chapter 18 the heart and cardiovascular function lecture 3

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Chapter 18The Heart and Cardiovascular Function

Lecture 3

Martini’s VisualAnatomy and Physiology

First Edition

Martini Ober

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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)

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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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Summary of Factors Affecting Cardiac OutputFactor 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

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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