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Summary of Heart Failure and Therapy (AB_1211) - minor Biomedical Topics in Health Care €6,96
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  3. Vrije Universiteit Amsterdam (VU)
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  5. Heart Failure and Therapy (AB_1211)

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Summary of Heart Failure and Therapy (AB_1211) - minor Biomedical Topics in Health Care
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Summary of the course Heart Failure and Therapy; part of the minor Biomedical Topics in Health Care. This course aims to provide insights into the pathophysiologic mechanisms, diagnostic approaches and therapies and societal impacts of cardiovascular diseases. Cardiac diseases that will be highligh...

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  • 4 januari 2025
  • 29
  • 2023/2024
  • Samenvatting

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Voorbeeld van de inhoud

Heart Failure and Therapy

Lecture 1. Physiology of the cardiovascular system.
- 1.1 excitation-contraction coupling
- 1.2 cardiac cycle

1.1
- pumping deoxygenated blood to the lungs:
o RA, TV, RV, PV, PA, lungs
- Pumping oxygenated blood to all organs in the body:
o LA, MV, LV, AV, aorta, body




→ to provide adequate perfusion of all organs + tissues of the body.

X Function of the heart:
Contraction and relaxation determine cardiac output.
- Cardiac output: pumping activity of the heart = stroke volume x heart rate.
→ realized by 2-3 billion cardiomyocytes.

X Excitation-contraction coupling
= coupling between myocyte action potentials and contraction.

When an action potential causes depolarization of a myocyte, it initiates excitation-
contraction coupling. When a myocyte is depolarized, calcium ions enter the cell during the
action potential through long-lasting calcium channels.

,X automation of the heart
The heart can also beat without input from the central nervous system. The heart has a
natural rhythm of 100bpm, because of its pacemaker cells.
→ The heart rate is determined by these specialized cells within the heart that act as
electrical pacemakers, and their activity is increased or decreased nu autonomic nerves and
hormones. The action potentials generated by these pacemaker cells are conducted
throughout the heart and trigger contraction of cardiac myocytes → results in ventricular
contraction and ejection of blood.

Resting membrane cannot be regulated (threshold), but your starting point can be regulated.
So you can create an action potential earlier, so you raise your heart rate. → reduced
repolarization. ((nor)adrenaline), which opens your sodium channel → to raise the
prepotential → channels open earlier.

Decreasing heart rate: acetylcholine, does the opposite to adrenaline → it opens the
potassium channels → it will take longer to reach the threshold.

X pacemaker cells
Pacemakers have specific action potentials → sodium enters, calcium enters, potassium
leaves.
Ions that enter are higher outside than inside, and those that leave the cell are higher on the
inside than on the outside.

→ Opening and closing of ion channels generate action potentials.

two general types of ion channels exist:
- Voltage-gated ion channels: open and close in response to changes in membrane
potential → channels involved in cardiac action potentials.
- Receptor-gated ion channels: open and close in response to chemical signals
operating through membrane receptors.

The response of the activation and inactivation gates occurs when the resting membrane
potential is normal (about -90mV) and a rapid depolarization of the membrane occurs, as
happens when a normal depolarization current spreads from one cardiac cell to another
during electrical activation of the heart.

X action potentials
Action potentials occur when the membrane potential suddenly depolarizes and then
repolarizes back to its resting state.
→ Nonpacemaker action potentials are triggered by depolarizing currents from adjacent
cells, whereas pacemaker cells are capable of spontaneous action potentials generation.

, X pacemaker action potentials
Pacemaker cells:




Step 1. Sodium enters the cell (sodium channel opens) → during resting membrane.
Sodium is positive → membrane potential more positive. Until they reach a threshold. Which
is depended by calcium.
Step 2. Calcium senses the membrane potential → they open when the membrane potential
rises above -40mV. When it is too positive they close.
Step 3. Potassium will leave the cell.

Pacemaker cells have no true resting membrane potential, but instead generate regular,
spontaneous action potentials → unlike most other cells that exhibit action potentials, the
depolarizing current of the action potential is carried primarily by relatively slow, inward
Calcium currents instead of by fast sodium currents.
The rate of depolarization is relatively slow compared to nonpacemaker cells.

SA nodal action potential are divided into three phases:
- Phase 0: upstroke of the action potential → depolarization due to increased calcium;
These voltage-operated channels open when the membrane is depolarized to a
threshold voltage of about -40mV.
- Phase 3: the period of repolarization → Depolarization causes voltage-operated,
delayed rectifier potassium channels to open, and the increased gK+ repolarizes the
cell toward the equilibrium potential for K+. At the same time, the slow inward
calcium channels that opened during phase 0 becomes inactivated, thereby
decreasing gCa++ and contributing to the repolarization. Phase 3 ends when the
membrane potential reached about -65mV. The phase of repolarization is self-limited
because the potassium channels begin to close again as the cell becomes repolarized.
- Phase 4: the period of spontaneous depolarization that leads to subsequent
generation of a new action potential → gK+ is still declining . This fall in gK+
contributes to depolarization. This depolarizing current involves, in part, a slow
inward movement of sodium. In the second half of phase 4, there is a small increase
in gCa++. As the depolarization begins to reach threshold, L-type calcium begin to
open, causing a further increase in gCa++ until threshold is reached and phase 0 is
initiated.

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