THE HEART
* Major Function: Propulsion of blood through the body
* Size: Approximately the size of a fist, weighs less than a pound
* Location: The mediastinum (the medial cavity of the thorax)
* Orientation: Apex points towards the left hip; base points towards the right shoulder
* Tissue Composition:
o PERICARDIUM – Covers the heart
+ Fibrous pericardium – superficial portion
# Composed of dense connective tissue
# Protects and anchors the heart; prevents overfilling of heart
+ Serous pericardium – deep portion
# Composed of squamous epithelium and areolar connective tissue
# Two layers of serous pericardium:
* Parietal layer – lines internal face of fibrous pericardium
* Visceral layer (Aka, epicardium) – lines the external heart surface
# Between the parietal and visceral layer is the pericardial cavity, containing the serous fluid that reduces friction.
o LAYERS OF THE HEART WALL
+ Epicardium – superficial layer infiltrated with adipose tissue
+ Myocardium – middle layer
# Composed of:
* Cardiac muscle – contraction
* Connective tissue fibers – reinforces cardiac muscles; provides structural support and resists stretching; limits the direct spread of action potentials across the heart to specific pathways (the intrinsic conduction system)
+ Endocardium – innermost layer
# Composed of squamous epithelium and connective tissue
# Lines the heart chambers and covers the fibrous skeleton of valves
# Continuous with the endothelial linings of the blood vessels
* Chambers of the Heart
o The heart has four chambers: 2 receiving and 2 discharging
+ Receiving Chambers – The atria
# Relatively small and thin-walled
# Atria are separated by the interatrial septum (the fossa ovalis is found here)
# Each atrium is covered by an auricle, which increases the volume of the chambers
# The anterior walls of each atrium is contains the ridged pectinate mucles
+ Discharging Chambers – The ventricles
# The ventricular walls are thicker due to their role in blood propulsion
* Right ventricle
o Relatively smaller than the left ventricle
o Forms most of the heart’s anterior surface
* Left ventricle
o Larger than the right ventricle
o Forms most of the heart’s posterorinferior surface
o Walls are thicker because it must pump blood to the systemic circulation
# The ventricles make up most of the heart volume
# Ventricles are separated by the interventricular septum
# Ventricular walls contain:
* Trabeculae carnea – irregular ridges of mucle
* Papillary muscles – fingerlike projections of muscle that aid in valve function
* Heart Valves
o The major function of heart valves is to prevent the backflow of blood.
o The heart contains two sets of valves: atrioventricular valves and semilunar valves.
o Atrioventricular (AV) valves – located at the atrial-ventricular junctions
+ The heart has two AV valves:
# Tricuspid valve – located on the right
# Bicuspid (mitral) valve – located on the left
+ When the heart is relaxed, the AV valves are open; when the heart contracts, the AV valves are closed
o Semilunar (SL) valves – located at the bases of the large arteries issuing from the ventricles
+ The heart has two semilunar valves:
# Pulmonary semilunar (SL) valve – guards the entrance of the pulmonary trunk
# Aortic semilunar (SL) valve – guards the entrance of the aorta
+ When the heart is relaxed, the SL valves are closed; when the heart contracts, the SL valves are open
* Coronary circulation – the functional blood supply of the heart
o Provides the nourishment to heart tissue
o Divided into the left and right coronary arteries and veins
o The coronary arteries deliver blood when the heart is relaxed.
o The coronary sinus delivers poorly oxygenated blood from the myocardium to the right atrium.
* Pulmonary vs. Systemic Circulation
o Pulmonary circulation – right side of the heart; responsible for gas exchange
o Systemic circulation – left side of the heart; it is responsible for transporting blood to and from the tissues of the body.
+ Walls of the left ventricle are thicker and can generate high pressure
* Pathway of Blood through the Heart
o The right atrium receives poorly oxygenated blood from the inferior and superior vena cava and the coronary sinus.
o The blood from the right atrium drains into the right ventricle. (Tricuspid valve open/Pulmonary SL valve closed)
o Following ventricular filling, the blood is forced through the pulmonary trunk. (Tricuspid valve closed/Pulmonary SL valve open)
o The blood flows from the pulmonary trunk to the lungs where it is oxygenated.
o Oxygenated blood is delivered to the heart via the pulmonary arteries.
o The pulmonary arteries deliver blood to the left atrium.
o The blood in the left atrium drains into the left ventricle. (Biscupid (mitral) valve open/Aortic SL valve closed)
o Following ventricular filling, the blood is forced through the aorta. (Bicuspid (mitral) valve closed/Aortic SL valve open)
o Once the blood leaves the aorta, it is carried to the rest to the body.
o Once depleted of the oxygen and nutrients it contains, the blood leaves the tissues and eventually drains into the superior or inferior vena cava or the coronary sinus.
* Properties of Cardiac Muscle Fibers
o Microscopic Anatomy
+ Cardiac cells are short, fat, branched, interconnected, and striated
+ Each cardiac muscle fiber contains one or two large, centrally located nuclei.
+ The sarcomeres of cardiac cells contain actin and myosin microfilaments
+ Intercellular spaces are filled with loose connective tissue and capillaries
+ Cardiac cells are connected by specialized cell junctions, called intercalated discs.
