Cardiovascular System: Anatomy, Function, and Blood Flow
General Function of the Cardiovascular System
Components: Heart + blood vessels
Functions:
Transport blood throughout the body.
Deliver O2 and nutrients.
Remove CO2 and waste products.
Ensure adequate perfusion: delivery of blood per time per gram of tissue (mL/min/g).
Adequate perfusion is essential for cellular health, requiring a constantly pumping heart and open, healthy vessels.
Components of the Cardiovascular System
Blood Vessels:
Arteries: Carry blood away from the heart; most carry oxygenated blood. Veins: Carry blood back to the heart; most carry deoxygenated blood. Capillaries: Exchange sites for gases (e.g., in lungs and body cells).
Two Sides of the Heart:
Right Side: Receives deoxygenated blood and pumps it to the lungs.
Left Side: Receives oxygenated blood and pumps it to the body.
Heart’s Four Chambers:
Atria: Superior chambers, receive blood, send to ventricles.
Ventricles: Inferior chambers, pump blood away.
Great Vessels: Transport blood to/from heart chambers.
Superior & Inferior Vena Cava: Drain deoxygenated blood into the right atrium.
Pulmonary Trunk: Transports blood from the right ventricle, splits into pulmonary arteries.
Pulmonary Veins: Drain oxygenated blood into the left atrium.
Aorta: Transports blood from the left ventricle.
Heart Valves: Ensure one-way blood flow.
Atrioventricular (AV) Valves: Between atria and ventricles.
Right AV Valve (Tricuspid): Between right atrium and ventricle.
Left AV Valve (Bicuspid/Mitral): Between left atrium and ventricle.
Semilunar Valves: At the boundary of ventricles and arterial trunks.
Pulmonary Semilunar Valve: Between right ventricle and pulmonary trunk.
Aortic Semilunar Valve: Between left ventricle and aorta.
Pulmonary and Systemic Circulation
Pulmonary Circulation:
Deoxygenated blood from the right heart to lungs.
Blood picks up oxygen, releases CO2 in the lungs.
Blood returns to the left side of the heart.
Systemic Circulation:
Oxygenated blood from the left heart to systemic cells.
Exchanges gases, nutrients, and wastes at systemic cells.
Blood returns to the right heart.
Basic Blood Flow Pattern:
Right heart → Lungs → Left heart → Systemic tissues → Right heart.
Location and Position of the Heart
Heart’s Position:
Enclosed in the pericardium within the thoracic cavity.
Positioned posterior to the sternum, left of the body midline.
Located between the lungs in the mediastinum.
Slightly rotated with the right side more anterior than the left.
Base: Postero-superior surface.
Apex: Inferior, conical end projecting slightly anteroinferiorly toward the left side of the body
The Pericardium
Pericardium Layers:
Fibrous Pericardium: Outermost layer, dense irregular connective tissue.
Attaches to diaphragm, aorta, and pulmonary trunk.
Anchors the heart and prevents overfilling.
Parietal Layer of Serous Pericardium:
Simple squamous epithelium and areolar connective tissue.
Attaches to the fibrous pericardium.
Visceral Layer of Serous Pericardium (Epicardium):
Directly attaches to the heart.
Continuous with the parietal layer, separated by the pericardial cavity.
Superficial Features of the Heart
Anterior View Highlights:
Right atrium and ventricle are prominent.
Noticeable right auricle (wrinkled extension of the atrium).
Portions of the left auricle and ventricle visible.
Pulmonary trunk splits into right and left pulmonary arteries.
Visible aorta components: ascending, arch, and descending.
Posterior View Highlights:
Left atrium and ventricle are prominent.
Pulmonary veins, superior and inferior vena cava, and pulmonary arteries are visible.
Posterior interventricular sulcus and coronary sulcus housing the coronary sinus are present.
Sulci of the Heart:
Coronary Sulcus: Separates atria from ventricles, encircles the heart.
Interventricular Sulci: Separate the left and right ventricles.
Anterior Interventricular Sulcus: Anterior side.
Posterior Interventricular Sulcus: Posterior side.
Extend from the coronary sulcus to the apex.
Grooves contain coronary vessels supplying blood to the heart wall.
Layers of the Heart Wall
Wall Thickness:
Ventricles (pumping chambers) have thicker walls than atria.
The left ventricle wall is thicker than the right.
Reason: The left ventricle generates high pressure for systemic circulation, while the right ventricle pumps to nearby lungs.
Heart Wall Layers:
Epicardium (Visceral Pericardium): Outermost layer, simple squamous epithelium, and areolar connective tissue.
Myocardium: Middle layer, thickest, cardiac muscle tissue for pumping blood.
Endocardium: Covers internal surfaces of the heart and valves, continuous with blood vessel linings.
Heart Chambers
Chamber Separation:
Interatrial Septum: Between left and right atria.
Interventricular Septum: Between left and right ventricles.
Right Atrium:
Pectinate Muscles: Ridges on anterior wall and auricle.
Fossa Ovalis: Remnant of the fetal foramen ovale.
Receives blood from coronary sinus, superior vena cava, and inferior vena cava.
Exits to the right ventricle through the right AV valve.
Left Atrium:
Pectinate muscles in the auricle.
Receives blood from pulmonary veins.
Exits to the left ventricle through the left AV valve.
Right Ventricle:
Trabeculae Carneae: Irregular muscular ridges.
Papillary Muscles: Cone-shaped projections, usually three in the right ventricle.
Chordae Tendineae: Collagen fibers attaching to the AV valve.
Exits to the pulmonary trunk through the pulmonary semilunar valve.
Left Ventricle:
Similar trabeculae carneae.
Two papillary muscles.
Exits to the aorta through the aortic semilunar valve.
Heart Valves
Valve Functions: Ensure one-way blood flow.
Atrioventricular (AV) Valves: Prevent backflow to atria.
Right AV (Tricuspid) Valve: Three flaps.
Left AV (Mitral/Bicuspid) Valve: Two flaps.
Valves close during ventricular contraction, with papillary muscles and tendinous cords preventing inversion into atria.
Semilunar Valves:
Prevent backflow to ventricles.
Open during ventricular contraction to allow blood flow into arteries.
Close during ventricular relaxation when arterial pressure exceeds ventricular pressure.
Both semilunar valves have three cusps.
Pulmonary Semilunar Valve: Between right ventricle and pulmonary trunk.
Aortic Semilunar Valve: Between left ventricle and aorta.
Fibrous Skeleton of the Heart
Composition: Dense irregular connective tissue.
Functions:
Provides structural support at the boundary of atria and ventricles.
Forms fibrous rings to anchor heart valves.
Offers a framework for cardiac muscle attachment.
Acts as an electrical insulator, preventing simultaneous contraction of atria and ventricles.
Arrangement of Cardiac Muscle Around Fibrous Skeleton
Muscle Arrangement:
Spiral arrangement of cardiac tissue.
Muscle cells are attached to the fibrous skeleton and arranged in spiral bundles.
Atrial contraction: Moves walls inward.
Ventricular contraction: Similar to wringing a mop, starting at the apex and compressing superiorly.
Coronary Vessels: Blood Supply Within the Heart Wall
Coronary Circulation: Delivers blood to the heart’s thick wall.
Coronary Arteries: Transport oxygenated blood to the heart wall.
Coronary Veins: Transport deoxygenated blood away from the heart wall to the right atrium.
Functional End Arteries:
Blockage in a coronary artery can lead to insufficient blood flow to the heart wall.
Arterial Anastomoses: Connections between vessels providing alternate blood flow routes.
Coronary Anastomoses: Too small to act as effective alternates.
Blood Flow in Coronary Vessels:
Intermittent Flow: Varies with heart contractions.
Vessels open (patent) when the heart is relaxed.
Vessels compressed, interrupting flow when the heart contracts.
Coronary Veins and Drainage:
Great Cardiac Vein: In the anterior interventricular sulcus.
Middle Cardiac Vein: In the posterior interventricular sulcus.
Small Cardiac Vein: Next to the right marginal artery.
Coronary Sinus: Located in the posterior coronary sulcus, receives blood from cardiac veins, and drains into the right atrium.
Microscopic Structure of Cardiac Muscle
Myocardium: Composed of cardiac muscle tissue.
Cardiac Muscle Cells:
Short, branched.
Contain one or two central nuclei.
Supported by areolar connective tissue (endomysium).
Sarcolemma (plasma membrane): Forms T-tubules extending into the sarcoplasmic reticulum (SR).
Myofilaments: Arranged in sarcomeres, giving the striated appearance under a microscope.
Optimal Length: Allows greater contraction force with more blood filling the chamber.
Intercellular Structures:
Sarcolemma Folds: Increase structural stability and cell communication.
Intercalated Discs: Connect cells.
Desmosomes: Mechanically join cells with protein filaments.
Gap Junctions: Electrically join cells, allowing ion flow, creating a functional syncytium (each chamber functions as a unit).
Metabolism of Cardiac Muscle
High Energy Demand:
Extensive blood supply.
Numerous mitochondria.
Presence of myoglobin and creatine kinase.
Fuel Molecules: Can use fatty acids, glucose, lactic acid, amino acids, and ketone bodies.
Aerobic Metabolism:
Relies heavily on oxygen, making the heart susceptible to ischemia (low oxygen).
Blood flow interruption can lead to cell death.
