This document provides an overview of cardiac anatomy and physiology. It identifies the venous system of the heart including the coronary sinus. It describes the specialized conduction system including the sinoatrial node, atrioventricular node, His bundle, and Purkinje fibers. It lists the properties of cardiac cells and identifies the internal structures of the atria and ventricles. It also describes cardiac innervation and how the autonomic nervous system influences heart rate, conductivity and contractility. Key concepts covered include cardiac output, stroke volume, preload, afterload, and the Frank-Starling law of the heart.
there is detailed analysis of mitral valve segments by 2d transesophageal echo cardiography. There is a review on this and simplified approach how one can identify the pathological segment with great accuracy using two dimensional tee.
there is detailed analysis of mitral valve segments by 2d transesophageal echo cardiography. There is a review on this and simplified approach how one can identify the pathological segment with great accuracy using two dimensional tee.
Idiopathic VT refers to VT occurring in structurally normal hearts in the absence of myocardial scarring. Classification of monomorphic idiopathic VT includes outflow tract VT, fascicular VT, papillary muscle VT,annular VT, and miscellaneous (VT from the body of the RV and crux of
the heart). It is commonly seen in young patients and usually has a benign course. The 12-lead lectrocardiogram is critical in distinguishing the specific form and locations of idiopathic VT. Treatment options include medical therapy specific to the underlying mechanism of VT or catheter
ablation.
Idiopathic VT refers to VT occurring in structurally normal hearts in the absence of myocardial scarring. Classification of monomorphic idiopathic VT includes outflow tract VT, fascicular VT, papillary muscle VT,annular VT, and miscellaneous (VT from the body of the RV and crux of
the heart). It is commonly seen in young patients and usually has a benign course. The 12-lead lectrocardiogram is critical in distinguishing the specific form and locations of idiopathic VT. Treatment options include medical therapy specific to the underlying mechanism of VT or catheter
ablation.
A PowerPoint Presentation on Basic Electrophysiology of Heart and Angiotensin Converting Enzymes and their Inhibitors suitable for Undergraduate MBBS level Students
Conductive system of heart by Dr. Pandian M Pandian M
The student will be able to: (MUST KNOW)
Name the parts of conducting system of the heart.
Appreciate the importance of AV nodal delay.
Explain the mechanism of AV nodal delay.
Give the conduction velocity in different cardiac tissues.
Understand the propagation of electrical impulse in conducting system of heart.
CONDUCTIVE SYSTEM OF HEART .pptx BY MRS. WINCY THIRUMURUGAN .PROFESSOR.NURSIN...WINCY THIRUMURUGAN
MEANING.
The conducting system of the heart consists of cardiac muscle cells and conducting fibers (not nervous tissue) that are specialized for initiating impulses and conducting them rapidly through the heart.
It provides the heart its automatic rhythmic beat.
The purpose is to
Generating rhythmical electrical impulses to cause rhythmical contraction of the heart muscle. Conducting these impulses rapidly throughout the heart.
This pathway is made up of 5 elements:
The sino-atrial (SA) node.
The atrio-ventricular (AV) node.
The bundle of His.
The left and right bundle branches.
The Purkinje fibers.
SINOATRIAL NODE
The sinoatrial (SA) node is a collection of specialized cells (pacemaker cells), and is located in the upper wall of the right atrium, at the junction where the superior vena cava enters.
These pacemaker cells can spontaneously generate electrical impulses. The wave of excitation created by the SA node spreads via gap junctions across both atria, resulting in atrial contraction (atrial systole) – with blood moving from the atria into the ventricles.
The SA node is supraventricular and is sensitive to parasympathetic and sympathetic influence.
The SA node generates impulses and influenced by the Autonomic Nervous System:
Sympathetic nervous system – increases firing rate of the SA node, and thus increases heart rate.
Parasympathetic nervous system – decreases firing rate of the SA node, and thus decreases heart rate
THE INTER NODAL PATHWAYS consist of three bands (anterior, middle, and posterior) that lead directly from the SA node to the next node in the conduction system, the atrioventricular node. The impulse takes approximately 50 m s (milliseconds) to travel between these two nodes.
Bachmann's bundle (BB), also known as the interatrial bundle, myocardial strands connecting the right and left atrial walls and is considered to be the main pathway of interatrial conduction.
