Description

Complete Cheat Code for Heart Physiology:

• 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.

What is Cardiac Output?

Definition: The amount of blood ejected from each ventricle per minute.

Formula: Cardiac Output = Heart Rate (bpm) × Stroke Volume (L/beat)

Units: Measured in liters per minute (L/min).

Visualizing Cardiac Output

• Heart Anatomy: Right and left atria, ventricles, aorta.
• Cardiac Cycle Phases:
  • Atrial systole
  • Isovolumetric contraction
  • Ejection phase (systolic phase)
  • Isovolumetric relaxation
  • Passive filling phase (common diastolic phase)
• Stroke Volume: Amount of blood ejected per beat (~50-100 ml).
• Heart Rate: Number of beats per minute.

Factors Determining Cardiac Output

• Heart Rate: Increased HR typically increases cardiac output, but >150 bpm may reduce it due to inadequate ventricular filling.
• Stroke Volume: Depends on:
  • Venous Return: More blood entering the heart leads to greater output.
  • Contractility: Stronger contractions eject more blood.
  • Aortic Resistance: Higher resistance (hypertension, plaque) reduces stroke volume.

Normal Cardiac Output

• At Rest: ~5-7 L/min
• During Exercise: ~15-30 L/min

Pressure-Volume Relationship

• Diastolic Phase: Ventricular filling, gradual pressure increase.
• Systolic Phase: Ventricular contraction, pressure rises then falls.
• Isovolumetric Phases: Contraction and relaxation phases with no volume change.

Clinical Relevance

• Pressure-Volume Curves: Assess heart function, muscle efficiency, and valve health.
• Abnormal PV Loops:
  • Right Shift: Increased preload (more blood in, more ejected).
  • Increased Afterload: Higher aortic pressure, harder for the heart to eject blood.
  • Increased Contractility: Stronger contractions, more blood ejected.

Factors Affecting Cardiac Output

• Preload: Volume of blood before contraction.
• Afterload: Resistance ventricles overcome to eject blood.
• Contractility: Strength of ventricular contraction.

Regulation of Heartbeat

• Mechanisms: Myogenic, neural, and humoral regulation.

Conclusion

Summary: Discussed cardiac output, pressure-volume curve, and effects of preload, afterload, and contractility.

Next Video: Regulation of heartbeat.