Microscopic Structure of Cardiac Muscle
Myocardium: Composed of cardiac muscle tissue.
Cardiac Muscle Cells:
Short, branched with one or two central nuclei.
Supported by areolar connective tissue called endomysium.
Sarcolemma (plasma membrane): Forms T-tubules extending into the sarcoplasmic reticulum (SR).
Myofilaments: Arranged in sarcomeres, giving a striated appearance under a microscope.
Optimal Length: Allows greater contraction force when the heart chamber fills with blood.
Intercellular Structures:
Folded Sarcolemma: Increases structural stability and communication between cells.
Intercalated Discs: Connect cells through:
Desmosomes: Mechanically join cells with protein filaments.
Gap Junctions: Electrically join cells, allowing ion flow and enabling each chamber to function as a unit (functional syncytium).
Longitudinal View of Cardiac Muscle Cell
Likely a visual representation showing:
Sarcomeres, intercalated discs, desmosomes, gap junctions, and T-tubules.
High Energy Demand:
Extensive blood supply, numerous mitochondria.
Presence of myoglobin and creatine kinase.
Fuel Molecules: Can use fatty acids, glucose, lactic acid, amino acids, and ketone bodies.
Metabolism:
Relies mostly on aerobic metabolism, making the heart susceptible to ischemia (low oxygen).
Blood flow interruption can lead to cell death.
Pathway of Blood Flow Through the Heart
Right Atrium → Tricuspid Valve → Right Ventricle → Pulmonary Semilunar Valve → Pulmonary Arteries → Lungs → Pulmonary Veins → Left Atrium → Bicuspid (Mitral) Valve → Left Ventricle → Aortic Semilunar Valve → Aorta → Systemic Circulation.
The Heart’s Conduction System
Conduction System:
Function: Initiates and conducts electrical events for proper timing of contractions.
Specialized Cardiac Muscle Cells: Generate action potentials (APs) but do not contract.
Autonomic Nervous System Influence: Modulates activity.
Components of the Conduction System:
Sinoatrial (SA) Node:
Pacemaker of the heart, initiates heartbeat.
Located in the posterior wall of the right atrium.
Atrioventricular (AV) Node:
Located in the floor of the right atrium, near the right AV valve.
Atrioventricular (AV) Bundle (Bundle of His):
Extends from the AV node through the interventricular septum, dividing into left and right bundles.
Purkinje Fibers:
Extend from the bundles at the heart’s apex.
Spread through ventricle walls to facilitate contraction.
Innervation of the Heart
Cardiac Center of Medulla Oblongata:
Contains cardioacceleratory and cardioinhibitory centers.
Receives signals from baroreceptors and chemoreceptors in the cardiovascular system.
Sends signals via sympathetic and parasympathetic pathways.
Modifies cardiac activity but does not initiate it.
Influences the rate and force of heart contractions.
Parasympathetic Innervation:
Function: Decreases heart rate.
Pathway:
Starts at the medulla’s cardioinhibitory center.
Relayed via vagus nerves (CN X):
Right vagus: Innervates SA node.
Left vagus: Innervates AV node.
Sympathetic Innervation:
Function: Increases heart rate and force of contraction.
Pathway:
Starts at the medulla’s cardioacceleratory center.
Relayed via T1–T5 segments of the spinal cord.
Extends to SA node, AV node, myocardium, and coronary arteries.
Results in increased coronary vessel dilation.
Stimulation of the Heart
Heart Contraction Involves Two Events:
Conduction System: Initiates and propagates an action potential.
Cardiac Muscle Cells: Initiate action potentials and contract.
Atria contract first, followed by ventricles.
SA Nodal Cells at Rest
SA Nodal Cells:
Function: Initiate heartbeat, spontaneously depolarize, and generate action potential.
Resting Membrane Potential (RMP): ~ -60mV, but not stable.
Pacemaker Potential: Ability to reach threshold without stimulation.
Membrane Proteins:
Common: Na+/K+ pumps, Ca2+ pumps, leak channels.
Specific Channels:
Slow V-gated Na+ channels.
Fast V-gated Ca2+ channels.
V-gated K+ channels.
Electrical Events at the SA Node: Initiation of AP
Autorhythmicity: SA node cells exhibit spontaneous firing.
Reaching Threshold:
Slow V-gated Na+ channels open, Na+ flows in.
Membrane potential changes from -60 mV to -40 mV (threshold).
Depolarization:
Fast V-gated Ca2+ channels open, Ca2+ flows in.
Membrane potential changes from -40 mV to just above 0 mV.
Repolarization:
Calcium channels close, V-gated K+ channels open, K+ flows out.
Membrane potential returns to RMP = -60 mV.
Cycle Restarts: Voltage-gated Na+ channels open at -60 mV.
At Rest: One SA node action potential starts about 0.8 sec after the last:
This translates to 75 heartbeats per minute.
Inherently: SA node would fire faster (100 per minute) in heart tissue culture.
Vagal Tone: Parasympathetic activity (via vagus nerve) slows the resting heart rate.
Conduction System of the Heart: Spread of the Action Potential
Action Potential (AP) Spread:
Distribution Through Atria:
Excitation travels via gap junctions, both atria contract together.
Delay at the AV Node:
AV Nodal Cells: Slow due to small diameter and few gap junctions.
Fibrous Skeleton: Insulates, making the AV node a bottleneck.
Delay Function: Allows ventricles to fill before they contract.
Travel Through AV Bundle to Purkinje Fibers:
Pathway: AV Node → AV Bundle → Bundle Branches → Purkinje Fibers.
Spread Through Ventricles:
Gap Junctions: Enable impulse spread through cardiac muscle fibers.
Nearly Simultaneous Contraction of both ventricles.
Specialized Ventricular Features:
Purkinje Fibers:
Larger Diameter: Allows rapid action potential conduction.
Ensures synchronized ventricular contraction.
Papillary Muscles:
Contract Immediately: Anchors chordae tendineae of AV cusps.
Function: Prevents valve prolapse during ventricular contraction.
Apex Stimulation:
Blood Ejection: Contraction begins at the heart apex, ensuring efficient ejection toward arterial trunks.
Cardiac Muscle Cells at Rest
Membrane Components:
Na+/K+ pumps, Ca2+ pumps, leakage channels for Na+ and K+.
Resting Membrane Potential (RMP): -90 mV.
Voltage-Gated Channels:
Fast V-gated Na+ channels.
Slow V-gated Ca2+ channels.
V-gated K+ channels.
Channel State at Rest: All voltage channels are closed.
Electrical Events of Cardiac Muscle Action Potential:
Depolarization:
Impulse from conduction system (or gap junctions) opens fast V-gated Na+ channels.
Na+ enters, changing membrane potential from -90 mV to +30 mV.
Voltage-gated Na+ channels begin to inactivate.
Plateau Phase:
Depolarization opens V-gated K+ and slow V-gated Ca2+ channels.
K+ leaves while Ca2+ enters, stimulating the sarcoplasmic reticulum (SR) to release more Ca2+.
Membrane potential remains depolarized.
Repolarization:
Ca2+ channels close, K+ channels remain open.
Membrane potential returns to -90 mV
Mechanical Events (Crossbridge Cycling):
Contraction Process:
Ca2+ enters sarcoplasm from interstitial fluid and SR, leading to contraction.
Ca2+ binds to troponin, initiating crossbridge cycling.
Steps:
Crossbridge formation.
Power stroke.
Myosin head release and reset.
Relaxation:
Ca2+ levels decrease, leading to muscle relaxation.
Channels close, and pumps move Ca2+ into the SR and out of the cell.
Repolarization and the Refractory Period
Tetany Prevention:
Cardiac Muscle vs. Skeletal Muscle:
Cardiac Muscle: Cannot exhibit tetany.
Refractory Period: 250 ms, due to the plateau phase.
Ensures heart contracts and relaxes before it can be stimulated again.
Prevents sustained (tetanic) contraction.
Electrocardiogram (ECG)
ECG Basics: ECG (EKG): Detects electrical signals of cardiac muscle cells using skin electrodes.
ECG Waves Segments and Intervals
P Wave: Represents atrial depolarization originating in the SA node.
QRS Complex: Represents ventricular depolarization, Atrial repolarization occurs simultaneously but is not visible.
T Wave: Represents ventricular repolarization.
P-Q Segment:Associated with atrial plateau, indicating atria contracting.
S-T Segment: Associated with ventricular plateau, indicating ventricles contracting.ECG Intervals:
P-R Interval: Time from P wave to QRS deflection. Measures atrial depolarization to ventricular depolarization. Indicates AP transmission through the entire conduction system.
Q-T Interval: Time from QRS to end of T wave. Reflects the duration of ventricular action potentials. Length varies with heart rate.
Prolongation: May indicate tachyarrhythmia (rapid, irregular heart rate).
Electrical Events of the Heart and an ECG:
Atria:
Atrial Depolarization: P wave, muscle cells stimulated to contract.
Atrial Plateau: PQ segment, muscle cells contract and relax.
Atrial Repolarization: Not visible on ECG.
Ventricles:
Ventricular Depolarization: QRS complex, muscle cells contract.
Ventricular Plateau: ST segment, muscle cells contract and relax.
Ventricular Repolarization: T wave.
Clinical View: Cardiac Arrhythmia:
Definition: Abnormality in heart’s electrical activity.
