Lecture 19 : Anatomy & Electrical Properties of the Heart Flashcards

1
Q

Describe the flow of blood through the CVS from when blood first enters the heart:

A

Heart:
1. Right atrium
2. Right AV (tricuspid) valve
3. Right ventricle
4. Pulmonary valve
Pulmonary circuit:
1. Pulmonary trunk
2. Pulmonary arteries
3. Capillaries of lungs
4. Pulmonary veins
Heart:
1. Left atrium
2. Left AV (bicuspid) valve
3. Left ventricle
4. Aortic valve
Systemic circuit:
1. Aorta
2. Arteries
3. Arterioles
4. Capillaries
5. Venules
6. Veins
7. Venae cavae

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2
Q

Name the 2 main cardiac cells:

A
  1. Contractile myocardial cells
  2. Nodal tissue (SA & AV node)
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3
Q

What are contractile myocardial cells?

A
  • Arranged in layers, associated at the intercalated disc, and form the bulk of the atria and ventricles
  • All myocardial cells contract with every beat due to gap junctions
  • Filaments of actin and myosin are arranged with a striated appearance
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4
Q

Describe the role of gap junctions within the contractile myocardial cells:

A
  • Low electrical resistance
  • Present in the intercalated disc
  • Allows the passage of ions and small molecules of up to 1KDa
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5
Q

What is nodal tissue?

A
  • 1% of the cardiac cells
  • Contains small round cells with no, or little, contractile protein
  • Specialised for the generation and conduction of action potentials in the atria
  • Gap junctions are present
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6
Q

Where are action potentials generated in the heart?

A

Sino-atrial (SA) node - pace maker of the heart

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7
Q

How do action potentials spread around the heart?

A

Spread from cell to cell by gap junctions determined by the location of intercalated discs

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8
Q

What structure do action potentials have to pass through to get to the ventricles?

A

Atrioventricular ring via AV node

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9
Q

How fast are APs generated at the SA node?

A

100-110 min-1

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10
Q

How fast is an AP conducted through atrial muscle?

A

~0.5 ms-1

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11
Q

How fast is an AP conducted through the AV node and what is the role of this?

A

Slowly ~0.05 ms-1
* Provides a delay for full depolarisation and contraction of the atria before the ventricles are depolarised

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12
Q

How fast are APs conducted through the bundle of His, bundle branches, and Purkinje system?

A

Rapidly ~5 ms-1

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13
Q

How fast are the APs spread at the ventricular myocardium?

A

~0.5 ms-1

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14
Q

What is the purpose of the speed of the APs from the bundle of His to the ventricular myocardium?

A

Allows synchronous depolarisation and contraction of all regions of the ventricles

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15
Q

Describe the basis of resting and action potentials:

A

The resting membrane potential (RMP) of nodal and myocardial cells depends upon a high resting permeability to K+
(PK )
- K+ moves out of cell making inside more negative

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16
Q

What is the PK and RMP of nodal tissue relative to myocardial cells?

A
  • PK is lower in nodal tissue than myocardial cells and the RMP is less negative
  • The RMP of the SA nodal cells is unstable
17
Q

What occurs to PK within pacemaker cells:

A

PK gradually reduces, and this combined with an increasing permeability to Na+ and Ca2+, causes the gradual decrease in RMP

18
Q

What is the gradual decrease in RMP in pacemaker cells called?

A

This slow depolarisation is called the pacemaker potential

19
Q

What happens when threshold voltage is reached in a pacemaker cell?

A

Other Ca2+ channels open, and a relatively ‘slow’ AP occurs
- A similar AP occurs in AV nodal cells
- Other cells may spontaneously depolarise -> ectopic pacemakers/arrhythmias

20
Q

Describe the action potentials within ventricular cells:

A
  • PK is higher and hence the RMP is more negative
  • Depolarization phase of AP is due to the opening of the voltage-gated Na+ channels
21
Q

Describe the process of excitation contraction coupling:

A
  • “Excitation” - depolarisation of plasma membrane
  • Opening of plasma membrane, L-type Ca2+ channels in T-tubules
  • Flow of Ca2+ into cytosol
  • Ca2+ binds to Ca2+ receptors (ryanodine receptors) on the outside of the sarcoplasmic reticulum
  • Opening Ca2+ channels intrinsic to these receptors
  • Flow of Ca2+ into cytosol
  • Increase cytosolic Ca2+
  • Calcium triggers contraction (via troponin) - contraction lasts for as long as the plateau of the AP
  • Normally about 30% maximal effect -> if more calcium can get stronger contraction
22
Q

What is a refractory period?

A

A time between which an AP arrives at the cell to trigger contraction and the next AP arriving at the cell

23
Q

What do long absolute and relative refractory periods prevent?

A
  • Prevent re-excitation of heart muscle during most of the contraction period
  • Also prevent circuitous recycling of the action potential
24
Q

Does tetanus normally occur in heart muscle?

A

No - summation of contractions isn’t possible

25
Q

What is an ECG?

A

A recording of potential changes at the skin surface that result from the depolarization and repolarization of the heart muscle

26
Q

What are the different waves on an ECG?

A

P - Atrial depolarisation; precedes atrial contraction
QRS - Ventricular depolarisation; precedes ventricular contraction
T - Ventricular repolarization; ventricular relaxation

27
Q

What are the electrical events causing the ECG?

A
  • Depolarisation toward +ve electrode = +ve bump
  • Depolarisation away from +ve electrode = -ve bump
  • Repolarisation away from +ve electrode = +ve bump
  • Shape of waves depends where you “look at” heart from
28
Q

What is Einthoven’s triangle?

A

LA-RA = lead I
LL-RA = lead II “classic” ECG
LL-LA = lead III

29
Q

What are the augmented leads?

A
  1. Lead AVL heart from left shoulder; left free wall
  2. Lead AVR heart from right shoulder; cavity of the heart
  3. Lead AVF heart from foot; inferior surface of the heart