Flashcards in IHD 2 - Coronary revascularisation Deck (71):
What are the 4 main progressive steps involved in atherogenesis?
Normal -> fatty streak -> atheromatous plaque -> atherosclerotic plaque
What is atherosclerosis?
A disease of the arteries characterized by the deposition of fatty material on their inner walls causing progressive narrowing and hardening
What is an atheroma?
A fatty deposit in the intima
Risk factors for coronary heart disease?
Gender AgeDrug abusealcoholSmokingStressHypertensionHigh cholesterolObesityFamily history
What is chronic stable angina?
Chest pain caused by demand led ischaemia due to fixed stenosis which occurs in a predictable manner
What is the immediate treatment of chest pain due to chronic stable angina?
What is an acute coronary syndrome in general?
Any acute presentation of coronary artery diseaseOnly a provisional diagnosis that covers a spectrum of conditionsLike stable angina it is caused by ischaemia caused by atherosclerosis
What conditions are classified as acute coronary syndromes?
What are 2 older alternative names for a NSTEMI?
Non-Q waveSub-endocardial MI
What are 2 older alternative names for a STEMI?
Acute MI (not called this anymore)Q wave MI
What are the 2 types of MI?
ST elevation MI Non ST elevation MI
Does a fatty streak cause symptoms?
No - it is clinically silent
What is the pathogenesis surrounding unstable coronary syndrome?
Plaque rupture/ fissure and thrombosis
What can happen to the plaque which bridges between an atherosclerotic plaque and plaque rupture/ fissure and thrombosis?
Fibrous cap forms over the fatty core
What type of stenosis does acute coronary syndrome have?Type of ischaemia?
Dynamic stenosis (subtotal or complete occlusion)Supply led ischaemia
What are the stages of the platelet cascade?
What causes initiation of the platelet cascade?
Spontaneous plaque rupture which leads to exposed tissue elements (sub endothelial collagen and Von Willebrand factor)
What are factors affecting plaque rupture/ fissure? (6)
Lipid content of plaqueThickness of fibrous capSudden changes in intraluminal pressure or toneBending and twisting of an artery during each heart contractionPlaque shapeMechanical injury
What is von willebrand factor?
A glycoprotein that plays an important role in stopping the escape of blood from vessels
What is involved in adhesion (platelet cascade)?
Platelet recruitment and adhesion at the site of injury forming a monolayer
What is involved in activation (platelet cascade)?
Activators are released (ADP and Thromboxane A2)They bind to surface receptors on plateletsPlatelet activation accelerates resulting in platelet aggregationActivated platelets express adhesion receptors for leukocytes (P-selectin and CD40 ligand) = inflammationOrganised fibrin-rich thrombus forms(This leads to vascular blockage = acute MI/ stroke)
How is ADP and other activators released during platelet cascade?
How is thromboxane A2 generated?
What adhesion receptors for leukocytes do activated platelets express (2)?
Difference between unstable angina and NSTEMI?
There is no elevation in cardiac enzymes in unstable angina where as there will be an elevation in cardiac enzymes in an NSTEMI (infarction does not occur- pre-MI which can lead to an MI)
Difference between a STEMI and NSTEMI?
There is only partial damage in heart muscle with an NSTEMI compared to full thickness damage to heart muscle with a STEMI - due to this full thickness damage ST elevation occurs on the ECG
What are ECG changes that are seen with a STEMI?
ST elevationT wave inversionPathological Q waves
What must be present on an ECG to confirm a STEMI? (either one of 3 of)
Greater than or equal to 1mm ST elevation in 2 adjacent limb leadsGreater than or equal to 2mm elevation in at least 2 adjacent precordial leadsNew onset bundle branch block (usually left bundle branch block)
What changes in Q waves indicate a problem?
> 40 ms (1 mm) wide> 2 mm deep> 25% of depth of QRS complex-Seen in leads V1-3
What changes in ECG are seen in the first few hours of a STEMI?
What changes in ECG are seen in the first day?
pathological Q wave formation and T wave inversion
What ECG changes are suggestive of an old MI?
Q waves +/- inverted T waves
What leads have pathologies that indicate an inferior MI?
II, III and aVF
What leads have pathologies which indicate an anteroseptal MI?
What leads have pathologies indicating an anterolateral MI?
I, aVL, V1-V6
What is the cardiac enzyme?When does its levels peak post-MI?Where is this also present?
CK (creatinine kinase)24 hoursIn skeletal muscle and brain
What is the cardiac protein marker?Specific/ not specific?Sensitive/ not sensitive?
TroponinHighly specificCan detect tiny small amounts of myocardial necrosis
Is CK or Tn better?
Difference between NSTEMI and UA?
NSTEMI will cause an elevation in cardiac enzymes due to necrosis, which will not be present in UA (as the muscle is not dying)
Management of acute coronary syndrome pre-hospital?
