Heartbeat&ECG Flashcards
Excitable cells
How heart cells are excitable: what causes this
Characteristics of cardiac excitabitiliy
Intrinsic rhythm
External autonomic system
- Some cells can be electrically excited causing generation of action potentials (propagated electrical signals along cell membranes to adjacent cells) and an action
- Heart cells (cardiac cells: cardiac myocytes) are excitable
- Cardiac excitability characterized by cardiac cell membrane sequential depolarisation and repolarisation, communication with adjacent cells and propagation of electrical activity
- Our heart has an intrinsic rhythm-if supported with ions and energy it can beat outside our body
- the external autonomic system affects the rate of heart beat but it is mainly done on its own
Cardiac myocytes-intercalated discs
ICD
Gap junctions
Desmosomes
Sacromere
Cardiac myocytes
Cardiac myocytes: one nucleus in the middle
ICD: sites of thickening of sarcolemma (plasma membrane) where the cell are joined together
Gap junctions: enable action potentials (ions) to spread from cell to cell throughout atria then ventricles
Desmosomes: sites of adhesion between cardiac muscle cells-connected when they contract
- pacemaker communicates with desmosomes
Sacromere: basic contractile unit -> bundle of myosin -> containing thick filaments flanked and interdigitated with bundles of actin-containing thin filaments
Cardiac Conduction System-Specialised Conducting system
- Consists of SAN, AVN, bundle of His, Purkinje fibres
- Begins with primary cardiac pacemaker cells located SAN in RA
- SAN cells modified cardiac muscle cells not nerve cells
- It(?) suppresses other pacemaker cells except when the SAN fails
- The heart pauses because the blood needs to fill up the atria
Function of annualis fibrosis:
1. Anchoring point of cardiac msucle
2. Stops the randon transmission of electrical activity
Cellular electrical acitivity-cardiac action potentials
Size and shape
What generates action potentials?
- Size and shape of APs differ betwen cell types-pacemaker cells vs contraction cells
- Cells have different kinds of voltage-dependent ion channels
- Voltage-dependent ion channel proteins opening and closing in plasma membrane generate action potentials
SAN depolarisation
Pacemaker cells in SAN spotaneously active-automacity
1. Action potentials initiated by opening of sodium channels (funny current): open when membrane potential is less than -50mV
2. Sodium ions enter cell and depolarisation starts
3. Threshold reached which then opens voltage-gated calcium channels
4. Calcium enters cell causing further depolarization and action potential
SAN repolarisation
- Calcium channesl close
- Potassium channels open and potassium leaves cells-cell repolarises (negative internal charge relative to ouside restored)
- After each actional potential, potassium channels which had opened during action potential during action potential now slowly spontaenously close
- Once cell membrane potential back to -50mV, funny current sodium channels open
-AVN action potential looks almost the same but intrinsic rate is slower
Ventricular myocyte cells’ action potential: depolarisation&plateau
- Cell starts to depolarise intiated by neighboring cell action potential
- After threshold reached cells’ own action potential is initiated by opening of voltage gate sodium channels that depolarise cell
- Voltage gated Na+ channels close.Voltage gated potassium channels start to open
- Finally L voltage gated calcium channels (L for long-sustained) open-plateau
- K+ efflux continues
- myocytes contration
Refractory period: Once an action potential is initiated there is a period of time (effective refractory period, ERP)- in which new stimulation of cell does not produce new, propagated action potentials
Prevents muscle contracting prematurely and keeps all cells synchronous
Ventricular myocyte cells’ action potential: repolarisation
- Rapid repolarization: L voltage gated calcium channels close
- Cell repolarises: voltage gated potassium channels stil open and
- now unopposed and more voltage gate potassium channels open
- Resting potential: high K+ permeability, return to resting cell membrane potential
Cardiac cell refractory period
- Allows heart to empty and then fill: ventricle is contracting when they dont have a rhythm and quivering randomly and not pumping blood
- If cells get out of synchronisation then fibrillation can occur, when different parts of the ventricle are contracting at different times. Ventricular pressure does not rise enough to generate any cardiac output and death results.
- Defibrillator shocks all cardiac cells into refractory period-can then all start to contract synchronously and rhythm is restored.
