Note
Studied by 97 peopleCh 13
Comprehensive Cardiovascular Physiology Lecture Notes
Chapter Overview
Course: BIO 403 - Physiology I
Lecturer: Katerina Tsouma, Ph.D.
Department of Biology, University of Dayton
Cardiovascular System Components
Primary Components
Heart (Pump)
Located in center of thorax
Ventrally positioned between two lungs
Separated by septum into left and right halves
Anatomical Features:
Base
Apex
Encased in tough membranous sac (pericardium)
Pericarditis: Inflammation of the pericardium
Composed mainly of cardiac muscle (myocardium)
Major blood vessels emerge from heart base
Blood Vessels (Vasculature)
Types of Vessels:
Arteries
Arterioles
Capillaries
Venules
Veins
Blood (Fluid)
Composed of:
Cells
Plasma
Primary Function
Transport of materials:
Materials entering the body
Materials transferred between cells
Cellular waste products
Circulatory Circuits
Pulmonary Circuit
Blood pathway between:
Right side of heart
Lungs
Left atrium
Involves blood oxygenation
Systemic Circuit
Pathway between left and right heart sides
Distributes blood throughout body
Portal Systems
Types:
Hepatic
Renal
Hypophyseal
Supplies specific organ systems
Blood Flow Mechanics
Pressure Dynamics
Fundamental Principle: Liquids move from high to low-pressure regions
Pressure Creation:
Heart contracts, creating high pressure
Pressure lost due to friction
Pressure Gradient:
Highest pressure: Aorta
Lowest pressure: Venae cavae
Heart Valves
Atrioventricular (AV) Valves
Right Side: Tricuspid valve
Three flaps
Left Side: Bicuspid (mitral) valve
Two flaps
Structural Details
Chordae tendineae prevent valve eversion
Attached to valve flaps from papillary muscles
Prevent backward blood flow
Semilunar Valves
Pulmonary Valve
Between right ventricle and pulmonary trunk
Aortic Valve
Between left ventricle and aorta
Characteristics:
Three cuplike leaflets each
No connective tendons needed
Cardiac Muscle Cells
Types of Cardiac Muscle Cells
Contractile Cells (99% of cardiac muscle)
Characteristics:
Striated fibers
Organized into sarcomeres
Smaller and uninucleate
Branch and join neighboring cells via intercalated disks
Larger, branching T-tubules
Smaller sarcoplasmic reticulum
Partially depend on extracellular Ca2+
Mitochondria occupy 1/3 cell volume (high energy demand)
Cellular Connections:
Gap junctions provide electrical connection
Desmosomes allow force transfer
Autorhythmic Cells (1% of cardiac muscle)
Pacemaker cells
Characteristics:
Smaller
Fewer contractile fibers
No organized sarcomeres
Spontaneous signal generation (myogenic)
Muscle Cell Comparison
Muscle Types Comparison
Feature | Skeletal Muscle | Smooth Muscle | Cardiac Muscle |
Microscopic Appearance | Striated | Smooth | Striated |
Fiber Arrangement | Sarcomeres | No Sarcomeres | Sarcomeres |
Location | Attached to bones | Hollow organ walls | Heart |
Tissue Morphology | Multinucleate, large cylindrical fibers | Uninucleate, small spindle-shaped | Uninucleate, short branching fibers |
Ca2+ Control | Troponin, independent fibers | Calmodulin | Troponin, electrically linked |
Electrical Conduction in Heart
Conduction System
Sinoatrial (SA) Node
Main heart pacemaker
Located in right atrium
Sets baseline heart rhythm (approximately 70 beats per minute)
Atrioventricular (AV) Node
Located on right atrium floor
Slows action potential transmission
Allows atrial contraction before ventricular contraction
Alternative pacemaker (around 50 bpm)
Additional Components
AV bundle (bundle of His)
Purkinje fibers (25-40 bpm pacemaker potential)
Internodal pathway
Action Potential Characteristics
Contractile Cells Action Potential
Phase 0: Depolarization
Na+ influx
Phase 1: Initial repolarization
K+ efflux
Phase 2: Plateau
Ca2+ influx
Decreased K+ efflux
Phase 3: Rapid repolarization
Increased K+ efflux
Phase 4: Resting membrane potential
