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Block 2 > The Heart As An Electrical Pump > Flashcards

The Heart As An Electrical Pump Flashcards

1
Q

How are cardiac myocytes arranged? Why?

A

Into syncytium of cells which branch + interdigitate

Intercalated disks provide mechanical + electrical interconnection between myocytes

-> low threshold all or nothing response with rapid propagation of electrical activity

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2
Q

What makes up myocytes?

A

Composed of myofibrils which contain myofilaments (actin + myosin)

Myofilament interdigitation forms repeating microanatomical units (sarcomeres)

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3
Q

What aspect of myocytes is responsible for contraction? How does contraction occur?

A

Sarcomeres

Slide along each other shortening the muscle during contraction

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4
Q

What is a sarcomere?

A

Region of myofibril between 2 Z lines

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5
Q

What is a sarcomere made up of?

A

Thick (myosin) + thin (actin) myofilaments which interdigitate

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6
Q

What aspects of the heart are involved in the conduction system in order of where electrical activity begins in the left atrium?

A 
Sino-Atrial (SA) node
Atrio-ventricular (AV) node
Bundle of His
L bundle branch
R bundle branch
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7
Q

Why is the Sinoatrial (SA) node important?

A

Source of action potential that drives cardiac contraction in normal individuals

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8
Q

Why is the Atrio Ventricular (AV) node important?

A

Delays the passage of electrical activity between atria + ventricles to ensure coordinated chamber contraction

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9
Q

What happens if the Sinoatrial (SA) node stops working?

A

Another conductor will take over; AV node -> Bundle of His etc.

The lower you get in the conduction system, the slower the replacement rhythm generator is

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10
Q

What is the Sinoatrial (SA) node?

A

Primary pacemaker but any muscle cell can take over this role

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11
Q

What are the features of Sinoatrial (SA) node cells?

A

Modified muscle cells characterized by:

  • No true resting potential
  • Generation of regular + spontaneous APs
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12
Q

What is pacemaker activity usually like?

A

Spontaneously generated

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13
Q

What can modify pacemaker activity?

A

Autonomic nerves (e.g. SNS), hormones or drugs

Ions, ischaemia or hypoxia

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14
Q

What ion movements occur during an action potential (AP)?

A
  1. Slow influx of Na+ from adjacent AP (prepotential)
  2. Threshold membrane potential reached
  3. Rapid influx of Ca2+ (depolarization)
  4. Outflow of K+ (repolarization)
  5. Membrane potential drops below threshold
  6. Refractory period in this cell + cycle starts again in next adjacent muscle cell
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15
Q

How are the ion concentrations of Na+ and K+ maintained in the ECF and ICF?

A

Na+/K+ return Na+ to the ECF and K+ to ICF returning concentrations back to baseline after an AP

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16
Q

How are action potentials (APs) propagated?

A
  1. Change in potential difference across the cell surface
  2. Reaches AP threshold
  3. AP modifies adjacent membrane by cytosolic ion flux (movement facilitated by desmosomes) in direction opposite to refractory zone
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17
Q

Why is it not possible for action potentials (APs) to move backwards along the muscle cells?

A

Refractory period where cells that have just experienced an AP, cannot have another one for a short period of time

18
Q

What is the difference between refractory periods in skeletal and cardiac muscle?

A

Skeletal: does not extend long or much into contraction so APs + contractions can occur rapidly causing a build-up of muscle taut (sustanic state)

Cardiac: longer extending to end of contraction i.e. cannot contract muscle until one contraction is done

19
Q

What are the 2 myocardial syncytia and what separates them?

A

Atrial + ventricular

Separated by AV node

20
Q

What is excitation-contraction coupling?

A

Excitation: AP originates in SA node pacemaker cells + passes along myocyte syncytium membranes

Coupling: membrane depolarization initiates release of Ca2+ into myocyte cytoplasm

-> Ca2+ facilitates CONTRACTION

21
Q

How does the coupling process increase intracellular calcium concentration?

A

AP propagates along sarcolemma + enter cells via T tubule system -> Ca2+ enters sarcoplasm from T-tubules, SR + cell membrane = increased [Ca2+]ic

22
Q

How can increased intracellular calcium concentration cause muscle contraction?

A
  1. Ca2+ binds troponin on thin actin filament
  2. Tropomyosin moves revealing an actin binding site for myosin heads
  3. ATP is bound + hydrolysed to ADP via ATPase in myosin head providing energy
  4. ATP hydrolysis drives repeated cycle of interaction between myosin heads + actin
  5. Conformational changes in myosin result in movement of myosin heads along actin filaments
  6. Movement causes muscle fibre shortening
23
Q

What is calciums role within the heart?