THE AV NODEThe AV node is located in the posterior wall of the right atrium immediately behind the tricuspid valve.
Cause of Slow Conduction in the A-V Node
What is the significance of AV nodal delay?
The cardiac impulse does not travel from the atria to the ventricles too rapidly.
It is primarily the AV node and it’s adjacent fibers that delay this transmission into the ventricles
AV BUNDLE OR BUNDLE OF HIS
From the AV node arises a special conducting pathway .
RIGHT AND LEFT BUNDLE BRANCHES
FASCICLE
The right bundle branch contains one fascicle.
The left bundle branch into three fascicles:
The left anterior,
The left posterior, and
The left septal fascicle.
PURKINJE FIBRES
The LT and RT bundle branches divides in turn course sidewise around each ventricular chamber and back toward the base of heart.
The ends of Purkinje fibers penetrate about one third of the way into muscle mass and finally become continuous with cardiac muscle fibers
,abundant with glycogen and extensive gap junctions, rapidly transmit cardiac action potentials in 0.03sec
Cardiac muscle has three types of membrane ion channels that play important roles in causing the voltage changes of the action potential. They are (1) fast sodium channels, (2) slow sodium-calcium channels, and (3) potassium channels
Depolarization: First, the action potential of cardiac muscle is caused almost entirely by sudden opening of large numbers of so-called fast sodium channels that allow tremendous numbers of sodium ions to enter the cardiac muscle fiber from the extracellular fluid. These channels are called “fast” channels because they remain open for only a few thousandths of a second and then abruptly close. After depolarization, there's a brief repolarization that takes place with the efflux of potassium through fast acting potassium channels.
Plateau: Secondly, another entirely different population of slow calcium channels, which are also called calcium-sodium channels. This second population of channels differs from the fast sodium channels in that they are slower to open and, even more important, remain open for several tenths of a second. During this time, a large quantity of both calcium and sodium ions flows through these channels to the interior of the cardiac muscle fiber, and this maintains a prolonged period of depolarization, causing the plateau in the action potential.
Repolarization: When the slow calcium-sodium channels do close at the end of 0.2 to 0.3 second and the influx of calcium and sodium ions ceases, the membrane permeability for potassium ions also increases rapidly; this rapid loss of potassium from the fiber immediately returns the membrane potential to its resting level, thus ending the action potential.
definition of conductive system of heart brief explanation of components of conductive system
ECG interpretations major waves of ECG ,intervals of ECG ,
segments of ECG brief explanation
Similar to Anatomy & physiology for the EP professional part II 8.4.14 (20)
Synthetic Fiber Construction in lab .pptxPavel ( NSTU)
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This will be used as part of your Personal Professional Portfolio once graded.
Objective:
Prepare a presentation or a paper using research, basic comparative analysis, data organization and application of economic information. You will make an informed assessment of an economic climate outside of the United States to accomplish an entertainment industry objective.
June 3, 2024 Anti-Semitism Letter Sent to MIT President Kornbluth and MIT Cor...Levi Shapiro
Letter from the Congress of the United States regarding Anti-Semitism sent June 3rd to MIT President Sally Kornbluth, MIT Corp Chair, Mark Gorenberg
Dear Dr. Kornbluth and Mr. Gorenberg,
The US House of Representatives is deeply concerned by ongoing and pervasive acts of antisemitic
harassment and intimidation at the Massachusetts Institute of Technology (MIT). Failing to act decisively to ensure a safe learning environment for all students would be a grave dereliction of your responsibilities as President of MIT and Chair of the MIT Corporation.
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Exploiting Artificial Intelligence for Empowering Researchers and Faculty,
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2. ObjectivesObjectives
• Identify the venous system of the heart
• Identify the electrophysiology properties of the heart
• Describe the flow of conduction through the heart
• List the properties of cardiac cells
• Identify the internal structures of the heart
• Describe cardiac innervation and the effects on heart
rate.
• Identify the components of cardiac output
• Describe preload and afterload
3. Cardiac Venous SystemCardiac Venous System
• Cardiac veins lie next to the arteries.
• Coronary sinus (CS) is the largest vein
– Traverses posterior in the AV sulcus and lies next to the
LCX.