Unique Characteristics
Longer action potential (200 msec vs. 1-5 msec in other tissues)
Prevents tetanus
Ensures heart muscle relaxation between contractions
Autorhythmic Cells
Use "If" channels (funny current)
Unstable membrane potential
Spontaneous depolarization mechanism
Electrocardiogram (ECG)
Definition
Summed electrical activity of heart cells
Not identical to action potential
Provides information on:
Heart rate
Rhythm
Conduction velocity
Tissue condition
ECG Waves
P-Wave: Atrial depolarization
QRS Complex: Ventricular depolarization
T-Wave: Ventricular repolarization
Einthoven Triangle
Hypothetical triangle around heart
Electrodes placed on arms and left leg
Triangles sides numbered corresponding to electrode leads
Cardiac Cycle
Mechanical Events
Systole: Muscle contraction
Diastole: Muscle relaxation
Cycle Stages
Heart at rest
Ventricular filling
Atrial contraction
Ventricular contraction
Arterial blood ejection
Ventricular relaxation
Heart Sounds
First sound ("Lub"): AV valve closure
Second sound ("Dup"): Semilunar valve closure
Cardiac Output
Key Metrics
Stroke Volume: Blood pumped per ventricle contraction
Cardiac Output: Blood volume per time period
Calculation: Heart Rate × Stroke Volume
Average Values:
Heart Rate: 72 beats/minute
Stroke Volume: 70 mL/beat
Cardiac Output: ~5 L/minute
Factors Affecting Stroke Volume
Muscle fiber length
Contractility
Preload (ventricular wall stretch)
Frank-Starling Law
Autonomic Control
Heart Rate Regulation
Sympathetic Nervous System:
Increases heart rate
Positive inotropic effects
Parasympathetic Nervous System:
Decreases heart rate
Typically dominates tonic control
Additional Physiological Mechanisms
Contractility Factors
Positive Inotropic Agents:
Epinephrine
Norepinephrine
Digitalis
Negative Inotropic Agents: Decrease contractility
Cardiac Glycosides
Examples: Digitoxin, Ouabain
Increase contractility by:
Slowing Ca2+ removal from cytosol
Depressing Na+/K+ ATPase
Increasing intracellular Ca2+
1 OVERVIEW OF THE CARDIOVASCULAR SYSTEM
In simplest terms, describe the basic structure of a cardiovascular (CV) system.
The cardiovascular system consists of the heart, blood vessels, and blood, working together to transport oxygen, nutrients, hormones, and waste products throughout the body.
List at least five substances transported by the blood.
Oxygen, carbon dioxide, nutrients (like glucose and amino acids), hormones, and waste products (such as urea).
What are the key functions of the CV system?
The cardiovascular system transports substances, regulates body temperature and pH, protects against disease, and helps maintain fluid balance.
How do arteries differ from veins?
Arteries carry blood away from the heart under high pressure and have thick muscular walls. Veins carry blood back to the heart under low pressure and have thinner walls with valves to prevent backflow.
What ensures one-way flow of blood through the system?
Valves in veins and the heart ensure one-way flow of blood by preventing backflow.
Diagram the structure of the heart.
The heart consists of four chambers: two atria (upper chambers) and two ventricles (lower chambers). It is divided into a right and left side by the septum.
Trace a drop of blood from the left ventricle to the stomach and back to the left ventricle.
From the left ventricle, blood is pumped through the aortic valve into the aorta. It travels through the mesenteric arteries to the stomach. After nutrient absorption, blood returns to the heart through the mesenteric veins, the inferior vena cava, and into the right atrium, then passes into the right ventricle, and is pumped to the lungs for oxygenation. Oxygenated blood returns to the left atrium, and then to the left ventricle.
Compare the pulmonary circulation with the systemic circulation.
