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Case 3: Physiology 2 - Coggle Diagram
Case 3: Physiology 2
Intrinsic Factors and Extrinsic FactorsDefine Intrinsic and Extrinsic Factors
- Intrinsic Control
- Intrinsic Factors are those inbuilt mechanisms found inside the heart
- They give the heart it's Automaticity
- Example: Rate and Rhythm, Preload, Contractility and Afterload
- Extrinsic Control
- Extrinsic control mechanisms are factors outside the heart
- Hearts response to the Autonomic nervous system
- The Extrinsic and Intrinsic Control Mechanisms are integrated
Regulation of the Cardiac Output
- In order to regulate the heart, you need to regulate the Stroke Volume and Heart Rate
- These are the main Determinants of Cardiac Output
- Heart Rate depends on the
- Rate which is the Number of Beats per Minute
- Rhythm which is the initiation and regularity of the beats
- Stroke Volume depends on the:
- Preload which is the filling volume or stretch or initial fibre length
- Afterload which is the resistance to ventricular flow
- Contractility which is the capacity of the Myocardium to generate force
Intrinsic factorsList the Intrinsic Factors
- Rate
- Rhythm
Intrinsic Factors: Rate and Rhythm (Automaticity and Conduction System
- The Heart Rate and Rhythm are determined by the different parts of the Conduction System
- For example SA Node beats the fastest at a rate of 100/min, AV Node and Bundle of His beat at a rate of 40-60 and the Purkinje Fibres beat at a rate of 20-40
- The heart rate is determined by the Fastest Pacemaker Site.
- Therefore, the Sinoatrial Node determines the Heart Rate because it creates a Refractory period for the slower Pacemaker Sites
- ONLY when the SA Node is not fully functional will the other Pacemaker Sites takeover the Heart Rate at a SLOWER Rate
Outline the Chronotropic Effects
- Chronotropic effect involves the rate of change of the heart rate
- There are Positive and Negative Chronotropics
Outline the Dromotropic Effects
Rate and Rhythm: ArrhythmogenesisOutline Arrhythmogenesis with regards Rate and Rhythm
- The abnormalities of the Heart Rate, Rhythm and the Conduction System produces Arrhythmias.
- Arrhythmias may be caused by the following:
- Pacemaker dysfunction
- Conduction Defects such as Heart blocks
- Re-entry Pathways also known as Pre-excitation phenomenon
- Bundle Branch block
- Ectopic excitation by damaged site
Intrinsic Control Mechanisms
- Preload
- Preload is the End-Diastolic Volume which is the volume of blood remaining in the ventricle, after the previous ventricular contraction.
List the Factors that control PreloadFactors that affect Preload
Outline the Frank Starling Principle GRAPH
- If we look at a graphical relationship between Stroke Volume and Ventricular Preload:
- Stroke Volume (SV) is the volume of blood in millilitres ejected from the each ventricle due to the contraction of the heart muscle which compresses these ventricles.
- We start off at a Normal Stroke Volume determined by a normal Ventricular preload
- If we change the Ventricular Preload we get relationship seen in the graph where:
- A High Ventricular Preload results in a Higher Stroke Volume
- A Low Ventricular Preload results in a too Low Stroke Volume
- However, if the Ventricular Preload is too High it results in a Lower Stroke Volume
- The Resulting curve represents the Frank-Starling Principle of Contraction
- If a Patient is Hypovolaemic with a Low Ventricular Preload, they will have a Low Stroke Volume and will require Blood replacement
- If a patient has an overfilled circulation (Hypervolemia) then their Stroke Volume will decrease
- At Normal Contract, Ventricular Preload and Stroke Volume, the Sarcomere length is Optimum so that there is efficient interaction between the Myofilaments
- At a Low Ventricular preload, and Stroke Volume, the Sarcomere length is Shortened. As a result the interaction between the Myofilaments is not optimum due too Congestion. Resulting in decreased Contraction
- At an abnormally high Ventricular Preload and decreased Stroke Volume, the Sarcomere length is Overstretched. As a result the areas of interaction between the Myofilaments are SMALL
Preload (End-Diastolic Volume)List the Determinants of Right Ventricular Preload
- The Determinants of Right Ventricular preload are as follows:
- Venous Return, which is the blood coming back into the heart.