• The CS receives blood from the Great, middle and small
cardiac veins, the oblique vein of the LA and posterior vein of
the LV.
• Anterior cardiac venules drain directly into the RA.
• Ostium of the CS is located in the RA posterior and slightly
inferior to the MV structure.
9. Anatomy of specialized conduction system
Specialized conduction
system
• Sinoatrial (SA), or
Sinus Node
• Atrioventricular
(AV) Node
• His Bundle
• Left Bundle
Branch
• Right Bundle
Branch
10. Conduction SystemConduction System
• Electrophysiology properties
– SA Node
– AV Node
– His Bundle
– Right and left bundle branches to
include the Purkinje fibers
11. Normal sinus rhythm
Intracardiac tracings show
the normal intervals
between
•initiation of atrial
depolarization A
•His bundle activation H
•ventricular depolarization V
• AH + HV = PR interval
12. Right Atrium conductionRight Atrium conduction
• Right Atrium
–SA node (SAN)
–Internodal pathways
–Interatrial pathways
–Bachmann’s Bundle
–AV node
• Triangle of Koch
13. Right Atrium – SA nodeRight Atrium – SA node
conductionconduction
• Located in the RA at the junction of the anterior RA and
the SVC
• 2 cm long and .05 cm wide
• Thought to extend inferiorly in to the Christa trerminalis
• SA node has the fastest automaticity generating
impulses at 100-110 bpm
– vagal tone suppresses this… 60-100bpm
– Conduction speed w/i SAN: 0.05m/sec
• Calcium dependent action potential
• Transitional cells at the border of the node.
14. SA Node CellsSA Node Cells
• P cells (pole cells)
– main characteristic: automaticity
– the fastest depolarizing conduction system cells
– aka. pacemaker cells
• Transitional cells
– form a network of fibers
– mainly found on the SA node periphery (border)
– attached to the P cells on one side and to the
atrial myocardium on the other side
– transmits activation from the SA node to the
atrium
15. SA Node - stained cross-SA Node - stained cross-
sectionsection
atrial myocytes
Cross section RA wall
epicardium
endocardium
adipose
SAN artery SA node
16. 3 Internodal Tracks3 Internodal Tracks
• There is evidence for preferential spread of atrial activation
between SA & AV nodes by way of intranodal pathways but
whether these are distinct “true” tracts or simply areas of
preferential conduction is unclear
• Text have described 3 Internodal tracks:
– Anterior – Bachman’s Bundle –Travels concurrently from
the SA node to the left atrium and AV node. (white arrows)
– Middle -Travels from the SA node posteriorly around the
SVC, down the inter-atrial septum to the AV node, (red
arrows)
– Posterior -Travels from the SA node posteriorly through
the Crista Terminalis, to the posterior interatrial septum to
the AV node. (yellow arrow)
17. SA Node & Internodal tracksSA Node & Internodal tracks
18. AV NodeAV Node
• Impulse reaches the AV Node.
– AV node is located at the base of the RA at the
apex of the Triangle of Koch.
• Triangle of Koch comprised of the Tendon of Todaro,
septal leaflet of the Tricuspid valve and the Os of the CS
– AV node is comprised of specialized conducting
tissue allowing the impulse to travel through the
fibrous septum.
– The AV node is slower to conduct (calcium
dependent).
– Acts as the “gate Keeper”
19. AV nodeAV node
• Specialized collection of conducting cells provide the only link
between the A & V passage of a wave of depolarization
• Oval-shaped, 60 x 30mm in size
• Located subendocardially on the interatrial septum
– RA side: within the triangle of Koch.
– LA side: next to the base of the mitral valve annulus
• Anteriorly and inferiorly, continuous with the His bundle
• Rich blood supply from AV nodal artery branch of RCA in 90%
• 2 types of cells
– rod-shaped: contains Na channels
– ovoid-shaped: responsible for spontaneous activity
20. AV nodeAV node
• AVN conduction speed is approximately 0.1msec
• AVN conduction speed is inversely proportional to
prematurity of the impulse received
• The cells of the AV node are responsible for the
slowing of conduction between atria and ventricles
• This functions to permit sequential atrial then
ventricular contraction
• AVN node is richly innervated…
– sympathetic fibers: increase the speed of conduction
– parasympathetic fibers: have the opposite effect
21. Cells of the AV JunctionCells of the AV Junction
•AN (atrio-nodal) cells
•in the transitional region
•activated shortly after the atrial cells
•Action potential (AP) visual appearance is between
the fast & brief atrial AP and the slower nodal APs
•N (nodal) cells
•"most typical" of the nodal cells
•have slow rising and longer AP duration
•the site of Wenckebach
•NH (nodal-His) cells
•typically distal to the site of Wenckebach block
•AP’s closer in visual appearance to the fast rising
and long AP of the His bundle.
