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cardiology > acute coronary syndromes > Flashcards

acute coronary syndromes Flashcards

1
Q

coronary blood flow to the myocardium may be reduced by mechanical obstruction that is due to …

A

atheroma, thrombosis, spasm, embolus, coronary postal stenosis, coronary arteritis

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2
Q

what does primary prevention and secondary prevention mean in regards to cardiovascular disease (atherosclerosis)

A 
primary= prevention of the atherosclerotic process
secondary= treatment of the atherosclerotic disease process
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3
Q

what drug is recommended in the primary prevention of cardiovascular disease in people with a 10 year risk of cardiovascular disease or 10% higher

A

Atorvastatin 20mg

in patients with established cardiovascular disease 80mg is recommended

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4
Q

explain classical or typical angina

A

Characterised by chest pain which is heavy, tight or gripping, central or retrosternal pain may radiate to the jaw. Pain occurs at emotional stress or with exercise. pain eases with rest or with GTN

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5
Q

explain atypical angina

A

chest pain with 2 out of the 3 features of classical angina.

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6
Q

explain non-angina chest pain

A

described by NICE as having 1 out of 3 of the features of angina

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7
Q

explain stable angina

A 
Is classified by the Canadian Cardiovascular Society guidelines 
ie 
class 1 = no angina with ordinary activity: angina with strenuous activity 
class 2 = angina during ordinary activity eg walking up hills with mild limitation of activity 
class 3 = angina with low levels of activity eg walking 50-100m with marked restrictions on activity 
class 4= angina at rest or with any level of exercise
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8
Q

explain unstable angina

A

Refers to angina of recent onset (<24hours) or deterioration in previous stable angina, with symptoms frequently occurring at rest: that is acute coronary syndrome

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9
Q

explain refractory angina

A

Patients with sever coronary disease in whom revascularation is not possible and angina is not controlled by medical therapy

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10
Q

explain vasospastic or variant (Prinzmetals) angina

A

Angina that occurs without provocation, usually at rest, as a result of coronary artery spasm. it occurs more frequently in women. Characteristically there is ST segment elevation on the ECG during this pain

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11
Q

explain microvascular angina

A

Patients have exercised induced angina but normal or unobstructed coronary arteries. Intracoronary acetylcholine may cause coronary spasm.

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12
Q

how should stable angina be treated

A
  1. information, lifestyle modifications, short acting nitrates, secondary prevention
  2. beta blocker or calcium channel blocker
    3a. If not tolerated then move to long acting nitrates, Ivabradine, Nicorandil, Ranolazine.
    3b. if symptomatic switch to the other (ie if using beta blocker switch to calcium channel blocker) or use both a beta blocker and a calcium channel blocker
  3. if symptomatic on 2 anti-anginals consider revascularation
    5a. PCI = single vessel disease. multi vessel disease <65years
    5b. CABG = unsuitable anatomy. multi vessel >65 years. diabetes
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13
Q

what is the process of percutaneous coronary intervention (PCI) for angina

A

the process dilates a coronary artery stenosis by introducing an inflatable balloon and metallic stent into the arterial circulation via the femoral, radial or brachial artery
- dual anti platelet therapy should continue for 6-12 months (aspirin and P2Y12 inhibitor)

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14
Q

what is coronary artery bypass grafting (CABG)

A

autologous veins or arteries are anastomosed to the ascending aorta and to the native coronary arteries distal to the area of stenosis (ie blood bypasses the obstructed area)

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15
Q

explain the factors that influence PCI vs CABG

A
  • PCI is proffered to CABG in patients with single or doubled vessel disease not involving the proximal left anterior descending or left main stem.
  • CABG and PCI are both appropriate in patients with proximal LAD stenosis, LMS or three vessel disease and a low SYNTAX score
  • CABG is preferred to PCI in patients with three vessel disease and diabetes or elevated SYNTAX (>22) and in patients of a SYNTAX or LMS score of more than 22
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16
Q

what types of drug are used in the pharmacological therapy of stable angina

A
  • vasodilator eg glycerol trinitrate = prophylaxis and treatment- rapid onset and repeat after 5 min is symptomatic
  • beta blocker eg bisoprolol = reduces heart rate and BP, reduces myocardial oxygen consumption
  • calcium channel blocker eg verapamil = inhibits calcium channels in myocardium, cardiac conductive tissue and vascular smooth muscles
  • Ivabradine = inhibits pacemaker If current in SA node. Use in sinus rhythm with or without a beta blocker
  • Nicorandil = activates ATP sensitive potassium channels and has nitrate properties- peripheral and coronary vasodilation. Use as adjunctive therapy
17
Q

for stable angina what are some event reducing drugs

A
  • Antiplatelet eg aspirin = reversible inhibition of platelet COX-1 and thromboxane production
  • ACE inhibitor or ARB = indicated if treating other condition eg hypertension, heart failure
  • Statin eg Atorvastatin = use to reduce LDL cholesterol to <1.8mmol/L
18
Q

what does STEMI and NSTEMI stand for

A 
STEMI = ST-elevation myocardial infarction 
NSTEMI = non AT elevation myocardial infarction
19
Q

how does an MI occur

A

Mi occurs when cardiac myocytes die due to myocardial ischaemia

20
Q

what are the 5 types of myocardial infarction

A

1 = spontaneous MI with ischaemia due to primary coronary event

2 = MI secondary to ischaemia due to increased oxygen demand or decreased supply ie coronary spasm, coronary embolism, anaemia, arrhythmias..

