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(solved) Coronary Arteries - PDF

   

Added on  2020-11-02

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Scenario 1/ cardio:CVD lecture:Coronary arteries:Left CA – branch directly from the aortaRight CA – branch directly from the aortaRight marginal branch of RCALeft auricle (reflected)Circumflex branch of LCAPerfusion of the heart (blood going to the coronary arteries) cannot happen during systole and only occurs during diastole. The aortic valve cusps close off the coronary arteries during systole.Intramyocardial coronary vessels – blood also doesn’t flow during systole. Autoregulatory mechanisms tell vessels to contract or constrict, usually metabolic factors. If a cell has a higher level of activity more metabolic factors are released which tells the artery supplying that factor to dilate to get more blood and increase oxygen and nutrient absorption.When blood flows through the coronary arteries the muscle tissue extracts 60-80% of oxygen in that blood, skeletal only 20-40%. Meaning, the cells will die quickly if blood supplystops.Coronary Heart/Artery Disease:Involves narrowing of the lumen of one or more coronary arteries enough that the downstream myocardial perfusion is reduced.Clinical manifestations depend on:-Which artery-Transient or permanent obstruction (sometimes or always blocked)-Partial or complete obstruction (some blood flow or no blood flow)-Development of collateral blood supply (stimulate the growth of new blood vessels (anastomosis) to supply blood to cells, takes long time to occur)Ischemia: reduced blood flow to/in an areaHypoxia: low oxygenation in an areaCause of CHD:Hypertension and hyperlipidaemia, increases risk of atherosclerosis which increases risk of CAD.Atherosclerosis:Common site is proximal coronary arteries, carotid arteries, vertebral, basilic and cerebral arteries and abdominal, iliac, femoral and popliteal arteries.

It is the process of plaque building up in vessels with can obstruct the pathway of blood, causing primarily by hyperlipidaemia. The negative affecting cholesterol is a high level of low density lipoprotien.The process happens between the epithelium and the elastic layer of the blood vessel creating an overgrowth of muscle that is bumpy instead of smooth.Plaque results in a reduced luminal diameter and a reduced capacity to vasodilate. Chronic ischemic heart disease: Recurrent episodes of transient (happens every now and again) myocardial ischemia= partial obstruction to coronary blood flow causing imbalance between O2 supply and O2 demand.Heart doesn’t have a big stored source of energy in anerobic metabolism (60 seconds beforeit starts losing function)Types of CIHD:-Stable angina: occurs predictably with exertion or known stressors (temperature regulation), caused by atherosclerotic plaques in main coronary arteries. Meaning at rest the myocardium has adequate oxygen supply but with the known stressors the increased oxygen cannot be met.The pain is caused by biomechanical fatigue, switching to aerobic to anaerobic metabolism producing things like: adenosine, lactic acid, hydrogen ions, etc. Glyceryl trinitrate relieves it.-Variant angina: occurs unpredictably and can occur at rest. Caused by episodes of coronary arteries having vasospasms (contracting for no reason)-Silent myocardial angina: recurrent episodes of myocardial ischemia but no angina pectoris. Can be causes by autonomic sensory neuron loss like due to diabetes. Can be diagnosed by exercise stress test. Usually results in characteristic pain, angina pectoris (symptom) this is the pain associated with heart attack. Crushing pain in the left side of the chest radiating down the arm and into the jaw.This can cause arrhythmias: AF, VTTreatments:Statins are a medication that decrease the progression of atherosclerosis.Anti-platelets: When plaque ruptures platelets adhere to plaques and generate thrombus which blocks artery. Beta blockers: Glyceryl trinitrate: dilates veins, = decreased venous return, decreased energy and oxygen for heart to contract (decrease pre load). And dialates arterioles = decreased afterload. Organic nitrates decreased the work of the heart. Acute Coronary Syndrome: Chronic ischemic heart disease can develop into/cause acute coronary syndrome.Classification of ACS:

Distinguishing features: Onset: can occur when restingDuration: pain does not go away at rest, can go on for much longer. Intensity: Pain is worseMyocardial ischemia, resulting from acute coronary occlusion causing pain and or discomfort that is more severe, prolonged and or frequent or is not relieved by glyceryl trinitrate. Other clinical features:Diaphoresis – sympathetic nervous system gone into overdriveDyspnoea – alterations to breathing rateNausea/ and or vomiting – Feeling of impending doom – emotional response, fight or flight response into overdriveAngina pectoris: symptom, chest painAngina: atherosclerotic plaque-Unstable angina: this is commonly a progression of stable (plaque ruptures and platelets aggregate) or variant angina OR secondary to a non-cardiac condition such as severe anaemia or infection OR post MI.Pain is more persistent and severe than stable angina.To determine whether it is this or a non-STEMI is the absence of serum markers for myocardial damage.-No ST-segment elevation: no change on ECG, needs cardiac blood work to determine-ST-segment elevation: MI STEMI-Acute myocardial infarctionST segment can be depressed but is usually elevated in ACS. Either depression or elevation indicate ischemia within the ventricle wall and injury of the cells. Myocardial infarction type 1:Thrombus forms on atherosclerotic plaque blocking off blood flow causing ischemia and cell death. Process:Plaque rupturesThrombus is over the plaqueOcclusion of coronary artery (either all or partial blockage)Prolonged ischemia of the cells past the blockageHypoxic injury of myocardial cellsCell necrosis (infarction = tissue death)Cell membrane breaks down and the content is released into the bloodTroponin I and Troponin T are higher and indicate myocardial infarction, creatine kinases-MB and myoglobin can be tested also but aren’t as relevant. However, there are other caused of MI not atherosclerosis related.

Scenario:Stable angina – unstable angina – transient ischemia – sustained ischemia – myocardial infarction (STEMI) – myocardial inflammation and necrosis (can cause remodelling of the heart and lead to heart failure. Where in the patient’s heart will the ischemia be: because in the left anterior descending artery, the anterior (front) section of the intraventricular septum will become ischemic.Functional significance:Once cells start dying cells stop contracting, reduces stroke volume and leads to decreases in cardiac output or complete stoppages of cardiac output. Can also lead to arrhythmias.If the patients present to hospital with chest pain and persistent ST elevation on the ECG thediagnosis is ST elevation myocardial infarction (stemi). No biomarkers required.STEMI: Within less than 120 minutes reperfusion (return of blood flow) of the heart is the aim. Immediate management for chest pain admission as a nurse: Aim to re-establish to maintainmyocardial perfusion-ECG, Serum markers-IV Opioid to reduce pain and anxiety reduce sympathetic nervous system activation-O2 therapy if SaO2 below 93%-Nitrates such as glyceryl trinitrate, dilate blood vessels reduce workload of heart.-Aspirin to prevent thrombus formation-Angioplasty if STEMI is evidentAngioplasty:Catheter is threaded up through femoral artery through abdominal aorta to the heart and into the coronary artery where the blockage is found. A balloon is placed to reopen the coronary artery that is blocked.Coronary artery bypass graft: CABGJoin the aorta with a vein usually the saphenous vein from the leg and join the aorta to the coronary artery.What might happen to the patient if the treatment was prolonged:Heart Failure:Symptoms typically occur upon exertion but can also occur at rest. It is secondary to an abnormality of cardiac structure or function that impairs the ability of the heart to fill with blood at normal pressure to eject blood sufficiently to fulfil the needs of metabolising organs.

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