Questions on acute coronary syndrome (ACS)
Definition
- What is ACS? Why both of them known as collectively?
- What is unstable angina?
- What is myocardial infarction (MI)?
- What is silent MI?
Epidemiology
- –
Etiology and Pathophysiology
- What is the pathology of unstable angina?
- What is the pathology of MI?
- Who are more prone to develop silent MI?
- What is the cause of silent MI?
Clinical manifestations
- How may a patient with MI present to you?
Examinations
- –
Investigations
- How will you investigate this patient?
- What are the ECG findings in MI?
- In which leads do you expect changes of inferior MI?
- In which leads do you expect changes of anterior MI?
- In which leads do the ECG changes occur in acute anteroseptal MI?
- In which leads do the ECG changes occur in acute anterolateral MI?
- What are the criteria of pathological Q-wave?
- What are the cardiac markers?
Diagnosis
- A 50-year-male smoker develops sudden severe chest pain which radiates to neck. He vomited several times and now he is sweating. What is your diagnosis?
- Please tell WHO diagnostic criteria of MI.
Treatment
- How can you manage unstable angina?
- What is the early/immediate management of this patient?
- What drugs are used to relief pain in MI?
- What are the contraindications of morphine?
- What are the thrombolytic agents?
- Which is commonly used in our country?
- How is streptokinase given?
- What are the side effects/complications of streptokinase?
- What are the indications of thrombolytic therapy?
- What are the contraindications of thrombolytic therapy?
- What is the late management of MI?
- What are the roles of ACE inhibitor in MI?
- What are the roles of β-blocker in MI?
Complications
- What are the immediate complications of MI?
- What are the complications of MI?
Rimikri
SOLVES
What is ACS? Why both of them known as collectively?
ACS means acute coronary syndrome.
Acute coronary syndrome is a term that encompasses both unstable angina and MI (STEMI and NSTEMI).
These two are considered collectively as initial emergency management is same done by using ACS triage therapy. It is also a dynamic process, i.e. unstable angina if not treated appropriately in time, may progress to MI.
* Pre-exam preparation for medicine, HN Sarker
What is unstable angina?
Unstable angina is characterized by new-onset or rapidly worsening angina (crescendo angina), angina on minimal exertion or angina at rest in the absence of myocardial damage.
* Pre-exam preparation for medicine, HN Sarker; Davidson’s Principles and Practice of Medicine, 22nd edition Page: 589
What is myocardial infarction (MI)?
Acute ischemic necrosis of an area of myocardium is called myocardial infarction.
* Pre-exam preparation for medicine, HN Sarker
Figure: The time course of MI. The relative proportion of ischaemic, infarcting and infarcted tissue slowly changes over a period of 12 hours. In the early stages of MI, a significant proportion of the myocardium in jeopardy is potentially salvageable.
* Davidson’s Principles and Practice of Medicine, 22nd edition Page: 590
What is silent MI?
Painless MI is called silent MI.
* Pre-exam preparation for medicine, HN Sarker
Who are more prone to develop silent MI?
Older patients or those with diabetes mellitus.
* Pre-exam preparation for medicine, HN Sarker
What is the pathology of unstable angina?
Ischemia caused by dynamic obstruction of a coronary artery due to plaque rupture or erosion with superimposed thrombosis (supply-led angina).
* Pre-exam preparation for medicine, HN Sarker
What is the pathology of MI?
Myocardial necrosis caused by acute occlusion of a coronary artery due to plaque rupture or erosion with superimposed thrombosis.
* Pre-exam preparation for medicine, HN Sarker
What is the cause of silent MI?
Autonomic neuropathy.
* Pre-exam preparation for medicine, HN Sarker
How may a patient with MI present to you?
- Prolonged cardiac pain (>30 minutes): Chest, throat, arms, epigastrium or back
- Breathlessness
- Nausea and vomiting
- Collapse/syncope
- Anxiety and fear of impending death
* Pre-exam preparation for medicine, HN Sarker; Davidson’s Principles and Practice of Medicine, 22nd edition Page: 590
* Davidson’s Principles and Practice of Medicine, 22nd edition Page: 590
What are the characteristics of chest pain in MI?
Read more about chest pain at Symptoms of cardiovascular disease
* Macleod’s Clinical Examination, 13th Edition Page: 101
What are the physical signs you will get of a patient with ACS?
