Exam 3 BMS

Learning objectives for Jones content

List and define the function of the neural support tissues: oligodendrocytes, Schwann cells, ependymal cells, microglial and astrocytes

• Oligodendrocytes(CNS): Produce myelin in the central nervous system.

• Schwann cells(PNS): Produce myelin in the peripheral nervous system.

• Ependymal cells: Line the ventricles of the brain, involved in cerebrospinal fluid production.

• Microglial cells(Scavengers): Act as immune cells, removing debris and pathogens in the central nervous system.

• Astrocytes: Maintain the blood-brain barrier, provide structural support, and regulate nutrient and waste exchange.

Describe how a potential difference is generated between two charges.

When charges have different electric potential energy, a potential difference is created

Define current (I), voltage or potential difference (V) and resistance (R).

I: Current refers to the flow of electric charge in a circuit, measured in amperes (A).

V: Voltage or potential difference is the electrical potential energy per unit charge, measured in volts (V).

R: Resistance is the opposition to the flow of electric current, measured in ohms (Ω).

List the electrolyte concentrations of Na+, Cl- and K+ in the ECF and ICF.

ECF:

• Na+: High concentration 145

• Cl-: High concentration 120

• K+: Low concentration 5

ICF:

• Na+: Low concentration 15

• Cl-: Low concentration 10

• K+: High concentration 150

what equation to use to Calculate the equilibrium potential for an ion when given the extracellular and intracellular concentrations.

Nernst equation: Calculates equilibrium potential for an ion. E = 61 x log (out/in)

Describe the equilibrium potential of an ion in terms of ion flow and driving forces.

Equilibrium potential: The membrane potential at which the ion flow through channels is balanced by the electrical and chemical driving forces.

Discuss the role of K+ and Na+ channels and the Na+ /K+ ATPase in the generating the resting potential of a cell.

Role of K+ and Na+ channels and Na+/K+ ATPase in generating resting potential: K+ channels allow K+ ions to leave the cell, maintaining negative charge inside. Na+ channels permit Na+ ions to enter, but are mostly closed at rest. Na+/K+ ATPase pumps 3 Na+ out and 2 K+ in, establishing concentration gradients. Na+/K+ is secondary active transport.

what are the effects of changes in electrolyte concentration or permeability to the resting membrane potential and action potential of a cell

Effects of changes in electrolyte concentration or permeability on cell potentials:

1. ↑ Electrolyte concentration: Increases resting membrane potential and makes action potentials more likely to occur.

2. ↓ Electrolyte concentration: Decreases resting membrane potential and makes action potentials less likely to occur.

3. ↑ Permeability to positive ions: Depolarizes the cell, making it more likely to reach the threshold for an action potential.

4. ↑ Permeability to negative ions: Hyperpolarizes the cell, making it less likely to reach the threshold for an action potential.

How do changes in Na+ and K+ channel permeability cause potential difference changes seen during the action potential.

Changes in Na+ and K+ channel permeability cause potential difference changes during the action potential. Na+ channels open, allowing Na+ ions to enter the cell, depolarizing it. K+ channels then open, allowing K+ ions to exit the cell, repolarizing it.

What are the gating mechanisms of voltage-gated K+ and Na+ channels

Gating mechanisms of voltage-gated K+ channels: Activation gate (m) opens when membrane is depolarized, allowing K+ ions to flow out. Inactivation gate(h) closes shortly after, preventing further ion flow.

Gating mechanisms of voltage-gated Na+ channels: Activation gate opens when membrane is depolarizing, allowing Na+ ions to flow in. Inactivation gate closes shortly after, preventing further ion flow.

what are the variables of the GHK equation and how the variables generate the resting membrane potential.

Variables of the GHK equation: Permeabilities (P) of ions (K+, Na+, Cl-), Concentrations (C) of ions inside and outside the cell, and the Temperature (T). The equation calculates the resting membrane potential by considering the influence of these variables on ion movement across the cell membrane.

Vm = 61 x log (Pna (Na)o + Pk (K)o + Pcl (Cl)i / Pna (Na)i + Pk(K)i + Pcl (Cl)o)

Define the all-or-none principle and relate to the action potential.

