CVS 2 Flashcards
(22 cards)
What is Cardiac Output (CO)?
The volume of blood pumped by each ventricle per minute
What is the equation for CO?
CO = HR x SV
What is average HR?
70bpm
What is stroke volume?
The volume of blood ejected per contraction
SV = EDV-ESV
What is the average SV?
70ml
What is a normal CO?
5l/min
What controls CO?
Physiological requirements (control of HR and SV)
Describe the relationship between EDV and SV
If you increase EDV you increase SV as if more blood returns to the hearts more is pumped out, but this is not a simple relationship ship because the heart does not eject all blood.
What does the Frank Starling curve show?
The effect of increase EDV on SV
What causes cardiac muscle fibres to vary in length before contraction?
The degree of diastolic filling
Describe the Frank-Stirling Law of the heart
The heart normally pumps out during systole the volume of blood returned to it during diastole; increased venous return results in increased stroke volume
- It describes the intrinsic relationship between EVD and SV
- Increased EDV, the heart is more stretched
- The more the heart is stretched, the longer the initial cardiac fibre length before contraction
- The increased length results in a greater force on the subsequent cardiac contraction and thus a greater SV
What effect does sympathetic stimulation have on the frank-stirling curve?
Shifts it to the left, increased SV at the same EDV
Describe Tachycardia:
Increased activity in the sympathetic nerves to the heart, increasing HR
Describe Bradycardia:
Increased activity in the parasympathetic nerves to the heart, decreasing HR
Describe the advantages of the intrinsic relationship of matching SV with venous return
- Equalising output between the left and right sides of the heart
- When a larger CO is required (during exercise) venous return is increased though the action of the sympathetic NS, resulting in increased EDV and therefore, SV
What is the effect of extrinsic control (symp. stim. and adrenaline) on SV
They both enhance the heart’s contractility (strength of contraction at any EDV)
How does symp. stim. and adrenaline increase heart’s contractility?
= Increased Ca2+ entry by NorAd/Ad
Increase in inward Ca2+ flux during plateau phase of the action potential enhances th intracellular calcium store
Ca2+ is require for the excitation-contraction coupling in cardiac muscle cells
Increase rate if relaxation of cardiac muscle cells by stimulating Ca2+ pumps - take up Ca2+ from cytoplasms more rapidly - shortening systole
(inotropic actions)
Wha does the Parasympathetic NS release?
Acetylcholine
what is the effect of the Parasympathetic NS on the SA node?
decreases HR by
-Hyperpolarisation of the SA node membrane (longer to reach threshold)
- Decreases rate of spontaneous depolarisation
ACh increases K+ permeability by slowing closure of K+ channels
What are other effects of Parasympathetic NS on heart activity
- Weakens atrial contraction
- Increases time between atrial and ventricular contraction
- Decreases HR
What is the effect of sympathetic stimulation on the Sa node?
Speeds up depolarisation so the threshold is reached more rapidly
What are the other effects of sympathetic stimulation on heart activity?
-reduces AV nodal delay by increasing conduct velocity
-Speeds up the spread of the AP thorough the specialised conduction pathway
-Increased contractile strength of the atrial and ventricular contractile close
Speeds up relaxation