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CVS > Cardiovascular Mechanics > Flashcards

Cardiovascular Mechanics Flashcards

1
Q

Single cell structure

A

Ventricular cells 100μm long, 15μm wide, mainly made of myofibrils
T tubules from cell surface (gaps)
Each T tubule spaced so it lies alongside each Z line of every myofibril
Sarcoplasmic reticulum
Mitchondria

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2
Q

Exitation-contraction coupling in heart

A

Ca2+ = messenger , goes through VGCC
Conformational change in Ryanodine receptor on the SR
Causes Calcium Induced Calcium Release
Na+/ Ca2+ exchanger on membrane uses Na energy gradient to efflux Ca from cell
Ca enters back into SR through Ca2+ ATPase
Increase intracellular Ca= increase force (sigmoidal log curve)

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3
Q

Length-tension relation in cardiac muscle

A 
Increased stretching of the same cardiac muscle= increase baseline of force that can be produced (passive/ recoil force)+ increases active force production when contraction is stimulated
Isometric contraction (no shortening)
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4
Q

Length-tension relation cardiac vs skeletal

A

Passive force+ Active Force= total force
Cardiac muscle= less compliant/ stretchy so produces more passive force because of properties of ECM compared to skeletal muscle
Skeletal+ Cardiac have same active force properties
Therefore total force produced by cardiac when stretched= more
After a certain point, overstretching= rapid decrease in active force in skeletal but cardiac muscle can’t be overstretched because contained in pericardial sac.

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5
Q

Two types of contraction

A

Isometric- Muscle fibres don’t change length but pressures increase in both ventricles
Isotonic- shortening of fibres+ blood is ejected from ventricles

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6
Q

Preload definition

A

Weight that stretches muscle before it’s stimulated to contract

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7
Q

Afterload definition

A

Weight that is not apparent to muscles in the resting state only when the muscle has started to contract

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8
Q

Isometric contraction, preload, force

A

Increase preload= increase force until a certain point when it decreases sharply in isometric contraction

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9
Q

Isotonic contraction, afterload, force, velocity of force

A

Increase afterload= decrease shortening
At a longer muscle length, less of a decrease in shortening at the same afterload
Increase afterload= sharp decrease in velocity of shortening then flattens out
At a longer muscle length, less of a sharp decrease in velocity of shortening at the same afterload and hits 0 at a higher afterload

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10
Q

Measures of preload

A

End diastolic volume
End diastolic pressure
Right Atrial pressure

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11
Q

What is preload on the ventricles dependent on?

A

Stretching of resting ventricular walls

That is dependent on venous return

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12
Q

Afterload in the heart

A

Load against which LV ejects blood after the opening of the aortic valve
(Increase afterload= decrease shortening+ decrease velocity of shortening)

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13
Q

Measure of afterload

A

Diastolic blood pressure

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14
Q

What affects isometric contraction?

What affects isotonic contraction?

A 
Ventricular filling (Increase stretch= increase force)
Pressure in aorta (Increase afterload= decrease shortening+ decrease velocity of shortening)
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15
Q

Frank-Starling relationship+ consequence

A

Increased diastolic fibre length= increase ventricular contraction
Consequence= ventricles pump greater stroke volume so at equilibrium, the CO balances augmented venous return

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16
Q

Causes of Frank- Starling relationship

A
  1. Changes in number of myofilament cross bridges interacting
    At longer lengths the actin filaments don’t overlap on themselves as much= increase myosin cross bridges that can be made
  2. Changes in Ca2+ sensitivity of myofilaments (unclear)
    Hypothesis 1: Ca2+ required for myofilament activation, troponin C which binds to Ca2+ regulates formation of cross bridges between actin+ myosin. At longer sarcomere lengths, increase affinity of troponin C to Ca2+ due to conformational change in protein. Therefore less Ca required for same amount of force
    Hypothesis 2: Stretching= spacing between actin+ myosin decreases= increased probability of forming strong binding cross-bridges= more force for same amount of Ca2+
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17
Q

Stroke work definition+ equation

A

Work done by heart to eject blood under pressure into aorta+ pulmonary artery
Stroke work= Stroke Volume x Pressure
Stroke Volume= influenced by preload and afterload
Pressure= influenced by cardiac structure

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18
Q

Law of LaPlace+ equation

Also equates to?