#cardiacphysiology #heartfunction #cardiacoutput #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
0:08
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,
0:18
the action potentials of pace maker cells and contractile myocardium, and the general
0:22
properties of our cardiomyocytes. In the 2nd video we looked detailed into the cardiac cycle. In this
0:28
video we’re gonna cover everything you need to know regarding the cardiac output. And in
0:33
the next video we’ll cover the regulation of the Heartbeat, covering all the most
0:38
important mechanisms that actually change the contractility and heart rate. Alright awesome.
What is Cardiac Output?
0:44
Now how do we define cardiac output? Cardiac output is the mount of blood that is ejected
0:50
from each ventricle during one contraction. Let’s visualize this. Here’s the heart. We got
0:56
the right and the left atria, the right and the left ventricles, and the aorta.
1:00
In the previous video we went through something called a cardiac cycle, which is basically all
1:05
the mechanics that actually happen in each phase of one cardiac cycle. Which is atrial systole,
1:11
then we got the isovolumetric contraction, and the ejection phase which we call Systolic phase,
1:16
then there’s the isovolumetric relaxation and passive filling phase which we call common
1:21
diastolic phase, then we’re back to atrial systole again. All that happens in one contraction.
1:27
So with each contraction, you’ll get a certain amount of blood out from each ventricle,
1:33
that amount is called Stroke Volume, and it’s about, roughly about 50-100 ml of blood equal
1:38
for both sides. So again stroke volume is the amount of blood that is ejected from
1:44
the ventricles during the ejection phase of one cardiac cycle. So you see here there’s one cardiac
1:51
cycle happening again and again and again. There’s a term we use. If you combine the
1:57
amount of cardiac cycles within a span of one minute, we call this a heart rate.
2:02
So again heart rate are all the cardiac cycles within one minute. So beats per minute.
The Equation
2:09
We say, that Cardiac Output is equal to, Heart Rate multiplied by Stroke Volume.
2:16
So again heart rate is characterized as beats per minute, Stroke Volume is characterized as
2:22
liters per beat. And for those of you who likes math, you know that if you take beats per minute,
2:28
and multiply it with liters per beat, you can remove beats, and you end up with liter/minute.
2:34
And that’s how we define Cardiac Output. Cardiac Output is defined as the amount of blood,
2:40
either in ml or in L, ejected out per minute. Alright what are the factors
Changes in Heart Rate
2:46
that determine the cardiac output? Example. We increase the heart rate, what happens
2:51
with the cardiac output? It increases. Now we increase the heart rate to 150
2:58
beats per minute, what happens now? You might think it increases but that is not actually
3:04
correct. There’s a paradoxical effect here with this equation because imagine if the heart pumps
3:09
so fast it reaches a heart rate of above 150 times per minute, the cardiac cycle becomes
3:16
so short that the ventricles won’t be able to be filled with blood properly. So the cardiac
3:21
output now might decrease or stagnate. Now, what if the stroke volume increase,
Changes in Stroke Volume
3:27
the actual blood that is ejected out during each contraction? Well then naturally the
3:32
Cardiac Output will increase aswell. Stroke volume depend on three factors.
3:37
First one is the venous return, so if more blood comes into the heart, then more blood
3:43
can be ejected out during the next systole. Second one is the contractility of the cardiac muscle.
3:49
The stronger contraction means higher amount of blood can be pushed into the greater arteries,
3:54
remember in out last video we mentioned something called reserve volume, which are released
3:59
during a stronger contraction. We’ll mention all the most important things that can regulate this
4:04
contraction in the next video, but the third factor that influence the stroke volume is the
4:09
resistance in the aorta. If a patient has chronic hypertension, it can stiffen up the aorta and not
4:17
make it as elastic anymore. If there’s a patient with a high cholesterol, then he’s at risk for
4:22
plaque build-up in the aortic wall. That can stiffen the aorta. So if there’s any factor
4:27
that causes a higher pressure in the aorta, then less blood is going to be able to move from the
4:33
ventricle into the aorta during the ejection phase. That’s why we say that the stroke volume
4:39
generally is dependent upon these three factors. So what’s the normal Cardiac Output. At rest,
Normal Values of CO
4:46
we say about 5-7 liters of blood is ejected per minute given there’s no
Left Ventricular Pressure-Volume Diagram
4:51
pathology. During physical activity, it rises to about 15-30 liters per minute.
4:58
Now, let’s visualize this, specifically for the left ventricle because that is what we’re usually
5:03
interested in. So here in the vertical axis we see the left ventricular pressure expressed in mmHg,
5:11
and in the horizontal axis we see the volume within the left ventricle expressed
5:16
in ml. So we’re interested in the relation between pressure and volume. We call this
5:22
graph the pressure volume curve. We’ll do this in two segments.
5:26
First I’ll show the maximum pressure volume relationship, then the relation under normal
5:32
resting conditions. Okay let’s break this down. When the left ventricle is undergoing a diastolic
Maximum Pressure-Volume Relationship
5:39
phase, it’s getting progressively filled with a great volume of blood. And naturally since it’s
5:45
receiving a lot of blood, then the pressure within the ventricle increases. Notice that until about
5:51
the end diastolic volume of 150 ml, pressure in left ventricle remains almost stable. But
5:58
when the volume rises above 150ml, the pressure rises drastically. This is because the ventricles,
6:05
after getting filled with a certain amount of blood, in this case 150ml,
6:10
the ventricle is not very stretchable anymore it cant expand due to fibrous tissues within
6:16
the wall and also due to the limitations of pericardium. Just keep in mind that the values
6:21
of 150ml is very individual and it depends upon the individual. These numbers are just average.
6:28
