126 - Angina Flashcards
Define stable angina
Reversible ischaemia to the myocardium brought on by increased work load. It is relieved by rest.
What presenting complaint might someone with angina have?
Retrosternal pain
Tight, crushing over chest
Radiation to arm/jaw
Lasts minutes
When suspecting angina, what serious conditions must you be careful not to miss?
MI (pain longer?)
PE (pain when breathing)
Tension Pneumothorax (pain when breathing)
Dissecting aneurysm
Someone comes in with pain in their chest in the early afternoon, he works in an office and usually eats lunch with colleagues. What might you suspect?
Reflux not angina?
Someone presents with chest pain and tightness of breath. They mention they have had a bit of a rash. What might it be?
Varicella Zoster
What routine investigations would you begin with when investigating for angina?
ECG
Routine bloods
Chest X ray
If you wanted to learn more about the anatomical issues going on in someones angina, what investigations could you do?
CT Coronary angiogram Invasive angiogram with IVUS Functional Flow Reserve Virtual histololgy
To stimulate angina and see how someones heart reacts, what type of tests would you suggest, name some examples?
Functional tests:
- ETT : exercise tolerance test
- Dobutamine stress + echo
- Adenosine stress + nuclear imagine/MRI/PET
What race of people are at a higher risk of angina?
South west asians
In the 65-75 year old population, what proportion of men and women have angina?
14% of men
8% of women
Why are coronary angiograms performed?
They are the gold standard technique at investigating coronary artery disease.
Help plan treatment - crucial before surgery
Where is access usually made for a coronary angiogram?
Femoral artery or vein
Brachial or radial artery (easy to get to)
Internal jugular or subclavian - eg. obese patient, hard to get jugular.
What are the key areas of focus in management of angina?
Lifestyle advice
Medical management
Revascularisation - percutaneous or surgically
What two first line drugs would you give in angina?
Nitrates - eg. GTN
B-blockers - eg. Bisoprolol
If B-blockers were contraindicated in a patient with angina, what 2nd line alternative could you use?
Calcium channel blockers - eg. Amlodipine or Verapamil
There are 4 3rd line drugs that can be used in angina, if symptoms persist of patients have many contraindications. What are they?
Longer acting Nitrates - eg. isosobide mononitrate
Potassium channel activators eg. Nicorandil
Ivabradine (blocks pacemaker channel in SA node)
Ranolazine (add on by cardiologist only)
As well as GTN and a B blocker, what else may you prescribe someone with angina?
Statins - stabalise plaques
ACE inhibitors - reduce BP
Antiplatelets - eg. asprin
What acronym + drugs would use use int he initial management of someone with suspected acute coronary syndrome?
MONA Morphine Oxygen therapy Nitrates Antiplatelets
What acronym and drugs should all patients post MI be given?
MI 5 drugs: Aspirin Clopidogrel ACE inhibitor B-Blocker Statin
What does aspirin do?
It inhibits COX1 and COX2 enzymes, inhibiting platelet aggregation
What does clopidogrel do?
It is an antiplatelet
It blocks P2Y12 part of adenosine receptor on platelet surfaces
What do ACE-inhibitors do?
The lower BP by prefenting angiotensin I becomeing angiotensin II, which prevents vasoconstriction. IT also prevents aldosterone production which reduces sodium and water retention.
What side effect may you get on ramipril?
A ACE-inhibitor. Dry cough
How do B-Blockers work?
They reduce HR and contractility by reducing the sympathetic drive to the heart.
How do statins work?
They reduce lipid and slow cholesterol production. They stablise plaques.
What drink is contraindicated if you are taking statins?
Grapefruit juice!
Define hypoxia
Lack of O2, causes reduced aerobic respiration causing cell injury
Define ischaemia
Lack of blood supply means there is a lack of O2 and essential metabolites - causing cell injury (more rapidly than just hypoxia)
What is infarction?
Irreversible cell damage and death due to ischemia and hypoxia
What 4 changes occur in cell injury pathophysiology?
Decreased ATP
Membrane damage
Increased intracellular Ca
Increased O2 derived free radicles
What is ischaemia-re-perfusion injury?
When blood is restored to a ischaemic tissue is may resolve, or the cells may die despite the damage being reversible - as cells have high levels of O2 free radicals, complements and inflammation.