- Venous Return is determined by mechanisms that pull blood from the Periphery back to the heart such as:
- Muscle Compression action
- Respiratory Pump action
- Diastolic Filling Time
- If an individual has Tachycardia their diastolic filling time is shortened resulting in less time for the heart to fill up
- If an individual as Bradycardia their diastolic filling time is increased resulting in the heart having more time to fill up
- Right Atrial pressure
- Right atrial pressure level determines if the blood can freely flow back to the Atria
- Ventricular Compliance (Distensibility)
- Ventricular compliance is whether or not the ventricles are compliant to fill up with blood.
Intrinsic Control Mechanisms
- Contractility
- Contractility is the capacity of the Myocardium to generate force
List the Factors which determine Contractility
- Factors which determine Contractility:
- Inotropism
- Force-Frequency Relationship (Treppe Effect)
- Effects of Changes in the Afterload (Anrep's Effect)
Outline Inotropism GRAPH
- Contractility can also be changed by the concept of Inotropism
- If we look at the Tension Generated by the Heart as a Function of Time the following may occur:
- If the heart contracts normally, the maximum tension generated by the Heart will be Normal.
- If a Positive Inotropic Drug is given such as catecholamines (Adrenaline) the maximum Tension generated by the Heart will be Increased.
- If a Negative Inotropic Drug is given such as Voltage Gated Calcium Channel Blockers the maximum Tension generated by the Heart will decrease below the Normal Tension generated by the Heart.
Contractility: Force-Frequency Relationship (Treppe Effect) / Staircase PhenomenonOutline the Treppe Effect
- Contractility can also be changed by a change in Heart Rate this is known as the Force-Frequency Relationship or the Treppe effect
Outline the Force-Frequency Relationship (Treppe Effect) GRAPH
- If we look at the Force/Tension generated by the Ventricle as a Function of Heart Rate the following may occur:
- If the Heart Rate Increases the Force/Tension generated by the Ventricle also Increases
- If the Heart Rate is increased again there will be a steady Increase in the Force/Tension generated by the Ventricles thus creating a "Staircase" Graph
- Therefore, as the Heart Rate increases there will be a Steady increase in the Tension/Force generated by the Ventricles.
- This is known as the Staircase Phenomenon, in which case human beings have a Positive Staircase Phenomenon or a Positive Force-Frequency Relationship
- This is due to the accumulation of Ca2+ Ion as a result of the Na+/Ca2+ Exchanger Slowing Down, as the Na+/K+ ATPase gets Saturated
- Therefore, more Ca2+ Ions are remaining in the Cytoplasm to interact with the myofilaments
Contractility: Effects of Changes in the Afterload (Anrep's Effect)
- Afterload is the resistance to the Ventricular flow of blood or the Resistance the heart experiences when ejecting blood
- Contractility can also be effected by the Effects of Changes in the Afterload (Anrep's Effect)
Outline the Anrep's Effect
- If we look at Tension generated by the Heart as a Function of Afterload the following may occur:
- As the Afterload increases, the Tension Generated by the heart also Increases till a certain point.
- This is to ensure that the Force Generated by the Heart can compensate for Changes in the Aortic Pressure so that there is no decrease in the Cardiac Output (Stroke Volume)
- However, when the Afterload is too HIGH, the Tension Compensation Mechanism of the Heart fails resulting in Heart Failure
- Therefore, the Anrep's Effect is to ensure that the Stroke Volume (Cardiac Output) is maintained even at HIGHER Aortic Pressures
Intrinsic Control Mechanism
- Afterload (outflow Resistance)
- Afterload is the resistance to ventricular outflow or the Outflow Resistance that the Heart experiences when ejecting blood through the Valves or Blood Vessels
List the Factors which affect Afterload
- Factors which affect Afterload:
- Blood vessels and Valves (Mainly the Radius)
- Quality of Flow (Laminar and Turbulence)
- Arterial Elastic Rebound (The Winkessel Effect)
- Vascular Tone of Blood Vessels
Outline the effects of Blood Vessels and Valves on the Afterload EQUATION & GRAPH
- Mathematically, the Blood flow depends on:
- Whether there is Pressure to drive the blood
- Whether the Diameter of the Blood Vessels and Valves is open
- With an Inverse Relationship to:
- Length of the Blood Vessels and Valves
- Viscosity: whether or not the Blood being driven is Viscos
- Therefore, according to Poiseuille's equation, the Flow of Blood is