All-or-none principle: Neurons either fire at full strength or do not fire at all. It applies to the action potential, where a stimulus must reach a certain threshold to trigger an all-or-none response. If the threshold is not met, no action potential occurs.

Describe the effects of increasing depolarizing stimulus strength on the action potential.

As depolarizing stimulus strength increases, the action potential amplitude also increases. This phenomenon is known as amplitude modulation. Additionally, the duration of the action potential remains relatively constant regardless of the stimulus strength.

Define relative and absolute refractory period in terms of ability to fire an action potential.

Relative refractory period: Time after firing an action potential when a stronger stimulus is needed to fire another action potential due to partially repolarized membrane.

Absolute refractory period: Time after firing an action potential when no stimulus, no matter how strong, can fire another action potential due to inactivated sodium channels.

Discuss how voltage-gated ion channel permeability changes lead to the refractory periods of an action potential.

Voltage-gated ion channel permeability changes during an action potential because of refractory periods. These periods prevent immediate re-stimulation of the neuron.

Contrast chemical and electrical synapse.

Chemical Synapse:

• Communication between neurons via chemical signals (neurotransmitters)

• Slower transmission

• Allows for modulation and integration of signals

• Examples: synapses in the brain

Electrical Synapse:

• Direct electrical connection between neurons

• Faster transmission

• Synchronizes activity between neurons

• Examples: synapses in the heart and some parts of the brain

Describe the cellular events which lead to the release of neurotransmitters from the axon terminals at a chemical synapse.

Cellular events leading to neurotransmitter release at a synapse: 1) Action potential (Na+ channels depolarization of axon) arrives at axon terminal. 2) Voltage-gated calcium channels open. 3) Calcium ions enter the terminal. 4) Calcium triggers synaptic vesicles to fuse with the membrane. 5) Neurotransmitters are released into the synaptic cleft.

List the action of neurotransmitters on the post-synaptic membrane.

Neurotransmitters act on the post-synaptic membrane by binding to specific receptors, either excitatory or inhibitory. Excitatory neurotransmitters increase the chances of an action potential occurring, while inhibitory neurotransmitters decrease the chances. This interaction determines whether the post-synaptic neuron will be activated or inhibited.

Contrast metabotropic and inotropic receptors.

Metabotropic Receptors: Indirectly linked to ion channels. Activation triggers a series of intracellular events, leading to slower and longer-lasting responses. Examples include G-protein coupled receptors (GPCRs).

Inotropic Receptors: Directly linked to ion channels. Activation causes rapid changes in ion flow across the cell membrane, leading to fast and short-lived responses. Examples include ligand-gated ion channels.

which post-synaptic ion channel permeable changes will lead to inhibitory or excitatory potentials.

Excitatory: Na+ channels open, depolarizing the membrane.

Inhibitory: Cl- channels open, hyperpolarizing the membrane. K+ channels open repolarizing the membrane.

Define spatial and temporal summation of synapses and their role in excitatory or inhibitory signaling.

Spatial summation occurs when multiple synapses stimulate a neuron simultaneously, increasing the overall signal strength.

Temporal summation happens when a single synapse fires rapidly, creating a cumulative effect.

Both summation processes play a role in excitatory or inhibitory signaling by determining whether the combined input is strong enough to trigger an action potential in the receiving neuron.

Describe the sequence of events by which an action potential in a motor neuron produces an action potential in the plasma membrane of a skeletal muscle fiber through synaptic transmission at the neuromuscular junction.

Sequence of events in motor neuron to skeletal muscle fiber action potential:

1. Action potential reaches axon terminal of motor neuron.

2. Voltage-gated calcium channels open, allowing calcium ions to enter.

3. Calcium influx triggers release of acetylcholine (ACh) into synaptic cleft.

4. ACh binds to receptors on motor end plate of muscle fiber.

5. Binding of ACh opens ion channels, allowing sodium ions to enter muscle fiber.

6. Sodium influx depolarizes muscle fiber, generating an action potential.

7. Action potential travels along plasma membrane of muscle fiber, initiating muscle contraction.

Explain the process of excitation-contraction coupling in skeletal muscles by describing the role and source of calcium ions and the mechanism by which they initiate contraction in skeletal muscle.

