Description

Complete Cheat Code for Heart Physiology Series:

• 1st Video: Types of cardiac muscle, action potentials of pacemaker cells and contractile myocardium, and general properties of cardiomyocytes.
• 2nd Video: Detailed exploration of the cardiac cycle, including phase-by-phase events, valve operations, and pressure differences.
• 3rd Video: Cardiac output.
• 4th Video: Regulation of heartbeat.

Key Concepts Covered:

1. Overview of Cardiac Output (CO):

• Formula: CO = Heart Rate (HR) × Stroke Volume (SV).
• Regulation affects pacemaker activity or myocardial contraction.

2. Regulation Categories:

Myogenic Regulation:

• Heterometric Regulation:
  • Frank-Starling Mechanism: Increased end-diastolic volume (EDV) stretches cardiomyocytes, enhancing contraction and increasing SV.
• Homeometric Regulation:
  • Bowditch Effect (Staircase Effect): Increased HR strengthens contractions due to enhanced calcium handling in cells.

Neural Regulation:

• Involves the nervous system, divided into extracardiac and intracardiac regulation.
• Extracardiac Regulation:
  • Sympathetic Nervous System: Increases HR, contractility, and CO via norepinephrine and epinephrine acting on β1-adrenergic receptors.
  • Activates ion channels to enhance calcium influx, increasing contraction strength and speed.
  • Parasympathetic Nervous System: Reduces HR and conduction velocity via acetylcholine on muscarinic receptors.
  • Inhibits adenylyl cyclase, decreasing cAMP levels and activating K+ channels to hyperpolarize the membrane.
• Medullary Control: Integrates input from baroreceptors and chemoreceptors to modulate autonomic nervous system activity.
• Intracardiac Regulation: Intramural ganglia modulate cardiac function independent of direct CNS control.

Humoral Regulation:

• Involves hormones in the blood influencing HR, contractility, and CO.
• Epinephrine: Released by adrenal medulla, activating β1-adrenergic receptors.
• Renin-Angiotensin-Aldosterone System (RAAS):
  • Angiotensin II increases contractility, vasoconstriction, and blood volume.
  • Aldosterone promotes sodium and water reabsorption, increasing blood pressure and CO.
• Thyroid Hormones (T3): Increase HR and contractility by influencing gene expression and ion channel activity.
• Glucocorticoids: Enhance myocardial contractility and adrenergic receptor sensitivity.
• Natriuretic Peptides (ANP, BNP): Reduce blood volume and pressure by promoting sodium and water excretion.

3. Ion Regulation:

• Calcium:
  • Hypercalcemia increases contractility, shortening the QT interval.
  • Hypocalcemia decreases contractility, prolonging the QT interval.
• Potassium:
  • Hyperkalemia depolarizes cells, increasing arrhythmia risk.
  • Hypokalemia reduces excitability, making depolarization more difficult.

By understanding these regulatory mechanisms, you’ll gain a comprehensive understanding of how the body maintains cardiac function under various physiological conditions.

#cardiacphysiology #heartfunction #extracardiac #ecg #medicaleducation #usmlepreparation #nursingeducation #premed #heartanatomy

Sources:

• University lectures and notes
• Barrett, K. E., Barman, S. M., Boitano, S., & Brooks, H. L. (2016). Ganong’s Review of Medical Physiology (25th ed.). McGraw-Hill Education.
• Hall, J. E. (2016). Guyton and Hall Textbook of Medical Physiology (13th ed.). Elsevier.
• Mohrman, D. E., & Heller, L. J. (2014). Cardiovascular Physiology (11th ed.). McGraw-Hill Education.
• Biorender

