Cardiovascular System pt 2

Conduction System of the Heart

• Heart contraction relies on electrical stimulation of myocardial cells.

Key Components of the Conduction System

• Sinoatrial (SA) Node:

  • Acts as the heart’s pacemaker, initiating depolarization of the atria.

• Atrioventricular (AV) Node:

  • Passes depolarization signals to the ventricles.

  • Includes a brief delay allowing for ventricular filling.

• Bundle Branches:

  • Conduct impulses to the left and right ventricles.

• Purkinje Fibers:

  • Extend throughout the ventricles, allowing both atria to receive signals at the same time.

Cardiac Electrical Conduction

1. Sinoatrial (SA) Node:

   • Generates electrical impulses, acts as the "pacemaker" of the heart, and is autorhythmic.

   • Regulates atrial depolarization rate.

2. AV Node & Bundle of His:

   • Serves as the sole pathway for impulse transmission from atria to ventricles.

   • Controls ventricular depolarization rate and facilitates rapid impulse transmission.

Right & Left Bundle Branches

3. Right & Left Bundle Branches:

   • The AV bundle splits into two branches down the interventricular septum, facilitating rapid impulse transmission.

4. Purkinje Fiber Network:

   • Completes transmission of impulses to myocardial cells, causing ventricular depolarization and contraction.

Summary of Cardiac Conduction Components

• SA Node

• AV Node & AV Bundle

• Right and Left Bundle Branches

• Purkinje Fiber Network

Regulation of Heart Rate

• Autonomic Nervous System (ANS) plays a key role in regulating heart rate (HR):

  • Influenced by factors such as stress hormones (epinephrine), caffeine, and aging.

• The SA node has a self-depolarization capacity, but its rate is influenced by various external factors.

Abnormal Cardiac Rhythms

• Normal

• Atrial Fibrillation (A-Fib)

• Bradycardia

• Tachycardia

• Ventricular Fibrillation (V-Fib)

Electrocardiogram (ECG or EKG)

• Monitors electrical activity during one heartbeat and can identify heart problems such as arrhythmias and past heart attacks.

• P wave: Indicates atrial depolarization.

• PR segment: Time for impulse travel through AV node, Bundle Branches, and Purkinje network.

• QRS complex: Represents ventricular depolarization.

• T wave: Reflects ventricular repolarization.

Factors Affecting Blood Volume Delivery

• Cardiac Output (Q) is determined by:

  • Heart Rate (HR): Rates can increase demand for oxygen 15-25 times during intense exercise compared to rest.

  • Stroke Volume (SV): More blood per heartbeat impacts overall blood delivery.

Formula:

• Q = HR x SV

Cardiac Output Regulation

• Affected by:

  • Contraction Strength

  • End-Diastolic Volume (EDV)

  • Mean Arterial Pressure (MAP)

  • Parasympathetic and Sympathetic Nerves

  • Frank-Starling Mechanism (the principle that increased preload results in increased contraction strength).

Factors Regulating Stroke Volume (SV)

1. Venous Return:

   • Refers to blood returning to the heart from peripheral veins. Increased venous return elevates SV.

2. Frank-Starling Law:

   • As ventricular stretch increases (preload), stronger contractions occur, boosting SV.

3. Plasma Volume:

   • Dehydration reduces plasma volume, subsequently lowering venous return and ventricular filling pressure, which decreases EDV and preload.

4. Ventricular Filling Time:

   • At a Resting Heart Rate (RHR) of 70 bpm, one cardiac cycle lasts 0.8 seconds (0.5 seconds for filling and 0.3 seconds for ejection).

5. Ventricular Chamber Size:

   • Greater chamber size can accommodate larger volumes of blood, thus increasing SV.

Frank-Starling Mechanism

• States that increased filling leads to a stronger contraction, resulting in a more forceful ejection of blood per heartbeat.

Blood Flow and Resistance

• Blood flow (BF) is directly proportional to pressure difference across the system and inversely proportional to resistance.

Factors Impacting Resistance

• Length of vessel

• Viscosity of blood

• Vessel radius (radius is the primary factor affecting resistance).

Mean Arterial Pressure (MAP)

• MAP, cardiac output, and total peripheral resistance (TPR) determine blood flow from the heart to tissues.

• Increases in CO or TPR raise blood pressure (BP).

• Note: Decrease in vessel radius (vasoconstriction) raises resistance; increase in radius (vasodilation) lowers resistance.

Neural Control of Heart Rate

• The Central Nervous System coordinates heart rate and blood pressure.

• Sympathetic Nervous System (SNS): Increases HR and BP through norepinephrine release.

• Parasympathetic Nervous System (PNS): Decreases HR via the vagus nerve, keeping it below 100 bpm.

Peripheral Control Mechanisms

1. Mechanical receptors: Sense changes in blood pressure and volume.

2. Chemical receptors: Monitor blood gases and pH levels.

3. Thermoreceptors: Detect temperature deviations in the body.

Parasympathetic Control

• Achieved via the vagus nerve to slow HR at rest.

• Acetylcholine acts on the SA and AV nodes, facilitating parasympathetic tone.

Sympathetic Control

• Stimulates HR above 100 bpm due to norepinephrine release, which enhances SA and AV node activity.

Autonomic Nervous System Control During Exercise

• Parasympathetic System: Decreases intrinsic HR initially during rest.

• Sympathetic System: After 100 bpm, further increases in HR result from enhanced sympathetic stimulation.

Humoral Control

• Influences aspects like HR, myocardial function, vasodilation/vasoconstriction, and BP through the release of substances:

  • Norepinephrine (NE): Increases HR and myocardial contractility during stress.

  • Epinephrine: Enhances HR and contractility, influencing blood flow distribution.

  • Angiotensin II: Raises blood pressure by vasoconstriction in response to lowered BP.

Impact of Exercise on Venous Return

• Venous return can be enhanced via:

  1. Venoconstriction: Sympathetic control of veins.

  2. Skeletal Muscle Pump: Muscle action aids in blood return.

  3. Respiratory Pump: Abdominal pressure increases during inspiration, propelling blood volume towards the heart.