The pulmonary circulation carries deoxygenated blood from the heart to the lungs for oxygenation. The systemic circulation carries oxygenated blood from the heart to the rest of the body.
What is a portal system?
A portal system is a set of blood vessels that carries blood from one capillary bed to another, bypassing the general circulation.
Name the three portal systems of the body.
Hepatic portal system (liver), renal portal system (kidneys), and hypophyseal portal system (pituitary gland).
14.2 PRESSURE, VOLUME, FLOW, AND RESISTANCE
Liquids and gases flow from areas of _________________ pressure to areas of ________________ pressure.
High pressure to low pressure.
How does the cardiovascular system create a region of higher pressure?
The heart generates high pressure through ventricular contraction, pushing blood into the arteries.
As blood moves away from the heart, what happens to the pressure? Why?
Pressure decreases as blood moves away from the heart because energy is lost due to friction in the blood vessels.
The highest pressure in the blood vessels is found in the ______________________ and the lowest pressures are found in the _____________________________________.
Arteries; veins.
14.3 CARDIAC MUSCLE AND THE HEART
The heart is a muscle that lies in the center of the __________________ cavity, surrounded by a membrane called the _________________________.
Thoracic; pericardium.
True or false: The base of the heart is the pointed end that angles downward. Defend your answer.
False. The base of the heart is the top, where the major blood vessels attach, while the apex is the pointed end that angles downward.
The medical term for cardiac muscle is _____________.
Myocardium.
The left and right sides of the heart are separated by a wall known as the _______________.
Septum.
The ____________________ are the lower chambers and the ____________________ are the upper chambers. Which chambers have the thickest walls?
Ventricles; atria. The left ventricle has the thickest walls.
Diagram the blood vessels that connect to each chamber and tell from where or to where they are carrying blood.
Right atrium: Receives blood from the superior and inferior vena cava (deoxygenated blood from the body).
Right ventricle: Pumps blood through the pulmonary artery to the lungs.
Left atrium: Receives oxygenated blood from the pulmonary veins.
Left ventricle: Pumps oxygenated blood through the aorta to the body.
Name the vessels that supply blood to the heart muscle itself.
Coronary arteries supply oxygenated blood, while the coronary veins drain deoxygenated blood.
Heart Valves Ensure One-Way Flow in the Heart
Diagram the location of the heart valves.
Atrioventricular (AV) valves: Between atria and ventricles.
Semilunar valves: Between ventricles and arteries (pulmonary and aortic).
What are the chordae tendineae and what is their function? How are chordae tendineae related to papillary muscles?
Chordae tendineae are fibrous strings that prevent AV valves from inverting. They are attached to papillary muscles, which contract to tighten the chordae tendineae.
Compare and contrast the two AV valves and two semilunar valves.
AV valves: The tricuspid valve (right) has three cusps, and the bicuspid (mitral) valve (left) has two. They prevent backflow from the ventricles to the atria.
Semilunar valves: The pulmonary valve controls blood flow from the right ventricle to the pulmonary artery, and the aortic valve controls blood flow from the left ventricle to the aorta.
Cardiac Muscle Cells Contract without Innervation
Describe the differences between myocardial autorhythmic cells and myocardial contractile cells.
Autorhythmic cells generate their own action potentials and control heart rhythm.
Contractile cells contract to pump blood, and their action potentials are triggered by autorhythmic cells.
What are intercalated disks? What role do desmosomes and gap junctions play?
Intercalated disks are specialized connections between cardiac cells. Desmosomes anchor cells together, while gap junctions allow electrical signals to pass between cells, enabling coordinated contraction.
Compare myocardial contractile cells to skeletal muscle cells.
Both have striations and contract via sliding filaments, but myocardial cells are branched and connected by gap junctions, while skeletal muscle cells are multinucleated and do not have gap junctions.
Why do myocardial cells have a high rate of oxygen consumption? Because of this, what organelle occupies about one-third of the cell volume?
Myocardial cells have high oxygen demands due to constant activity. The organelle that occupies about one-third of the cell volume is the mitochondrion.