Physical signs
- Signs of sympathetic activation
- pallor, sweating, tachycardia
- Signs of vagal activation
- vomiting, bradycardia
- Signs of impaired myocardial function
- Hypotension, oliguria, cold peripheries
- Narrow pulse pressure
- Raised JVP
- Third heart sound
- Quiet first heart sound
- Diffuse apical impulse
- Lung crepitations
- Signs of tissue damage
- fever
- Signs of complications
- e.g. mitral regurgitation, pericarditis
* Davidson’s Principles and Practice of Medicine, 22nd edition Page: 590
How will you investigate this patient?
Investigate the patient by:
- ECG
- Cardiac markers
- In unstable angina, there is no detectable rise in plasma cardiac biomarkers or enzymes.
- In contrast, MI causes a rise in the plasma concentration of enzymes and proteins that are normally concentrated within cardiac cells.
- Blood tests—CBC, ESR, CRP, blood sugar, and lipid profile
- A leucocytosis is usual, reaching a peak on the first day.
- The erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are also elevated.
- X-ray chest PA view
- This may demonstrate pulmonary oedema
- The heart size is often normal but there may be cardiomegaly due to pre-existing myocardial damage.
- Echocardiography
- For assessing ventricular function
- For detecting important complications, such as mural thrombus, cardiac rupture, ventricular septal defect, mitral regurgitation and pericardial effusion.
* Pre-exam preparation for medicine, HN Sarker; Davidson’s Principles and Practice of Medicine, 22nd edition Page: 592, 593
What are the ECG findings in MI?
The ECG findings in MI are:
- ST segment elevation with convexity upward > 1mm in limb leads, and >2 mm in chest leads
- Diminution of R-wave
- Pathological Q-wave
- Symmetrical T-wave inversion.
Normal ECG complex. |
Acute ST elevation (‘the current of injury’). |
Progressive loss of the R wave, developing Q wave, resolution of the ST elevation and terminal T-wave inversion. |
Deep Q wave and T-wave inversion. |
Old or established infarct pattern; the Q wave tends to persist but the T-wave changes become less marked. |
Figure: The serial evolution of ECG changes in transmural MI.
* Pre-exam preparation for medicine, HN Sarker; Davidson’s Principles and Practice of Medicine, 22nd edition Page: 592
What are the criteria of pathological Q-wave?
The criteria of pathological Q-wave are:
- Q-wave height >3 mm
- Q-wave wide >1 mm
- Q-wave is more than 25% of the succeeding R-wave.
* Pre-exam preparation for medicine, HN Sarker
Note:
Normal Q wave:
- Usually absent
- Depth: <2mm & width: 1 small sq
In which leads do you expect changes of anterior MI?
V1–6, I, and AVL.
* Netter’s Internal Medicine, 2nd Edition Page: 197
In which leads do you expect changes of inferior MI?
Lead II, III, and AVF.
* Netter’s Internal Medicine, 2nd Edition Page: 197
In which leads do the ECG changes occur in acute anteroseptal MI?
In which leads do the ECG changes occur in acute anterolateral MI?
V4-6
Note:
In true posterior infract:
* Netter’s Internal Medicine, 2nd Edition Page: 197
What are the cardiac markers?
Commonly used cardiac markers are (according to time of appearance):
- Troponin T/I
- CK-MB (cardio-specific isoform of creatine kinase)
- AST (aspartate aminotransferase)
- LDH (lactate (hydroxybutyrate) dehydrogenase)
* Pre-exam preparation for medicine, HN Sarker
Note:
- CK starts to rise at 4–6 hours, peaks at about 12 hours and falls to normal within 48–72 hours.
- CK is also present in skeletal muscle, and a modest rise in CK (but not CK-MB) may sometimes be due to an intramuscular injection, vigorous physical exercise or, particularly in older people, a fall.
- Defibrillation causes significant release of CK but not CK-MB or troponins.
- The most sensitive markers of myocardial cell damage are the cardiac troponins T and I, which are released within 4–6 hours and remain elevated for up to 2 weeks.
Figure: Changes in plasma cardiac biomarker concentrations after MI. CK and troponin I (Tn I) are the first to rise, followed by AST and then LDH. In patients treated with reperfusion therapy, a rapid rise in plasma creatine kinase (curve CK (R)) occurs, due to a washout effect.
* Davidson’s Principles and Practice of Medicine, 22nd edition Page: 593
A 50-year-male smoker develops sudden severe chest pain which radiates to neck. He vomited several times and now he is sweating. What is your diagnosis?
Please tell WHO diagnostic criteria of MI.
