heart Flashcards
adaptation of cardiac myocytes for electrical conduction
-Cardiac muscle is myogenic: It is able to generate & propagate its own electrical activity
independent of the nervous system
-intercalated discs: Allows for spread of electrical activity & flow of nutrients between cardiac myocytes
-Gap junctions: cluster of ion channels at
intercalated discs provides low resistance
path between myocytes
-Cardiac muscle is myogenic: It is able to generate & propagate its own electrical activity
independent of the nervous system
What constitutes the cardiac conduction system?
-Sinoatrial node (SAN):
Dominant pacemaker in the heart Where electrical activity within the heart is originated
-Atrioventricular node (AVN): Transmits impulses from SAN to ventricles with a delay
-Ventricular conduction system - bundle of His, and the
Purkinje fibres: Fast conduction which delivers impulses
to ventricles
sinatrial node action potential phases:
-Phase 0: Action potential upstroke Involves Ca2+ influx which depolarises Vm from
-30mV to ~ 20mV. due to the l type volage gated channels on the membrane of calcium channels opening
-phase 3 involves K+ efflux which hyperpolarises Vm to ~
-60mV. due to iIKs channels
phase 4 of the SAN
-Phase 4: Pacemaker depolarisation
Exclusive to SAN – Unstable & constantly depolarising resting membrane potential
Allows automaticity
Involves a combination of depolarising & hyperpolarising currents, with a net overall
depolarising effect on Vm from -60mV to -30mV
Currents involved:
Depolarising – INCX, ICaT2+, If
Hyperpolarising - I
SAN phase 4 channels involved
- NCX (Na+/Ca²⁺ Exchanger):
Removes 1 Ca²⁺ ion in exchange for bringing in 3 Na⁺ ions.
Net effect: Depolarizing current (makes the cell more positive).
2. Depolarizing Currents:
I_CaT²⁺: Influx of Ca²⁺ ions (via T-type Ca²⁺ channels).
If (“Funny Current”):
Movement of K⁺ and Na⁺ through HCN channels.
Drives membrane potential (Vm) toward ~ -20mV (midway between Na⁺ and K⁺ potentials).
3. Hyperpolarizing Current (I_K⁺):
Outward flow of K⁺ ions (via I_Ks channels).
During Phase 4 of the sinoatrial node action potential (SAN AP):
I_Ks amplitude decreases as channels deactivate.
Key Concepts for Depolarization and Hyperpolarization:
Depolarization = Makes the cell more positive (due to Na⁺ or Ca²⁺ inflow).
Hyperpolarization = Makes the cell more negative (due to K⁺ outflow).
ventricular action potential phases
-Phase 0: Action potential upstroke
Involves Na+ influx which depolarises Vm from -
85mV to ~ 40mV
Phase 3: Action potential repolarisation
Involves K+ efflux which hyperpolarises Vm to ~
-85mV
Currents involved:
Phase 0 – INa+
Phases 3 & 4 – IK+
Phase 4: Resting potential
Involves K+ efflux maintaining Vm at ~ -85mV
venticular action potential phases
-Currents during Phase 0:
INa+ – Due to influx of Na+ ions through voltage gated Na+ channels
Na+ channels’ activation threshold is ~ -60mV
Na+ influx during phase 0 drives Vm of ventricular cells towards ENa+ at ~ 60mV
Currents during Phases 3 & 4:
IK+ – Due to efflux of K+ ions through voltage gated K+ channels
rapid and slow delayed rectifier K+ channels (IKr & IKs)
& inward rectifying K+ channel (IK1)
K+ efflux during phase 3 drives Vm of ventricular cells towards EK+ at ~ -90mV
IKr channels:
Fast gating kinetics –
Responsible for Vm
repolarisation during earlier
parts of phase 3 ventricular AP
IKs channels:
Slow gating kinetics –
responsible for Vm
hyperpolarisation later during
phase 3 ventricular AP
IK1 channels:
Activate at more negative Vm (<-40mV)
– so during the late stages of
ventricular AP phase 3 & phase 4
Responsible for maintaining &
stabilising Vm at -85mV
ventricular action potential phase 1 and 2
Phase 1: Initial repolarisation
Involves K+ efflux which repolarises Vm from
~40mV to ~ 20mV
Phase 2: Plateau phase
Involves a combination of K+ efflux and Ca2+
influx with no net overall change in Vm.
Currents involved:
Phase 1 – IK+
Phase 2 – IK+ & ICa2+
Functional organsiation of T-tubules
Function of T-tubules (with SERCA and RYR):
T-tubules deliver the action potential deep into muscle cells.
This activates voltage-gated L-type Ca²⁺ channels, causing Ca²⁺ influx.
The Ca²⁺ influx activates ryanodine receptors (RYR) on the sarcoplasmic reticulum (SR), releasing more Ca²⁺ into the cytoplasm (Ca²⁺-induced Ca²⁺ release).
After contraction, SERCA pumps Ca²⁺ back into the SR, helping reset the system for the next contraction.
Sliding Filament Model of Contraction:
-Calcium binds to troponin, causing tropomyosin to move and expose binding sites on actin.
-Myosin heads attach to actin, forming cross-bridges.
Power stroke: Myosin pulls actin toward the center of the sarcomere, shortening the muscle.
ATP binds to myosin, causing it to detach from actin.
ATP is hydrolyzed, resetting the myosin head for the next cycle.
This process repeats, sliding the filaments past each other, causing muscle contraction.
rise in intracellular Ca2+ concentration
Membrane Depolarization activates voltage-gated L-type Ca²⁺ channels, allowing Ca²⁺ influx into the cell.
This triggers ryanodine receptors (RYR) on the sarcoplasmic reticulum (SR), releasing more Ca²⁺ into the cytoplasm (Ca²⁺-induced Ca²⁺ release).
The rise in intracellular Ca²⁺ causes muscle contraction.
After contraction, SERCA pumps Ca²⁺ back into the SR, and the Na⁺/Ca²⁺ exchanger and Na⁺/K⁺ ATPase help restore ion balance.
Muscle relaxation and reduction in intracellular Ca2+ concentration
Membrane repolarization stops Ca²⁺ influx through L-type Ca²⁺ channels.
SERCA pumps Ca²⁺ back into the sarcoplasmic reticulum (SR).
The Na⁺/Ca²⁺ exchanger (NCX) and Na⁺/K⁺ ATPase help remove Ca²⁺ from the cytoplasm.
The reduction in intracellular Ca²⁺ causes muscle relaxation.
have the structure of the heart up when doing exam
the right side of the heart
-contains deoxygenated blodd
-operates at low pressure due to small capilaries in the lungs
-responsible for the pulmonary circulation
the left side of the heart
-contains oxygenated blood
-responsible for the systematic circulation
