Cardiac Output and Heart Rate Regulation

Cardiac Output (CO) is a crucial indicator of cardiovascular health, measuring the volume of blood pumped by each ventricle of the heart per minute. It is a key determinant of the heart's efficiency in supplying oxygen and nutrients to the tissues and organs throughout the body, making it an essential parameter in assessing the cardiac function in both resting and exercising states.

Formula:

\text{Cardiac Output} = \text{Stroke Volume} \times \text{Heart Rate}

Key Relationships:

CO is composed of two fundamental components:

• Stroke Volume (SV): The amount of blood ejected by the ventricle with each heartbeat.

• Heart Rate (HR): The number of heartbeats per minute.

The relationship between SV and HR is direct; an increase in either component typically results in an increase in CO, which allows the body to meet higher oxygen demands during physical activity.

Cardiac Output at Rest and During Exercise

At Rest:

• Typical CO is approximately 5 L/min.

• Stroke Volume (SV) is around 70 mL/beat, which indicates the efficiency of the heart at rest.

• Heart Rate (HR) usually ranges from 60-80 bpm, reflecting a lower demand for oxygen and nutrients when the body is at rest.

During Exercise:

• CO can increase to about 20-25 L/min.

• This increase is achieved through enhancements in both HR (up to 180 bpm or more) and SV (which can reach 100-120 mL/beat) to accommodate the elevated metabolic needs of the muscles.

Heart Rate Regulation

Central Control:

The cardiac control center is located in the Medulla Oblongata, which integrates signals from the body to regulate heart function appropriately.

Autonomic Nervous System (ANS):

• Sympathetic Division:

  • Increases Heart Rate (HR) through the release of norepinephrine.

  • Norepinephrine binds to beta-1 adrenergic receptors, triggering a positive chronotropic effect via cAMP signaling pathways that enhance the pacemaker activity of the sinoatrial node.

• Parasympathetic Division:

  • Decreases HR via the Vagus Nerve, which releases acetylcholine that binds to muscarinic cholinergic receptors, leading to a negative chronotropic effect that slows the heart rate for energy conservation.

Stroke Volume Regulation

Several components influence Stroke Volume, including:

• End-Diastolic Volume (EDV): The volume of blood in the ventricles just before contraction, reflecting pre-load.

• End-Systolic Volume (ESV): The volume of blood remaining in the ventricle after contraction, demonstrating the heart's efficiency with each heartbeat.

Frank-Starling Law

The Frank-Starling Law describes how increasing EDV leads to enhanced contraction and stroke volume:

• More stretch in myocardial walls results in increased contractile force, optimizing the heart's output in response to varying venous return levels.

• This intrinsic control of the myocardium permits adjustments to SV based on the amount of blood filling the heart.

Contractility and Autonomic Control

Contractility:

• Refers to the inherent strength of contraction at any given fiber length within cardiac muscle cells.

Sympathetic’s Role:

• Increases contractility via norepinephrine, boosting calcium availability within sarcomeres, which leads to a positive inotropic effect, allowing for more forceful heart contractions.

Parasympathetic’s Role:

• The parasympathetic division has minimal effect on contractility but significantly influences the rate of contraction.

Afterload and Its Effects on Stroke Volume

Definition:

Afterload represents the frictional resistance that the heart must overcome to circulate blood effectively. It is often quantified as Total Peripheral Resistance (TPR).

Impact on SV:

• There exists an inverse relationship; as afterload increases due to factors like hypertension or arteriosclerosis, stroke volume decreases, which can hinder cardiac efficiency and increase the workload on the heart.

Venous Return and Preload

Venous Return:

• The return of blood to the heart via veins is significantly influenced by:

  • Blood volume and venous pressure.

  • Venoconstriction and the action of skeletal muscle pumps acting during movement.

  • Respiratory pump, which aids in enhancing venous return during breathing phases.

Role in Preload:

• Preload increases with increased venous return, raising the EDV and consequently influencing stroke volume, thus playing a critical role in cardiac output control.

Clinical Relevance

• Caffeine: Stimulant that notably increases heart rate and contractility by altering signaling pathways in cardiac muscle, thereby affecting CO for improved physical performance and alertness.

• Left Ventricular Hypertrophy: A pathological condition where the left ventricle's muscle walls thicken, reducing the chamber's capacity for optimal filling and ultimately impairing cardiac output and efficiency, leading to heart disease over time.

• Atherosclerosis: A condition characterized by the buildup of plaques in the arteries, which narrows the arterial lumen and increases afterload, critically affecting both stroke volume and cardiac output due to elevated pressure demands on the heart.

Diagram Notes

• ECG and Heart Sounds: Provide essential visualization of heart sounds, pressures within the heart chambers, and phases of the cardiac cycle, useful in diagnosing various cardiac conditions.

• Clinical Situations: Conditions like left ventricular overstretch can disallow optimal filling and may lead to heart failure, indicating the importance of monitoring and managing cardiovascular health effectively.