Cardiac cycle Flashcards

1
Q

Describe the mechanisms of excitation- contraction coupling

A

Trigger: Action potential opens L-type Ca²⁺ channels in the sarcolemma.
Calcium-Induced Calcium Release: Ca²⁺ enters and triggers release from sarcoplasmic reticulum via ryanodine receptors.
Contraction: Ca²⁺ binds troponin, enabling actin-myosin cross-bridge cycling.
Relaxation: Ca²⁺ reuptake by SERCA and extrusion via Na⁺/Ca²⁺ exchanger.

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2
Q

Describe the architecture and micro-artitecture of cardiac muscle

A

Architecture: Branched, striated fibers with intercalated discs for mechanical and electrical coupling.
Micro-architecture: Sarcomeres composed of myofilaments (actin and myosin) arranged in repeating units.

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3
Q

What is the myofilament structure? describe the individual structure of both parts?

A

Thin Filaments: Actin, troponin (T, I, C subunits), and tropomyosin.
Thick Filaments: Myosin with globular heads for ATP hydrolysis and actin binding.

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4
Q

What actin-myosin interactions and the role of troponin?

A

Troponin C: Binds Ca²⁺, causing conformational change.
Troponin I: Inhibits actin-myosin binding in the absence of Ca²⁺.
Troponin T: Anchors troponin complex to tropomyosin.
Interaction: Ca²⁺ binding exposes actin binding sites for myosin heads.

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5
Q

What is cross bridge cycle?

A

Attachment: Myosin head binds actin (cross-bridge forms).
Power Stroke: ADP + Pi released; myosin pulls actin.
Detachment: ATP binds myosin, releasing it from actin.
Reactivation: ATP hydrolysis repositions myosin head.

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6
Q

Define cardiac output

A

Definition: Volume of blood pumped by each ventricle per minute.
Formula: Cardiac Output = Heart Rate × Stroke Volume.

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7
Q

What factors are affecting cardiac output?

A

Heart Rate: Influenced by autonomic input and hormones.
Stroke Volume: Dependent on preload, afterload, and contractility.

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8
Q

What does it mean when we talk about the autonomic innervation of the heart?

A

Sympathetic: Increases heart rate (SA node) and contractility (ventricles).
Parasympathetic: Decreases heart rate via vagus nerve (SA and AV nodes).

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9
Q
A
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10
Q

Describe the mechanisms of excitation-contraction coupling

A

Trigger: Action potential opens L-type Ca²⁺ channels in the sarcolemma.
Calcium-Induced Calcium Release: Ca²⁺ enters and triggers release from sarcoplasmic reticulum via ryanodine receptors.
Contraction: Ca²⁺ binds troponin, enabling actin-myosin cross-bridge cycling.
Relaxation: Ca²⁺ reuptake by SERCA and extrusion via Na⁺/Ca²⁺ exchanger.

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11
Q

What is the architecture and micro-architecture of cardiac muscle?

A

Architecture: Branched, striated fibers with intercalated discs for mechanical and electrical coupling.
Micro-architecture: Sarcomeres composed of myofilaments (actin and myosin) arranged in repeating units.

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12
Q

What is the myofilament structure?

A

Thin Filaments: Actin, troponin (T, I, C subunits), and tropomyosin.
Thick Filaments: Myosin with globular heads for ATP hydrolysis and actin binding.

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13
Q

What are the actin-myosin interactions and role of troponin?

A

Troponin C: Binds Ca²⁺, causing conformational change.
Troponin I: Inhibits actin-myosin binding in the absence of Ca²⁺.
Troponin T: Anchors troponin complex to tropomyosin.
Interaction: Ca²⁺ binding exposes actin binding sites for myosin heads

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14
Q

Describe the cross bridge cycle

A

Attachment: Myosin head binds actin (cross-bridge forms).
Power Stroke: ADP + Pi released; myosin pulls actin.
Detachment: ATP binds myosin, releasing it from actin.
Reactivation: ATP hydrolysis repositions myosin head.

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15
Q

Define cardiac output

A

Definition: Volume of blood pumped by each ventricle per minute.
Formula: Cardiac Output = Heart Rate × Stroke Volume.

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16
Q

What factors affect cardiac output?

A

Heart Rate: Influenced by autonomic input and hormones.
Stroke Volume: Dependent on preload, afterload, and contractility

17
Q

What is the autonomic innervation of the heart?

A

Sympathetic: Increases heart rate (SA node) and contractility (ventricles).
Parasympathetic: Decreases heart rate via vagus nerve (SA and AV nodes).

18
Q

What is the effects of sympathetic and parasympathetic stimulation?

A

Sympathetic: ↑ Heart rate, ↑ force of contraction, ↓ AV nodal delay.
Parasympathetic: ↓ Heart rate, ↓ conduction velocity, ↑ AV nodal delay.

19
Q

Define valve operation, blood volume and blood pressure

A

Valve Operation: Opens/closes due to pressure differences between chambers.
Blood Volume: End-diastolic and end-systolic volumes affect stroke volume.
Blood Pressure: Maintained by cardiac output and systemic vascular resistance.

20
Q

what are the main events within the ecg? (pqrst wave)

A

P Wave: Atrial depolarization; precedes atrial contraction.
QRS Complex: Ventricular depolarization; triggers ventricular contraction.
T Wave: Ventricular repolarization; precedes ventricular relaxation.
Valve Timing:
AV valves close: Start of QRS (ventricular systole).
Semilunar valves open: During ventricular ejection.

21
Q

What are the events of the cardiac cycle?

A

Atrial Systole: Atria contract to fill ventricles.
Ventricular Systole: Ventricles contract; blood ejected into aorta/pulmonary artery.
Diastole: Chambers relax and fill with blood.

22
Q

What is the valve operation within the heart?

A

Atrioventricular (AV) Valves: Open during diastole; close during ventricular systole.
Semilunar Valves: Open during systole; close during diastole.

23
Q

What is the blood volume and pressure changes in the cardiac cycle?

A

Peaks during systole; lowest during diastole.
End-diastolic volume (EDV) and end-systolic volume (ESV) define stroke volume.

24
Q

what is the ecg correlation?

A

P Wave: Atrial depolarisation (atrial systole).
QRS Complex: Ventricular depolarisation (ventricular systole).
T Wave: Ventricular repolarisation (diastole).