Ischaemic Heart Disease And ACS Flashcards
Development of atherosclerosis
Plaque morphology
Plaque development
Migration of LDL which becomes oxidised which is inflammatory provoking - so monocytes migrate into the tissue and become macrophages they segregate in vesicles - foam cells
May then die forming a necrotic core surrounding inflammation tissues which secreting MMPs so there is active low grade inflammation disease
Which then becomes calcified
Plaque evolution
Lipid accumulates Ruptured and erosion Thrombin and platelets are activated Rupture can lead to stenosis of the vessel Or emboli
Stable angina history
Retro sternal (neck /shoulders/Jaw/arms) -tightness/heaviness/crushing Associated SOB Important-exertion induced Relived by rest or GTN Exacerbated -after meals -emotion -cold weather
NOT continuous or prolonged
Related to respiration or posture
Risk factors
Smoking, FHx/inc BP/lipids/DM
Past history MI PCI or CABG Other vascular disease -renal disease
Stable angina signs
Usually no abnormal findings Exclude -aortic valve disease -LV outflow obstruction HCM -anaemia -arrhythmia
Investigations of stable angina
First you need to estimate the probability of CAD History of Pain chest neck,shoulder, jaw Pain in exertion Rest GTN better Risk factors Sex age
Use NICE guideline scoring system to risk stratify patients
With increasing risk
Reassure—> CT coronary calcium score —> functional imaging —> angiography
Reliability of a calcium score
Clarified plaque doesn’t mean that it will stenose but the more calcium more likely it’ll stenose
More calcium on the scan inc stenosis likelihood
In younger patients who have a plaque
Would not be calcified yet but still a possibility of it stenosing
What happens in stable angina to the demand of the muscle
On exertion the muscle needs more oxygen due to the stenosis it cannot inc supply to the demand this means the area becomes ischaemic
At rest adequate supply for metabolic need
On exertion not adequate supply to meet metabolic need cannot inc flow so you get symptoms
What is the ischaemic cascade is stable angina
Normal LV function Perfusion abnormality Regional diastolic dysfunction RegioNal systolic dysfunction ST shift on ECG Chest pain
What can an exercise test induce in stable angina
Induces ischaemia
There is ST segment depression
On the cascade this is a late sign
Want to ta test to detect earlier
What test detects changes earlier in the ischaemic cascade
Stress test with exercise or adenosine or dobutamine
You can scan wall motion in an echo or MRI
Perfusion in a MIBI and SPECT
Gd and MRI
Last test in the risk stratified testing is angiography when to do an angiogram
When there is a 61% to 91% likelihood of CAD Uncertain diagnosis Inadequate symptoms control -Sx in spite of medication -SE from meds If non invasive tests suggest a high risk - revascularisation for prognosis -stable -Unstable
What is the treatment of stable angina
Drugs lipid control BP control antiplatelets beta blockers
CCB
PCI
CABG
What happens in ACS
Sudden change in coronary flow Leading to Chest pain ECG changes Subsequent release of cardiac markers -creatinine kinase -cardiac troponins
What are the 3 acs
STEMI
NSTEMI
UA
What happens in a stemi
The plaque ruptured thrombosis occluded the artery totally
This leads to a trans mural affect which leads to pain
Raised ST segment
And raised trops
What happens in an NSTEMI
The clot ruptured and embolises This causes ischaemia and some infarction but is not transmural This leads to pain No ST elevation Inc trops
What happens in unstable angina
The plaque is platelet rich there is no occlusion
No ischaemia or infarction
There is pain
No ST segment elevation
No CK or trip inc
ECG can be normal but can show some t wave inversion or ST depression
Adrian chest pain in a STEMI
Retro sternal chest pain. At rest Prodrome in 20-60 % Characteristic pain Associated SOB Sweating Nausea Palpitations and syncope
What scan should be done immediately in cardiac chest pain
Immediate ECG
If STEMI emergency treatment pathway
Everything else non emergency
What other ecg abnormality can be triggered by a MI
Ventricular fibrillation
Can be triggered by an MI that did not cause much damage
Need to be treated with defibrillation
What is the aim of Stemi treatment
Reopen the vessel to allow the myocardium to repercussion before necrosis
Primary PCI
Pre Tx with ASA + clopidogrel prasugrel/ticagralor
Or thrombolysis
tPA. Fibrinolytic
Transfer to PCI centre ASAP
Time dependent affect with treatment
Sooner the better
What is the strategy for rapid diagnosis of ischaemic like chest pain
ECG
Aspirin 300mg po
Plus one other antipletelt
Prasugrel 60mg po
Clopidogrel 600mg po
IV cannula No routine O2 only if SATs below 94 Analgesia Diamorphine 5mg iv Metocloperamide 10 mg iv
Complications of stemi
these complications can occur following MI even after successful treatment Acute LVF
Can lead to pulmonary oedema or cardiogenic shock which need to be managed accordingly
Necrotic muscle - mitral regurg - wall lead to a tamponade , septum VSD
Pericarditis -dresslers
Post STEMI MANAGEMENT
After PCI
Bystander disease with staged revascularisation ? Assessment of LV function 2ndary prev -drugs Aspirin + clopidogrel /ticagralor HMGCoA reductase inhib -statin ACEi Beta blocker
If LV impaired
Eplerine/spironolactone
Warfarin
Implantable defibrillators or resynch
