Cardiac understand cardiac muscle contraction. 

We need to know how a skeletal muscle contract first, and then we compare 

At the neuromuscular junction

the action potential arrives and 

Acetylcholine is released .

acts on receptors on the muscle membrane. Sodium enters the muscle cell and there’s generation of an end plate potential when that potential reaches threshold. There’s an action potential action potential propagate along the membrane, I am down the Tea, which are tips from the memory That stimulates dihydropyridine receptor, which is a voltage calcium is mechanically, coupled to receptor on the surface of the plasma reticular when that channel opened the store calcium, exoplasm reticulum, and the intra cellular calcium levels rise, the calcium, then bind to troponin see which is a part of the Thin element. This moves tropin out of the way, allowing my son to act. Myosin has ATP From breaking down, the ATP had hello, welcome to bite Ti man this video is on the at the region, dragging the Ayehnin filament along with Thin

 And then we compare, so in the next few minutes, I’m gonna very quickly go over the steps of skeletal muscle contraction just to give this video a little orientation. It starts at the neuromuscular junction. The action potential ar arrives acetylcholine  is released it actionAnd there’s generation of an endplate potential when that potential reaches receptors on the muscle membrane sodium enters the muscle cells there is generation of an end plate potential when that potential reaches threshold. There’s an action potential action, potential propagate along the membrane and down the Tea, which which are dips from the membrane that stimulates a dihydropyridine receptor, which is a voltage calcium is mechanically, coupled to run receptor on the surface of the sarcoplasmic reticular when that channel opens the store calcium exits, the circle plasmic reticulum, and the intra cellular calcium levels risecalcium then bone which is a part of the Thin element. This moves out of the way, allowing Ayehnin has ATP activity the energy from breaking down the ATP causes the myosin head, the bend at the hinge region, dragging the thin filament along with. there’s a calcium ATP pump on the surface of the sarcoplasmic reticular pump calcium back into the circle plasmic reticular. This is the sarcoplasmic endoplasmic reticulum calcium ATP once the intra cellular calcium levels come back down once again muscle muscle contraction is very similar to skeletal muscle contraction.

 Different is a nice muscle. The impulse tells the cardiac contract doesn’t come from Nwe Nwe. It comes from the pacemaker of the heart that’s the signal at that generates an action potential in the HL and the particular muscle action potential in the contract. It was inlet there’s a plateau, during which calcium enters the cell that is a voltage gated type calcium on the membrane of the teacher Calcium move along gradient entering the cellular calcium concentration rises. This calcium is insufficient to cause contraction on its own. What it does is it also triggers a calcium release channel on the surface of the plasma. This is calcium induced calcium release, so the calcium inside the cell has two extra cellular fluid and sarcoplasmic Calcium sliding over the thick short muscle at the end of the plateau calcium what happens to the calcium inside the ions pumped out of the circle plasm into the circle plasm reticulum and out into the cellular space plasma reticulum has a calcium uses ATP calcium against its gradient inside the plasma is the Kho Kho plasmic, endoplasmic reticulum calcium ATP Plasmic membrane which plasma membrane has calcium sodium along it gradient would enter the cell in exchange for calcium leaving the cell so you can see how calcium gets out of the cell through this exchanger that sodium is gonna be pumped out by sodium potassium ATP, so the calcium level in the cell comes back down again, and when another action potential arrives, the process repeats That in the cardial cell depends on the intra cellular calcium concentration ability of the myocardial cells to contract and generate force is contractility. If there’s increased calcium through the calcium &channels, there’s more cellular calcium so there’s increased contract. There’s increased calcium into plasma reticulum and there’s more calcium being stored which can get released during the next contraction again increasing contract. This can happen with phosphorylation of these channels with sympathetic stimulation Remember that the hardest applied by autonomic nerves the sympathetic parasympathetic nervous system sympathetic stimulation increase contract, said a positive ironic effect is the term that used for contract so More contract means a positive tropic effect parasympathetic opposite effect has a negative tropic reduces contractibility more, so in the Than in the ventricles cause, they innovate the atrium more This other factors which can either increase or decrease cardiac contract and this contract together with preload, and after our important factors that determines stroke volume of the heart and the cardiac output muscle

AFib

 Certainly! Atrial fibrillation (AFib) is an irregular heart rhythm characterized by chaotic and often rapid contractions of the heart’s upper chambers (atria). While some people with AFib experience noticeable symptoms, others may remain asymptomatic or attribute their symptoms to other causes. Let’s explore when symptoms are likely to occur and why:

1. Symptoms of Atrial Fibrillation:

   • Palpitations: A sensation of a fast, fluttering, or pounding heartbeat.
   • Chest Pain: Some individuals may experience discomfort or pressure in the chest.
   • Dizziness: Feeling lightheaded or dizzy.
   • Fatigue: General tiredness or weakness.
   • Shortness of Breath: Difficulty breathing.
   • Reduced Exercise Tolerance: Inability to engage in physical activity as usual.