A

[Ca2+]ec determines strength of cardiac muscle contraction

24
Q

What happens to calcium concentration in the extracellular fluid at the end of an action potential?

A

Ca2+ flow reversed (back into SR + T-tubules via Ca/Mg ATPase) which stops actin-myosin interaction causing relaxation

25
Q

How does blood pass through the heart?

A

SVC -> R atrium -> tricuspid valve -> R ventricle -> pulmonary valve -> pulmonary artery -> pulmonary system (lungs) -> pulmonary vein -> L atrium -> mitral valve -> L ventricle -> aortic valve -> aorta -> systemic system

26
Q

What are the steps of the cardiac cycle?

A
  1. Ventricular pressure falls below atrial pressure
  2. MV + TV open
  3. Passive ventricular filling
  4. Atrial systole (corresponds to ‘a’ wave on JVP + P ECG wave)
  5. Small ‘hump’ in L ventricular pressure due to volume increase
  6. Ventricular + atrial pressure equalize so MV + TV close
  7. QRS ECG complex
  8. Isovolumic ventricular contraction causes big increase in ventricular pressure above that of great vessels
  9. AV + PV open so blood flows into aorta + PA
  10. ‘c’ wave on JVP (tricuspid bulging back due to pressure)
  11. Ventricular contraction finishes + pressure falls
  12. Aortic pressure follows ventricular
  13. T ECG wave (ventricular repolarisation)
  14. Ventricular pressure falls below aortic pressure
  15. AV + PV shut at beginning of dichrotic notch
  16. Ventricular isovolumic relaxation
  17. Ventricular pressure falls below atria which has been slowly rising due to venous return
  18. ‘v’ wave on JVP (atrial filling)
  19. MV + TV open
  20. ‘y’ descent (atrial emptying)
27
Q

What does a pressure volume loop of left ventricular pressure (y-axis) and volume (x-axis) show?

A
  1. Initial diastole when the MV is closed + L atrium is filling
  2. Ventricular isovolumetric relaxation
  3. When ventricular pressure < atrial pressure MV opens
  4. Initial rapid ventricular filling + sharp increase in volume
  5. Diastasis
  6. Atrial contraction
  7. Ventricular isovolumetric contraction
  8. When ventricular > atrial pressure MV closes
  9. AV opens when ventricular > aortic pressure
  10. Rapid ejection of blood accounting for 1st 1/3rd of ejection time
  11. Blood flow slows as potential energy stored in elastic walls of aorta
  12. Aortic > ventricular pressure so AV closes
28
Q

What does valve stenosis cause? What is its compensation?

A

Ventricular outflow obstruction (i.e. restriction to forward flow into systemic circulation) + fixed CO placing pressure load on the ventricle so ventricles hypertrophy

29
Q

What does regurgitation cause? What is its compensation?

A

Increased volume load (due to backflow) so there is increased sarcomere length + cavity volume, increases SV + eccentric hypertrophy to compensate for further wall stress

30
Q

What happens to the affected ventricle as valvular pathology worsens?

A

Will functionally decompensate + dilate

31
Q

What are the 4 heart sounds and what causes them?

A

S1: MV + TV closure

S2: AV + PV closure

S3: Rapid passive phase of ventricular filling (coincides with ‘y’ descent in JVP)

S4: Atrial contraction phase of ventricular filling (coincides with ‘a’ atrial systole wave in JVP)

32
Q

What will mitral stenosis sound like?

A

Opening snap + loud 1st heart sound that both quieten as valve becomes rigid

Low frequency diastolic rumble

Does not radiate but palpable thrill at apex in severe disease

33
Q

What can cause mitral stenosis?

A

Rheumatic fever
Sclerosis
Endocarditis
Congenital disease

34
Q

What can occur in mitral stenosis?

A

Reduction in flow + increased ventricular filling time -> pulmonary hypertension -> L atrium increases in size -> increased tendency for atrial arrhythmia

35
Q

What can exacerbate mitral stenosis?

A

Increased HR

36
Q

Why can atrial fibrillation by catastrophic in stenotic patients?

A

As they are dependent for atrial kick for ventricular filling

37
Q

What can cause mitral regurgitation?

A

Degenerative
Rheumatic
Congenital prolapse (esp. Marfans syndrome)
MI + chordae tendinae rupture (acute emergency)

38
Q

What sound can occur in aortic stenosis?

A

Midsystolic murmur may radiate to carotid pulse

39
Q

What causes aortic regurgitation?

A 
Endocarditis
Marfan's disease
Ankylosing spondylitis
Dissection
Trauma
40
Q

What will aortic regurgitation sound like?

A

Early diastolic murmur + high pitched

Block 2 (45 decks)

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