# Intercalated discs contain:
* Desmosomes – prevent adjacent cells from separating during contraction
* Gap junctions – allow ions to pass from cell to cell
* Causes the myocardium to act as a functional syncytium (a single coordinated unit).
o Energy requirements
+ Cardiac cells are highly dependent on oxygen for metabolic needs
+ Cardiac muscle relies almost exclusively on aerobic respiration
+ Cardiac muscle is able to utilize multiple fuel sources (ex. Glucose, fatty acids, and even lactic acid for a short period of time)
* Mechanisms and Events of Contraction
o The autorhythmic cells of the heart are able to initiate their own depolarization.
o The action potential in cardiac muscle cells:
+ Normally cardiac cells have a resting membrane potential of approximately –90mV.
+ The action potential in cardiac muscle cells begins when the membrane potential is brought down to approximately –75mV.
+ The stimulus of an action potential is usually the excitation of an adjacent muscle cell.
+ Once threshold has been reached, the action potential proceeds as follows:
# RAPID DEPOLARIZATION - Voltage-regulated sodium channels open, and the membrane becomes permeable to sodium ions. This results in the rapid depolarization of the sarcolemma.
* The sodium channels are called fast channels because they open quickly and remain open for only a few milliseconds.
# THE PLATEAU –
* As the transmembrane potential approaches +30mV, the voltage-regulated sodium channels close. They will remain closed and inactivated until the membrane potential reaches –60mV.
* As the sodium channels are closing, calcium channels begin to open and calcium enters the cardiac cells. The calcium channels are called slow channels because they open slowly and remain open for a relatively long period (~175 ms). This causes the transmembrane potential to remain near 0mV for an extended period of time – this is called the plateau.
o This increase in calcium ions around the myofibrils (from the calcium ions entering the cell and the release of additional calcium ions from the sarcoplasmic reticulum) generates a contraction.
# RAPID REPOLARIZATION - As the plateau continues, slow calcium channels begin closing and slow potassium channels begin opening. This restores the resting membrane potential.
# REFRACTORY PERIOD – For some time after an action potential begins, the membrane will not respond to a second stimulus. The length of this refractory period is approximately 250ms.
* In cardiac muscle the refractory period continues until the muscle begins to relax. Summation of action potentials is not possible at this point and this prevents tetanic contractions in cardiac cells.
* Intrinsic Conduction System of the Heart
o The cardiac conduction system coordinates and synchronizes heart activity and forces the heart to beat faster
o The intrinsic conduction system of the heart consists of noncontractile cardiac cells that are able to generate and distribute electrical impulses.
+ The autorhythmic cells of the heart do not have a stable resting potential. Instead, they have spontaneously changing membrane potentials called pacemaker potentials.
# The influx of calcium ions generates the action potential, not sodium ions
# The rate of spontaneous depolarization varies in different portions of the conduction system
* Sinoatrial node – generates action potentials at a rate of 75-100 per minute
* Atrioventricular node – generates action potentials at a rate of 40-60 per minute
* Most cells of the AV bundle and Purkinje fibers do not depolarize spontaneously. Those that do depolarize at the rate of about 30 times per minute
o Components of the intrinsic conduction system:
+ The sinoatrial (SA) node – cells of the SA node reach threshold first, so they establish the heart rate
# Aka, the cardiac pacemaker
# Located in the posterior wall of the right atrium
# Contains pacemaker cells which establish the heart rate
# Generates impulses about 75 times every minute (~100 per minute, in the absence of neural and hormonal factors) – this is called the sinus rhythm
+ The atrioventricular (AV) node
# Connected to the SA node via the internodal pathway
# Located in the inferior portion of the interatrial septum, immediately above the tricuspid valve
# The impulse is delayed for about 100ms to allow for completion of the atrial contraction before ventricular contraction
* The delay is due to the smaller diameter of the fibers and the presence of fewer gap junctions
+ The atrioventricular (AV) bundle
# Aka, the Bundle of His
# Impulse travels from here to the right and left bundle branches
# The only electrical connection between the atria and the ventricles
+ The Bundle branches
# Divide into right and left bundle branches
# Run along the interventricular septum toward the heart apex
+ The Purkinje fibers
# Penetrate into the heart apex and into the ventricular walls
# The Purkinje fibers are more elaborate in the left side of the heart
# Directly supply the papillary muscles
# Ventricular contraction follows depolarization by the Purkinje fibers
* Electrocardiography
o An electrocardiogram is a graphic recording of heart activity.
+ Aka, ECG or EKG
+ 3 distinguishable deflection waves are present:
# P wave – depicts movement of the depolarization wave from the SA node to the atria.
* The atria begin to contract approximately 100ms after the start of the P wave.
# QRS complex – depicts ventricular depolarization.
* The ventricles begin contracting shortly after the peak of the R wave.
* Atrial repolarization takes place at this time, but the wave is obscured by the QRS complex.
# T wave – depicts ventricular repolarization.
* The Cardiac Cycle – All of the events associated with blood flow through the heart during one complete heartbeat.
o 2 phases:
+ Systole – Contraction
+ Diastole - Relaxtion
o Atrial Systole
+ Atria contract; increase in atrial pressures push residual blood into ventricles through the open right and left AV valves.
+ At the end of atrial systole, each ventricle contains the maximum amount of blood that it will hold in this cardiac cycle. This quantity is called the end-diastolic volume (EDV).
o Ventricular Systole
+ As the pressure inside the ventricles rise above those in the atria, the AV valves swing shut.