Calcium Entry Is a Feature of Cardiac EC Coupling
In what ways does cardiac muscle E-C coupling blend aspects of skeletal muscle and smooth muscle?
Like skeletal muscle, cardiac muscle has T-tubules and sarcomeres. Like smooth muscle, it uses calcium from both the extracellular fluid and the sarcoplasmic reticulum for contraction.
Diagram the mechanism for E-C coupling in cardiac muscle. Why is this also called Ca²⁺-induced Ca²⁺ release?
Calcium enters the cardiac muscle cell, triggering the release of more calcium from the sarcoplasmic reticulum, which initiates contraction. This process is called Ca²⁺-induced Ca²⁺ release.
Diagram the mechanism for cardiac muscle relaxation.
Calcium is pumped back into the sarcoplasmic reticulum and out of the cell, leading to muscle relaxation.
Myocardial Action Potentials Vary
What ion is important in cardiac muscle action potentials but plays no significant role in skeletal muscle or neuronal action potentials?
Calcium (Ca²⁺) is crucial for myocardial action potentials.
Do myocardial contractile cells have a stable or unstable membrane potential?
Unstable.
In the myocardial contractile cell, the rapid depolarization phase is due to __________.
Sodium (Na⁺) influx.
The rapid repolarization phase is due to ____________.
Potassium (K⁺) efflux.
In Figure 14.11, what causes the small repolarization in the membrane potential between points 1 and 2?
The potassium (K⁺) efflux before the plateau phase.
How does a longer action potential in cardiac muscle (compared to skeletal muscle) prevent tetanus?
The extended refractory period in cardiac muscle prevents additional stimuli from causing continuous contraction (tetanus).
Myocardial Autorhythmic Cells
Diagram the generation of pacemaker potentials and action potentials in autorhythmic cells.
Pacemaker potentials gradually depolarize due to sodium (Na⁺) influx through funny channels (If), followed by rapid depolarization due to calcium (Ca²⁺) entry and repolarization due to potassium (K⁺) efflux.
The rapid depolarization phase is due to _________. How does this compare with a contractile cell?
Calcium (Ca²⁺). In contractile cells, rapid depolarization is caused by sodium (Na⁺).
The repolarization phase in autorhythmic cells is due to _____________. How does this compare to a contractile cell?
Potassium (K⁺). In contractile cells, repolarization is also due to potassium (K⁺) but follows a longer plateau phase.
Here are detailed answers for the section "14.4 THE HEART AS A PUMP":
Electrical Signals Coordinate Contraction
41. Where do electrical signals in the heart originate? (Figs. 14.14, 14.15)
Electrical signals in the heart originate in the sinoatrial (SA) node, which is located in the right atrium near the opening of the superior vena cava. The SA node functions as the natural pacemaker of the heart, generating electrical impulses that initiate the heart's rhythm. These impulses spread through the atria, causing them to contract and send blood into the ventricles.
42. If you cut all nerves leading to the heart, will it continue to beat? Explain.
Yes, the heart will continue to beat even if all nerves leading to it are cut. The heart has its own intrinsic pacemaker activity, primarily controlled by the SA node. This means the heart can continue to generate electrical signals and contract rhythmically without external nervous input. However, the rate and strength of the heart's beat would be less regulated, and it would beat at its intrinsic rate (usually around 100 beats per minute for the SA node) rather than the modified rate determined by autonomic nervous input.
43. What cell structures allow electrical signals to spread quickly to adjacent cells? (Fig. 14.14)
Electrical signals spread quickly to adjacent cells in the heart through gap junctions, which are found in intercalated discs between cardiac muscle cells. These gap junctions allow ions to pass directly from one cell to another, enabling rapid electrical communication and coordinated contraction across the heart muscle.
44. Starting at the sinoatrial (SA) node, diagram the spread of electrical activity through the heart. (Fig. 14.15)
SA Node: Electrical impulses are generated here.
Atria: The impulse spreads through both atria, causing them to contract and push blood into the ventricles.
Atrioventricular (AV) Node: The electrical signal arrives at the AV node, where it is briefly delayed to allow the ventricles to fill with blood.