Calcium ions are released from the sarcoplasmic reticulum in response to an action potential. They bind to troponin, causing a conformational change that moves tropomyosin away from the myosin binding sites on actin. This allows myosin heads to bind to actin, forming cross-bridges. ATP is hydrolyzed, providing energy for the myosin heads to pull on actin, resulting in muscle contraction.

Describe the pathophysiological basis of myasthenia gravis and Lambert Eaton Syndrome

Myasthenia Gravis: Autoimmune disorder where antibodies attack acetylcholine receptors, leading to muscle weakness and fatigue.

Lambert Eaton Syndrome: Autoimmune disorder where antibodies attack presynaptic voltage-gated calcium channels, impairing neurotransmitter release and causing muscle weakness.

Describe the structure and function of the transverse tubules and sarcoplasmic reticulum in skeletal muscle fibers and how they play a critical role in the excitation-contraction coupling.

T-tubules are invaginations of the cell membrane that allow for rapid transmission of electrical impulses.

Sarcoplasmic reticulum is a specialized network of membrane-enclosed tubules that stores and releases calcium ions.

Together, they enable excitation-contraction coupling by coordinating the depolarization of the cell membrane with the release of calcium ions, triggering muscle contraction.

Describe the organization of myosin, actin, tropomyosin, and troponin molecules in the thick and thin filaments.

Myosin: Motor protein in thick filaments that binds to actin.

Actin: Protein in thin filaments that interacts with myosin.

Tropomyosin: Covers myosin binding sites on actin in relaxed muscle.

Troponin: Regulates muscle contraction by controlling tropomyosin's position. When Ca2+ binds it will shift tropomyosin to allow myosin to bind actin.

Summarize the steps in excitation contraction coupling in skeletal muscle

1. Action potential travels down the motor neuron.

2. Acetylcholine is released at the neuromuscular junction.

3. Acetylcholine binds to receptors on the muscle cell membrane.

4. This triggers an action potential in the muscle cell.

5. Action potential spreads along the sarcolemma and T-tubules.

6. Calcium ions are released from the sarcoplasmic reticulum.

7. Calcium binds to troponin, causing tropomyosin to move.

8. Myosin heads bind to actin, forming cross-bridges.

9. Myosin heads undergo a power stroke, pulling actin filaments.

10. Muscle contraction occurs as sarcomeres shorten.

explain the steps of the cross-bridge cycle and explain how the cross-bridge cycle results in an increase in tension in the muscle fibers

Cross-bridge Cycle:

1. Calcium ions bind to troponin, exposing myosin binding sites on actin.

2. Myosin heads attach to actin, forming cross-bridges.

3. Power stroke: Myosin heads pivot, pulling actin towards the center of the sarcomere.

4. ADP and Pi are released, causing the myosin head to change shape.

5. New ATP binds to myosin, breaking the cross-bridge.

6. ATP hydrolysis re-energizes the myosin head. Result: Cross-bridge cycling increases tension in muscle fibers by repeatedly pulling actin filaments towards the center, shortening the sarcomere.

Explain how a lack of ATP results in rigor mortis.

Rigor mortis: Stiffening of muscles after death due to lack of ATP. ATP is needed for muscle relaxation, but without it, myosin and actin filaments remain bonded, causing muscles to become locked in a contracted state. Begins 2-6 hours after death and lasts up to 48 hours.

Discuss how skeletal muscle relaxation can occur

When a nerve signal stops, calcium ions are pumped back into the sarcoplasmic reticulum. This decreases calcium concentration in the cytoplasm, causing troponin and tropomyosin to block the myosin binding sites on actin. This prevents cross-bridge formation and muscle contraction, leading to relaxation.

Compare and contrast the differences in structure between skeletal muscle fibers and smooth muscle fibers

Differences between skeletal and smooth muscle fibers:

1. Skeletal fibers: multinucleated,

   smooth fibers: single nucleus.

2. Skeletal fibers: striated,

   smooth fibers: no striations.

3. Skeletal fibers: long and cylindrical,

   smooth fibers: shorter and spindle-shaped.

4. Skeletal fibers: voluntary control,

   smooth fibers: involuntary control.