Heart Blocks: Impaired conduction.
First-Degree AV Block: PR prolongation, slow conduction between atria and ventricles.
Second-Degree AV Block: Failure of some atrial APs to reach ventricles.
Third-Degree AV Block:Complete failure of AP transmission to ventricle
Types of Cardiac Arrhythmias:
Premature Ventricular Contractions:
Caused by stress, stimulants, or sleep deprivation.
Abnormal action potential in AV node or ventricles.
Generally not harmful unless frequent.
Atrial Fibrillation:
Chaotic timing of atrial action potentials.
Ventricular Fibrillation:
Chaotic electrical activity in ventricles.
Leads to uncoordinated contraction and pump failure.
Risk: Can lead to death of heart cells.
Treatment:
Paddle electrode defibrillator.
Automated External Defibrillator (AED).
Overview of the Cardiac Cycle
Cardiac Cycle: All heart events from the start of one heartbeat to the start of the next.
Includes systole (contraction) and diastole (relaxation).
Contraction increases pressure, relaxation decreases it.
Blood moves down its pressure gradient (high to low).
Valves ensure forward flow, preventing backflow.
Ventricular Contraction: Increases pressure, pushing AV valves closed and semilunar valves open.Blood ejected to artery.
Ventricular Relaxation:Decreases pressure, causing semilunar valves to close.nAV valves open, allowing ventricular filling.
Events of the Cardiac Cycle
1. Atrial Contraction and Ventricular Filling:
SA Node Initiates Atrial Excitation:
Atria contract, pushing remaining blood into ventricles.
Ventricles fill to end-diastolic volume (EDV).
Atria relax for the remainder of the cycle.
2. Isovolumic Contraction:
Purkinje Fibers Initiate Ventricular Excitation:
Ventricles contract, pressure rises, AV valves close.
Ventricular pressure
3. Ventricular Ejection:
Ventricular Contraction:
Pressure rises above arterial pressure, forcing semilunar valves open.
Stroke Volume (SV): Amount of blood ejected by ventricle.
End Systolic Volume (ESV): Blood remaining in ventricle after contraction.
ESV = EDV − SV (e.g., 60 mL = 130 mL − 70 mL).
4. Isovolumic Relaxation:
Ventricles Relax and Expand:
Pressure decreases, arterial pressure > ventricular pressure.
Blood closes semilunar valves, AV valves remain closed.
Isovolumic Phase: All valves closed, no blood flow in/out.
5. Atrial Relaxation and Ventricular Filling:
All Chambers Relaxed:
Atrial pressure opens AV valves, allowing ventricular filling.
Semilunar valves remain closed (arterial pressure > ventricular pressure).
Ventricular Balance:
Equal Blood Pumping:
Both left and right sides of the heart pump equal volumes of blood.
Left heart is stronger to pump blood farther (e.g., to systemic circulation).
Imbalance: May lead to edema (swelling) if volumes are unequal.
Introduction to Cardiac Output
Cardiac Output (CO):
Definition: Amount of blood pumped by a single ventricle in one minute.
Measured in liters per minute (L/min).
Significance:
Indicates the effectiveness of the cardiovascular system.
Increases during exercise in healthy individuals.
Calculation:
CO = Heart Rate (HR) × Stroke Volume (SV).
Example: 75 beats/min × 70 ml/beat = 5.25 L/min.
Maintaining Resting Cardiac Output:
Tissue Needs: CO must match the body’s metabolic demands.
Heart Size and CO:
Smaller Hearts: Smaller SV, higher HR (e.g., women and children).
Stronger Hearts: Larger SV, lower HR (e.g., endurance athletes with thicker heart walls).
Cardiac Reserve:
Definition: Ability to increase CO above resting level.
Formula: CO during exercise − CO at rest.
Exercise Effects:
HR increases, SV increases.
CO increases 4-fold in non-athletes and up to 7-fold in athletes.
Variables That Influence Heart Rate
Chronotropic Agents:
Function: Change heart rate by altering nodal cell activity (SA and/or AV node).
Mechanism: Typically through the autonomic nervous system or hormones.
Positive Chronotropic Agents: Increase heart rate.
Sympathetic Stimulation:
Norepinephrine (NE) release on heart.
Adrenal glands release epinephrine (EPI) and NE.
NE and EPI bind to β1-adrenergic receptors, increasing nodal cell firing rate.
Pathway: G-protein → adenylate cyclase → cAMP → protein kinase cascade.
Ca2+ Channels: Phosphorylation enhances Ca2+ influx, nodal cells fire sooner.
Additional Positive Chronotropic Agents:
Thyroid Hormone: Increases β1-adrenergic receptors on nodal cells.
Caffeine: Inhibits breakdown of cAMP, prolonging stimulation.
Nicotine: Increases release of norepinephrine.
Cocaine: Inhibits norepinephrine reuptake, extending its effects.
Negative Chronotropic Agents: Decrease heart rate.
Parasympathetic Activity:
Acetylcholine (ACh) binds to muscarinic receptors (K+ channels).
K+ exits cells, making membrane more negative (hyperpolarization).
Longer time to reach threshold, slows heart rate.
Beta-Blocker Drugs:
Block EPI and NE from binding to β-receptors.
Used to treat high blood pressure.
Autonomic Reflexes:
Input from Baroreceptors and Chemoreceptors:
Signals sent to the cardiac center.
Influence sympathetic and parasympathetic systems to adjust CO as needed.
Atrial Reflex (Bainbridge Reflex):
Prevents Overfilling of Heart:
Baroreceptors in atrial walls respond to increased venous return.
Increased signals to the cardioacceleratory center.
Sympathetic stimulation increases, heart rate rises to reduce atrial stretch.
Stroke Volume (SV):
Definition: Amount of blood ejected per beat.
Influencing Factors:
Venous Return, Inotropic Agents, Afterload.
Variables That Influence Stroke Volume Venous Return, Inotropic, Afterload
Venous Return:
Definition: Volume of blood returning to the heart.
Directly related to stroke volume.
Determines end-diastolic volume (EDV).
Frank-Starling Law:
As EDV increases:
Greater stretch of the heart wall, leading to optimal overlap of filaments.
Stronger contraction, increased SV.
Factors Affecting Venous Return:
Increased Venous Pressure: During exercise, muscles squeeze veins.
Increased Filling Time: Slow heart rate (e.g., in athletes).
Decreased Venous Return: With low blood volume (hemorrhage) or high heart rate.
Relationship of EDV, ESV, and SV
Formulas:
EDV (End-Diastolic Volume): Blood in ventricle before contraction.
ESV (End-Systolic Volume): Blood remaining after contraction.
SV = EDV – ESV.
Balanced Ventricular Output:
As one side receives more blood, it contracts more forcefully, leading to balanced blood flow.
Prevents edema and ensures stable circulation.
Inotropic Agents:
Change Stroke Volume by altering contractility (force of contraction).
Positive Inotropic Agents: Increase Ca2+ availability in sarcoplasm, boosting crossbridge formation.
EPI, NE: Increase Ca2+ via β1-adrenergic receptors.
Thyroid Hormone: Increases β1 receptors.
Digitalis (Drug): Boosts cardiac output by enhancing contractility.
Negative Inotropic Agents: Decrease contractility by lowering Ca2+ levels.
Electrolyte Imbalances: Increased K+ or H+.
Ca2+ Channel Blockers: Reduce contractility, lower blood pressure.
Afterload:
Definition: Resistance in arteries to ejection of blood by ventricles.
Effect: Pressure must be exceeded before ventricular blood is ejected.
Clinical Relevance:
Atherosclerosis: Plaque build-up increases afterload, reducing stroke volume.
Common in Aging: Leads to smaller arterial lumen, greater resistance.
Variables That Influence Cardiac Output
Cardiac Output (CO) Relationship:
CO = HR × SV.
Direct relationship: As HR and SV increase, CO increases.
Heart Rate:
Influenced by chronotropic agents.
SA node firing rate and AV node delay are modulated.
Stroke Volume:
Venous Return: Alters heart stretch.
Inotropic Agents: Influence crossbridge formation.
Afterload: Increased arterial resistance decreases SV, relevant in elderly.
Bradycardia: Persistently low resting heart rate (
Normal in Athletes: Due to increased cardiac efficiency.
Abnormal Causes:
Hypothyroidism: Reduced metabolism, slowed heart rate.
Electrolyte Imbalance: Affects cardiac cell depolarization.
Congestive Heart Failure: Inefficient heart pumping, reduced cardiac output.
Tachycardia: Persistently high resting heart rate (>100 beats per minute).
Potential Causes:
Heart Disease: Affects heart rhythm and strength.
Fever: Increases metabolic demand, requiring higher cardiac output.
Anxiety: Sympathetic activation, increased norepinephrine and epinephrine release.
Development of the Heart: Begins in the third week
Formation of two heart tubes from mesoderm in the embryo.
Fusion of Heart Tubes: Creates a single primitive heart tube.
Heartbeat Starts: Around day 22.
Heart Tube Bending and Folding: Occurs during the fourth week.
Develops Expansions:
Sinus Venosus & Primitive Atrium: Form parts of left and right atria.
Primitive Ventricle: Forms most of the left ventricle.
Bulbus Cordis:
Trabeculated Part of Right Ventricle: Forms most of the right ventricle.