2. When Symptoms Occur:

   • Occasional (Paroxysmal) AFib:
     • Symptoms come and go.
     • Episodes may last from a few minutes to several hours.
     • Some people have symptoms for up to a week.
     • Symptoms might spontaneously resolve.
   • Persistent AFib:
     • The irregular heartbeat is constant.
     • Symptoms persist until treated.
   • Long-Standing Persistent AFib:
     • Continuous AFib lasting longer than 12 months.
     • Requires medical intervention to correct the rhythm.
   • Permanent AFib:
     • Irregular rhythm cannot be reset.
     • Medications are used to control heart rate and prevent blood clots.

3. Why Symptoms Vary:

   • Atrial Function: During AFib, the atria quiver chaotically and irregularly. The loss of coordinated atrial contraction affects blood flow and can lead to symptoms.
   • Individual Differences: Some people are more sensitive to irregular heart rhythms and notice symptoms, while others may not.
   • Underlying Health: Factors like age, overall health, and other heart conditions influence symptom perception.
   • Stress and Triggers: Stress, fatigue, caffeine, alcohol, and other triggers can exacerbate symptoms.

4. When to Seek Medical Attention:

   • If you experience symptoms of AFib, consider the following:
     • Palpitations: Especially if they are severe or persistent.
     • Chest Pain: Seek immediate medical help, as it could indicate a heart attack.
     • Shortness of Breath: Especially during physical activity.
   • Regular health checkups are essential, especially if you suspect any heart-related symptoms.

Remember that AFib, although not always life-threatening, requires proper evaluation and management to prevent complications such as stroke. If you have concerns, consult a cardiologist. 😊

ECG

 

Chronic hypertension

 

lecture week 8 extra credit

 

Baroreceptor

 

Cardiac output

 Hello in this video, we’re going to talk about cardiac output so cut output is the output is defined as the amount of body ejected by the heart in one minute so here is a hot in Sicily and the ventricles are contracting injecting blood out to the Toyota and the pulmonary trunk Cut output is defined by the amount of blood ejected by each ventricle in one minute and there are two factors that are used to calculate the output. These are your heart rate and stroke your heart rate is essentially your conduction system of the heart. Your heart rate is how many beats per minutes so beats over minute  

The other factor is your stroke volume 

The factor is your stroke volume which is the volume of blood pumped by each ventricle with each beat so this is ML per beat so 

cardiac output =stroke volume heart rate beat per minute 

therefore cardiac output is equal to multiplied by heart rate and stroke volume ML/ minutes and heart rate is beats per minutes so as 

an example a normal stroke volume would be about 70 mils per beat and heart rate about 75 each per minute cross the beats out and your cardiac output is 5250 mils per minute and this is about 5 L per minute which is about right because the amount of blood passing through the heart minute is about 4 to 6 L and things that can influence your heart rate known as chronotropic factors so you can have positive Cronogropes which increase your heart rate and negative chronotropes which decrease your heart rate, and example of Positive chronotropes is your sympathetic stimulation your adrenaline adrenaline epinephrine epinephrine these guys will increase your heart rate. 

Some drugs can also increase your heart rate such as atropine.

Cardiac output

 Output output is defined as the amount of blood ejected by the heart in one minute

