Anatomy of the heart Flashcards

1
Q

Role of the heart

A

The heart pumps blood through the circulatory system, delivering oxygen and nutrients to tissues and removing waste products

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2
Q

Whats the gross structure of the heart?

A

Structure: A four-chambered organ (2 atria, 2 ventricles).
Location: Located in the thoracic cavity, between the lungs, slightly left of the midline.

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3
Q

Whats the location and role of the heart valves?

A

Valves:
Atrioventricular (AV) valves:
Tricuspid (right) and mitral (left) valves.
Prevent backflow from ventricles to atria during systole.
Semilunar valves:
Pulmonary and aortic valves.
Prevent backflow from arteries to ventricles during diastole.

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4
Q

cellular structure of cardiac muscle

A

Structure:
Striated, branched cells.
Single nucleus per cell.
Contains sarcomeres for contraction.
Abundant mitochondria for energy.

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5
Q

How are individual heart cells are coupled

A

Mechanical coupling:
Intercalated discs contain desmosomes that anchor cells together during contraction.
Electrical coupling:
Gap junctions in intercalated discs allow ions to pass, enabling synchronized contraction.

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6
Q

What ionic gradients are across the heart cell membrane?

A

Key Ions: Na⁺ (high extracellular), K⁺ (high intracellular), Ca²⁺ (high extracellular).
Resting Potential: Maintained by Na⁺/K⁺ ATPase and selective membrane permeability, with K⁺ contributing most to the resting membrane potential (~ -90 mV in ventricular cells).

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7
Q

What are the main classes of ion channels in the heart?

A

-Voltage-Gated Channels:
Na⁺ channels: Rapid depolarization.
-Ca²⁺ channels (L-type): Plateau phase and contraction.
-K⁺ channels: Repolarization and resting potential maintenance.
-Pacemaker Channels (If): Allow slow depolarization in SA node cells.
-Ligand-Gated Channels: Modulated by neurotransmitters.

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8
Q

What creates the initiation of the cardiac action potential?

A

Site: SA node (primary pacemaker).
Mechanism:
Pacemaker potential: Slow depolarization via If (Na⁺/K⁺ influx).
Threshold: Activation of Ca²⁺ channels (L-type) for rapid depolarization.
Repolarization: K⁺ efflux through voltage-gated K⁺ channels.

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9
Q

What is the ionic basis of the action potential in SA node and ventricular muscle

A

SA Node:
Phase 4: Pacemaker potential (If channels, T-type Ca²⁺ channels).
Phase 0: L-type Ca²⁺ channel activation.
Phase 3: K⁺ efflux for repolarization.
Ventricular Muscle:
Phase 0: Rapid Na⁺ influx.
Phase 1: Transient K⁺ efflux.
Phase 2: Ca²⁺ influx (plateau phase).
Phase 3: K⁺ efflux for repolarization.
Phase 4: Resting potential (K⁺ channels).

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10
Q

Describe the configuration of action potential as it spreads through the heart muscle

A

SA Node to Atria: Gradual depolarization; slower upstroke.
AV Node: Delayed conduction for ventricular filling.
Purkinje Fibers: Rapid conduction, ensuring synchronized ventricular contraction.
Ventricles: Strong, sustained action potential with prominent plateau phase for efficient contraction.

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11
Q

Describe the implications of the absolute refractory period

A

Definition: Period during which no new action potential can be initiated.
Importance:
Prevents tetany in cardiac muscle.
Ensures unidirectional propagation of the action potential.
Allows time for ventricular filling before the next contraction.

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12
Q
A
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13
Q

Whats the role of heart?

A

Role: The heart pumps blood through the circulatory system, delivering oxygen and nutrients to tissues and removing waste products.

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14
Q

Describe the gross structure of the heart

A

Structure: A four-chambered organ (2 atria, 2 ventricles).
Location: Located in the thoracic cavity, between the lungs, slightly left of the midline.

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15
Q

Describe the location and role of the heart valves

A

Valves:
Atrioventricular (AV) valves:
Tricuspid (right) and mitral (left) valves.
Prevent backflow from ventricles to atria during systole.
Semilunar valves:
Pulmonary and aortic valves.
Prevent backflow from arteries to ventricles during diastole.

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16
Q

Cellular structure of cardiac muscle

A

Structure:
Striated, branched cells.
Single nucleus per cell.
Contains sarcomeres for contraction.
Abundant mitochondria for energy.

17
Q

How are individual heart cells are coupled?

