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Physiology for Anaesthetists > Neurophysiology - Cardiac muscle > Flashcards

Neurophysiology - Cardiac muscle Flashcards

1
Q

What similarities does cardiac muscle share with skeletal muscle

A
  1. Striated appearance

2. Sarcotubular system: T-tubules and sarcoplasmic reticulum (although less developed in cardiac muscle)

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2
Q

What similarities does cardiac muscle have to smooth muscle

A
  1. Involuntary control (ANS and Endocrine axes)

2. Cells connected by low resistance gap junctions forming a functional syncytium.

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3
Q

How is the resting membrane established in cardiac muscle cells and how does this differ from neurons?

A

Neurons: K+ leak channels always open

Cardiac myocytes: K inward rectifying channels which open at negative membrane potentials but close with depolarisation –> K+ diffuses out the cardiac myocytes down its electrochemical gradient resulting in the cell interior becoming negatively charged with respect to the cell exterior.

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4
Q

What is the RMP in the heart

A

Varies depending on cardiac region

Sino-Atrial node = ± - 50 mV (but unstable)
Atrial myocyte = -70 mV
Purkinje fibre = - 90 mV
Ventricular myocyte = -90 mV

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5
Q

How do cardiac and nerve action potentials differ

A
  1. RMP: Cardiac - variable depending on cardiac region (SA -50 mV, Atria -70 mV, Purkinje/Ventricular myocyte -90mV). Nerve - - 70mV
  2. Duration: Cardiac (ventricular myocyte/purkinje) 200 - 400 ms. Nerve - 1 -2 ms
  3. Morphology: Atrial myocyte - triagular waveform. Ventricular myocyte prolonged plateau phase.
    Nerve - Single spike
  4. The Role of Ca++
    - Ca++ influx in cardiac cells prolongs the duration of the action potential –> plateau phase.
    - Nerve: Ca++ plays no role
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6
Q

How many phases does the cardiac action potential have - describe what happens in each phase

Draw the cardiac action potential in a ventricular myocyte

A

Phase 0
- V gated Na channels open

Phase 1

  • V gated Na channels close
  • Fast V gated K channels transiently open

Phase 2

  • Fast V gated K channels close
  • Slow V gated L-type Ca channels open
  • Slow delayed rectifier K channels open
  • —> Plateau

Phase 3

  • Slow V gated L-type Ca channels close
  • Rapid delayed rectifier K channels open

Phase 4
- Ca, Na and K conductance have returned to resting levels with K conductance exceeding Na and Ca. –> RMP

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7
Q

What are the durations of each phase of the cardiac action potnetial and how do the phases of the cardiac action potential correspond to the ECG waveforms

A

Phases 0 and 1 have a duration of 1 - 2 ms similar to the AP in a nerve. This corresponds to the QRS complex

Phases 2 duration 200ms and corresponds to the ST segment

Phase 3 duration 50ms and corresponds to T wave

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8
Q

How does the duration of the cardiac action potential vary with heart rate

A

Increasing heart rate –> decreased duration of cardiac AP

HR = 75 bpm --> ventricular AP lasts 250 ms
HR = 200 bpm --> ventricular AP lasts 150 ms
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9
Q

Describe the absolute and relative refractory periods of the cardiac action potential

A

ARP –> crom phase 1 to half way through phase 3

RRP –> halfway through phase 3 and phase 4.

ARP prevents cardiac tetany which would be incompatible with diastolic filling

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10
Q

What is meant by automaticity

A

Spontaneous decay of membrane potential of a pacemaker cell.

In the SA node this is spontaneous decay from -60 mV to - 40 mV.

The rate of the decay of membrane potential determines the heart rate

This property of the pacemaker cell is called automaticity

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11
Q

What is the historical name for the physiology of automaticity. Describe the physiology that brings about automaticity

A

The ‘funny’ current (If)

Slow depolarization of the membrane brought about by intracellular movement of Na ions exceeding the extracellular movement of K ions.

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12
Q

Describe the action potential of pacemaker currents

A

PHASE 4: Action potential leads to hyperpolarization
–> Hyperpolarization-activated cyclic nucleotide gated channels (HCN) - permeable to both Na and K. Na . K –> gradual depolarization towards threshold

PHASE 4: @ - 50 mV –> T-type Ca channels open –>Ca moves into cells –> enhancing membrane depolarization

PHASE 0: -40 mV is then reached –> Action potential: L-V gated L-Type Ca+ channels open

PHASE 3: L-Type Ca channels close. V gated K channels open –> Repolarisation and then hyperpolarization

PHASE 4…

The cycle repeats
= automaticity

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13
Q

Describe the electrical conducting system in the heart starting at the SA node

A

SA Node

Internodal pathways

  1. Anterior (Bachmann)
  2. Middle (Wenckebach)
  3. Posterior (Thorel)

AV node

Bundle of His

Left bundle branch

  1. Left anterior
  2. Left posterior

Right bundle branch

Purkinje fibres

Cardiac myocytes

  • -> intercalated discs between myocytes allow them to contract as one unit or a functional syncytium.
  • -> Adjacent to the intercalated discs are gap junctions which allow the AP to pass from one myocyte to the next
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14
Q

Why is the AV node the only place where action potentials from the atria can be conducted to the ventricles

A

Elsewhere the junction between the ventricles is insulated by the ANNULUS FIBROSIS

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15
Q

What part of the ECG is represented by the delay at the AV node

A

The PR interval

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16
Q

Draw the graph that demonstrates the cardiac action potential and muscle contraction in the ventricle

A

Page 254 Chambers

17
Q

Draw the pacemaker action potential and annotate the graph to explain the physiology

