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