Lecture - CVS (Bevin Physiology 11 Ischaemia)

Question 1

Coronary circulation:

1. What does the right coronary artery supply and what does the left coronary artery supply?
2. What’s the coronary sinus and where does it drain?
3. What’s the pressure like in the left coronary artery and the right coronary artery as compared with aorta?
4. So the coronary circulation exhibits marked fluctuations in flow rate which depend on what?
   - The _______ _______ in ______ pressure are partly responsible for these phasic fluctuations.
   - What’s the other main contributor to the variations in the coronary blood flow during the cardiac cycle?
5. Okay so you know that when the left ventricle squeezes (systole), the _______ myocardial pressure rises - what does this do to the coronary blood vessels and whereabouts it most?
   - why is there complete interruption of blood flow into the left artery during early systole?
   - during which phase (systole/diastole) is the flow through the left artery proportional to aortic pressure
6. So in which phase does the left artery get the blood flow? (therefore the left ventricle gets its blood flow)
7. Why the right coronary artery not have such a fluctuation in pressure?
   - when does the blood flow through the right coronary artery? (like which phase)
   - the right coronary artery blood flow follows the fluctuations in what?
8. Coronary sinus: when (systole/diastole) is there a surge of venous blood flow out of the coronary sinus? What is this due to?
   - what happens during diastole?

Answer 1

7. Bc the right intramural pressure is lower - RV goes 25 to 8

Question 2

Blood supply to the ventricular muscle:

1. How does the nutrient blood flow reach the myocardium?
   - how is this good for surgery or grafts?
   - what about chronic low grade atherosclerosis?
   - why is the subendocardium vulnerable?

Answer 2

-

Question 3

Regulation of coronary blood flow:

1. The role of vasodilators, invluding _____ and ______, in local metabolic control of the coronary circulation. As a result of heart ______ or _______, the rate at which the oxygen supply to the mitochondria can synthesise ATP is temporarily exceeded so that ______ ______ ______ __ _____ _______. NO is relased from the healthy _______. Neurogenic factors are both vasodilatory (___-adrenergic) and vasoconstrictiory (___-adrenergic)
2. What is the most lilely candidate in the metabolic control of coronary blood flow?
   - when is it produced?

0produced by what?

• so it leaves the cell to reach what and acts on what as a vasodilator?
  3. Another big player is ____
• where is it synthesised?
• diffuses where?
• does what 4 things?
  4. What’s the neurogenic effect on regulation of coronary blood flow? Direct and indirect

Answer 3

1. The role of vasodilators, invluding adenosine and NO, in local metabolic control of the coronary circulation. As a result of heart work or ischemia, the rate at which the oxygen supply to the mitochondria can synthesise ATP is temporarily exceeded so that ATP breaks down to form adenosine. NO is relased from the healthy endothelium. Neurogenic factors are both vasodilatory (B-adrenergic) and vasoconstrictiory (a-adrenergic)

Question 4

Coronary artery disease

1. Coronary artery disease can lead to coronary artery ______
   - what does this reduce to the distal segment of the diseased artery?
   - induces what? and what does that lead to?
2. To reduce the coronary blood flow by stensosis, how much of a drop in arterial diameter do you need?
   - what law is this related to?
   - so can you just keep eating bad food until 70%?

Complete coronary occlusion:

1. Does the sub-endocardial or the epicardial zone have a lower O2 tension? Why’s this?
2. When the coronary blood flow is reduced, which of the sub-endocardial or epicardial suffers more?
   - so where will the ischemia begin?

Answer 4

2. No, eat better so you dont get to 71 and die

Question 5

Ischaemia and contractile failure:

1. Overview but what does it do to: contractility, SV, ESV, EDV, ED pressure
   - what does the EDP do to the subendocardial tissue?
   - what happens to the blood flow following this? So increased ischaemia
2. So increased pressure on the endocardium with contractile failure makes the ischaemia spread where?
3. The major effect of ischamia is a decline in what?
   - the loss in ____ function happens how fast or slow after the onset of severe ischaemia?
4. The reduced myocardial contractility is due to what 3 things?
   - why is ocidative metabolism inhibited?
   - what channels lead to the K leaking out? What happens to the extracellular K+ for surrounding cardiac muscle cells
   - what does lactate do?
5. What is the effect of the high extracellular K+ on the cardiac AP?
   - normally the conc is 3.5-5.5mM but if it gets to 7.5mM, what will happen to the heart in diastole?
   - what happens to RMP? How does this relate to the K equil potential?
   - how exactly is the AP in the ischaemic heart altered? (2 things on slide 39) and why do both happen?
   - so what’s the relationship between contractility and ischaemia?

Answer 5

4. Lactate increased H+ so you get acidic environment and that’s not good for the cell
5. Okay so you increase extracellular K+ and that will depolarise the RMP so it’s less negative (lower the K equi potential). The Phase 0 (upstroke) of the AP becomes less steep and the amplitute of AP reduces. Less steep phase 0 because since the cell membrane potential is less negative in ischarmic cardiac cells, some fast Na channels remain inactive and so during depol, fewer Na+ channels open and the inward Na+ current isn’t as strong and the upstroke of the AP is smaller + less perpendicular (i.e. slower). Also, the plateau phase is shortened, late repol occurs earlier than normal, so less Ca++ and that means less contractility all because the ATP-senstivie K+ channels opened and that pulls the AP down the page faster

Question 6

Current of injury:

1. Normally all areas in the ventricles depolarise/repolarise ______
2. When the muscle is fully depolarised or repolarised:
   - what happens to the current flow?
   - what’s seen on the ECG? Eg which segment?
3. But when one part of the muscle is ischaemic and the other part if normal, what develops? Overview of how that works pls
4. During mid-systole, what voltage relatively is the normal vs ischaemic tissue?
   - so a current of injury flows from the _____ to the _____ tissue, towards the _____ ______
   - what’s the major ECG change you see?
5. During diastole, which tissue (ischaemia or normal) is more positive?
   - so a current of injury flows from the _____ to the ______, _____ from the detecting electrode
   - what’s the jaor ECG change seen?
6. On the ECG, what change do we actually see?
7. What leads can we see the ST segment elevation? ST depression?
8. What are addiotional changes that are seen?

Answer 6

3. Whole lot shorter AP so at various phases, you have tissues at various voltages - not really a current of injury - it’s just to decribe the different electrical tissue