The Heart as a Pump, Blood Vessels, and Blood Pressure: Structure and Function

14.4 The Heart as a Pump

Electrical Conduction System of the Heart

The heart's rhythmic contractions are coordinated by a specialized conduction system that ensures efficient pumping of blood. This system consists of pacemaker cells and conducting fibers that generate and transmit electrical impulses.

• Sinoatrial (SA) Node: The primary pacemaker of the heart, located in the right atrium, sets the heart rate at approximately 70 beats per minute (bpm).

• Internodal Pathway: Conducts impulses from the SA node to the atrioventricular (AV) node, ensuring the signal travels from the atrial apex to the base.

• Atrioventricular (AV) Node: Delays the impulse (AV node delay) to allow complete ventricular filling; can act as a secondary pacemaker (50 bpm).

• AV Bundle (Bundle of His) and Bundle Branches: Transmit impulses from the AV node to the ventricles via left and right bundle branches.

• Purkinje Fibers: Distribute the impulse throughout the ventricles; can act as pacemakers (25–40 bpm) if higher centers fail.

Pacemakers set the heart rate, with the SA node normally dominating.

Figure 14.14 & 14.15: Electrical Conduction and Conducting System

• Illustrate the pathway of electrical signals through the heart, from the SA node to the Purkinje fibers.

• Show how action potentials spread through gap junctions in myocardial cells.

The Electrocardiogram (ECG)

An electrocardiogram (ECG) records the summed electrical activity of all heart cells. It is not the same as a single action potential but reflects the overall electrical events of the cardiac cycle.

• P wave: Depolarization of the atria.

• QRS complex: Ventricular depolarization (and atrial repolarization).

• T wave: Ventricular repolarization.

• P-R segment: AV nodal delay.

• T-P segment: Ventricular and atrial relaxation.

The Cardiac Cycle

The cardiac cycle describes the sequence of events during one heartbeat, including periods of contraction (systole) and relaxation (diastole).

1. Atrial and Ventricular Diastole: Both chambers are relaxed; atria fill with blood from veins, AV valves open, ventricles fill.

2. Atrial Systole: Atria contract, pushing the last 20% of blood into the ventricles. End-diastolic volume (EDV) is the volume in the ventricle at the end of relaxation.

3. Early Ventricular Contraction: AV valves close, no blood enters or leaves (isovolumic contraction), pressure rises, atria relax.

4. Ventricular Ejection: Semilunar valves open, blood is ejected into arteries. End-systolic volume (ESV) is the volume in the ventricle at the end of contraction.

5. Ventricular Relaxation: Semilunar valves shut, ventricular pressure drops, AV valves open when ventricular pressure falls below atrial pressure.

Pressure-volume curves represent the changes in pressure and volume during one cardiac cycle.

Stroke Volume and Cardiac Output

• Stroke Volume (SV): The volume of blood pumped by one ventricle per contraction.

$\text{Stroke Volume (SV)} = \text{EDV} - \text{ESV}$

• Average SV ≈ 70 mL (for a 70-kg man at rest).

• Cardiac Output (CO): The volume of blood pumped by one ventricle per minute.

$\text{Cardiac Output (CO)} = \text{Heart Rate} \times \text{Stroke Volume}$

• Average CO ≈ 5 L/min.

Autonomic Regulation of Heart Rate

The autonomic nervous system modulates heart rate through parasympathetic and sympathetic divisions.

• Parasympathetic Control: Decreases heart rate by increasing K+ permeability (hyperpolarization) and decreasing Ca2+ permeability (slower depolarization).

• Sympathetic Control: Increases heart rate via β1-adrenergic receptors, increasing Na+ and Ca2+ permeability (faster depolarization).

• Tonic Control: Under normal conditions, parasympathetic activity predominates.

Factors Influencing Stroke Volume

• Contractility: The intrinsic ability of cardiac muscle to contract at any given fiber length.

• Length-Tension Relationship: The force of contraction is proportional to the initial length of the muscle fiber (preload).

• Frank-Starling Law: Stroke volume is proportional to EDV; the heart pumps all the blood returned to it.

• Venous Return: EDV is determined by venous return, which is affected by the skeletal muscle pump, respiratory pump, and sympathetic innervation of veins.

Regulation by Nervous and Endocrine Systems

• Inotropic Agents: Chemicals that affect contractility.

• Positive Inotropes: Increase contractility (e.g., epinephrine, norepinephrine, digitalis).

• Negative Inotropes: Decrease contractility.

• Afterload: The combined load of EDV and arterial resistance during ventricular contraction.

• Ejection Fraction: Percentage of EDV ejected with one contraction.

