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+ CAPS 301: Muscle, Bodily Fluid, Cardio > Cardiac Output > Flashcards

Cardiac Output Flashcards

1
Q

What is cardiac output?

A

volume of blood ejected from heart every minute (ml/min)

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2
Q

What is the equation for cardiac output?

A

CO = heart rate x

stroke volume

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3
Q

What is cardiac output regulated by?

A

heart rate

stroke volume

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4
Q

What is heart rate regulated by?

A
  • parasympathetic activity

- sympathetic activity (and epinephrine)

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5
Q

What does increased parasympathetic activity do to heart rate?

A

decreases HR

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6
Q

What is sympathetic activity controlled by?

A

norepinephrine and epinephrine

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7
Q

What does increased sympathetic activity do to heart rate?

A

increases HR

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8
Q

What is stroke volume regulated by?

A
  • sympathetic activity (extrinsic control)

- diastolic volume (intrinsic control)

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9
Q

What does increased sympathetic activity do to stroke volume?

A

increases SV

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10
Q

What does increased EDV do to stroke volume?

A

increases SV

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11
Q

What does increased sympathetic activity also control?

A

moves blood from venous system into heart

  • increases EDV
  • increases SV
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12
Q

What regulates the sympathetic nervous system?

A

noradrenaline/adrenaline acting on β1 receptors on nodal cells

  • increases slope of phase 4
  • increases HR
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13
Q

What regulates the parasympathetic nervous system?

A

acetylcholine acting on muscarinic receptors on nodal cells

  • decreases slope of phase 4
  • decreases HR
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14
Q

Extrinsic Control of Stroke Volume

A
  1. sympathetic nerves release NA that acts on β1 adrenergic receptors on muscle cells found in ventricle
  2. increases intracellular cAMP, which activates PKA
  3. PKA catalytic subunit phosphorylates proteins, which increases intracellular Ca2+
    - ↑ entry from outside cell into myocyte from outside cell
    - ↑ Ca2+ release from intracellular stores
  4. increased stroke volume – contraction of ventricle
    muscles contract more forcefully
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15
Q

What is the Frank Starling Law of the Heart?

A

SV of left ventricle will increase as left ventricular volume increases due to myocyte stretch, causing more forceful systolic contraction

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16
Q

Starling Law of the Heart

What is the strength of contraction related to?

A

initial length of cardiac muscle fibers

muscle is more stretched initially = stronger contraction

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17
Q

What is the initial length of heart muscle before contraction equivalent to?

A

EDV

18
Q

What is the strength of contraction equivalent to during systole?

A

SV

19
Q

What is end diastolic volume (EDV or preload)?

A

how filled the heart is at end of diastole

20
Q

How does EDV increase SV?

A

mobilization of more blood that increases EDV results in increase in SV

21
Q

What is stroke volume related to in regards to muscle?

A

muscle tension

22
Q

What is EDV related to in regards to muscle?

A

cardiac

muscle fibre length

23
Q

Starling Curve

What is EDV at rest?

A

~ 140 ml

24
Q

Starling Curve

What is SV at rest?

A

~ 70 ml

25
Q

What is the relationship between EDV and SV?

A

increase in EDV = increase in SV

  • more blood is pumped out (within reason – heart will pump what it receives)
  • if heart receives more but is not pumping out more, will get build-up of blood
26
Q

What is the equation for blood pressure?

A

blood pressure = CO x SVR

27
Q

What determines SVR?

A

radius of blood vessels

resistance ∝ 1/radius4

  • if radius is halved (ie. vasoconstriction), resistance increases by factor of 16 → flow decreases by 16x
28
Q

What is the equation for arterial pressure?

A

arterial pressure = CO

x SVR

29
Q

What are the vasoactive hormone constrictors?

A
  • angiotensin II (AII) – converted from angiotensinogen (liver) in response to renin from kidney
  • arginine vasopressin (AVP) – from brain
30
Q

What do hormones AII and AVP act on?

A

receptors (each have different ones) linked to Gq proteins (like NA)

31
Q

What is the vasoactive hormone dilator?

A

atrial natriuretic peptide (ANP) – from heart

32
Q

What does the hormone ANP act on?

A

receptor linked to GI protein

33
Q

ANP Vasodilation Pathway in Vascular Smooth Muscle Cell

A
  1. ANP acts on receptor linked to GI protein
  2. GI leads to activation and production of cGMP
  3. cGMP phosphorylates MLCK
  4. phosphorylated MLCK inhibits contraction

**not same vasodilation as 𝛽2 adrenergic receptor

34
Q

What is afterload?

A

pressure that ventricle must generate in order to eject cardiac output

  • when heart pushes, it pushes against pressure in aorta
  • ie. chronic high arterial pressure – high afterload
35
Q

What are the 2 Starling forces?

A

force of filtration: capillary hydrostatic pressure (CHP)
- move fluid out of capillaries

force of reabsorption: capillary oncotic pressure (COP)
- draw fluid into capillaries

36
Q

What increases filtration?

A

things that increase CHP

37
Q

What increases reabsorption?

A

things that increase COP

38
Q

Starling Forces Across Entire Length of Capillary

What occurs at arterial end?

A

CHP > COP

fluid moving out of vessel

  • CHP depends on arterial end (high blood pressure)
39
Q

Starling Forces Across Entire Length of Capillary

What occurs at venous end?

A

CHP < COP

fluid moving into vessel

blood pressure decreases as blood travels down capillary into venous end

40
Q

How does blood pressure change as it travels through capillary?

A

blood pressure decreases as blood travels down capillary into venous end

41
Q

Starling Forces Across Entire Length of Capillary

What occurs when venous pressure is too high (ie. heart failure)?

A
  • filtration on both ends of vessel
  • no reabsorption
  • results in edema – accumulation of fluid in tissue
42
Q

What happens during heart failure?

A
  • blood can’t get pumped efficiently
  • blood builds up in right side of heart, and pushes back against pulmonary veins
  • increases venous pressure and CHP on venous end

+ CAPS 301: Muscle, Bodily Fluid, Cardio (13 decks)

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