Cardio Introduction Flashcards
What are the functions of the cardiovascular system?
- Transports oxygen and nutrients to the cells
- Removes waste products from the body
- Transports hormones
- Maintain body temperature through homeostasis
Characteristics of Cardiac Muscle Cells
- Intercalating bundles of cardiac muscle arranged spirally around the circumference of the heart
- Abundance of mitochondria
- Receive rich blood supply
- Joined at Intercalating discs
Function of the Spiral muscle fiber arrangement
So that when the ventricles contract, a wringing effect is exerted. This ensures that the pressure exerted on the blood within the enclosed chambers would be directed upwards toward the major arteries that exit at the base of the ventricles.
Function of intercalating discs
When one of the cardiac cells spontaneously undergo action potential, the electrical impulse spreads to all other cells, allowing them to contract as a single, functional syncytium.
What are the mechanisms that cause pacemaker potentials?
- Na+ entry through funny channels
- Progressive reduction of passive efflux of K+
- Increased Ca2+ entry through T-type Ca2+ channels
Describe the events that occur in the pacemaker activity of cardiac autorhythmic cells
A: Na+ funny channels open in response to hyperpolarisation. This allows Na+ to enter, causing slow depolarisation to threshold. K+ permeability is low.
B: As the potential begins to reach to threshold, T-type Ca2+ channels open as Na+ funny channels begin to close. This allows Ca2+ to enter the cell, causing depolarisation to threshold.
C: At threshold, T-type Ca2+ channels close. L-type Ca2+ channel opens, causing a large and quick influx of Ca2+, resulting in rapid depolarisation of the membrane
D: At the peak of the action potential, the L-type Ca2+ channels close, which causes the permeability of K+ to increase. This results in K+ efflux due to rapid repolarisation.
Explain how the SA node is the main pacemaker of the heart
- SA node has the fastest rate of autorhythmicity
- When heart becomes excited, it triggers the contractile cells to contract and the heart to beat at the pace set by SA node.
- Other autorhythmic tissues cannot assume their own naturally slower rates because they are activated by action potentials that originate from the faster SA node, before they can reach threshold.
What are the criterion for efficient cardiac function
- Atrial contraction should complete before onset of ventricular contraction. This is to allow complete ventricular filling
- Excitation of cardiac muscle fibers should be. coordinated to ensure that each heart chamber contracts as a unit. This is to ensure a smooth, uniform ventricular contraction, which is essential to squeeze out the blood.
- Atrias and ventricles should be functionally coordinated to ensure that each heart chamber contracts as a unit.
What happens if atrial and ventricular contraction occur simultaneously?
- AV valves would close immediately because ventricular pressure far exceeds the atrial pressure as the walls of the ventricles are thicker.
- As a result, the contracted atrium cannot squeeze blood into the ventricles because the valves only permit one-way flow of blood.
- This results in decreased cardiac output
What happens if there is unsynchronised contraction of the cardiac muscle
Fibrillation will occur, which would cause inefficient filling of the heart, causing a reduction of cardiac output.
Characteristics of electrical conduction through the heart
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Atrial excitation
* *-Interatrial pathway** as wave of excitation can spread across gap junctions through the left atrium while excitation is spreading through the right atrium. This ensures that the atrium contracts simultaneously.
* *-Internodal pathway** which extends from SA node to AV node. The only way an action potential in the atria can spread to ventricles is by passing through the AV node. This ensures that there is sequential contraction of ventricles after the atria contracts. - Slow conduction between atria and ventricles (AV nodal delay)
- Allows atria to become completely depolarised and contract, emptying contents into the ventricles before ventricular depolarisation and contraction occurs. -
Ventricular excitation as the impulse travels rapidly down the septum via left and right bundle branches and throughout the ventricular myocardium via purkinje fibers
- Specialised for rapid propagation of action potentials
- Hastens and coordinates spread of ventricular excitation to ensure that ventricles contract as a unit
What happens if ventricular depolarisation depended on spread of impulse via gap junctions?
Ventricular tissue right next to the AV node would contract before the impulse is passed to the apex, causing inefficient pumping.
What are the events of action potential in cardiac contractile cells
A: During the rising phase of the action potential, voltage-gated Na+ channels open and Na+ enters the cell rapidly. Membrane potential goes from -90mV to -70mV (threshold) and rapid depolarisation occurs at threshold potential.
