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

Question 1

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?

Answer 1

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

Question 2

Where does excitation of the hear originate? Where is this located?

Answer 2

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

Question 3

When the heart is controlled by the SA node, what is it said to be in?

Answer 3

The heart is said to be in normal sinus rhythm

Question 4

How does the SA node cause the generation of regular spontaneous action potetnials?

Answer 4

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

Question 5

What generates the pacemaker potential in the SA node? (asking about the ionic basis for the spontaneous pacemaker potential)

Answer 5

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)

Question 6

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?

Answer 6

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

Question 7

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

Answer 7

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

Question 8

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?

Answer 8

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

Question 9

What is the only point of electrical contact between atria and ventricles and where is it located? Why is cardiac conduction delayed here?

Answer 9

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)

Question 10

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?

Answer 10

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

Question 11

What is the purpose of the plateua phase of the cardiac myocytes?

Answer 11

Plateua phase allows for membrane potential to remain near the peak of action potential prolonging depolarisation of the mycoytes

Question 12

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?

Answer 12

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

Question 13

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?

Answer 13

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

Question 14

What parts of the heart do the parasympathetic and sympathetics supply? What effect does this have?

Answer 14

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

Question 15

Do parasympathetic and sympathetic innervation to the heart have chronotropic or inotropic effects? What is the neurotransmitters and what receptors do they work through?

Answer 15

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

Question 16

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)

Answer 16

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

Question 17

Describe the different types of muscle fibres? Which muscle fibre type has no neuromuscular junctions? Name 2 diseases that affect the NMJ

Answer 17

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

Question 18

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?

Answer 18

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

Question 19

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?

Answer 19

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

Question 20

What are the actin and myosin filaments inisde each myofibril arranged into?

Answer 20

Actin and myosin filaments inside the myofibirls are arranged into sarcomeres

Question 21

The desmosomes ensure that the tension developed between cardiac myocytes is transmitted on to the next mycoyte How is this tension produced?

Answer 21

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

Question 22

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?

Answer 22

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)

Question 23

* What does the release of calcium in the sarcoplasmic reticulum cause? * How does this allww for cross bridge formation between actin and myosin filaments?

Answer 23

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

Question 24

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?

Answer 24

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)

Question 25

Why is the refractory period important?

Answer 25

The refractory period prevents too many action potentials being produced which would cause tetanic contractions in the cardiac muscle (sustained muscle contraction)

Question 26

Define stroke volume Define end diastolic volume Define end systolic volume How is the stroke volume using the other two volumes?

Answer 26

* Stroke volume is the volume of blood ejected by each ventricle per heart beat * End diastolic volume is the volume of blood within each ventricle at the end of diastole * End systolic volume is the volume of blood within each ventricle at the end of systole Stroke volume = end diastolic volume minus end systolic volume

Question 27

What can bring about changes to the stroke volume? (volume of blood pumped by each ventricle per heart beat)

Answer 27

Changes in stroke volume are brought about by changes in the diastolic length / diastolic stretch of mycoardial fibres (more time/space to fill will increase SV)

Question 28

What is the end diastolic volume determined by? What does the end diastolic volume detemrine?

Answer 28

The EDV is determined by the VENOUS RETURN to the heart The EDV determines the cardiac preload

Question 29

What is the difference between cardiac preload and cardiac afterload?

Answer 29

Cardiac preload is the initial stretching of the cardiac myocytes (muscle cells) prior to contraction. It is related to ventricular filling. - it is determined by the EDV which is determine by the venous return to the heart Cardiac afterload is the force or load against which the heart has to contract to eject the blood

Question 30

What affect does the stretch of cardiac fibres due to an increased end diastolic volume have on excitation contraction coupling?

Answer 30

Increased stretch of cardiac fibres cause an increase in the affinity of troponin for Calcium (remember calcium binds to troponin pulling troponin-tropmyosin complex aside exposing cross-bridge binding site of actin/yosin)

Question 31

What does The Frank-Starling Mechanism or the Starling’s Law of the Heart describe?

