Chapter 18 Heart Lecture 3 Marieb’s Human Anatomy and Physiology Marieb Hoehn.
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Transcript of Chapter 18 Heart Lecture 3 Marieb’s Human Anatomy and Physiology Marieb Hoehn.
Chapter 18Heart
Lecture 3
Marieb’s HumanAnatomy and
Physiology
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)
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