+ The ventricles contract, but blood flow does not occur because the pressure isn’t high enough to force open the semilunar valves – this is the period of isometric contraction.
# During isometric contraction, all of the heart valves are closed, the volume of the ventricle remains constant, and the ventricular pressure rises.
+ Once ventricular pressure exceeds that in the arterial trunks, the semilunar valves open and push blood into the pulmonary and aortic trunks – this is the beginning of the period of ventricular ejection.
+ At the end of ventricular systole, ventricular pressures fall rapidly. Blood starts to flow back toward the ventricles and it is this backward movement that closes the semilunar valves.
# When the semilunar valves close, this increases the pressure in the arterial walls and they recoil.
# The blood remaining in the ventricle when the semilunar valves close, is the end-systolic volume.
o Ventricular Diastole
+ The ventricular myocardium is resting at this point and all the heart valves are closed.
+ When ventricular pressures fall bellow those of the atria, the atrial pressure forces the AV valves to open. Blood flows from the atria to the ventricles and both the atria and ventricles are in diastole.
# The ventricular pressures continue to fall as the chambers expand.
# Because of this passive filling, the ventricles will be nearly ¾ full before the cardiac cycle ends.
* Heart Sounds (lub-dup)
o 1st sound (lub) – closing of the AV valves
+ Louder and longer than the second sound
o 2nd sound (dup) – closing of the semilunar valves
+ Short, sharp sound
* Cardiodynamics – the movements and forces generated during cardiac contractions.
o Important Terms
+ End-diastolic volume – The amount of blood in each ventricle at the end of ventricular diastole
+ End-systolic volume – The amount of blood remaining in each ventricle ate the end of ventricular systole
+ Stroke volume – The amount of blood pumped out of each ventricle during a single beat. (SV = EDV – ESV)
+ Ejection fraction – The percentage of the EDV represented by the SV.
o Stroke volume (SV) is the most important factor in an examination of a single cardiac cycle. SV is relatively constant in healthy individuals
+ Factors Controlling Stroke Volume
# The EDV
* EDV is affected by 2 factors:
o Filling time – during ventricular diastole
+ Entirely dependent upon heart rate.
# TREND: Increase in heart rate = Decrease in the available filling time; Decrease in heart rate = Increase in the available filling time
o Venous return – the rate of blood flow over this period
+ Changes in venous return can be caused by exercise, alterations in blood volume, skeletal muscle activity, patterns in peripheral ciruclation
# The ESV
* ESV is affected by 3 factors:
o Preload – the degree of stretching experienced during ventricular diastole
+ The greater the EDV, the larger the preload
# EDV is lowest during period of rest; highest during exercise
+ The greater the stretch, the greater the force of contraction (Frank-Starling law of the heart)
# Cardiac muscle cells are stretched more when there is more blood in the chambers
o Contractility – the amount of force produced during a contraction, at a given preload
+ Positive inotropic agents – increase contractility
# Ex., increase in calcium ion concentration, glucagons, thyroxine, epinephrine (sympathetic nervous system stimulation), digitalis
+ Negative inotropic agents decrease contractility
# Ex. Acidosis, elevated potassium ion levels, calcium channel blockers, parasympathetic nervous system stimulation &nbs p; &nb sp; & nbsp; ; &nb sp;
o Afterload – the amount of tension the contracting ventricle must produce to force open the semilunar valve and eject blood.
+ Relatively constant in health individuals
+ Individuals with hypertension – reduced ability to eject blood
o Cardiac output (CO) – the amount of blood pumped by each ventricle in 1 minute.
+ Examination of cardiac function over time
+ CO = Stroke Volume x Heart Rate
# Factors affecting heart rate
* Autonomic Nervous System Regulation
o Sympathetic stimulation – increases heart rate
o Parasympathetic stimulation – decreases heart rate
* Chemical Regulation
o Hormones
+ Epinephrine & thyroxine – increase heart rate
o Ions
Lecture 16: Cardiovascular System
The Heart as a Pump
The Right and Left Hearts are Connected in Series, but are Folded Together to Form a Single Unit
+ The right heart pumps blood only to the lungs; its output is low pressure (25 mm Hg)
+ The left heart pumps blood to the rest of the body; its output is high pressure (120 mm Hg)
+ Because the 2 hearts are attached they beat in synchrony
+ The 2 atria receive the incoming blood- they pump extra blood into the ventricles
+ The 2 ventricles produce enough pressure to push blood through the pulmonary and systemic circulations
This diagram is modified from one in The Sourcebook of Medical Illustration, edited by Peter Cull (Park Ridge, NJ: Parthenon, 1989).
+ The right side of the heart has been colored blue to indicate deoxygenated blood; the red color of the left side indicates oxygenated blood that has come from the lung.
+ There are no valves where the vena cavae and join the right atrium or where the pulmonary veins enter the left atrium. Pressures in the atria are small and valves are not needed.
+ Click to get a blank diagram of the heart for practice in learning the parts.
