CFB L5 Flashcards
State the average resting heart rate in adults
70 bpm
Very Variable
Is average resting heart rate higher in children or adults? Explain why?
Higher in children
Rapid growth, high metabolic rate
State two factors affecting average resting heart rate
Excitement
Anxiety
Can cause HR to raise to 125 bpm or higher
Why do athletes have a average resting heart rate of 50 bpm or less
Increased stroke volume
Exactly where in the heart is heart rate initiated and how is it modulated?
Initiated: Autorythmic cells in Sinoatrial node / pacemaker in right atrium
Modulated : By neural, hormonal, local factors (sympathetic + parasympathetic modulate heart rate through antagonistic control)
Parasympathetic (VAGUS NERVE) - decreases heart rate
Sympathetic (Sympathetic cardiac nerves) o increases heart rate
Describe the events that take place during parasympathetic control of heart rate
Parasympathetic control is via vagus nerve + parasympathetic neurotransmitter is ACh - SLOWS HEART RATE
ACh binds to muscarinic cholinergic receptors activating them, in sinoatrial node - opens K+ and funny current channels in pacemaker cells (in autoryhmic cells)
Increases K+ permeability, more K+ efflux, hyperpolarising cell, pacemaker potential starts at more -ve value
Also decreases funny current channel activity, less responsive to pacemaker potential
Therefore, increased conductance of K+ and decreased If channel activity, slow firing of action potentials
Simultaneously, Ca2+ channel activity is reduced (T type, L type), Ca2+ permeability of pacemaker reduced
Therefore, reduced rate of depolaristion of pacemaker cells / autorythmic cells
THIS ALL CAUSES CELL TO TAKE LONGER TO REACH THRESHOLD - DELAYING AUTORYTHMIC CELLS FROM PRODUCING ACTION POTENTIALS
SLOWER HEART RATE
Describe the events which take place during sympathetic control of heart rate
Sympathetic control via spinal nerves (cervical to upper thoracic T1-T4)
-Sympathetic neurotransmitters - noradrenaline, adrenaline - catecholamines, from adrenal medulla and sympathetic neurones
Noradrenaline binds to beta1 adrenergic receptors, activiating them, in sinoatrial node (on autoryhthmic cells)
-Activates cAMP system
-Causes Ca2+ and funny current channels to remain open for longer
-Increases transport proteins of ion channels
-Increases permeability to Na and Ca
-Greater influx of Na and Ca
-More rapid depolarisation of cell
-Reaches threshold faster
-Action potential occurs sooner
-Whole process is quicker
ADRENALINE HAS SAME AFFECT
-Heart rate goes up
What are the 2 nerves which link SAN in right atrium of heart to cardiovascular centre in medulla oblongata?
- Accelerator nerve: sympathetic NS. When stimulated, releses neurotransmitter (noradrenaline) at SA node to increase heart rate
- Vagus nerve: Parasympathetic NS. When stimulated, releases neurotransmitter ACh at SA node to decrease heart rate
Numerous sympathetic nerves link to the walls of the two ventricles where they increase contraction force of ventricles
What effects AV nodal conduction?
- ACh - slows conduction of action potentials through AV node. Increases AV nodal delay, decreasing heart rate
ACh binds to muscarinic cholinergic receptors, decreases intracellular cAMP, decrease in Ca2+, reduced conduction velocity through AVN
Therefore, excessive vagal activation / drugs enhancing vagal activity can produce AVN blockage, therefore, lower heart rate
- Catecholamines (adrenaline, noradrenaline) enhance conduction of action potentials through AV node, reducing AVN delay, increasing heart rate
Noradrenaline binds to beta1 adrenergic recpetors, increases intracellular cAMP, increase inCa2+, increased conduction through AVN
Explain how drugs which enhance vagal activity can lower heart rate
Enhanced vagal activity, more ACh produced
ACh binds to muscarinic cholinergic receptors, decreases intracellular cAMP, decrease in Ca2+, reduced conduction velocity through AVN
AVN blockage / increased AVN delay, decreases heart rate
Explain how “beta blocker” drugs can reduce heart rate
Drugs that block beta1 adrenergic receptors
Noradrenaline cannot bind, decreases intracellular cAMP, decrease inCa2+, decreased conduction through AVN, more AVN delay, lower heart rate
AGAIN, AVN BLOCK
Stroke volume
Vol of blood ejeceted by each ventricle in one contraction
Directly related to force generated by cardiac muscle during contraction
Therefore, as force of contraction increases, so does stroke volume
State two factors affecting force of contraction of cardiac muscle when ventricles contract
Length of muscle fibres (AT BEGINNING OF CONTRACTION): Determined by how much fibre is stretched as a result of volume of blood in ventricle at beginning of contraction (end diastolic vol)
Contractility of heart - affected by drugs, neurotransmitters
What is contractility of the heart?