5. Skeletal fibers: organized in bundles,

   smooth fibers: found in sheets or layers.

Compare and contrast the process for excitation-contraction coupling in skeletal, cardiac, and smooth muscles by discussing the two sources of Ca2+ that triggers contraction in smooth muscle and the mechanism by which a rise in cytosolic calcium initiates contractile activity in smooth muscle.

Sources of Ca2+ in smooth muscle:

1) Extracellular Ca2+ influx through voltage-gated Ca2+ channels.

2) Release of Ca2+ from the sarcoplasmic reticulum (SR) via IP3 receptors.

Rise in cytosolic calcium initiates contraction: Ca2+ binds to calmodulin, activating myosin light chain kinase (MLCK). MLCK phosphorylates myosin light chains, allowing actin and myosin to interact and generate force for contraction.

Define latch state in smooth muscles and explain why smooth muscles can develop and maintain force with a much lower rate of ATP hydrolysis than skeletal muscles.

Latch state in smooth muscles is a sustained contraction without ATP usage. This mechanism allows myosin heads to remain attached to actin for longer periods, reducing the need for ATP to detach and reattach.

Describe the actions of drugs that can be used to modify events at the neuromuscular junction and how they affect muscle contraction.

Acetylcholinesterase inhibitors prevent ACh breakdown, prolonging muscle stimulation.

Nondepolarizing blockers compete with ACh for receptor binding, preventing muscle contraction.

Depolarizing blockers cause prolonged depolarization, leading to muscle paralysis.

Generalize the functions of the parasympathetic and sympathetic nervous systems

Parasympathetic Nervous System: Rest and Digest. Slows heart rate, stimulates digestion, constricts pupils, and promotes relaxation.

Sympathetic Nervous System: Fight or Flight. Increases heart rate, dilates pupils, inhibits digestion, and prepares body for action.

Differentiate the anatomy of the autonomic nervous system with the somatic nervous system and sensory nervous systems in terms anatomy, neurotransmitters, receptors and muscles controlled.

Autonomic Nervous System (ANS):

• Controls involuntary actions

• Divided into sympathetic and parasympathetic branches

• Uses neurotransmitters like norepinephrine and acetylcholine

• Receptors include adrenergic and cholinergic receptors

• Controls smooth muscles, cardiac muscles, and glands

Somatic Nervous System (SNS):

• Controls voluntary actions

• Uses acetylcholine as the neurotransmitter

• Receptors include nicotinic receptors

• Controls skeletal muscles

Sensory Nervous System:

• Collects sensory information from the body

• Transmits signals to the central nervous system (CNS)

• Involves sensory receptors and sensory neurons

Compare and contrast the anatomy parasympathetic and sympathetic nervous systems in terms of: origin and length of preganglionic neurons, location of ganglia and length of post-ganglionic neurons.

Origin and length of pre and postganglionic neurons:

• Parasympathetic: Originates from cranial and sacral regions of the spinal cord. Preganglionic neurons are long. Postgang = short

• Sympathetic: Originates from thoracic and lumbar regions of the spinal cord. Preganglionic neurons are short. Postgang = long

Location of ganglia:

• Parasympathetic: Ganglia are located near or within target organs.

• Sympathetic: Ganglia are located close to the spinal cord, forming a chain called sympathetic chain ganglia.

Define cholinergic and adrenergic and use these terms to describe the neurotransmitters of different autonomic nerve fibers.

Cholinergic refers to nerve fibers that release acetylcholine as their neurotransmitter, while adrenergic refers to fibers that release norepinephrine.

Cholinergic fibers are found in the parasympathetic division of the autonomic nervous system, promoting rest and digestion.

Adrenergic fibers are found in the sympathetic division, responsible for the fight-or-flight response.

Describe the receptors used by the autonomic nervous system in the sympathetic and parasympathetic nervous system in the ganglion and target tissues

Sympathetic ganglion receptors: Nicotinic receptors.

Sympathetic target tissue receptors: Adrenergic receptors (α and β).

Parasympathetic ganglion receptors: Nicotinic receptors.

Parasympathetic target tissue receptors: Muscarinic receptors.