Pressure Causes Valves to Open and Close in the Heart Cycle
+ The heart has 2 sets of valves:
# AV valves: between atria and ventricles
* Flap type
* Chorda tendinae & papillary muscles keep them from being pushed too far
* Left heart: bicuspid or mitral (2 flaps)
* Right heart: tricuspid: (3 flaps)
# Semilunar valves: where arteries leave heart
* Blood caught in the 3 cusps pushes them closed
o Right heart: pulmonary semilunar
o Left heart: aortic semilunar
# Leaks in valves -> murmurs
# Usually there are no valves where veins enter the atria
* Not needed, low pressure
* Exception is a valve between the inferior vena cava and right atrium, but this is missing in many adults
+ When the heart contracts pressure builds up, forcing the valves to close
# Muscles are not required to close the valves
+ Valves in the cardiac cycle:
Event AV Valves:
Right: Tricuspid
Left: Mitral Semilunar Valves:
Right: Pulmonary
Left: Aortic
Filling of ventricle Open Closed
Building up pressure Closed Closed
Expelling blood Closed Open
+ Opening and closing of valves depends upon the pressures on opposite sides
# Example: aortic valve
# Closed during filling and building up of pressure in the left ventricle because pressure in the aorta is higher than pressure in the ventricle
# When pressure in the left ventricle becomes higher than pressure in the aorta the aortic valve opens and blood is expelled from the heart
Heart Sounds are Produced by the Closing of the Valves
+ Normal heart sounds are produced when valves snap closed: LUB-DUP
+ LUB = closing of AV valves: beginning of systole
+ DUP = closing of semilunar valves: end of systole
+ Abnormal valve sounds:
# Leakage of valve -> swishing sound (murmur)
# Narrowing of valve (stenosis) -> high pitched sound
The Cardiac Output is the Product of Heart Rate and Stroke Volume
+ Normally about 5 liters/min
+ The cardiac output per minute (CO) is the product of the size of a single output, the stroke volume (SV), and the heat rate (HR) in beats/minute:
# CO = HR X SV
# = 70 beats/min X .07 liters/beat = 5 liters/min
+ If the SV is constant, doubling the HR will double the CO
Heart Rate Can be Increased From About 70 to 200 Beats/Minute
+ Resting heart rate is about 60-80 beats/min (lower in athletes because they have large stroke volumes)
+ The HR can be increased about 3 times in exercise
+ Above about 200 beats/min the heart would not have time to fill properly- therefore nature limits the rate
+ Rate is controlled by the autonomic nervous system
Stroke Volume is Controlled by Sarcomere Length
+ When the venous return of blood to the heart increases the heart beats more forcefully and puts out more blood: Frank- Starling's law of the heart
+ Can be explained by sarcomere length:
# Cardiac muscle is like skeletal muscle: there is an optimum length for the sarcomeres
# At rest heart sarcomeres are too short to give maximum tension
# Filling heart to a greater volume stretches sarcomeres- they become more efficient and contract more strongly
# More input -> sarcomeres stretch -> stronger contraction -> more output
+ Mechanism allows SV to increase about 1.5 to 2X.
Blood Pressure is Caused by Cardiac Contraction
+ Blood pressure at the output of the left heart alternates between a high pressure (systole) and a lower pressure (diastole)
+ Systole:
# When the heart beats (systole) the pressure in the arteries leaving the heart rises to about 120 millimeters of mercury (mm Hg)
+ Diastole:
# Between beats (diastole) the arterial pressure drops to about 80 mm Hg
# The diastolic pressure does not drop to 0 because the arterial walls are elastic
# A force due to wall elasticity pushes on the arterial blood between beats
# The 80 mm Hg diastolic pressure keeps the blood flowing between beats
+ Blood pressure is reported as systolic pressure over diastolic pressure
# Example: 120/80
+ Pressure is a force per unit area. In engineering pressure is often given in pounds per square inch (PSI) or in dynes per square centimeter. Why then is blood pressure reported as millimeters of mercury? That seems to be the height of a column, not a pressure at all. Click to see an explanation of mm Hg pressure units.
Systemic Blood Pressure Depends Upon Cardiac Output and Resistance to Flow
+ The more blood pumped into the arteries the higher the pressure
+ Pressure also goes up if there is more resistance to flow- this occurs when large numbers of arterioles constrict
+ The body changes both CO and resistance to adjust blood pressure
+ The higher the blood pressure the more work the heart must do to pump blood
Blood Pressure is Regulated by Reflexes and the Kidney
+ Blood pressure must be closely regulated
# If too low circulation will be poor;
# If too high there is danger of arterial damage or hemorrhage
+ Short term regulation (seconds -> minutes): baroreceptor reflex
# Example:
* If you are lying down and suddenly stand up the pressure in the aorta will fall as blood flows to the lower limbs.
* The baroreceptor reflex will cause the heart to speed up and increase its stroke volume.
* This raises the cardiac output and the blood pressure will go up
# Components of the reflex:
* Pressure is measured by sensors in the arch of the aorta and in the carotid sinus (the carotids are the major arteries supplying blood to the brain)
* The control center is in the medulla of the brain
* Two nerves control the heart rate:
o Vagus nerve: slows the heart
o Accelerator nerve: speeds it up
+ Long term regulation (days -> years) is mainly by the kidney
# Kidney regulates the salt and water content of the body, and these substances control the blood pressure
* The more fluid in the blood vessels the higher the pressure
# Salt:
* Sodium retention is controlled by the Na pump
* The hormone aldosterone increases Na pump activity in the kidney
* The hormones renin and angiotensin control the amount of aldosterone secreted into the blood
# Water:
* If Na is retained the blood osmotic pressure rises and this causes water to be retained also- by osmosis in the kidney
* Water reabsorption in the kidney requires water channels in the kidney tubules
* The water channels are controlled by the antidiuretic hormone (ADH)
* If ADH is present at high concent
* Major Function: Propulsion of blood through the body
* Size: Approximately the size of a fist, weighs less than a pound
* Location: The mediastinum (the medial cavity of the thorax)
* Orientation: Apex points towards the left hip; base points towards the right shoulder
* Tissue Composition:
o PERICARDIUM – Covers the heart
+ Fibrous pericardium – superficial portion
# Composed of dense connective tissue
# Protects and anchors the heart; prevents overfilling of heart
+ Serous pericardium – deep portion
# Composed of squamous epithelium and areolar connective tissue
# Two layers of serous pericardium:
* Parietal layer – lines internal face of fibrous pericardium
* Visceral layer (Aka, epicardium) – lines the external heart surface
# Between the parietal and visceral layer is the pericardial cavity, containing the serous fluid that reduces friction.
o LAYERS OF THE HEART WALL
+ Epicardium – superficial layer infiltrated with adipose tissue
+ Myocardium – middle layer
# Composed of:
* Cardiac muscle – contraction
* Connective tissue fibers – reinforces cardiac muscles; provides structural support and resists stretching; limits the direct spread of action potentials across the heart to specific pathways (the intrinsic conduction system)
+ Endocardium – innermost layer
# Composed of squamous epithelium and connective tissue
# Lines the heart chambers and covers the fibrous skeleton of valves
# Continuous with the endothelial linings of the blood vessels
* Chambers of the Heart
o The heart has four chambers: 2 receiving and 2 discharging
+ Receiving Chambers – The atria
# Relatively small and thin-walled
# Atria are separated by the interatrial septum (the fossa ovalis is found here)
# Each atrium is covered by an auricle, which increases the volume of the chambers
# The anterior walls of each atrium is contains the ridged pectinate mucles
+ Discharging Chambers – The ventricles
# The ventricular walls are thicker due to their role in blood propulsion
* Right ventricle
o Relatively smaller than the left ventricle
o Forms most of the heart’s anterior surface
* Left ventricle
o Larger than the right ventricle
o Forms most of the heart’s posterorinferior surface
o Walls are thicker because it must pump blood to the systemic circulation
# The ventricles make up most of the heart volume
# Ventricles are separated by the interventricular septum
# Ventricular walls contain:
* Trabeculae carnea – irregular ridges of mucle
* Papillary muscles – fingerlike projections of muscle that aid in valve function
* Heart Valves
o The major function of heart valves is to prevent the backflow of blood.
o The heart contains two sets of valves: atrioventricular valves and semilunar valves.
o Atrioventricular (AV) valves – located at the atrial-ventricular junctions
+ The heart has two AV valves:
# Tricuspid valve – located on the right
# Bicuspid (mitral) valve – located on the left
+ When the heart is relaxed, the AV valves are open; when the heart contracts, the AV valves are closed
o Semilunar (SL) valves – located at the bases of the large arteries issuing from the ventricles
+ The heart has two semilunar valves:
# Pulmonary semilunar (SL) valve – guards the entrance of the pulmonary trunk
# Aortic semilunar (SL) valve – guards the entrance of the aorta
+ When the heart is relaxed, the SL valves are closed; when the heart contracts, the SL valves are open
* Coronary circulation – the functional blood supply of the heart
o Provides the nourishment to heart tissue
o Divided into the left and right coronary arteries and veins
o The coronary arteries deliver blood when the heart is relaxed.
o The coronary sinus delivers poorly oxygenated blood from the myocardium to the right atrium.
* Pulmonary vs. Systemic Circulation
o Pulmonary circulation – right side of the heart; responsible for gas exchange
o Systemic circulation – left side of the heart; it is responsible for transporting blood to and from the tissues of the body.
+ Walls of the left ventricle are thicker and can generate high pressure
* Pathway of Blood through the Heart
o The right atrium receives poorly oxygenated blood from the inferior and superior vena cava and the coronary sinus.
o The blood from the right atrium drains into the right ventricle. (Tricuspid valve open/Pulmonary SL valve closed)
o Following ventricular filling, the blood is forced through the pulmonary trunk. (Tricuspid valve closed/Pulmonary SL valve open)
o The blood flows from the pulmonary trunk to the lungs where it is oxygenated.
o Oxygenated blood is delivered to the heart via the pulmonary arteries.
o The pulmonary arteries deliver blood to the left atrium.
o The blood in the left atrium drains into the left ventricle. (Biscupid (mitral) valve open/Aortic SL valve closed)
o Following ventricular filling, the blood is forced through the aorta. (Bicuspid (mitral) valve closed/Aortic SL valve open)
o Once the blood leaves the aorta, it is carried to the rest to the body.
o Once depleted of the oxygen and nutrients it contains, the blood leaves the tissues and eventually drains into the superior or inferior vena cava or the coronary sinus.
* Properties of Cardiac Muscle Fibers
o Microscopic Anatomy
+ Cardiac cells are short, fat, branched, interconnected, and striated
+ Each cardiac muscle fiber contains one or two large, centrally located nuclei.
+ The sarcomeres of cardiac cells contain actin and myosin microfilaments
+ Intercellular spaces are filled with loose connective tissue and capillaries
+ Cardiac cells are connected by specialized cell junctions, called intercalated discs.
