Week 1/2 - B(1) - Physiology 1,2,3, - Electrical acitvity, Action potential, Sarcomere, S.V/E.D.V/E.S.V, Pre/after load, Cardiac Cycle Flashcards
(41 cards)
PHYSIOLOGY 1 The heart is an electrically controlled musuclar pump which sucks and pumps blood What is the capability of the heart to continue beating rhythmically in the asbence of external stimuli known as?
This is called autorhymicity Automaticity is the ability to spontaneously depolarize and generate an action potential and the heart can do this rhymically in the absenec of external stimuli - autorhymicity
Where does excitation of the hear originate? Where is this located?
Excitation of the heart normally originates in the SA node (where the cluster of specialised pacemaker cells of heart are found) The SA node is located in the upper right atrium close to where the SVC enters
When the heart is controlled by the SA node, what is it said to be in?
The heart is said to be in normal sinus rhythm
How does the SA node cause the generation of regular spontaneous action potetnials?
The cells in the SA node generate regular spontaneous pacemaker potentials and this takes the membrane to a threshold - everythime the threshold is reached an ACTION potential is generated - the regular spontaneous action potentials
What generates the pacemaker potential in the SA node? (asking about the ionic basis for the spontaneous pacemaker potential)
The spontaneous pacemaker potential is due to a A decrease in K+ efflux superimposed on a slow Na+ influx - this is known as the funny current There is also a transient Ca+ influx taking place (T-type calcium channels are open)
Once the membrane threshold is reach, what causes the rising phase of the action potential? - is this depolarisation or repolarisation What then causes the falling phase of the action potential?
The rising phase of the action potential in the SA node is caused by the activation of L-type calcium channels allowing calcium influx - depolarisation The falling phase occurs due to closure of the L-type calcium channels and opening of potassium channels allowing potassium efflux - repolarisation
State the ionic basis for: * Spontaneous pacemaker potential in the SA node * Rising phase of the action potential in the SA node * Falling phase of the action potential in the SA node
SA NODE Spontaneous pacemaker potential - K+ efflux superimposed on a slow Na+ influx (funny current), transient Ca++ influx through T-type Ca channels Rising phase -Ca++ influx (L-type channels) Falling phase - closure of L-type channels and potasium efflux
What is the pathway of cardiac excitation across the heart? What are the cell structures known as that anchor adjacent cardiac muscle fibres to one another so cell to cell spread can occur? What allows for the cell-to-cell spread of excitation?
Cardiac excitation SA node->AV node->Bundle of His (Right + Left Bundle branch blocks) -> Purkinje fibres Desmosome are cellular structures that anchor the ends of cardiac muscle fibres together. This allows for Cell-to-cell current flows via gap junctions
What is the only point of electrical contact between atria and ventricles and where is it located? Why is cardiac conduction delayed here?
The only point of electrical conduction between atria and ventricles is the AV node, located at the base of the right ventricle Conduction is delayed at the AV node to allow the atrial contraction to precede ventricular contraction (allows for ventricular filling)
The action potential in contractile cardiac muscle cells differs considerably from the action potential in pacemaker cells SA NODE * Spontaneous pacemaker potential - K+ efflux superimposed on a slow Na+ influx (funny current), transient Ca++ influx through T-type Ca channels * Rising phase -Ca++ influx (L-type channels) * Falling phase-closure of L-type channels & K+ efflux What causes the different stages of the atrial and ventricular myocytes? Which phase is the plateua phase?
Phase 0 - Fast sodium influx Phase 1 - Closure of Na+ channels and transient K+ efflux Phase 2 - Mainly Ca++ influx - plateau phase Phase 3 - Closure of Ca++ channels and K+ efflux Phase 4 - back to resting membrane potential
What is the purpose of the plateua phase of the cardiac myocytes?
Plateua phase allows for membrane potential to remain near the peak of action potential prolonging depolarisation of the mycoytes
The heart rate is mainly influenced by the autonomic nervous system What effect does the parasympathetic and sympathetic system have on the heart? What is the difference between a chronotopic effect and an inotropic effect?
