electrical activity of the heart Flashcards

1
Q

T tubule

A

invagination of the sarcolemma deep into the muscle

AP travels down the T tubules

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2
Q

sarcolemma

A

muscle membrane

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3
Q

sarcoplasmic reticulum

A

calcium store inside the skeletal muscle

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4
Q

gap junction

A

electrical connection

NOT FOUND IN SKELETAL MUSCLE

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5
Q

desmosome

A

physical connection

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6
Q

which of skeletal and cardiac muscle can exhibit tetanus?

A

skeletal: can - contractions add up, sustained contraction
cardiac: can’t

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7
Q

why can’t cardiac muscle exhibit tetanus

A

long AP and long refractory period

this is good because we need the heart to contract then relax, not be continuously contracted

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8
Q

how does cardiac muscle form a functional syncytium

A

electrical connection: gap junctions
physical connection: desmosomes
these form intercalated discs

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9
Q

what is a functional syncytium

A

the cells act together as if they are one cell due to their electrical and physical connection

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10
Q

what is the length of a cardiac action potential and why is this important

A

~250ms compared to ~2ms in skeletal muscle
long AP and refractory period to inhibit tetanic contraction
Ca entry can regulate contraction

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11
Q

how does Ca entry from outside the cell regulate contraction strength

A

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

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12
Q

unstable resting membrane potentials

A

some cardiac muscle cells have unstable resting membrane potentials and act as pacemakers
they continuously depolarise towards threshold

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13
Q

non pacemaker vs pacemaker action potentials

A

the majority of cardiac muscle cells stay at -90 until they are told to depolarise
some cells are pacemakers and spontaneously depolarise to threshold

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14
Q

non-pacemaker action potential electrophysiology

A

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)

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15
Q

pacemaker AP

A

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

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16
Q

modulators of electrical activity (5)

A
symp and parasymp NS
drugs
temperature
blood K levels 
blood Ca levels
17
Q

how to drugs modulate electrical activity

A

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

18
Q

how does temperature modulate electrical activity

A

increases ~10bpm/C

19
Q

how does hyperkalemia modulate electrical activity

A

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

20
Q

how does hypokalemia modulate electrical activity

A

fibrillation and heart block

anomalous

21
Q

how does hypercalcaemia modulate electrical activity

A

increased HR and force of contraction

22
Q

how does hypocalcaemia modulate electrical activity

A

decreased HR and force of contraction

23
Q

Sino-atrial node

A

fastest pacemaker cells are located here
pacemaker region of the heart
~0.5m/s spread of contraction over the walls of the atria

24
Q

Annulus firbosis

A

division between the atria and ventricles
non-conducting
made of fibrous connective tissue

25
Q

atrioventricular node

A

delay box
slows things down until the atria have finished contracting
conducts very slowly ~0.05m/s

26
Q

purkinje fibres

A

rapid conduction system
~5m/s
allows depolarisation to spread through the heart muscle so it all contracts roughly at the same time

27
Q

how is electrical activity recorded as an ECG

A

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

28
Q

what does ECG tell you about the heart

A

only disorders of conduction or rhythm

doesnt tell you about the pumping ability of the heart

29
Q

disorders of conduction

A

heart block - 1st/2nd/3rd degree

30
Q

3 examples disorders of rhythm

A

atrial flutter
atrial fibrillation
ventricular fibrillation

31
Q

1st degree block

A

longer interval between P wave and QRS complex

depolarisation spreading too slowly between atria and ventricle

32
Q

2nd degree block

A

AP doesnt get through

increasingly longer gap between P and QRS then P followed by no QRS

33
Q

3rd degree block

A

no transmission between atria and ventricle
P waves are followed in any sensible way by QRS
QRS is very slow and large

34
Q

atrial flutter

A

SVT
QRS complex preceded by p wave, sits on the back of previous T wave
150bpm
normal conduction but too frequent

35
Q

atrial fibrillation

A

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

36
Q

ventricular fibrillation

A

no coordinating QRS complexes
contracting in different parts at different times
treat by defibrillation

37
Q

P wave

A

corresponds to atrial depolarisation

38
Q

QRS complex

A

corresponds to ventricular depolarisation

39
Q

T wave

A

corresponds to ventricular repolarisation