Cardio 5 Flashcards
Define stroke volume and its equation.
volume of blood ejected in ventricles
[Stroke volume = EDV - ESV]
Define ejection fraction and its equation.
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]
Describe cardiac output and its equation.
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)
Describe factors affecting stroke volume.
-SV can only be increased by increasing EDV or decreasing ESV
-factors that affect SV:
1. Preload
2. Contractility
3. After load
Describe preload.
- End-diastolic fiber length
>stretching of cardiac myocytes prior to contraction
>resting length - Estimated by EDV
- Determined by:
>diastolic filling
>Venus return
Describe the optimal cardiac muscle fiber length.
-resting cardiac muscle fiber length = not optimal (unlike in skeletal muscle)
-increase in cardiac muscle fiber = increases contractile force of heart
Describe diastolic filling & Venus return.
-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
Describe the frank-starling law.
-relationship between EDV & SV
-greater the heart muscle stretched during filling = greater force of contraction = greater amount of blood pumped into aorta
Describe contractility or inotropism.
-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
Describe the factors that increase contractility.
-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
Describe the role of EPI & NE in contractility/inotropism.
-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
Describe afterload.
-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
Describe the anrep effect.
-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
Describe the factors affecting the HR.
-HR affected by ANS
(parasympathetic activity predominates in heart)
Describe the sympathetic factors affecting the HR. (Beta 1)
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
Describe the sympathetic factors affecting the HR. (Beta 2)
-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
How does beta 1 increase the HR?
B1 receptor activation increases:
1. Inward Na current in the pacemaker cell (funny Na channels)
2. Inward Ca current in pacemaker cell
What happens when HR is increased?
-contractility increases
>more AP per unit of time
>more Ca entering cell during plateau phase
>more Ca accumulation by SR
Describe positive inotropic effect, positive dromotropic effect, & positive chronotropic effect.
- Positive inotropic effect = Beta receptors enhance myocardial contractility
- Positive dromotropic effect = speed AV conduction
- Positive chronotropic effect = increase automaticity
& dilate coronary arteries
Describe parasympathetic affecting the HR.
-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
Describe reciprocal sympathetic vagal activity.
-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
