Coronary Artery Disease Flashcards
Discuss the basic epidemiology & pathophysiology of acute coronary syndromes
80,000 admissions a year in the UK
PMHX - Hypertension, Diabetes, Tobacco use, FHX, Dyslipidemia
Pathophysiology - Formation of Atheroscelorisis
Epithelium damage leads to increased LDL entering the tunica intima. Macrophages follow targeting and oxidising the LDL attracting more WBCs casuing a positive feedback loop and producing a Foam cell which builds up and forms a plaque with endothelial covering it.
The thombus forms by one of two ways - most commonly plaque rupure but also endothelial dysfunction
Nonsclerotic causes of ACS is a mismatch between supply and demand
Dyslipidemia = high cholesterol & lipids
Atherosclerosis in more detail on another card
Discuss the basic investigation of acute coronary syndromes
Initial investigation - 12 lead ECG within 10 mins of arriving, with a focused History and examination after
PC
* Chest pain - Worsens w/Exertion and not relieved w/Rest and no change w/Body position
* The signs of Cardiogenic shock
* Hypotension
* Tachycardia
* Diaphoresis
* Cool pale skin
Troponin - Only seen in NSTEMI and STEMI not in a UA as there is no ischaemia, needs to be done within 3 hours of admission
ECG - ST elevation in 2 Contigous leads
Or a New Left bundle branch block can mask the ST elevation so if that shows with the history it is diagnostic
In a NSTEMI the ECG might show a Pathological q-wave, ST depressions or T wave inversions
Discuss the basic management and prognosis of acute coronary syndromes
Initial management:
1. Insert IV access
2. Cardiac and 02 SAT monitoring
3. Morphine
4. Oxygen supplementation
5. Nitrates - Sublingual - vasodialation
6. Asprin & Ticagrelor
Also add High intensity atorvastatin and a Beta Blocker such as Metroprolol as these decrease Myocardial oxygen demand
After this initial Managment you need to do Reperfusion therapy which effecitivley means resupplying the myocardium with blood flow.
There are 2 key ways to do this
* Coronary angiography inserting a Stent which is often done in NSTEMI or UA.
* Coronary artery bypass grafting when you take a branch from the Aorta and supply in past the occluded artery of artery. Which is more often done in a STEMI as the coronary artery is often totally occluded.
If neither of these options are available you can do thrombolysis such as fibriolytics
SYNTAX score determines prognosis
Discuss the impact on daily life of coronary artery disease
Chanegs to lifestyle & diet
Fatigue
Limit physical activity
Causes health anxiety & depression
Impact social interactions
Smoking and Alcohol
Discuss the initial investigation of chest pain
- ECG - determine underlying cardiac involvement
- CXR- extremely versatile
- Bloods- Troponin, Inflammatory markers
- CT angiography
- CTPA- essential to rule out a PE.
- ABG
Identify the system affected first then the condition
What are the main 3 coronary arteries?
- The left anterior descending artery
- The circumflex artery
- The right coronary artery
1 & 2 are part of The left main coronary artery
List the radiological investigations used to assess the heart
CXR. Echo, Angiogram, Myocardial Perfusion imaging and Cardiac MRI
What are the 2 types of echocardiography
- Transthoracic echo
- Transoesophageal echo
Discuss angiography
The use of contrast to visualize regions of the cardiovascular system. A catheter is introduced into an appropriate vessel and guided under fluoroscopy to the site of injection. Contrast is then administered and a continuous series of x-rays are take to produce a motion picture angiogram.
In a coronary artery angiogram each patient is imaged in several standard views to provide a comprehensive view of the location and severity of coronary atherosclerotic lesions.
Discuss myocardial perfusion imaging
- detects Ischemia and infarction
- Greater sensitivity than standard exercise electrocardiography
- more expensive so are appropriate in patients with certain baseline ECG abnormalities such as left bundle branch block and electronic pacemakers.