Transcript

Introduction
0:06
Regulation of the Heartbeat Physiology What’s up, Taim talks med here. Let’s continue our Complete Cheat Code for Heart Physiology.
0:13
We’re doing this in 4 segments. The 1st video was about the different types of cardiac muscle, the action potentials of pace maker cells and contractile myocardium,
0:22
and the general properties of our cardiomyocytes. The 2nd video was about the cardiac cycle where we
0:28
made an easy diagram illustrating what actually happens at each phase. The 3rd video covered
0:33
everything you need to know regarding the cardiac output. This is the 4th video where we’ll cover the regulation of the Heartbeat, covering all the most important mechanisms that actually change the
0:44
contractility and heart rate. Alright awesome. Before we dive into the actual regulation,
Principles Behind Regulating the Heartbeat
0:50
I wanna just quickly remind you again about this equation because it’s so important to know that the quantity of blood pumped by the heart each minute, that is CO,
1:01
is influenced by the heart rate, that is changes in beats per minute, or the volume ejected per
1:07
each stroke, that is stroke volume. Therefore when we talk about the control of cardiac activity,
1:13
we always mention how it affects either the pacemaker activity or the myocardial contraction.
1:19
Now, we are quite complex organisms and a change in the function of one of these features almost
1:25
always changes the other one. Some factors can favour one of these more than the other,
1:30
like if the temperature changes the heart rate increases, and if the myocardium is stretched the contraction increases, but inevitably all factors influence both of these to
1:41
a certain degree. And there are a whole lot of factors that can influence the CO,
1:46
so I’ll give you the most important ways that the body regulate our heartbeat. And we can divide
1:52
them into Myogenic regulation, Neural regulation, and Humoral regulation. There are many ways to
1:58
classify this but I find this method the easiest. I’m gonna give you just enough info about each of
2:04
these so you become an expert in how our body actually regulate the CO. Let’s now quickly go
Myogenic Regulation
2:09
through the myogenic regulation first. Myogenic regulation is defined as the
2:14
autoregulated mechanism involving the cardiomyocytes. So basically
2:19
the cardiomyocytes are the ones who affect the CO. How? There are two ways.
Heterometric Autoregulation
2:25
First one is the Heterometric regulation. Now stay with me. Heterometric Regulation means the hearts
2:32
ability to adjust its contractility based on the length change of cardiomyocyte. Here’s the heart,
2:39
we take out one contractile myocardium which has you know the actin myosin and tropomyosin.
2:45
If the ventricles gets filles with blood, the ventricles and gonna stretch a little bit, leading
2:50
to a slight length change of the cardiomyocytes. Imagine now that during the same cardiac cycle,
2:57
the end diastolic volume is increased, so we get more blood filling up the ventricle. What’s gonna
3:03
happen now? Cardiomyocytes are stretched even more, allowing more crossbridge formation. Now
3:10
when it ejects the force of contraction is gonna be much higher, increasing the stroke volume,
3:15
thereby increasing the CO. That is called Frank-Starling mechanism. So Frank Starlings
Frank Starling Mechanism
3:21
mechanism says, the greater the heart muscle is stretched during filling, the greater is the
3:27
force of contraction and the greater the volume of blood pumped into the aorta. This is because the
3:32
actin and the myosin filaments are brought to a more nearly optimal degree of overlap to generate
3:38
a strong force. So the force of contraction increases based on the position of the actin
3:44
and myosin to each other during the stretch. And this is just up to a certain degree, If the EDV is
3:51
too much, too much stretch can lead to less actin and myosin being able to meet. So Frank Starling
3:58
Mechanism is up to a certain degree. Now, what if we reduce the EDV, what happens to the contractile
4:06
myocardium now? It stretched just a little bit. So the force of contraction is also not so strong.
4:12
So. Preload decrease leads to a decrease in stroke volume, causing lower CO. High preload, higher
4:21
stroke volume, higher CO. That is the heterometric regulation, based on Frank Starlings mechanism.
