Chapter 18Heart

Lecture 3

Marieb’s HumanAnatomy and

PhysiologyNinth Edition

Marieb Hoehn

2

Lecture Overview

• Physiology of cardiac muscle contraction

• The electrocardiogram

• Cardiac Output

• Regulation of the cardiac cycle and cardiac output

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Comparison of Skeletal and Cardiac Muscle

Cardiac and skeletal muscle differ in:

1. Nature of action potential

2. Source of Ca2+

3. Duration of contraction

Figure from: Martini, Anatomy & Physiology, Prentice Hall, 2001

Let’s look at this more closely

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The Cardiac Muscle Action Potential

Figure from: Martini, Anatomy & Physiology, Prentice Hall, 2001

Ca2+ ions enter from

1. Extracellular fluid (20%)

2. Sarcoplasmic reticulum (80%)

** Cardiac muscle is very sensitive to Ca2+ changes in extracellular fluid

Recall that tetanic contractions usually cannot occur in a normal cardiac muscle cell

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Electrocardiogram• recording of electrical changes that occur in the myocardium during the cardiac cycle

• used to assess heart’s ability to conduct impulses, heart enlargement, and myocardial damage

P wave – atrial depolarizationQRS wave – ventricular depolarizationT wave – ventricular repolarization

Important points to remember:

- Depolarization precedes contraction- Repolarization precedes relaxation

Three waves per heartbeat

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Electrocardiogram

Figure from: Martini, Anatomy & Physiology, Prentice Hall, 2001

PR Interval: 0.12 – 0.20 sec

QT Interval: 0.20 – 0.40 sec

QRS Interval: < 0.10 sec

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Review of Events of the Cardiac CycleFigure from: Martini, Anatomy & Physiology, Prentice Hall, 2004

1. Atrial contraction begins

2. Atria eject blood into ventricles

3. Atrial systole ends; AV valves close (S1)

4. Isovolumetric ventricular contraction

5. Ventricular ejection occurs

6. Semilunar valves close (S2)

7. Isovolumetric relaxation occurs

8. AV valves open; passive atrial filling

S1

S2

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Cardiodynamics – Important terms

• End-diastolic volume (EDV) – amount of blood present in the ventricles at end of ventricular diastole (~ 120 ml)

• End-systolic volume (ESV) – amount of blood left in ventricles at end of ventricular systole (~ 50 ml)

• Stroke volume (SV) – amount of blood pumped out of each ventricle during a single beat (SV = EDV – ESV) (~ 70 ml)

• Ejection fraction – Percentage of EDV represented by the SV (SV/EDV) (~ 55%)

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Cardiac Output (CO)

• The volume of blood pumped by each ventricle in one minute

CO = heart rate (HR) x stroke volume (SV)

Normal CO 5-6 liters (5,000-6,000 ml) per minute

ml/min beats/min ml/beat

Example: CO = 72 bpm x 75ml/beat 5,500 ml/min

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Regulation of Cardiac Output

• physical exercise• body temperature• concentration of various ions

• calcium• potassium

• parasympathetic impulses (vagus nerves) decrease heart action• sympathetic impulses increase heart action; epinephrine

Figure from: Martini, Anatomy & Physiology, Prentice Hall, 2001

CO = heart rate (HR) x stroke volume (SV)

SV = EDV – ESV

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Regulation of Cardiac RateAutonomic nerve impulses alter the activities of the S-A and A-V nodes

Rising blood pressure stimulates baroreceptors to reduce cardiac output via parasympathetic stimulation

Stretching of vena cava near right atrium leads to increased cardiac output via sympathetic stimulation

Figure from: Hole’s Human A&P, 12th edition, 2010

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Regulation of Cardiac Rate

Parasympathetic impulses reduce CO, sympathetic impulses increase CO

**ANS activity does not ‘make’ the heart beat, it only regulates its beat

Figure from: Martini, Anatomy & Physiology, Prentice Hall, 2004

Tachycardia > 100 bpmBradycardia < 60 bpm

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Additional Terms to Know…

• Preload– Degree of tension on heart muscle before it

contracts (i.e., length of sarcomeres)– The end diastolic pressure (EDP)

• Afterload– Load against which the cardiac muscle exerts

its contractile force– Pressure in the artery leading from the ventricle

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The Frank-Starling Mechanism• Amount of blood pumped by the heart each minute (CO) is almost

entirely determined by the venous return

• Frank-Starling mechanism – Intrinsic ability of the heart to adapt to increasing volumes of inflowing blood

– Cardiac muscle reacts to increased stretching (venous filling) by contracting more forcefully

– Increased stretch of cardiac muscle causes optimum overlap of cardiac muscle (length-tension relationship)

Figure from: Understanding Pathophysiology, Heuther & McCance, 5th ed, Elsevier, 2011.