- Directly proportional to the Pressure and Radius of the Tubes
- Inversely Proportional to the Length of the Tube and Viscosity of the Blood
- It is important to note that the Radius of the Blood Vessels and Valves is critical to the Blood Flow as any changes to the Radius result in great Changes in the Blood Flow
Outline the Structure of the Blood Vessels and Valve Lumen
- Valve has an Outer Annulus and Inner Orifice
- Therefore, the Radius of Valves would change if there is a change in the Annulus or Orifice of the Valve as a result of a Valvular disease
- Blood Vessels has three layers:
- Outer Adventitia Layer
- Middle Media (Elastic) Layer
- Inner Intima (Cellular) Layer
- Therefore, the Radius of the Blood Vessels will change if the Architecture (Adventitia, Media and Intima) of the Blood Vessels changes resulting in changes in the Vascular Tone
Afterload: Quality of the Flow
- Afterload is also affected by the types of Quality of Flow through the Blood Vessels
List the types of Quality of Flow
- Laminar Flow
- Turbulent Flow
Outline how the Types of Quality of Flow affect Afterload
- Laminar Flow
- When Blood flows through a Blood Vessels that is fully open with no structural obstructions the resulting flow of fluid is smooth, this is known as Laminar Flow (Tubular Flow)
- Turbulent Flow
- When Blood flows through a Blood Vessels that is clogged with Atherosclerotic plaque or nay other Debris the resulting flow of fluid is Turbulent, this is known as Turbulent Flow
- This Turbulence creates Eddy Currents due to the Non-linear Flow
- Resulting in the Murmurs and Bruits heard in the blood vessels when blood flow through
- Therefore, whenever there is Turbulent Flow the heart has to work harder due to the increased Afterload
- The occurrence of the Turbulent Flow is predicted through the Reynold's Number equation
- Reynold's Number = ρ D v/ η where
- ρ is Density
- D is Diameter
- v is Velocity
- η is Viscosity
Afterload Arterial Elastic Rebound (The Windkessel Effect)
- Afterload is also altered by the Arterial elastic rebound also known as the Windkessel Effect
Outline the Windkessel Effect DIAGRAM
- According to the Windkessels Effect: Changes in Afterload in Large Vessels such as the Aorta can give us the Coronary Circulation
- During Systole, Blood is ejected out of the Heart and Temporarily Accumulates in the Aorta because of the Aortic Systolic Stretch
- During Diastole, the Blood in the Aortic Systolic Stretch will be pushed forward to provide Diastolic Perfusion
- However, this some of the blood will also be pushed Backwards towards the Heart, and cause the Aortic Semilunar Valves to close.
- Since the Aortic Valves are closed and the blood has nowhere to go, the Blood goes into the Right and Left Coronary Arteries via the Right and left Coronary Leaflets.
- This results in Coronary Perfusion in Diastole due to the Arterial Elastic Rebound
Afterload and Cardiac Blood SupplyOutline The Coronary Circulation
- Coronary Flow is Diastole-dependent
- Coronary blood flow makes up 5% of Cardiac Output
- During Diastole, blood remaining in the Aorta will go into the Rights and Left Main Coronary Arteries
- The Left Main Coronary Artery will split into 2 Big Branches:
- Circumflex Artery which goes around the Left Atria and to the Posterior Surface of the Heart
- Anterior Interventricular Artery (Left Anterior Descending Artery)
- The Right Main Coronary Artery gives off 1 Main Branch called the Posterior Descending Artery
- The ECG and Echocardiography can provide an idea of which Coronary vessel damaged by recognizing what part of the Heart they supply
- Coronary Vasodilation is important during increased cardiac work since the heart already has a High Oxygen extraction rate at Rest
Cardiac Blood Supply: Ventricular WallsDescribe the parts of the Heart that are supplied by the Coronary vessels
- The ECG and Echocardiography is able to give an idea on which Coronary vessel is damaged by recognizing the part of the Heart it supplies.
- Anterior Wall of the heart is supplied by the Left Anterior Descending Artery (Anterior Interventricular Artery)
- Septal Wall of the heart is supplied by the Left Anterior Descending Septal Branch
- Left lateral Wall of the heart is supplied by the Left Circumflex Artery
- Inferior Wall of heart is supplied by the Right Coronary Artery branch - Posterior Descending
Cardiac Blood Supply: Ventricular Wall Motion (Echocardiography) DIAGRAM
- When looking at the Cross-section of the Heart, we will be able to identify the Left Ventricle with Thick walls and the Right Ventricle with Thinner walls.
