CVS Angina and acute coronary syndrome Flashcards
How many times more supply does coronary circulation require than unstimulated skeletal muscle does?
Needs a high supply of O2 – 20x of unstimulated skeletal muscle
What do cardiac muscles have a high density of and how does this impact diffusion?
-Cardiac muscle has high density of fibres and capillaries
-Shorter passive diffusion distances
What does a high capillary density and a large surface area do together in cardiac muscle?
-High capillary density
-Large surface area for O2 transfer
-Together these reduce diffusion
distance of O2 to myocyte
What times the blood flow is present in coronary circulation during normal activity?
- 10x the flow per weight of rest of body
How much O2 extraction is there in comparison to the average body in coronary circulation?
High O2 extraction (75%) - average body is 25%
What happens to coronary circulation during increased demand and how?
-Coronary blood 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 vessels due to beta-2 adrenoceptors on coronary artery vascular smooth muscle cells
When does coronary blood flow occur and when is it obstructed?
-Systole obstructs coronary blood flow
-Coronary blood flow only occurs during diastole
What are sudden obstructions that can occur in the heart?
Acute thrombosis, Acute Coronary Syndrome (ACS) including myocardial infarction
What are slow obstructions that can occur in the heart?
Atheroma (sub-endothelium lipid plaques)
chronic narrowing of lumen, produces angina
Why is coronary blood flow restricted during diastole?
Pressure in ventricles is = or > aorta
-Poor coronary perfusion
What are mechanical factors reducing coronary flow?
(1) Shortening diastole, e.g., high heart rate
(2) Increased ventricular end-diastolic pressure, e.g., volume-overload heart failure
(3) Reduced diastolic arterial pressure, e.g., hypotension
What type of arteries are the coronary artery?
Human coronary arteries are functional end-arteries
What happens when there is a total occlusion of left anterior descending coronary artery?
-Leads to ischemic area resulting in myocardial infarction
Steps involved from ischaemic tissue till cell death?
ischemic tissue, acidosis, pain (stimulation of C-fibres) –> impaired contractility –> sympathetic activation –> arrhythmias –> cell death (necrosis)
What does it mean by functional end arteries?
Low numbers of cross-branching collateral vessels (Arterio-arterial anastomoses)
What are the symptoms of angina pectoris?
Pain, crushing sensation in the chest
Radiates to neck, arms, jaw with shortness of breath, dizziness
How does angina pectoris feel like?
‘’Strangulation of the chest’’
What are the 3 forms of angina pectoris?
Stable, unstable and variant
What are the causes of angina pectoris?
Causes are ischaemia
What is ischemia in angina pectoris due to?
due to O2 and nutrient demands of cardiac tissue
not being met due to partial occlusion of coronary arteries
What are the causes of increased demands of cardiac tissue
Increased heart rate / left ventricular contractility / wall stress
such as triggers like:
Exercise (increased heart rate, contractility)
hypertension (afterload), left ventricular dilatation (heart failure)
What is stenosis?
partial occlusion
due to plaque formation
What happens to coronary arterioles during exercise in a healthy individual?
In exercise, metabolic vasodilation of
arterioles reduce total R
Increased blood flow to meet
increased O2 demands
What happens in stable angina to coronary arteries and arterioles during rest?
With stenosis in large coronary
artery - Resistance to flow increases
Metabolic vasodilation of arterioles occurs at
rest, so blood flow meets needs
What happens to coronary arterioles during exercise in an individual with stable angina?
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 NOT be met, angina develops
When do symptoms for stable angina appear?
symptoms appear after certain demand reached
How is relief given for stable angina?
Relief with nitrates (e.g., GTN spray)
What method of imaging is used for stable angina?
Coronary angiography
What is variant angina caused by?
caused by vasospasm
When does variant angina occur?
Occurs at rest
What is variant vagina often not linked to?
Often not linked to coronary artery occlusion
What are the causes of variant angina?
-Excessive responses to vasoconstrictors
-Endothelium dysfunction
What is the management of stable/variant angina?
-CCB
-Beta blockers
-Nitrates
What do CCBs do in the management of stable/variant angina?
-Decrease HR/Afterload
What do beta blockers do in the management of stable/variant angina?
Reduce heart rate
What do nitrates do in the management of stable/variant angina?
-Open up coronary
circulation increasing collateral flow
-Decrease afterload/preload
How does stable angina present on an ECG in an exercise stress test?
Exercise stress test produces symptoms and ST depression
What are the 3 types of acute coronary syndrome?
-NSTEMI (non-ST segment elevation myocardial infarction)
-STEMI (ST segment elevation myocardial infarction)
-Unstable Angina
What initiates acute coronary syndrome?
Initiated by a rupture of an atherosclerotic plaque produces a thrombus in a coronary artery which reduces blood flow
What is the presentation for acute coronary syndrome?
-unpredictable,
-sudden,
-lasts for >30 min,
-not relieved by GTN spray
What is the investigation for acute coronary syndrome?
-ECGs – NSTEMI or STEMI
-Troponins T and I measured (often raised in NSTEMI and STEMI)
How would an NSTEMI appear on an ECG and why?
In partial/less severe occlusion of a
coronary artery, small area of ischemia
which does not depolarize
- leads to injury current and depression
of ST segment on ECG -
How would a STEMI appear on an ECG and why?
In total/severe occlusion of a coronary
artery there is full wall thickness
ischemia which does not depolarize
- leads to injury current and elevation of
ST segment on ECG -
What is troponin T and I raised in and not raised in ACS?
-Often raised in NSTEMI and STEMI
-Not raised in unstable angina
What is the pharmacological therapy for unstable angina and NSTEMI?
-Morphine
-Anti-platelet - aspirin, clopidogrel
-Anti-thrombin - heparins, NOACs
-Long term - beta-blockers, CCBs, statins, ACEi
Based on what decisions is revascularisation needed?
Decision based upon:
Risk of future STEMI, symptoms persist, angiography shows occlusions
When would percutaneous coronary intervention(PCI, stents) be considered for the management of unstable angina and NSTEMI?
When 1 or 2 arteries are diseased
When would coronary artery bypass grafting(CABG) be considered for the management of unstable angina and NSTEMI?
-Greater than or equal to 3 main coronary arteries diseased,
-main left CA occluded,
-occlusion position not appropriate for PCI
How does PCI work?
balloon catheter inflated
in area of blockage, increase luminal size
What is the pharmacological treatment for STEMI
Morphine
Anti-platelet, aspirin, heparins
Thrombolytics – streptokinase, tissue plasminogen activators
Cause fibrinolysis, break down fibrin-clot, increase reperfusion zone
Long-term - beta-blockers, CCBs, statins, ACEi
What is the time frame for the preferred treatment for STEMI and what is it?
Preferred treatment within 2 hours of symptom onset – PCI or CABG
What are the life-threatening complications with STEMI?
Cardiac failure
Rupture of ventricular septal leads to blood leakage between ventricles
Arrhythmias