23. The His BundleThe His Bundle
• The impulse reaches the His bundle.
– The His bundle is the most proximal
portion of the His Purkinje System
– Rapidly conducting
– Branches to form the right bundle branch,
and left anterior and posterior bundle
branches, located within the AV septum
– Further branches to Purkinje fibers within
the ventricular myocardium
24. Bundle BranchesBundle Branches
• His purkinje trifurcates
• Right bundle within the membranous
septum
• Exits septum via the moderator band
• Moderator band attaches to the RV free
wall
25. Bundle branchesBundle branches
• At trifurcation of the His...
• Left bundle further bifurcates
• Anterior bundle traverses the
interventricular septum to the apex
• Posterior bundle traverses posteriorly,
in a fan like fashion, innervating the
basilar portion of the LV
26. His Purkinje systemHis Purkinje system
• specialized heart muscle cells for electrical
conduction
• Diameter: 3 mm
• Length: 12 to 40 mm
– (penetrating 8-10 mm)
• begins at the AV node and passes through the right
annulus fibrosis to the membranous part of the
interventricular septum
• starts to branch at the lower part of the membranous
septum
• named after the Swiss cardiologist Wilhelm His, Jr.,
who discovered them in 1893
28. Purkinje fibersPurkinje fibers
peripheral branching of the bundle branches
made up of individual myofibrils
divided by collagen fibers that prevent the lateral
spread of activation
form a subendocardial network that spreads among
the ventricular muscle fibers
directly innervate the myocardial cells and initiate the
ventricular depolarization cycle
Purkinje conduction speed
subendocardial: 2-10m/sec
ventricular muscle proper: 0.3m/sec
29. Four Properties of CardiacFour Properties of Cardiac
CellsCells
• Rhythmicity (Automaticity)
• Excitability
• Conductivity
• Contractility
30. Rhythmicity:Rhythmicity: (Automaticity)(Automaticity)
• Pacemaker cells can discharge an
electrical current without an
external stimulus.
• Once the cells are stimulated, the
flow is passed from one to another
in the conduction system until the
muscle contracts.
31. ExcitabilityExcitability
The ability of the cardiac cell to
respond to an electrical stimulus
with an abrupt change in its
electrical potential. (All or none
phenomenon)
35. Right Atrium internal -Right Atrium internal -
StructuresStructures
• Tendon of Todaro-
– Fibrous strand from the union of the Eustachian and
Thebesian valves which inserts into the AO root
passing thru the atrial wall myocardium.
• Triangle of Koch-
– Comprised of the membranous septum, the Os of
the CS and the tricuspid annulus
– Location of the AV Node
• Eustachian Ridge –
– fold of tissue at the anterior of the IVC
• Thebesian Valve –
– Fold of tissue that guards the Coronary Sinus
37. Right Ventricle internalRight Ventricle internal
structuresstructures
• Divided into the postero-inferior portion and the
antero-superior outflow portion.
• Demarcated by prominent muscle bands
• Parietal band, septal band and the moderator band.
• Inflow wall is heavily trebeculated
• Outflow portion few trebeculae
• Sub-Pulmonic area smooth muscled
• Papillary muscles anchor to ventricular myocardium
• Chordae tendonae anchor papillary muscles to the
valve leaflets.
39. Left Atrium internalLeft Atrium internal
StructuresStructures
• Mainly smooth walled structure
– Atrial septal surface smooth
– Left appendage offers small pectinate muscle
• Posterior wall may be .05 – 4.0 mm thick
• On the right – two, sometimes, three
pulmonary veins enter
• On the left – two, sometimes one, pulmonary
veins enter.