What is an atheroma?
an accumulation of lipid and fibrous tissue within the intima of arteries - form plaques
What are the characteristics of a stable plaque?
Concentric shape
High proportion of fibrous stroma
Lots of smooth muscle
What are the characteristics of an unstable plaque?
Eccentric shape
Lots of lipid, macrophages and inflammation
Endothelial cell injury.
What is in the core of an atheroma plaque?
Lipid, cholesterol, cellular debris, crystals, foam cells
What covers the core of an atheroma plaque?
A fibrous cap - made of collagen, elastin, smooth muscle and stroma (supportive tissue of epithelial tissue)
What is found between the layers of an atheromatous plaque?
A cellular area of T lymphocytes and macrophages
What are the complications of atherosclerosis?
Gradual narrowing of the artery
Ulceration of the plaque
Rupture and fissuring of the plaque - emboli
Superimposed thrombus
Plaque could rupture - thrombosis - occlusion of the coronary artery - MI
What complications are there from having an MI?
Death! Arrhythmias Left ventricular failure Ventricular wall rupture Aneurysms
What is blood flow driven by?
Pressure difference
What is darcy’s law?
Flow is proportional to change in pressure / resistance
What type of flow does darcy’s law apply to? Where is this flow found?
Laminar flow - in arteries, veins.
Not in the heart or diseased vessels - turbulant flow
What causes resistance in vessels?
Depends on the viscosity of fluid and the radius of the vessel.
No-slip condition
- The speed of flow depends on how close to the edge of the vessel you are, with the layer directly touching the wall being static, and the middle section moving fastest with least resistance.
When darcy’s law is combined with the variables of resistance, what is it called?
Poiseuilles law
What is the Fahraeus-Lindquist effect?
The viscosity of blood depends on the width/radius of the vessel - at the width of a capillary the viscosity is lowest, as the width increases or decreases from that side it gets more viscous.
Why does the Fahraeus-Lindquist effect occur?
Due to axial streaming
There is a cell free zone on the edge of fluid in vessels, so cells can go quickly down the middle.
In capillaries there is bolus flow, which reduces friction.
What is the sheer rate?
The rate of change of velocity between teo fluid layers moving over the top of each other
How is viscosity related to sheer rate?
Increase sheer rate - decrease viscosity
Decrease sheer rate - increase viscosity
As RBC form rouleux piles at slower speeds, so become more viscous
How is haemocrit involved in viscosity?
Increasing heamocrit increases the bloods viscosity - so must be careful in anaemia, as reduced heamocrit, reduced viscosity, so need to increase cardiac output for BP to remain stable.
Describe 3 ways to measure local blood flow
Kety’s tissue clearance - inject radioactive material, see how levels fall.
Venous occlusion plethysmography - Inflate a cuff, occlude the vein, use a strain gauge to measure swelling - estimate arterial supply.
Flick’s principle: of pulmonary blood flow can be adapted to any organ.
What extrinsic and intrinsic methods does the body have to regulate blood flow?
Extrinsic = nerves, hormones, human altering response
Intrinsic = Autoregulation, active hyperaemia, NO
How does autoregulation of local blood flow work?
The heart, kidneys and brain are able to stablise blood flow despite a rnage of BPs.
Direct response in arterioles to increased pressure - stretch vessel - Ca released - they vasoconstrict
- If blood flow flass, metabolic waste builds up, which dilates vessels
How does active hyperaemia of local blood flow work?
Flow is dependant on metabolic rate of an organ, so cardiac output is spread amongst organs. Due to vasodilator metabolites eg. CO2, O2, Lactate, adenosine, H+, K+, Po4-.
Autacoids (lik local enzymes) from damaged tissue also causes dilation
How does the human alerting response work? How did they test it?
Shows extrinsic can override intrinsic. The ANS vasomotor nerves cause dilation or constriction.
- sympathetic vasoconstrictors - innervate vessles, noradrenaline acts on alpha1 vascular smooth muscle, which dilates or constricts.
- Parasymphathetic vasoconstrictors and vasodilatoes also act.
Test: told a man he was having a massive blood leak from his arm during a procedure (despite there not really being one). Blood flow increased to this arm.