Homeometric Autoregulation
4:28
The other type of Myogenic regulation is homeometric regulation, which means the
4:34
hearts ability to adjust its contractility based on other factors than the length change for
4:40
cardiomyocytes. Which means, how do we change the CO, or afterload, without changing the preload. One way to do that is through the different ways calcium can be handled within the cell. And it can
4:47
be explained using the Bowditch effect, or the staircase effect. Bowditch effect is basically
Bowditch effect
4:53
says as the heart rate increases, the force of each contraction also increases, up to a certain
4:59
point. And this is due to the way the cells handle calcium. Let’s see how. Just to give you
5:05
a quick recap on how the contractile myocardium is depolarized. You first get a neural stimulus from
5:12
the previous cell, it positively charges the cell membrane, activates voltage gated sodium channels
5:17
at the threshold potential. Once the cell reach about +40 mV, it’ll activate potassium channels
5:24
pumping potassium ions out. That positive charge will still continue along the cell
5:30
membrane activating L-type calcium channels. I’m just running through here since we already went through the depolarization steps in details in the first video about cardiomyocytes. So,
5:40
calcium comes in, triggering ryanodine receptors to open, which’ll give off stored calcium within
5:46
the sarcoplasmic reticulum. This calcium will now sit on Troponin C, which eventually leads
5:53
to tropomyosin leaving the binding site for myosin on actin leading to contraction of
5:58
muscle. To relax the muscle, Calcium goes into he sarcoplasmic reticulum through calcium atp pump,
6:07
it can be pushed out of the cell through calcium ATP pump, or we can exchange sodium with calcium,
6:14
facilitated by the sodium potassium pump, by pumping sodium out so more sodium can be pushin in
6:21
in exchange to calcium. And we got a lot of these sodium calcium exchangers. Now. In a situation
6:29
where we have a high heart rate, maybe due to a sympathetic stimulation for example. That
6:35
increase in heart rate is going to fire lots of neural stimuli. That is going to cause the
6:40
voltage gated sodium channel to work more, in a higher frequency, filling up the cell with sodium.
6:46
Because we now have a high amount of sodium within the cell, this sodium calcium exchanger won’t be
6:52
as active anymore because what’s the point of exchanging calcium with sodium when you already have a lot of sodium inside the cell? So now, when the cardiac muscle needs to relax,
7:02
it needs to put the calcium somewhere. So more calcium is pushed into the sarcoplasmic reticulum.
7:09
Now during the next contraction – more calcium is pushed into the cell from the sarcoplasmic
7:15
reticulum, which leads to a stronger contraction. So If you look here, because the cardiomyocytes
Staircase effect
7:21
puts more calcium within the sarcoplasmic reticulum with increase in heart rate,
7:27
the contraction becomes stronger, but then reach a maximum contraction force.
7:32
This increase in contraction with every beat is called staircase effect. So that was the
7:39
myogenic autoregulation of the heart pumping. Now what about the neural regulation? Neural
Neural Regulation
7:45
regulation means the autoregulation concerning the nervous system, and it’s divided into extracardiac
7:52
regulation, and intracardiac regulation. Extracardiac regulation involve sympathetic
7:57
and parasympathetic involvement. I can’t express how important this is, to know the mechanism of
8:03
how these systems can regulate the heart. Let’s look into the sympathetic nervous system first.
Sympathetic Regulation of the Heart
8:10
The sympathetic nervous system is our fight or flight response. So you wanna increase the heart rate, increase contractility, increase cardiac output.
8:20
Now. The sympathetic nerves that innervate the heart primarily originate from the upper thoracic
8:26
segments of the spinal cord, approximately T1 to T5. These preganglionic fibers exit the spinal
8:33
cord to reach the paravertebral ganglia. The paravertebral ganglia will now give off
8:39
postganglionic sympathetic fibers towards the heart, specifically targeting the nodal cells
8:44
and the contractile cardiomyocytes, releasing primarily norepinephrine, but also a little bit of epi aswell. Most of the epinephrine comes from the adrenal medulla.
