Cardiovascular health & Health Promotion HH2602 & HH5607

Transcription

1 Cardiovascular health & Health Promotion HH2602 & HH5607 Lecture 2: Microscopic Structure and Function of the Heart 2pm ESGW Teaching Aims To introduce you to the microstructure of heart muscle. To highlight the link between cardiac structure and cardiac function Learning Out-comes: At the end of the session you will be able to: Outline the structure of cardiac muscle Identify the unique functions and properties of heart cells, and link structure to function. 1

2 The Myocardium: Consists of 3 types of excitable cells 1. myocardial cells pace-maker cells 3. cells of the intrinsic cardiac conducting system 2

3 Cardiac cytoskeleton : Figure 18.8 a, b Function of cardiac cytoskeleton: 1. Orientates muscle fibres 2. Acts as a tendon 2. Re-enforces vessel entry / exit points 3. Re-enforces valves 4. Forms a non- excitable zone between atria & ventricles to safe-guard the independent electrical and mechanical activity of the 2 hemispheres Cardiac cytoskeleton : 3

4 The innervation of the heart: SNS muscle fibres generally esp Ventricular fibres, PM cells, cells of the intrinsic conducting system all via β 1 receptors (+ coronary arteries via α receptors) Paraympathetic n.s. predominantly PM cells, few atrial fibres virtually NO ventricular fibres Myocardial Cells: Cardiac muscle is structurally similar to skeletal muscle. However there are some important anatomical and physiological distinctions that account for the different behaviour of cardiac & skeletal muscle 4

5 Fibre structure: Intercalated Discs: Intercalated discs contain: Desmosomes Gap junctions / nexi 5

6 Desmosomes: provide cell to cell cohesion (rivets) optimise force transmission Provide attachment site for actin Gap Junctions: (nexi) Gap junctions form: Low resistance - high conductance channels thro which ions can flow from fibre to fibre to i.e. AP propagation - in an All or none manner. Mass excitation of a hemisphere mass contraction of each hemisphere in turn Mitochondria: What does the table suggest? Cell type % cell volume Type II Skeletal mm 2% Type I Skeletal mm 12 15% Cardiac mm 25 35% 6

7 What is the sarcoplasmic reticulum? What function does it serve? How is this function slightly different in cardiac muscle? And what is the significance of the difference? SR in skeletal mm Arrival of an AP in the t-tubule causes the terminal cisternae of the SR to release Ca2+ into mm cytoplasm. This Ca2+ binds to troponin This sequence of events also happens in cardiac mm But its also a little bit different massive functional significance Cardiac Sarcoplasmic Reticulum: Arrival of an AP at the sarcolemma opening of sarcolemmal Ca2+ channels influx of a small amt Ca2+ from the ECF causing the SR to release larger amts of Ca2+ - amplifying effect binding with troponin contraction Calcuim induced calcium release - CICR 7

8 Ca 2+ induced Ca 2+ release; (CICR) sarcolemma ECF CICR happens when? All the time / every time an AP depolarises the sarcolemma. Its just how cardiac muscle works day in day out! BUT CICR can be enhanced to our advantage when necessary A couple of thoughts. What would happen if the ECF Ca2+ influx was increased? How might the ECF influx be increased? 8

9 CICR is a useful means of increasing the FORCE of contraction. So how does that work?? When activated sympathetic nerves & sympathetic hormones (catecholamines) can cause more sarcolemmal Ca2+ channels to open than usual. What is the consequence of sympathetic n.s action? Significance of CICR SNS opening of more SL Ca2+ channels than normal ECF SNS opening more Ca2+ channels in cell membrane than usual Means more Ca2+ enters the cell Causes the release of more Ca2+ from SR Ca2+ availability to troponin more XB than usual more force larger volume of blood ejected 9

10 An increased force of contraction caused by a sympathetically increased Ca2+ influx is known as.. Inotropy or contractility Drugs to manipulate inotropy: e.g blockers: Atenol, Propanol, Sotalol, Nadolol, Metrolol effect is to Used in those in whom cardiac work in excess of blood supply capacity myocardial ischaemia i.e those with e.g inotropic support critically ill e.g acute heart failure, septicaemia, AMI etc.. effect is to. Pacemaker Cells PM cells 10

11 Myogenicity: Skeletal mm Cardiac mm = neurogenic = myogenic auto-rhythmicity = inherent ability to spontaneously depolarise and create APs contraction Figure SAN inherent rate of depolarisation = ~ 100 bpm What is your resting HR now? Is it close to 100bpm? If not why not? 11

12 Myogenic rates of depolarisation are modulated by the ANS i.e by both the sympathetic & the parasympathetic n.s. Sympathetic n.s speeds up HR Parasympathetic n.s slows down HR The ANS & HRs: Parasympathetic n.s (vagus nerve) slows rate of SAN depolarisation HR / HR rest (negative chronotropy) Sympathetic n.s. - speeds up SAN depolarisation HR e.g. exercise (positive chronotropy) Both PNS & SNS nerves must synapse directly with the PM cells Also - SNS hormones esp. epinephrine must also make contact with β1 PM cells. Where does SNS or PNS activation come from? 12

13 Sympathetic n.s also force of contraction by increasing CICR Inotropy or increased contractility To cause inotropy the sympathetic nerves together with epinephrine must make direct contact / synapse with the myocardial muscle cells Note epinephrine adrenal medulla Can cardiac contractions be summated? Sk mm twitches can be summated because APs are v. short cf to the twitch. Twitch summation but Cardiac APs are as long as the twitch Refractory periods are long Twitch summation 13

14 Summation & tetanisation At high stimulation frequencies Sk mm can tetanise force But the heart can t. What would happen to cardiac output if the heart were capable of summation / tetanisation? Conclusion: Highlighted the main physiological differences between cardiac muscle and skeletal muscle namely: Branching structure of cardiac fibres Presence of intercalated discs, gap junctions and desmosomes 14

15 Interconnectivity: Branching & desmosomes = physical interconnectivity between all fibres a structural entity Gap junctions / nexi = electrical interconnectivity between all fibres in a hemisphere electrical coupling a functional entity High aerobic capacity, poor anaerobic capacity of cardiac muscle Dependence on external sources of Ca2+ in addition to SR supplies Myogenic properties particularly of the pace-maker zones Role of the ANS in modulating pacemaker activity & therefore HR the role of the sympathetic n.s in modulating force Long cardiac refractory periods prevent summation Next session ICS & cardiac cycle. 15

16 Knowledge check: What would happen to your HR rest if the ANS supply to your PM cells was cut now? What would happen to your HR if the SAN gave up now? When SNS activity is increased what changes HR (& how)? Or force of contraction (& how)? Possible Viva Qs? Describe how the Autonomic nervous system (ANS) influences i) pace-maker cell function (5 marks) and ii) force production ( 5 marks) Describe how the microscopic structure of heart muscle facilitates the unique function of the heart 16