A

Page 255 Chambers

18
Q

How is cardiac contraction terminated

A

Active removal of Ca from the cell
During diastole the IC Ca conc. is extremely low. Achieved via the following mechanisms

  1. Plasma membrane Ca ATPase pump
  2. Ca/Na exchanger (3:1. Depends NA/K ATPase)
  3. SERCA ATPase pump –> uses ATP to sequester Ca into SR
19
Q

What structures give the heart the property of automaticity

A

Hyperpolarisation-activated cyclic nucleotide channels (HCN channels)

20
Q

Describe the effects of the PSNS on the heart

A

Right vagus supplies SA node
Left vagus supplies AV node

SA node –> pacemaker activity slowed
AV node –> conduction reduced
No affect on contractility

21
Q

What is the intrinsic rate of the SA node and how is this affected by the PSNS

A

Intrinsic rate: 90 - 120

Continuous PSNS input to SA node = vagal tone –> HR 60 - 80 bpm

22
Q

What is the cellular mechanism for vagal tone on the SA node

A
  1. Ach released from postganglionic PSNS fibre
  2. Binds G protein coupled receptor on post synaptic membrane
  3. G protein activated: Gai and GBy divide
  4. Gai –> inhibit adenylate cyclase –> decrease IC cAMP –> decreased activation HCN channels –> reduced Na influx and reduced If (funny current) –> reduced heart rate.
  5. GBy –> Activated inward rectifying K channels –> K efflux –> membrane hyperpolarization –> counteracts pacemaker current –> slows HR
23
Q

How does the SNS innervate the heart

A

SNS fibres from T1 - T3 innervate the heart myocardium and conducting system.

These fibres synapse with B1 adrenergic receptors - a G protein coupled receptor –> Increased cAMP IC and Protein kinase A:

  1. Positive chronotropy
    SA node: cAMP opens HCN –> increased Na influx i.e. increased ‘funny current’ –> threshold reached faster
  2. Positive inotropy
    Cardiac myocytes: Protein kinase A phosphorylates L-type Ca+ channels –> increased Ca+ influx during plateau phase –> increase IC Ca+ –> increased strength of contraction
  3. Shorter AP duration
    Protein kinase A increases opening of delayed rectifier K channels during phase 3 –> shortening repolarization time.
  4. Increased rate of transmission through AV node
    Opposite effect of PSNS.
24
Q

Summarize the PSNS and SNS effect on heart rate with regard to overall mechanism of increased and decreased heart rate

A

PSNS

  • -> Gai–> Reduced cAMP –> slowed HCN channels –> slowed pacemaker potential
  • -> GBy –> Protein kinase A–> + Kir –> Hyperpolarization (distant from threshold)
  • -> slowed conduction through AV node

SNS

  • -> B1 –> Gs –> increased cAMP –> +HCN channels –> faster (steeper) pacemaker potential –> faster HR
  • -> B1 –> Gs –> Protein kinase A –> P of L-Type Ca channels –> increase Ca influx –> increased inotropy
  • -> B1 –> Gs –> Protein kinase A –> open delayed K rectifier channels (phase 3) –> shortening repolarization time
  • -> B1 –> increased rate conduction through AV node
25
Q

Describe immunological complications associated with local anaesthetics

A

Allergic: local and systemic

Especially ester local anaesthetics
Cocaine
Procaine
Amethocaine

26
Q

Describe the mechanism and phases of CNS toxicity with local anaesthetics

A
  1. EXCITATORY PHASE
    V gated Na channels blocked in inhibitory interneurons first –> tinnitus, circumoral paraesthesia, seizures.
  2. DEPRESSIVE PHASE
    V gated Na channels blocked in excitatory interneurons –> coma, respiratory depression
27
Q

Describe the mechanism for CVS toxicity with local anaesthetics

A

Local anaesthetics block: Na, K and Ca channels in the heart.

Initial signs: bradycardia / refractory VF

28
Q

List the following in order of CVS toxicity and explain:

  1. Lignocaine
  2. Racemic Bupivacaine
  3. Levobupivacaine
A

Most to least toxic

  1. Racemic bupivacaine (S and R enantiomers present)
  2. Levobupivacaine (S - bupivacaine)
  3. Lignocaine

Ion channels are stereospecific and the S-enantiomer, levobupivacaine is less toxic

Bupivacaine is more CVS toxic than other local anaesthetics because of higher affinity for Na channels in the heart and due to the fact that bupivacaine also binds Ca channels preventing Ca release from SR.

29
Q

Describe the effects of the denervation in the transplanted donor heart

A

Heart relies on automaticity and Starlings law only

  1. Loss of vagal tone: HR = 100 bpm
  2. Loss of CVS reflexes
    - Laryngoscopy response lost
    - Peritoneal traction response lost
    - Anaesthetic drug related fall in SVR is poorly tolerated
    (dramatic hypotension if preload is not maintained.
  3. Blunted CVS response to exercise
    - HR gradually increases with exercise
    - HR gradually decreases with rest
    (B1 adrenoreceptors on heart still sensitive to circulating adrenalin released by adrenal glands during exercise)
30
Q

What is the Bainbridge reflex

A

Increase heart rate in response to stretch of the atria (increased venous return/preload)

31
Q

What are the pharmacological implications after heart transplant

A
  1. Atropine and glycopyrrolate have no effect
    - No PSNS innervation therefore atropine has no M to block
    (use isoprenaline B1 agonist)
  2. Adrenalin and noradrenalin have increased effect
    - Denervation causes upregulation of B1 adrenergic receptors –> exaggerated response to catecholamines

Physiology for Anaesthetists (61 decks)

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