Conus Cordis: Becomes outflow tracts for ventricles.
Truncus Arteriosus: Forms the ascending aorta and pulmonary trunk.
Weeks 5 to 8: Heart is partitioned into four chambers, and great vessels form.
Chamber Division:
Common Atrium: Subdivided into left and right atrium by the interatrial septum.
Septum Components:
Septum Primum and Septum Secundum.
Foramen Ovale: Opening in septum secundum, allows blood shunting from right to left atrium in the fetus.
At Birth: The foramen ovale closes, forming the fossa ovalis.
Interventricular Septum Formation:
Divides left and right ventricles, grows superiorly from the ventricular floor.
Formation of AV Valves, Papillary Muscles, and Chordae Tendineae:
Develop from portions of the ventricular walls.
Congenital Heart Defects:
Atrial Septal Defect:
Opening between left and right atria.
Blood shunting from left to right atrium, leading to right heart enlargement.
Ventricular Septal Defect:
Occurs if the interventricular septum is incompletely formed.
Tetralogy of Fallot:
Aorticopulmonary septum divides truncus arteriosus unevenly, causing:
Ventricular septal defect.
Narrow pulmonary trunk.
Overlapping aorta over both ventricles.
Right ventricular hypertrophy (enlargement).
Structure and Function of Blood Vessels
Three Main Types of Blood Vessels:
Arteries: Transport blood from the heart to capillaries.
Capillaries: Microscopic, porous blood vessels that allow substance exchange between blood and tissues.
Veins: Carry blood from capillaries back to the heart.
General Structure of Blood Vessels
Blood Vessel Wall Composition:
Three Layers (Tunics):
Tunica Intima:
Innermost layer.
Endothelium: Simple squamous epithelium.
Subendothelial Layer: Areolar connective tissue.
Tunica Media:
Middle layer.
Smooth Muscle Cells: Circularly arranged with elastic fibers.
Function:
Vasoconstriction: Narrows lumen.
Vasodilation: Widens lumen.
Tunica Externa:
Outermost layer.
Composition: Areolar connective tissue with elastic and collagen fibers.
Role: Anchors vessel to other structures.
Vasa Vasorum: Small arteries that supply large vessels.
Lumen: The space inside a blood vessel where blood flows.
Walls of an Artery, a Capillary, and a Vein
Visual Comparison:
Arteries: Thick walls with high elasticity.
Capillaries: Thin walls to facilitate exchange.
Veins: Larger lumen with valves to prevent backflow.
Companion Vessels:
Definition: Arteries and veins that lie next to each other, serving the same body region.
Structural Differences:
Arteries:
Thicker tunica media, narrower lumen.
More elastic and collagen fibers, allowing spring back to shape.
Resilient and resistant to blood pressure changes.
Veins:
Thicker tunica externa, larger lumen.
Fewer elastic and collagen fibers.
Walls collapse if there is no blood.
Capillaries:
Only have the tunica intima, composed of endothelium and basement membrane.
Thin wall: Allows rapid exchange of gases and nutrients.
Comparison of Companion Vessels
Side-by-Side Comparison:
Arteries: Thicker walls, smaller lumen, withstand high pressure.
Veins: Thinner walls, larger lumen, valves to prevent blood pooling.
Capillaries: Single layer of endothelial cells, ideal for exchange.
Artery vs. Vein Histology
Histological Differences:
Arteries: Prominent tunica media with smooth muscle.
Veins: Dominant tunica externa, thin tunica media.
Capillaries: Only endothelium, suitable for diffusion.
Arteries
Arterial System:
Arteries Branch Into Smaller Vessels: As they move away from the heart:
Lumen Diameter Decreases.
Elastic Fibers Decrease.
Smooth Muscle Increases.
Three Types of Arteries:
Elastic Arteries: Largest, conduct blood from heart to muscular arteries.
Muscular Arteries: Distribute blood to specific body regions.
Arterioles: Smallest arteries, regulate systemic blood pressure and blood flow.
Elastic (Conducting) Arteries
Characteristics:
Diameter: 2.5 to 1 cm.
Function: Conduct blood from heart to muscular arteries. Elastic fibers allow stretch and recoil. Helps propel blood during diastole.
ex) Aorta, pulmonary trunk, common carotid, common iliac arteries.
Muscular (Distributing) Arteries
Diameter: 1 cm to 0.3 mm.
Function: Distribute blood to specific body regions.
Muscular Wall: Allows vasoconstriction and vasodilation.
Elastic Tissue:
Internal Elastic Lamina: Between tunica intima and tunica media.
External Elastic Lamina: Between tunica media and tunica externa.
Examples: Brachial artery, coronary arteries.
Arterioles
Diameter: 0.3 mm to 10 µm.
Structure:Larger arterioles: Have all three tunics. Smaller arterioles: Only endothelium and smooth muscle.
Vasomotor Tone: Smooth muscle is usually somewhat constricted.Regulated by the vasomotor center in the brainstem.
Function: Regulate systemic blood pressure and Controls blood flow to capillaries.
Continuous Capillaries
Structure: Endothelial cells form a continuous lining.
Tight Junctions: Connect cells but do not completely seal.
Intercellular Clefts: Allow small molecule passage (e.g., glucose).
Barrier Function: Large particles (e.g., proteins) cannot pass.
Locations: Muscle, skin, lungs, central nervous system.
Atherosclerosis
Progressive disease of elastic and muscular arteries.
Plaque Formation (Atheroma):
Thickening of tunica intima.
Narrowing of arterial lumen.
Response-to-Injury Hypothesis:
Injury to endothelium due to infection, trauma, or hypertension.
Inflammatory reaction leads to atheroma development.
Enlarging plaques restrict blood flow to affected regions.
Risk Factors:
Hypercholesterolemia: High cholesterol levels.
Gender: Males more affected than females.
Lifestyle Factors: Smoking, hypertension increase vascular injury.
Treatment:
Angioplasty: Expands narrowed regions of the artery.
Coronary Bypass Surgery: Creates alternate routes for blood flow.
Aneurism:
Condition: Thinning and ballooning of the arterial wall.
Risks: Prone to rupture, leading to massive bleeding and death.
Affected Vessels: Elastic and muscular arteries. Aorta and arteries at the base of the brain are most susceptible.
Age Factor: With aging, arteries lose elasticity. Less able to withstand pulsating blood flow.
Risk Increases: With age and hypertension.
Capillaries
Function: Connect arterioles to venules.
Size:
Length: ~1 mm.
Diameter: 8 to 10 µm (RBCs pass in single file—rouleau).
Structure:
Endothelial layer on basement membrane.
Thin wall allows efficient exchange between blood and tissue fluid.
Types of Capillaries:
Continuous Capillaries
Fenestrated Capillaries
Sinusoids
Continuous Capillaries
Structure: Endothelial cells form a continuous lining.
Tight Junctions: Connect cells but do not form a complete seal.
Intercellular Clefts:Gaps between endothelial cells.
Allow small molecules (e.g., glucose) to pass.
Large particles (e.g., proteins, cells) cannot pass.
Common Locations: Muscle, skin, lungs, central nervous system.
Fenestrated Capillaries
Structure: Endothelial cells form a continuous lining with fenestrations (pores).
Fenestrations: Allow movement of smaller plasma proteins.
Function: Efficient fluid transport across the capillary wall.
Common Locations: Intestine Capillaries: For nutrient absorption.
Kidney Capillaries: For blood filtration to form urine.
Sinusoids
Structure:
Endothelial cells form an incomplete lining with large gaps.
Basement membrane: Incomplete or absent.
Function:
Allow transport of large substances, including formed elements and large proteins.
Common Locations:
Bone Marrow, Spleen, Some Endocrine Glands.
Capillary Beds: Groups of capillaries functioning together.
Blood Flow Pathway:
Fed by Metarteriole:
Proximal part: Contains scattered smooth muscle cells.
Distal part: Forms a thoroughfare channel (no smooth muscle).
Connects to postcapillary venule, which drains the bed.
True Capillaries:
Branch from metarteriole, forming the bulk of the capillary bed.
Precapillary Sphincter:
Smooth muscle ring at the origin of true capillaries.
Relaxation: Allows blood flow into true capillaries.
Contraction: Causes blood to bypass the capillary bed.
Physiological Concepts:
Vasomotion: Cycle of contraction and relaxation of precapillary sphincters.
Perfusion:
Definition: Amount of blood entering capillaries per unit time per gram of tissue (mL/min/g).
At Any Time: Only 1/4 of capillary beds are open.
Capillary Bed Structure: Sphincters Relaxed
Visual Representation:
Sphincters relaxed: Blood flows into true capillaries.
Allows nutrient exchange and waste removal in tissues.
Capillary Bed Structure: Sphincters Contracted
Visual Representation:
Sphincters contracted: Blood bypasses the capillary bed.
Shunting blood directly from arteriole to venule.
Common in:
Cold environments: To conserve heat.
Exercise: To prioritize blood flow to essential organs.
Venules and Veins
Venules: Smallest veins, diameters 8 to 100 µm.
Companion vessels to arterioles.
Smallest Venules: Known as postcapillary venules.
Largest Venules: Contain all three tunics.
Merge to Form Veins.
Small, Medium-Sized, and Large Veins:
Companion Vessels:
Small and Medium Veins: Accompany muscular arteries.