8:54
Alrigh. Let’s zoom into one pacemaker cell and see what happens. We already went through this
8:59
in a previous video, but remember pacemaker cells has funny sodium channels leaking sodium into the
9:06
cell all the time, depolarizing it. As its getting more and more depolarized T-type
9:12
calcium channels starts opening, letting calcium into the cell. Once it hits threshold potential,
9:18
L-type calcium channels starts opening up, giving us a massive influx of calcium. Once
9:24
it’s done depolarizing, the cell now repolarizes by opening potassium channels letting potassium
9:30
out, getting it back to its resting membrane potential. On the cell wall of pacemaker cells,
9:37
we have b1-adrenerig receptors, which Epinephrine and Norepinephrine bind to. These are g-protein
9:44
coupled receptors which activate when Epi and Norepi binds. Activated g-protein will activate
9:53
adenylyl cyclase, which increases cyclic amp production, to then activate protein
9:59
kinase. What protein kinase is gonna do now is that it’s going to phosphorylate and activate
10:05
ion channels, specifically the L-type calcium channels, leading to more calcium into the cell,
10:11
as well as phosphorylating the funny sodium channels, leading to more sodium into the cell.
10:17
What happens now is that we get an accelerated depolarization during the pacemaker potential,
10:22
increasing the heart rate. So we get a positive Chronotropic action,
10:28
What about the contractile myocardium? Again Sodium comes in, depolarizing the cell. Potassium channels open, potassium goes out, while the sodium channels close. L-type
10:38
calcium channels open leading to a calcium influx giving us the plateau phase. On the sarcoplasmic
10:44
reticulum we got ryanodine receptors which open in a response to calcium influx from the
10:49
dihydropyridine receptors. Calcium will flow from Sarcoplasmic reticulum into the cell,
10:55
increasing the intracellular calcium levels. Now calcium can bind to the Troponin C,
11:01
which eventually leads to contraction. When the cell repolarizes, it gets rid of intracellular
11:08
calcium using using Ca2+ ATP pumps located in the Sarcoplasmic reticulum and also in the cell
11:14
membrane. Now, the contractile myocardium also has B1 adrenergic receptors, which follow the same
11:22
pathway once Epi and Norepi binds. G-protein gets activated, which will activate adenylyl cyclase,
11:29
which increases cyclic amp production, to then activate protein kinase. What protein kinase is
11:35
gonna do now is that it’s going to phosphorylate the L-type calcium channels to enhance calcium
11:41
influx during the plateau phase. What it also is going to do is that it’s going to phosphorylate
11:47
phospholamban, and relive its inhibitory effect on SERCA, the sarcoplasmic reticulum Ca2+-ATPase,
11:54
enhancing calcium reuptake into the SR. Remember phospholamban acts as an inhibitor of the SERCA
12:02
pump under normal conditions, reducing its affinity for Ca2+. This means that while the SERCA
12:08
pump is still active, its efficiency is lower compared to when phospholamban is phosphorylated.
12:15
What happens now? Now we have so much calcium within the sarcoplasmic reticulum. For the next
12:21
depolarization, we released out more calcium into the cytoplasm. More calcium, means more
12:27
interaction with the troponin, which moves the tropomyosin. If you move the tropomyosin you’re gonna have more actin and myosine interaction, so you’re gonna have significantly more crossbridge
12:38
formations. If you have more crossbridge formation you have more power strokes. More sliding of the
12:45
myofilaments, so that’s gonna increase the actual contractions. So we’ll have an increase inotropic
12:51
action. And since it enhances the reuptake of the calcium by phosphorylating phospholamban,
12:58
we’ll have an increase rate of myocardial relaxation as well, so increase lusitropic
13:04
action. All that will essentially increase the stroke volume, and increase the cardiac output.
13:10
So the overall effect of sympathetic nervous system is a positive chronotropic action because
13:16
you increase heart rate in the pacemaker cells. We’ll get a positive dromotropic action, meaning
13:22
the conduction velocity, Sympathetic stimulation increases the conduction velocity of electrical
13:28
