Week 10: Ischaemic Heart Disease Flashcards
What is cardiac ischaemia?
- Cardiac ischemia is therefore the inadequate blood supply to meet the oxygen requirements of the heart or the imbalance between myocardial oxygen supply and the myocardial oxygen demand
where does cardiac ischaemia predominantly cause in the heart?
- Predominately occurs to the left ventricle as its myocardium is much thicker, and requires a great deal more oxygen (isolated right ventricular ischemia is very rare at only about 1-2%)
Describe the left blood supply of the heart
- Left coronary artery
- Divides immediately into two branches;
- Left anterior descending: Which supplies the anterior wall of the left ventricle, the anterior 2/3rd of the interventricular septum
- Circumflex artery: Supplies the lateral wall of the left ventricle
Describe the blood supply of the right side of the heart
- Right coronary artery
- Predominately supplies the right atrium and right ventricle
- Supplies the SA and AV nodes
- It does also supply the inferior and posterior wall of the left ventricle
- Supplies 1/3rd of the interventricular septum
Why does the coronary blood flow decrease during systole?
Coronary arteries send perforating / penetrating branches of their vessels into the myocardium itself (the inner endocardial region to supply the inner part of the heart)
as a consequence of the contractions of the heart that push blood along, these penetrating branches are compressed during systole
- Thus, the coronary circulation shows phasic changes, with less blood flow during systole and high blood flow during diastole due to the compression of the vessels during contraction
What parts of an ECG become wrong with ischemic heart disease?
ST segment, T wave, Q wave
What is the ST segment in an ECG and what happens to it during ischemic heart disease
- Starts at the end of the S wave and at the beginning of the T wave
- This is the region which shows all of the ventricular myocytes to be in the depolarised state
- No electrical gradient will occur during this segment
- In a normal person, this ST segment will be in line with the PR and TP segments (on the same level)
- In ischemia this segment can deviate, either upwards or downwards
What is the T segment in an ECG and what happens to it during ischemic heart disease
Repolaristation of ventricles
- The T wave is normally upright in leads I, II, V3-6
- In some ischemic patients, this T wave can be inverted
What is the Q segment in an ECG and what happens to it during ischemic heart disease
Depolarisation moving from left branch to right branch
- Is due to the depolarisation of the intraventricular septum
- Normally, the duration of the Q wave is less than one small box (0.04)
- Normally, the amplitude of the Q wave is small (less than 25% of QRS)
- In ischemic patients, the Q wave will be longer and with a deeper amplitude
What are the two determinants for cardiac ischaemia and explain them
- Determinants of myocardial oxygen supply
- The oxygen content of the blood (which depends on the amount and type of haemoglobin as well as lung function)
- Rate of coronary blood flow (this should be high enough to supply enough oxygen and nutrients to the myocardium and is dependant on coronary perfusion pressure
- Resistance of coronary arteries (obviously a smaller diameter from plaque etc. will reduce lumen size and increase resistance diminishing oxygen supply) - Determinants of myocardial oxygen demand
- Is determined largely cardiac output (If heart rate is increased, oxygen demand will increase. If stroke volume increases, the heart has to work harder thus requires more oxygen)
- If the preload increases (the ventricle has a higher volume, meaning a greater force of contraction is required, meaning more oxygen is required)
- If the afterload increases (More pressure is required to pump the blood out, meaning a greater force of contraction is required, meaning more oxygen is required)
- In most cases, it is the supply of oxygen to the myocardium that goes wrong as a result of plaque build-up on coronary arteries
What are the 3 main disturbances that cardiac ischaemia causes to the heart
- mechanical
- biochemical
- electrical
cardiac ischaemia causes 3 main disturbances to the heart, mechanical, biochemical and electrical. Explain mechanical and biochemica
- Mechanical
- Is the contraction and relaxation of the myocardium
- This is caused by the reduced ATP (from lack of oxygen) - Biochemical
- Because of anaerobic metabolism, there will be the accumulation of metabolites
- E.g. lactic acid, serotonin, adenosine etc.
- These metabolites are also known to stimulate the pain nerve endings between the myocytes
- It is the accumulation of these which cause the patient to experience pain and discomfort
cardiac ischaemia causes 3 main disturbances to the heart, mechanical, biochemical and electrical. Explain electrical disturbance
ischaem causes lack of ATP
- Ischemia will result in an abnormality in the Action Potential (AP) as well as the Resting Membrane Potential (RMP) of myocytes within the ischemic region
- The AP duration becomes less with ischemia. This is caused by ATP sensitive Potassium channels that start to open with the onset of ischemia. Potassium then leaves the cell, causing early repolarisation (potassium leaving the cell is the cause)
- The RMP becomes less negative (doesn’t repolarise). This is caused by the lack of ATP, the power source for a number of pumps (especially Na/K ATPase) that mediate the appropriate RMP. The other reason is due to the accumulation of calcium within the cell, caused by a lack of ATP to drive the calcium ATPase. These combined raise the RMP.