A

When the pressure within a cylinder is constant, increase radius= increase tension (P x r)
Wall tension= (Pressure in vessel x Radius of vessel)/wall thickness (h)
Circumferential stress in a vessel= same thing (persistent high circumferential stress= vessel distension because radius increases= more stress on outside of vessel)

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19
Q

Implication of LaPlace on ventricles

Failing hearts?

A

Radius of LV curvature less than RV= LV can generate higher pressures with similar wall stress
Failing hearts often become dialated= increased wall stress

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20
Q

Stages of cardiac cycle

A

Diastole- Ventricular relaxation (1st step+ last 3)
Systole- Ventricular contraction
1. Atrial systole
2. Isovolumetric contraction (End-diastolic volume- volume in ventricles just before about to contract)
3. Rapid ejection
4. Slow ejection (End-systolic volume- volume left in ventricles after contraction)
5. Isovolumetric relaxation
6. Rapid passive filling
7. Slow passive filling

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21
Q

Stroke volume+ ejection fraction equation

A 
Stroke Volume= End diastolic volume - End systolic volume
Ejection fraction (%) = (100 x Stroke Volume) / End diastolic volume
Ejection fraction= amount of blood being ejected by heart in relation to amount during filling (ratio) (clinical relevance)
EDV= volume in ventricles when the heart has relaxed 
ESV= volume in ventricles when heart has contracted
SV= amount of blood being ejected from heart
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22
Q

Changes in ECG, Aorta pressure, Ventricle pressure, Atrium pressure, Ventricle volume in cardiac cycle
Slide 7 lecture 2 onwards

A

-

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23
Q

Atrial systole

A

SA node stimulates action potentials flowing over atria
P wave signals atria depolarisation
Atria almost full from passive filling from pressure gradient (increase atrial pressure)
Contraction= blood ‘tops up’ ventricular volume (increase ventricular volume)
Sound= abnormal, indicates heart failure/ pulmonary embolism/ tricuspid defect

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24
Q

Isovolumetric contraction

A

Waves of depolarisation conducted to ventricular cells= contraction + CICR
QRS= start of ventricular depolarisation
Interval between AV valves (mitral+ tricuspid) closing and semi-lunar valves (pulmonary+ aortic) opening
No change in ventricular volume but still contraction so increase ventricular pressure
1st heart sound (lub) because of closure of AV valves

25
Q

Rapid ejection

A

Start= opening of aortic+ pulmonary valves
Ventricular contraction exceeds aortic+ pulmonary artery pressure
Semilunar valves open+ blood pumped out
Volume of ventricles decreases because of isotonic contraction
Increase in ventricular+ aortic pressure

26
Q

Reduced ejection

A

Ventricles begin to repolarise= T wave
End of systole
Decrease pressure gradient (pressures start to decrease) = aortic+ pulmonary valves begin to close
Ventricular volume+ blood flow out decreases more slowly
As pressure in ventricles falls below arteries, blood flows back= semilunar valves start to close

27
Q

Isovolumetric relaxation

A

Aortic+ pulmonary valves shut
AV valves remain closed until ventricular pressure drops below atrial pressure
All valves closed= no change in ventricular volume
Atrial pressure increases
Slight increase in aortic pressure because rebound pressure against aortic valve as distended aortic wall relaxes
2nd heart sound (dub) because of closure of semilunar valves
Ventricular pressure decreases

28
Q

Rapid passive filling

A

Occurs during flat ECG between cardiac cycles (relaxation of cardiac tissue)
Pressures of everything don’t change much
Once AV valves open, blood from atria flows into ventricles= increase ventricular volume rapidly
Heart sound= abnormal, may signify turbulent ventricular filling/ severe hypertension/ mitral defect

29
Q

Reduced passive filling/ Diastasis

A

Ventricular volume fills more slowly but can fill quite a lot without atrial contraction= increase ventricular volume but not as fast as rapid passive filling
However much they fill defines preload= defines stretch= defines contraction strength
Aorta pressure continues to steadily decrease, other pressures don’t change
No electrical effects
Longest phase of cardiac cycle

