Flashcards in Angina and ACS Deck (57):
What is the most common site of infarction
What is meant by coronary artery dominance?
The dominant coronary artery is that which gives rise to the posterior descending artery and thereby supplies the posterior septum
80% of people exhibit RCA dominance
20% exhibit circumflex dominance
What three conditions comprise acute coronary syndrome (ACS)
3. Unstable angina
What are the characteristics of classical/exertional angina?
Constricting discomfort in the chest, arms, neck and jaw
Provoked by physical exertion, especially after meals and in cold windy weather, or by anger or excitement
Relieved (usually within minutes) with rest or GTN
What is meant by the term stable angina?
Angina is stable when it is not a new symptom and there is no change in the frequency or severity of the attacks
What is meant by the term unstable angina?
Angina of recent onset (<24 hr) or a deterioration in a previous stable angina with symptoms frequently occuring at rest (i.e. ACS)
What is variant (Prinzmental's angina)?
Angina that occurs without provocation, usually at rest, as a result of coronary artery spasm. More common in women
Describe the physiological process of atheromatous formation
Damage to vessel wall is caused by mechanical stresses (e.g. from morbid hypertension), biochemical abnormalities (e.g. elevated LDL, diabetes mellitus), immunological factors (e.g. free radicals from smoking) or inflammation. This initial endothelial injury or dysfunction triggers the development of atherosclerosis. There is increased permeability to and accumulation of oxidized lipoproteins, which are taken up by macrophages at focal sites within the endothelium to produce lipid-laden foam cells. Macroscopically these lesions are seen as flat yellow lines on the endothelium called 'fatty streaks'. Release of cytokines by the damaged endothelium promotes further platelet adhesion and accumulation of macrophages as well as smooth muscle proliferation. This leads to formation of an atheroma
How much of the artery is occluded in stable angina?
How much of the artery is occluded in unstable angina?
What is the most common cause of angina?
Myocardial ischaemia due to atheroma
What are the major causes of ischaemia?
Decrease in the flow of oxygenated blood to the mycoadrium due to anaemia
Increased demand for oxygen due to increase cardiac output e.g. hyperthyroid or myocardial hypertrophy (due to aortic stenosis or hypertension)
How are patients with stable angina managed? (N.B 5 drug types used)
1. Modify risk factors: stop smoking, encourage exercise, encourage weight loss, control hypertension, control diabetes, give statins if cholesterol is raised
2. Aspirin (75-150mg/24 hr)
3. Beta blocker (e.g. atenolol 50-100mg/24 hours) unless contraindicated e.g. COPD, asthma
For symptom relief GTN spray
For prophylaxis oral isosobide mononitrate (N.B. 8hr nitrate free period to prevent tolerance)
5. Calcium channel blocker (useful if beta-blockers are contraindicated)
6. If still not controlled, try a potassium channel activator e.g. nicorandil
Blockage of which artery causes anterior MI? What leads are affected on the ECG?
ST elevation in V1-V4
Blockage of which artery causes lateral MI? What leads are effected on the ECG?
ST elevation in I, aVL, V5 and V6
Blockage of which artery causes posterior MI? Which leads are effected on the ECG?
RCA or circumflex
Reciprocal ST depression in V1-V3
(ST elevation in V7-V9)
Blockage of which coronary artery causes inferior MI? Which leads are effected on the ECG?
RCA or circumflex
ST elevation in II, III, aVF
What is the most common complication(s) of an anterior MI?
1, Cardiac tampenade
2. Mitral regurgitation
What is the most common complication(s) of a posterior MI?
What is Dresner's syndrome?
Pericarditis following MI
What are the non-modifiable risk factors of ACS?
2. Male gender
3. Family history (MI in first degree relative)
What are the modifiable risk factors of ACS?
6. sedentary lifestyle
7. cocaine use
How is acute MI diagnosed?