Contracting ejecting blood out to the Aorta and the pulmonary trunk. The cardiac output is defined by the amount of blood ejected by each ventricle in one minute and there are two factor. Is that are used to calculate the cutting output these are your heart rate and stroke volume. Your heart rate is essentially your conduction system of the heart. Your heart rate is how many beats permitted so beats over minute. The other factor is a stroke volume. The factor is a stroke volume which is the volume of blood humped by each ventricle with each heat so this is Mills per beat so therefore output is equal to multiplied by heart rate and stroke volume is Mills per beat and heart rate is beats permitted so as an example a normal stroke volume would be about 70 mil per beat and heart rate about 75 ft./m cross the beats out and your cardiac output is 5250 mils per minute And this is about 5 L per minute which is about right because the amount of blood passing through the heart is about 4 to 6 L, so the heart rate and stroke volume is used to calculate it output, but there’s another three factors which influence/volume and so in topic factors we put but there’s another 34 to 6 L Heart rate volume is Used to calculate cut it output, but there’s another three factors which influence/volume and so in total. There are four determinants of credit output. Let’s take a look at these so the first determinant, which we talked about his heart rate which is your conduction system this is how many beats per minute And things that can influence your heart rate known as chronic factors so you can have positive Kron which increase your heart rate and negative chronic which decrease your heart rate example of positive Cron is your sympathetic stimulation your adrenaline adrenaline epinephrine epinephrine. These guys will increase your heart rate. Some drugs can also increase your heart rate such as atropine Negative decrease your heart rate. This is your parasympathetic activity so this is your acetyl colon some drugs such as a dentist can also decrease your heart rate. The determinants of output are the things that influence your preload preload is essentially the amount of blood entering the ventricles during Gast so it’s also known as I guess and diastolic again the pillow is the amount of blood, the volume entering the ventricles, and this is during diastole Preload can be influenced by Venus return the blood and also The preload again occurs during diastole, because this is when your ventricles are being filled with blood output, which essentially occurs during cyst. When ventricles are contracting injecting blood out of the aorta and into the pit trunk is essentially the resistant ventricles must overcome to circulate. The blood can imagine things can increase these things such as hypertension sclerosis and laser construction, because because these things will increase the resistance and therefore increase after the fourth determine of output. This is hardcard contract for a preload And things that influence these are tropic factors which increase contract, and then there is negative trips which decreased contractility so positive again is your sympathetic stimulation, nor adrenaline or nor epinephrine. Some drugs can also increase contractility making it a more powerful contraction negative things parasympathetic stimulation, so you’re still calling again, and some drugs can also decrease Output heart rate. Nephritis can be a complication 

 
sidebar interaction. Press tab to begin.

In previous quarters where I teach 2 lectures a week in person, the students learn about different capillaries before this lecture. This quarter, this is your pre-class work so it's okay if you didn't know the answer before I covered it!

I'll link a short video on the different types of capillaries for you to review if needed (see it under the instructions for this assignment in "extra resources"

9 regions

 

 

Electrocardiography (ECG/EKG) - basics

Arrhythmias - What is an arrhythmia and how is it treated?

The different types of heart arrhythmia

two different pressures

physio flip

muscle or nervous tissue 

capillary wit hthe thin wall exchange nutrients

get stuff into the blood 

get stuff out of the blood 

swell up -edema 

fluid stay outside the blood  vessel 

normally reabsorb 

fluid been out of the blood 

hydrostatic pressure 

straw - fill up the straw with water ( water is being pull down by hydrostatic pressure ) 

basic the same thing happen in the capillaries

in the capillaries-CVS system fluid is force out through capillary wall 

just about all the time 

osmotic pressure 

water always flow towards 

higher concentration 

small hole - allow small perticle to pass 

much higher 

protein molecule 

concentration protein molecule 

water always flow 

water reabsorb to the vessel

blood serum protein compre outside the 

driven by osmotic or osmotic pressure ( tend to drive back in ) 

colloid -oncotic pressure 

protein 

ion sodium 

do not contribute the osmotic fluid 

filter 

reabsorb 

osmotic 

interstitial 

capillary 

equal to 

hydrostatic pressure 

small fraction 

final player 

lympatic system 

helping gup prevent or  

 sympathetic nervous system increase Beta 1 adrnergic receptors on contractile cell 

calcium can combine to troponin tropomyosin which mean that we can get stronger contraction or contractile cell increase contraction 

less calcium flow in  ( concentration gradient distrupt ) so that not true 

hyperkalemia tends to block depolarization ( pacemaker cell ) K want to leave the cell 

not contract contractile cell not depolarize

 preload 

contract 

all the step of the cardiac cycle

diastolic volume 

systolic volume

two cardiac out put 

regular stroke volume '

remember your rule 

big picture 

blood flow from high to low 

all about pressure 

cotracting either atria or ventricle 

get to the lung 

get out  from the lung 

valve 

prevent back from 

when ventricle  are ontracting 

prevent from improper blood flow 

all the blood pump out to the body

definition 

1. stroke volume: the volume of blood pump out the left ventricle of the heart during each systolic cardiac contraction (SV)
2. end diastolic volume (EDV) the amount of blood that is in the ventricles before the heart contracts 
3. the volume of blood in one ventricle at the end of the systolic ejection phase immediately before diastole (ESV)
4. the amount of blood pumped by the heart minute by one ventricle (cardiac output )

