Flashcards in Ischaemic Heart Disease Deck (17):
What are common causes of Chest pain?
Heart related such as angina, MI and pericarditis, Respiratory such as pneumonia, pulmonary embolism and pneumothorax, GI problems such as acid reflux and cholecystitis and finally muscular or skeletal issues.
Which layer of the heart is most vulnerable to ischaemia?
Subendocardial tissue is last layer to be fed by blood vessels so is most vulnerable.
Why can't coronary arteries perfuse any blood during systole?
During systole coronary arteries are compressed.
Why are blockages or narrowing's in the coronary arteries very costly to heart tissue?
There are very few collateral arteries in the heart and cardiac myocytes have a very high metabolic rate.
What is myocardial oxygen supply dependant on?
Myocardial supply is dependent upon: coronary flow, perfusion pressure, coronary resistance and oxygen carrying capacity.
How does myocardial oxygen demand change
Myocardial oxygen demand changes with contractility so: heart rate, wall tension, pre load and after load.
What are the risk factors for IHD?
Risk factors for IHD: age, sex, race, family history, hyperlipidaemia, smoking, hypertension, diabetes and obesity.
Describe an atheromatous plaque and the difference between an unstable and stable plaque.
Atheromatous plaques have a necrotic core and fibrous cap surrounding. Unstable plaques have a thin fibrous cap whilst stable ones are thick – the necrotic core is thrombogenic.
What is stable angina and how do you test for it?
In stable angina chest pain appears only during exercise and can be relieved by rest or nitrates. Exercise stress test can be done to test for this and you get a transient subendocardial ischaemia which manifests itself as pain and ST segment depression.
What is acute coronary syndrome?
Acute coronary syndrome occurs when there is pain at rest, no relief with nitrates and it lasts a while and occurs due to plaque fissuring. There are three types: Unstable Angina, NSTEMI and STEMI.
Describe unstable Angina
Unstable Angina happens due to incomplete thrombus occlusion, there will be ST depression or T inversion and negative lab tests. Can occur with no ECG changes.
NSTEMI occurs again due to partial thrombus occlusion there will be some death of tissue limited to deeper regions which will cause positive lab results, there will again be ST depression, T inversion but no ST elevation. Can occur with no ECG changes.
STEMI occurs due to full occlusion and death of myocardium resulting in ST elevation due to injury, Q waves due to necrosis and T wave inversion due to ischaemia.
STEMI can also be caused by a new left bundle branch block (double R peak).
During an MI what observations will you make and why?
In an MI sympathetic pathways are overstimulated resulting in sweating and pallor and parasympathetic over stimulation causing nausea and vomiting. They will also have low BP, be out of breath due to LV failures, tachycardic and feel faint.
After an MI what are the timing of the rise in Troponin and Creatine Kinase?
Troponin starts to rise 4 hours after MI, peaks between 18-26 hours and declines slowly over the next 10-14 days. Creatine Kinase starts after 2-8 hours, peaks at 24 hours and is back to normal within 3 days.
What are the complications of an MI?
Sudden death, cardiogenic shock, arrhythmias, heart blocks, heart failure and ventricular tachycardia due to re-entry circuits.