- The Left Ventricle has special markers which we can identify such as the Papillary Muscles and the Thick Ventricular wall
- By looking at the different parts of the Walls we are able to identify where the Left Anterior Descending Artery supplies, where the Left Circumflex Artery supplies and where the Right Coronary supplies
- This is the view seen on an Echocardiogram and is used to tell where Wall Motion Abnormality is located
Afterload and Blood Vessels: Changes in Vascular Resistance (Vascular Tone)
- Afterload is determined by the Vascular Tone of the Blood vessels
List the components of the Blood Vessel that determine the Vascular Tone
- Smooth Muscle Layer of the Blood Vessel
- Inner Endothelial Layer of the Blood Vessel
- The combination of Smooth Muscle activity and the Endothelial cells can change the Vascular Tone of Blood Vessels.
Outline the Components of the Blood Vessel that determine the Vascular Tone
- Within the layers of the Blood vessels are Smooth Muscles that have Gap Junctions between the Smooth Muscle Cells that permit coordinated contraction.
- Therefore, the Smooth Muscles can Contract or Relax and change the Tone of the Blood vessels
Outline the characteristics of Smooth Muscles
- Smooth muscles have a IP3 -Mediated Ca2+ Ion release from Endoplasmic Reticulum
- Myosin head is phosphorylated by MLCK
- Smooth muscles are Non-Striated Muscles and work slightly differently to Skeletal and Cardiac Muscles
- Calcium ion will bind to Calmodulin and NOT Troponin C of the Actin Filament
- Termination occurs by way of Myosin Phosphatase rather than ATP Hydrolysis by ATPase
- Endothelial Layer contains endothelial cells.
- Therefore, there is Endothelial Cell-dependent Vasoreactivity
- This is because Endothelial Cells can produce Vasoactive Substances such as:
- Nitric Oxide (vasodilator)
- Prostacyclin (Vasodilator)
- Endothelin-1 (Vasoconstrictor)
Afterload: Changes in the Vascular Tone alter Regional Blood Flow
- Changes in the Vascular Tone are important because they determine the amount of blood going into an organ which is called a Regional Blood Flow
- For example: In the heart:
- Coronary Arteries are End-Arteries, there are NO Collaterals
- At rest the Heart has a High Oxygen Extraction Ratio of 60-70% meaning that it utilizes a large amount of Oxygen available in the blood vessel.
- Therefore, in order to increase the Coronary Blood Flow, the vessels need to undergo Coronary Vasodilation and create a Coronary Flow Reserve.
- Therefore, Coronary Vasoreactivity is important for increasing the Coronary blood flow when more blood is required in the heart.
Control of the Vascular Tone: Autoregulation
- In certain organs the Vascular Tone changes to ensure that there is a constant flow of blood to that organ this is known as Autoregulation.
Outline the role of Autoregulation in the Control of the Vascular Tone GRAPH
- Autoregulation is when the blood flow to an organ is kept constant over a range of Arterial Blood Pressures
- When looking at a graph which shows Blood Flow(ml/min) as a function of Mean Arterial pressure (MAP):
- There is a Range of Mean Arterial Pressures where the Blood Flow to an organ remains constant this is known as the Autoregulation Range
- Example: In Renal Blood Flow or Cerebral Blood Flow the blood flow to the Kidneys or Brain remains constant over a range of Arterial blood Pressures
- When the Mean Arterial Pressure (MAP is higher than the Autoregulation Range, the Blood Flow (ml/min) will increase
- When the mean Arterial pressure is lower than the Autoregulation Range, the Blood Flow (ml/min) will decrease
Mechanisms of AutoregulationList the Mechanisms of Autoregulation/ Vascular Tone
- Mechanism of Autoregulation include:
- Myogenic Reflexes
- Local Responses (Tubulo-Glomerular Feedback) - Vasoactive Substances eg: Nitric Oxide, Adenosine/ Prostacyclin
- Local Metabolic Factors (i.e.: CO2, O2, H+, Electrolytes)
Mechanisms of Autoregulation/ Vascular Tone: Myogenic ReflexesOutline the Myogenic Reflexes DIAGRAM
- In Myogenic Reflexes, Smooth Muscle Tension in the blood vessels varies with blood pressure changes thus allowing the smooth muscles to adjust the Radius of the blood vessels to Transluminal Pressure Changes
- For example:
- Smooth muscles contain Stretch-activated Calcium (Ca2+) Ion Channels with pressure sensors
- At a Relaxed State the Stretch-activated Ca2+ Channel of the smooth muscle is closed
- However, when there is Increased Transluminal Pressure, the Stretch-activated Ca2+ Ion Channels will be activated and Open.