1. Initial increase in troponin. Serum levels increase within 3-12 hours, peak at 24-48 hours and return to baseline over 5-14 days. Normal troponin levels= <0.01. N.B. takes a few hours after MI for troponin to rise. Peak levels are useful for risk stratification
2.ECG changes- ST elevation, development of pathological Q waves. In 20% of MI, ECG is normal initially
3. CXR: cardiomegaly, pulmonary oedema, widened mediastinum due to aortic rupture
What factors determine treatment of an MI?
1. Is the ST segment elevation
2. Is there a rise in cardiac troponin (if there is no rise in cardiac troponin 6 hours after onset of symptoms, no cardiac damage has occurred and prognosis is good)
What is the pre-hospital treatment of suspected ACS
1. Aspirin 300mg chewed (unless absolute contraindication)
2. Nitrate- GTN sublingual
3. Analgesia e.g. morphine 5-10mg IV+metoclopramide (anti-emetic) 10mg IV (not IM due to risk of bleeding with thrombolysis)
What initial tests should be done upon admission of suspected STEMI?
1. 12 lead ECG
What is the initial treatment of confirmed STEMI?
1. Aspirin 300mg PO (if not already given)
2. Morphine 5-10mg IV + anti-emetic e.g. metoclopramide 10mg IV
3. GTN: routine use no longer recommended in the acute setting unless the patient is hypertensive or in acute LV failure
4, Oxygen if patients have O2 saturations <95%, are breathless or in acute LVF
5. Restore coronary perfusion by PCI (if available) or thrombolysis
6. Anticoagulation using injectable anticoagulant. Preferably bivalirudin, if not available use enoxaparin
How quickly should a patient be transferred for PCI in STEMI? What should happen if a PCI is not available within this time frame?
1. Transferred within 120 minutes of first medical contact
2. If this is not possible, patients should receive fibrinolysis and be transferred subsequently to a primary PCI centre for rescue PCI if fibrinolysis is unsuccessful or for angiography if fibrinolysis is successful
What is the target time for administering fibrinolytics in STEMI? At what point does it become contraindicated?
Target time is within 30 minutes of admission. Benefit then reduces steadily and it is contraindicated >24 hours after onset of symptoms
What fibrinolytic is used first line in STEMI?
What is the major difference in the pathophysiology of STEMI and NSTEMI?
Full thickness damage of heart muscle in STEMI vs. partial thickness damage of heart muscle in NSTEMI
Briefly describe the acute management of ACS without ST elevation?
Medical management until symptoms settle unless patient is high risk
Admit patient to CCU and monitor closely
Oxygen (if sats <40%. Use calcium antagonist e.g. verapamil if beta-blocker contra-indicated
ACE inhibitor for all patients unless contraindicated
Fondaparinux or LMWH
IV nitrate if pain continues
Record ECG while in pain. If patient is high risk pursue invasive strategy; if low risk pursue conservative strategy
What factors identify a "high risk" NSTEMI patient?
1. Rise in troponin
2. Dynamic ST or T wave changes
3. Secondary criteria: diabetes; chronic kidney disease; LVEF <40%; early angina post MI; recent PCI; prior CABG; intermediate to high GRACE score
What factors identify a "low risk" STEMI?
1. No recurrence of chest pain
2. No signs of heart failure
3. Normal ECG
4. Negative baseline and 6-9 hour troponin
5. No inducible ischaemia
What is a GRACE score?
Global registry of acute coronary events
Risk is scored based on:
2. Heart rate
4. Renal function
5. Killip class of heart failure
6. ST segement deviation
7. Cardiac arrest at admission
8. Elevated troponin
How is high risk NSTEMI managed?
Infusion of a GPIIb/IIIa antagonist e.g. tirofiban and refer for angiography as in patient (invasive strategy)
1. Urgent (140
3. Within 72 hr in lower risk patient
When discharged following NSTEMI, what drugs should a patient be prescribed?
1. Dual antiplatelet therapy (aspiring + clopidogrel/ticagrelor/prasugrel)
2. Beta blocker (if depressed LV function)
3. ACE inhibitor
How is STEMI treated?
1. Primary angioplasty or thrombolysis
2. Beta-blocker unless contraindicated e.g. asthma
3. ACEi in all normotensive patients within 24 hours of MI eso. if there is clinical evidence of heart failure or echo evidence of LV dysfunction
4. Consider clopidogrel- 300mg loading followed by 75mg/day for 30 days
How is NSTEMI treated?
