1. The Human Body in Health and
Illness,
4th edition
Barbara Herlihy
Chapter 17:
Function of the Heart

2. Lesson 17-1 Objectives
Define cardiac cycle with respect to systole and diastole.
Describe the autonomic innervation of the heart.
Define cardiac output and explain how changes in heart rate and/or stroke volume change cardiac output.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

3. Lesson 17-1 Objectives (cont’d.)
Describe the effect of Starling’s law of the heart on myocardial contraction.
Define preload and explain how it affects cardiac output.
Define afterload and identify the major factors that determine afterload.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

4. Lesson 17-1 Objectives (cont’d.)
Describe the inotropic effect on myocardial contraction.
Define the special clinical vocabulary used to describe cardiac function.
Define heart failure and differentiate between right-sided and left-sided heart failure.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

5. Cardiac Cycle: One Heartbeat
Systole (contraction) and diastole (relaxation) act in coordination.
The cardiac cycle is a coordinated contraction and relaxation of the chambers of the heart for proper blood flow through the heart.
Systole is the contraction of the heart muscle (myocardium). Diastole is the relaxation of the heart muscle. During atrial systole (Figure A), the ventricles are relaxed to receive blood from the atria. During ventricular systole (Figure B), the blood is pumped out of the ventricles into the pulmonary artery and aorta. During diastole (Figure C), the entire heart is in diastole and fills with blood.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

6. Autonomic Control of the Heart
Allows heart to respond to changing body needs
Involves sympathetic and parasympathetic (vagal) nerves
The ANS helps coordinate and adapt cardiac function to the changing needs of the body. It can affect the rate of firing of the cardiac impulse (heart rate), the speed at which the impulse travels through the heart, and the force of myocardial contraction.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

7. Autonomic Wiring Sympathetics Parasympathetics SA node AV node
Ventricular myocardium
Parasympathetics
The sympathetics innervate the SA node (pacemaker), the AV node, and the ventricular myocardium. The parasympathetics (vagus) innervate the SA and AV nodes. There is no parasympathetic innervation to the ventricular myocardium.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

8. Autonomic Neurotransmitters
Sympathetics
Adrenergics
Norepinephrine (NE)
Parasympathetics
Cholinergic
Acetylcholine (ACh)
The sympathetics secrete norepinephrine, which activates beta1-adrenergic receptors on the heart. The parasympathetics secrete Ach, which activates muscarinic receptors on the heart.
The receptors are not shown on the diagram, but are located in the general areas where the neurotransmitters (NE and ACh) are noted.
This might be a good time to review Figure 12-3 regarding adrenergic and cholinergic receptors.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

9. Firing of the Sympathetic System
SA node activity and heart rate
Speed of cardiac impulse through conduction system
Force of myocardial contraction
The sympathetics fire when the demands of the body increase, as in exercise. This firing is also part of the fight-or-flight response.
Excess sympathetic activity causes tachydysrhythmias.
Drugs or hormones that mimic the effects of the sympathetic nervous system are called sympathomimetics.
When a person is in shock, the sympathetics can fire to attempt to compensate by raising blood pressure.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

10. Firing of the Parasympathetic System
SA node activity and heart rate
Speed of cardiac impulse from SA to AV node
No effect on strength of contraction
In the resting state, the SA node is dominated by the vagus, producing a resting heart rate of about 72 beats/min. If vagal discharge is interrupted, the heart rate increases. Intense vagal discharge can decrease heart rate and the speed of impulse conduction. This causes bradydysrhythmias, such as heart block.
A vagomimetic drug, such as digoxin, slows heart rate and the speed of impulse conduction.
A vagolytic drug, such as atropine, increases heart rate and the speed of impulse conduction through the heart. Thus, atropine can reverse the effects of intense vagal discharge.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

11. Cardiac Output (CO)
CO is amount of blood pumped by each ventricle in 1 minute (mL/min).
CO = heart rate × stroke volume
CO in the healthy heart can increase four to five times; called the cardiac reserve
Total blood volume is about 5 liters, so the entire blood volume passes through the heart every minute in the average resting human body.
Patients with heart disease often have little or no cardiac reserve. Predict such patients’ response to exercise.
They will first feel fatigue and then pain (angina) if they persist with exercise.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

12. Heart Rate and Stroke Volume
Heart rate: Number of times the heart beats each minute caused by SA node’s firing
Stroke volume: Amount of blood pumped by the ventricle per beat
CO can be altered by changing heart rate and/or stroke volume
The normal range of adult resting heart rates is from 60 to 100 beats/min, with an average rate of 72 beats/min.
Stroke volume can be changed by changing the force of contraction.
Heart rates can change for many reasons. Predict three reasons.
Exercise, fight-or-flight response, and certain drugs, including caffeine and street drugs, can increase heart rate. Intense firing of the vagus, or vagomimetic drugs, can also decrease heart rate.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

13. How to Change Stroke Volume
Starling’s law of the heart
Changes the force of contraction by stretching the myocardium
Mechanism: Aligns the sarcomeres for greater interaction between actin and myosin
Inotropic effect
Changes the force of contraction without stretching the myocardium
Mechanism: Makes calcium more available to the contractile proteins
Changes in the volume of blood in the heart activate Starling’s law of the heart. A greater volume of blood increases the force of contraction and stroke volume, whereas a smaller volume of blood does the opposite. On a beat-to-beat basis, Starling’s law matches venous return and cardiac output.
Explain what is meant by saying that “sympathetic discharge (NE) causes a positive inotropic effect?”
The NE stimulates the heart muscle in a way that makes more calcium available to the contractile proteins, actin and myosin. No stretch of the myocardium is involved.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