According to the WHO the diagnostic criteria of MI as revised in 2000 –
- A cardiac troponin rise,
- Accompanied by either
- typical symptoms,
- pathological Q-waves, and
- ST elevation or depression or
- coronary intervention .
* Pre-exam preparation for medicine, HN Sarker
Figure: Universal definition of myocardial infarction
* Davidson’s Principles and Practice of Medicine, 22nd edition Page: 590
How can you manage unstable angina/non ST elevated MI?
To manage unstable angina:
- Patient should be hospitalized
- Bed rest
- Anti-ischemic treatment
- Nitrates
- These should first be given sublingually or by buccal spray (0.3–0.6 mg) if the patient is experiencing ischemic pain.
- If pain persists after three doses given 5 min apart, intravenous nitroglycerin (5–10 μg/min using nonabsorbing tubing) is recommended.
- β blockers
- Atenolol—50–100 mg daily or,
- Metoprolol— 50–100 mg 12 hourly
- Calcium channel blockers
- Patients whose symptoms are not relieved by adequate doses of nitrates and beta blockers, or in patients unable to tolerate adequate doses of one or both of these agents, or in patients with variant angina
- Morphine sulfate
- Patients whose symptoms are not relieved after three serial sublingual nitroglycerin tablets or whose symptoms recur with adequate anti-ischemic therapy
- Nitrates
- Antithrombotic therapy
- Antiplatelet Drugs
- Aspirin—300 mg stat, then 75 mg daily
- Clopidogrel—300 mg stat, then 75 mg daily
- Anticoagulants
- Subcutaneous low molecular weight heparin (enoxaparin 1mg/kg 12 hourly).
- Antiplatelet Drugs
- If medical treatment fails
- PCI (primary percutaneous coronary intervention)
- CABG (coronary artery bypass grafting).
* Pre-exam preparation for medicine, HN Sarker; Harrison’s Principles of Internal Medicine, 19th Edition Page: 1595-1597
Note: Q. In CABG which vessels are used?
- Great saphenous vein,
- Internal mammary artery.
What is the early/immediate management of ACS/ST elevated MI?
Management protocol of acute myocardial infraction:
- Complete bed rest
- Oxygen inhalation – High flow (3-4 L/min)
- Open an I/V channel with 5% DA at 3-5 dpm (if patient nondiabetic and without HF)
- Keep the patient in cardiac monitor
- Tab. Aspirin 300mg – crushing/ chewing stat
- Tab. Clopidogrel 600mg / Tab. Parsugrel 60 mg orally stat
- Spray GTN 2 puff sublingual – stat and SOS
- No I/M injection
- Inj. Pethidine 100mg dissolved in 5ml d/w – I/V stat slowly Or,
- Inj. Morphine sulphate after dilution – 1ml (15mg) dissolved with 14ml d/w. I/V 3ml (mg)/dose, if chest pain doesn’t subside
- Inj. Prochlorprazine 12.5 mg I/V stat
- Inj. Streptokinase – 1.5 million units mixed with 100 cc NS I/V infusion within 1 hour + Inj. Hydrocortisone 2 vials I/V stat before starting streptokinase – If criteria fulfilled
- Inj. Enoxaparine 1 mg/kg of body weight subcutaneous around the umbilicus 12 hourly (5-7 days)
- Tab. Aspirin 75 mg, 0+1+0 (after meal)
- Tab. Clopidogrel 75mg 0+1+0
- Tab. GTN 2.6 mg 1+0+1+0
- Tab. Atorvastatine 20mg/ Rosuvastatine 10mg, 2 tabs stat then 0+0+1
- Cap. Omeprazole/ Pantoprazole 20mg, 20mg stat then 1+0+1 (before meal)
- Anxiolytics (Clonazepam, Bromazepam, Diazepam) 0+0+1
- Beta blocker – Tab. Metoprolol 25mg 12 hourly – if not contraindicated
- ACE inhibitor/ ARB – if failure is impending in anterior MI
What is the late management of MI?
- Risk stratification and further investigation.
- Lifestyle modification
- Cessation of smoking
- Regular exercise
- Diet (weight control, lipid-lowering, ‘Mediterranean diet’).
- Secondary prevention drug therapy
- Antiplatelet therapy (aspirin and/or clopidogrel)
- β -blocker
- ACE inhibitor/ARB
- Statin
- Additional therapy for control of diabetes and hypertension.
- Mineralocorticoid (Aldosterone) receptor antagonist.
- Rehabilitation
- Devices
- Implantable cardiac defibrillator for high-risk patients.