# Intercalated discs contain:
* Desmosomes – prevent adjacent cells from separating during contraction
* Gap junctions – allow ions to pass from cell to cell
* Causes the myocardium to act as a functional syncytium (a single coordinated unit).
o Energy requirements
+ Cardiac cells are highly dependent on oxygen for metabolic needs
+ Cardiac muscle relies almost exclusively on aerobic respiration
+ Cardiac muscle is able to utilize multiple fuel sources (ex. Glucose, fatty acids, and even lactic acid for a short period of time)
* Mechanisms and Events of Contraction
o The autorhythmic cells of the heart are able to initiate their own depolarization.
o The action potential in cardiac muscle cells:
+ Normally cardiac cells have a resting membrane potential of approximately –90mV.
+ The action potential in cardiac muscle cells begins when the membrane potential is brought down to approximately –75mV.
+ The stimulus of an action potential is usually the excitation of an adjacent muscle cell.
+ Once threshold has been reached, the action potential proceeds as follows:
# RAPID DEPOLARIZATION - Voltage-regulated sodium channels open, and the membrane becomes permeable to sodium ions. This results in the rapid depolarization of the sarcolemma.
* The sodium channels are called fast channels because they open quickly and remain open for only a few milliseconds.
# THE PLATEAU –
* As the transmembrane potential approaches +30mV, the voltage-regulated sodium channels close. They will remain closed and inactivated until the membrane potential reaches –60mV.
* As the sodium channels are closing, calcium channels begin to open and calcium enters the cardiac cells. The calcium channels are called slow channels because they open slowly and remain open for a relatively long period (~175 ms). This causes the transmembrane potential to remain near 0mV for an extended period of time – this is called the plateau.
o This increase in calcium ions around the myofibrils (from the calcium ions entering the cell and the release of additional calcium ions from the sarcoplasmic reticulum) generates a contraction.
# RAPID REPOLARIZATION - As the plateau continues, slow calcium channels begin closing and slow potassium channels begin opening. This restores the resting membrane potential.
# REFRACTORY PERIOD – For some time after an action potential begins, the membrane will not respond to a second stimulus. The length of this refractory period is approximately 250ms.
* In cardiac muscle the refractory period continues until the muscle begins to relax. Summation of action potentials is not possible at this point and this prevents tetanic contractions in cardiac cells.
* Intrinsic Conduction System of the Heart
o The cardiac conduction system coordinates and synchronizes heart activity and forces the heart to beat faster
o The intrinsic conduction system of the heart consists of noncontractile cardiac cells that are able to generate and distribute electrical impulses.
+ The autorhythmic cells of the heart do not have a stable resting potential. Instead, they have spontaneously changing membrane potentials called pacemaker potentials.
# The influx of calcium ions generates the action potential, not sodium ions
# The rate of spontaneous depolarization varies in different portions of the conduction system
* Sinoatrial node – generates action potentials at a rate of 75-100 per minute
* Atrioventricular node – generates action potentials at a rate of 40-60 per minute
* Most cells of the AV bundle and Purkinje fibers do not depolarize spontaneously. Those that do depolarize at the rate of about 30 times per minute
o Components of the intrinsic conduction system:
+ The sinoatrial (SA) node – cells of the SA node reach threshold first, so they establish the heart rate
# Aka, the cardiac pacemaker
# Located in the posterior wall of the right atrium
# Contains pacemaker cells which establish the heart rate
# Generates impulses about 75 times every minute (~100 per minute, in the absence of neural and hormonal factors) – this is called the sinus rhythm
+ The atrioventricular (AV) node
# Connected to the SA node via the internodal pathway
# Located in the inferior portion of the interatrial septum, immediately above the tricuspid valve
# The impulse is delayed for about 100ms to allow for completion of the atrial contraction before ventricular contraction
* The delay is due to the smaller diameter of the fibers and the presence of fewer gap junctions
+ The atrioventricular (AV) bundle
# Aka, the Bundle of His
# Impulse travels from here to the right and left bundle branches
# The only electrical connection between the atria and the ventricles
+ The Bundle branches
# Divide into right and left bundle branches
# Run along the interventricular septum toward the heart apex
+ The Purkinje fibers
# Penetrate into the heart apex and into the ventricular walls
# The Purkinje fibers are more elaborate in the left side of the heart
# Directly supply the papillary muscles
# Ventricular contraction follows depolarization by the Purkinje fibers
* Electrocardiography
o An electrocardiogram is a graphic recording of heart activity.
+ Aka, ECG or EKG
+ 3 distinguishable deflection waves are present:
# P wave – depicts movement of the depolarization wave from the SA node to the atria.
* The atria begin to contract approximately 100ms after the start of the P wave.
# QRS complex – depicts ventricular depolarization.
* The ventricles begin contracting shortly after the peak of the R wave.
* Atrial repolarization takes place at this time, but the wave is obscured by the QRS complex.
# T wave – depicts ventricular repolarization.
* The Cardiac Cycle – All of the events associated with blood flow through the heart during one complete heartbeat.
o 2 phases:
+ Systole – Contraction
+ Diastole - Relaxtion
o Atrial Systole
+ Atria contract; increase in atrial pressures push residual blood into ventricles through the open right and left AV valves.
+ At the end of atrial systole, each ventricle contains the maximum amount of blood that it will hold in this cardiac cycle. This quantity is called the end-diastolic volume (EDV).
o Ventricular Systole
+ As the pressure inside the ventricles rise above those in the atria, the AV valves swing shut.
+ The ventricles contract, but blood flow does not occur because the pressure isn’t high enough to force open the semilunar valves – this is the period of isometric contraction.