5-6 liter of pump 

heart rate 

10 L 

how much blood 

3 key factor 

preload -how much fill the ventricle during diastolic 

force of contract- the more blood push

 - after load -certain amount of resistant 

ventricle has to overcome out through the aorta

second-Heart rate 

Heart rate is higher - the more blood volume to the heart 

if we increase - cardiac output will be increase 

double heart rate 

equation - double the cardiac output 

average heart rate 70 to 72 perminute 

18-40years of age 

infant and toddler

normal average is faster than adult (100-150)

greater than 60 years old 

number of beat per minute 

range from 100 to 130 per minutes 

how heart rates changes 

brady cardia 

slower heart rate 

for average adult ( less than 60perminute ) 

lower than 60 when sleeping heart rate can be slow down 

slower heart rate

the other term 

tachy cardia 

fast than normal heart rate 

over the 100 beat per minute (during exercise to deliver more oxygen ) 

higher metabolic activity

especially aerobic or running 

blood is red 

second set of exercise 

effectors heart rate in two ways - 

positive chronotropic effector- increase the heart rate 

negative chronotropic effector - decrease the heart rate 

tachycardia - decrease preload (fast heart rate ) filled before ventricle contract 

ventricle never fully filled 

start to contract before fully full 

Cardiovascular System Physiology - Cardiac Output (stroke volume, heart ...

Muscle contraction

 

CPR can result in broken ribs

 When performed by untrained or overzealous individuals, CPR can result in broken ribs or a broken sternum, and can inflict additional severe damage on the patient. It is also possible, if the hands are placed too low on the sternum, to manually drive the xiphoid process into the liver, a consequence that may prove fatal for the patient. Proper training is essential.

“Staying Alive,” song recorded in 1977 by the Bee Gees

 “Staying Alive,” recorded in 1977 by the Bee Gees. If you are unfamiliar with this song, a version is available on www.youtube.com. 

Subvalvular apparatus: The papillary muscles and the chordae tendineae, known as the subvalvular apparatus, hold the valves closed so that they do not prolapse.

Papillary muscles, together with the chordae tendineae, make up the subvalvular apparatus. 

Blood flows through an atrioventricular (AV) valve Blood flows through an atrioventricular (AV) valve when blood pressure in the atria becomes high during atrial systole and blood pressure in the ventricles becomes low enough during ventricular diastole, creating a blood pressure gradient.

Papillary muscles, finger-like projections from the wall of the ventricles, connect the chordae tendineae (heartstrings) to the cusps of the atrioventricular valves. This connection prevents the valve from prolapsing under pressure.

 Guiding Questions

Cardiac Cycle: Conduction & Mechanical Events

Explain how pressure gradients drive blood flow in the cardiovascular system.

Ventricular contraction ejects blood into the major arteries, resulting in flow from regions of higher pressure to regions of lower pressure.

Identify the location of high pressure and low pressure during systole and diastole.

Outline the steps of the cardiovascular cycle and describe what happens to pressure and blood flow in each chamber at each step of the cycle. Be sure to identify the status of the AV and semilunar valves during each stage of the cycle.

Explain how the pressure gradients cause the valves open and close during the cardiac cycle.

What is the importance of the gap junctions that connect the autorhythmic cells with the contractile cells?

Outline the steps of the intrinsic conducting system and associate them with the steps of the cardiac cycle.

Describe how the SA node controls heart rate. What happens when the SA node is damaged?

Explain how heart rate is controlled by the parasympathetic system and the sympathetic system. Be sure to discuss the intrinsic heart rate, the neurotransmitters and receptors that operate during control of heart rate.

What is an ECG and what kind of information can be gathered from it?

Draw an ECG trace. Identify the P wave, the QRS complex, and the T wave.

Draw another ECG trace. Identify the part of the ECG trace that correlates with atrial depolarization, atrial hyperpolarization, ventricular depolarization and ventricular hyperpolarization.

Now draw a third trace. Identify the part of the ECG trace that correlates with atrial systole, atrial diastole, ventricular diastole, and ventricular systole (remember that physical events happen AFTER the electrical events).

