatory markers, weak, constant pain
What are some of the examination findings of a patient with ACS?
- May seem distressed or may be completely normal if not in pain at that moment
- Pallor/ Diaphoresis/ cold/ clammy - SNS activation
- Peripheral or central cyanosis- ↓ oxygen saturation
- Hypotension- ↓CO
- Dizziness, weak
- Chest discomfort, dysponea
- Bibasal crackles- pulmonary oedema due to Left sided dysfunction
- Raised JVP, hepatomegaly, peripheral oedema due to right sided dysfunction
- Auscultation:
- Mitral stenosis
- S3 / S4 sounds or gallop rhythm
- extra systoles- AF/ ventricular tachycardia and fibrillation (sudden death risk).
Describe the major features of Unstable angina and how this differs to NSTEMI
Unstable angina:
- Clincal entity- symptoms correlate with clinical condition
- Ischaemia without infarction (unlike NSTEMI)
- Hypoxia which causes chest discomfort and ischaemia
- No necrosis of myocytes and therefore no release of biomarkers
- First presentation or worsening of stable angina, pain now more frequent/ at rest/ minimal exertion
- Usually no ECG changes
- Ischaemia of myocardium only due to partial occlusion of CA.
Describe the major features of NSTEMI
NSTEMI:
- Clinicopathological entity- symptoms, signs and lab results fit with clinical syndrome and pathology
- Ischaemia and infarction (more severe than UA as infarction, infarction less severe than STEMI).
- Myocardial damage and necrosis
- Release of biomarkers: ckMB (creatinine kinase muscle/ bone) and Troponin ( raised 6 hrs after presentation).
-
ECG changes:
- ST segment depression
- T wave inversion
- Non specific ECG changes
- Due to severe occlusion of coronary artery, often by plaque rupture causing partial occlusion of CA via thrombus formation.
- Ischaemia proximally to occluded artery
- Infarcation distally- subendocarial infarction characteristic of NSTEMI.
Describe the major features of STEMI:
STEMI:
- Raised Troponin (6 Hrs after presentation) and ckMB
- ECG changes: ST segement elevation
- Full occlusion of coronary artery
- Plaque rupture and thrombus fully occluding blood flow
- Ischaemia proximally initially with infarction distally
- Infarction spreads proximally- becomes a transmural infarction.
- More severe symptoms
List the complications of ACS:
Transmural infarction (STEMI)
- Damage to the papillary muscles:
- Valvular dysfunction
- Regurgitation
- Prolapse
- Damage to heart wall:
- Cardiac Rupture
- Ventricular aneurysm ( wall bulges outwards)
- Right ventricular infarction from left MI
- Reccurrent ischaemia
- Damage to conduction system:
- Tachycardia
- Bradycardia
- Bradycardia leads to low CO
- Low CO leads to hypotension
- Hypotension leads to hypoperfusion:
- Cardiogenic shock
- Acute kidney injury
- Damage to pericardium- pericarditis
- Mural thrombosis- thrombus sticks to wall of atria/ ventricles
What are the steps in the diagnosis of ACS?
ACS:
-
Cardiac enzymes:
-
Troponin - released by myocardial damage
- Raised 6 hours after presentation
- Peaks 24-96 hours after
- Remains elevated 14 days
- Creatine kinase MB:
- Rises after 12 hours to clinically significant level
- Only remains raised for ~2 days
- Not specific also raised with skeletal muscle damage
-
Troponin - released by myocardial damage
-
ECG: (may be normal in 20% P’s initially)
- Unstable angina- usually no change, could be T wave inversion
- NSTEMI- ST segement depression, T wave inversion
- STEMI- elevated ST segment
-
Full blood count:
- U and E’s - AKI
- inflammatory markers- CRP
- Blood glucose - hyperglycaemia common in ACS patients
- Lipids- Hyperlipidaemia
-
Chest Xray:
- looking for cardiomegaly, pulmonary oedema, widened mediastinum.
- DO NOT DELAY TREATMENT FOR CXR.
Why does ischaemia cause pain?
- O2 unavailable to tissues
- Tissues survive using anaerobic metabolism
- Produces lactic acid
- Activates chemical pain receptors
- Damaged cells produce bradykinin
- Bradykinin activates chemical pain receptors
Explain pathophysiology of cardiac ischaemia:
How does the coronary artery become occluded?
(Atherosclerosis process)
- By the development of an atherosclerotic lesion in the coronary artery, rupture of the plaque and thrombus formation that occludes blood flow.
Atherosclerosis:
- Damage to tunica intima endothelial cells:
- Hyperlipidaemia, ↑ cholesterol / LDL
- Hyperglycaemia
- Hypertension ( turbulent blood flow)
- Bacterial/ viral toxins
- Toxins from smoking
- Damaged endothelium become dysfunctional endothelium that release inflammatory cytokines and express adhesion molecules for monocytes and T lymphocytes.
- Endothelial dysfunction allows LDL to enter tunica intima
- Dysfunctional endothelium also releases ROS
- Oxidises LDL which induces monocytes to infiltrate and become macrophages
- Macrophages ingest oxLDL becoming Foam cell.
- Foam cells and T lymphocytes form inital fatty streak.
- Foam cells release GF’s which stimulate SMC’s in media to infilitrate intima and divide.
- SMC’s migrate over fatty core forming a fibrous cap. - Stable Plaque.
- Plaque rupture- balance of collagen production vs protease release from foam cells. Proteases degrade the ECM of the fibrous cap
- Loss integrity of endothelium and fibrous cap exposes blood to highly thrombogenic subendothelium:
- Collagen/ vWF/ TF.
- Platelet activation and adhesion- primary haemostatic plug
- TF- coagulation cascade- formation of secondary haemostatic plug with crosslinked fibrin.
Fill in the blanks
Delineate phases of MI
- Ischaemic phase:
- blockage of CA, no O2 supply
- myocardium survives on anaerobic respiration
- Cannot keep up with demands
- Infarct phase:
- Irreversible cell damage
- Myocardial necrosis
- Affected area contributes less to depolarisation
What are the following indicative ECG changes for:
Ischaemia?
Injury?
Infarction/ Scar?
Ischaemia:
- T wave inversion
- ST depression
Injury:
- ST elevation - reflects dying myocardium
Infarction/ scar:
- Pathological Q wave preceeding QRS complex
- Large inversion of Q wave