Illustrate how adrenergic receptors with different signaling pathways can generate different physiological functions in response to the same adrenergic agonists

Agonists binding to α1 receptors activate Gq proteins, causing vasoconstriction.

β1(heart) receptors couple to Gs proteins, increasing heart rate and contractility.

β2(lungs) receptors activate Gs proteins, promoting bronchodilation and vasodilation.

β3(tissues) receptors, coupled to Gi proteins, enhance lipolysis.

Describe the effects of the sympathetic and parasympathetic nervous systems on various organs and know the receptors used for these actions

Effects of sympathetic and parasympathetic systems on organs:

1. Sympathetic: Increases heart rate, dilates pupils, inhibits digestion, stimulates glucose release. Uses adrenergic receptors.

2. Parasympathetic: Decreases heart rate, constricts pupils, stimulates digestion, promotes urination. Uses cholinergic receptors.

Summarize the dual innervation of the heart, salivary gland, bladder and pupil

In the heart, sympathetic stimulation increases heart rate and contraction force, while parasympathetic stimulation decreases heart rate.

Salivary glands receive both sympathetic and parasympathetic innervation, with sympathetic activation reducing saliva production and parasympathetic activation increasing it.

The bladder experiences sympathetic stimulation for muscle relaxation and internal sphincter contraction, while parasympathetic stimulation causes muscle contraction and internal sphincter relaxation.

The pupil also receives dual innervation, with sympathetic stimulation causing pupil dilation and parasympathetic stimulation leading to pupil constriction.

Identify the central control centers of the autonomic nervous system and the organs they control

Central control centers of the autonomic nervous system:

1. Hypothalamus: Regulates body temperature, hunger, thirst, and controls the pituitary gland.

2. Brainstem: Controls basic functions like breathing, heart rate, and blood pressure.

3. Spinal cord: Coordinates reflex actions and controls bladder, bowel, and sexual functions.

Discuss the effects of autonomic agonists or antagonists on function and the value of their use in treating or assessing physiology dysfunction

• Agonists mimic neurotransmitters, boosting autonomic activity.

• Agonists increase heart rate, bronchodilation, and pupil dilation.

• Antagonists block receptors, reducing autonomic activity.

• Antagonists decrease heart rate, bronchoconstriction, and pupil constriction.

• They treat asthma, hypertension, and heart rhythm disorders.

• They help assess autonomic dysfunction by observing vital signs and organ function changes.

Compare and contrast the structure and function of arteries, arterioles, capillaries, venules and veins

Arteries carry oxygenated blood away from the heart

Veins carry deoxygenated blood back to the heart.

Arteries (lots of elastic fibers) and arterioles have thick muscular walls to withstand high pressure.

Capillaries are thin-walled and allow for gas exchange.

Venules collect blood from capillaries and lead to veins.

Veins have valves to prevent backflow and thinner walls than arteries.

Differentiate between the possible circulatory arrangements

Circulatory arrangements refer to the organization of blood vessels in an organism. Closed circulatory systems have blood confined to vessels, while open systems lack vessels. Single circulations pass blood through the heart once per circuit, while double circulations pass it twice.

Summarize the changes in Pressure, surface area, velocity, resistance throughout the circulatory system

Pressure: Force exerted by blood on the walls of blood vessels. Increases in arteries, decreases in veins.

Surface area: Total area available for blood exchange. Increases as blood moves from arteries to capillaries. Decreases from capillaries to veins.

Velocity: Speed at which blood flows. Decreases in capillaries due to increased surface area.

Resistance: Opposition to blood flow. Increases in arterioles, decreases in capillaries and venules.

Define diastolic and systolic pressure comparing pressures in the vessels during systole and diastole

Diastolic pressure: The lowest pressure in the arteries during the heart's relaxation phase (diastole), when the heart is refilling with blood.

Systolic pressure: The highest pressure in the arteries during the heart's contraction phase (systole), when the heart is pumping blood out.

Define hypertension and hypotension

Hypertension: High blood pressure, a condition where the force of blood against artery walls is consistently too high, increasing the risk of heart disease and stroke.

Hypotension: Low blood pressure, a condition where the force of blood against artery walls is consistently too low, leading to dizziness, fainting, and inadequate blood flow to organs.

how do you Calculate MAP and PP given diastolic and systolic pressure

MAP (Mean Arterial Pressure) is calculated by adding two times the diastolic pressure to the systolic pressure, and then dividing the sum by three.