Describe what is happening to both pressure and volume during each stage of the cardiac cycle. Be sure to use the following terms: Ventricular filling, end diastolic volume, isovolumetric contraction, ejection, and end systolic volume, isovolumetric relaxation.

How does ESV change during exercise?

What is stroke volume? What is the average stroke volume? How does stroke volume change?

 

Cardiac Output

Define cardiac output. How do I determine cardiac output?

Explain how altering heart rate (via sympathetic or parasympathetic stimulation) alters cardiac output.

What is afterload and how does it affect cardiac output? Give an example of how afterload alters cardiac output. 

What is preload and how does it affect cardiac output? Why does EDV determine the force of contraction?

What are some ways that I can alter EDV (and therefore alter stroke volume)?

Describe how the skeletal muscle pump and the respiratory pump affect EDV **(we'll cover this when we discuss blood vessels)

How does total blood volume affect EDV?

How much of the blood is contained in the venous circulation? How can I send more of the blood in the veins to the heart, and how does this affect EDV? **(we'll cover this when we discuss blood vessels)

Define contractility and explain how an inotropic agent affects contractility.

Explain how the sympathetic system modulates contractility. Be sure to name the neurotransmitters and receptors involved.

In a fight or flight response, explain what happens to the following factors and why they are affected this way (be sure to discuss neurotransmitters and receptors): heart rate, venous return, EDV, contractility, stroke volume, cardiac output.

The Cerebellar GABAAR System as a Potential Target for Treating Alcohol Use Disorder

 The Cerebellar GABAAR System as a Potential Target for Treating Alcohol Use Disorder 

The Cerebellar GABAAR System as a Potential Target for Treating Alcohol Use Disorder

refractory period

 The refractory period is a state of recovery that occurs after a neuron has fired an action potential. 

During this period, another action potential cannot be easily produced. 

This encourages unidirectional flow of action potentials because they cannot travel backwards to inactive neurons.

The depolarization that produces Na+ channel opening also causes delayed activation of K+ channels and Na+ channel inactivation, leading to repolarization of the membrane potential as the action potential sweeps along the length of an axon (see Figure 3.12). In its wake, the action potential leaves the Na+ channels inactivated and K+ channels activated for a brief time. These transitory changes make it harder for the axon to produce subsequent action potentials during this interval, which is called the refractory period. Thus, the refractory period limits the number of action potentials that a given nerve cell can produce per unit time. As might be expected, different types of neurons have different maximum rates of action potential firing due to different types and densities of ion channels. The refractoriness of the membrane in the wake of the action potential explains why action potentials do not propagate back toward the point of their initiation as they travel along an axon.

What happens during the refractory period of a neuron?

In its wake, the action potential leaves the Na+ channels inactivated and K+ channels activated for a brief time. These transitory changes make it harder for the axon to produce subsequent action potentials during this interval, which is called the refractory period.

By definition, the refractory period is a period of time during which a cell is incapable of repeating an action potential. In terms of action potentials, it refers to the amount of time it takes for an excitable membrane to be ready to respond to a second stimulus once it returns to a resting state.

Aorta

 The aorta holds the distinction of being the largest artery in the human body. Its significance lies in serving as the initial pathway for blood leaving the heart and distributing it to various organs through smaller, branching arteries. Without the aorta, our body’s tissues wouldn’t receive the vital oxygen and nutrients they need 1. Let’s delve into more details about this remarkable vessel:

• Anatomy of the Aorta:

  • The aorta starts at the left ventricle of the heart, where it receives oxygenated blood.
  • It then arches upward toward the neck (forming the aortic arch), before curving back downward and extending into the abdomen.
  • Structurally, the aorta is a big tube-like structure, typically about 1 inch wide in diameter. However, its size can vary based on an individual’s height and weight.
  • The aorta is widest at its connection to the heart’s left ventricle through the aortic valve. As it descends into the abdomen, it gradually narrows.

• Four Parts of the Aorta:

  1. Ascending Aorta:
     • The first part of the aorta, connected to the left ventricle.
     • Originates at the aortic valve, which regulates blood flow from the heart into the aorta.
  2. Aortic Arch:
     • Curves upward toward the head and neck.
     • Begins where the ascending aorta ends.
  3. Descending Aorta:
     • Travels downward from the aortic arch through the chest.
     • Also known as the descending thoracic aorta.
  4. Abdominal Aorta:
     • The final part of the aorta.
     • Starts at the diaphragm and ends where it splits into the two iliac arteries that extend into the legs.