Bundle of His: The signal travels from the AV node to the Bundle of His, located in the interventricular septum.
Bundle Branches: The impulse is transmitted down the left and right bundle branches toward the apex of the heart.
Purkinje Fibers: These fibers spread the impulse throughout the ventricles, causing them to contract from the bottom up (starting from the apex), which pushes blood into the pulmonary artery and aorta.
45. Why is it necessary to direct the electrical signals through the AV node?
It is necessary to direct the electrical signals through the AV node because the AV node introduces a slight delay between atrial and ventricular contraction. This delay allows the atria to complete their contraction and fully empty into the ventricles before the ventricles begin to contract, ensuring efficient blood flow into the next chamber.
46. What is the purpose of AV node delay?
The purpose of the AV node delay is to allow the atria to contract and fully empty their blood into the ventricles before the ventricles contract. This delay ensures that the ventricles are adequately filled with blood before they pump it out to the lungs and the rest of the body.
Pacemakers Set the Heart Rate
47. If the SA node is damaged, will the heart continue to beat? At the same rate? Explain.
Yes, the heart will continue to beat if the SA node is damaged, but it will not beat at the same rate. The SA node is the natural pacemaker, but if it is damaged, other pacemaker cells in the heart (such as those in the AV node) will take over. However, the AV node typically has a slower intrinsic rate (about 40-60 beats per minute), so the heart will beat more slowly than normal without the influence of the SA node.
The Electrocardiogram Reflects Electrical Activity
48. What is an electrocardiogram (ECG)? What information does an ECG show? (Fig. 14.16)
An electrocardiogram (ECG) is a recording of the electrical activity of the heart over time. It shows the timing and sequence of electrical events that occur during the cardiac cycle, including depolarization and repolarization of the heart's chambers. The ECG is valuable for diagnosing arrhythmias, heart attacks, and other cardiac abnormalities.
49. Name the waves of the ECG, tell what electrical event they represent, and name the mechanical event with which each wave is associated. (Figs. 14.16, 14.17)
P wave: Represents atrial depolarization (the electrical impulse moving through the atria, causing them to contract). It is associated with atrial contraction.
QRS complex: Represents ventricular depolarization (the electrical impulse moving through the ventricles, causing them to contract). It is associated with ventricular contraction.
T wave: Represents ventricular repolarization (the electrical recovery of the ventricles). It is associated with ventricular relaxation.
50. Does the ECG directly show ventricular contraction? (Fig. 14.17)
No, the ECG does not directly show ventricular contraction. The QRS complex represents the depolarization of the ventricles, which triggers ventricular contraction, but the mechanical contraction occurs slightly after the electrical signal is recorded. The actual contraction happens after the QRS wave, as the ventricles respond to the depolarization.
51. Can you tell if an ECG is showing depolarization or repolarization simply by looking at the shape of a wave relative to the baseline? Why or why not?
Yes, you can tell if an ECG is showing depolarization or repolarization by looking at the shape of the wave. Depolarization is typically associated with a positive deflection (moving upward from the baseline) because it is an electrical activation of the muscle fibers, while repolarization is associated with a negative deflection (moving downward from the baseline) because it represents the recovery phase of the muscle fibers.
The Heart Contracts and Relaxes during a Cardiac Cycle
52. Define systole and diastole.
Systole is the phase of the cardiac cycle when the heart muscle contracts, pumping blood out of the heart chambers (ventricular systole pushes blood into the arteries).
Diastole is the phase of the cardiac cycle when the heart muscle relaxes and the chambers fill with blood.
53. Is the heart in atrial and ventricular systole at the same time? Explain.
No, the heart is not in atrial and ventricular systole at the same time. Atrial systole occurs just before ventricular systole. The atria contract to push blood into the ventricles, and then the ventricles contract to push blood into the pulmonary artery and aorta.
54. Briefly describe the major events that happen during each phase of the cardiac cycle. Indicate contraction and relaxation states for the chambers, pressure-volume changes for the chambers, heart sounds, and whether heart valves are open or closed.