PP (Pulse Pressure) is calculated by subtracting the diastolic pressure from the systolic pressure.

List the factors which determine mean arterial pressure

Factors determining mean arterial pressure include cardiac output, total peripheral resistance, and blood volume.

Describe how cardiac output and total peripheral resistance effect mean arterial pressure and blood flow

Cardiac output is the amount of blood pumped by the heart per minute,

Total peripheral resistance is the resistance to blood flow in the blood vessels.

An increase in cardiac output or a decrease in total peripheral resistance will result in an increase in mean arterial pressure and blood flow.

Conversely, a decrease in cardiac output or an increase in total peripheral resistance will lead to a decrease in mean arterial pressure and blood flow.

Apply changes in the Poiseuille equation to vascular resistance and flow

Changes in vessel length, radius, or viscosity alter resistance.

Longer vessels or smaller radii increase resistance, while shorter vessels or larger radii decrease resistance.

Higher viscosity also increases resistance.

Flow is directly proportional to the pressure gradient and inversely proportional to resistance. F= Delta P/ R

Describe the effects of arteriole smooth muscle on mean blood pressure and local blood pressure in the downstream capillaries

Effects of arteriole smooth muscle on mean blood pressure: Constriction increases resistance, raising mean blood pressure. Dilation decreases resistance, lowering mean blood pressure.

Effects of arteriole smooth muscle on local blood pressure in downstream capillaries: Constriction reduces blood flow, decreasing local blood pressure. Dilation increases blood flow, increasing local blood pressure.

Summarize the local mechanisms for controlling blood flow to a capillary defining active and reactive hyperemia

Active hyperemia: Increased blood flow to a capillary due to increased metabolic activity in the tissue.

Reactive hyperemia: Increased blood flow to a capillary after a period of reduced blood flow.

Describe the baroreceptor reflex and it regulation of the autonomic nervous system control of vascular smooth muscle

Baroreceptor Reflex: Mechanism regulating autonomic control of vascular smooth muscle. Baroreceptors in the carotid sinus and aortic arch detect changes in blood pressure. Increased pressure triggers inhibition of sympathetic activity and stimulation of parasympathetic activity. This leads to vasodilation and decreased heart rate, reducing blood pressure.

List the factors which regulate capillary filtration

Factors regulating capillary filtration:

1. Hydrostatic pressure: force exerted by fluid against capillary walls.

2. Colloid osmotic pressure: pressure created by proteins in the blood.

3. Capillary permeability: ability of capillary walls to allow fluid and solutes to pass through.

4. Lymphatic drainage: removal of excess fluid by the lymphatic system.

5. Arteriolar constriction/dilation: changes in diameter of arterioles affecting blood flow to capillaries.

6. Venous pressure: pressure in veins affecting fluid return to the heart. Remember these factors to understand capillary filtration in the body.

how do you Calculate the net filtration pressure across a capillary bed

Net filtration pressure (NFP) across a capillary bed is calculated by subtracting the sum of the hydrostatic pressure (HP) and the colloid osmotic pressure (COP) of the blood from the hydrostatic pressure (HP) and the colloid osmotic pressure (COP) of the interstitial fluid.

NFP = (Pc + PIi)-(PIc + Pi)

Define edema

Excess accumulation of fluid in body tissues, causing swelling and puffiness. Commonly seen in conditions like heart failure, kidney disease, and lymphatic obstruction.

Compare the three conditions which can result in edema and suggest therapeutic strategies for each

1. Cardiac edema: Result of heart failure, causing fluid accumulation. Therapeutic strategies: Diuretics, sodium restriction, cardiac medications.

2. Renal edema: Caused by kidney dysfunction, leading to fluid retention. Therapeutic strategies: Diuretics, treating underlying kidney disease, fluid restriction.

3. Lymphatic edema: Occurs due to lymphatic system impairment, causing fluid buildup. Therapeutic strategies: Compression therapy, lymphatic drainage massage, elevation of affected limb.

