9 - ELECTROPHYSIOLOGY Flashcards
CARDIAC MUSCLE
Heart pumps 5 L of blood round the body 1000x a day
• Cells contract spontaneously
• Spontaneous contraction (depolarisation ) creates a need for a pacemaker
• Need regulation to co-ordinate
• Adapted to conduct signals rapidly across the cardiac tissue
CARDIAC MUSCLE: STRUCTURE
- Mononucleated cells. 100µm in length
- Striated: crossbands of the muscle contraction apparatus are visible (z-bands)
- Intercalated discs between: made up of gap junctions, which allow the transmission of ions and the action potential
- This arrangement means that the muscle works as a functional syncytium: it works as one unit.
SPECIALIST FEATURES FOR CONDUCTION IN THE CARDIAC MUSCLE.
Desmosomes, intercalated discs and gap junctions allow rapid communication from one cardiomyocyte to the next.
- Desmosomes hold the muscle cells together tightly
- Gap junctions allow passage of action potentials from one cell to the next, very quickly – allows the cardiac muscle to function together as a syncytium
- Intercalated discs link muscle cells together and contain desmosomes and gap junctions
STIMULATION OF CONTRACTION: ACTION POTENTIALS
- As in skeletal muscle, electrical signals are passed via action potentials.
- Cardiac cell APs are slightly different to those elsewhere.
- Cardiac resting potential : -90mV (not -70mV)
- Resting potential is higher (less negative) if cardiac cells are hypoxic and this inactivates some Na channels. This has consequences for AP generation.
CARDIAC ACTION POTENTIALS
Non-pacemaker cardiomyocyte action potentials are slower: • Nerve: 1-2 millisecs • Skeletal muscle: 2-5 millisecs • Ventricular: 200-400 millisecs • 5 phases Period of depolarisation is extended
CARDIAC ACTION POTENTIALS EXPLAINED
- Rapid depolarisation due to Na+ inflow when voltage-gated fast Na+ open
- Plateau (maintained depolarization) due to Ca2+ inflow when voltage gated slow Ca2+ channels open and K+ outflow when some K+ channels open
- Repolarization due to closure of Ca2+ channels and K+ outflow when additional voltage-gated K+ channels open
Why is a long refractory period essential?
The long refractory period is essential to allow relaxation (and filling) of ventricles between contractions – if further action potentials were triggered too quickly, the heart would not function effectively as a pump.
CONTROL OF CONTRACTION
• Action Potential stimulates contraction: AP allows Ca to enter the cells to stimulate excitation-contraction coupling: the contraction of the cardiomyocytes.
• Cardiac cells in aorta would beat at 60/min, ventricles at 20-40/min.
Heart beats at 70b/min - Slowing allows for ventricles to be filled.
• Need a regulation system to co-ordinate: autonomic nervous control
(parasympathetic and sympathetic nervous system)
• External influences can interrupt rhythm. ie exposure to high levels of
caffeine or nicotine.
IN-HEART REGULATION: NODAL SYSTEM
A network of structures sets up a conduction system to control heart rate.
- Sinoatrial (SA) Node: pacemaker
- Atrioventricular Node
- Bundle of His (and branches) in septum
- Purkinje fibres in ventricular walls
CARDIAC CONDUCTION SYSTEM
- Specialised cells of the SAN produce electrical impulses at a rate of 100 per minute
- Impulses spread through Atria - contraction
- Impulse moves through AV node towards ventricles. Delay of signal here
• Allows time for atria to completely depolarise, contract and empty - Impulse transmitted to ventricular muscle via Purkinje fibres to stimulate contraction
CARDIAC PACEMAKERS
- SAN cells slowly depolarize spontaneously
- Causes the resting membrane potential to decrease (pacemaker potential)
- Once the threshold is reached, an AP is stimulated
- AVN cells also spontaneously depolarize slowly. BUT they are usually triggered by AVN activity before they can depolarize on their own.
> Co-ordination
> SAN activity can be influenced by the Autonomic Nervous System
PACEMAKER POTENTIALS: A LITTLE MORE DETAIL
- Influx of Calcium through L-channels
- Potassium (K+) channels open, repolarising cell
- 2-step process:
i. Funny current of Na+ enters through funny channels (pacemaker current)
ii. T-channels let Ca2+ in until the threshold is reached
• Phase 4 is the pacemaker potential and mediated by movement of Ca2+ and Na+
NEURAL CONTROL OF HEART RATE
- Sensory information from sensors (eg chemo and baro) is processed in the medulla oblongata
- Triggers an ANS response
i. Sympathetic NS (cardiac accelerator nerves) increase HR and contractility. Physical and emotional stress will increase HR
ii. Parasympathetic NS (Vagus nerves) decrease HR
FACTORS AFFECTING SA NODE FIRING - Increasing
Sympathetic stimulation • Muscarinic receptor antagonist • β Adrenergic receptor agonists • Circulating catecholamines • Hypokalemia • Hyperthyroidism • Hyperthermia
FACTORS AFFECTING SA NODE FIRING - Decreasing
Parasympathetic stimulation • Muscarinic receptor agonist • β blockers • Ischaemia/hypoxia • Hyperkalemia • Sodium and calcium channel blockers • Hypothermia