30
Q

Difference in pressure and volume changes between RV and LV

A

Pattern of pressure changes= same
Pressures in right heart+ pulmonary circulation = lower than left
BUT RV ejects same amount of blood as LV (pumping same quantity of blood into lower pressure circuit)

31
Q

Pulmonary circuit pressures

Slide 15, lecture 2

A

Same pattern for R+ L side but R side has lower magnitude

-

32
Q

Pressure Volume Loops

A

X axis= Left Ventricular volume
Y axis= Left Ventricular pressure
Start at bottom right corner= end diastolic volume: haven’t activated ventricles yet so no contraction, blood filling here determines preload that stretches ventricular muscle
Top right= isovolumetric contraction, aortic pressure encountered: increase pressure without changing volume (ventricle activation). Ventricles encounter afterload at this point, afterload represented by pressure in aorta+ pulmonary artery
Top left= end systolic volume: ventricular pressure overcomes back pressure in aorta+ aortic valve opens allowing blood to flow out= volume decreases
Bottom left= isovolumetric relaxation, no volume change but decrease in pressure

33
Q

Preload+ afterload effect on PV loop

A

Bottom of PV loop runs along line of passive force with increasing muscle fibre length
Top left of PV loop intersects with active force line of same x axis as above.
Active force line= end-systolic PV line
Increase amount of volume entering heart= increase preload+ end diastolic volume= increase width of PV loop= increase stroke volume as a result (Frank-Starling relationship)
Increase afterload/ back-pressure= need greater pressure in ventricle to overcome it+ open aortic valve= decreased shortening of muscle fibre= less stroke volume= PV loop is narrower, increased pressure at top side of PV loop= PV loop is taller (top left of PV loop still intersects with a higher section of the end systolic PV line)

34
Q

Cardiact Output equation

A

Cardiac output= Heart Rate x Stroke Volume

35
Q

What is stroke volume affected by?

A

Preload: stretch of cardiac myocytes, Inadequate venous return can compromise SV
Afterload: force with which the ventricles have to contract against to eject the blood out of the ventricles, Excessive resistance compromises ejection volume
Contractility: intrinsic muscle strength, Inadequate contractility can compromise SV

36
Q

Contractility definition, measure + influences

A

Contractile capability of heart
Measure= ejection fraction
Increased by sympathetic stimulation (Noradrenaline binds to muscle cells= increase in phosphorylation levels= increase in calcium delivery to myofilaments= increase in force of muscle fibres

37
Q

Hardening and narrowing aortic valve effect on PV loop

A

Hardening= less easy to drive blood through= increased afterload+ reduces flow= need to produce more pressure to overcome back pressure
PV loop is taller, narrower, and lined up with the right border of a normal PV loop

38
Q

Acute blood loss effect on PV loop

A

Decreased venous return= decreased ventricular filling= decreases preload= decreased SV
PV loop is taller, narrower and lined up with left border of normal PV loop

39
Q

Exercise effect on PV loop

A

Exercise= increased blood flow back to heart+ increased BP because of venoconstriction+ skeletal muscle pump= increased venous return= increased preload. Increased contractions (increased sympathetic nervous system)
PV loop is taller, wider on both sides and in line with bottom line of normal PV loop

40
Q

Effect of adrenaline secretion on preload

A

Decreases amount of blood stored in veins= increases blood to heart = increase preload

41
Q

Purpose of circulation

A

To transport blood around body

Regulate temperature

42
Q

Principles of circulation

A 
Two circulations (pulmonary+ systemic) each with own pump that are physically linked together
Pump generates pressure gradient that propels blood which flows through vessels
Highly branched structure required because diffusion only effective over short distances
43
Q

Change in the following over circulation:
SA of vessels
Mean pressure
Proportion of systemic blood volume

A

Increases sharply at capillaries then decreases sharply by venules
High at arteries, decreasing at arterioles then decreases sharply by end of capillaries (pressure difference allows blood to flow through capillaries) then stays low (venules+ veins have valves)
Low until end of capillaries, increases by veins and stays high (proportion of blood remaining depends on pressure)

44
Q

Darcy’s Law

A 
∆P= Q x R
∆P= Pressure difference
Q= Volumetric flow
R= Resistance
Similar to V= IR
45
Q

MAP equations+ assumptions

How is regulation of flow achieved?