14. How to Change Stroke Volume
Starling’s law of the heart: What goes in, comes out
Why does a high venous return result in a high cardiac output?
The increased blood volume stretches the myocardium, activating Starling’s law and increasing the force of myocardial contraction. This, in turn, increases cardiac output.
Why does a low venous return result in a low cardiac output?
A lesser volume of blood does not stretch the heart muscle, so the stroke volume and cardiac output are not as great.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

15. Stroke Volume: Ejection Fraction
Ejection fraction is the percentage of blood volume in the ventricle that is pumped by the heart.
Normal ejection fraction is about 67%.
Exercise can increase ejection fraction.
Heart failure decreases ejection fraction.
Both stroke volume and ejection fraction are terms used to describe the amount of blood pumped from the ventricles in one beat.
Stroke volume expresses this idea with the number of mL/beat, about 80 mL.
Ejection expresses the idea as the percentage of the contents of the ventricle that was pumped out, about 67%.
What does an ejection fraction of 35% indicate?
Such a fraction indicates a weakened heart muscle that is capable of pumping only 35% of ventricular volume.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

16. Heart Talk: Clinical Terms
Preload: EDV
Amount of blood in ventricle at the end of diastole (EDV)
Basis of Starling’s law of the heart
Afterload: Resistance
Caused by blood pressure
End-diastolic volume (EDV) refers to the amount of blood in the ventricle at the end of diastole. This term expresses the amount of blood that has filled the ventricle immediately before systole. EDV is also called preload. Because it talks about ventricular volume, EDV (preload) is the basis of Starling’s law.
The term afterload refers to the amount of work that the myocardium must exert to pump blood against resistance, illustrated by the gremlin pinching the aorta. Aortic blood pressure is the left ventricle’s afterload. Chronic hypertension increases afterload, causes left ventricular hypertrophy and eventually heart failure.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

17. Heart Talk: Clinical Terms (cont’d.)
Inotropic effect: Change in myocardial contraction not caused by stretch
Chronotropic effect: Change in heart rate
Dromotropic effect: Change in the speed at which the cardiac impulse travels from the SA node through the AV node and His-Purkinje system
A positive inotropic effect increases force of contraction, and a negative one decreases force of contraction. A positive chronotropic effect increases heart rate, and a negative one decreases heart rate. A positive dromotropic effect increases the speed with which the cardiac impulse travels through the heart.
Digoxin exerts a positive inotropic effect and negative chronotropic and dromotropic effects. Why would you check the patient’s heart rate prior to administering digoxin?
Digoxin slows the heart, and we want to avoid a heart rate of less than 60 beats/min.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

18. Heart Talk: Beta1-Adrenergic Receptors
Locations
 SA node
 AV node
Myocardium
Activated by NE
The receptors are not shown on the figure, so point out their locations.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

19. Effects of Beta1-Adrenergic Receptors
Effect of Activating
Effect of Blocking
(+) Chronotropic
(+) Dromotropic
(+) Inotropic
() Chronotropic
() Dromotropic
() Inotropic
A beta1-adrenergic agonist activates the receptors. A beta1-adrenergic antagonist or blocker blocks activation of the receptors.
Predict the effect on heart rate if you administer a beta blocker drug, such as propranolol.
The heart rate will decrease.
Why might a beta blocker be administered to someone having a panic attack?
The drug will block the response to the firing of the sympathetics, thus slowing the heart rate.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

20. Heart Talk: Muscarinic Receptors
Locations
 SA node
AV node
Activated by ACh
The receptors are not shown on the figure, so point out their locations. It is also important to note that there are no muscarinic receptors in the ventricular myocardium.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

21. Effects of Muscarinic Receptors
Effects of Activating
Effects of Blocking
(+) Chronotropic (+) Dromotropic
() Chronotropic
() Dromotropic
Why does muscarinic activation not result in decreased force of contraction?
There are no muscarinic receptors on the ventricular myocardium.
A patient has had a heart attack and is severely bradycardic. Why could an antimuscarinic drug be administered?
The antimuscarinic drug, such as atropine, blocks vagal discharge, which is the cause of the bradycardia. This increases heart rate.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

22. Heart Failure: Left-Sided
Backward
Poor left ventricular function
Fluid backs up into lungs
Forward
Decreases blood flow to systemic circulation
Why is the heart red in the figure?
The left heart carries oxygenated blood.
Why is the character in the diagram cyanotic?
Fluid has backed up into his lungs, diminishing the movement of oxygen into the blood. The unoxygenated blood causes cyanosis.
In left-sided heart failure, why might a person have poor blood flow to the kidneys?
Poor ventricular contraction diminishes the pumping of blood to vital organs, such as the kidney. The kidneys respond to poor blood flow by retaining excess fluid, causing edema.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

23. Heart Failure: Right-Sided
Backward
Blood backs up into veins that drain blood to the right heart
Explain why the character in the slide has distention in his neck vein, an enlarged liver, and ankle edema.
Poor right ventricular contraction causes blood to back up in the veins draining the head, liver, and feet. The accumulated blood in these areas causes distention of the veins and edema.
Why is the heart blue in the figure?
The right heart carries unoxygenated blood.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

24. Heart Failure: Treatment Goals
Strengthen myocardial contractile force
Remove excess water
Decrease work of the heart
Protect the heart from excess sympathetic nerve activity
Predict the types of drugs that would be used in treating heart failure. What effects would be desired from the drugs?
The drugs used in treatment will be positive inotropic agents, diuretics, beta blockers, or other drugs that block sympathetic effects.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.