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Block 2 Week 3 > Cardiac Metabolism & Coronary Circulation > Flashcards

Cardiac Metabolism & Coronary Circulation Flashcards

1
Q

Work equation

A 
Work= Force Applied x Distance 
Work= Pressure x Area x distance 
Work= Pressure x volume x HR
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2
Q

minute work equation

A

-work performed by heart each minute

minute work= presure work + vol per minute

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3
Q

How does heart maintain huge, continuous energy supply?

A

1) ATP pool generation by oxidative phophosphorylation (requires lots of mito & O2, pool runs out ~12sec if ischemic conditions occur)
2) Creatine Phosphate Pool- transfers a Phos. to ADP to make ATP and restore deprived pool. Creatine only last ~2 min
* is why heart can only survive 2-5 min in ischemic conditions*

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4
Q

What are the hearts fuel sources?

A
  • Fatty acids, ketone bodies (kept acid), AA & glucose
  • heart= an omnivore uses many substances to meet high energy demands
  • allows heart to quickly respond to varying energy demands
  • FA and glucose/lactate are 2 major energy sources*
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5
Q

How does cardiac myocyte structure help its high energy consumption?

A
  • have a network of mito surrounding myofibrils in close proximity
  • allows rapid ATP regeneration & rapid diffusion
  • as ATP made in mito, immediately diffuses and ready for use by myocytes
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6
Q

How are fatty acids used as energy in cardiac myocytes?

A
  • Free FA chain is broken down into 2 carbon chains by beta-oxidation and fed into TCA cycle to make 129 ATP units per glucose
  • is preferred method
  • downside: requires ALOT of O2 and FA, if lacking turn to anaerobic methods
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7
Q

How anaeobic glycolysis used to make energy for the cardiac myocytes?

A
  • glucose (stored as glycogen) & lactate are broken down via anaerobic glycolysis
  • doesn’t require any O2, but only makes 38 ATP/glucose
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8
Q

What does it mean when say heart is an oxygen hog?

A
  • working myocardium consumes ATP rapidly and beta-oxidation/ oxidative phosphorylation require a fuck ton of O2
  • means for its relatively small size, it consumes an insane proportion of O2 from blood
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9
Q

What is the myocardial oxygen consumption (MVO2)?

A
  • the rate at which the heart consumes O2 or the amount of O2 that must be consumed to perform work
  • directly correlates with cardiac minute work
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10
Q

What does the PV loop show?

A
  • the workload of the ventricle throughout the cardiac cycle as they convert chemical to mechanical energy
  • ventrciles impart momentum and pressure to blood
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11
Q

What is work? How show external work on the PV loop?

A
  • work= the displacement (ejection) of a volume under pressure
  • the area within the PV loop= external work done by ventricle (basically CO)
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12
Q

What does the area below the PV loop represent?

A
  • the amount of work (displacement of a vol under pressure) expended when filling the ventricles
  • this is due to atrial contraction, ventricle compliance, and venous return
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13
Q

What is stroke work and it’s equation?

A
  • the external work done by ventricle (CO) or amount of energy transferred to the ejected blood
  • SW= change in pressure x change in volume
  • so depends on both pressure work and volume work
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14
Q

what is pressure work?

A
  • the work expended to pressurize the blood, dependent on after load (arterial BP)
  • equivalent to aortic pressure or internal work
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15
Q

What is volume work?

A
  • the work expended to move (displace) the blood
  • dependent on how much blood filled heart before contraction (preload)
  • equivalent to CO or external work
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16
Q

Which is more costly in terms of MVO2 between pressure and volume work?

A
  • pressure work (after load effects) are more costly

- in IHD want to transfer pressure work into volume work to lessen demand of heart

17
Q

What is the Law of LaPlace?

A
  • defines relationship between tension, radius, wall thickness and pressure
  • cylinder: tension= (pressure x radius)/ wall thickness
  • spherical: tension= (pressure x radius)/ 2x wall thickness
18
Q

What is wall tension in the heart? And what is it correlated with?

A
  • it is equivalent to the wall stress,
  • wall stress is directly correlated w/ MVO2, HR, and contractility
  • and Law of LaPlace equation
19
Q

How does Law of LaPlace relate to aneurysms?

A
  • once begin they only get worse due to LaPlace Law
  • positive feedback cycle, increased wall pressure (dilation) increases the tension which increases dilation (pressure)
  • continues until rupture
  • aneurisms form due to bulging of a weekend aortic wall (increased radius)
20
Q

How do capillaries relate to the Law of LaPlace?

A
  • are fragile but can withstand high pressure due to LaPlace
  • thin walls BUT tiny radius so tiny radius outweighs thin walls and get low tension
21
Q

Heart failure and the Starling Function Curve?