Phase 1: The heart at rest: atrial and ventricular diastole (Fig. 14.18)
Atria and ventricles are relaxed. Blood fills the atria from the veins.
The AV valves are open, and semilunar valves are closed.
Heart sounds: None (no contraction).
Phase 2: Completion of ventricular filling: atrial systole (Fig. 14.18)
The atria contract, pushing the remaining blood into the ventricles.
The AV valves remain open, and the semilunar valves stay closed.
Heart sound: First heart sound (S1) marks the beginning of systole.
Phase 3: Early ventricular contraction and the first heart sound (Fig. 14.18)
Ventricles contract, and pressure builds. The AV valves close.
Semilunar valves are still closed.
Heart sound: The first heart sound (S1) is heard when the AV valves close.
Phase 4: The heart pumps: ventricular ejection (Fig. 14.18)
The ventricles contract fully, and the semilunar valves open, ejecting blood.
AV valves remain closed.
Heart sounds: None (ventricular contraction).
Phase 5: Ventricular relaxation and the second heart sound (Fig. 14.18)
The ventricles relax, and the semilunar valves close.
The AV valves open to allow filling of the ventricles.
Heart sound: Second heart sound (S2) marks the closing of the semilunar valves.
Pressure-Volume Curves Represent One Cardiac Cycle
55. Use the pressure-volume graph shown in Figure 14.18b to describe the cardiac cycle. For each graph section listed below, briefly describe the corresponding cardiac cycle event(s)
Point A: The end-diastolic volume (EDV), which is the amount of blood in the ventricles at the end of diastole, just before the ventricles contract. The atria have just finished contracting, and the ventricles are relaxed.
Point A to A’: This marks the isovolumetric contraction phase, where the ventricles start contracting, causing pressure to rise, but the AV valves and semilunar valves are closed, so no blood is ejected yet. The volume remains constant, but pressure increases.
Point A’ to B: This is the phase of ventricular ejection, where the pressure in the ventricles exceeds the pressure in the arteries, opening the semilunar valves, and blood is pumped into the aorta and pulmonary artery. The volume in the ventricles decreases as blood is ejected.
Point B: This marks the end-systolic volume (ESV), which is the volume of blood left in the ventricles after contraction. This is the lowest point of the volume in the cycle.
Point B to C: This is the isovolumetric relaxation phase, where the ventricles begin to relax. The semilunar valves close, but the AV valves remain closed, so the volume stays constant while the pressure in the ventricles drops.
Point C: This is when the AV valves open, allowing blood to flow from the atria to the ventricles. This marks the beginning of ventricular filling.
Point C to D: This is the rapid ventricular filling phase, where blood flows quickly into the ventricles due to the pressure difference between the atria and ventricles.
Point D: The cycle returns to Point A, completing one full cycle. This is the end-diastolic volume again, just before the next contraction begins.
Cardiac Volumes and Stroke Volume
56. Define end-diastolic volume (EDV). What is the EDV for our 70-kg man at rest?
End-diastolic volume (EDV) is the volume of blood in the ventricles at the end of diastole, just before the ventricles contract. It is typically around 120 mL for an average adult at rest.
57. Define end-systolic volume (ESV). What is the ESV for our 70-kg man at rest?
End-systolic volume (ESV) is the volume of blood left in the ventricles after systole, i.e., after the ventricles have contracted and ejected blood. It is typically around 50 mL for an average adult at rest.
58. At what point(s) on the graph are both the AV and semilunar valve closed? What happens to ventricular pressure? Volume?
Both the AV valves and semilunar valves are closed during the isovolumetric contraction and isovolumetric relaxation phases of the cardiac cycle (from Point A to A’ and from Point B to C on the graph).
During isovolumetric contraction, the ventricular pressure increases as the ventricles contract, but the volume remains the same because no valves are open.
During isovolumetric relaxation, the pressure in the ventricles decreases, and the volume remains constant because both sets of valves are still closed.
Stroke Volume Is the Volume of Blood Pumped per Contraction
59. Define stroke volume. How do you calculate it? (Give units.)
Stroke volume (SV) is the amount of blood pumped by the left ventricle in one contraction.