• Layers of the Aorta Wall:

  • The aorta has three layers in its wall:
    1. Tunica Intima: The innermost layer, providing a smooth surface for blood flow. Composed of endothelial cells and supporting tissue.
    2. Tunica Media: The middle layer, consisting of smooth muscle, elastic tissue, and collagen.
    3. Tunica Adventitia: The outer layer made of connective tissue (collagen) and a network of small blood vessels (vasa vasorum) that nourish the aorta.

• Variations and Anomalies:

  • In some conditions (such as dextrocardia or situs invertus), the aorta may be on the right side instead of the left.
  • Coarctation of the aorta is a birth defect where a part of the aorta is significantly narrower than usual.

In summary, the aorta’s essential role as the largest artery ensures efficient oxygen and nutrient distribution throughout our body, making it a vital conduit for life-sustaining blood flow 234. If you have more questions or need further information, feel free to ask! 😊

lab exit

What Is Aortic Stenosis? Your aortic valve keeps blood flowing from your heart's lower left chamber (left ventricle) to the aorta which is the main artery bringing blood from the heart to the body. Aortic stenosis occurs when the aortic valve narrows and blood cannot flow normally.

regurgitation?

Mitral valve regurgitation is a problem that occurs when there is a valve leak, leading to blood flowing back into the left atrium. The incomplete valve closure may produce a softer S1 sound. Symptoms that may arise in people with this valve problem include: dizziness.

 

check in question week 7

 

tetrodotoxin TXX blocks voltage gated sodium channel which part of action potential graph is affected by TXX discuss the activation and inactivation status of channel the key channel involved and the refractory period

 Tetrodotoxin (TTX) is a potent neurotoxin that specifically targets voltage-gated sodium channels. Let’s explore how TTX affects the different phases of the action potential graph:

Activation and Inactivation of Sodium Channels:

Voltage-gated sodium channels play a crucial role in generating action potentials.

These channels have two main states: closed (resting state) and open (activated state).

When a neuron is at rest, sodium channels are predominantly in the closed state.

Upon depolarization (due to an incoming stimulus), some sodium channels open, allowing sodium ions (Na⁺) to flow into the cell. This is the activation phase.

However, sodium channels also have an inactivation gate that can close the channel shortly after it opens. This prevents continuous sodium influx.

Tetrodotoxin’s Mechanism of Action:

TTX binds to the extracellular pore opening of voltage-gated sodium channels.

By binding to site 1 of the sodium channel, TTX temporarily disables the channel’s function.

Specifically, it prevents the passage of sodium ions into the neuron during the rising phase of an action potential.

As a result, the nervous system cannot transmit messages effectively, leading to muscle paralysis.

Key Channel Involved:

The primary sodium channel affected by TTX is the fast voltage-gated sodium channel.

These channels are responsible for the rapid depolarization phase of the action potential.

Refractory Period:

The refractory period is a critical aspect of action potentials.

After an action potential, sodium channels enter a refractory state:

Absolute refractory period: During this phase, sodium channels are completely closed and cannot be activated, regardless of the stimulus.

Relative refractory period: In this phase, some sodium channels have recovered from inactivation, but the membrane potential is still below the resting level. A stronger stimulus can trigger another action potential.

TTX prolongs the refractory period by preventing sodium channels from reopening promptly.

In summary, TTX disrupts the normal function of sodium channels, leading to the inhibition of action potentials and muscle paralysis. Its selective blocking action makes it a valuable tool for studying neuronal excitability and pain pathways12. 🧪🔬

If you have more questions or need further clarification, feel free to ask! 😊

what is the concentration gradient for the ion at the resting membrane potential what happen ion flow once the drug added and how the drug change the memembrane potential

 what is the concentration gradient for the ion at the resting membrane potential what happen ion flow once the drug added and how the drug change the memembrane potential

Copilot

Certainly! Let’s break down the impact of a drug on the resting membrane potential (RMP) and how it affects ion flow.

Concentration Gradient at RMP:

At the resting membrane potential, there is a concentration gradient for both sodium ions (Na⁺) and potassium ions (K⁺).

Inside the cell, the concentration of potassium ions is higher than outside, while the concentration of sodium ions is higher outside the cell.

This concentration gradient is maintained by the sodium-potassium pump and leak channels.

Ion Flow Once the Drug Is Added:

When a drug is introduced, it can alter the permeability of the cell membrane to specific ions.