Parasympathetic stimulation decreases the heart rate Sympathetic stimulation increases the heart rate Chronotropes effect the heart heart rate * Positive increase heart rate * Negative decrease heart rate Intropres effect contraction force of the heart - * positive effect increases contraction force * negative effect decreases contraction force
Which nerve provides parasympathetic innervation to the heart? Do parasympathetics or sympathetics dominate under resting conditions? What is a bradycardia and tachycardia said to be?
The vagus nerve provides parasympathetic innervation to the heart - parasympathetics dominate over sympathetic under resting conditions Bradycardia is a heart rate less than 60bpm Tachycardia is a heart rate more than 100bpmp
What parts of the heart do the parasympathetic and sympathetics supply? What effect does this have?
Parasympathetic nerve (Vagus nerve) supplies the SA node and AV node * Vagus nerve stimulation decreases heart rate and increases AV nodal delay Sympathetic nerves supply the SA node, AV node and myocardium * Sympathetic stimulation increases heart rate, decreases AV nodal delay and increases the force of contraction
Do parasympathetic and sympathetic innervation to the heart have chronotropic or inotropic effects? What is the neurotransmitters and what receptors do they work through?
Parasympathetic nerve supply * Negative chronotropic effect - decreases heart rate * Neurotransmitter is acetylcholine working through M2-muscarinic receptors Sympathetic supply * Positive chronotropic effect - increases heart rate * Positive inotropic effect - increases contraction force * Neurotransmitter is noradrenaline working though B1 adrenoreceptors
What effects do the sympathetic and parasymapethtics have on the ionic factors involved in heart rate (this is discussing the SA node pacemaker cell action potentials)
Sympathetic - increases slope - decreases K+ efflux, increases Na+ influx, also increases transient Ca++ influx. Increases HR & decreases AV nodal delay Parasympathetic -decreases slope - increases K+ efflux, decreases Na+ influx & transient Ca++ influx. Decreases HRe and increases AV nodal delay
Describe the different types of muscle fibres? Which muscle fibre type has no neuromuscular junctions? Name 2 diseases that affect the NMJ
Cardiac muscle fibres- striated, single nucleus, branched and involuntary Smooth muscle fibres - non-striated, tapered, single nucleus and inovluntary Skeletal muscle fibres - striated, multinucleus and voluntary - has NMJs NMJ - affects skeletal muscle eg MG and LEMS
What are the cell structures known as that anchor adjacent cardiac muscle fibres to one another so cell to cell spread can occur? What allows for the cell-to-cell spread of excitation?
Cell structures that anchor adjacent cardiac cells to one another are known as desmosomes Cell to cell spread of electrical excitation allowed for by gap junctions
Each muscle fibre contains many many contractile units What are the contractile units of the heart? What are the alternating thick and thin protein filaments in the contractile units?
Each muscle fibre contains many myofibrils. The myofibrils have alternating segments * Myosin - thick protein filament giving a darker appearance * Actin - thin protein filament giving a lighter appearance
What are the actin and myosin filaments inisde each myofibril arranged into?
Actin and myosin filaments inside the myofibirls are arranged into sarcomeres
The desmosomes ensure that the tension developed between cardiac myocytes is transmitted on to the next mycoyte How is this tension produced?
Cardiac myocyte tension is produced by the sliding of the thin actin filaents on th thick myocin filaments - this explains how the muscles shorten and produces force
Excitation contraction coupling is the process by which an electrical stimulus triggers the release of calcium resulting in contraction of cardiac muscle fibres by sarcomere shortening. * What stimulates calcium release and where is it released from?
Ca2+ is released from the extracellular fluid in cardiac muscle which cause Ca2+ release from the sarcoplasmic reticulum In skeletal muslce, Ca2+ is simply released from the sarcoplasmic reticulum As the action potential travels down the transverse (T) tubules of the sarcoplsmic reticulum, Ca is released from the lateral sacs (terminal cisternae)
* What does the release of calcium in the sarcoplasmic reticulum cause? * How does this allww for cross bridge formation between actin and myosin filaments?
Ca++ released from SR binds to troponin pulling troponin-tropomycoin complexes aside exposing active sites on actin filaments - This allows myosin to bind to actin - resulting in cross bridge binding inducing contraction
The refractory period is a period following an action potential in which it is not possible to produce another action potential What causes the refractory period?
The refractory period is caused by sodium channels being closed after phase 0 of ventricular action potential meaning another action potential cannot be generated (unable to depolarize the heart again)