impulses through its action on the AV node. So phosphorylation of L-type calcium channels in
13:34
the AV node speeds up the depolarization phase, reducing the delay of impulse
13:40
transmission from the atria to the ventricles. We also get positive Bathmotropic action, because
13:47
if you increase the calcium and sodium currents within the pacemaker and contractile cells,
13:52
you increasing their excitability aswell. And as we just said we get a stronger contraction
13:58
and enhanced relaxation speed through the sarcoplasmic reticulum calcium channels.
Parasympathetic Regulation of the Heart
14:03
How does the parasympathetic nervous system act on the cells then? The parasympathetic nervous system is our rest and digest system. Now,
14:13
the sympathetic comes from the thoracic spinal segments, The parasympathetic innervation of
14:18
the heart primarily comes from the vagus nerve, the 10th cranial nerve, And it originates in the
14:24
medulla oblongata, and then goes to innervate the heart through the right and the left vagus
14:29
nerves, and it’s going to give off acetylcholine. Acetylcholine will bind to muscarinic receptors on
14:35
the SA node, activating g inhibitory protein. G inhibitory protein will inhibit adenylyl cyclase
14:43
activity, leading to a decrease in cyclic AMP (cAMP) levels opposing the actions of
14:48
sympathetic activity. What it’s also going to do is that it’s going to activate the K+ Channels,
14:55
leading to an efflux of K+ ions, hyperpolarizing the cell membrane.
15:00
What’s that going to do? It’s going to decrease the heart rate, negative chronotropic action
15:06
and decrease conduction velocity, negative dromotropic action. Because muscarinic receptors,
15:12
specifically M2 receptors, are densely populated in the sinoatrial (SA) node and atrioventricular
15:18
(AV) node. This explains the significant effects on the heart rate and conduction velocity. The
15:25
density of M2 receptors in atrial contractile myocardium and especially ventricular myocytes
15:31
is relatively lower. That’s why the direct effect of acetylcholine on the contractile strength of
15:37
the heart muscle is less pronounced, but it do cause a light decrease in inotropy aswell.
15:43
So that was the overall effect of these two systems. Another system that’s really
15:49
important to mention here is the medullary control of the cardiovascular system. One of the major sources of excitatory input to the sympathetic nerves is a group of neurons
Medullary Control of the Cardiovascular System
15:59
located near the outer surface of the medulla, in the rostral ventrolateral medulla. These neurons
16:05
have axons that descend in the lateral column of the spinal cord to the thoracolumbar area,
16:11
giving off sympathetic innervation to the paravertebral ganglia, to then give postganglionic
16:17
innervation to the heart, again increasing the HR and CO, like we just saw. It’s also
16:23
going to cause vasoconstriction, and stimulate the adrenal medulla in releasing epinephrine.
16:29
So what is it that stimulate these nerves? We got chemoreceptors in the carotid and aortic bodies.
16:36
We got Baroreceptors, which are stretch receptors in the walls of the heart and blood vessels. There
16:42
are descending tracts from the limbic cortex aswell that are responsible for rise in blood
16:47
pressure and tachycardia produced by emotions such as stress and anger and sexual excitement.
16:54
Pain usually cause a rise in blood pressure also by sending signals to this area as well.
17:00
Now the medulla is also a major site of origin of excitatory input to cardiac vagal motor neurons
17:07
in the nucleus ambiguous and the Dorsal Motor Nucleus of the Vagus, which give off
17:12
parasympathetic innervation. Things like inflation of the lungs causes vasodilation and a decrease
17:19
in blood pressure. This response is mediated via vagal afferents from the lungs that inhibit RVLM
17:26
and sympathetic nerve activities. I’m not gonna confuse you too much with this, I just wanna show
17:31
you how baroreceptors and chemoreceptors affect these systems and essentially the CO of the heart.
Chemoreceptors
17:39
Within our body, we have something called peripheral chemoreceptors. These are receptos
17:45
that are located within the aortic body and the carotid bodies, and they have a very high rate of
17:51
blood flow. These receptors are very sensitive to changes in partial pressure of oxygen,