Largest Veins: Travel with elastic arteries.
Valves:
Function: Prevent blood pooling in the limbs.
Structure: Made of tunica intima, elastic, and collagen fibers.
Similarity: Structure resembles semilunar valves in the heart.
Blood Distribution at Rest:
Systemic Circulation: 70% of blood:
Systemic Veins: 55%.
Systemic Arteries: 10%.
Systemic Capillaries: 5%.
Pulmonary Circulation: 18% of blood.
Heart: 12% of blood.
Blood Redistribution:
Vasoconstriction of Veins:
Moves blood into circulation when more blood needed (during exertion).
Vasodilation:
Shifts blood back into reservoirs when less blood is needed (during rest).
Systemic Veins as Blood Reservoirs
Blood Distribution at Rest:
70% of Blood in Systemic Circulation:
Systemic Veins: 55%.
Systemic Arteries: 10%.
Systemic Capillaries: 5%.
Pulmonary Circulation: 18% of blood.
Heart: 12% of blood.
Blood Mobilization:
Vasoconstriction:
Moves blood into circulation when needed, such as during exertion.
Vasodilation:
Returns blood to reservoirs when less blood is needed, like during rest.
Pathways of Blood Vessels
Simple Blood Flow Pathway:
One Major Artery delivers blood to an organ or region.
End Artery:
Provides only one path for blood to reach an organ/region.
Branches into smaller arteries, which become arterioles.
Flow Path:
Arteriole → Capillary Bed → Venule → Major Vein.
Example:
Splenic Artery: Delivers blood to the spleen.
Splenic Vein: Drains blood from the spleen.
Types of Alternative Pathways:
Arterial Anastomosis (Arterial Joining):
Two or more arteries converge to supply the same region.
Example: Superior and inferior epigastric arteries supplying the abdominal wall.
Functional End Arteries: If junction is small, arteries may not supply sufficient blood alone.
Venous Anastomosis:
More common than arterial anastomoses.
Definition: Two or more veins drain the same body region.
Example: Basilic, brachial, and cephalic veins in the upper limb.
Arteriovenous Anastomosis (Shunt):
Directly transports blood from artery to vein, bypassing the capillary bed.
Examples: Fingers, toes, palms, ears.
Purpose: Prevents heat loss by shunting blood away from extremities during hypothermia.
Portal System:
Pathway: Artery → Capillary Bed → Portal Vein → Capillary Bed → Vein.
Example: Hypothalamo-hypophyseal portal system.
Total Cross-Sectional Area and Blood Flow Velocity
Cross-Sectional Area:
Definition: The lumen diameter of a single vessel.
Total Cross-Sectional Area:
Sum of diameters of all vessels of a type (artery, capillary, or vein).
Capillaries: Have the largest total cross-sectional area due to their sheer number.
Blood Flow Velocity:
Relationship: Inversely related to total cross-sectional area.
Clinical Implication:
Slowest Flow in Capillaries: Allows efficient exchange between blood and tissue fluid.
Relationship of Total Cross-Sectional Area and Velocity of Blood Flow
Graphical Representation:
Large Cross-Sectional Area: Leads to reduced flow velocity (e.g., capillaries).
Small Cross-Sectional Area: Results in faster blood flow (e.g., arteries).
Capillary Exchange
Capillary Function:
Primary Role: Exchange substances between blood and tissues.
Exchanged Substances:
Gases: Oxygen, Carbon Dioxide.
Nutrients, Wastes, Hormones.
Exchange Processes:
Diffusion:
Movement along concentration gradient (high to low).
Small Solutes: Pass through endothelial cells or clefts.
Large Solutes: Pass through fenestrations or sinusoids.
Vesicular Transport:
Mechanism: Pinocytosis and exocytosis.
Transported Molecules: Certain hormones, fatty acids.
Bulk Flow:
Definition: Fluids move down pressure gradients.
Processes:
Filtration: Fluid exits blood at arterial end of capillary.
Reabsorption: Fluid re-enters blood at venous end.
Forces Involved:
Hydrostatic Pressure (HP):
Force exerted by a fluid.
Blood Hydrostatic Pressure (HPb): Promotes filtration out of capillaries.
Interstitial Fluid Hydrostatic Pressure (HPif): Minimal in most tissues.
Colloid Osmotic Pressure (COP):
“Pull” on water due to proteins.
Blood Colloid Osmotic Pressure (COPb):
Promotes reabsorption, opposes hydrostatic pressure.
Clinical Term: Oncotic pressure.
Interstitial Fluid Colloid Osmotic Pressure (COPif):
Low due to few proteins in interstitial fluid.
Filtration Pressure (NFP)
NFP=(HPb−HPif)−(COPb−COPif)NFP = (HP_b – HP_{if}) – (COP_b – COP_{if})NFP=(HPb−HPif)−(COPb−COPif)
Arterial End: NFP favors filtration.
Venous End: NFP favors reabsorption.
Lymphatic System:
Collects 15% of excess fluid not reabsorbed by capillaries.
Returns fluid to venous circulation.
Bulk Flow at Capillaries
Visual Summary:
Shows movement of fluids and solutes through capillary walls.
Highlights: Filtration and reabsorption processes.
Net Filtration Pressure (NFP): Difference between net hydrostatic pressure and net colloid osmotic pressure.
NFP=(HPb−HPif)−(COPb−COPif)NFP = (HP_b – HP_{if}) – (COP_b – COP_{if})
Net Hydrostatic Pressure: Difference between blood and interstitial fluid hydrostatic pressures.
Net Colloid Osmotic Pressure: Difference between blood and interstitial fluid osmotic pressures.
NFP Dynamics:
Arterial End: NFP favors filtration.
Venous End: NFP favors reabsorption.
Lymphatic System:
Collects 15% of excess fluid not reabsorbed by the capillary.
Filters fluid and returns it to venous circulation.
Bulk Flow at Capillaries
Bulk Flow: The mass movement of fluids and solutes based on pressure gradients.
Key Processes:
Filtration: Fluid moves out of the blood at the arterial end.
Reabsorption: Fluid moves back into the blood at the venous end.
Capillary Exchange
Questions for Review:
Diffusion: Oxygen, hormones, nutrients move from blood to tissues; Carbon dioxide and wastes move from tissues to blood.
Vesicular Transport: Used for hormones and fatty acids.
Hydrostatic vs. Osmotic Pressure:
Hydrostatic Pressure: Pushes fluid out.
Osmotic Pressure: Pulls fluid in.
Pressure Changes:
Hydrostatic Pressure: Decreases from arterial to venous end.
Colloid Osmotic Pressure: Remains relatively constant.
Lymphatic Dysfunction: Would lead to fluid accumulation in interstitial spaces (edema).
Local Blood Flow
Not All Capillaries Are Filled Simultaneously: Blood flow is variable.
Measured in: mL/min.
Local Blood Flow Depends On:
Degree of Tissue Vascularity
Myogenic Response
Local Regulatory Factors
Total Blood Flow
Degree of Vascularization and Angiogenesis
Degree of Vascularization:
Highly Metabolic Tissues: High vascularity (e.g., brain, skeletal muscle, heart, liver).
Low Vascularity: Tendons, ligaments, epithelia, cartilage, cornea, lens of the eye.
Angiogenesis: Formation of new blood vessels over weeks to months.
Examples:
Skeletal Muscle: During aerobic training.
Adipose Tissue: With weight gain.
Coronary Vessels: Response to blockage.
Regression: Return to previous state of blood vessels.
Examples:
Sedentary Lifestyle: Reduces skeletal muscle vasculature.
Weight Loss: Reduces adipose tissue vasculature.
Tumor Angiogenesis
Cancer Cells: Require oxygen and nutrients.
Process:
Cancer cells secrete molecules to stimulate host cells to release growth factors.
Goal of Research: Inhibit angiogenesis to starve tumors
Myogenic Response
Definition: Smooth muscle in blood vessel wall maintains constant blood flow.
Responses to Blood Pressure Changes:
Increased Blood Pressure:
Arteriole Stretch: Causes smooth muscle contraction.
Result: Flow returns to original levels.
Decreased Blood Pressure:
Less Stretch: Leads to smooth muscle relaxation.
Result: Flow returns to normal.
Local, Short-Term Regulation of Blood Flow
Local Regulation: Adjusts blood flow based on tissue needs.
Vasoactive Chemicals:
Vasodilators: Increase blood flow by dilating arterioles and relaxing precapillary sphincters.
Vasoconstrictors: Decrease blood flow by constricting arterioles and contracting precapillary sphincters.
Autoregulation: Tissues control local blood flow.
Metabolic Activity Changes:
Increased Activity:
Oxygen/Nutrient Levels Drop, CO₂, lactic acid, H+, and K+ increase.
Vasodilation: Increases perfusion.
Negative Feedback: Vessel constriction when perfusion increases.
Reactive Hyperemia:
Increased Blood Flow: After a temporary disruption.
Example: Entering a warm room after being in the cold.
Tissue Damage and Defense Response:
Inflammation:
Vasoactive Chemicals: Released by damaged tissue, leukocytes, platelets.
Vasodilators:
Histamine, bradykinin, and nitric oxide.
Trigger: Trauma, allergy, infection, exercise.
Vasoconstrictors:
Leukotrienes and thromboxanes.
Function: Prevent blood loss through damaged vessels.