A

Mechanical coupling:
Intercalated discs contain desmosomes that anchor cells together during contraction.
Electrical coupling:
Gap junctions in intercalated discs allow ions to pass, enabling synchronized contraction.

18
Q

What are the ionic gradients across the heart cell membrane?

A

Key Ions: Na⁺ (high extracellular), K⁺ (high intracellular), Ca²⁺ (high extracellular).
Resting Potential: Maintained by Na⁺/K⁺ ATPase and selective membrane permeability, with K⁺ contributing most to the resting membrane potential (~ -90 mV in ventricular cells).

19
Q

What are the main classes of ion channels in the heart?

A

Voltage-Gated Channels:
Na⁺ channels: Rapid depolarization.
Ca²⁺ channels (L-type): Plateau phase and contraction.
K⁺ channels: Repolarization and resting potential maintenance.
Pacemaker Channels (If): Allow slow depolarization in SA node cells.
Ligand-Gated Channels: Modulated by neurotransmitters.

20
Q

Describe the initiation of the cardiac action potential

A

Site: SA node (primary pacemaker).
Mechanism:
Pacemaker potential: Slow depolarization via If (Na⁺/K⁺ influx).
Threshold: Activation of Ca²⁺ channels (L-type) for rapid depolarization.
Repolarization: K⁺ efflux through voltage-gated K⁺ channels.

21
Q

What is the ionic basis of the action potential in as node and ventricular muscle?

A

SA Node:
Phase 4: Pacemaker potential (If channels, T-type Ca²⁺ channels).
Phase 0: L-type Ca²⁺ channel activation.
Phase 3: K⁺ efflux for repolarization.
Ventricular Muscle:
Phase 0: Rapid Na⁺ influx.
Phase 1: Transient K⁺ efflux.
Phase 2: Ca²⁺ influx (plateau phase).
Phase 3: K⁺ efflux for repolarization.
Phase 4: Resting potential (K⁺ channels).

22
Q

describe the configuration of the action potential as it spreads through the heart muscle

A

SA Node to Atria: Gradual depolarization; slower upstroke.
AV Node: Delayed conduction for ventricular filling.
Purkinje Fibers: Rapid conduction, ensuring synchronized ventricular contraction.
Ventricles: Strong, sustained action potential with prominent plateau phase for efficient contraction.

23
Q

the definiton and implications of the absolute refractory period

A

Definition: Period during which no new action potential can be initiated.
Importance:
Prevents tetany in cardiac muscle.
Ensures unidirectional propagation of the action potential.
Allows time for ventricular filling before the next contraction.

24
Q

definition of dysrhythmias

A

Dysrhythmias: Abnormal heart rhythms caused by disturbances in electrical activity of the heart, affecting rate, rhythm, or conduction.

25
Q

Types of dysrhythmias

A

Bradycardia: Slow heart rate (<60 bpm).
Causes: SA node dysfunction, AV block.
Tachycardia: Fast heart rate (>100 bpm).
Causes: Increased sympathetic tone, ectopic pacemaker activity.
Fibrillation: Disorganized electrical activity.
Atrial fibrillation (AF): Rapid, irregular atrial activity.
Ventricular fibrillation (VF): Life-threatening; uncoordinated ventricular contractions.
Heart Block: Impaired conduction between atria and ventricles.
First-degree: Prolonged PR interval.
Second-degree: Intermittent conduction failure.
Third-degree: Complete block; atria and ventricles beat independently.

26
Q

What are the mechanisms of dysrhymias?

A

Abnormal automaticity: Ectopic pacemaker activity (e.g., ischemia, hypoxia).
Triggered activity: Afterdepolarizations due to ion channel dysfunction (early or delayed).
Reentry circuits: Circular propagation of impulses (e.g., AV nodal reentrant tachycardia).

27
Q

What are the risk factors of dysrhythmias

A

Structural heart disease (e.g., myocardial infarction, cardiomyopathy).
Electrolyte imbalances (e.g., K⁺, Mg²⁺).
Drugs (e.g., antiarrhythmics, stimulants).
Systemic conditions (e.g., thyroid disorders, fever)

28
Q

What is treatment for dysrhythmias ?

A

Lifestyle modifications: Reduce triggers (e.g., caffeine, stress).
Pharmacological:
Beta-blockers (rate control).
Antiarrhythmics (e.g., amiodarone, flecainide).
Non-Pharmacological:
Electrical cardioversion.
Pacemaker or defibrillator implantation.
Catheter ablation (for reentry circuits).