Cardiac (Heart) Physiology

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Outline

Overview

    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
            1. 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)
            1. → Stronger stretch of myocardium
            2. → Stronger force of contraction
            3. → Greater stroke volume
            4. WITHIN LIMITS:
              1. 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
            1. Parasympathetic
            2. Neurotransmitter = Acetylcholine (Ach)
            3. R. Vagus → SA node
            4. L. Vagus → AV node & ventricles
          2. T1 – T6 spinal nerves
            1. Sympathetic
            2. Neurotransmitter = Norepinephrine (NE)
            3. SA node, AV node, lots to atrial & ventricular myocardium
        2. Mechanisms of actions
          1. To affect Cardiac Output
            1. Increase or Decrease Heart Rate
            2. Increase or Decrease Stroke Volume
            3. In disease processes:
              1. Opposite force will change to compensate
                1. SV decreased → HR increases to compensate
          2. Decrease Heart Rate
            1. Increased vagus input to SA node
              1. More Ach at SA node
            2. ↓ Rate of depolarization of SA node
            3. Decreased HR → Decreased CO
            4. Vagal tone = the normal supply of Ach at rest to keep HR normal
          3. Increase Heart Rate
            1. Increased sympathetic input
              1. More norepinephrine at SA node
            2. ↑ Rate of depolarization at SA node
            3. Increased HR → Increased CO
          4. Decrease Stroke Volume
            1. Increased parasympathetic input to ventricular myocardium
            2. Slightly decreased force of contraction in the ventricles
            3. Decreased SV → Decreased CO
          5. Increase Stroke Volume
            1. Increased sympathetic stimulation to atrial and ventricular myocardium
            2. Increased force of contraction
            3. Increased SV → Increased CO

Assessment

  1. 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

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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

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Concepts Covered:

  • Gastrointestinal
  • Newborn Complications
  • Pregnancy Risks
  • Labor Complications
  • Fetal Development
  • Terminology
  • Prenatal Concepts
  • Noninfectious Respiratory Disorder
  • Newborn Care
  • Labor and Delivery
  • Postpartum Care
  • Postpartum Complications
  • Medication Administration
  • Studying
  • Communication
  • Prefixes
  • Suffixes
  • Proteins
  • Statistics
  • Med Term Basic
  • Med Term Whole
  • Cardiovascular
  • Circulatory System
  • Nervous System
  • Skeletal System
  • Emergency Care of the Cardiac Patient
  • Neurological
  • Respiratory
  • Urinary System
  • Respiratory System
  • Endocrine System
  • Tissues and Glands
  • Hematologic System
  • Digestive System
  • Reproductive System
  • Endocrine and Metabolic Disorders
  • Preoperative Nursing
  • Integumentary Disorders
  • Urinary Disorders
  • Muscular System
  • Sensory System
  • Basics of Human Biology
  • Test Taking Strategies
  • Adult
  • Intraoperative Nursing
  • Microbiology
  • Cardiac Disorders
  • Anxiety Disorders
  • Depressive Disorders
  • Vascular Disorders
  • Upper GI Disorders
  • Central Nervous System Disorders – Brain
  • Gastrointestinal Disorders
  • Immunological Disorders
  • Fundamentals of Emergency Nursing
  • Dosage Calculations
  • Understanding Society
  • Concepts of Pharmacology
  • Hematologic Disorders
  • Adulthood Growth and Development
  • Disorders of Pancreas
  • Respiratory Disorders
  • Postoperative Nursing
  • Substance Abuse Disorders
  • Bipolar Disorders
  • Peripheral Nervous System Disorders
  • Learning Pharmacology
  • Psychotic Disorders

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Needle Safety
Neostigmine (Prostigmin) Nursing Considerations
NG Tube Med Administration (Nasogastric)
NG Tube Medication Administration
Nitro Compounds
NRSNG Live | The S.O.C.K Method for Mastering Nursing Pharmacology and Never Forgetting a Medication Again
Nystatin (Mycostatin) Nursing Considerations
OB Pharm and What Drugs You HAVE to Know – Live Tutoring Archive
Olanzapine (Zyprexa) Nursing Considerations
Opioid Analgesics in Pregnancy
Oral Medications
Oxycodone (OxyContin) Nursing Considerations
Pain Management for the Older Adult – Live Tutoring Archive
Pain Management Meds – Live Tutoring Archive
Parasympathomimetics (Cholinergics) Nursing Considerations
Patient Controlled Analgesia (PCA)
Pediatric Dosage Calculations
Pentobarbital (Nembutal) Nursing Considerations
Pharmacodynamics
Pharmacokinetics
Pharmacokinetics Nursing Mnemonic (ADME)
Pharmacology Course Introduction
Phenobarbital (Luminal) Nursing Considerations
Phytonadione (Vitamin K) for Newborn
Pill Crushing & Cutting
Positioning
Procainamide (Pronestyl) Nursing Considerations
Propofol (Diprivan) Nursing Considerations
Quetiapine (Seroquel) Nursing Considerations
Ranitidine (Zantac) Nursing Considerations
Rh Immune Globulin in Pregnancy
Sedatives-Hypnotics
Sedatives-Hypnotics
Selecting THE vein
Spiking & Priming IV Bags
Starting an IV
Streptokinase (Streptase) Nursing Considerations
Struggling with Dimensional Analysis? – Live Tutoring Archive
SubQ Injections
Supplies Needed
Tattoos IV Insertion
TCAs
The SOCK Method – C
The SOCK Method – K
The SOCK Method – O
The SOCK Method – Overview
The SOCK Method – S
The SOCK Method of Pharmacology 1 – Live Tutoring Archive
The SOCK Method of Pharmacology 2 – Live Tutoring Archive
The SOCK Method of Pharmacology 3 – Live Tutoring Archive
Tips & Tricks
Tips & Advice for Newborns (Neonatal IV Insertion)
Tips & Advice for Pediatric IV
Understanding All The IV Set Ports
Using Aseptic Technique
Verapamil (Calan) Nursing Considerations