Total Blood Flow
Definition: Amount of blood transported through vasculature per unit time.
Equal to: Cardiac Output (approx. 5.25 L/min at rest).
Exercise Effects:
Significant Increase: More blood available to tissues.
Regulation: Involves both the heart and blood vessels.
Blood Pressure
Blood Pressure (BP): Force of blood against vessel walls.
Blood Pressure Gradient: Change in pressure along a vessel, driving blood flow.
Highest pressure in arteries, lowest in veins.
Arterial Blood Pressure:
Systolic Pressure: Occurs during ventricular contraction.
Highest pressure, arteries are stretched.
Upper number in BP ratio, e.g., 120 mm Hg in 120/80.
Diastolic Pressure: Occurs during ventricular relaxation.
Lowest pressure, arteries recoil.
Lower number in BP ratio, e.g., 80 mm Hg in 120/80.
Pulse Pressure:
Calculation: Systolic – Diastolic pressure.
Example: 40 mm Hg if BP is 120/80.
Significance: Reflects artery elasticity and recoil.
Clinical Relevance: Allows palpation of a throbbing pulse.
Mean Arterial Pressure (MAP):
Formula: MAP = Diastolic pressure + 1/3 Pulse pressure.
Example: If BP is 120/80, MAP = 80 + 40/3 = 93 mm Hg.
Indicator of Perfusion: MAP
Pulse: Throbbing of the arterial wall, useful for determining heartbeat.
Forceful Pulse: Indicates higher pressure.
Pulse Points: Where arteries can be compressed (e.g., radial, carotid, femoral).
Clinical Tip: Absence of a pulse suggests impaired blood flow to a body part.
Capillary Blood Pressure:
No Fluctuation: Between systolic and diastolic pressures.
Requirements: High enough for substance exchange, low enough to avoid vessel damage.
Pressure Ranges: 40 mm Hg (arterial end) to
Facilitates: Filtration and reabsorption.
Venous Blood Pressure: Low and Non-Pulsatile
Venous Return to Heart: Depends on:
Pressure Gradient: BP drops from 20 mm Hg in venules to almost 0 in the vena cava.
Skeletal Muscle Pump: Assists blood return from limbs.
Respiratory Pump: Pressure changes in thorax during breathing drive venous return.
Skeletal Muscle Pump:
Mechanism: Muscle contraction squeezes veins, pushing blood forward. Valves prevent backflow.
Exercise: Increases blood flow speed.
Prolonged Inactivity: Can cause blood pooling in leg veins.
Respiratory Pump:
During Inspiration: Diaphragm contracts, increasing abdominal pressure and decreasing thoracic pressure, driving blood towards the thoracic cavity.
During Expiration: Diaphragm relaxes, thoracic pressure increases, moving blood towards the heart.
Faster Breathing: Enhances blood movement.
Clinical Condition: Cerebral Edema
Cause: MAP > 160 mm Hg.
Effect: Increased filtration in brain capillaries, leading to fluid accumulation.
Systemic Blood Pressure Gradient:
Systemic Gradient: Difference in pressure between arteries near the heart (MAP = 93 mm Hg) and the vena cava (0 mm Hg).
Significance: Drives blood flow through vasculature.
Increased Gradient: Leads to increased total blood flow, often via increased cardiac output.
Resistance
Resistance: Friction blood encounters in vessels.
Peripheral Resistance: Specifically refers to resistance in blood vessels (not the heart).
Factors Affecting Resistance:
Blood Viscosity
Higher Viscosity: Increases resistance (e.g., blood is ~5x more viscous than water).
Decreased Viscosity: Seen in anemia.
Increased Viscosity: Occurs in blood doping or dehydration.
Vessel Length
Longer Vessels: Increase resistance.
Body Weight Changes: Affect vessel length through angiogenesis or regression.
Vessel Radius
Smaller Radius: Higher resistance.
Laminar Flow: Blood flows faster in the center of the vessel lumen.
Flow Relation: Flow (F) ∝ radius (r) to the fourth power (F ∝ r⁴).
Example: Doubling radius from 1 mm to 2 mm increases flow 16 times.
Relationship of Blood Flow to BP Gradients and Resistance:
Total Blood Flow: Amount of blood moving through the system per unit time.
Blood Flow Formula: F ∝ ΔP/R.
Systemic Blood Pressure Gradient (ΔP):
Higher Gradient: Leads to increased total blood flow, usually by increasing cardiac output.
Resistance (R):
Increased Resistance: Decreases total blood flow.
Influenced By: Viscosity, vessel length, and vessel lumen diameter.
Relationship of Blood Flow to BP Gradients and Resistance
Total Blood Flow: Directly proportional to blood pressure gradient and inversely proportional to resistance.
Regulation of Flow: Through changes in cardiac output and vessel diameter.
Clinical Application: Understanding how changes in resistance or pressure gradients affect perfusion.
Factors That Influence Total Blood Flow
Key Variables: Cardiac output, blood volume, and resistance.
Regulatory Systems:
Nervous System: Quick adjustments.
Endocrine System: Longer-term regulation.
Blood Flow Formula: Flow (F) = Pressure Gradient (ΔP) / Resistance (R).
Increased Gradient: Increases flow.
Increased Resistance: Decreases flow.
Clinical Example: High resistance in atherosclerosis reduces blood flow.
Regulation of Blood Pressure and Blood Flow
Blood Pressure (BP) Requirements:
High Enough: To maintain tissue perfusion.
Not Excessive: To avoid vessel damage.
Determinants of BP:
Cardiac Output: Heart rate and stroke volume.
Resistance: Vessel diameter, blood viscosity, and vessel length.
Blood Volume: Influences venous return and cardiac output.
Regulatory Systems:
Nervous System: Fast, moment-to-moment adjustments.
Autonomic Reflexes: Maintain short-term BP control.
Control Center: Medulla oblongata.
Functions: Adjust cardiac output and resistance as needed.
Situational Need: E.g., rapid adjustment when standing up.
Cardiovascular Center:
Cardiac Center: Influences cardiac output.
Cardioacceleratory Center: Sympathetic stimulation increases heart rate and force of contraction (increases BP).
Cardioinhibitory Center: Parasympathetic stimulation decreases heart rate and slows electrical conduction (decreases BP).
Vasomotor Center: Influences vessel diameter.
Sympathetic Pathways: Affect blood vessels by releasing norepinephrine (NE).
Adrenal Secretion: Epinephrine (EPI) and NE amplify effects.
Receptor Types:
α1 Receptors: NE and EPI cause vessel constriction.
β2 Receptors: NE and EPI cause vasodilation.
Sympathetic Activation Effects:
Increased Peripheral Resistance: More vessels constrict than dilate, raising BP.
Blood Volume Shift: Venous constriction moves blood to arterial circulation.
Blood Redistribution: More flow to skeletal muscles and heart, less to non-essential organs.
Sympathetic Inhibition: Reverses these effects, reducing BP.
Baroreceptors: Detect changes in vessel wall stretch.
Locations:
Aortic Arch: Systemic BP regulation via vagus nerve (CN X).
Carotid Sinuses: Monitor blood flow to the brain, using glossopharyngeal nerve (CN IX).
Sensitivity: Carotid receptors are more sensitive to BP changes.
Autonomic Reflexes:
When BP Decreases:
Decreased Vessel Stretch: Lowers baroreceptor firing rate.
Cardiovascular Center Responses:
Cardioacceleratory Center: Boosts sympathetic output to increase heart rate and contraction strength.
Cardioinhibitory Center: Reduces parasympathetic activity.
Vasomotor Center: Increases vasoconstriction.
Overall Effect: Raises cardiac output and resistance, restoring BP.
When BP Increases:
Increased Stretch: Heightens baroreceptor firing.
Cardiovascular Center Adjustments:
Cardioacceleratory Center: Reduces sympathetic signals.
Cardioinhibitory Center: Activates parasympathetic pathways to the heart.
Vasomotor Center: Decreases sympathetic signals to blood vessels.
Result: Decreased cardiac output and resistance, lowering BP.
Clinical Note: Baroreceptor reflexes are effective for quick changes (e.g., postural adjustments) but not for long-term BP management.
Neural Regulation of BP-
Chemoreceptor Reflexes:
Purpose: Maintain normal blood chemistry.
Main Peripheral Chemoreceptors: Located in aortic and carotid bodies.
Aortic Bodies: Send signals via the vagus nerve.
Carotid Bodies: Use the glossopharyngeal nerve.
Triggers: High CO₂, low pH, and very low O₂.
Response: Activates the vasomotor center to increase BP and redirect blood to the lungs, enhancing CO₂ expulsion and normalizing pH.
Cardiovascular Center
Higher Brain Centers Influence BP:
Hypothalamus: Modifies cardiac output and resistance during situations like increased body temperature or stress (fight-or-flight).
Limbic System: Alters BP in response to emotions or memories.
Hormonal Regulation of Blood Pressure
Renin-Angiotensin System:
Angiotensinogen: Produced by the liver, released into the blood.
Renin: Released by kidneys in response to low BP or sympathetic activity.
Function: Converts angiotensinogen to angiotensin I.
Angiotensin-Converting Enzyme (ACE): Found in lung capillaries.
Function: Converts angiotensin I to angiotensin II.
Effects of Angiotensin II:
Vasoconstriction: Increases resistance.