B: At peak potential, Na+ permeability plummets while Transient K+ channels opens. This allows K+ to move out of the cell. This causes a brief, small repolarisation as membrane becomes slightly less positive.
C: At the plateau phase, 2 voltage-dependent permeability changes occur. Activation of L-type Ca2+ channels that cause slow, inward diffusion as Ca2+ is in a greater concentration in the ECF. This prolongs the positivity inside the cell, thus primarily responsible for plateau part of the action potential. K+ permeability also decreases as the transient and leaky K+ channels close. This prevents rapid repolarisation and prolongs the plateau phase
D: Rapid repolatisation occurs as Ca2+ channels become inactivated while there is a delayed activation of voltage-gated K+ channels. Inward movement of Ca2+ decreases while there is a rapid outward diffusion of K+
E: As membrane returns to its resting potential, voltage-gated K+ channels begin to close while leaky K+ channels begin to open.
Describe how action potential results in contraction of the cardiac muscle
- Action potential travels down the transverse tubules, where L-type Ca2+ channels can mostly be found.
- Ca2+ diffuses into the cytosol from ECF across the T-tubule membrane, triggering the sarcoplasmic reticulum to release a large amount of Ca2+
- There is a further increase of cytosolic Ca2+
- Ca2+ binds to troponin-tropomyosin complex (similar to skeletal muscle). This allows cross-bridge cycling, resulting in contraction
Identify the stages in the cardiac cycle
- Mid Ventricular Diastole
- Late Ventricular Diastole
- End Ventricular Diastole
- Onset of Ventricular Systole
- Isovolumetric Ventricular Contraction
- Ventricular Ejection
- End of Ventricular Systole
- Onset of Ventricular Diastole
- Isovolumetric Ventricular Relaxation
- Ventricular Filling
- Atrial Repolarisation and Ventricular Depolarisation occur simultaneously
Identify the events occurring at each point in the cardiac cycle (Points 1-24)
1. Atrial pressure slightly higher than the ventricular pressure as the AV valve opens so that blood flows from the atrium to the ventricle throughout filling phase of ventricular diastole
2. Ventricular volume begins to rise before atrial contraction takes place
3. SA node reaches threshold and fires, causing P wave to appear on the ECG
4. Atrial pressure increases as atrial depolarisation causes atrial contraction
5 and 6. Blood begins to be added to the ventricle as atria contracts, elevating the ventricular and atrial pressure
7. The maximum amount of blood left in the ventricle at the end of diastole is the EDV
8. Ventricular excitation is represented by QRS complex in the ECG and induces ventricular contraction
9. Ventricular pressure sharply increases, indicating the onset of ventricular systole. When the ventricle begins to contract, the ventricular pressure exceeds the atrial pressure, forcing the AV valve shut.
10. The ventricle briefly remains a closed chamber after the AV valves shut and before the aortic valves open. As a result, no blood can enter or leave the ventricle
11. This results in the volume of blood in the left ventricle to remain the same.
12. When ventricular pressure exceeds aortic pressure, aortic valve is forced open, ejection of blood begins. The amount of blood pumped out of the ventricle at each contraction is called the stroke volume.
13. Aortic pressure rises as blood is forced into the aorta from the ventricle faster than draining the blood. This phase is called the ejection phase.
14. As the blood is being pumped out, the volume of blood in the ventricle begins to fall.
15. End systolic volume is the amount of blood at the end of systole when ejection is complete.
16. T wave indicates ventricular repolarisation at the end of ventricular systole
17. As the ventricle repolarises and start to relax, ventricular pressure falls below aortic pressure, causing the aortic valve to close
18. Close of aortic valve produces a dicrotic notch on the aortic pressure curve
19. Ventricular pressure still exceeds atrial pressure. This means that all the valves are closed again. This is known as isovolumetric ventricular relaxation as there is no change in the blood volume.
20. The length of the muscle fibers remain constant
21. AV valve opens as ventricular pressure falls below atrial pressure and ventricular filling occurs again.
22. Blood flows from pulmonary veins into left atrium as the atrium is in diastole during ventricular systole. The incoming blood pooling in the left atrium causes the atrial pressure to rise
23. When the AV valve opens at the end of ventricular systole, blood that accumulated in the atrium empties into the ventricle. This causes rapid ventricular filling.
24. As the pressure begins to decrease, ventricular filling slows down. Blood continues to flow from pulmonary veins into the left atrium and through the open AV valve into the left ventricles.