Describe the normal histology of the cardiac muscle
The Wall consists of 3 Layers
Describe the 3 layers of the blood vessels
- Tunica intima
- Tunica Media
- Tunica Adventitia
Describe the pathological process of thrombosis
- Over time, foam cells within the lipid core undergo necrosis (ulceration) and release enzymes
- These enzymes begin breaking down the fibrous cap, making it thinner and thinner until it ruptures
- When this happens, platelets respond by forming a fibrin clot at the site of the rupture
- These clots can occlude the lumen of the artery even more or they may detach and obstruct other blood vessels
Describe the pathological process of atherosclerosis - Fatty Streaks
- The endothelium is injured by stress against the arterial wall e.g. in hypertension
This is more prominent at arterial bifurcations where there is more turbulent flow - When the endothelium is injured, this causes increased vascular permeability, so LDL (cholesterol) particles are allowed to leak into the intimal layer where they get oxidised
- When LDL is oxidised, it becomes a pro-inflammatory antigen which induces an immune response
- Monocytes migrate into the intima and transform into macrophages
- Macrophages engulf the oxidised LDL particles which causes them to turn into foam cells
- Accumulation of foam cells underneath the endothelium creates a fatty streak
These are not raised meaning they don’t obstruct the lumen, so they don’t produce clinical symptoms like angina
These fatty streaks can develop in adolescence, but they don’t always develop into plaques
Describe the pathological process of atherosclerosis - Plaques
- Damage to the endothelium causes platelets and endothelial cells to release factors e.g. platelet derived growth factor and fibroblast growth factor
- These factors stimulate smooth muscle proliferation and migration from the tunica media to the tunica intima as well as production of extracellular matrix
- This results in the formation of a fibrous cap overlying a lipid core in the centre – this structure is called a plaque
This plaque can obstruct the lumen and produce symptoms
Vulnerable plaques: those with a thin fibrous cap and rich lipid core so are more likely to rupture and incite thrombosis
Stable plaques: have thick fibrous cap and small lipid core so less likely to rupture - Neovascularization: periphery of the lesions show proliferating small blood vessels due to increased oxygen demand
Describe the pathological process of infarction
Non-ST elevation myocardial infarction is caused by severe but incomplete occlusion of a coronary artery
- Poor oxygen supply to myocardium causing infarction distally and ischaemia proximally to the artery supply
- The infarcted area is called a subendocardial infarction
ST elevation myocardial infarction is caused by complete occlusion of a coronary artery
- This means there is no blood supply to the myocardium, and this means you have a transmural infarction which is when there is infarction and death through the full thickness of the myocardium
Describe how the coronary circulation adapts to meet its metabolic demand
- High density of myocardial capillaies - one per myocyte for skeletal and cardiac muscle
- Higher blood flow
- Higher O2 extraction - 75% vs 25% average
- metabolic Hyperaemia - coronary arteries dilate releasing metabolites and increasing blood flow to the heart. It is proprtionate to how hard the body is working
- Autoregulation - blood flow kept constant despite blood pressure fluctuation
High BP = Vasoconstriction
Low BP = Vasodilation
Discuss how the cardiovascular system adapts to exercise
- Increases Cardiac Output by increasing stoke volume and increasing heart rate.
- Increases blood flow to active muscles
- Peripheral vasodiliation to cool
- Stabilisation of BP
- Compensatory vasoconstriction in non active tissues to counterbalance hypotension
What are the stages of the cardiac cycle
- Atrial Contraction
- Isovolumetric Contraction
- Rapid Ejection
- Reduced Ejection
- Isovolumetric Relaxation
- Rapid Ventricular Filling
- Reduced Ventricular Filling (Diastasis)
What is Atherosclerosis?
A chronic inflammatory disorder which affects the endothelium of medium and large arteries and is characterised by the build-up of cholesterol plaques within the arterial lumen.
What are the complications of Atherosclerosis?
- Thrombus - see other card
- Aneurysm-The atheroma may weaken the vessel wall, causing an aneurysm
- Cholesterol emboli - When the atherosclerotic plaque itself is dislodged and travels in the circulation as a cholesterol embolus
Plaque may be dislodged accidentally during a cardiac procedure
& Can cause livedo reticularis, acute kidney injury, gangrene - Haemorrhage - Rupture of the overlying fibrous cap or of thin-walled vessels can cause intra-plaque haemorrhage. A haematoma may expand the plaque or induce plaque rupture
- Calcification - This may increase its fragility
What increases Stroke Volume?
Faster ejection and relaxation
1. Noradrenaline released by sympathetic fibres
2. Myocardial fibre b1 adrenoreceptors activated
3. Increased contractility
4. Resulting biochemical changes raise the ejection fraction and speed up the rate of contraction and relaxation
Small increase in end-diastolic volume in upright exercise
1. Due to small increase in CVP and filling pressure
* Caused by peripheral venoconstriction and calf muscle pump
2. Activates Starling’s law of the heart and increases contractile force of the heart
Substantial decrease in end-systolic volume
* Due further increase in contractile energy brought about by cardiac
sympathetic fibres