List the major characteristics of veins

• Carry deoxygenated blood back to the heart

• Have thinner walls compared to arteries

• Contain valves to prevent backflow of blood

• Have larger lumen for easier blood flow

• Often located closer to the body surface compared to arteries

Compare venous return to cardiac output

• Venous Return: Amount of blood returning to the heart from the body's veins per minute.

• Cardiac Output: Volume of blood pumped by the heart per minute.

• Venous Return depends on factors like blood volume, venous tone, and skeletal muscle contraction.

• Cardiac Output depends on heart rate and stroke volume.

• Both are measured in liters per minute.

• Venous Return supplies blood to the heart, while Cardiac Output delivers blood to the body's organs and tissues.

Summarize the effects of gravity, respiration, and muscle activity on venous return

• Gravity: Decreases venous return from lower extremities, as blood has to work against gravity to return to the heart.

• Respiration: Increases venous return during inspiration due to negative intrathoracic pressure, aiding blood flow towards the heart.

• Muscle activity: Enhances venous return by compressing veins, propelling blood towards the heart, especially during exercise or movement.

Summarize the factors which maintain venous return and can be increased to increase stroke volume

Factors maintaining venous return and increasing stroke volume:

1. Venous tone: Constriction of veins by sympathetic stimulation.

2. Skeletal muscle pump: Contraction of muscles compresses veins, aiding blood flow.

3. Respiratory pump: Inhalation lowers thoracic pressure, aiding venous return.

4. Blood volume: Higher volume increases venous return and stroke volume.

5. Sympathetic activity: Increased sympathetic activity constricts veins, enhancing venous return.

6. Hormonal regulation: Hormones like adrenaline can increase venous tone and stroke volume.

Define the factors which control cardiac out put

Factors controlling cardiac output:

1. Heart rate: the number of times the heart beats per minute.

2. Stroke volume: the amount of blood pumped out of the heart with each beat.

3. Preload: the degree of stretch in the heart muscle before it contracts.

4. Afterload: the resistance the heart must overcome to eject blood.

5. Contractility: the strength of the heart's contraction. Remember, cardiac output is the amount of blood pumped by the heart per minute.

Define the three factors which control blood pressure (HR, SV and TPR)

Factors controlling blood pressure:

1. Heart Rate (HR): Number of times the heart beats per minute.

2. Stroke Volume (SV): Amount of blood pumped by the heart with each beat.

3. Total Peripheral Resistance (TPR): Resistance to blood flow in the arteries.

Summarize the baroreceptor reflex

Automatic response to changes in blood pressure. Baroreceptors in arteries detect pressure changes and send signals to the brain. Brain then adjusts heart rate and blood vessel diameter to maintain stable blood pressure.

Describe the effects of the autonomic nervous system on heart rate including the receptors and ion channels effected

1. Sympathetic stimulation: Increases heart rate.

2. Parasympathetic stimulation: Decreases heart rate.

3. Receptors involved: Sympathetic - β1 adrenergic receptors. Parasympathetic - muscarinic receptors.

4. Ion channels affected: Sympathetic - Ca2+ channels increase, K+ channels decrease. Parasympathetic - K+ channels increase.

Describe the factors which can change stroke volume

Preload is the volume of blood in the ventricles before contraction.

Contractility is the force of ventricular contraction.

Afterload is the resistance the heart must overcome to pump blood out of the ventricles.

Discuss the effects of sympathetic stimulation on cardiac muscle and how that will change cardiac output and mean arterial pressure

1. Increased contractility: Enhances force of heart contractions.

2. Increased heart rate: Speeds up heart rhythm.

3. Increased conduction velocity: Accelerates electrical impulses. These changes lead to:

4. Increased cardiac output: More blood pumped per minute.

5. Increased mean arterial pressure: Higher pressure in arteries. Sympathetic stimulation prepares the body for physical activity or stress response.

Review the effects of blood loss (hemorrhage) and exercise on the cardiovascular system and mean arterial pressure. Focus on the changes to the autonomic nervous system

1. Blood loss: Sympathetic NS activation, increased heart rate & vasoconstriction.

2. Exercise: Parasympathetic NS suppression, increased heart rate & vasodilation.

3. Mean arterial pressure: Blood loss decreases MAP, exercise increases MAP.