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Flashcards in The Heart as an Electrical Pump Deck (19)
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1

Describe the arrangement of cardiac muscle 

Cardiac myocytes are arranged into a syncytium of cells which branch and interdigitate. 

Intercalated discs provide electrical and mechanical interconnection between myocytes. 

Myocytes are composed of myofibrils which are composed of sarcomeres

Sarcomeres are composed of actin and myosin filaments: these filaments sliding over eachother results in contraction. 

2

Where is the usual source of the action potential that drives cardiac muscle contraction?

What are pacemaker cells? What alters their activity?

Sinoatrial node (primary pacemaker)

  • Pacemaker cells are modified muscle cells characterised by:
    • No true resting potential
    • Generation of spontanous regular action potentials.
  • Activity can be modified by:
    • Hormones
    • Ions
    • Autonomic nerves 
    • Hypoxia
    • Ischaemia

 

 

3

What occurs if the sino-atrial node stops working?

Pacemaker cells take over, often in the atria but can be in the AV node or bundle of His.

The further away from the AV node the action potential is generated, the slower the rhythm generated. 

4

Describe the process of action potential generation in cardiac muscle cells

  1. Phase 0: Slow influx of Nafrom previous action potential gets membrane to threshold. Rapid depolarisation: voltage gated Na+ channels open, rapid influx of Na+
  2. Phase 1: 
  • Na+channels close
  • K+channels open- rapid K+ efflux out of cell. 
  • Slow Ca2+ channels open-slow influx of Ca2+ into cell.
  1. Phase 2: Slow influx of calcium prevents rapid repolarisation by Kand causes the plateau​​
  2. Phase 3: Slow Ca2+ channels close and rapid repolarisation begins by rapid efflux of Kfrom cell. (muscle contraction stops)
  3. Phase 4: K+ channels close, Na+/K+ pump returns Kto ICF and Na+ to ECF. 

5

Describe the propagation of the AP along cardiac muscle

AP travels in one direction only due to the refractory period, in which the muscle cell that generated the action potential cannot generate another one. 

Initial uslow influx of Na+ that gets membrane potential to the threshold is due to the sodium from the previous action potential. 

6

Describe the process of action potential generation in the sinoatrial node

  1. Slow influx of Naup to the threshold
  2. Rapid influx of Ca2+- depolarisation
  3. Outflow of K+- repolarisation

Phase 1 and 2 seen in action potential in cardiac muscle cells not seen in SA node. 

7

Why is the refractory period in cardiac muscle necessary?

Why is this different from skeletal muscle?

The action potential in skeletal muscle is short and does not extend to the end of muscle contraction. This allows repeated action potentials which causes a build up of muscle power and sustained muscle contraction.

The relatively long refractory period in cardiac muscle allows the cell to full repolarise as it extends to the end of muscle contraction, preventing sustained contraction. 

8

What are the 2 cardiac syncytia?

What is the role of the AV node?

Atrial and ventricular syncytia are separated by the AV node. 

 

Prevents the action potential from reaching the ventricle too quickly- coordinates contraction so that the atria contract just before the ventricles. 

9

How does the action potential cause muscle contraction?

Excitation-contraction coupling

Excitation: action potential is generated in pacemaker cells, passes along membranes of myocyte syncytium. 

Coupling: Action potential propagates along sarcolemma entering the cell via the t-tubule system. This causes Ca2+ to enter the sarcoplasm from t-tubules, sarcoplasmic reticulum and cell membrane. Intracellular Ca2+ increases.  

Contraction: Calcium facilitates the process of contraction by binding to troponin on the actin (thin) filaments. This binding causes tropomyosin to move, revealing actin binding site for myosin heads. ATP is hydrolysed by ATPase in the myosin head producing energy. Myosin heads attach to binding site on actin. 

Cycle of repeated interactions between myosin and actin is driven by hydrolysis of ATP. 

During each cycle, conformational changes in myosin heads result movement of myosin heads along actin filament. 

10

What occurs in isovolumic contraction and relaxation?

Isovolumic contraction:

  • Ventricle is contracting but volume is staying the same as the pressure has not yet exceeded that of the aorta/pulmonary arteries. 
  • Pressure increases to the point where it forces the valves open and blood is ejected from the ventricles (end of isovolumic contraction) 

Isovolumic relaxation:

  • Ventricular contraction ceases due to repolarisation
  • Aortic/pulmonary artery pressure exceeds that of ventricular pressure closing the aortic and pulmonary valves.
  • Volume remains constant as the AV valves are not yet open- ventricular pressure drops as the volume remains constant and the muscle relaxes. 

11

Which stage of the cardiac cycle are the first and second heart sounds?

1st sound: AV valve closing at the beginning of ventricular systole

2nd sound: aortic valve closing at the beginning of isovolumic relaxation

 

 

12

What occurs in stage 1 of the cardiac cycle?

  • Ventricular pressure falls below atrial pressure
  • Tricuspid and mitral valves open
  • Passive ventricular filling followed by atrial systole
    • = a wave on JVP
    • = p wave on ECG
  • Small increased in ventricular pressure as volume increases
  • Ventricular and atrial pressures equalise and mitral and tricuspid valves close. 

13

What occurs in stage 2 of the cardiac cycle?

  • Ventricular systole begins which initiates the start of isovolumic contraction (ventricular pressure increases due to contraction but volume remains the same as valves not yet open)
  • Ventricular pressure exceeds aortic and pulmonary artery pressure- aortic and pulmonary valves open, blood ejected frm ventricles
  • = QRS complex on ECG
  • = c wave on JVP (due to tricuspid bulging under back pressure)

14

What occurs in the 3rd stage of the cardiac cycle?

  • Ventricular contraction finishes, ventricular pressure falls.
  • = T wave on ECG, ventricular repolarisation
  • Aortic pressure initially follows ventricular 
  • Ventricular pressure falls below aortic pressure
  • Aortic and pulmonary valves close (dichrotic notch)

15

What occurs in the 4th stage of the cardiac cycle?

  • Ventricular pressure falls while volume remains constant (isovolumic relaxation)
  • Ventricular pressure falls below that of the atria which has been slowly rising due to venous return
    • = v wave on JVP (atrial filling) 
  • Mitral and tricuspid valves open 
  • y descent- atrial emptying 

16

What occurs in the first stage of the pressure volume loop?

Initial diastole:

MV closed, atrial filling.

Ventricular pressure decreases without volume change – isovolumic relaxation (d)

When ventricular pressure < atrial pressure, MV opens. Initial rapid ventricular filling and increase in volume (a)

17

What occurs in the second stage of the pressure volume loop?

Diastasis: following initial passive filling, blood flow slows, ventricle 70% full.

Atrial contraction

When ventricular pressure exceeds atrial, mitral valve closes. 

Ventricular systole- isovolumic contraction

 

18

What occurs in the 3rd stage of the pressure volume loop?

  • Ventricular pressure exceeds aortic pressure- aortic valve opens.
  • Rapid ejection of blood (c)
  • Accounts for first 1/3 of ejection time
  • Blood flow slows as potential energy stored in elastic walls of aorta
  • When aortic pressure exceeds ventricular, aortic valve closes

19

What is valvular disease?

  • Stenosis of valves places obstruction to ventricular outflow and a fixed cardiac output. 
    • This places excess pressure on ventricles
    • Compensation: ventricular hypertrophy
  • Regurgitation causes increased volume load (allows backflow of blood during diastole)
    • Compensation: increased sarcomere length and cavity volume, increased stroke volume and eccentric hypetrophy to compensate for further wall stress.

As valvular pathology worsens, the affected ventricle will dilate and functionally decompensate.