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Chapter 18 Heart Lecture 3 Marieb’s Human Anatomy and Physiology Ninth Edition Marieb Hoehn.
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Transcript of Chapter 18 Heart Lecture 3 Marieb’s Human Anatomy and Physiology Ninth Edition Marieb Hoehn.
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
3
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
4
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
5
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
6
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
12
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
13
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%)
14
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
15
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
16
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
17
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
18
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
19
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.
20
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
21
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)
22
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
24
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
25
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
26
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
27
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
28
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
29
Review
• Regulation of Cardiac Output– Heart Rate
• Autonomic tone
• Hormones
• Venous return
– Stroke Volume• Autonomic tone
• Hormones
• Venous return
• Afterload