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The Heart Muscle

Created: 2/11/2004
 
 

Cardiac muscle

  • Striated myofibrils composed of sarcomere units (same as skeletal)
  • Thick and thin filaments giving Z, A & I bands
  • Thick: myosin strands with actin binding sites at their heads
  • Six thin actin filaments surround each thick one
  • Contraction involves coupling and de-coupling fuelled by ATP and Ca
  • Sarcolemma surrounds the muscle fibre, and has invaginations (T-tubules) passing deep into cell (at Z-lines): spreads action potential
  • Sarcoplasmic reticulum (SR; Ca store) surrounds the myofibrils

Differences between cardiac and skeletal muscle

  • Cardiac muscle forms a functional syncitium: all or nothing response achieved by branching and interdigitation
  • Cardiac muscle has a low threshold for propagation
  • Cardiac muscle has many more mitochondria
  • Cardiac muscle has more capillaries (cannot incur hypoxia)

Excitation-contraction coupling

  • Triggered by an action potential through the T-tubule, which causes Ca ions to enter the cell (voltage- and receptor-mediated channels)
  • Trigger of further Ca release from the SR
  • Ca binds to troponin on actin causing tropomyosin to move, revealing binding sites for myosin heads
  • Contraction proceeds by walk-along process and ATP is used up (converted to ADP)
  • Ca pumped back into SR by Ca/Mg pump

Cardiac action potential

  • Spontaneous
  • Two different types:

    Fast (contractile myocardial cells and conducting pathways)

    Slow (pacemaker cells) exhibiting automaticity

Resting membrane potential (RMP)

  • About –90 mV
  • Maintained by three mechanisms:

Retention of many intracellular anions to which the cell membrane is not permeable

Resting cell membrane is 100 x more permeable to K allowing it to flow down its concentration gradient outwards

           Maintenance by the Na/K ATPase (3Na/2K)

Slow potentials

  • Pacemaker cells depolarise spontaneously
  • Most negative potential is only –60 mV (cf –90 mV)
  • This is because the membranes are more permeable to Na ions in their resting state; therefore the RMP tends more towards ENa

Summary of differences

  • Pacemaker cells differ in the following ways:
  • Less negative phase 4 membrane potential
  • Less negative threshold potential
  • Spontaneous depolarisation
  • Less steep slope in phase 0 (T-type Ca channels)
  • Absence of phase 2 (plateau)

Automaticity

  • Depends mainly on the ability to maintain a spontaneous rhythm due to leakage of Na into the cell in phase 4
  • Influenced by autonomic nervous system and various drugs
  • Can also have less negative threshold (quinidine/procainamide) or increased hyperpolarisation (increased ACh), which both cause a decrease in firing

ECG changes

  • Sinus bradycardia: <60 bpm
  • Sinus tachycardia: >100 bpm (compromised over 140 ?why)
  • HypoK: RMP more negative, so heart less excitable but automaticity increases
  • Prolonged PR, QT, flat T (can invert), prom U
  • HyperK: RMP towards TP heart more excitable and then poor contraction occurs
  • Short QT, peaked T, QRS can widen, PR can lengthen
  • HypoCa: prolonged PR, QRS, prolonged QT interval
  • HypoMg: promotes tachyarrhythmias
  • HyperMg: delayed AV conduction, prolonged PR, QRS, can lead to heart block

Control of cardiac pump function

CO = SV X HR

Pre-load

  • Synonymous with:

Central venous pressure (CVP)

Venous return

Pulmonary capillary wedge pressure (PCWP)

  • Definition: pre-load is the initial length of the muscle fibre before contraction
  • In the intact ventricle, the pre-load is proportional to end-diastolic volume (EDV)

Measurement of pre-load

  • No practical methods of reliable assessment
  • Therefore end-diastolic pressure (EDP) is often used which is related to EDV by the ventricular end-diastolic pressure-volume curve
  • Practical index: CVP or PVWP

Factors affecting EDV

  • Total blood volume
  • Body position
  • Intrathoracic/intrapericardial pressures
  • Venous tone and compliance
  • Pumping action of skeletal muscles
  • Synchronous atrial contribution to ventricular filling
  • Ventricular end-diastolic compliance

ArticleDate:20041102
SiteSection: Article
 
   
    
                                            
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