3 = diagnosis of MI in sudden cardiac death

4a = MI related to PCI 
4b = MI related to stent thrombosis

5 = MI related to CABG

21
Q

What follows the rupture or erosion in a fibrous cap of a coronary artery plaque ( in acute coronary syndromes)

A
  • Platelet aggregation and adhesion, localised thrombosis, vasoconstriction and distil thrombus embolisation
  • Thrombus formation and the vasoconstriction produced by platelet release of serotonin and thromboxane A2 result in myocardial ischaemia due to reduction of coronary blood flow
22
Q

on an ECG what is suggestive of an acute coronary syndrome

A
  • ST depression
  • T-wave inversion
  • with STEMI complete occlusion of the vessel will result in persistent ST elevation or left bundle branch block pattern, although transient ST elevation is seen with coronary vasospasm or Prinzmetals angina
23
Q

what are the functions of cardiac troponin I, T and C

A 
I = inhibits the myosin binding site on the actin 
T = attaches the complex to tropomyosin 
C = binds calcium during excitation-contraction coupling

A high troponin levels carries an increased mortality risk in ACS

24
Q

what pharmacological therapies should be given in acute coronary syndrome

A
  • Anti platelet drugs eg aspirin = platelet activation stimulates the expression of glycoprotein IIb/IIIa receptors on the platelet surface. These receptors bridge fibrinogen between adjacent platelets causing platelet aggregation. ACS patients should be treated with dual anti platelet agents
  • Antithrombin drugs eg heparin, low molecular weight heparins (enoxaparin)
  • Glycoprotein IIb/IIIA inhibitors eg Abciximab = inhibit platelet coagulation
  • Analgesia eg Diamorphine = painkiller
  • Plaque stabilisation/ventricular remodelling = HMG-CoA reductase inhibitors (statins) eg rosuvastatin and ACE inhibitors = these agents provide stabilisation, improve vascular and myocardial remodelling, and reduce future cardiovascular
25
Q

at what stages do very high, hight, intermediate and low risk patients require a coronary angiography

A
  • Very high risk = require urgent coronary angiography (<2 hours)
  • High risk = with rising and falling cardiac troponin levels dynamic ST or T-wave changes, or elevated GRACE score requires coronary angiogram within 24 hours
  • Intermediate risk = patients with diabetes mellitus, renal impairment… require angiography within 72 hours
  • Low risk = can be managed initially with medical therapy but an invasive strategy with cardiac catheterisation is preferred in almost all patients
26
Q

what are clinical features of an ST elevated MI

A
  • Severe chest pain for more than 20 minutes
  • The pain doest respond to sublingual glyceryl trinitrate, and opiate analgesia is required
  • Pain may radiate to the left arm, neck or jaw
  • Patient may be pale, clammy and marked sweating
  • Pulse may be thready with significant hypotension, bradycardia or tachycardia
27
Q

what limb leads produce a anterior MI, inferior MI, lateral MI, posterior MI

A
  • anterior MI = at the J point in leads V1-V3
  • inferior MI = at leads II, III AVF
  • lateral MI = at lead I, AVL, V5/V6
  • posterior MI = ST depression at V1-V3 with a new dominant R wave and ST elevation in V5/V6
28
Q

what is the early medical management for STEMI

A
  • Rapid triage for chest pain and referral for repercussion therapy
  • Oxygen, iV opioids and aspirin
  • Primary percutaneous coronary intervention - target of 60 minutes for wire crossing of the culprit vessel
  • Thrombolysis is appropriate if primary PCI isn’t available within 120 minutes of STEMI diagnosis. It includes thrombolytic agents that enhance the breakdown of occlusive thrombosis by the activation of plasminogen to form plasmin.
  • Coronary artery bypass surgery = usually reserved for the complications of MI
29
Q

what can be the complications of MI

A
  • Heart failure
  • Myocardial rupture and aneurysmal dilation
  • Ventricular septal defect
  • Mitral regurgitation
  • Cardiac arrhythmias
  • Conduction disturbances
30
Q

What is the post- acute coronary syndrome drug therapy and assessment

A
  • Aspirin 75mg daily
  • ADP-receptor blocker
  • Oral beta blocker to maintain heart rate
  • Proton pump inhibitor for patients at high risk of bleeding while on dual antiplatelet therapy
  • ACE inhibitor or angiotensin receptor blocker
  • High intensity statin with target LDL cholesterol <1.8mmol/L
  • Aldesterone antagonist

cardiology (13 decks)

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