2.2 - Control of Cardiac Output Flashcards

1
Q

Definition: afterload + preload

A

afterload
The load the heart must eject blood against (roughly equivalent to aortic pressure)

preload
Amount the ventricles are stretched (filled) in diastole – related to the end diastolic volume or central venous pressure

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2
Q

Defintion: central venous pressure + arterial pressure

A

CVP
The pressure in the large veins draining into the heart (the greater the CVP = the more blood will drain into the heart)

AP
Pressure in the large arteries

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3
Q

What is total peripheral resistance

A

Aka systemic vascular resistance
resistance to blood flow offered by all the systemic vasculature

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4
Q

What happens to pressure of fluid in a tube as it encounters resistance

A
  • The pressure that the blood exerts drops as it flows through a resistance
  • The arterioles offer the greatest resistance
  • constriction of arterioles → increased resistance
  • This causes capillary pressure to fall, but increased pressure on arterial side
  • Arterioles can constrict due to having smooth muscle
  • This means arterioles can constrict to alter their resistance
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5
Q

What is the effect of arterial + venous pressure if total peripheral resistance (TPR) is decreased (and CO is unchanged)

A
  • Peripheral resistance falls
  • This makes it easier for blood to flow through to the venous side
  • Pressure on arteriole side drops a bit, but venous side pressure increases (relatively)
  • Relative increase in central venous pressure (where blood is returning to heart)
    arterial pressure falls
    venous pressure increases
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6
Q

What is the effect of arterial + venous pressure if total peripheral resistance (TPR) is increased (and CO is unchanged)

A
  • Peripheral resistance increases
  • This makes it more difficult for blood to flow through to the venous side
  • Pressure on arteriole side increases a bit, but venous side pressure decreases (relatively)
  • Relative decrease in central venous pressure (where blood is returning to the heart)
    arterial pressure increases
    venous pressure decreases
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7
Q

What is the effect of arterial + venous pressure if cardiac output (CO) is increased (and TPR is unchanged)

A
  • Heart is pumping out more blood
  • This means that emptying the heart more
  • This means its easier for blood to flow into the heart (reduction in central venous pressure)
  • Pumping out more blood (so increase in arterial pressure)
    increased arterial pressure
    decreased venous pressure
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8
Q

What is the effect of arterial + venous pressure if cardiac output (CO) is decreased (and TPR is unchanged)

A
  • Heart is pumping out less blood
  • This means that heart is less empty after each contraction (more full)
  • This makes it less easy for venous blood to get back into the heart
  • This means there is increased venous pressure
  • As less blood is being pumped into arteries, decreases arterial pressure
    decreased arterial pressure
    increased venous pressure
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9
Q

Changes in demand for blood

A
  • The heart must meet changes in demand for blood (increased CO for activity etc)
  • If the tissues need more blood, arterioles and precapillary sphincters will dilate → allows for more blood flow → peripheral resistance falls
  • This occurs to make sure it remains balanced, so that arterial pressure doesn’t fall (need to maintain for perfusion) and venous pressure doesn’t rise
  • The heart detects changes in demand via changes in arterial blood pressure (aBP) and central venous pressure (CVP) by baroreceptors
  • The heart responds to changes in aBP and CVP by intrinsic and extrinsic mechanisms (next card)
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10
Q

What does intrinsic and extrinsic mechanisms mean

A

intrinsic = how the heart responds itself
extrinsic = neuro-humoral effects, eg hormones, effects of sympathetic / parasympathetic innervation

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11
Q

Equations – cardiac output and stroke volume

A

CO = Stroke Volume x Heart rate
CO is cardiac output (the amount of blood pumped out of the heart per unit time L/min)

SV = EDV – ESV
SV is the volume of blood ejected by the heart each time it beats
EDV is end diastolic volume (volume at end of diastole when heart finished filling)
ESV is end systolic volume (blood volume left in heart after it has finished contracting)

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12
Q

What’s the average cardiac output and stroke volume for a 70kg man at rest

A

CO = 5 L/min
SV = about 70ml

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13
Q

Ventricular filling

A
  • This occurs during diastole
  • The AV valves are open but the aortic and pulmonary valves are closed
  • The ventricle fills until the walls stretch enough to produces an intraventricular pressure equal to the venous pressure
  • This is because blood is flowing down pressure gradient (don’t want backflow)
  • The higher the venous pressure → more the heart fills → higher left ventricular pressure
  • This relationship is the ventricular compliance curve (more on next card)
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14
Q

The ventricular compliance curve + diseased hearts

A

increased venous pressure → heart fills more → increased left ventricular pressure

☞ decreased compliance: ie in hypertrophied hearts that can’t stretch as much as it fills → LV pressure increases more steeply with increasing volume
☞ increased compliance: ie in dilated hearts where walls are thinner → heart stretches too much as it fills → LV pressure doesn’t increase as much with volume

(need to be somewhere in the middle for normal hearts)

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15
Q

Frank-starling law of the heart

A
  • If you stretch the fibres of the heart before contracting, it will contract harder
  • This is the same as skeletal muscle, but more extreme in cardiac muscle
  • **the more the heart fills, the harder it contracts (up to a limit - plateau)
  • The harder the heart contracts → the greater the stroke volume
  • An increase in venous pressure will fill the heart more
  • How much the ventricles fill depends on the compliance
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16
Q