40. Structures that are external toStructures that are external to
the Left Atriumthe Left Atrium
• External structures to the LA
– Right superior PV – Aorta
– Right & Left Superior PV – Pulmonary
Artery
– Posterior medial to lateral atrial wall –
Esophagus
42. Left Ventricle internalLeft Ventricle internal
StructuresStructures
• Thickness 3 times greater than RV
• Majority of LV trebeculated
• Basilar third is smooth walled
• Two papillary muscles anchor the Mitral
Valve
• Ventricular septum muscular.
52. ChemoreceptorsChemoreceptors
– Located in internal carotid arteries and
aortic arch
• Detect and respond to changes in:
–Oxygen content of the blood
–pH
–Carbon dioxide tension
53. Cardiac OutputCardiac Output
• Volume of blood ejected from the
heart over 1 minute
• RV and LV output usually equal
• CO = HR X SV
54. SSx of Decreased COSSx of Decreased CO
• Cold, clammy
skin
• Color changes in
skin/mucous
membranes
• Dyspnea
• Orthopnea
• Crackles (rales)
• Changes in
mental status
• Changes in blood
pressure
• Arrhythmias
• JVD
• Fatigue
• Restlessness
55. Stroke VolumeStroke Volume
• Amount of blood ejected during
one contraction
• Dependent on:
–Preload
–Afterload
–Myocardial contractility
56. PreloadPreload
• Force exerted by the walls of the
ventricles at the end of diastole
• Influenced by venous return
–Hypovolemia decreases preload
–Heart failure increases preload
57. Frank-Starling Law of theFrank-Starling Law of the
HeartHeart
• Up to a limit, the more a myocardial
muscle is stretched, the greater the
force of contraction (and thus
stroke volume)
–Influenced by both preload and
afterload
59. AfterloadAfterload
• Afterload is the pressure or
resistance against which the
ventricles must pump to eject
blood
–Results in
• Increased myocardial workload
• Increased myocardial O2 demand
60. AfterloadAfterload
• Vasoconstriction results in
increased afterload and increased
myocardial work and O2 demand
• Vasodilation results in decreased
afterload decreased myocardial
work and O2 demand
61. Blood PressureBlood Pressure
• Force exerted by circulating blood
volume on arterial walls
• Influenced by peripheral vascular
resistance (PVR)
–Resistance to blood
–Determined by vessel diameter and
muscle tone
• BP = CO X PVR
62. Normal Heart PressuresNormal Heart Pressures
Pressure Measurement Normal
RA Mean 2-8 mm Hg
RV Systolic 25-35mm Hg
End Diastolic 2 -8 mm Hg
PA Systolic 25-35mm Hg
End Diastolic 8-12mm Hg
63. Normal Heart PressuresNormal Heart Pressures
Pressure Measurement Normal
PCW Mean 8-12mm Hg
Aorta Systolic 90-140mm Hg
Diastolic 60-90mm Hg
LV Systolic 90-140mm Hg
End Diastolic 8-12mm Hg
64. ReferencesReferences
• Netter, F H (1987) The CIBA collection of medical Illustrations.
Volume 5 The heart. Colorpress, New York NY
• Mazgalev, T.N., Tchou, P.J. (2000) Atrial AV Nodal
Electrophysiology; A view from the millennium. Futura, Armonk,
NY
• Podrid, P.J., Kowey, P.R. (2001) Cardiac Arrhythmia,
Mechanisms, Diagnosis & Management, 2nd
Ed. Lippincott,
Williams & Wilkins. Philadelphia PA
• Anderson, R.H. (2000) Electrical Anatomy of the Atrial
Chambers. Medtronic USA
• Anderson R.H., Ho, S.W. ( n.d.) The Anatomy of the
Atrioventricular Node. Article review by Sechler, D.A., RN
Triangle of Koch comprised of the Tendon of Todaro, septal leaflet of the Tricuspid valve and the Os of the CS
The heart is innervated by both the sympathetic and parasympathetic divisions of the autonomic nervous system. The sympathetic division mobilizes the body, allowing the body to function under stress (“fight or flight” response). The parasympathetic division is responsible for the conservation and restoration of body resources (“feed and breed” response). Autonomic regulation of the cardiovascular system requires sensors, afferent pathways, an integration center, efferent pathways, and receptors.