- These ischemic cells have a shorter AP and less negative RMP
- Changes to the myocytes electrical activity will be reflected in the patients ECG
- The ST segment will have deviated (either up or down), the T wave changes and the Q waves may also be abnormal (occurs alter if the myocytes die and are replaced with fibrous tissue)
Explain what will happen to electrical activity of the heart with severe ischaemia
- With severe ischemia, the various pumps are inhibited caused abnormally high intracellular Sodium and calcium (causing intracellular edema), and high potassium levels outside the cell (causing arrhythmia)
- Severe, irreversible injury and myocyte death will occur in the myocytes if they are deprived of oxygen for longer than 20 – 40 minutes
- If this occurs, myocardial necrosis (cell death / injury through failure of the blood supply) will occur. As necrotic muscle does not generate electrical forces, it will cause a pathological Q wave in ECG
- Furthermore, as a result of the anaerobic metabolism there will be increased hydrogen ions within the cell causing protein denaturisation (destroying the actin and myosin function)
What is angina pectoris and what is it caused by?
uncomfortable sensation in the chest and neighbouring structures (burning, heaviness, pressure, crushing, squeezing or choking in the chest)
caused by the build up of biochemical metabolites which irritate the pain receptors with the myocardium to cause chest discomfort
Explain pathogenesis of CHRONIC CORONARY SYNDROME – STABLE ANGINA PECTORIS, clinical presentation and how to treat it.
- It is most commonly caused within patients by the chronic obstruction of stable atherosclerotic plaque
- This usually looks like a fixed obstruction with 75% or more lumen encroachment, which is sufficient to serve the cardiac oxygen needs at rest (thanks to the adaption of compensatory collateral arteries)
- The cardiac ischemia is intermittent, non-progressive and brief. It is not enough to cause myocyte death and so only occurs during times of increased oxygen demand like exercise, stress and sympathetic nervous activation
- Put simply, it is impaired blood flow at times of higher demand which causes ischemia and hence pain
- Symptoms include: angina pectoris, tachycardia, nausea, dyspnoea, transient fatigue and weakness- The characteristic symptom of stable angina is no pain at rest, but pain during exercise that is relieved by rest and / or nitro-glycerine
Treatment: - by rest or nitro-glycerine (which increases nitric oxide production, which is vasodilator) within 5 to 10 minutes
Explain myocardial infarction pathogenesis, clinical presentation
- Also known as a heart attack, myocardial infarction is an irreversible injury to, and the eventual death of myocardial tissue that results from ischemia and hypoxia due to a complete / partial prolonged occlusion of a vessel
- This irreversible myocardial injury and cell death (necrosis) occurs after 20 – 40 minutes of severe ischemia
crushing chest pain, more severe and wider radiation than usual angina
what are the two categories of myocardial infarction
- Subendocardial MI
- Is characterised by injury to the myocytes being limited to the subendocardial area because the occlusion of a major coronary artery is only partial
- Occurs if the damage is not to severe, or the therapy is started early
- NSTEMI ECG changes are indicative of subendocardial MI - Transmural MI
- Is characterised by ischemic necrosis of the full thickness of the affected muscle segment
- The irreversible myocardial cell damage extends from the endocardium through the myocardium to the epicardium
- This is caused by total prolonged occlusion and produces far more severe symptoms
- STEMI ECG changes are indicative of transmural MI
what are the two ECG changes in a myocardial infarction
- STEMI
- Is a wave form characterised by an elevated ST segment in the leads overlying severe ischemia
- Is indicative of a transmural MI, and requires immediate help as a large percentage of the ventricular wall has been damaged
- Immediate reperfusion therapy (restore blood flow) is likely to help or fibrinolytic therapy (disrupts the clot) - NSTEMI
- Is a wave form characterised by a depressed ST segment or T wave inversion in the overlying leads
- Is indicative of a subendocardial MI, which means the ischemic zone has been limited to the inner third or one half of the ventricular wall (sometimes can arise in unstable Angina patients)
- Usually fibrinolytic therapy is commenced
What are the 3 factors used to diagnose between unstable angina, stemi and nstemi
- Clinical presentation
- Severity and duration of chest pain (prolonged in MI)
- However most patients present very very similarly - ECG findings
- Is the main differential tool
- ST segment deviation changes indicate
- T wave inversion
- Q waves (however only develop later on and indicate an old MI) - Serum biomarker proteins of myocardial necrosis
- Are not always helpful in initial indications of MI
- When cardiac ischemia occurs, the membrane is damaged releasing its contents
- Cardiac specific proteins only will reach peripheral circulation after 3 – 6 hours
- If we are too wait this long, damage to a significant portion of the myocardium will already have occurred
What are the serum markers present in a blood test of a patient who has suffered an MI
- Cardiac troponin T and Cardiac troponin I and Troponin C
- T and I are very specific for the cardiac myocytes
- These are the proteins that come from broken down actin and myosin
- If these are present in peripheral circulation, MI has occurred, it is the gold stand in serum marker diagnosis
- Remains in the circulation for around 2 weeks, making it a useful marker - Creatine kinase MB
- Is a specific enzyme that is more concentrated in the cardiac muscle
- Levels subside very quickly - CK-MB:CK
- Myoglobin
- However due to its reduced specificity, and the potential for it to come from skeletal muscle this isn’t as preferred
- Reaches circulation very early