It can be calculated as:
SV=EDV−ESVSV = EDV - ESV
Where EDV is the end-diastolic volume and ESV is the end-systolic volume.
Units: mL per beat (milliliters per beat).
Cardiac Output Is a Measure of Cardiac Performance
60. Define cardiac output (CO). What information does CO tell us?
Cardiac output (CO) is the volume of blood pumped by the heart per minute. It is an indicator of the heart’s performance and can be calculated by:
CO=SV×HRCO = SV \times HR
Where SV is stroke volume (mL per beat) and HR is heart rate (beats per minute). Cardiac output tells us how efficiently the heart is pumping blood to meet the body’s demands for oxygen and nutrients.
61. Using the average resting values for stroke volume and heart rate as given in the textbook, show how you would calculate CO. (Give units.)
At rest, typical values are:
Stroke volume (SV) = 70 mL/beat
Heart rate (HR) = 70 beats/min
To calculate cardiac output (CO):
CO=70 mL/beat×70 beats/min=4900 mL/min=4.9 L/minCO = 70 \, \text{mL/beat} \times 70 \, \text{beats/min} = 4900 \, \text{mL/min} = 4.9 \, \text{L/min}
So, the cardiac output at rest is 4.9 L/min.
62. True or false: The right side of the heart pumps blood only to the lungs, so its CO is less than that of the left side of the heart, which must pump blood to many more tissues. Defend your answer.
False. The cardiac output (CO) of the right and left sides of the heart is equal. While the left side pumps blood to the entire body and the right side pumps blood to the lungs, the volume of blood pumped by both sides is the same, ensuring that the amount of blood entering the lungs is equal to the amount being circulated through the body.
The Autonomic Division Modulates Heart Rate
63. Identify the mechanisms by which the parasympathetic and sympathetic divisions control heart rate. Specify the neurotransmitters/neurohormones, receptors, ions, and any second messengers that might be involved. (Fig. 14.20)
Parasympathetic Control:
Neurotransmitter: Acetylcholine (ACh)
Receptor: Muscarinic receptors (M2)
Mechanism: ACh binding to muscarinic receptors opens K+ channels, which hyperpolarizes the cell, decreasing the rate of depolarization and slowing heart rate (negative chronotropy).
Sympathetic Control:
Neurotransmitter: Norepinephrine (NE)
Receptor: Beta-1 adrenergic receptors
Mechanism: NE binding to beta-1 receptors activates cAMP and protein kinase A (PKA), leading to the opening of Na+ and Ca2+ channels, increasing the rate of depolarization and heart rate (positive chronotropy).
Tonic Control: Both parasympathetic and sympathetic divisions provide tonic control of heart rate, meaning both systems are active at rest, balancing the overall heart rate. The parasympathetic division usually dominates at rest, slowing the heart rate.
64. If you were to block all autonomic input to the heart, what would happen to heart rate? What does this reveal about the tonic autonomic control of heart rate?
If all autonomic input to the heart were blocked, the heart would beat at its intrinsic rate set by the SA node (typically around 100 beats per minute). This reveals that the autonomic nervous system provides tonic control over the heart rate: the parasympathetic system normally slows it down, while the sympathetic system can increase it. Without autonomic input, the heart rate would be governed purely by the pacemaker activity of the SA node.
Multiple Factors Influence Stroke Volume
65. Stroke volume is directly related to the ______________ generated by cardiac muscle during contraction. It is affected by (1) length of the muscle fibers at the beginning of contraction and (2) the contractility of the heart.
Stroke volume is directly related to the force generated by cardiac muscle during contraction. It is affected by:
Preload (the length of the muscle fibers at the beginning of contraction, which relates to the volume of blood in the ventricles before contraction).
Contractility (the intrinsic ability of the heart muscle to contract forcefully at a given fiber length).