$\text{Ejection Fraction} = \frac{\text{Stroke Volume}}{\text{EDV}}$

15.1 The Blood Vessels

Structure of Blood Vessels

Blood vessels are composed of layers of smooth muscle, elastic tissue, and fibrous connective tissue. The structure varies depending on the vessel type and function.

• Endothelium: The innermost layer, secretes paracrine factors, regulates blood pressure, vessel growth, and absorption.

• Vascular Smooth Muscle: Arranged in circular or spiral layers, responsible for vasoconstriction and vasodilation. Muscle tone refers to a state of partial contraction.

Vessel Type	Main Features
Arteries	Thick smooth muscle, elastic and fibrous tissue, act as pressure reservoir
Arterioles	Variable resistance, part of microcirculation, more muscular
Capillaries	Single layer of endothelium, site of exchange, no smooth muscle
Venules	Thin exchange epithelium, little connective tissue
Veins	Thin smooth muscle, act as volume reservoir, contain valves

Arteries, Arterioles, and Metarterioles

• Arteries: Carry blood away from the heart, act as pressure reservoirs, thick muscular walls.

• Arterioles: Control blood flow to capillaries, site of variable resistance.

• Metarterioles: Branch from arterioles, have partial smooth muscle, contain precapillary sphincters to regulate flow into capillaries.

Capillaries and Exchange

• Capillaries: Smallest blood vessels, primary site of exchange between blood and interstitial fluid, composed of a single layer of endothelium and basal lamina.

• Pericytes: Contractile cells associated with capillaries, regulate permeability, secrete factors for vascular growth and differentiation.

Venules and Veins

• Venules: Receive blood from capillaries, thin walls, little connective tissue, convergent flow.

• Veins: Return blood to the heart, act as volume reservoirs, thin walls, contain one-way valves to prevent backflow, more numerous and closer to the body surface than arteries.

15.2 Blood Pressure

Blood Pressure Gradients

Blood pressure is highest in arteries and lowest in veins, creating a pressure gradient that drives blood flow through the systemic circulation.

• Pulse Pressure: The difference between systolic and diastolic pressure.

$\text{Pulse Pressure} = \text{Systolic Pressure} - \text{Diastolic Pressure}$

• Pulse pressure decreases with distance from the heart due to friction.

• Venous return is aided by valves, the skeletal muscle pump, and the respiratory pump.

Mean Arterial Pressure (MAP)

• MAP: Represents the average driving pressure for blood flow.

$\text{MAP} = \text{Diastolic Pressure} + \frac{1}{3}(\text{Systolic Pressure} - \text{Diastolic Pressure})$

• Hypotension: Lower than normal MAP.

• Hypertension: Higher than normal MAP.

• Blood pressure is measured using a sphygmomanometer and Korotkoff sounds.

Determinants of Mean Arterial Pressure

• MAP is determined by cardiac output (CO) and peripheral resistance (Rarterioles).

$\text{MAP} \propto \text{CO} \times R_{\text{arterioles}}$

• If blood flow into the aorta exceeds outflow, blood volume and MAP increase; if outflow exceeds inflow, MAP decreases.

• Blood volume is regulated by the kidneys and can be adjusted by fluid intake or loss.

• Vasoconstriction and sympathetic stimulation compensate for decreased blood volume.

Summary Table: Factors Influencing Mean Arterial Pressure

Factor	Effect on MAP
Blood Volume	Increased volume raises MAP; decreased volume lowers MAP
Cardiac Output	Increased CO raises MAP
Peripheral Resistance	Increased resistance raises MAP
Distribution of Blood	Constriction of veins increases venous return and MAP

Key Terms

• Sinoatrial node (SA node)

• Atrioventricular node (AV node)

• Bundle of His

• Purkinje fibers

• Cardiac cycle

• Diastole, Systole

• End-diastolic volume (EDV)

• End-systolic volume (ESV)

• Stroke volume (SV)

• Cardiac output (CO)

• Frank-Starling law

• Perfusion

• Vascular smooth muscle

• Vasoconstriction, Vasodilation

• Pulse pressure

• Mean arterial pressure (MAP)

• Skeletal muscle pump

• Respiratory pump

Learning Outcomes

• Describe the conduction of electrical signals through the heart.

• Explain the pressure changes during the cardiac cycle and their relationship to blood flow.

• Relate heart rate, cardiac output, and stroke volume.

• Explain autonomic control of heart rate.

• Discuss factors influencing stroke volume: venous return, preload, afterload, contractility.

• Compare the structure and function of the five major types of blood vessels.

• Explain what creates blood pressure and how it changes as blood flows through the systemic circulation.

• Explain the relationship between blood flow, pressure gradients, and resistance.

• Calculate mean arterial pressure and explain its determinants.