Let’s consider a hypothetical drug that selectively increases the permeability of sodium ions (Na⁺) through the membrane.

Impact of the Drug on Membrane Potential:

If the drug enhances sodium ion permeability, more sodium ions will flow into the cell.

This influx of positive charges will depolarize the cell membrane (make it less negative).

As a result, the resting membrane potential will shift toward a less negative value (e.g., from -70 mV to a less negative value).

Overall Effect:

The drug disrupts the balance between sodium and potassium ions, altering the resting membrane potential.

Depending on the drug’s mechanism, it could lead to hyperpolarization (more negative potential) or depolarization (less negative potential).

Remember that the specific effects of a drug depend on its properties and the type of ion channels it interacts with. Real-world drugs can have complex interactions, affecting various ion channels and receptors.

If you have any further questions or need additional details, feel free to ask! 🧪🔬

explain how each of the choices selected above RMP K leack channel and sodium and potassium pump and concentration gradient and membrane permeablity why RMP is -70

 

the factors that contribute to the resting membrane potential (RMP) of a neuron and why it is typically around -70 mV.

Leak Channels:

Neurons have leak channels (also known as non-gated channels) that allow ions (such as potassium and sodium) to passively move across the cell membrane.

These channels are always open and contribute to the resting membrane potential.

The most important leak channel for RMP is the potassium leak channel (K⁺ channel). It allows potassium ions (K⁺) to move out of the cell, making the inside of the cell more negative.

Sodium-Potassium Pump (Na⁺/K⁺ Pump):

The sodium-potassium pump actively transports sodium ions (Na⁺) out of the cell and potassium ions (K⁺) into the cell.

For every three sodium ions pumped out, two potassium ions are pumped in.

This pump helps maintain the concentration gradients of sodium and potassium across the cell membrane, which is crucial for RMP.

Concentration Gradient:

The concentration gradient refers to the difference in ion concentrations between the inside and outside of the cell.

At rest, there is a higher concentration of potassium ions (K⁺) inside the cell and a higher concentration of sodium ions (Na⁺) outside the cell.

The potassium leak channel allows potassium ions to move out of the cell along their concentration gradient, contributing to the negative RMP.

Membrane Permeability:

The permeability of the cell membrane to different ions affects RMP.

The cell membrane is more permeable to potassium ions (K⁺) due to the abundance of potassium leak channels.

Sodium ions (Na⁺) have fewer leak channels, so their contribution to RMP is smaller.

Now, let’s tie it all together:

The potassium leak channel allows potassium ions to leak out of the cell, making the inside more negative.

The sodium-potassium pump maintains the concentration gradients by actively pumping sodium out and potassium in.

The net effect of these processes results in an RMP of approximately -70 mV.

Remember that RMP can vary slightly depending on the specific type of neuron and its environment, but -70 mV is a common value. 

If you have any more questions or need further clarification, feel free to ask! 😊

 The first heart sound "lubb" (or S1) corresponds to AV valves closing. The second heart sound "dubb" (or S2) corresponds to the closing of semilunar valves closing.

 

The closing of these valves are so forceful that you can hear these when you are listening to heart beats of a person/patient and this is what we refer to when we are listening to someones heart beat!

Answer 1:

AV

 

Answer 2:

semilunar

 

The Cardiac Cycle, Animation

Cardiac Cycle | Wiggers Diagram | Part 5 | Summary | Cardiac Physiology

Muscle Contraction - Cross Bridge Cycle, Animation.

Lecture 6: Cardiac Cycle Conduction Friday 5/17

 Lecture 6: Cardiac Cycle Conduction

Friday 5/17

Pre-Class SlidesDownload Pre-Class Slides

Take notes with me using this handoutDownload Take notes with me using this handout

Lecture 6 (5/17) Exit Ticket (opens when I open it during class!)

Post-class slidesDownload Post-class slides

RecordingLinks to an external site.

This is actually a really nice summary of the whole cardiovascular section we'll cover over the next few weeks. For pre-nursing folks, this is actually put together for their Associate degree in nursing (so this stuff is quite relevant!). I'll leave this here in case folks like a one-stop resource of helpful diagrams & text. Otherwise feel-free to review lecture recordings & pre-class videos: https://www.austincc.edu/apreview/PhysText/Cardiac.htmlLinks to an external site.