Intrinsic ability of a cardiac muscle fibre to contract at any given fibre length. Contractility is a function of Ca2+ interaction with the contractile filaments which determine the number of active cross bridges being formed
Explain length-tension (length-force) relationships + Frank-Starling Law of the Heart
Force created by muscle fibres directly related to length of sarcomere (in turn represents initial length of musccle fibre)
The longer the fibre when the contraction starts, greater the force
The relationship between length and tension in muscle fibres also applies to ventricle muscle
When ventricles stretched, contraction force increases, therefore, stroke volume also increases
If additional blood flows into ventricles, muscle fibres stretch further, increased force of contraction, pumping more blood out
What does the Frank-Starling curve show?
Relationship between length and force
Shows stroke volume directly proportional to end diastolic volume
Therefore, as more blood flows into the heart, the heart contracts more forcefully to eject more blood
This is the Frank-Starling Mechanism
What is pre-load?
Amount of myocardial stretch before contraction begins / EDV
Explain the Frank-Starling Curve
X axis - EDV - vol of blood in ventricles at beginning of contraction, measure of stretch in ventricles, therefore, detrmines sarcomere length
Y axis - Stroke volume, indicates force of contraction
What factors affect EDV ?
Determined by venous return (vol of blood returning to heart)
Factors affecting venous return:
- Skeletal muscle pump: Contraction / compression of systemic veins returning blood to heart - particularly in legs during exercise
- Respiratory pump - pressure changes in abdomen + thorax during breathing
- Sympathetic innervation of veins
- Blood volume - affecting by drinking, bleeding, urine volume, tissue fluid volume
Tissue fluid volume affected by oncotic pressures e.g. albumin
How does the skeletal muscle pump facilitate venous return to the heart?
Skeletal muscle contracts, compresses systemic veins (mostly in legs), pushes blood twards heart (during exercise)
Promotes return of more blood to heart during exercise - increasing EDV - stretching myocardial fibres - increasing force of contraction - increasing SV
How does the respiratory pump facilitate venous return to the heart?*
Respiratory pump - pressure changes in abdomen and thorax during breathing in
During inspiration, chest expands, diaphragm moves towards abdomen
Thoraciv cavity enlarges, lowers pressure in chest, producing sub-atmospheric pressure
This low pressure decreases pressure in IVC as it passes through thorax, therefore higher pressure in veins in abdomen helps draw more blood into IVC from these veins
This allows venous return, during inspiration
How does sympathetic innervation of veins facilitate venous return to the heart ?
Sympathetic activity = vasocontriction of veins
Diameter of veins decreases
Squeezes mroe blood towards + into heart, increasing EDV - stretching myocardial fibres - increasing force of contraction - increasing SV
Therefore, sympathetic innervation of veins allows redistrobution of venous blood to arterial circulation
What are Inotropic agents?
Chemicals that affect contractiity
What are Positive inotropes?
Chemicals that increase contractiity
-Adrenaline
-Noradrenaline
-Dopamine
-Digoxin
-Glucagon
-Insulin
-Dobutamine
-Amiodarone
Increase contractility and therefore, SV, independent of EDV + muscle fibre lenghth
What are negative inotropes?
Chemicals that decrease contractility
Beta blockers
Calcium channel blockers
Antiarrythmics
Graph showing effects of positive and negative inotropic effects
Increase / decrease in contractility
No change in muscle length, therefore, same EDV
NOT FRANK-STARLING EFFECT
How to catecholamines work as positive inotropes?
Catecholamines - adrenaline, noradrenaline, sympathetic neurotransmitters - increase Ca2+ entry + storage
Bind to beta1 adrenergic receptors, activating them on membrane of contractile cardiomyocytes, increases intracellular cAMP, leads to phosphorylation of voltage gated Ca2+ channels, which stay open for longer, so more Ca2+ enter cells
More Ca2+ is concentrated in sarcoplasmic reticulum
Give an example of a cardiac glycoside and explain how they work as positice inotropes
Digoxin
Less Na+ removed from cell
Na+ build up in cytosol
Electochemical conc gradient across membrane decreases
Reduces ability of cell to remove Ca using Na-Ca exchanger
More Ca stays in cell
Increased contraction
How do negative inotropes decrease contractility of muscle fibres?
Two methods:
- Beta blockers block action of catecholamines
Block beta1 adrenergic receptors of contractile cells
Inhibits intracellular cAMP
No phosphorylation of voltage gated Ca2+ channels
Therefore, do not open
No intracellular Ca2+
Decreased contration
- Ca2+ channel blockers - block Ca2+ channels on autoryhtmic cells