A 
MAP= CO - PVR
PVR= Pulmonary Vascular Resistance
Assumptions= Steady flow (doesn't happen because intermittent pumping of heart)
Rigid vessels (actually change)
Right atrial pressure= negligible (sometimes it's not)
Regulation achieved by variation in vessel resistance (BP= constant)
Second equation:
Pulse Pressure (PP)= Systolic BP- Diastolic BP
MAP= DBP + PP/3
46
Q

What does resistance to blood flow depend on?

Equation?

A

Fluid viscosity (η) (doesn’t usually change except high altitude)
Length of the tube (L) (doesn’t change)
Inner radius of the tube (r)
R= (8Lη)/ πr^4
Principle= small changes in vascular tone= large changes in flow (halving radius= 16times less flow)

47
Q

Cardiac output normal vs exercise

A

Normal= 5L/min
Exercise= 20L/min (more blood to heart= more blood pumped= more can be diverted to muscles)
Same principle of exercise for any other organ that needs more blood (e.g. skin)

48
Q

Types of blood flow

A

Laminar: velocity of fluid= constant+ flows in layers.
Blood flows fastest at centre of lumen (adhesive forces at sides) (Parabolic velocity profile, if you draw a tangent to the profile at any rate that gives you the shear rate)
Turbulent: blood flows erratically+ prone to pooling, associated with pathophysiological changes to endothelial lining

49
Q

Shear stress equation

A

Shear stress= Shear rate x viscosity

50
Q

Laminar shear stress

A

High shear stress
Promotes endothelial survival+ quiescence (inactivity)
Cells aligned in direction of flow
Secretions promote vasodialation+ anticoagulation

51
Q

Turbulent shear stress

A

Low shear stress
Promotes endothelial proliferation, apoptosis and shape change
Secretions promote vasoconstriction, coagulation and platelet aggregation

52
Q

Blood pressure measuring mechanism

A

Slow deflation= turbulent flow that can be heard with stethoscope

53
Q

How and why do ventricular and aortic pressures differ?

A

When aortic valve closes, ventricular pressure falls more rapidly but aortic pressure falls more slowly
Because of elasticity of aorta+ large arteries which buffer pulse pressure changes (Windkessel effect)

54
Q

Windkessel effect

A

Blood enters aorta+ arteries faster than it leaves them
When aortic valve closes, ejection stops but still diastolic flow in downstream circulation because of recoil of elastic arteries leading to pressure to fall slowly
Decrease in arterial compliance= decrease of Windkessel effect= increase pulse pressure

55
Q

Aneurysm explanation

A

Weakening of vessel walls= balloon-like distension
Relates to LaPlace
Vascular aneurysm= increase radius of vessel= for same internal pressure, inward force exerted by muscular wall needs to increase but if fibres have weakened force can’t be produced so keeps expanding
Same thing happens in intestine (diverticuli)

56
Q

Compliance
Arteries vs Veins?
Increasing smooth muscle contraction in veins?

A

Relationship between transmural pressure+ vessel volume
Depends on vessel elasticity
At low pressures, venous compliance= much greater than arterial compliance= veins can hold more blood than arteries
Increase smooth muscle contraction= decrease radius= decrease venous volume+ increase venous pressure= decreased storage of blood
Vein distension= increase amount of blood stored in them

57
Q

Effect of gravity

A

Standing up= increased hydrostatic pressure= blood tends to pool in veins because of high compliance= reduced venous return
Therefore decreased CO and blood pressure would occur without compensatory mechanisms
Gravity mainly effects leg veins
Prolonged elevation of venous pressure= oedema in feet

58
Q

Skeletal muscle pump

A

Pushes blood through veins back to heart
Valves allow unidirectional blood flow
Defect in valves= dialated varicose veins in legs

59
Q

Respiratory pump

A

As you breath= negative intrathoracic pressure (diaphragm has moved down)= blood can flow back to heart more easily (more space in cavity)

CVS (10 decks)

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