1. Beta blocker
2. Antithrombotic e.g. fondaparinux if low bleeding risk and no angiography planned for 24 hours, otherwise LMWH
3. Assess risk e.g. GRACE score
4. High risk patients: glycoprotein II/IIIa antagonist; angiography within 96 hours
5. Low risk: clopidogrel. Discharge if repeat troponin is negative. Treat medically and arrange further investigation if recurrent ischaemia
How is ACS managed following PCI?
1. Bed rest with continuous ECG monitoring for 48 hours
2. Prophylaxis against thromboembolism until fully mobile. If large, anterior MI, consider warfarin for 3 months as prophylaxis against systemic embolism from LV wall thrombus
3. Aspirin 75 mg/day
4. Long term beta-blocker e.g. bisoprolol. If contraindicated consider verapamil or diltiazem
5. Continue ACEi in all patients
6. Start a statin
7. General advice:
Reduce modifiable risk factors (e.g. stop smoking; encourage exercise);
Discharge after 5-7 days in uncomplicated cases
Patient may return to work after 2 months
Encourage healthy diet and exercise
Avoid air travel for 2 month
Review at 5w and 3m
What are the main complications of MI?
Left ventricular failure
DVT and PE
How should sinus bradycardia be treatment if it occurs following MI or during PCI?
1. Atropine IV
2. Consider temporary pacing if no response or poorly tolerated
With which type of MI is 1st degree heart block most commonly seen?
Which types of heart block require pacing?
Mobitz type II
Complete AV block
Bundle branch block
What electrolyte or pH changes predispose to tachyarrhytmias?
How does pericarditis present? What is shown on the ECG? How is it treated?
1. Central chest pain relieved by sitting forwards
2. Saddle shaped, global ST elevation
What is cardiac tamponade? How does it present? How is it treated?
1. An acute type of pericardial effusion in which fluid, pus, blood, clots, or gas accumulates in the pericardium
2. Low cardiac output, pulsus paradoxus, raised JVP, muffled heart sounds
3. Pericardial aspiration
How does Dressler's syndrome present? How is it treated?
1. Recurrent pericarditis; pleural effusion; fever; anemia; and increased ESR 1-3 weeks post MI
2. NSAIDS; steroids if severe
When might a CABG be performed?
1. LMS disease (to improve survival)
2. Triple vessel disease involving the proximal part of the LAD (to improve survival)
3. Patients unsuitable for angioplasty
4. Failed angioplasty
5. Refractory angina- angina which is unresponsive to drugs (symptom relief)
With the availability of new stent technology, NICE recommends that PCI is general the preferable treatment for ACS as it is less invasive. When might patients undergo CABG as opposed to PCI?
1. Triple vessel disease
2. Abnormal LV function
Patients with single vessel CAD and normal LV function almost always undergo PCI
Which vessels are commonly used for the graft in a CABG? Which last longer?
1. Great saphenous vein
2. Internal mammary artery (tend to last longer but may cause chest wall numbness)
What is pulsus paradoxus?
An abnormally large decrease in systolic blood pressure and pulse wave amplitude during inspiration. The normal fall in pressure is less than 10 mmHg. When the drop is more than 10mm Hg, it is referred to as pulsus paradoxus
What 5 drugs are used for secondary prevention following ACS?
1. Beta blocker
What are contraindications for thrombolysis following STEMI?
1. Previous intracranial haemorrhage
2. Iscahemic stroke
3. Recent injury/surgery/head trauma <24 hours e.g. liver biopsy, lumbar puncture
What is the acute care for someone who has had a stemi?
M: Morphine (5-10mg) + Metoclopramide
O: Oxygen (ONLY if sats <94%)
N: GTN spray
A: Aspirin- 300mg
C: Clopidogrel- 300mg
Why are anti-platelets used in STEMI over anti-coagulants?
Anti-coagulants are used to treat venous clots (DVT) anti-platelets are used to treat arterial clots