- Opening of the Stretch-activated Ca2+ Ion Channels allows Ca2+ ions to enter the Smooth muscles cells resulting in the contraction of the Smooth Muscle
- In the Contracted State, the Contraction of the smooth muscle will result in a shorter and contracted Smooth muscle cell with a changed Lumen. This is known as Vasoconstriction
- This means that when there is increased pressure within a Blood Vessels the smooth muscles will react by contracting, in order to limit the amount of blood flow in that vessel to ensure that the Distal Flow is kept Constant
- Local Response (Tubulo-Glomerular Feedback) DIAGRAM
Outline the Autoregulation mechanism/ Vascular Tone: Local Response called the Tubulo-Glomerular Feedback
- Another mechanism of autoregulation is Local Responses such a the Tubulo-Glomerular Feedback in the Renal Corpuscle
- Renal corpuscle is an area of the nephron where the Blood vessels such as the Afferent Arteriole enter the Filtration mechanism of the Bowman's Capsule and exit via the Efferent Arteriole
- Vascular Tone (Vascular Caliber) of these blood vessels can be altered by interacting with the Tubular Mechanisms such as the Distal Tubule
- The Distal Tubule contains Specialized Epithelial called the Macula Densa
- The Macula Densa senses the Concentration of NaCl (Sodium Chloride) returning back into the Distal Tubule via Osmolarity or Tubular Flow
- The Macula Densa will then produce Vasoactive Substances such as Adenosine (Vasodilation) or Nitric Oxide (Vasodilation) that will alter the Arterial (Blood vessel) Vascular Tone (Vascular caliber)
Control of Vascular Tone: Local Metabolic Factors
- Vascular tone is also regulated by Local Metabolic Factors such as Carbon Dioxide (CO2), Hydrogen Cation (H+) and Oxygen (O2)
- For example: Carbon Dioxide-Induced Cerebral vasodilation
Outline Carbon Dioxide (CO2)-Induced Cerebral Vasodilation
- In Carbon Dioxide- Induced Cerebral Vasodilation, Carbon Dioxide in the Plasma is able to act through the Blood Brain Barrier and cause changes in the Cerebral Arteries
- So the Carbon Dioxide will diffuse through the Blood Brain barrier into the Cerebrospinal Fluid (CSF).
- Once in the Cerebrospinal Fluid (CSF) the Carbon Dioxide will react with Water (H2O) and form Carbonic Acid, which will eventually form Bicarb- and Hydrogen cation (H+)
- The Hydrogen Cation is able to interact with the Cerebral Arteries and cause H+ - mediated Vasodilation of the Cerebral Arteries
Control of Vascular Tone: Carbon Dioxide & Cerebral Steel SyndromeOutline the Cerebral Steel Syndrome DIAGRAM
- The action of Carbon Dioxide on Cerebral Blood Vessels is important as it can cause the phenomenon, Cerebral Steal Syndrome
- This is because when there is a High Concentration of Carbon Dioxide known as Hypercarbia.
- The Hypercarbia can cause Hypercarbia-Induced Hypoperfusion of Ischaemic Tissue
- For example: Blood flows into 2 areas, where the one are is Ischaemic and the other area is Normal.
- There may be an Increased Concentration of carbon Dioxide known as Hypercarbia.
- The Area that is Normal may react through Hydrogen ions (H+) and undergo Vasodilation. The Area that is Ischaemic may not react and will remain with a decreased blood supply.
- Therefore, the blood will be preferentially distributed to the Normal Area, and less blood will be distributed to the Ischaemic Area causing the Ischaemic Area to undergo Hypoperfusion and further damage.
