electrical activity of the heart Flashcards
T tubule
invagination of the sarcolemma deep into the muscle
AP travels down the T tubules
sarcolemma
muscle membrane
sarcoplasmic reticulum
calcium store inside the skeletal muscle
gap junction
electrical connection
NOT FOUND IN SKELETAL MUSCLE
desmosome
physical connection
which of skeletal and cardiac muscle can exhibit tetanus?
skeletal: can - contractions add up, sustained contraction
cardiac: can’t
why can’t cardiac muscle exhibit tetanus
long AP and long refractory period
this is good because we need the heart to contract then relax, not be continuously contracted
how does cardiac muscle form a functional syncytium
electrical connection: gap junctions
physical connection: desmosomes
these form intercalated discs
what is a functional syncytium
the cells act together as if they are one cell due to their electrical and physical connection
what is the length of a cardiac action potential and why is this important
~250ms compared to ~2ms in skeletal muscle
long AP and refractory period to inhibit tetanic contraction
Ca entry can regulate contraction
how does Ca entry from outside the cell regulate contraction strength
ca release doesnt saturate the troponin so regulation of ca release can be used to vary the strength of the contraction which therefore regulates stroke volume
unstable resting membrane potentials
some cardiac muscle cells have unstable resting membrane potentials and act as pacemakers
they continuously depolarise towards threshold
non pacemaker vs pacemaker action potentials
the majority of cardiac muscle cells stay at -90 until they are told to depolarise
some cells are pacemakers and spontaneously depolarise to threshold
non-pacemaker action potential electrophysiology
resting membrane potential: high resting PK+ due to leaky K channels
initial depolarisation: triggered by neighbouring cells depolarising, increase in PNa+ due to VG Na channels
plateau: increase in PCa2+ (L type channels: open slower but stay open for longer) and decrease in PK+
repolarisation: decrease in PCa2+ (channels shut) and increase in PK+ (leaky K channels open again)
pacemaker AP
AP: increase in PCa2+ by L type VG Ca channels, no sharp increase in MP
pacemaker potential: gradual decrease in PK+ (leaky channels shut)
early increase in PNa+ (PF, some Na moves in through unusual Na channels)
late increase in PCa2+ (T type, only lets in a small amount of Ca)
pacemaker explains autorhythmicity of the heart
modulators of electrical activity (5)
symp and parasymp NS drugs temperature blood K levels blood Ca levels
how to drugs modulate electrical activity
Ca2+ channel blockers: decrease force of contraction, mainly work on L type, reduce amount of Ca coming in during the AP
cardiac glycosides: increase force of contraction, increase amount of Ca being released, mainly from internal stored
how does temperature modulate electrical activity
increases ~10bpm/C
how does hyperkalemia modulate electrical activity
fibrillation: K depolarises cells, cells are pushed towards threshold and fire on their own in an uncoordinated manner
heart block: cells are depolarised, smaller electrical gradient so things happen slower, in some areas of the heart it is so slow that the heart stops
how does hypokalemia modulate electrical activity
fibrillation and heart block
anomalous
how does hypercalcaemia modulate electrical activity
increased HR and force of contraction
how does hypocalcaemia modulate electrical activity
decreased HR and force of contraction
Sino-atrial node
fastest pacemaker cells are located here
pacemaker region of the heart
~0.5m/s spread of contraction over the walls of the atria
Annulus firbosis
division between the atria and ventricles
non-conducting
made of fibrous connective tissue
atrioventricular node
delay box
slows things down until the atria have finished contracting
conducts very slowly ~0.05m/s
purkinje fibres
rapid conduction system
~5m/s
allows depolarisation to spread through the heart muscle so it all contracts roughly at the same time
how is electrical activity recorded as an ECG
an AP in a single myocyte evokes a very small extracellular electrical potential
lots of small extracellular potentials evoked by many cells depolarising and repolarising at the same time can summate to create large extracellular waves
these can be recorded at the periphery as the ECG
what does ECG tell you about the heart
only disorders of conduction or rhythm
doesnt tell you about the pumping ability of the heart
disorders of conduction
heart block - 1st/2nd/3rd degree
3 examples disorders of rhythm
atrial flutter
atrial fibrillation
ventricular fibrillation
1st degree block
longer interval between P wave and QRS complex
depolarisation spreading too slowly between atria and ventricle
2nd degree block
AP doesnt get through
increasingly longer gap between P and QRS then P followed by no QRS
3rd degree block
no transmission between atria and ventricle
P waves are followed in any sensible way by QRS
QRS is very slow and large
atrial flutter
SVT
QRS complex preceded by p wave, sits on the back of previous T wave
150bpm
normal conduction but too frequent
atrial fibrillation
no P waves
parts of the atria are depolarising and contracting at different points
some QRS complexes if the wave gets through to the ventricle
not a major problem at rest
ventricular fibrillation
no coordinating QRS complexes
contracting in different parts at different times
treat by defibrillation
P wave
corresponds to atrial depolarisation
QRS complex
corresponds to ventricular depolarisation
T wave
corresponds to ventricular repolarisation