Answer 31

Frank Starling mechanism states that the more the ventricle is filled with blood during diastole (increasing EDV), the greater the volume that will be ejected during the resulting systolic contraction (Stroke volume)

Question 32

As said, afterload means the resistance into which the heart is pumping If the afterload increases ie so that the heart is unable to eject the full stroke volume, what will this cause? - this is the compensatory mechanism If the afterload continues to exist (eg in untreated hypertension), what occurs to overcome the resistance?

Answer 32

If the afterload increases so that the heart is unable to eject the full SV, the frank starling mechanism partially compensates by increasing the end diastolic volume If the afterload continues to exist (eg untreated hypertension cause the resistiance in which the heart is pumping to remain), eventually the ventricular mass will increase (ventricular hypertrophy) to overcome the resistance

Question 33

Which autonomic nervous system can affect the contractility of the heart?

Answer 33

The sympathetic nervous system innervates the SA node, AV node and mycoardium Therefore sympathetic stiimulation cause noradrenaline to act via B1 adrenoreceptors to have a positive inotropic (contractile) and chrontropic (heart rate) effect

Question 34

The orderly depolarisation/ repolarisation sequence triggers a recurring CARDIAC CYCLE of atrial and ventricular contractions and relaxations The CARDIAC CYCLE refers to all events that occur from the beginning of one heart beat to the beginning of the next What are the 5 phases of the cardiac cycle?

Answer 34

1. Passive filling 2. Atrial contraction 3. Isovolumetric ventricular contraction 4. Ventricular ejection 5. Isovolmetric ventricular relaxation

Question 35

What happens during passive filling? How full do the ventricles become due to passive filling?

Answer 35

During passive filling the Atrioventricular valves (tricuspid right side and mitral valve left side) are open allowing for venous return into the ventricles - ventricles become ~ 80% full during passive filling

Question 36

What happens during atrial contraction, where is this contraction on the ECG?

Answer 36

Atrial depolarisation takes place in the p-wave of the ECG Atrial contraction happens between the p-wave and QRS (ventricles don’t contract here due to AV nodal delay remember) Atril contraction completes the end diastolic volume (volume in ventricle at end of diastole)

Question 37

What is stage 3 of the cardiac cycle? Which valves are open at the beginning and why? Why is the first heart sound heard here?

Answer 37

At the beginning of isovolumetric contraction (Stage 3) * atrial pressure > ventricular pressure Ventricular contraction starts after the ventricle has depolarised (QRS complex) and pressure rises. Once ventricular pressure > atrial, then the AV valves shut and the 1st heart sound is heart (LUB)

Question 38

Why is stage 3 called isovolumetric contraction?

Answer 38

Termed isovolumetric contraction because once the AV valves have closed due to rising ventricular pressure, the aorto-pulomonary valves are still closed - therefore tension rises in a closed volume

Question 39

What happens in stage 4 of the cardiac cycle? Which valves open and why? What volume is ejected? Why is a second heart sound?

Answer 39

Ventricular ejection * In stage 4 of the cardiac cycle, the ventricular pressure exceeds the aorta/pulmonary pressure and these valves therefore oopen - the stroke volume is ejected by each ventricle leaving behind the ESV and the aorta pressure rises * The ventricles begin to relax the ventricular pressure now relaxes. * Once the pressure is below that of the aorta, the aortic/pulmonary valves shut - SECOND HEART SOUND (DUB)

Question 40

* Passive filling * Atrial contraction * Isovolumetric ventricular contraction * Ventricular ejection What happens in the 5th stage of the cardiac cycle?

Answer 40

The final stage - isovolumetric ventricular relaxation * Closure of aorta/pulmonary valves allows for ventricular pressure to start falling. * At this point AV valves are still closed therefore pressure falls in a closed volume - isovolumetric ventricular relaxation * When ventricular pressure falls below atrial, AV valves open again * NEW CYCLE BEGINS

Question 41

Why does the arterial blood pressure not fall to zero during diastole? - when there is no blood being contracted from the ventricles (isovolumetric ventricular relaxation)

Answer 41

This is due to the outwards (hydrostatic) pressure exerted on blood vessels walls - known as the blood pressure