Cardio 5 Flashcards

1
Q

Define stroke volume and its equation.

A

volume of blood ejected in ventricles
[Stroke volume = EDV - ESV]

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2
Q

Define ejection fraction and its equation.

A

fraction (%) of the EDV that is ejected in one stroke volume = 60% (0.6)
-describes effectiveness of ventricles ejecting blood
-indicator of contractility
>the increasing in ejection fraction = increase in contractility (vice versa)
[ejection fraction = stroke volume/EDV]

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3
Q

Describe cardiac output and its equation.

A

total volume of blood ejected per time (mL/min)
-varies with levels of activity in body
>body metabolism, exercise, age, size of body
-can be increased if SV or HR increases, or both
[cardiac output = stroke volume X heart rate)

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4
Q

Describe factors affecting stroke volume.

A

-SV can only be increased by increasing EDV or decreasing ESV
-factors that affect SV:
1. Preload
2. Contractility
3. After load

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5
Q

Describe preload.

A
  1. End-diastolic fiber length
    >stretching of cardiac myocytes prior to contraction
    >resting length
  2. Estimated by EDV
  3. Determined by:
    >diastolic filling
    >Venus return
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6
Q

Describe the optimal cardiac muscle fiber length.

A

-resting cardiac muscle fiber length = not optimal (unlike in skeletal muscle)
-increase in cardiac muscle fiber = increases contractile force of heart

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7
Q

Describe diastolic filling & Venus return.

A

-greater the diastolic filling = larger the EDV = more the heart is stretched
-more heart is stretched = longer the initial cardiac fiber before contraction
-increased length = greater force of contraction = greater SV

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8
Q

Describe the frank-starling law.

A

-relationship between EDV & SV
-greater the heart muscle stretched during filling = greater force of contraction = greater amount of blood pumped into aorta

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9
Q

Describe contractility or inotropism.

A

-pumping ability of a ventricle
-ability of myocardial cells to develop force at a muscle length
-increase in contractility = complete emptying of ventricle during systole = decrease in ESV
>increase in SV without increasing EDV

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10
Q

Describe the factors that increase contractility.

A

-correlated with intracellular calcium concentration
>larger inward Ca current & larger intracellular stores = greater the increase in Ca & greater contractility
-extrinsic factors increase contractility = positive iontropic effect
>sympathetic stimulation
>cathecolamines

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11
Q

Describe the role of EPI & NE in contractility/inotropism.

A

-increase contractile force & velocity by B1
-increase Ca influx & activation of Ryanodine receptors = increase SR Ca release
>through protein phosphorylation of L-type Ca channels
-speed up Ca accumulation in SR to allow faster cardiomyocyte relaxation

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12
Q

Describe afterload.

A

-resistance that the ventricles must overcome to empty its contents
>force opposing ejection
>afterload for left ventricle = aortic pressure
>when aortic pressure increases
—SV decreases
—ESV/pressure increases

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13
Q

Describe the anrep effect.

A

-allows myocardium to compensate for an increased ESV & decreased SV when aortic BP rises
>increase in afterload = stimulates release of catecholamines
>increase in ventricular contractility (inotropy)
-without this effect = every increase in aortic BP = drop in SV = compromise circulation to peripheral & visceral tissue

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14
Q

Describe the factors affecting the HR.

A

-HR affected by ANS
(parasympathetic activity predominates in heart)

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15
Q

Describe the sympathetic factors affecting the HR. (Beta 1)

A

Beta receptors in cardiac tissue
1. Beta 1
-expressed in the heart
-GPCR = couple to Gs -> activates cAMP
>activation of cAMP = enhance cardiac myocyte contraction
-NE = primary endogenous agonist
>released from postganglionic neurons
-found in SA node, AV node, & myocardial cells (atria & ventricles)
-increase HR, SV, & cardiac output

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16
Q

Describe the sympathetic factors affecting the HR. (Beta 2)

A

-expressed in arterioles of coronaries
-GPCR = couple to Gs = activates cAMP
>activation of cAMP = smooth muscle relaxation
-EPI is primary endogenous agonist
>released from adrenal gland
-found in vascular smooth muscle
-causes vasodilation = relax
sympathetic = increase in blood to heart, skeletal muscle, & liver

17
Q

How does beta 1 increase the HR?

A

B1 receptor activation increases:
1. Inward Na current in the pacemaker cell (funny Na channels)
2. Inward Ca current in pacemaker cell

18
Q

What happens when HR is increased?

A

-contractility increases
>more AP per unit of time
>more Ca entering cell during plateau phase
>more Ca accumulation by SR

19
Q

Describe positive inotropic effect, positive dromotropic effect, & positive chronotropic effect.

A
  1. Positive inotropic effect = Beta receptors enhance myocardial contractility
  2. Positive dromotropic effect = speed AV conduction
  3. Positive chronotropic effect = increase automaticity
    & dilate coronary arteries
20
Q

Describe parasympathetic affecting the HR.

A

-M2 receptors = expressed in the heart
>GPCR = couple to Gi = inhibits cAMP
(Inhibition of cAMP = decreases cardiac HR & output)
>acetylcholine = endogenous agonist
(Released from postganglionic neurons)
>found in SA node, AV node, & myocardial cells (mainly atria)
>slows down discharge rate of SA node & slows/blocks AV conduction & decrease atrial/ventricular contractility

21
Q

Describe reciprocal sympathetic vagal activity.

A

-parasympathetic activity predominates in heart, but both systems act in a reciprocal manner
-sympathetic activation increases HR while parasympathetic activation decreases
>blockade of sympathetic B1 receptors decrease HR while blockade of parasympathetic M2 receptors increases HR
-increase in HR = results from both removal of vagal tone & increase in sympathetic drive