* Pre-exam preparation for medicine, HN Sarker; Davidson’s Principles and Practice of Medicine, 22nd edition Page: 598
What drugs are used to relief pain in MI?
Opiate, e.g. morphine or diamorphine.
* Pre-exam preparation for medicine, HN Sarker
What are the contraindications of morphine?
The contraindications of morphine are –
- bronchial asthma,
- COPD,
- respiratory depression, and
- profound hypotension.
* Pre-exam preparation for medicine, HN Sarker
What are the indications of thrombolytic therapy?
Patients with MI presenting within 12 hours of the onset of symptoms and PCI is unavailable.
ECG shows—
- New onset left bundle branch block or
- Characteristic ST segment elevation > 1 mm in the limb leads or 2 mm in the chest leads.
* Pre-exam preparation for medicine, HN Sarker
What are the thrombolytic agents?
Streptokinase, alteplase,reteplase and tenecteplase.
* Pre-exam preparation for medicine, HN Sarker
Which is commonly used in our country?
Streptokinase.
* Pre-exam preparation for medicine, HN Sarker
How is streptokinase given?
1.5 million units mixed in 100 mL of normal saline infuse intravenously over 1 hour.
* Pre-exam preparation for medicine, HN Sarker
What are the side effects/complications of streptokinase?
The side effects/complications of streptokinase are:
- Bleeding such as stroke.
- Transient hypotension.
* Pre-exam preparation for medicine, HN Sarker
What are the contraindications of thrombolytic therapy?
The contraindications of thrombolytic therapy / Relative contraindications to thrombolytic therapy: potential candidates for primary PCI –
- Active internal bleeding
- Previous subarachnoid or intracerebral hemorrhage
- Uncontrolled hypertension
- Recent surgery (within 1 month)
- Recent trauma (including traumatic resuscitation)
- High probability of active peptic ulcer
- Pregnancy
* Pre-exam preparation for medicine, HN Sarker; Davidson’s Principles and Practice of Medicine, 22nd edition Page: 596
What are the roles of ACE inhibitor in MI?
ACE inhibitor can counteract ventricular remodelling and thus –
- Prevent the onset of heart failure
- Improve survival
- Reduce recurrent MI
- Avoid rehospitalization.
* Pre-exam preparation for medicine, HN Sarker
Figure: Infarct expansion and ventricular remodelling. Full-thickness Ml causes thinning and stretching of the infarcted segment (infarct expansion), which leads to increased wall stress with progressive dilatation and hypertrophy of the remaining ventricle (ventricular remodelling). |
*Davidson’s Principles and Practice of Medicine, 22nd edition Page: 596, 597
What are the roles of β-blocker in MI?
β-blocker can –
- Relieve pain
- Reduce arrhythmias
- Reduce blood pressure
- Improve short-term mortality in patients who present within 12 hours of the onset of symptoms.
* Pre-exam preparation for medicine, HN Sarker
What are the immediate complications of MI?
- Arrhythmia
- Ischemia
- Cardiogenic shock.
* Pre-exam preparation for medicine, HN Sarker
What are the complications of MI?
- Early complications are:
- Arrhythmia—All types of arrhythmia
- Ischemia
- Cardiogenic shock
- Pericarditis
- Thromboembolism
- Mechanical complications are:
- Rupture of chorda tendinae or papillary muscle damage leading to MR
- Rupture of interventricular septum leading to VSD.
- Late complications are:
- Ventricular aneurysm
- Dressler’s syndrome (pleurisy, pericarditis, and pyrexia-3P)
- Shoulder hand syndrome.
* Pre-exam preparation for medicine, HN Sarker
* Davidson’s Principles and Practice of Medicine, 22nd edition Page: 596
Points to be noted
- Most dangerous complication of MI is ventricular fibrillation.
- Immediate cause of death after MI is ventricular fibrillation and cardiac arrest/ asystole.
- Anterior MI is worse, because it causes arrhythmia.
- Inferior MI causes bradycardia.
- In inferior MI, heart failure is common.
Q. How will you understand that streptokinase is working?
A. By sing the ECG, reperfusion arrhythmia.
Q. A patient was administered streptokinase 2 years back. Now he developed MI. Can he take streptokinase again? If not which drug should be given?
A. No. As he take streptokinase 2 years back, there is developed antibody against streptokinase. In that we can give him Alteplase (tissue plasminogen activator).
Q. For how long the antibody against streptokinase persists?
A. Upto 5 years.