Chest Pain Flashcards
Describe the blood supply to the heart i.e. coronary arteries.
Blood supply - two coronary ostia (origins of coronary arteries) – above aortic valve - branch off left and right to form the left and right coronary arteries
Right coronary divides into the posterior descending artery and right marginal artery
Left coronary divides into the left circumflex artery, anterior descending artery and left marginal artery
Left coronary artery – occlusion – sudden death - right artery is not sufficient to sustain life - Why? Left artery feeds the left circumflex and anterior descending artery
This sits on the surface of the heart so that is is not subject to pressure created by the heart
What do we call the fatty deposits that build up in our blood vessels?
Atheroma - fatty deposits which start to build up around the age of 18-20
Common in western societies
The rate of build-up progression is a big concern as it can lead to the occlusion of blood flow
Goal – keep it stable
What are the main independent risk factors for a myocardial infarct?
Independent risk –> factors that can predict the incidence of MI in isolation
Main 5 independent risk factors are…
1. Smoking (includes passive smoking)
2. Diabetes (type I and II - diabetes for more than 10 years significantly increases risk)
3. Hypertension
4. Family history (if someone in your family had MI below the age of 60)
5. Hyperlipidemia
What is an myocardial infarction?
A myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops to the coronary artery of the heart, causing damage to the heart muscle (differentiating factor from angina)
Basically, blood supply to the heart muscle is blocked - leading to the death of cardiac cells
On a cellular level in heart muscles - what are two key energy dependent processes require for muscular contraction?
Two key energy dependent process ….
1. Calcium pumping - in and out of sarcoplasmic reticulum - Ca2+ bind to troponin, freeing the actin binding sites for the myosin heads.
2. Myosin head release - ATP hydrolysis
What two investigations are normally used to investigate whether someone has had an MI?
- First investigation - Electrocardiogram
- Second investigation - blood test looking at serum troponin levels - cardiac troponin is specific to the cardiac muscle - hence, we use an immunoassay to measure levels of troponin
Detection of elevated serum troponin is more important than ECG changes. However, they often can only be detected in the hours after the onset of the myocardial infarction. So, especially in the first few hours after the myocardial infarction, the ECG can be crucial.
What are the different stages of an ECG?
U wave - sometimes present - to the right of the T-wave -
What does sinus rhythm, sinus tachycardia and sinus bradycardia look like on an ECG?
Sinus rhythm - Regular p waves, and each p wave is followed by a QRS - 60-100bpm
Sinus Tachycardia - Same as above, except >100bpm - Does not represent cardiac patholoy. May be a sign of anxiety, dehydration, recent exercise, or general illness
Sinus bradycardia - Same as above except <60bpm - normal in young fit people
Outline the conduction system of the heart.
SA Node - AV node- Right and left bundle branches - Purkinje fibres
How much does a big and small box in an ECG represent - time wise?
What changes in the ECG can be observed in MI patients?
- ECG shows ST segment elevation or depression
- Pathological Q waves develop on the ECG - small little wave in QRS complex - elevation, excessive depression and width
What is the difference between an ECG lead and electrode? What are the different ECG leads?
ECG lead is a graphical representation of the heart’s electrical activity.
ECG electrode - is a conductive pad that is attached to the skin to record electrical activity
Only 10 physical electrodes are attached to the patient, to generate the 12 leads, which consists of…
Six chest electrodes - V1-V6
Four limb electrodes - RA, LA, LL and RL
Where is the pain for MI’s typically localized and how it is typically described? What are some associated features?
Pain secondary to myocardial ischaemia is typically located in the centre of the chest - It may radiate to the neck, jaw, and upper or even lower arms and sometimes it may only be experienced at the radiation sites or in the back.
Myocardial Ischaemia - typically dull, constricting, choking or ‘heavy’, and is usually described as squeezing, crushing, burning or aching - patients emphasize this to be a discomfort rather than pain.
Myocardial infarction (MI) pain - typically takes several minutes or even longer to develop to its maximal intensity
Associated features - accompanied by autonomic disturbance, including sweating, nausea and vomiting.
What is angina? Where is the pain normally experienced? How is it described as? What are its associated features?
Stable Angina (Angina Pectoris) - common presentation of CHD - insufficient oxygen supply to the heart to meet demand i.e. when there is myocardial ischaemia without infarct (death/necrosis of tissue)
Basically the heart isn’t receiving enough oxygen
Angina typically presents as central or left sided chest pain, with or without radiation to the neck, arm or jaw.
Pain is described as tight, dull or heavy
Angina builds up gradually in proportion to the intensity of exertion and is generally transient and is releived by rest, but can also be triggered by emotion.
Other symptoms - breathlessness, feeling sick and fatigue
What is myocarditis and pericarditis? Where is pain localized? How is it described?
Myocarditis is an inflammation of the myocardial layer of heart muscle
Pericarditis refers to inflammation of the pericardium, a fibrous sac surrounding the heart.
Location - characteristically felt retrosternally (behind the sternum), radiates to the left/right shoulder or neck
Pain - often also described as ‘sharp’ and may ‘catch’ during inspiration, coughing or lying flat. It typically varies in intensity with movement and the phase of respiration.
What is coronary artery disease? What are the most common presentations/clinical manifestations of coronary artery disease?
Coronary artery disease - disease caused by the narrowing and blockage of the coronary artery - atherosclerosis
Note - sometimes CAD can also rarely occur due to aortitis, vasculitis and autoimmune connective tissue diseases
Outline the pathognesis of atherosclerotic plaque formation.
Atherosclerosis - progressive inflammatory condition whereby we get a build-up of lipid rich deposits (atheroma) along the arterial wall. It is clinically silent, unless they become large enough to cause tissue perfusion or until ulceration and disruption of the atheroma causes thrombotic occlusion or distal embolization
- Begins early in life - build-up of fatty deposits at site of arterial shear stress, e.g. bifurcations, and are associated with abnormalities of endothelial function at these sites
- During evolution of the plaque - monocytes and other inflammatory cells bind to receptors expressed by the endothelial cells and migrate into the intima. These cells phagocytose the LDL-cholesterol that has built up to become lipid laden macrophages and foam cells
- Extracellular pools of lipids build up when the foam cells die and release their contents
- Activated macrophages - release cytokine and growth factors - smooth muscle cells migrate from the arterial wall into the intima – change from a contractile to fibroblastic phenotype – stabilises the atherosclerotic lesion - clinically silent unless its very big
- In established plaque – macrophages mediate inflammation and smooth muscle cells promote repair
- If inflammation predominates - the plaque becomes active and unstable
- This increase the risk of ulceration and thrombosis – breach in integrity of plaque causes platelet aggregation (clot formaiton) and thrombosis (block veins and arteries)