# During isometric contraction, all of the heart valves are closed, the volume of the ventricle remains constant, and the ventricular pressure rises.
+ Once ventricular pressure exceeds that in the arterial trunks, the semilunar valves open and push blood into the pulmonary and aortic trunks – this is the beginning of the period of ventricular ejection.
+ At the end of ventricular systole, ventricular pressures fall rapidly. Blood starts to flow back toward the ventricles and it is this backward movement that closes the semilunar valves.
# When the semilunar valves close, this increases the pressure in the arterial walls and they recoil.
# The blood remaining in the ventricle when the semilunar valves close, is the end-systolic volume.
o Ventricular Diastole
+ The ventricular myocardium is resting at this point and all the heart valves are closed.
+ When ventricular pressures fall bellow those of the atria, the atrial pressure forces the AV valves to open. Blood flows from the atria to the ventricles and both the atria and ventricles are in diastole.
# The ventricular pressures continue to fall as the chambers expand.
# Because of this passive filling, the ventricles will be nearly ¾ full before the cardiac cycle ends.
* Heart Sounds (lub-dup)
o 1st sound (lub) – closing of the AV valves
+ Louder and longer than the second sound
o 2nd sound (dup) – closing of the semilunar valves
+ Short, sharp sound
* Cardiodynamics – the movements and forces generated during cardiac contractions.
o Important Terms
+ End-diastolic volume – The amount of blood in each ventricle at the end of ventricular diastole
+ End-systolic volume – The amount of blood remaining in each ventricle ate the end of ventricular systole
+ Stroke volume – The amount of blood pumped out of each ventricle during a single beat. (SV = EDV – ESV)
+ Ejection fraction – The percentage of the EDV represented by the SV.
o Stroke volume (SV) is the most important factor in an examination of a single cardiac cycle. SV is relatively constant in healthy individuals
+ Factors Controlling Stroke Volume
# The EDV
* EDV is affected by 2 factors:
o Filling time – during ventricular diastole
+ Entirely dependent upon heart rate.
# TREND: Increase in heart rate = Decrease in the available filling time; Decrease in heart rate = Increase in the available filling time
o Venous return – the rate of blood flow over this period
+ Changes in venous return can be caused by exercise, alterations in blood volume, skeletal muscle activity, patterns in peripheral ciruclation
# The ESV
* ESV is affected by 3 factors:
o Preload – the degree of stretching experienced during ventricular diastole
+ The greater the EDV, the larger the preload
# EDV is lowest during period of rest; highest during exercise
+ The greater the stretch, the greater the force of contraction (Frank-Starling law of the heart)
# Cardiac muscle cells are stretched more when there is more blood in the chambers
o Contractility – the amount of force produced during a contraction, at a given preload
+ Positive inotropic agents – increase contractility
# Ex., increase in calcium ion concentration, glucagons, thyroxine, epinephrine (sympathetic nervous system stimulation), digitalis
+ Negative inotropic agents decrease contractility
# Ex. Acidosis, elevated potassium ion levels, calcium channel blockers, parasympathetic nervous system stimulation &nbs p; &nb sp; & nbsp; ; &nb sp;
o Afterload – the amount of tension the contracting ventricle must produce to force open the semilunar valve and eject blood.
+ Relatively constant in health individuals
+ Individuals with hypertension – reduced ability to eject blood
o Cardiac output (CO) – the amount of blood pumped by each ventricle in 1 minute.
+ Examination of cardiac function over time
+ CO = Stroke Volume x Heart Rate
# Factors affecting heart rate
* Autonomic Nervous System Regulation
o Sympathetic stimulation – increases heart rate
o Parasympathetic stimulation – decreases heart rate
* Chemical Regulation
o Hormones
+ Epinephrine & thyroxine – increase heart rate
o Ions
Lecture 16: Cardiovascular System
The Heart as a Pump
The Right and Left Hearts are Connected in Series, but are Folded Together to Form a Single Unit
+ The right heart pumps blood only to the lungs; its output is low pressure (25 mm Hg)
+ The left heart pumps blood to the rest of the body; its output is high pressure (120 mm Hg)
+ Because the 2 hearts are attached they beat in synchrony
+ The 2 atria receive the incoming blood- they pump extra blood into the ventricles
+ The 2 ventricles produce enough pressure to push blood through the pulmonary and systemic circulations
This diagram is modified from one in The Sourcebook of Medical Illustration, edited by Peter Cull (Park Ridge, NJ: Parthenon, 1989).
+ The right side of the heart has been colored blue to indicate deoxygenated blood; the red color of the left side indicates oxygenated blood that has come from the lung.
+ There are no valves where the vena cavae and join the right atrium or where the pulmonary veins enter the left atrium. Pressures in the atria are small and valves are not needed.
+ Click to get a blank diagram of the heart for practice in learning the parts.
