ACS, angina, UA, STEMI, NSTEMI Flashcards
List the modifiable and unmodifiable RFs for ischaemic heart disease
Unmodifiable risk factors:
Increasing age
Male gender
Family history
Modifiable risk factors:
Smoking
Diabetes mellitus
Hypertension
Hypercholesterolaemia
Obesity
Explain the pathophysiology of ischaemic heart disease listing some of the cells involved
- ENDOTHEILIAL DYSFUNCTION triggered by smoking/HTN/DM
- fatty infiltration of subendothelial space by LDL particles [low-density lipoproteins]
- Monocytes migrate over from blood and differentiate into macrophages
- Macrophafes phagocytose oxidised LDLs –> become large foam cells fomring fatty plaques. Death of macrophages increases inflammation.
- Smooth muscle cells migrate from tunica media –> intima and form fibrous capsules around the fatty plaques
- Plaques cause narrowing of coronay arteries (angina), and can also rupture and occlude the cornary artery (MI)
Signs and symptoms of ACS
- left-sided chest pain
- radiating to jaw or left arm
- heavy, crushing
- dyspnoea
- sweating
- N+V
Which patients may have ACS without chesy pain?
elderly, DM, females
What are the 2 most important Ix for someone presenting with chest pain?
- ECG
- Troponin
Which leads are associated with which territors of the heart? (HINT: visualise 3D model of heart)
Anterior: V1-V4
Inferior: ll. aVF, lll
Lateral: l, V5-V6, aVL
Which leads are associated with which coronaty arteries? (HINT: visualise 3D model of heart)
V1-V4: left ANTERIOR descending
ll. lll. aVF: right coronary
l. V5-V^: left circumflex
Expected Ix results for angina, unstable angina, STEMI and NSTEMI
Angina: changes only seen in exercise ECG
UA: ECG changes but normal trop
NSTEMI: increased trop, widespread ST depression and/or inverted T-waves
STEMI: increased trop, persistent ST elevation in leads V2-V3 + new LBBB
Common management in all patients presenting with ACS (with key dose)
MONA
1. Morphine (if pt is in severe pain)
2. Oxygen (Only if sats are <94%)
3. Nitrates (cautious if Pt is hypotensive)
4. aspirin 300mg
Drugs used in longterm Mx of pt with ACS
aspirin + statins for all
sublingual GTN to abort attacks
1st line: BB/CCB monotherapy
2nd line: BB/CCB combination therapy
3rd line: atypical drugs
Which CCB should be used as monotherapy for angina and which can be used with a BB?
Alone: verapamil, diltiazem (will cause complete block if used with BB)
With BB: long-acting dihydropyridine like amlododipine, nifedipine
if a patient is on monotherapy and cannot tolerate the addition of a calcium channel blocker or a beta-blocker then consider less common antianginals like:
- a long-acting nitrate(isobromide mononitrate)
- ivabradine (reduced HR)
- nicorandil (vasodilator)
- ranolazine
Mx of STEMI once confirmed by ECG
- Is pt presenting with 12h of onset of symptoms?
- Can PCI be done in 120 min?
If yes, do PCI.
If PCI cannot be done in 120 min, do fibrinolysis
What drugs are used for fibronlysis?
tPA (good mortality outcomes!)e.g alteplase, streptokinase
Drugs given to pt prior to PCI (for pts on/not on anticoag)
Prior: needed to do dual antiplatelet therapy (aspirin has been given already under MONA)
if the patient is not taking an oral anticoagulant: prasugrel (higher bleeding risk)
if pt is taking anticoag: clopidogrel
Which acceess is prefered for PCI?
radial over femoral
Drugs given to Pt during PCI (radial/femoral access)
patients undergoing PCI with radial access:
unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI) - this is the action of using a GPI during the procedure when it was not intended from the outset, e.g. because of worsening or persistent thrombus. GPI prevents platelet aggregation and thrombus formation.
patients undergoing PCI with femoral access:
bivalirudin with bailout GPI
When would you do a CABG?
Mulltivessel coronary arterty disease
What should be given along with and following fibrinolysis?
Along with: antithrombin (fondaparinux, edoxaban)
Following: tricagrelor (antiplatelet)
antiplatelets vs anticoagulants
Both classes of medications are antithrombotic agents.
Plarelets are the primary mediators that trigger the mechanical pathway of the coagulation cascade. Platelets + fibrin (product of CC) form the clot in a vascular wall.
Anticoagulants disrupt the CC and include Vitamin K antagonists (warfarin), DOACs and LMWH.
Antiplatelets prevent platelet formation and include clopidogrel, ticagrelor, prasugrel.
Mx once NSTEMI/UA is confirmed (including score)
- Aspirin 300mg
- Fondaparinux if no immediate PCI
- Calculate GRACE Score
If <3% - Give tricagrelor
If >3% - coronary angiography + PCI within 72h if necessary
What are the criteria of the GRACE Score?
Gold standard biomarker: troponin
Renal (serum creatinine) and cardiac (killip class) function
Age
Cardiac arrest on presentation
ECG findings
Pt comes in with NSTEMI/UA, GRACE score <3% but hypotensive - what is the mx?
immediate CA + PCI
clopidogrel vs ticagrelor - how do you decide which to use?
higher bleeding risk = use clopidogrel