17:57
carbon dioxide and pH levels. And they are activated if there’s a reduction in PaO2,
18:04
Increase in PaCo2 or and decrease in pH. So if you’re on a mountain, or a place with
18:12
high altitudes where atmospheric oxygen levels are lower, peripheral chemoreceptors detect the
18:19
decrease in arterial oxygen (PaO2), if there’re conditions such as chronic obstructive pulmonary
18:25
disease (COPD) or pneumonia can lead to hypoxemia, stimulating peripheral chemoreceptors. If there’s
18:32
a respiratory failure, peripheral chemoreceptors respond to the increase in arterial CO2 levels
18:39
(PaCO2). Or conditions such as diabetic ketoacidosis or severe diarrhea can cause an increase in blood acidity aswell. Afferent nerve fibers will now travel from peripheral
18:50
chemoreceptors via the glossopharyngeal nerve (CN IX) from the carotid bodies and via the
18:56
vagus nerve (CN X) from the aortic bodies. And they will go to Nucleus Tractus Solitarius, The
19:04
NTS integrates incoming sensory information from peripheral chemoreceptors, and then it tells that
19:10
information to the rostral ventrolateral medulla (RVLM), which is also called the cardioaccelerator
19:16
area and the vasomotor area, to initiate a sympathetic activity, primarily, increasing
19:22
the heart rate and CO, causing vasoconstriction, and stimulating the adrenal medulla. All this
19:28
is to ensures coordinated reflex responses to optimize oxygen delivery, carbon dioxide removal,
19:35
and acid-base balance in the body. Now, we do also have something called
Baroreceptors
19:41
baroreceptors. These are stretch receptors that react to stretch of the arterial walls,
19:47
located in the same area approximately as the peripheral chemorecep-tors. Specifically,
19:52
they are located in the walls of the heart and in the carotid sinus and aortic arch.
19:59
They respond to stretch caused by changes in blood pressure. So when there’s a sudden increase in
20:05
blood pressure, it’ll increase the baroreceptor activity, and if there’s a decrease in BP,
20:11
it’ll reduce the baroreceptor activity. Makes sense? Alright. Now when they’re activated,
20:18
signals will pass on via the glossopharyngeal and vagus nerves to the nucleus of the tractus
20:24
solitarius (NTS). NTS will do two things now. It’ll go to neurons in the Caudal ventrolateral
20:30
medulla and release glutamate. CVLM will go to the cardioaccelerator and vasomotor area
20:40
and release the inhibitory neurotrans-mitter GABA. This leads to a reduction in sympathetic activity.
20:48
NTS is also going to give off gluta-mate and activate the cardioinhibitory areas,
20:54
and activate the parasympathetic activity towards the heart, reducing CO and blood pressure. So
21:03
you have a set-point or desired range for BP. If the BP deviates from the set-point,
21:10
meaning it gets either too high or too low, the NTS initiates appropri-ate reflex responses to
21:18
restore BP to normal levels. So that is mainly the extracardiac regulation. We do have some neural
21:26
intracardiac regulation aswell, I’m not gonna go in too much details into it. But we have something
Intracardiac nervous system
21:31
called intramural ganglia imbedded within the myocardium itself, con-sisting of a cluster of
21:37
nerve cell bodies, and they’re all interconnected via nerve fibers to form a network that spans
21:44
throughout the heart. They’re classified as intrinsic cardiac nervous system be-cause
21:50
they regulate the cardiac function independent of the direct CNS control. So what they do is that
21:56
they receive signals from the sympathetic and the parasympathetic nervous system, and they integrate and modulate the response to ensure coordinated cardiac functioning. And
22:07
often if something happens to these ganglia, that can contribute to developing arrythmias.
22:13
And we have low pressure baroreceptors here aswell, sensing stretch within the
22:19
walls of the heart. I’m just gonna keep it at that for the intracardiac regulation.
22:28
So that was, the neural autoregulation. Then we got humoral regulation. Humoral regulation are
Humoral Regulation
22:35
hormones within the blood that influence the heart rate, contractility and overall cardiac output.
22:42
One of the main ones are the epinephrine released by the adrenal medulla as a sympathetic con-trol,
22:47