A
  • failign heart can’t contract well enough to supply body with enough blood (SV decreases)
  • due to residual blood (increased ESV, decreased SV) plus normal added pre-load, the heart now has a larger volume and can provide a SV sufficient to avoid shock but still to low and are at risk of pulmonary edema
  • this shifts the Starling Curve (ventricle function curve/P-V loop) DOWN and to the right (reduced inotropy)
22
Q

2 downsides of the adaptive responses of a failing heart and how do they relate to Law of LaPlace?

A

1) the excess blood in pre-load causes pooling and can be transmitted back into pulmonary capillaries to causing pulmonary edema & gas exchange impairment
2) Law of LaPlace shows that as wall tension increases (due to increased preload) the radius of the wall will increase (dilate) which means contractility blows and SV decreases

23
Q

what are the 2 main goals in CHF treatment

A

1) improve contractility so ventricles can operate at a smaller volume, which means smaller radius and less wall stress
2) reduce required wall stress and energy expensive pressure workload of sick ventricle

24
Q

ventricular remodeling in CHF over time and end consequence?

A

1) initially heart hypertrophies to decrease tension of the heart, put had poor relaxation
2) bombarding heart with AT-II, SNS & high filling pressures (large pre-load) leads to thinning of walls and dilated cardiomyopathy
3) Law of LaPlace shows that thin walls= high tension to eject, but walls too thin to do this work so get low SV, low CO, decreased PP, low renal perfusion (hold more H20)

25
Q

How does heart receive blood and nutrients?

A
  • via the coronary circulation, left and right coronary arteries are first to branch off aorta
  • arteries move along surface of heart & penetrate myocardium, bifurcating progressively as weave into the endocardium to make smaller vessels in larger numbers
26
Q

Left and Right Coronary arteries?

A

1) Right: projects along right side of heart, supplies inferior walls/right heart (due to weird heart angle)
2) Left Main branches into Left anterior descending (LAD)and left circumflex

27
Q

Left anterior descending (LAD )and left circumflex arteries feed what?

A

a) LAD= feeds anterior wall and septum (widow maker)

b) LCA= feeds lateral wall

28
Q

Capillary density and perfusion in the heart?

A
  • cap density in the heart large compared to sk muscle due to thin-ness of cardiac cells (more cells per area so more capillaries per area)
  • cap perfuse heart continuously (in sk. muscle only 15% perfused at time)
  • cap density & perfusion vary regional in the heart with inner endocardium&raquo_space; epicardium
29
Q

How does heart respond to an increased workload (exercise)?

A
  • O2 extraction from blood in cardiac myocytes is maxed out at rest
  • so need increased coronary blood flow to meet increased demand
  • means coronary blood flow increases as MVO2 (work) increases
30
Q

Challenges of high myocardial O2 requirement?

A
  • ATP demand is high and continuous so require almost exclusive aerobic metabolism (require O2) via oxidative phosphorylation & beta oxidation
  • coronary flow is suspended during systole so loose O2 each cycle
31
Q

Reactive Hyperemia in the heart?

A

-heart is ischemic briefly during systole, and have compensatory hyperemia (increased flow) in diastole
-O2 debt made in systole, repaid in diastole
-NO (dilates coronary arteries) and adenosine have major role in this, they are metabolites that increase and tell capiallris to dilate to get increased blood flow when ischemic
-

32
Q

How trick heart into vasodilation?

A

-with organic nitrate Nitroglycerin

33
Q

How do you restore normal supply and demand of the cardiac myocyte?

A
  • supply= O2 conc. in blood, perfusion into tissue, and blood flow
  • demand= work= pressure (after load) X volume (preload) X HR (SNS)
  • more effective to decrease demand because even if give 100% O2…wont make huge difference
34
Q

What causes the phasic (cyclic) perfusion pressure of blood flow through coronary vessels? What chamber of heart feels the effect the most?

A

-extravascualr compression during systole, when ventricle contracts squeezes blood vessels & chokes flow creates a nutritional debt repaid by reactive hyperemia in diastole
-effects in LV are much greater than anywhere else
CHECK NOTES

35
Q

how calculate the max coronary perfusion pressure?

A
  • diffeence in aorta pressure- left ventricle pressure gives you CPP max
  • CHECK NOTES
36
Q

What happens in tachycardia?

A
  • decrease the supply since more frequent coronary vascular compression (extravascualr compression) so less time spent in diastole to provide a coronary flow
  • increase demand, increase workload & MVO2 since body tissues need more O2 to meet demand of exercise
  • limits performance of the heart
37
Q

What re the 3 determinants of MVO2?

A
  • the oxygen demand of the heart to do work
    1) Heart rate
    2) contractility
    3) wall stress= after load and preload effects

Block 2 Week 3 (6 decks)

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