Lecture 10 handout Key (will post at the end of the week :) have some folks making up the lecture)

 

Guiding Questions:

1. Lay out the steps of myocardial cell contraction. Describe carefully what happens in each step.

What is the Ca2+ spark (rush of calcium into the cell)? Where does the Ca2+ come from?

Lay out the steps that lead to relaxation of the myocardial cell after contraction.

How is Ca2+ removed in a contractile myocardial cell?

3. What is the resting membrane potential of a contractile myocardial cell?

What is the trigger for the action potential in contractile myocardial cells? What is the source of that stimulus?

What type of channel activity results in the rising phase, plateau phase and falling phase of the action potential? What is the trigger for each of these types of channel activity?

4. Why is the refractory period in contractile cells so much longer than that in skeletal muscle cells? (covered in post-class week 6, not lecture)

How does the refractory period for myocardial cells prevent summation of force in these cells*****

What would the impact of summation be if it could happen in these cells? Where does the Ca2+ come from to lengthen the refractory period so much? ****These questions will actually be answered during your pre-class week 7! Feel free to skip for now and make sure they are answered by next week!

5. Describe the origin of the pacemaker potential found in autorhythmic cells.

How does the pacemaker potential trigger the rising phase in autorhythmic cells?

What causes the falling phase in autorhythmic cells?

Compare and contrast the rising phase of the autorhythmic cells with the rising phase of the contractile cells, the rising phase in skeletal muscles and the rising phase in neurons.

6. How do action potentials in autorhythmic cells translate to the contraction of the contractile cells?

 

. What is the function of the cardiovascular system? Give some examples of materials transported by the system.

Describe the organization, pattern of blood flow and the major function of the cardiovascular system using the following terms: heart, arteries, capillaries, and veins.

Describe the structure of the heart and pattern of blood flow through the heart using the following terms: atria, ventricles, septum, vena cava, aorta, pulmonary veins, pulmonary arteries, AV valves, papillary muscle*, chordae tendineae*, semilunar valves.

What is the function of the valves in the heart? Where does the energy come from to open and close the valves? (*covered in lab Week 6)

2. What is the importance of the gap junctions that connect the autorhythmic cells with the contractile cells?

Outline the steps of the intrinsic conducting system and associate them with the steps of the cardiac cycle.

Describe how the SA node controls heart rate. What would happen when the SA node is damaged?

Explain how heart rate is controlled by the parasympathetic system and the sympathetic system. Be sure to discuss the intrinsic heart rate, the neurotransmitters and receptors that operate during control of heart rate

3. Define the terms systole and diastole in terms of the cardiovascular system.****

Explain how pressure gradients drive blood flow in the cardiovascular system. Identify the location of high pressure and low pressure during systole and diastole.*** these questions will be covered next Tuesday's lecture

week 2 preclass activity quizz

 

Question 2

0 / 1 pts

When I teach this in person, I like to make an analogy between pacemaker cells, contractile cells, and the autonomic nervous system (ANS). Remember that the ANS is divided into sympathetic (speeds up heart rate) and parasympathetic (slows down heart rate).

 

Consider how lights can be turned on/off and that some have a dimmer switch:

 

I would argue that each component: pacemaker, contractile cells and autonomic nervous system match the way this lighting system works. Check your understanding by matching the terms below.

Correct!

Pacemakers are autorhythmic and determine when contractile cells will depolarize.

 

               Light switch on/off             

Correct!

ANS can determine how fast or slow pacemaker and contractile cells depolarize and therefore speed up/slow down heart rate.

 

               Dimmer switch (controls how bright/dim lights are)             

Correct!

Contractile cells are THE cardiac muscle cells that generate contractions (pumping/beating) of the heart. They follow the pace set by pacemakers & ANS.

 

               The actual light (how bright or on/off)             

How are contractile and pacemaker cells connected? Select all

Correct!

  

They have continuous channels and share ions, forming a network of cells called a syncytium.

 

  

There are two syncytia: atrial and ventricular. This explains why the atria contract at once and the ventricles contract second.

 

You Answered

  

If connections between pacemaker & contractile cells are most similar to a chemical synapse.

 

Correct Answer

  

If connections between pacemaker & contractile cells are most similar to an electrical synapse.

 

How does the heart pump? How does it know when to beat?

  

Contractile cells set the pace/rhythm of beats. Autorhythmic cells cause cardiac muscle contractions

 

Correct!

  

Autorhythmic cells set the pace/rhythm of beats. Contractile cells cause cardiac muscle contractions