Contractility Is Controlled by the Nervous and Endocrine Systems
66. Define contractility.
Contractility is the ability of the heart muscle to contract with force, independent of preload or afterload. It refers to the intrinsic strength of the cardiac muscle fibers to generate force and is influenced by factors such as sympathetic stimulation and the availability of calcium ions.
Length-Tension Relationships and the Frank-Starling Law of the Heart
67. As sarcomere length increases, what happens to the force of contraction? (Fig. 14.21a)
As sarcomere length increases, the force of contraction also increases—up to an optimal point. This is because the overlap between actin and myosin filaments increases, allowing more cross-bridges to form, resulting in stronger contractions. If the sarcomere is stretched too far (beyond the optimal length), the force of contraction will decrease because the overlap between actin and myosin decreases.
68. In the intact heart we cannot measure sarcomere length directly. What parameter do we use as an indicator of sarcomere length? (Fig. 14.21b)
In the intact heart, end-diastolic volume (EDV) is used as an indicator of sarcomere length. The higher the EDV, the more the ventricles are stretched, which corresponds to an increased sarcomere length, and therefore a stronger contraction, as described by the Frank-Starling law.
69. Describe the Frank-Starling law of the heart.
The Frank-Starling law of the heart states that the more the heart muscle is stretched (due to increased venous return and higher EDV), the greater the force of contraction, up to an optimal point. This allows the heart to pump out more blood in response to increased filling (preload), ensuring that the output of both ventricles is balanced.
Stroke Volume and Venous Return
70. Define venous return. What cardiac volume does it determine?
Venous return is the volume of blood returned to the heart via the veins, primarily into the right atrium. It determines the end-diastolic volume (EDV), which, in turn, affects stroke volume according to the Frank-Starling mechanism. Increased venous return leads to increased EDV and, consequently, a higher stroke volume.
71. What are three factors that affect venous return? Name them and briefly describe how they influence venous return.
Skeletal muscle pump: Muscle contractions help propel blood through veins toward the heart, enhancing venous return.
Respiratory pump: Inhalation decreases thoracic pressure and increases abdominal pressure, helping to push blood toward the heart.
Sympathetic nervous system activation: Sympathetic stimulation causes vasoconstriction, increasing the pressure gradient for blood to flow toward the heart, thus increasing venous return.
Contractility Is Controlled by the Nervous and Endocrine Systems
72. What is an inotropic agent? If a chemical has a positive inotropic effect, what does that mean? (Fig. 14.21c)
An inotropic agent is a substance that affects the contractility of the heart muscle. A positive inotropic effect means that the agent increases the force of contraction of the heart muscle. This can be caused by agents that increase calcium availability to the muscle fibers (e.g., catecholamines such as norepinephrine).
73. At the molecular level, contractility increases as ____________ available for contraction increases.
At the molecular level, contractility increases as calcium available for contraction increases. Calcium ions bind to troponin on the actin filaments, allowing the myosin heads to interact with actin, which leads to contraction.
74. Diagram the mechanisms by which catecholamines enhance the force of cardiac muscle contraction. (Fig. 14.22)
Catecholamines (such as norepinephrine and epinephrine) enhance the force of cardiac muscle contraction through the following mechanisms:
Norepinephrine binds to beta-1 adrenergic receptors on cardiac muscle cells.
This activates adenylyl cyclase, increasing cAMP levels inside the cells.
Increased cAMP activates protein kinase A (PKA).
PKA phosphorylates calcium channels, increasing Ca2+ influx into the cells during each action potential.
More calcium is available for the contractile proteins, enhancing the force of contraction.
75. How do cardiac glycosides affect contractility? Name an example of a cardiac glycoside. What are the dangers associated with these compounds?
Cardiac glycosides, such as digoxin, increase contractility by inhibiting the Na+/K+ ATPase pump. This results in an increase in intracellular Na+, which in turn reduces the activity of the Na+/Ca2+ exchanger, leading to an increase in intracellular calcium. This boosts the force of contraction.
Dangers: These drugs have a narrow therapeutic window, meaning that overdosing can lead to toxicity, which may cause arrhythmias, nausea, vomiting, and other symptoms. They should be carefully monitored.