Pressure Causes Valves to Open and Close in the Heart Cycle
+ The heart has 2 sets of valves:
# AV valves: between atria and ventricles
* Flap type
* Chorda tendinae & papillary muscles keep them from being pushed too far
* Left heart: bicuspid or mitral (2 flaps)
* Right heart: tricuspid: (3 flaps)
# Semilunar valves: where arteries leave heart
* Blood caught in the 3 cusps pushes them closed
o Right heart: pulmonary semilunar
o Left heart: aortic semilunar
# Leaks in valves -> murmurs
# Usually there are no valves where veins enter the atria
* Not needed, low pressure
* Exception is a valve between the inferior vena cava and right atrium, but this is missing in many adults
+ When the heart contracts pressure builds up, forcing the valves to close
# Muscles are not required to close the valves
+ Valves in the cardiac cycle:
Event AV Valves:
Right: Tricuspid
Left: Mitral Semilunar Valves:
Right: Pulmonary
Left: Aortic
Filling of ventricle Open Closed
Building up pressure Closed Closed
Expelling blood Closed Open
+ Opening and closing of valves depends upon the pressures on opposite sides
# Example: aortic valve
# Closed during filling and building up of pressure in the left ventricle because pressure in the aorta is higher than pressure in the ventricle
# When pressure in the left ventricle becomes higher than pressure in the aorta the aortic valve opens and blood is expelled from the heart
Heart Sounds are Produced by the Closing of the Valves
+ Normal heart sounds are produced when valves snap closed: LUB-DUP
+ LUB = closing of AV valves: beginning of systole
+ DUP = closing of semilunar valves: end of systole
+ Abnormal valve sounds:
# Leakage of valve -> swishing sound (murmur)
# Narrowing of valve (stenosis) -> high pitched sound
The Cardiac Output is the Product of Heart Rate and Stroke Volume
+ Normally about 5 liters/min
+ The cardiac output per minute (CO) is the product of the size of a single output, the stroke volume (SV), and the heat rate (HR) in beats/minute:
# CO = HR X SV
# = 70 beats/min X .07 liters/beat = 5 liters/min
+ If the SV is constant, doubling the HR will double the CO
Heart Rate Can be Increased From About 70 to 200 Beats/Minute
+ Resting heart rate is about 60-80 beats/min (lower in athletes because they have large stroke volumes)
+ The HR can be increased about 3 times in exercise
+ Above about 200 beats/min the heart would not have time to fill properly- therefore nature limits the rate
+ Rate is controlled by the autonomic nervous system
Stroke Volume is Controlled by Sarcomere Length
+ When the venous return of blood to the heart increases the heart beats more forcefully and puts out more blood: Frank- Starling's law of the heart
+ Can be explained by sarcomere length:
# Cardiac muscle is like skeletal muscle: there is an optimum length for the sarcomeres
# At rest heart sarcomeres are too short to give maximum tension
# Filling heart to a greater volume stretches sarcomeres- they become more efficient and contract more strongly
# More input -> sarcomeres stretch -> stronger contraction -> more output
+ Mechanism allows SV to increase about 1.5 to 2X.
Blood Pressure is Caused by Cardiac Contraction
+ Blood pressure at the output of the left heart alternates between a high pressure (systole) and a lower pressure (diastole)
+ Systole:
# When the heart beats (systole) the pressure in the arteries leaving the heart rises to about 120 millimeters of mercury (mm Hg)
+ Diastole:
# Between beats (diastole) the arterial pressure drops to about 80 mm Hg
# The diastolic pressure does not drop to 0 because the arterial walls are elastic
# A force due to wall elasticity pushes on the arterial blood between beats
# The 80 mm Hg diastolic pressure keeps the blood flowing between beats
+ Blood pressure is reported as systolic pressure over diastolic pressure
# Example: 120/80
+ Pressure is a force per unit area. In engineering pressure is often given in pounds per square inch (PSI) or in dynes per square centimeter. Why then is blood pressure reported as millimeters of mercury? That seems to be the height of a column, not a pressure at all. Click to see an explanation of mm Hg pressure units.
Systemic Blood Pressure Depends Upon Cardiac Output and Resistance to Flow
+ The more blood pumped into the arteries the higher the pressure
+ Pressure also goes up if there is more resistance to flow- this occurs when large numbers of arterioles constrict
+ The body changes both CO and resistance to adjust blood pressure
+ The higher the blood pressure the more work the heart must do to pump blood
Blood Pressure is Regulated by Reflexes and the Kidney
+ Blood pressure must be closely regulated
# If too low circulation will be poor;
# If too high there is danger of arterial damage or hemorrhage
+ Short term regulation (seconds -> minutes): baroreceptor reflex
# Example:
* If you are lying down and suddenly stand up the pressure in the aorta will fall as blood flows to the lower limbs.
* The baroreceptor reflex will cause the heart to speed up and increase its stroke volume.
* This raises the cardiac output and the blood pressure will go up
# Components of the reflex:
* Pressure is measured by sensors in the arch of the aorta and in the carotid sinus (the carotids are the major arteries supplying blood to the brain)
* The control center is in the medulla of the brain
* Two nerves control the heart rate:
o Vagus nerve: slows the heart
o Accelerator nerve: speeds it up
+ Long term regulation (days -> years) is mainly by the kidney
# Kidney regulates the salt and water content of the body, and these substances control the blood pressure
* The more fluid in the blood vessels the higher the pressure
# Salt:
* Sodium retention is controlled by the Na pump
* The hormone aldosterone increases Na pump activity in the kidney
* The hormones renin and angiotensin control the amount of aldosterone secreted into the blood
# Water:
* If Na is retained the blood osmotic pressure rises and this causes water to be retained also- by osmosis in the kidney
* Water reabsorption in the kidney requires water channels in the kidney tubules
* The water channels are controlled by the antidiuretic hormone (ADH)
* If ADH is present at high concent
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