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Factors Affecting Cardiac Output

Contractility

Afterload

CVP

CO

HR

SV

ESV

EDV

ANSParasympathetic Sympathetic

CO – Cardiac Output (~5L/min). Dependent upon Stroke Volume (SV; ~70 ml) and Heart Rate (HR)

CVP – Central Venous Pressure; Pressure in vena cava near the right atrium (affects preload; Starling mechanism)

Contractility – Increase in force of muscle contraction without a change in starting length of sarcomeres

Afterload – Load against which the heart must pump, i.e., pressure in pulmonary artery or aorta

ESV – End Systolic Volume; Volume of blood left in heart after it has ejected blood (~50 ml)

EDV – End Diastolic Volume; Volume of blood in the ventricle before contraction (~120-140 ml)

= EDV - ESV

= HR x SV

Figure adapted from: Aaronson & Ward, The Cardiovascular System at a Glance, Blackwell Publishing, 2007

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Regulation of Cardiac OutputRecall: SV = EDV - ESV

Figure from: Martini, Anatomy & Physiology, Prentice Hall, 2001

Be sure to review, and be able to use, this summary chart

CO = heart rate (HR) x stroke volume (SV)

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Factor Effect on HR and/or SV Effect on Cardiac Output

 DECREASE  

Parasympathetic activity (vagus nerves)

HR

K+ (hyperkalemia) HR and SV (weak, irreg. beats)

K+ (hypokalemia) Irritability

Ca2+ (hypocalcemia) SV (flaccidity)

Decreased temperature HR

 INCREASE

Sympathetic activity HR and SV

Epinephrine HR and SV

Norepinephrine HR

Thyroid hormone HR

Ca2+ (hypercalcemia) SV (spastic contraction)

Rising temperature HR

Increased venous return HR and SV

Summary of Factors Influencing Cardiac Output

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Life-Span Changes• deposition of cholesterol in blood vessels

• cardiac muscle cells die

• heart enlarges

• fibrous connective tissue of heart increases

• adipose tissue of heart increases

• blood pressure increases

• resting heart rate decreases

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Review

• Cardiac muscle contraction differs in several important ways from skeletal muscle contraction– Duration of the action potential is longer

– Ca2+ for contraction is derived from the extracellular fluid as well as the sacroplasmic reticulum

– Length of contraction is longer

– Tetany cannot develop due to length of the absolute refractory period

• The electrocardiogram– Measures the electrical changes occurring in the heart

– Is used to assess heart’s ability to conduct impulses, heart enlargement, and myocardial damage

– Depolarization -> contraction, repolarization -> relaxation

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Review• There are three major events (waves) in the ECG

– P wave = atrial depolarization

– QRS complex = ventricular depolarization

– T wave = ventricular repolarization

• The different leads of an ECG can be used to localize heart muscle abnormalities

• Abnormalities in ECG presentation can be indicative of heart damage

• Several common cardiac abnormalities– Arrhythmia

– Tachycardia (and bradycardia)

– Atrial flutter

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Review

• Important cardiodynamic terminology– End-diastolic volume (EDV) – amount of blood

left in ventricles at end of ventricular diastole– End-systolic volume (ESV) – amount of blood

left in ventricles at end of ventricular systole– Stroke volume (SV) – amount of blood pumped

out of each ventricle during a single beat (EDV – ESV = SV)

– Ejection fraction – Percentage of EDV represented by the SV

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Review

• Cardiac output (CO)– Amount of blood pumped by the heart in one

minute– CO = stroke volume x heart rate– Normal (resting) CO 5-6 L/min

• Factors Affecting CO– Autonomic activity– Hormones– K+, Ca2+ – Venous return

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Review

• Regulation of Cardiac Output– Heart Rate

• Autonomic tone

• Hormones

• Venous return

– Stroke Volume• Autonomic tone

• Hormones

• Venous return

• Afterload