activating the b1 adrenergic receptors. Another way is through the Renin Angiotensin Aldoste-rone
Renin-Angiotensin-Aldosterone System (RAAS)
22:54
System. This is one of the most important system you need to know by heart. This
22:59
system is so important both in physiology and pathology. So what this system is essentially,
23:06
is that the liver secretes Angiotensinogen. If there’s low blood pressure, that’ll decrease the
23:13
perfusion to the jux-taglomerular cells of the kidneys, causing it to secrete renin. Renin acts
23:19
on angiotensinogen con-verting it into Angiotensin 1, Angiotensin 1 is converted to angiotensin 2
23:28
primarily by angiotensin converting enzyme, which is located predominantly in the lungs. Angiotensin
23:34
2 is so important in our body. It can directly act on the myocardial cells, increasing contractility
23:42
by enhancing calcium influx through L-type calcium channels, it can directly cause vasoconstriction,
23:49
increasing the sys-temic vascular resistance which increases afterload because remember the initial response was to low blood pressure. Angiotensin 2 also stimulate the release of ADH,
24:02
promoting water reabsorp-tion in the kidneys contributing to increase blood volume and thereby increase in preload. But what it also does, is that it can go to the adrenal cortex
24:13
and stimulate release of aldosterone. Al-dosterone will go to the nephrons and cause increase sodium
24:19
reabsorption and potassium secre-tion, wherever sodium goes, water will follow, so that’ll
24:27
essentially increase the blood pressure, which will increase the preload and increase the CO.
24:33
Aldosterone can also act directly on the heart by binding to mineralocorticoid
24:39
receptors (MR) es-sentially enhancing the force of cardiac contraction, and it also does something
24:45
called cardiac re-modelling, same with angiotensin 2, meaning a chronic, or prolonged expression of
24:51
these hor-mones can lead to cardiac hypertrophy, which is an adaptive response initially but can
24:57
progress to heart failure in the long term, and can also promote things like cardiac fibrosis. That’s why some-times the aim to treat heart failure is to bock aldosterone
25:07
action and reduction of blood pressure. Alright what else. Thyroid hormones, primarily t3 Is the active one. Thyroid hormones bind to thy-roid hormone receptors (TRs), which
Thyroid Hormones
25:18
are present in cardiac myocytes. What happens initially is that it’s going to influence the
25:24
gene expression, metabolism and ion channel activity, to increase the heartrate and enhance
25:30
contractility. Not to go into too much detail. But that’s why if there’s a hyperthyroidism, that can
25:36
lead to tachycardia and palpitations and increase cardiac output, and sometimes even arrythimias.
25:43
While in patients with hypothyroidism, can have things like bradycar-dia and decrease cardiac
25:48
output, or even symptoms of heart failure. Alright. Another hormone secreted by the
Glucocorticoid Hormones
25:56
adrenal cortex are glucocorticosteroids. What this hormone does is that it’s going to cause
26:02
increase in myocardial contractility and heart rate, and it does that by enhancing adrenergic
26:08
receptor sensitivity, and promote the pumping of calcium into the sarcoplasmic reticulum.
26:13
They also increase responsiveness to catecholamines in the blood vessels.
Natriuretic Hormones
26:30
Another humoral regulation we have, are through the natriuretic hormone, specifically atrial
26:36
natriuretic peptide (ANP) and B-type natriuretic peptide (BNP). If there’s an increase pressure
26:42
within the atria and the ventricles, the myocytes will get stretched, and release ANP and BNP. They
26:49
will then promote dilation of the arteries, reducing blood volume by removing sodium and
26:55
water through the kidneys, and thereby decreasing the cardiac preload and afterload. By doing that,
27:01
we get a reduced myocardial workload and lower blood pressure. If you get a patient with heart
27:07
failure, and you analyse their blood, you might sometimes see that they have an elevated levels of
27:12
BNP and ANP, so they can be used as a biomarkers for helping diagnosis of heart failure aswell.
Effects of Calcium and Potassium Levels
27:19
Now, you already know how important calcium and potassium are to the depolarization and
27:25
repolarization of both the contractile myocardium and the pacemaker cells, as well as how important