Stimulates Thirst Center: Enhances fluid intake, increasing blood volume.
Reduces Urine Formation: Conserves blood volume.
Triggers Hormone Release: Aldosterone and antidiuretic hormone (ADH).
Renin-Angiotensin System
Aldosterone:
Source: Adrenal cortex.
Trigger: Angiotensin II.
Effect: Increases sodium and water reabsorption in kidneys, reducing urine output.
Antidiuretic Hormone (ADH):
Source: Posterior pituitary.
Trigger: Hypothalamus signaling, high blood concentration, angiotensin II.
Effects:
Enhances water reabsorption in kidneys.
Stimulates thirst.
Causes vasoconstriction in large amounts (hence the name “vasopressin”).
Atrial Natriuretic Peptide (ANP):
Source: Atria of the heart, released when walls are stretched by high blood volume.
Effects:
Stimulates vasodilation (reduces resistance).
Increases urine output (lowers blood volume).
Blood Pressure Homeostasis:
Three Key Variables: Cardiac output, resistance, and blood volume.
Direct Relationship: Increasing any variable increases blood pressure.
Measuring Blood Pressure
Method: Sphygmomanometer.
Steps:
Cuff wrapped around the arm, over the brachial artery.
Inflate cuff to compress the artery completely.
Gradually release air and listen with a stethoscope.
BP Readings:
Systolic Pressure: Pressure when the heart contracts (first sound heard).
Diastolic Pressure: Pressure when the heart relaxes (sound stops as flow smooths out).
Blood Flow Distribution During Exercise
Increased Total Blood Flow: To meet increased metabolic demands.
Physiological Changes:
Heart beats faster and stronger.
Blood is drawn from venous reservoirs.
Blood redistribution prioritizes active tissues.
Examples:
Increased Flow: Coronary vessels, skeletal muscles, skin.
Decreased Flow: Abdomen and kidneys (to maintain blood volume and pressure).
Comparison of Systemic Circulation Blood Flow During Rest and Strenuous Exercise
Resting State: Blood is more evenly distributed across organs.
Exercise State: Blood flow increases significantly to skeletal muscles and skin for thermoregulation.
Clinical Insight: This redistribution supports higher oxygen demands and heat dissipation.
Blood Flow Through the Pulmonary Circulation
Pathway:
Deoxygenated blood is pumped from the right ventricle to the pulmonary trunk.
Pulmonary trunk divides into left and right pulmonary arteries.
Blood flows through arterioles and capillaries in the lungs.
Gas exchange occurs: O₂ enters blood, CO₂ exits.
Oxygenated blood returns to the left atrium via pulmonary veins.
Pulmonary Circulation and Blood Flow Through the Heart
Characteristics of Pulmonary Circulation:
Lower Pressure System: Systolic pressure 15-25 mm Hg, capillary pressure ~10 mm Hg.
Structural Differences: Vessels have less elastic tissue, wider lumens, shorter length due to proximity to the heart.
Purpose: Slow blood flow ensures efficient gas exchange.
General Arterial Flow Out of the Heart
Systemic Arteries: Branch off from the aorta.
Blood Pathway:
Ascending Aorta: Supplies coronary arteries (heart wall).
Aortic Arch: Gives rise to:
Brachiocephalic Trunk: Splits into right common carotid (head/neck) and right subclavian artery (upper limb, thoracic structures).
Left Common Carotid: Supplies the left side of the head and neck.
Left Subclavian Artery: Supplies the left upper limb and some thoracic structures.
Descending Aorta:
Thoracic Aorta: Supplies thoracic wall and viscera.
Abdominal Aorta: Supplies abdominal wall and organs.
At the Fourth Lumbar Vertebra: Splits into left and right common iliac arteries.
Internal Iliac Artery: Supplies pelvic structures.
External Iliac Artery: Supplies lower limbs.
General Venous Return to the Heart
Three Major Vessels to the Right Atrium:
Superior Vena Cava: Formed by left and right brachiocephalic veins. Drains the head, neck, upper limbs, thoracic and abdominal walls.
Inferior Vena Cava: Formed from veins below the diaphragm. Drains the lower limbs, pelvis, perineum, and abdominal structures.
Coronary Sinus: Returns deoxygenated blood from the myocardium.
Head and Neck
Common Carotid Arteries: Supply most of the blood to the head and neck.
Pathway: Travel parallel to the trachea, dividing into:
External Carotid Artery: Supplies structures external to the skull.
Internal Carotid Artery: Supplies internal skull structures.
Additional Arteries from Subclavian Artery:
Vertebral Artery: Supplies the brain.
Thyrocervical Trunk: Supplies the thyroid gland, neck, and shoulder.
Costocervical Trunk: Supplies the deep neck and upper intercostal spaces.
Branches of External Carotid Artery:
Superior Thyroid Artery: Thyroid gland and larynx.
Lingual Artery: Tongue.
Facial Artery: Face.
Occipital Artery: Posterior scalp.
Maxillary Artery: Teeth, gums, nasal cavity, muscles of mastication, meninges.
Superficial Temporal Artery: Parotid gland and part of the scalp.
Internal Carotid Branches:
Anterior and Middle Cerebral Arteries: Supply the brain.
Ophthalmic Artery: Supplies eyes and surrounding structures.
Vertebral Arteries:
Pathway: Branch off the subclavian arteries, travel through cervical vertebrae, enter the skull via the foramen magnum.
Merge to Form: The Basilar Artery, which then divides into the Posterior Cerebral Arteries (supply posterior cerebrum).
Cerebral Arterial Circle (Circle of Willis):
Significance: Provides collateral circulation in the brain.
Formation: Includes posterior cerebral, posterior communicating, internal carotid, anterior cerebral, and anterior communicating arteries.
Major Veins of the Head and Neck:
Vertebral Vein: Empties into the subclavian vein.
External Jugular Vein: Drains the superficial head and neck, empties into the subclavian vein.
Internal Jugular Vein: Drains blood from the cranial cavity, joins the subclavian vein to form the brachiocephalic vein.
Cranial Cavity Drainage:
Primary Route: Through dural venous sinuses (modified veins between dura mater layers).
Functions: Drain blood and excess cerebrospinal fluid.
Drainage Path: Primarily into internal jugular veins.
Arterial Supply:
Internal Thoracic Artery: Supplies anterior thoracic wall and mammary gland.
Branches: Six anterior intercostal arteries (intercostal spaces) and musculophrenic artery.
Inferior Epigastric Artery: Supplies the inferior abdominal wall.
Supreme Intercostal Artery: Branches into first and second posterior intercostal arteries.
Posterior Intercostal Arteries: Branch off the thoracic aorta.
Lumbar Arteries: Supply the posterolateral abdominal wall.
Median Sacral Artery: Supplies the sacrum and coccyx.
Venous Drainage:
Internal Thoracic Vein: Receives blood from anterior intercostal, musculophrenic, and superior epigastric veins.
Inferior Epigastric Vein: Merges with the external iliac vein.
Azygos System: Collects blood from lumbar and posterior intercostal veins.
Hemiazygos and Accessory Hemiazygos Veins: Drain left-side veins.
Azygos Vein: Drains right-side veins and empties into the superior vena cava.
Thoracic Organs and Spinal Cord
Lungs:
Bronchial Arteries: Supply bronchi and bronchioles.
Bronchial Veins: Drain into azygos and pulmonary veins.
Esophagus:
Arterial Supply: From descending thoracic aorta and left gastric artery.
Venous Drainage: Into the azygos or left gastric vein.
Diaphragm:
Arteries: Superior phrenic, inferior phrenic, musculophrenic, and pericardiacophrenic.
Veins: Drain into the inferior vena cava and internal thoracic veins.
Spinal Cord:
Arterial Supply: Anterior and posterior spinal arteries, with contributions from segmental medullar and radicular arteries.
Arterial Blood Supply: To the organs of the thoracic cavity and diaphragm.
Notable Arteries:
Anterior Spinal Artery: Supplies the superior part of the spinal cord.
Segmental Medullar and Radicular Arteries: Provide additional blood flow to the spinal cord
Gastrointestinal Tract
Arterial Supply: Provided by the abdominal aorta.
Three Unpaired Arteries Serving the GI Tract:
Celiac Trunk: Located just below the diaphragm, with three main branches:
Left Gastric Artery: Supplies part of the stomach and the esophagus.
Splenic Artery: Supplies the spleen, part of the stomach, and the pancreas.
Common Hepatic Artery: Has two main branches:
Hepatic Artery Proper: Supplies the liver, gallbladder, and part of the stomach.
Gastroduodenal Artery: Supplies part of the stomach, duodenum, and pancreas.
Superior Mesenteric Artery:
Location: Just below the celiac trunk.
Branches:
Intestinal Arteries: Supply the jejunum and ileum.
Middle Colic Artery: Supplies most of the transverse colon.
Right Colic Artery: Supplies the ascending colon.
Ileocolic Artery: Supplies the ileum, cecum, and appendix.
Inferior Mesenteric Artery:
Location: Just above the bifurcation of the aorta.
Branches:
Left Colic Artery: Supplies the distal transverse colon and descending colon.
Sigmoid Arteries: Supply part of the descending colon and the sigmoid colon.
Superior Rectal Artery: Supplies the rectum.
Superior and Inferior Mesenteric Arteries
Diagram likely showing:
Superior Mesenteric Artery: Branches extending to the small intestine and proximal large intestine.
