Cardiac (Heart) Physiology

1. Cardiac output (CO) = volume of blood pumped from LV to aorta per minute
  1. Determining factors
    1. CO = SV x HR
      1. SV = stroke volume
        
        Volume of blood ejected from LV with each systole
      2. HR = heart rate (bpm)
    2. Average at rest:
      1. CO = HR x SV
      2. 5.4 L/min = 72 bpm x 74 mL/beat
    3. Average CO during exercise = 30 L/min
    4. Cardiac reserve (capacity to increase from rest)
      1. Approximately 24.6 L/min
      2. Higher cardiac reserve = more physically fit

Nursing Points

General

1. Controlling Cardiac Output
  1. Intrinsic autoregulation – heart regulates itself
    1. Starling’s Law of the heart
      1. Greater volume of blood entering the heart during diastole (venous return)
        
        → Stronger stretch of myocardium
        
        → Stronger force of contraction
        
        → Greater stroke volume
        
        WITHIN LIMITS:
        
        Above a certain point, increased venous return does NOT result in greater stroke volume
  2. Nervous control of CO
    1. Nervous supply to heart
      1. Vagus nerve
        
        Parasympathetic
        
        Neurotransmitter = Acetylcholine (Ach)
        
        R. Vagus → SA node
        
        L. Vagus → AV node & ventricles
      2. T1 – T6 spinal nerves
        
        Sympathetic
        
        Neurotransmitter = Norepinephrine (NE)
        
        SA node, AV node, lots to atrial & ventricular myocardium
    2. Mechanisms of actions
      1. To affect Cardiac Output
        
        Increase or Decrease Heart Rate
        
        Increase or Decrease Stroke Volume
        
        In disease processes:
        
        Opposite force will change to compensate
        
        SV decreased → HR increases to compensate
      2. Decrease Heart Rate
        
        Increased vagus input to SA node
        
        More Ach at SA node
        
        ↓ Rate of depolarization of SA node
        
        Decreased HR → Decreased CO
        
        Vagal tone = the normal supply of Ach at rest to keep HR normal
      3. Increase Heart Rate
        
        Increased sympathetic input
        
        More norepinephrine at SA node
        
        ↑ Rate of depolarization at SA node
        
        Increased HR → Increased CO
      4. Decrease Stroke Volume
        
        Increased parasympathetic input to ventricular myocardium
        
        Slightly decreased force of contraction in the ventricles
        
        Decreased SV → Decreased CO
      5. Increase Stroke Volume
        
        Increased sympathetic stimulation to atrial and ventricular myocardium
        
        Increased force of contraction
        
        Increased SV → Increased CO

Assessment

Refer to Hemodynamics lesson in Cardiac (Med-Surg) course

References
Betts, J.G., et al. (2017). _Anatomy and physiology_. Houston, TX: OpenStax, Rice University. Retrieved from https://openstax.org/details/books/anatomy-and-physiology?Book%20details

Unlock the Complete Study System

Used by 300,000+ nursing students. 99.25% NCLEX pass rate.

200% NCLEX Pass Guarantee.
No Contract. Cancel Anytime.

Transcript

Okay, in this lesson we’re going to take a look at cardiac physiology, and the factors that affect cardiac output.

When were talking specifically about cardiac physiology, we’re looking at cardiac output. Cardiac output is the volume of blood pumped from the left ventricle all the way to the aorta per minute. Now there’s a formula for this.

That formula is heart rate, X stroke volume. Stroke volume is the amount of blood squeezed out of the ventricles per contraction. In that is in a volume. The average cardiac output is anywhere from 4 to 8 liters per minute so we’re just going to go at 6. As you can see in this particular formula, 75 beats per minute x 80 mL of blood per contraction equals 6000 ml per minute for 6 L per minute of cardiac output.

Here’s a fun fact for you though, the average cardiac output during exercise is over 30 liters per minute.

And we were talking about cardiac physiology we want to look at something called Starling’s law. This is an intrinsic factor. So as volume increases inside the ventricles the myocardium is stretched. What happens is as a response to this stretch the ventricles are going to create a stronger contraction. This is going to increase the stroke volume. In medicine, it’s very common for patients that we wanted increase a cardiac output on we will give them more fluid. But as a response at some point, increasing that fluid or increasing that venous return is not going to result in any greater stronger output.