- This is known as the Cerebral Steel Syndrome
Afterload: Control of Vascular ToneList all the factors which affect/regulate the Control of Vascular Tone
- Vascular Tone is regulated by:
- Local Factors
- Myogenic Reflexes: Such as Autoregulation
- Local Responses: Vasoactive Substances such as Nitric Oxide, Prostacyclin, Adenosine
- Local Metabolites: CO2, H+, H2O, Electrolytes
- Systemic Factors
- Sympathetic system
- Neuro - Humoral activation by way of Peptides
- Reflexes through various Chemoreceptors and Baroreceptors
Regulation of Vascular Tone: Extrinsic Factors
- Cardiac Autonomic Nervous System
Describe how the Cardiac Autonomic Nervous System regulates the Vascular Tone
- The Cardiac Autonomic Nervous System is made up of 2 Branches called the Sympathetic Nervous System and the Parasympathetic Nervous System
- The Sympathetic Outflow to the heart comes from the Spinal Cord via the Sympathetic Ganglion and is mediated by the nerves T1-T4
- These are the nerves which cause the Heart to beat at a Fast Rate and Strongly through the activation of various Channels and Proteins that promote the Heart to beat strongly
- L-Type Ca Channels
- Type 2 Ca Channels
- Pacemaker Channels
- Ryanodine Channels
- SERCA Pump
- Coronary Vessels
- The Sympathetic outflow also supplies Blood Vessels except Capillaries to cause Vasoconstriction. This is via the Thoracolumbar Outflow
- The Parasympathetic Outflow to the Heart is via the Vagus Nerve
- The Vagus Nerve acts through the Acetylcholine to cause changes in the Sinoatrial Node, Atria and Conduction System majority of which is to depress the activity of the heart
Regulation of Vascular Tone: Extrinsic Factors
- Sympathetic System
Describe how the Sympathetic Outflow acts on the Heart and blood Vessels
- In the Heart:
- The Cardiac myocyte membrane has Beta-adrenergic receptor
- Noradrenaline produced by the post-ganglionic neurons binds to Beta-adrenergic receptors
- The Beta-adrenergic receptor are coupled to G Proteins called Gs, which stimulate Adenyl Cyclase
- Adenyl Cyclase is an enzyme that facilitates the breakdown of ATP to cAMP
- This increases the concentration of cAMP in the Heart muscle
- Increased cAMP then modifies and regulates the various channels and proteins in the heart to cause the Beta-Adrenergic affect in the heart
- In the Blood vessels:
- Noradrenalin binds to Alpha1-receptor of the blood vessels
- The Alpha1-receptor is then coupled to a G protein called Gq, which couples an enzyme called Phospholipase C
- Phospholipase C mediates the breakdown of PIP2 to IP3 + DAG
- As a result, IP3 and DAG regulate the channels and proteins in the blood vessels
- Therefore the overall sympathetic effects are as follow:
- Beta1 cardiac positively inotropic, chronotropic and dromotropic
- Beta2 skeletal vasodilation
- Alpha1 peripheral vascular constriction
Regulation of Vascular Tone: Extrinsic Factors
- Parasympathetic System
Describe how the Parasympathetic Outflow acts on the Heart and blood Vessels
- In Parasympathetic system the Vagus nerve will secrete Acetylcholine
- Acetylcholine will then bind to muscarinic receptors on the cardiac tissue
- The Muscarinic receptors will then bind to a G Protein called Gk (G-potassium) as a result this an Acetylcholine-activated Potassium Channel
- Therefore, when the Acetylcholine-activated Potassium channel is activated, Potassium (K+) will move out of the cardiac cell
- The cell will become hyperpolarized due to the exit of the Potassium ions, and the membrane potential will move further away from the action potential
- Therefore, the cardiac muscle becomes difficult to stimulate
- In Parasympathetic system the Vagus nerve will secrete Acetylcholine
- Acetylcholine will bind to the Muscarinic receptor of the heart muscle
- The Muscarinic receptor will then bind to a G protein called Gi (inhibitory)
- The Gi protein is inhibitory for the Adenylyl Cyclase enzyme
- As a result the binding of the Gi protein to the enzyme Adenylyl Cyclase inhibits the conversion reaction of ATP to cAMP
- As a result the concentration of cAMP decreases causing the Heart rate to decrease and the heart to beat at a decreased force
- The cyclic AMP dependent proteins and channels are then down-regulated
- Therefore the overall Parasympathetic effects:
- Negative Chronotropism: Pacemaker channel inhibition
- Negative Inotropism: Low cAMP dependent effects on contractility
- Negative Domotropism: AV Node delay
Extrinsic FactorsAutonomic Tone and Lung Stretch ReceptorDescribe the activity of the Lung Stretch Receptors in the regulation of the Heart Rate
- Under normal conditions, during Inspiration the Heart rate goes faster and then during Expiration the Heart rate is slower
