P: Cardiac Output Flashcards
What is Stroke volume
EDV - ESV
Volume of blood ejected by each ventricle during systole
Cardiac output
stroke volume x cardiac rate
Normal at rest = 5-5.5 litre/min
Cardiovascular control centres
Sensory information relayed to hypothalamus, which regulates activity in CV control centres located in reticular regions of pons and medulla oblongata.
Sympathetic pre-ganglionic fibres originated in:
T1-T5 segments
Post-ganglionic sympathetic nerves innervations
- Innervate SA and AV nodes
- Innervate contractile atrial + ventricular tissue
Post-ganglionic parasympathetic (vagus) innervations
- Innervate SA and AV nodes
- Some innervation of contractile atrial + ventricular tissue
Vagal escape
- Reduction of heartrate making the HR = 0 triggers reflex stimulation of sympathetic nerves (baroreceptor reflex)
- Simultaneous sympathetic and vagal nerve activity results in a HR of 20-40bpm.
Sympathetic regulation of heart rate
- Sympathetic stimulation of pacemaker cells increases ion flow through ifNa+ channels and iCa Ca2+ channels.
- This increase rate of autorhythmic cell depolarizations and thus HR.
- Noradrenaline released from sympathetic nerve endings binds B1-adrenergic receptors on pacemaker cells.
- cAMP levels and PKA activity increases
- cAMP binds to ifNa+ channels and PKA phosphorylates iCa2+ channels
- Results in opening of these channels.
Vagal regulation of heart rate
- Release of acetylcholine from vagus nerves causes opening of K+ channels and closing of ifNa+ and iCa Ca2+ channels (HCN) on pacemaker cells
- Ach binds directly to and activates Ach-sensitive K+ channels
- Ach also minds M2 muscarinic receptors which inhibits cAMP production.
- Opening of ifNa+ and iCa Ca2+ channels is decreased, reducing their permeability.
- Increase K+ efflux during phase 4 causes Vm to become more negative –> dampens rate of generation of slow response Aps in autorhythmic cells + HR is reduced.
Regulation of conduction rate
- Vagal stimulation also decreases excitability of AV node cells, slowing transmission of cardiac impulse into ventricle: hyperpolarization slows generation of successive Aps required to Conduct electrical activity through AV node –> longer duration of diastole and ventricular filling.
- Sympathetic stimulation: increased sodium-calcium permeability makes It easier for AP to excited successive AV node cells, decreasing conduction time from atria to ventricles. Shortens duration of diastole and ventricular filling.
Frank-starling mechanism
ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return.
- Increased EDV increases resting sarcomere length in ventricular myocytes
- Allows optimum overlap of thick/thin filaments: maximum no. of cross bridges formed + increased affinity of troponin C for Ca2+
Ejection fraction
- EF = SV/EDV * 100
- % of EDV ejected from heart
- Normally EF > 60%
- Exercise EF > 90% due to increased inotropy (contractility)
How does an increase in EDV result in an increase of SV
- Increase in EDV increases ventricular pressure (preload) which stretches ventricular myocytes
- Increased stretch increases intrinsic contractility of myocytes
- Myocytes contraction is stronger –> increases SV
Preload in normal heart:
12mmHg
Contractility will peak at preload of:
30mmHg
Optimum length of sarcomeres:
2.4µm
Brachycardia effect on CO
- Brachycardia decreases CO initially
- Increased duration of diastole –> increased ventricular filling, so increased EDV
- Increased stretch + increased contractility results in increased SV
- Reduction of HR is compensated by increase in SV
- CO remains constant
Increase in afterload
- Increase in blood pressure increases afterload
- Increase in afterload delays opening of valves and ventricular ejection
- Ventricles have to contract for longer to open semilunar valves
- Reduction in stroke volume + increase in ESV.
How does increased heart rate increase contractility?
- Increased heart rate causes an increase in intracellular calcium in contractile myocytes.
- Calcium enters cell during each AP plateau phase –> more AP/min = rise in [Ca2+]
- Increased number of depolarizations also increases opening of Ca2+ channels.
- Increased intracellular calcium increases contractility.
Bowditch effect / Treppe phenomenon:
increased heart rate increases intracellular calcium, which increases contractility.
Intrinsic mechanism of an increase in HR
- Shortens diastolic time
- Reduces duration of ventricular filling
- Reduces EDV (preload)
- Reduces SV
Why does SV decrease as HR increases?
- Reduced time for ventricular filling
- Reduced EDV
- Reduced SV
Increasing influx of Ca2+ has 2 effects on fast response:
- Prolongs plateau phase of AP
- Increase i[Ca2+] induces stronger contraction of sarcomeres in myocytes.
Sympathetic regulation of contractility:
- Sympathetic nerves release noradrenaline which bind to B1 adrenergic receptors on myocytes
- cAMP levels increase, resulting in activation of PKA
- Phosphorylation of L-type Ca2+ channels increases opening time
- Contractile strength increases
- SV increases
Mechanisms of a stronger + more rapid ventricular contraction:
- Shortened systole
- Faster relaxation
- Diastole is longer
- Promotes increased ventricular filling
How vagus nerves regulate contractility:
- Vagus nerves release Ach which closes L-type Ca2+ channels by either:
- Ach binds to M2 muscarinic receptors + inhibits cAMP production, resulting in down-regulation of cAMP 2nd messenger system. Phosphorylation and opening of Ca2+ channels is reduced.
- Release of ACH from vagal endings inhibits release of noradrenaline from neighbouring sympathetic nerves.
- Contractile strength is decreased
- SV is decreased.
Cardiac output equation
(O2 absorbed per minute by the lungs)/(Arteriovenous O2 difference)
Doppler echocardiography
Measures cardiac output non-invasively.
Determines direction + velocity of blood flow; SV and therefore CO is calculated from velocity of blood + area of aorta.
Cardiac factors vs coupling factors
Cardiac factors: intrinsic to heart (e.g. heart rate + myocardial contractility)
Coupling factors: interaction of heart with blood vessels (preload + afterload)
____ stimulation also decreases excitability of __ node cells, slowing transmission of cardiac impulse into ___:
_____ slows generation of successive Aps required to Conduct electrical activity through AV node –> ___ duration of ___ and _____.
Vagal
AV
Ventricle
Hyperpolarization
Longer
Diastole
ventricular filling.
Increase in ____ increases afterload
Increase in afterload delays opening of ____ and ventricular ejection
Ventricles have to contract for longer to open ____ valves
Reduction in ____ + increase in ____
Blood pressure
Valves
Semilunar
Stoke volume
ESV