Systolic pressure now is when the heart contract. Notice how the left ventricular pressure during
6:35
systolic phase rises almost constantly as the end diastolic volume rises. But just
6:41
as we hit the volume of approx. 150-170ml of blood, the pressure generated during systole
6:49
starts to decrease. The reason for this is quite logical, a great volume of blood will
6:54
simply overstretch the cardiomyocytes, leading to a decrease in contacting
6:59
places between actin and myosin filaments. Less actin and myosin are able to connect,
7:05
less contraction, pressure decrease. These are the maximum pressure volume relationship where you can
7:11
see that the maximum pressure the left ventricle can be in during systole is up to approximately
7:18
250-300 mmHg, which varies between the individual. How does the pressure volume curve look like in
Normal Pressure-Volume Relationship
7:26
the resting state then? In a normal physiological state the left ventricular pressure volume curve
7:33
is located right around here, with each arrow showing each phase of the cardiac cycle. So
7:39
phase 1 includes both passive and active filling phase, phase 2 is the isovolumetric contraction,
7:45
followed by the ejection phase, and then phase 4 Is the isovolumetric relaxation.
7:51
Now let’s expand this graph, and look at pressure changes in each phase in a little more detail.
7:57
The first thing that happens is that the mitral valve opens, to which the filling phases start,
8:02
including both the active and passive filling. Notice that the filling phase starts with having
8:07
about 40 ml of blood within the ventricles already, so the end systolic volume is 40 ml,
8:13
while the pressure being very low, 2 or 3 mmHg. What happens is, when blood starts filling up, and
8:20
the end diastolic volume gets to about 140 ml, the pressure rises to about 10 mmHg. Now we’ve reached
8:29
the end of filling phase. And the mitral valve closes. The period after that is the isovolumetric
8:36
contraction. Meaning the walls of the ventricle is now contracting, but all the valves are closed. So
8:42
blood is not going anywhere, while the walls are contracting, increasing the pressure. The pressure
8:48
now will rise to around the diastolic pressure in the aorta, which is between 60-80 mmHg. And when
8:55
the pressure in the ventricle becomes higher than the pressure in the aorta, the aortic valve opens,
9:00
and we’re now in the ejection phase, where blood is being pushed out to the periphery,
9:05
where the pressure will continue to rise up until around 130 mmHg, and then decrease again to around
9:13
100 mmHg as the blood is getting squeezed out. Now once it reaches the end systolic volume of
9:20
about 40ml, the aortic valve will close, and we enter the isovolumetric relaxation,
9:27
where both valves are closed, and the ventricle is relaxing, reducing the pressure down to just
9:33
a few mmHg so the filling phase can start again. And again we can place the stroke volume here,
9:40
going from the end diastolic volume all the way back to the end systolic volume.
Why make graphs?
9:46
Now. Why are we making these graphs? What’s the purpose of them? Let’s say you get a patient
9:52
and you insert a catheter into the left ventricle through the blood vessels. That catheter contain a
9:58
pressure sensors which senses the pressure change within the ventricle through the cardiac cycle,
10:03
and you’ll get a graph like this. There are other non invasive methods as well like ultrasound with
10:08
doppler, but for simplicity, why do we test for it? Well for one thing the PV curves help
10:15
assessing things like how well the heart pumps blood, the efficiency of the cardiac muscle,
10:20
and the health of the heart valves in general. And if there’s an abnormal PV loops,
10:26
that can indicate things like heart failure, valve diseases, and cardiomyopathies which can
10:31
then further guide the steps in treatment. So what happens is, if the curve shifts to
Preload
10:37
the right side, that means the preload increases. Pre-load meaning pre- before
10:43
the contraction. To loading the heart before the contraction. So it fills up during the
10:48
diastolic phase. This is quite an effective work too because look, you get more blood in,
10:54
so more blood is ejected out of the heart. So now what happens if I draw the curve like
Afterload
11:00
this? It means that the afterload has increased. Because look the end diastolic volume is the same,
11:07
but the heart has to now push harder to eject less blood. Is it an effective work or not?
11:14
Absolutely not, the heart is straining itself to push a smaller amount of blood out. That’s why
11:20
we call it increase afterload. Because increased afterload mean increased pressure in aorta. And
11:27
if the pressure in the aorta is increased, the isovolumetric contraction phase has to go up
11:32
so high it has to have a higher pressure in the ventricle than in the aorta for the aortic valve
11:38
to open. And since the pressure in the aorta remains high, lesser volume can be ejected and
11:44
more volume of blood remains in the ventricle. That’s’ why we don’t like arterial hypertension,
11:49
it can stiffen the aorta and strain the heart. Another thing that can happen is that we can
Contractility
11:54
have an increased contractility, meaning the cardiomyocytes contracts harder from
11:59
the same amount of end diastolic volume, where we now eject the reserve volume aswell, having
12:05
a lower amount end systolic volume. So the heart has to use a higher amount of energy to contract
12:11
stronger to push more blood out. Is it effective work or not? It’s quite effective, because we’re
12:18
getting more blood pumped out of the ventricle. This is why preload, afterload and contractility
12:26
has a huge impact on the cardiac output. And generally there are three ways the
Next video
12:31
body and adjust the contractility, preload and afterload, regulating the heartbeat basically.
12:37
And that is through myogenic regulation, neural regulation and humoral regulation. We’ll cover
12:43
all that in the next video. So that was everything I
12:47
had for the cardiac cycle. So, we covered in this video
12:50
the Cardiac Output and the pressure volume curve along with how preload, afterload
12:54
and contractility affects the curve. In the next video we’ll cover the regulation of the heartbeat.
QUIZ
13:01
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