27:31
they are for contractility. But what happens if we have hypercalcemia? If a patient has high
27:37
calcium levels in their blood, you can expect the patient to have increased contractility. Because
27:43
elevated calcium levels can enhance myocardial contractility by increasing calcium availability
27:49
for each contraction. Now, we haven’t gone through the ECG yet, but on the ECG, you have PQRST, where
27:58
the QT interval shows the time from the beginning of depolarization to the end of repolarization
28:05
of the ventricles. In hypercalcemia, you’ll get a shortened QT interval, because the repolarization
28:14
phase becomes accelerated. They’re also at risk of arrythmias, any changes is any ions that the cell
28:21
utilizes for depolarization and repolarization are at risk of arrythmias, especially with potassium.
28:29
Now, in low calcium levels you’ll see the exact opposite. Decreased contractility, prolonged QT
28:35
interval. Sodium remember it maintains the resting membrane potential of contractile
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myocardium because K⁺ ions tend to leak out of the cell due to their concentration gradient,
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making the inside of the cell more negative. Potassium also helps with the repolarization phase
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of cardiomyocytes. If someone has hyperkalemia, the resting membrane potential now becomes less
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negative because less ions are able to leak out, making cardiac cells less negative and closer
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to the threshold for depolarization. And this is bad, really bad. If the contractile myocardium are
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close to depolarization, they’re more excitable and more prone to arrythmias. High potassium
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values also slows the conduction and can lead to bradycardia and conduction blocks. If you do
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an ECG, one of the earliest signs of hyperkalemia are peaked T-wave, because the increased potassium
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cause the process of repolarization faster and more pronounced, resulting in the characteristic
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peaked appearance of the T waves on the ECG, and since the conduction speed is slower,
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you’ll often see wider QRS complexes aswell. If the patient has low potassium, the contractile
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myocardium’s resting membrane potential will more negative, increasing the distance from
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the threshold for depolarization making it harder for the cell to contract. Hypokalemia
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also causes prolonged repolarization, which can increase the risk of early afterdepolarization.
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On the ECG you’ll see exact opposite of hyperkalemia, you’ll see a flattened T-wave
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because the repolarization phase is slow, and you can also see prolonget QT interval aswell
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because of the prolonged repolatization. Now, I don’t want to scare you with this
Summary Slide
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next slide. But I did make a quick ‘’summary’’ slide. It doesn’t contain all the information,
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I just tried to compress everything in case you wanna pause the video and take some notes. There’s
30:44
always something you can add to this list. So that was everything I had for the regulation of the heartbeat. So, we covered in this video the myogenic,
30:53
neural and the humoral regulation of the heart. Thank you all for watching! If you found this
QUIZ
30:58
information helpful and want a little extra practise on the regulation of the heartbeat, I’ve created a quick follow-up video with quizzes and questions. These resources
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Thank you again for watching and I hope that was helpful. See you in the next video! Peace.