L.27, 31, 34 : Chest pain, acute and chronic Flashcards
Coronary artery disease due to artherosclerosis can present as stable angina
Acute coronary syndrome - sudden cardiac death: sudden blockage.
Or stable angina:
How does chest pain present
- Visceral pain is more diffuse
- Cardiac pain is felt across the front of the chest, left arm to hand, throat and jaw.
- Pain can also be heaviness, tightness.
What does MI pain look like
MI- pain at rest, unstable angina, pain for heart . Arrhythmia, dizziness, short of breath, tachycardia.
What is the treadmill exercise test and what do you look for on the ecg. (Stemi , non stemi)
For stable coronary artery disease If the problem is due to fixed narrowing causing mismatch supply demand.
ST should be on the baseline
ST segment on ECG will be depressed if there is sub-endocardial ischaemia (first usually) and it will be elevated if it is Transmural myocardial ischaemia (second - complete blood loss)
When in doubt- if there is ST elevation it is never the reciprocal- this
-deep Q waves means one side of the heart has died, so mean vector points somewhere else
What are the focus for treatments of MI (resulting from coronary artery disease)
-improve coronary blood flow: Stent, angioplasty, CAbypass grafting the obstruction.
-reduce myocardial oxygen demand: betablockers,
calcium antagonists, nitrates : venodilation, reduce preload, increase flow, reduce afterload in arteries
- reduce LDL cholesterol to reduce atherosclerosis genesis: statins
- anti platelet treatment to prevent clotting in arteries
What do you use troponin blood test for
High troponin in the blood indicates myocardial injury
What are the signs accompanying pericarditis
- Pain is worse with breathing that is pulling on it, relieved when leaning forward
What are the signs of aortic dissection (Intimal tear in the aorta that tracks to the media.)
Sudden onset.
Pain radiating from front to back following the tear.
- continuous pain
-murmur - leaking aortic valve
-higher systolic and reduced diastolic: increased run off, ventricle has to pump harder
What are common thrombolytic drugs, also how they work given after 12 hours of chest pain onset for a STEMI
Streptokinase which activates plasminogen in blood and tenecte or alteplase which catalyse plasminogen on fibrin
Both catalyse plasminogen to plasmin which breaks down fibrin- clot.
What are the risks of thrombolytic drugs
They can reduce clotting so can illict local and intracerebral/GI bleeding.
Danger for surgery. Also streptokinase being derived from bacteria can case allergic reaction
What is the mechanism of action for Aspirin and its uses
Acutely, 1. It irrevesibly acetylates CycloOxygenase 1 enzyme which makes thromboxane/ prostaglandins which activates platelets. It is metabolised into salicyclic acid.
It also is part of secondary prevention of CA disease (MI, angina), stroke, periph vasc. disease by stopping long term clotting
What are the risks of anti-platelet drug - clopidogrel or aspirin use
- There is reduced production of protective prostaglandins in the gut, leading to upper GI ulcers, dyspepsia (asthma)
- increased broncho constrictor activity (lipo-oxygenase) make asthma control worse (asthma)
- GI bleeding, rash, Can’t go on warfarin (blood thinner)
What is the mechanism of clopidogrel- when used
ticagrelor also targets this
Antiplatelet drug that inhibits p2y 12 receptor preventing ADP induced thrombosis. Must be metabolised before active, time and dose dependent. Used for Acute coronary symptoms, aspirin allergy and with asthma vascular stenting
What is the mechanism of Low molec weight heparins-eg. enoxaparin anticoagulant.
Inhibit central clotting cascade factor Xa (can’t be given orally- has to subcut).
What is given as initial treatments for Non stemi and stemi and what are the differences?
pain relief, nitrate, aspirin + others, beta-blockers, stent
non-stemi: nonurgent: LMW heparin
urgent: Thrombolytic and LMWheparin
What is the risk of LMW heparins
- Bruising/ bleeding sites: intracrania , intracranial
- thrombocytopenia: autoimmune
What is the risk of nitrates
Headache, syncope: reduced blood pressure in the brain, nausea
- Can also have nitrate tolerance: loss of haemodynamic and anti-anginal efficacy if no nitrate free period.
What is the main function of beta-blockers, B1 and B2 receptors and the adverse effects
Antagonise B adrenoreceptors and reduce heart rate, reduce bp (afterload) reduce cardiac work inhibit sympathetic stimulation
Adverse:
Respiratory : asthma exacerbation - blocking the bronchi dilatiors. Hypotension, bradycardia
How does chronic chest pain (stable angina) present
Coronary artery disease due to artherosclerosis can present as stable angina
Predictable pain in central chest-tightness in relation to fixed stenosis causing reduced blood flow in comparison to increased demand - higher HR- less time to drain. So pain resolves with rest
Examinations performed for stable angina
Bruits: sounds over arteries show stenosis- indicate likelihood of it in the arteries
BP, Heart sounds, oedema,
ST depression in ecg changes in the treadmill test, stress echocardiogram looking for ischaemia areas in the left ventricle.
What is the management of stable angina
Lifestyle: low lipid diet, smoking,
Pharmacological reduction of symptoms/risk
Interventional surgery, percutaneous intervention stent – doesn’t have large effect on long term mortality
What are the drugs that reduce symptoms vs CVS risk (secondary prevention)
Need to have ongoing review
Symptoms: betablockers, nitrates, calcium channel blockers
CVS risk: antiplatelet, lipid lowering statins
What is the function of calcium channel blockers
Block voltage operated L type Ca2+ channels in cardiac and smooth muscle.
In resistance vessels, It inhibits calcium influx into the cell so cause reduced contractility, so vasodilation due to reduced tone in resistance vessels- dihydropyridine
Ones that target heart tissue, inhibits depolarisation slow HR, and is negative inotropic, reduces peristalsis in the gut.
How are nitrates administered
regular daily or plus as required (sublingual)
Nicorandil is what
Nitratelike, It helps to vasodilate and opens the K+ channel open to hyperpolarises cell, inactivates VGCa channel to decrease calcium influx. For symptom relief
What is the relationship between cholesterol and cvs risk
There is a linear relationship with reduced cholesterol, and reduced CVS risk
How do statins work
Inhibit an enzyme HMGcoa-reductase which is proximal in the synthetic pathway for cholesterol. This lack of cholesterol causes increased expression for LDL receptors for hepatocytes to get LDL from the circulation.
- Also reduce Isoprenoid production which are involved in inflammation, cells signalling, differentiation
What are side effects of statins (eg, Simvastatin
Skeletal muscle based: aches, inflammation of skeletal muscle (CK level measure). Rhabdomyolysis: denaturing of skeletal muscle- renal failure.
Calcium channel blockers interact to prevent breakdown
