CVS: Angina and Acute Coronary Syndrome Flashcards
Describe the special requirements of coronary circulation
- Need a high supply of O2 - 20% of unstimulated skeletal muscle
- Increase O2 supply in proportion to increased demand/cardiac work
- E.g. Exercise increases heart rate and contractility
What are the structural features of cardiac muscle that aid coronary circulation?
High density of fibres and capillaries, shorter diffusion distances
- High capillary density
- Large SA for O2 transfer
- Reduces diffusion distance of O2 to myocyte
- t ∝ X squared (X = distance)
So, transport O2 is fast over very short distances
Describe the functional features of coronary circulation
During normal activity:
- High blood flow - 10x the flow per weight of rest of body
- Sparse sympathetic-mediated vasoconstriction + high nitric oxide release = Low vascular tone, promotes vasodilation
- High O2 extraction (75%) - average body is 25%
During increased demand:
- Coronary blood flow increases in proportion to demands
- Production of vasodilator molecules from active cardiac muscle e.g. adenosine, K+, acidosis
- Produce local vasodilation
- Circulating adrenaline dilates coronary vesels due to B2 adrenoceptors on coronary artery VSMCs
What must be increased if O2 requirements increase?
Blood flow:
- Extraction near max during normal activity
- So, to provide more O2 during demand, blood flow need to increase
- Myocardium metabolism generates metabolites to produce vasodilation, increase blood flow (metabolic hyperaemia) e.g. adenosine, produced by ATP metabolism and is released from cardiac myocytes, also increase in PCO2, H+, K+ lvls.
This is known as metabolic hyperaemia
What are special problems faced by coronary circulation?
Systole obstructs coronary blood flow, coronary blood flow only occurs during diastole
Ischemic heart diseases:
- Coronary arteries are functional end-arteries and therefore decreased perfusion produces major problems
- Heart very susceptible to sudden + slow obstruction
- Sudden: Acute thrombosis, ACS, including MI
- Slow: Atheroma (sud-endothelium lipid plaques) chronic narrowing of lumen, produces angina
Describe the mechanical factors reducing coronary flow
- Shortening diastole, e.g. high HR
- Increased ventricular end-diastolic pressure, e.g. volume-overload HF
- Reduced diastolic arterial pressure, e.g. hypotension
What type of arteries are human coronary arteries?
Functional end-arteries
- Low numbers of cross-branching collateral vessels (arterio-arterial anastomoses)
- Other arteries cannot divert blood to area
Occlusion of left anterior descending artery:
- Leads to ischemic area:
- Ischemic tissue → acidosis, pain (stimulation of C fibres) → impaired contractility → sympathetic activation → arrhythmias → cell death (necrosis)
Describe angina pectoris
“Strangulation of chest”- Pain, crushing sensation in chest, radiates to neck, arms, jaw with SOB, dizziness
3 forms:
- Stable
- Variant
- Unstable (ACS)
Causes:
- Ischemia - Due to O2 nutrient demands of cardiac tissue not being met due to partial occlusion of coronary arteries
- Increased demand - Increased HR/ LV contractility/ wall stress such as triggers like:
- Exercise
- Hypertension
- LV dilatation (HF)
Describe the symptoms, diagnosis and pharmacological treatment of stable angina
Symptoms include:
- Chest pain that feels like pressure or indigestion.
- Pain that radiates to your left shoulder or down your left arm.
- Shortness of breath.
- Dizziness.
- Nausea.
- Exhaustion.
- Stenosis - Partial occlusion due to plaque formation
- Stable angina worsens during exercise as:
- Stenosis in large coronary artery - Greater resistance to flow
- Metabolic vasodilation occurs at rest, so blood flow meets needs
- During exercise, arterioles can dilate a little more to increase blood flow, but resistance is too high due to dominance of stenosis
- O2 demand can’t be met, angina develops
- Management:
- CCB (decrease HR/afterload)
- B-blockers (decrease HR)
- Nitrates (open up coronary circulation increasing collateral flow, decreased afterload/preload)
- Minimise risk factors - lifestyle, aspirin, statins
Compare stable and variant angina
Stable (Exertional, typical)
- Predictable - symptoms appear after certain demand reached, relief with nitrates (E.g. GTN spray)
- ECG - Exercise stress test produces symptoms and ST depression
- Coronary angiography
Variant (Vasopastic, prinzmetal)
- Uncommon, caused by vasopasm, occurs at rest, often not linked to coronary artery occlusion
- Excessive responses to vasoconstrictors, endothelium dysfunction (e.g. less NO produced)
- Managed same way to stable (same medications etc)
Outline unstable angina, NSTEMI and STEMI
- Different types of ACS
- Spectrum of potentially life-threatening conditions, medical emergency
- Sudden decrease in flow of blood through a coronary artery
- Initiated by a rupture of an atherosclerotic plaque produces a thrombus in a coronary artery which reduces blood flow
- Presentation - Unpredictable, sudden, last for >30 min, not relieved by GTN spray
- Investigation:
- ECGs - NSTEMI or STEMI
- Troponin T and I measured (often raised in NSTEMI and STEMI, not i unstable angina)
Describe NSTEMI and STEMI
In healthy tissue, ventricles uniformly depolarised, so no current on ECG, isoelectric ST line
NSTEMI:
- In partial/less severe occlusion of a coronary artery, small area of ischemia which doesn’t depolarise
- Leads to injury current and depression of ST on ECG
STEMI:
- In total/severe occlusion of coronary artery there is full wall thickness ischemia which doesn’t depolarise
- Leads to injury current and elevation of ST segment on ECG
How are unstable angina and NSTEMI managed?
Investigation:
- ECGs - Pick up NSTEMI
- Troponins T + I measured - Raised in NSTEMI, not used in UA
Pharmacological treatment:
- Morphine
- Anti-platelet - aspirin, clopidogrel
- Anti-thrombin - Heparins, NOACs
- B-blockers, CCBs, statins, ACEi (these are long term)
Revascularisation may be needed depending on risk of future STEMI, peristent symptoms, angiography showing occlusions
Percutaneous coronary intervention (PCI, stents) - 1 or 2 arteries diseased
CABG (coronary artery bypass grafting) - ≥ 3 main coronary arteries diseases, main left CA occluded, occlusion position not appropriate for PCI
Describe revascularisation
PCI:
- Less invasive
- Balloon catheter inflated in area of blockage
- Increase luminal size
- Restenosis can occur - thickening of internal area of vessel causing blockage
CABG:
- Invasive
- Patient on cardiopulmonary bypass
- Heart stopped
- Potential restenosis issues but less with mammary artery
How is STEMI managed?
Investigation:
- ECGS - STEMI (ST elevation)
- Troponins T and I measured - Often raised
Pharmacological therapy:
- Morphine
- Anti-platelet, aspirin, heparins
- Thrombolytics - Streptokinase, tPAs, cause fibrinolysis, break down fibrin-clot, increase reperfusion zone
- Long term - B-blockers, CCBs, statins, ACEi
Revascularisation - preferred treatment (PCI or CABG) within 2 hours of symptom onset
Life threatening conditions with STEMI - Cardiac failure, rupture of ventricular septal leads to blood leakage b/w ventricles, arrhythmias
Describe how coronary blood flow occurs during diastole
- During systole, pressure in ventricles is equal to or greater than the aorta, meaning there’s poor coronary perfusion as there’s no pressure gradient
- During diastole, pressure in the aorta is greater than the ventricles, and therefore also greater than in the coronaries, enables coronaries to open, so blood flows from aortic sinus into coronaries