Now when are we looking at how the nervous system controls cardiac output basically there are two ways that this happens. There’s a parasympathetic response, and a sympathetic response. Parasympathetic is the part that slow the heart rate down, and sympathetic is the fight-or-flight response. Acetylcholine is a neurotransmitter that is responsible for pushing out action potentials to the heart, and norepinephrine is the one that’s responsible for the sympathetic response. The vagus nerve innervates the SA node on the right side and it innervates the AV node and the ventricles on the left side.

For the sympathetic nervous system control, this comes from the T1 to T6 spinal nerves, and it innervates at the sa and AV node innervation and then it also has some atrial and ventricular myocardial innervation.

Another thing that you need to think about something called cardiac reserve. Cardiac reserve is basically the difference in the heart’s normal ability to pump and its maximum capacity. The reason want to know this is that some people as a response to fight or flight, can jump their heart rate from 6 minute to 30 minute. But some people don’t have that reserve and cardiac reserve is actually an indication of how physically fit a person is.

So the human body is a fascinating thing, and it compensate on a large scale. When I look at mechanisms of action what we’re looking at is how the body responds to that particular change. So let me explain.

We were talking about cardiac output we’re talking about what can a heart do as a response to different things. The heart can increase or decrease the rate, and it can also increase or decrease in stroke volume.

With disease the heart responds to compensate. It likes to keep a little bit of a balance. So if the stroke volume is increased, the heart rate increases to compensate for that, because the heart wants to keep that cardiac output within that good window of about 6 L of minute

So what’s happening in each specific situation? Well let’s take a look at that.

If we have a decrease heart rate, it’s going to be most likely from increased vagal nerve input into that sinoatrial node. More acetylcholine is being introduced. What happens is it rate of depolarization slows down, and you have a decrease heart rate. There’s also a decreased cardiac output. Remember cuz our cardiac output is our heart rate and stroke volume. There’s also something that’s really important to know and that’s something called vagal tone. This is a normal supply of acetylcholine address to keep the heart rate normal. So if you want to keep that heart rate in between 70 to 80 beats per minute, but there’s a certain amount of acetylcholine that has to be produced by the parasympathetic nervous system.

So what happens in the other instance? Well if there’s increased heart rate you have an increased sympathetic input. More epinephrine is being introduced into that sinoatrial node. That increases the heart rate of depolarization at the SA node, and a heartache it’s going to go up. That increases cardiac output.
So what happens in terms of stroke volume?

Just like with the heart rate, that increased Parasympathetic input into the ventricular myocardium is going to decrease the contraction in the ventricles. This is going to decrease in stroke volume and therefore decrease the cardiac output

Increasing the stroke volume is, just as we would expect an increase sympathetic stimulation. This is going to be specifically to The Atrium in The myocardium. This increases at force of contraction tear by increasing your stroke volume and cardiac output.
Okay so let’s recap.

Anytime you’re dealing with cardiac physiology you almost live and die by this formula. Heart rate times stroke volume equals cardiac output. Heart rate is the amount of beats per minute and stroke volume is the amount of blood ejected from the ventricles every time it squeezes.

Vagal tone is the normal amount of acetylcholine introduced by the parasympathetic nervous system at rest to keep that heart rate normal. As you have an increase in acetylcholine production by the parasympathetic nervous system it’s going to slow that heart rate down.

Sympathetic input increases the heart rate due to the increase in the Norepinephrine.

The body is a fascinating thing when it comes to convince attractions. The heart wants to maintain that normal cardiac output. If the heart rate is low, the stroke volume will increase, and if the stroke volume is low, the heart rate will increase. And if I either are too high, the other one will slow down.

Now that’s it for a lesson on cardiac physiology. Make sure you check on all the resources attached this lesson. Now go out and be your best selves today, and as always happy nursing

Cardiac (Heart) Physiology

You're watching a preview. 300,000+ students are watching the full lesson.

Included In This Lesson

Study Tools For Cardiac (Heart) Physiology

300,000+ Students Use These Cheatsheets To Pass NCLEX

NURSING.com students have a 99.25% NCLEX pass rate.

Outline

Overview

Nursing Points

General

Assessment

Unlock the Complete Study System

Used by 300,000+ nursing students. 99.25% NCLEX pass rate.

Transcript

Study Faster with Full Video Transcripts

Nursing School Doesn't Have To Be So Hard

Go from discouraged and stressed to motivated and passionate

Prep for PN Program

Study Plan Lessons

Welcome Back