Lecture 13: Regulation Of Cardiac Output Flashcards
How is cardiac output regulated?
Cardiac output is regulated by changing heart rate and or stroke volume
What is cardiac output. How do you calculate it?
Cardiac output = amount of blood pumped by each ventricle each minute
Cardiac output = HR X SV
Intrinsic vs extrinsic regulation of cardiac output
Intrinsic control = regulation of an organ by factors arising within that organ (autoregulation)
Extrinsic control = regulation of an organ by factors arising outside of that organ (neural of hormonal)
Regulation of heart rate
Sa node
Neuronal and hormonal
HR is determined by SA node which depolarises spontaneously
-HR is subject to both neuronal and hormonal regulation
Note: autonomic nerves modulate heart rate but don’t cause the heart beat
Neuronal control of hear rate
SA node is innervated by both sympathetic and parasympathetic nerves
-at rest, parasympathetic activity dominates
-intrinsic SA node firing rate + 100BPM
-normal resting HR = 75 BPM
Effects are mediated by adrenergic and cholinergic receptors on SA node
Autonomic innervation to the heart
Vagus nerve and cardiac nerve
Describe the parasympathetic effects on SA node firing
Parasympathetic nerve firing decreases HR and CO
Parasympathetic nerve firing (vagus) –> muscarinic cholinergic receptors –> opens K+ channels–> K+ efflux–> hyperpolarizes SA node cell –> decreases HR and CO
So it takes longer for the cells to reach its action potential level?
Sympathetic effects on SA node firing
Sympathetic nerve firing increases HR and CO
Sympathetic nerve firing –> adrenergic receptors –> open Na+ and Ca2+ channels –> Na+ and Ca2+ influx –> rate of depolarisation increases –> increases HR and CO
Hormonal control of heart rate
Adrenaline released from the adrenal medulla in response to sympathetic NS activation
-acts in adrenergic receptors –> increased HR
(Mimics sympathetic nerve action)
Regulation of stroke volume. What is it regulated by?
End diastolic volume (volume of blood in the heart before contraction starts)
Strength of ventricular contraction
After load (pressure ventricles have to work against to pump blood out)
Who does end diastolic volume affect stroke volume? The starling effect
- Force of contraction is related to amount of blood in ventricle.
- Intrinsic mechanism to match the amount of blood expelled to the amount of blood received, prevents blood pooling
- means that heart can match the output of the 2 ventricles, moment to moment, in the absence of external regulation.
Ie ⬆EDV ➡ ⬆ventricular contraction➡ ⬆stroke volume ➡ ⬆CO ➡ ⬇EDV etc
Cellular mechanisms:
⬆ EDV ➡stretching of heart muscle ➡more overlap between myosin heads and actin filaments ➡ more cross bridge formation ➡ stronger contraction
Explain how venous return effects end diastolic volume (EDV)
-its a major determinant of EDV
-increased venous return ➡ increased cardiac output
Venous return is determined by:
-skeletal muscle pump
-respiratory pump
-venoconstriction
-blood volume
How does skeletal muscle pump effect venous return?
- thickening if skeletal muscles during conaction increases pressure in veins
- venous valves ensure blood moves towards heart and does not flow back during relaxation
- contraction ➡ increased venous return ➡ increased CO
Respiratory pump and venous return
Inhalation decreases the ossified in the thorax, in cases venous return and increases cardiac output
Diaphragm drops during inhalation ➡reduced pressure around the heart➡ large veins distend ➡ blood drawn u towards the heart ➡ increased venous return
Venoconstriction and venous return
About 60% of blood is stored in the veins at rest
Sympathetic NS activation ➡ venous smooth muscle contraction ➡ venoconstriction ➡ blood forced towards heart ➡ venous return increases
Venous valves ensure blood moves towards the heart and does not flow backwards during inhalation
Venoconstriction ➡ increased venous return ➡ increased CO