Cardiac muscle
5 main characteristics
How it is similar to skeletal and smooth muscle
Definition of myofibrils and sacromeres and bands
Five main characteristics of cardiac myocytes:
1. Striated
2. Uninucleated
3. branched
4. connected by intercalated discs
5. high mitochondrial content
- shares important characteristics with both skeletal and smooth muscle
Skeletal muscle:
a. striated like skeletal muscle because of arrangement actin and myosin filmatents into sacromeres
b. produce strong contractions like skeletal muscle
Smooth muscle:
a. Automacity: rate and force of contraction not subject to voluntary control though is influenced by ANS and hormones
Myofibrils: series sarcomeres consisting of bands
Sacromere: the basic contractile units of cardiac muscle
Z-bands: lateral boundaries sarcomeres; actin attachment site
M-line: attachment site for myosin
A bands: myosin&overlapping actin filamebts
H bands: myosin alone
I bands: actin alone
Cardiomyocyte contractile cycle
- Calcium binds to troponin C, leading to a conformational change that displaces tropomyosin from the actin binding sites
- Crossbridge formation occurs with ATP hydrolyzation into ADP+Pi
- Power tsroke moves actin filament towards the centre of the sacromere. ADP+Pi are released from the myosin heads
- Actin released with ATP binding to myosin. Myosin heads cocked back into firing position, ready to make crossbridges further downstream
- Cycle continues until cellular calcium levels decrease, allowing calcium to dissociate from troponin. Tropomyosin returns to its original conformation that block actin binding stie.
How do these cardiac electrical events lead to cardiac muscle cell contraction?
Sarcolemma: cardiac cell membrane
Sarcoplasmic reticulum: specialized endoplasmic reticulum of cardiac muscle (storage and release area for calcium-surrounds sarcomere)
- Depolarisation of membrane (influx of sodium via sodium channels) opens voltage-gated calcium channels
- Influx of calcium through voltage-gated (L-type) calcium channels (LTCC) in the cell membrane into cell.
- The rise in intracellular calcium triggers further calcium relase from the sarcoplasmic reticulum (SR) by the ryanodine receptor (RyR)
the Ca 2+ is not enough for the cardiac contraction, calcium induced calcium release
4. Calcium then associates with troponin C in the sarcomere to intiate contraction in the cardiac muscle (systole)
These events are terminated by release of calcium from the sacromere (causing relaxation, diastole) and its reuptake into the sarcoplasmic reticulum.
Chronotropic effect: heart rate and autonomic nervous system
- SA node is richly innervated by vagal (PNS) and sympathetic autonomic nerve fibres
Parasympathetic nerves from vagus nerve act via interneurones in SAN
1. release acetyl choline athat acts on muscarinic receptors
2. Cause potassium channels to open
3. Potassium leaving cells (efflux) decreases depolarisation rate
4. Decrease action potential rate
5. Heart slows down
Sympathetic nerves at SAN
1. release norepinephrine
2. Acts on Beta 1 adrenoreceptors
3. Increase Ca2+ influx (speeds up depolarisation in pacemaker cells
4. Increase pacemaker rate
- chronotropic effect-> faster HR
Both systems also ahve (weaker) inputs to the AVN
Inotropic effects: heart contractility and ANS
Sympathetic nerves increase ventricular and atrial contraction force
- positive ionotropic effect
1. Increasing Ca2+ influx (via L type Ca2+ channels), primarily during phase 2
2. Increases sarcoplasmic calcium release
3. Mediated by Beta 1 adrenoreceptor responding to norepinephrine released by sympathetic neurons
Parasympathetic nerves (vagal efferents) only small negative ionotropic effect
- negative ionotropic effect
- vagal efferents
- primary effect on SAN/AVN (heart rate)
During exercise, stress and anxiety high levels of circulating epinephrine secreted by adrenal glands augment sympathetic NS direct noradrengergic effect on heart.
AVN conduction pathway
AVN located in inter-artrial septum near tricuspid valve
1. Action potential from SAN with have spread all over both atria and reached AVN by about 60ms after SAN activated
(delay of 60ms AVN allows time for atria to physically contract and so to push more blood into ventricles before ventricles start to contract)
2. However, AVN doesn’t start to transmit action potentials down into ventricles via bundle of His until about 120ms after start of SAN action potential
3. From AVN electrical activity conducted through bundle of His-wide,fast, conducting muscle fibres that travel through Annulus Fibrosis
4. Annulus Fibrosus connective tissue separates atria from ventricles.
5. Bundle of His-enters interventricular septum where divides into right and left
Right bundle branch: travels along right side of interventricular septum-> excites right ventricle (left branch for left ventricle)
6. RIght and left bundle branch terminate in extnesive network of large,fast conducting myocyte fibre
7. Purkinje fibres continue to condcut depolarization wave through the ventricles.