Sympathetic (accelerator) nerve fibers supply the sinoatrial (SA) node, the atrioventricular (AV) node, the atrial muscle, and the ventricular myocardium. Stimulation of sympathetic nerve fibers results in the release of norepinephrine, a neurotransmitter, which increases the force of ventricular contraction, heart rate, blood pressure, and cardiac output.
Parasympathetic (inhibitory) nerve fibers supply the SA node, the atrial muscle, and the AV junction of the heart by means of the vagus nerves. Acetylcholine, a neurotransmitter, is released when parasympathetic (cholinergic) nerve fibers are stimulated. Acetylcholine binds to parasympathetic receptors.
Parasympathetic stimulation slows the rate of discharge of the SA node, slows conduction through the AV node, decreases the strength of atrial contraction, and can cause a small decrease in the force of ventricular contraction. (There is little effect on the strength of ventricular contraction because of the minimal parasympathetic innervation of these chambers). The net effect of parasympathetic stimulation is a slowing of the heart rate.
Parasympathetic (inhibitory) nerve fibers supply the SA node, atrial muscle, and the AV junction of the heart by means of the vagus nerves. Acetylcholine, a neurotransmitter, is released when parasympathetic (cholinergic) nerve fibers are stimulated. Acetylcholine binds to parasympathetic receptors. The two main types of cholinergic receptors are nicotinic and muscarinic receptors. Nicotinic receptors are located in skeletal muscle, and muscarinic receptors are located in smooth muscle.
Sympathetic (accelerator) nerve fibers supply the SA node, the AV node, the atrial muscle, and the ventricular myocardium. Stimulation of sympathetic nerve fibers results in the release of norepinephrine, a neurotransmitter that increases the force of ventricular contraction, heart rate, blood pressure, and cardiac output.
Sympathetic (adrenergic) receptor sites are divided into alpha-, beta-, and dopaminergic receptors. Dopaminergic receptor sites are located in the coronary arteries, renal, mesenteric, and visceral blood vessels. Stimulation of dopaminergic receptor sites results in dilation.
Different body tissues have different proportions of alpha- and beta-receptors. In general, alpha-receptors are more sensitive to norepinephrine and beta-receptors are more sensitive to epinephrine. Stimulation of alpha-receptor sites results in the constriction of blood vessels in the skin, cerebral, and splanchnic circulation.
Beta-receptor sites are divided into beta-1 and beta-2 categories. Beta-1–receptors are found in the heart. Stimulation of beta-1–receptors results in an increased heart rate, contractility, and, ultimately, irritability of cardiac cells. Beta-2–receptor sites are found in the lungs and skeletal muscle blood vessels. Stimulation of these receptor sites results in dilation of the smooth muscle of the bronchi and blood vessel dilation.
Increases in heart rate shorten all phases of the cardiac cycle, but the most important is a decrease in the length of time spent in diastole. If the length of diastole is shortened, there is less time for adequate ventricular filling. In some cases of a rapid heart rate, vagal maneuvers (e.g., carotid sinus pressure) may be performed to attempt to slow the rate. When vagal maneuvers are performed, baroreceptors in the carotid arteries are stimulated to slow AV conduction, resulting in slowing of the heart rate.
Baroreceptors (pressoreceptors) are specialized nerve tissue (sensors) located in the internal carotid arteries and the aortic arch. These sensory receptors detect changes in blood pressure and cause a reflex response in either the sympathetic or parasympathetic divisions of the autonomic nervous system.
If the systolic blood pressure decreases, the body’s normal compensatory response to increase blood pressure is peripheral vasoconstriction, increased heart rate (chronotropy), and increased myocardial contractility (inotropy). In this example, the compensatory responses occur because of a reflex sympathetic response (also called adrenergic response). If the systolic blood pressure increases, the baroreceptor reflex response decreases sympathetic stimulation and increases parasympathetic stimulation (cholinergic response).
Chemoreceptors in the internal carotid arteries and aortic arch detect changes in the concentration of hydrogen ions (pH), oxygen, and carbon dioxide in the blood. The response to these changes by the autonomic nervous system can be sympathetic or parasympathetic. Decreased pH or oxygen levels or increases in carbon dioxide levels in the blood cause a sympathetic response, resulting in increased heart rate, contractility, and vasoconstriction.[i] Increased pH or decreased carbon dioxide levels in the blood causes a decrease in vasoconstrictor effects, leading to a general vasodilatory effect.