- This is normal because the Lung Stretch receptor send a feedback via the Vagus nerve to cause change of the heart rate
- This is known as Respiratory Sinus Arrhythmia
- In addition the balance between the Sympathetic and Parasympathetic outflow can change the heart rate and cause Heart rate variability (beat-to-beat variation) between beats
- As a result, between the previous heart beat and the next heart beat there is a tug of war between the Parasympathetic and Sympathetic outflow
- This is because the Sympathetic outflow is trying to increase the heart rate and the Parasympathetic outflow is trying to decrease the heart rate
- This is a normal Heart Rate Variability (HRV)
- Therefore, Heart rate variability (Beat-to-beat variation) is:
- Heart Rate variability (HRV) is normal
- A determinant of autonomic balance
- If it is absent then it indicates that there is a form of autonomic neuropathy where the tug of way between the Parasympathetic and Sympathetic outflow is upregulated
- Reduced HRV is a predictor of death in myocardial infarction
Extrinsic Factors: BaroreceptorDescribe the action of the Baroreceptor in the Regulation of the Heart Rate
- Baroreceptor (pressure receptors) are responsible for sensing the blood pressure
- Baroreceptors are Mean Arterial Pressure receptors, therefore they are sensitive to changes in blood pressure
- Baroreceptors are located on the Carotid Sinus, and the Aortic arch
- As the Blood flows through these large vessels, it causes a stretch of the vessels which is sensed by the stretch receptors which send an action potential to the Medulla (Brain)
- Feedback is then send via the IX nerve to the Baroreceptors of the Carotid sinus and the X nerve to the Baroreceptors of the Aortic arch
- This creates an Autonomic Feedback mechanism to change the activity of the heart depending on the Blood pressure experienced by the Blood vessels
Baroreceptors and Autonomic FeedbackDescribe the link between the Baroreceptors and Autonomic Feedback
- Therefore, changes in the Baroreceptor will cause changes in the Autonomic outflow
- Therefore, Blood pressure changes can change the heart rate
- If we take blood pressure from the Baseline (beginning) and an individual breaths in deeply, and then holds their breathe, the individual would have completed the Valsalva maneuver
- This is Forced expiration against a Closed glottis
- Therefore, the Blood pressure will rise when the individual breathes in deeply, as the blood is being forced out of the chest
- The Blood pressure will then drop when the individual holds their breath due to a decreased venous return
- These changes in Blood Pressure will then be detected by the Baroreceptors and send an autonomic outflow that may stimulate heart rate changes
- For Example: when the BP rises, there is a drop in the Heart Rate and then when the BP drops due to a decreased venous return, there is a compensatory increase in the Heart rate (Tachycardia)
- This autonomic response is normal. Therefore, that the Cardiac-autonomic innervation is intact
- In patients where the Cardiac-Autonomic innervation is disrupted such as in cardiac autonomic neuropathy there would be NO HEART RATE CHANGES due to changes in Blood Pressure
- Therefore, resulting in an abnormal cardiac autonomic response
Other Extrinsic Factors that regulate the Heart RateOutline other extrinsic factors that regulate the Heart rate
- Changes in Temperature (Hot and Cold)
- pH (Acidosis)
- Changes in Hormones (Thyroxine, Vasopressin, Angiotensin II)
- Changes in Humoral factors (Peptides, Transmitters)
- Stretch (Baroreceptors, Lung Receptors and Atrial)
- Metabolic byproducts (Chemoreceptors and Osmoreceptors)
Extrinsic Regulation of the Cardiovascular System
- Cardio-Respiratory control centre is the Medulla
- Cardio-Respiratory control centre receives feedback from the Hypothalamus and the Cortex
- Cardio-Respiratory control centre will send signals to an effector such as Heart and Blood Vessels
- Heart and Blood Vessels will change their activity resulting in a change in a Parameter such as the Blood Pressure
- The change in Blood Pressure will then be detected by a Receptor such as the Baroreceptor
- Baroreceptor will then send a feedback in the form of an action potential to the Cardio-Respiratory Control centre in the Medulla
- It is important to note that there are other Effectors:
- Kidneys which change the parameter called Osmolality
- Changes in Osmolality will then be detected by the Osmoreceptors which will send an action potential to the Medulla
- Lungs which change the pO2, pCO2 or pH
- Changes in the pO2, pCO2 or pH will be detected by the Chemoreceptors
- Muscles which change the Temperature
- Changes in Temperature will then be detected by Thermoreceptors