Inferior Mesenteric Artery: Branches extending to the distal large intestine and rectum.
Venous Return: The Hepatic Portal System
Function: Transports blood from the digestive organs to the liver for processing.
Blood from Digestive System: Comes from three main veins that merge into the hepatic portal vein:
Splenic Vein: Positioned horizontally.
Inferior Mesenteric Vein: Positioned vertically.
Superior Mesenteric Vein: Positioned vertically on the right side of the body.
Pathway:
Hepatic Portal Vein: Carries blood to liver sinusoids.
Hepatic Veins: Drain processed blood into the inferior vena cava.
Posterior Abdominal Organs, Pelvis, and Perineum
Posterior Abdominal Organs:
Arterial Supply:
Middle Suprarenal Artery: Supplies each adrenal gland.
Renal Artery: Supplies each kidney.
Gonadal Artery: Supplies the gonads (testes or ovaries).
Veins: Follow the same naming pattern as the arteries.
Pelvis and Perineum:
Common Iliac Arteries: Divide into internal and external iliac arteries.
Internal Iliac Artery: Primary supply to the pelvic region with branches to gluteal muscles, bladder, rectum, vagina, uterus, anal canal, perineum, and medial thigh muscles.
Pelvic and Perineal Arteries:
Branches of Internal Iliac Artery:
Superior Gluteal Artery: Supplies the gluteus medius and minimus.
Inferior Gluteal Artery: Supplies the gluteus maximus.
Superior Vesical Artery: Supplies the bladder.
Middle Rectal Artery: Supplies the rectum.
Vaginal and Uterine Arteries: Supply the vagina and uterus.
Internal Pudendal Artery: Supplies the anal canal and perineum.
Obturator Artery: Supplies the medial thigh muscles.
Venous Drainage:
Pelvic and Perineal Veins: Mirror the names of the supplying arteries and drain into the internal iliac vein.
Female Pelvis, Medial View
Anatomical Diagram: Likely demonstrates the arterial and venous supply within the female pelvic region.
Key Features:
Arteries: Highlight the uterine, vaginal, and internal pudendal arteries.
Veins: Show venous return to the internal iliac vein.
Upper Limb
Arterial Supply to the Upper Limb:
Subclavian Artery:
Left Subclavian Artery: Arises directly from the aortic arch.
Right Subclavian Artery: Branches from the brachiocephalic trunk.
Axillary Artery: Continuation of the subclavian artery past the first rib.
Supplies: Axilla (armpit), chest wall, shoulder, and humerus.
Brachial Artery: The axillary artery becomes the brachial artery past the teres major muscle.
Deep Brachial Artery: A major branch supplying most arm muscles.
Radial and Ulnar Arteries:
Divisions of the Brachial Artery: Supply the forearm and wrist.
Anastomosis: Form the deep palmar arch (primarily from the radial artery) and superficial palmar arch (primarily from the ulnar artery).
Digital Arteries: Emerge from these arches to supply the fingers.
Superficial Venous Drainage:
Highly Variable Among Individuals.
Dorsal Venous Network: Located on the dorsum of the hand.
Drains into:
Medial Basilic Vein.
Lateral Cephalic Vein.
Axillary Vein: Receives blood from basilic and cephalic veins.
Median Cubital Vein: Connects cephalic and basilic veins in the cubital region.
Clinical Relevance: Common site for venipuncture (drawing blood).
Deep Venous Drainage:
Digital Veins and Superficial Palmar Venous Arches: Drain into radial and ulnar veins.
Brachial Veins: Formed by the merger of radial and ulnar veins, travel with the brachial artery.
Axillary Vein:
Forms From: Brachial veins and basilic vein.
Becomes: Subclavian vein at the lateral border of the first rib.
Merges with: Internal jugular vein to form the brachiocephalic vein.
Lower Limb
Arterial Supply to the Lower Limb:
External Iliac Artery: Primary blood supply to the lower limb.
Becomes the Femoral Artery: As it passes the inguinal ligament.
Deep Femoral Artery:
Supplies: Hip joint and many thigh muscles.
Pathway: Branches off the femoral artery and travels posteromedially.
Popliteal Artery: Continuation of the femoral artery in the popliteal fossa (behind the knee)
Divides into:
Anterior Tibial Artery: Supplies the anterior leg, becomes the dorsalis pedis artery at the ankle.
Posterior Tibial Artery: Supplies the posterior leg, branches into:
Fibular Artery: Supplies the lateral leg.
Medial and Lateral Plantar Arteries: On the plantar side of the foot.
Plantar Arterial Arch: Formed from the dorsalis pedis and a branch of the lateral plantar artery.
Digital Arteries: Extend from the plantar arch to supply the toes.
Lower Limb Arteries – Anterior View
From external iliac artery → femoral artery → popliteal artery → anterior and posterior tibial arteries.
Shows the dorsalis pedis artery, plantar arteries, and digital arteries in the foot.
Superficial Veins of the Lower Limb
Key Superficial Veins:
Dorsal Venous Arch: On the dorsum of the foot.
Great Saphenous Vein:
Origin: Medial ankle.
Path: Extends along the medial surface of the entire lower limb.
Drains into: Femoral vein.
Small Saphenous Vein:
Origin: Lateral ankle.
Path: Travels along the posterior calf.
Drains into: Popliteal vein.
Deep Veins of the Lower Limb
Deep Vein Pathway:
Medial and Lateral Plantar Veins: Drain digital veins and deep veins of the foot.
Posterior Tibial Veins: Drain medial and lateral plantar veins, including fibular veins.
Anterior Tibial Veins: Drain deep veins of the foot and ankle.
Popliteal Vein:
Formed From: The merger of anterior and posterior tibial veins.
Becomes: Femoral vein in the anterior thigh.
Transitions to: External iliac vein superior to the inguinal ligament.
Common Iliac Vein:
Formed By: The merger of the external and internal iliac veins.
Veins of the Right Lower Limb – Anterior View
From digital veins → plantar veins → tibial veins → popliteal vein → femoral vein → external iliac vein.
Key Differences Between Fetal and Newborn Circulation:
Oxygen and Nutrient Source:
Fetus: Receives oxygen and nutrients through the placenta.
Newborn: Cardiovascular system becomes independent, and the lungs take over oxygen exchange.
Lung Function:
Fetus: Lungs are nonfunctional, and blood bypasses the lungs.
Blood Pressure: Higher on the right side of the heart than the left in the fetus.
Blood Flow Priorities:
Shunting Mechanism: Blood is directed toward developing organs and away from immature ones (e.g., lungs and liver).
Fetal Circulation
Fetal Circulatory Route:
Oxygenated Blood from Placenta: Enters the fetus through the umbilical vein.
Ductus Venosus: Shunts blood from the umbilical vein to the inferior vena cava, bypassing the liver.
Blood Mixing: Oxygenated blood in the ductus venosus mixes with deoxygenated blood in the inferior vena cava.
Right Atrium: Receives blood from the superior and inferior venae cavae.
Foramen Ovale: Shunts most blood from the right atrium to the left atrium, allowing blood to bypass the lungs.
Blood then flows into the left ventricle and is pumped out through the aorta.
Pulmonary Trunk to Aorta:mA small amount of blood enters the right ventricle and is pumped to the pulmonary trunk. Most of this blood is shunted to the aorta through the ductus arteriosus, avoiding the pulmonary circulation.
Systemic Circulation: Blood travels through the body and returns to the placenta through the umbilical arteries.
Gas Exchange at the Placenta: Blood is reoxygenated, and waste is removed.
Circulatory Changes at Birth:
First Breath:
Pulmonary Arteries: Dilate, reducing resistance in the lungs.
Pressure Shift: The left side of the heart now has higher pressure than the right.
Post-Birth Changes:
Umbilical Vein and Arteries: Become nonfunctional.
Umbilical Vein: Becomes the round ligament of the liver.
Umbilical Arteries: Become medial umbilical ligaments.
Ductus Venosus: Constricts and becomes the ligamentum venosum.
Foramen Ovale: Closes due to higher pressure on the left side of the heart.
Leaves a remnant known as the fossa ovalis, a small depression in the interatrial septum.
Ductus Arteriosus: Closes within 10 to 15 hours of birth. Becomes the ligamentum arteriosum, a fibrous structure.
Fetal Circulation
Visual Aid: Likely provides a diagram of fetal circulation, showing:
Umbilical Vessels: Umbilical vein and arteries connecting to the placenta.
Shunts: Ductus venosus, foramen ovale, and ductus arteriosus.
Blood Flow Pathways: From the placenta through the fetal heart and back.
Patent Ductus Arteriosus (PDA)
Definition: Failure of the ductus arteriosus to close after birth.
Pathophysiology:
Blood flows from the aorta into the pulmonary system, leading to:
Increased Pulmonary Pressure: High blood pressure in the pulmonary circulation.
Blood Mixing: Deoxygenated blood mixes with oxygenated blood.
Symptoms: Shortness of breath. Fatigue. Potential heart failure if untreated.
Treatment Options:
Medication: Prostaglandin-inhibiting drugs can help close the ductus arteriosus.
Prostaglandins: Keep the ductus arteriosus open during fetal life, so inhibiting them encourages closure.
Surgical Intervention: May be needed if medication is ineffective.