Nerve impulses are carried from the sensory receptors to the brain by means of the vagus and glossopharyngeal nerves (afferent pathways). The medulla of the brain serves as the integration center and interprets the sensory information received. The medulla determines what body parameters need adjustment (if any) and transmits that information to the heart and blood vessels by means of motor nerves (efferent pathways).
[i] Thibodeau GA, Patton KT: Anatomy & Physiology, ed 2, St. Louis, 1993, Mosby.
Cardiac output is the amount of blood pumped into the aorta each minute by the heart. It is defined as the stroke volume (amount of blood ejected from a ventricle with each heartbeat) multiplied by the heart rate. In the average adult, normal cardiac output is between 4 and 8 liters/min. The cardiac output at rest is approximately 5 liters/min (stroke volume of 70 mL times a heart rate of 70 beats/min).
Because the cardiovascular system is a closed system, the volume of blood leaving one part of the system must equal that entering another part. For example, if the left ventricle normally pumps 5 liters/min, the volume flowing through the arteries, capillaries, and veins must equal 5 liters/min. Thus, the cardiac output of the right ventricle (pulmonary blood flow) is normally equal to that of the left ventricle on a minute-to-minute basis.
Cardiac output varies depending on hormone balance, an individual’s activity level and body size, and the body’s metabolic needs. Factors that increase cardiac output include increased body metabolism, exercise, and the age and size of the body. Factors that may decrease cardiac output include shock, hypovolemia, and heart failure.
Signs and symptoms of decreased cardiac output include cold, clammy skin; color changes in the skin and mucous membranes; dyspnea, orthopnea, and crackles (rales); changes in mental status; changes in blood pressure; dysrhythmias; jugular venous distention; fatigue; and restlessness.
Cardiac output may be increased by an rise in heart rate or stroke volume.
An increase in myocardial contractility (and subsequently, stroke volume) may occur because of norepinephrine and epinephrine released from the adrenal medulla; thyroxin, insulin, and glucagon released from the pancreas; or medications such as calcium and digitalis.
A decrease in contractility may result from severe hypoxia, decreased pH, hypercapnea (elevated carbon dioxide levels), and medications such as propranolol (Inderal).
Stroke volume is determined by the degree of ventricular filling during diastole (preload), the pressure against which the ventricle must pump (afterload), and the myocardium’s contractile state.
Preload is the force exerted on the walls of the ventricles at the end of diastole. The volume of blood returning to the heart influences preload. More blood returning to the right atrium increases preload; less blood returning decreases preload.
According to the Frank-Starling law of the heart, to a point, the greater the volume of blood in the heart during diastole, the more forceful the cardiac contraction, and the more blood the ventricle will pump (stroke volume). This is important so that the heart can adjust its pumping capacity in response to changes in venous return, such as during exercise. If, however, the ventricle is stretched beyond its physiological limit, cardiac output may fall due to volume overload and overstretching of the muscle fibers.
Afterload is the pressure or resistance against which the ventricles must pump to eject blood. Afterload is influenced by arterial blood pressure, arterial distensibility (ability to become stretched), and arterial resistance. The less resistance there is (lower afterload), the more easily blood can be ejected. Increased afterload (increased resistance) results in increased cardiac workload. Conditions that contribute to increased afterload include increased blood viscosity, hypertension, and aortic stenosis.
The mechanical activity of the heart is reflected by the pulse and blood pressure.
Blood pressure is the force exerted by the circulating blood volume on the walls of the arteries.
Peripheral resistance is the resistance to the flow of blood determined by blood vessel diameter and the tone of the vascular musculature. Blood pressure is equal to cardiac output times peripheral resistance.
Blood pressure is affected by any condition that increases peripheral resistance or cardiac output. Thus, an increase in either cardiac output or peripheral resistance will result in an increase in blood pressure. Conversely, a decrease in either will result in a decrease in blood pressure.
Tone is a term that may be used when referring to the normal state of balanced tension in body tissues.
The heart functions as a pump to propel blood through the systemic and pulmonary circulations. As the heart chambers fill with blood, the heart muscle is stretched. The most important factor determining the amount of blood pumped by the heart is the amount of blood flowing into it from the systemic circulation (venous return).