Myocardial Infraction Flashcards
Describe the aetiology of CHD ?
Altherosclerosis accounts for >90% of coronary artery narrowing
Slowly progressing, pathological process involving the demise of the arterial wall
Non-modifiable risk factors for CHD ?
Male gender
Increased age
Ethnic origins
Low birth weights/prematurity
Family history of premature CHD
ACE’s
Modifiable risks for CHD ?
Cigarette smoking
Hyper-cholesterolaemia
Hypertension
Lack of exercise/sedentary lifestyle
Excess alcohol consumption
Smoking and how to effects the body towards CHD ?
Nicotine:
1. Constricts blood vessels
2. Increases catecholamine release from symphetic nervous system (NSN) & adrenaline medulla which increases heart rate
3. Encourages thrombin formation
4. Encourages platelets at adhere
5. Lowers vitamin C levels necessary for cholesterol metabolism
6. Lowers levels of high density lipoproteins (HDL)
Describe an NSTEMI
This MI occurs when the coronary artery becomes totally occluded leading to the progressive ischaemia of the myocardium and ultimately cells deal or infraction of the heart wall
Affects the three layers of the ventricular wall “transdermal”
ECG reading: pronounced ST elevation
Explain the pathophysiology of an MI
MI occurs because of plaque buildup causing plaque rupture
Rupture occurs the lipid core and form thrombus which suddenly occludes the coronary artery
Occlusion stops the blood flowing beyond this point , reduction in perfusion in myocardial muscle area
If no reperfusion myocardial cells die
The cells become ischaemia within 10 seconds
Can withstand 20 mins of ischaemia before metabolically altered cellular hypoxia
Describe cellular hypoxia leading to cell death
Interupted blood flow
Reduced oxygen/nutrients to cells
Reduced ATP production/energy deficit
Loss of Na/k pump
Na and water rush in/cell swells
Reduced protein synthesis
Calcium moves into cell and triggers further cell dysfunction
Mitochondria swells triggering signals for apoptosis
Cell death/necrosis
What happens when the myocardial is damaged ?
Reduced myocardial contractability
Reduced stroke volume
Reduced cardiac output
Reduced blood pressure
Reduced blood supply to organ sand tissues
What are the two types of compensatory mechanisms ?
Sympathetic nervous system (SNS) response
And
Renin angiotensin aldosterone system (RAAS)
What is the systematic nervous system (SNS) response ?
Reduced circulatory volume activates bars receptors in aortic arch/carotid sinus
Response to reduced stretch (Reduced CO and BP)
Medulla and sympathetic nerves stimulated
Adrenaline glands triggered to release catecholamines (adrenaline/nor adrenaline)
Increase HR, CO. Peripheral vasodilation, increased BP and persuasion to tissues
What is the Renin angiotensin system response ?
Reduced circulatory volume to kidneys (JGA)
Activation of the renin-angiotensin-aldosterone mechanism
Renin ( released by kidneys)
Converts angiotensinogen to Angiotensin 1
Angiotensin 1 converts to Angiotensin 2 in lung by ACE
Angiotensin 2 stimulates release of aldosterone from adrenal gland
Na+ and H2O retained
Vasoconstriction of arteries (increased BP)
Stimulates pituitary gland to release ADH (H2O retained)
Increased BP, increased circulating volume/venous return to heart increasing cardiac output
Name some of the signs and symptoms of an MI
Blood pressure changes
Dyspnoea
Nausea and vomiting
Referred pain - arm, neck and jaw
Severe chest pain/tightness/pressure
What is referred pain ?
This is a cardiac pain signal coming from the spinal cord, close proximity to the chest wall and arms are received
‘Spill over’ in these spinal fjord areas creat the perception of discomfort in the arms, chest, neck and sometimes back
What is the blood pressure changes ?
If tissue is not re-perfused then hypotension will happen, this follows as a result of cardiogenic shock
What is dyspnoea ?
May develop breathlessness in response to tissue ischaemia and an increased demand for oxygen