Length-tension curve for cardiac muscle

A

the more the heart fills, the more it contracts
- General pattern of contractile force being directly proportional to resting length of sarcomere
- The normal sarcomere length is 1.9μm and optimum is 2.2μm
- If sarcomere length is too short, filament overlap interferes with contraction (plateau)
- If sarcomere stretched too much, the number of cross bridges that can form is reduced (plateau)
- In cardiac muscle, also get an increase in Ca2+ sensitivity as the muscle fibers are stretched
- This allows more Ca2+ → more actin + myosin binding → more cross bridge formation
- The length-tension curve is steeper in cardiac muscle than it is in skeletal muscle

17
Q

What is the purpose of starling’s law of the heart

A

ensures both sides are balanced ☞ maintain pumping the same cardiac output as each other
- Increased stroke volume with increased filling of the heart is an intrinsic control mechanism
- The pulmonary + systemic circulations operate in series ☞ the same volume of blood pumped to the body must also be pumped to the lungs
- If the right side pumps more blood → inc CO → inc venous pressure → more blood pumped back into left → more stretch → higher LV output (vice versa etc)

18
Q

Contractility and force of contraction

A

contractility = force of contraction for a given fibre length
- Increase in contractility → greater force of contraction → greater stroke volume
- extrinsic factors eg sympathetic stimulation + circulating adrenaline can increase contractility
- Reducing sympathetic stimulation below normal levels will reduce contractility

19
Q

Effect of increasing arterial pressure on stroke volume

A
  • afterload = pressure that the heart has to pump against
  • This is the pressure in the aorta (aortic impedance)
  • If pressure in aorta increased → more difficult for ventricle to pump out → ventricles will have to contract at a higher pressure to pump blood out
  • If peripheral resistance increased → more difficult for blood to flow from arteriole to venous side of the capillaries → increased pressure on arteriole side → increased aortic pressure
  • Increased TPR also reduces venous pressure, reducing filling of the heart
20
Q

What are the factors determining cardiac output

A

how much the ventricle empties (end systolic volume) depends on…

how hard it contracts
- This affects stroke volume
- Determined by the end diastolic volume + contractility

how hard it is to eject blood
- Also affects stroke volume
- Determined by aortic impedance (roughly = arterial pressure)

21
Q

Baroreceptors + aortic blood pressure

A
  • Increase/decrease in arterial BP is detected by baroreceptors
  • baroreceptors = stretch receptors that are present in carotid + aorta
  • A decrease in aBP → reduce parasympathetic NS activity + stimulate sympathetic NS → increased HR + contractility
22
Q

How does the CVS respond to eating a meal

A

need to digest meal → need good blood supply to absorb nutrients → local vasodilation in gut → reduces total peripheral resistance

TPR causes drop in arterial pressure → sensed by baroreceptors → stimulate sympathetic NS → increased HR + increased contractility (so inc SV) → increased cardiac output → increased arterial pressure + decreased venous pressure
decreased TPR also causes increased venous pressure → more blood returning to heart → increased stroke volume… [same as above]

23
Q

How does the CVS respond to standing up

A

standing up → pooling of blood due to effect of gravity → makes it more difficult for blood to drain up to heart → decrease in venous pressure → filling heart less → decreased CO → decreased arterial pressure

  • Both arterial + venous pressure have decreased
  • Cannot adjust by intrinsic mechanisms
  • baroreceptor reflex detects drop in arterial pressure, decreasing parasympathetic activity + increasing sympathetic activity
  • Increased heart rate, contractility + increased TPR
  • This ensures that the arterial blood pressure is maintained enough so that it doesn’t compromise perfusion
  • If reflexes don’t work = postural hypotension
24
Q

How does the CVS respond to exercise

A
  • Calf muscle pumping + venoconstriction returns more blood to the heart (as veins have smooth muscle in tunica media)
  • Later, decreased TPR (as need to supply more blood to exercising tissues) increases venous return
  • Increased HR (to increase CO) increases the sympathetic drive → increased contractility

Therefore 3 factors contribute to increased cardiac output:
Increased venous pressure, heart rate and contractility

25
Q

Jugular venous pulse

A
  • Internal jugular vein is in direct contact with superior vena cava → drains into right atrium
  • Can estimate change in pressure in RA as it transmits up to the right internal jugular vein
  • Therefore can estimate central venous pressure
  • Pulse is seen behind the sternocleidomastoid muscle
  • Get patient to lie down at 45 degree angle and turn head to left
  • Estimate highest visible pulsations above sternal angle +4 cm
  • Can also be measured using a central line inserted into internal jugular vein
  • Biphasic (next card)
26
Q

Why is jugular venous pulse biphasic

A
  • Get patient to lie down at 45 degree angle and turn head to left
  • Estimate highest visible pulsations above sternal angle +4cm
  • Changes in pressure in RA is transmitted back to right internal jugular vein
  • First pulse seen after atrial systole = increase in pressure due to atria contracting
  • Second pulse seen at end of ventricular systole = due to increased pressure of atria filling from veins
27
Q

Conditions that will increase central venous pressure (and therefore jugular venous pressure)

A

if right side of heart doesn’t pump blood out properly
Eg heart failure → not pumping blood out properly → more blood left at end of systole → harder for veins to drain into heart

volume overload with IV infusion
Patient ends up with too much blood volume → central venous pressure increases → pulsations will rise up higher

if something impairs filling of the heart
Venous blood return to the heart builds up → can’t move so easily into right atrium → pressure increases