Emergency ambulance300mg aspirinGTN Morphine (e.g. 5-10mg morphine IV)Anti-emetics (e.g. 10mg IV metoclopramide)O2 if requiredIf 45 minutes or longer road time to hospital, pre-hospital thrombolysis
Management of STEMI?
300mg aspirinGTN (if BP greater than 90mmhg)Morphine (e.g. 5-10mg morphine IV)Anti-emetics (e.g. 10mg IV metoclopramide)O2 (if hypoxic)300mg clopidogrelPCIThrombolysis if angioplasty not available within 90 minutes
What are the indications for repercussion therapy (thrombolysis or PCI) for acute coronary syndrome?
Chest pain suggestive of acute MI (more than 20 minutes but less than 12 hours)Ecg changes (acute ST elevation/ new left bundle branch block)No contraindicaitons
When is thrombolysis performed instead of PCI?
Patients who can't undergo PCI in a timely fashion - diagnosis to angioplasty time is greater than 90 minutes
Risk of thrombolysis?
Failure to re-perfuseHaemorrhageHypersensitivity
What are the 4 categories of complications from an MI?
DeathArrhythmic complicaitonsStructural complicationsFunctional complications
Arrhythmic complications from a MI?
Structural complications from an MI?
Cardiac ruptureVentricular septal defectMitral valve regurgitationLeft ventricular aneurysmMural thrombus +/- systemic emboliInflammationAcute pericarditisDressler's syndrome
What are the functional complications of an MI?
Acute ventricular failure (left, right, both)Chronic cardiac failureCardiogenic shock
What classification system can be used to determine in-hospital mortality post-MI?
I = no signs of heart failure (6%)II = crepitations less than 50% of lung fields (17%)III = crepitations greater than 50% of lung fields (38%)IV = cardiogenic shock (81%)
Routine observations post-MI?
Cardiac monitor - rhythm?How does the patient feel?Pulse and blood pressureHeart sounds especially added soundsMurmurs especially new murmurspulmonary crepitationsFluid balance especially uric output
What is extremely important to remember about the ECG of a patient with an NSTEMI?
It may be normal
What are the different isotopes of troponin present in the body and where are these present?
Troponin C = heart and skeletal muscleTroponin I = cardiac specificTroponin T = cardiac specific
What are the preferred isoforms of troponin used as a biomarker?
TnT or TnI (high cardiac specificity)
What happens to the TnT or TnI levels over time?
Serum levels increase within 3-12 hours from the onset of chest pain, peak at 24-48 hours, and return to baseline over 5-14 days
What other conditions can cause an elevation in TnT levels?
CCFHypertensive crisisRenal failurePESepsisStroke/ TIAPericarditis/ myocarditisPost arrhythmia
How many different classifications of MI are there according to the new clinical classification of MI?
6 (1, 2, 3, 4a, 4b, 5)
What is a class 1 MI?
Spontaneous MI related to ischaemia due to a primary coronary event, such as plaque erosion and/or rupture, fissuring or dissection
What is a class 2 MI?
MI secondary to ischaemia due to an imbalance of O2 supply and demand, as from coronary spasm or embolic, anaemia, arrhythmias, hypertension or hypotension
What is a class 3 MI?
Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggesting ischaemia with new ST-segment elevation, ew left bundle branch block, or pathological or angiographic evidence of fresh coronary thrombus - in the absence of reliable biomarker findings
What is a class 4a MI?
MI associated with PCI
What is a class 4b MI?
MI associated with documented in-stent thrombosis
What is a class 5 MI?
MI associated with CABG surgery
Treatment of NSTEMI?
Long term aspirinClopidogrel therapy (continued for 3 months)Patients should receive coronary angioplasty within 72 hours of admission
How should patients with STEMI treated with thrombolysis be further treated?
Early coronary angiography and revasculirisation
What are the 4 phases of cardiac rehabilitation?
Phase 1 = in-patietnPhase 2 = early post discharge periodPhase 3 = structured exercise programme - usually hospital basedPhase 4 = long term maintenance of physical activity and lifestyle change - usually community based
What is the aim of blood pressure post MI?
Less than 140/85mmHg unless diabetic, renal disease or target organ damage = less than 130/80 mmHg
4 examples of thrombolytic drugs?
Apart from MONA-C, how is an NSTEMI treated?
Low weight heparin or fondaparinux givenAngiography within 72 hours to determine best next steps e.g. PCI, CABG
Management of UA once in hospital?
Aspirin and other anti-platlet agent e.g. clopidogrelLow weight heparin or factor Xa inhibitor e.g. fondaparinuxOpiates and anti-emeticsMay need IV nitrates for painSecondary prevention with statin, ACEI and beta blockerIf high risk of reoccurrence, revascularisaiton