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physiology > Electrical Activity and Muscle contraction L6 > Flashcards

Electrical Activity and Muscle contraction L6 Flashcards

1
Q

What is the structure of cardiac muscle

A

Cardiac muscle cells are striated, have T-tubules and SR, and have sarcomeres made up of myosin, actin, tropomyosin and troponin (TN), like skeletal muscle

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2
Q

what do neurons/skeletal muscle and cardiac muscles have in common

A

all are electrically excitable and generate action potentials

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3
Q

what is the purpose of action potentials

A

generate increase in cytoplasmic Ca+ which generates a contraction response
- This process is known as excitation-contraction (EC) coupling

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4
Q

what drives mechanical events

A

electrical activity

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5
Q

give 5 features of the heart

A
  1. it is autorhythmic
    - continues to beat outside the body if provided with oxygen and moisture
    - Group of cells that spontaneously fire APs which underlies autorhythmicity
  2. has a nerve supply
    - regulated heart beat but does not initiate heart beat
  3. two groups of myocytes
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6
Q

what are the two types of myocytes

A
  1. Conducting cells/system – used for fast spread of electrical activity (APs) throughout the heart
  2. Work cells – generate force in atria & ventricular cells
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7
Q

what are the two ways excitation spreads

A
  1. by specialised conducting fibres in atria and ventricles
  2. cell to cell via gap junctions
    - slower than fibres
    -
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8
Q

what is syncytium

A

Work cells are ‘stuck’ together by the intercalated discs to form a functional syncytium

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9
Q

where is depolarisation initiated in the heart

A

SA node in right atria

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10
Q

give the pathway of depolarisation

A
  1. SA node in right atria
  2. left atria
  3. AV node
  4. bundle of His
  5. purkinje fibres
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11
Q

why doesn’t depolarisation spread straight from atria to ventricles

A

There is a fibrous, non-conducting, layer between atria and ventricles which electrically insulates the chambers from each other

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12
Q

what is the pacemaker potential of SA node

A

an unstable membrane potential which spontaneously depolarises to threshold (-40), at which point an action potential (AP) is then generated

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13
Q

what determines heart rate

A

rate of action potential
- Rate can be altered by the ANS
- If the SAN is dysfunctional other conducting cells takeover the role, but these have a slower firing rate

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14
Q

what is Ionic basis of electrical activity in SA node

A
  1. pacemaker potential
    - slow initial depolarisation
    - Na+ moves into cell until threshold met
  2. action potential
    - at threshold, voltage gated calcium channels opens causing membrane to fully depolarise to 10mv
    - at 10mv, calcium channels close and voltage gated K+ channels open and K+ diffuses out - repolarisation
    - VGK channels remain open causing hyperpolarisation
    - VGNa channels open and cycle repeats
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15
Q

describe electrical activity in ventricular muscle cell
(look at pp for graph)

A
  1. resting membrane potential (-85)
  2. rapid depolarisation (20mv)
  3. Plato phase
  4. slow repolarisation
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16
Q

what is the Ionic basis of electrical activity in a ventricular muscle cell

A
  1. resting membrane potential
  2. rapid depolarisation
    - VGNa+ channels open, Na enters
  3. initial repolarisation phase
    - some Na channels inactive and some K+ channels open
    - K+ leak out causing initial repolarisation
  4. plato phase
    - Ca+ channels open and enter the cell equally to K+ leaving
    - prolongs depolarisation
  5. repolarisation phase
    - Na and Ca channels close, K+ continues to exit causing repolarisation
17
Q

what is the role of trigger calcium

A

The ‘trigger’ calcium entering the muscle cell through the voltage-gated Ca2+ channels during the plateau phase of the AP, leads to muscle contraction through a process known as calcium-induced calcium-release (CICR)
- trigger calcium causes calcium from SR to be released

18
Q

describe muscle contraction

A

Force of contraction is proportional to number of active crossbridges

This is determined by how much calcium is bound to troponin-C (TN-C), which is dependent on the amount of CICR

The more trigger calcium the more CICR

Sarcomere length also affects the force of contraction

19
Q

what is the benefit of having a refractory period that outlasts contraction period

A

it prevents tetanus
- As pulse frequency increases the twitches become more frequent until they merge into a sustained contraction known as tetanic contraction or spasm
if this happened in the heart, it would stop
- it can not contract again until it is full relaxed

20
Q

what is an EEG and what does it measure

A

electrocardiogram
measures The electrical changes in the atria and ventricles get conducted to the surface of the body
- uses electrodes to do this
records both depolarisation and repolarisation of the working muscle cells
The ECG is the summed electrical activity generated by all the working cells of the heart

21
Q

what are the 3 waves of an EEG
- use pp for diagram

A
  1. P wave: atrial depolarisation
  2. QRS complex: ventricular depolarisation
  3. T wave: ventricular repolarisation
22
Q

what is the isoelectric point on a EEG
use pp for diagram

A

the straight lines on diagram
- point where all cells are repolarised

23
Q

when does atrial repolarisation occur

A

occurs over QRS complex
- very minimal, unlikely to be able to see on EEG

24
Q

how many waves are there in QRS complex and what happens at each
what occurs before and after QRS wave

A

3
Q- AVN and bundle of HIS depolarisation
R- pukunji fibres depolarisation
S- depolarization spreads up ventricles
before: P-R segment
after: S-T segment

25
Q

what are Arrhythmias

A

abnormal or irregular heart rhythms

26
Q

what are the types of arrhythmias

A
  1. defects in impulse propagation
    - heart block
    - loose ability to electrically activate ventricles from atria
  2. defects in impulse initiation
    - fibrillation
    - too many action potentials resulting in rhythm being no existent

physiology (10 decks)

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