Title: Heart
1Mariebs Human Anatomy and Physiology Marieb w
Hoehn
- Chapter 18
- Heart
- Lecture 3
2Lecture Overview
- Physiology of cardiac muscle contraction
- The electrocardiogram
- Cardiac Output
- Regulation of the cardiac cycle and cardiac output
3Comparison of Skeletal and Cardiac Muscle
- Cardiac and skeletal muscle differ in
- Nature of action potential
- Source of Ca2
- Duration of contraction
Figure from Martini, Anatomy Physiology,
Prentice Hall, 2001
Lets look at this more closely
4The Cardiac Muscle Action Potential
- Ca2 ions enter from
- Extracellular fluid (20)
- 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
Figure from Martini, Anatomy Physiology,
Prentice Hall, 2001
5Electrocardiogram
- recording of electrical changes that occur in
the myocardium during the cardiac cycle - used to assess hearts ability to conduct
impulses, heart enlargement, and myocardial
damage
Important points to remember - Depolarization
precedes contraction - Repolarization precedes
relaxation
P wave atrial depolarization QRS wave
ventricular depolarization T wave ventricular
repolarization
Three waves per heartbeat
6Electrocardiogram
PR Interval 0.12 0.20 sec QT Interval 0.20
0.40 sec QRS Interval lt 0.10 sec
Figure from Martini, Anatomy Physiology,
Prentice Hall, 2001
7Electrocardiogram and Heart Events
Figure from Holes Human AP, 12th edition, 2010
8Electrocardiogram and Heart Events
Figure from Holes Human AP, 12th edition, 2010
9Different Leads for a 12-Lead ECG
10Different Leads Can Help Localize Abnormalities
EKG leads Location of MI Coronary Artery
II, III, aVF Inferior MI Right Coronary Artery
V1-V4 Anterior or Anteroseptal MI Left Anterior Descending Artery
V5-V6, I, aVL Lateral MI Left Circumflex Artery
ST depression in V1, V2 Posterior MI Left Circumflex Artery or Right Coronary Artery
11Normal and Pathological ECGs
Figures from Saladin, Anatomy Physiology,
McGraw Hill, 2007
12Review of Events of the Cardiac Cycle
Figure from Martini, Anatomy Physiology,
Prentice Hall, 2004
- Atrial contraction begins
- Atria eject blood into ventricles
- Atrial systole ends AV valves close (S1)
- Isovolumetric ventricular contraction
- Ventricular ejection occurs
- Semilunar valves close (S2)
- Isovolumetric relaxation occurs
- AV valves open passive atrial filling
S2
S1
13Cardiodynamics 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)
14Cardiac Output (CO)
- The volume of blood pumped by each ventricle in
one minute
CO heart rate (HR) x stroke
volume (SV)
ml/min beats/min
ml/beat
Example CO 72 bpm x 75ml/beat ? 5,500 ml/min
Normal CO ? 5-6 liters (5,000-6,000 ml) per minute
15Regulation of Cardiac Output
CO heart rate (HR) x stroke
volume (SV)
Figure from Martini, Anatomy Physiology,
Prentice Hall, 2001
SV EDV ESV
- physical exercise
- body temperature
- concentration of various ions
- calcium
- potassium
- parasympathetic impulses (vagus nerves) decrease
heart action - sympathetic impulses increase heart action
epinephrine
16Regulation of Cardiac Rate
Autonomic 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 Holes Human AP, 12th edition, 2010
17Regulation of Cardiac Rate
Tachycardia gt 100 bpmBradycardia lt 60 bpm
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
18Additional 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
19The 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)
20Regulation of Cardiac Output
Recall SV EDV - ESV
Figure from Martini, Anatomy Physiology,
Prentice Hall, 2001
CO heart rate (HR) x stroke
volume (SV)
Be sure to review, and be able to use, this
summary chart
21Factors Affecting Cardiac Output
Figure adapted from Aaronson Ward, The
Cardiovascular System at a Glance, Blackwell
Publishing, 2007
ANSParasympathetic Sympathetic
HR
Contractility
CO
HR x SV
ESV
Afterload
EDV - ESV
SV
EDV
CVP
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)
22Summary of Factors Influencing Cardiac Output
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 ?
23Summary of Factors Influencing CO Table Form
Effect on CO How? Affect HR, SV, or both?
INCREASE
Atrial reflex ? HR HR
Sympathetic stimulation ? HR, SV HR and SV
Epinephrine, thyroxin ? HR, SV HR and SV
? Preload (Frank-Starling Mechanism) ? EDV, ? ESV SV
? Contractility ? ESV SV
? Venous return, ? CVP ? Preload, ? atrial reflex HR and SV
? Ca2 (hypercalcemia) ? Contractility, ? ESV SV
? Temperature ? HR HR
DECREASE
Parasympathetic stimulation (vagus nerves) ? HR HR
? Afterload ? ESV SV
? Ca2 (hypocalcemia) ? Contractility, ? ESV SV
? K (hyperkalemia) Arrhythmia, cardiac arrest HR, SV
? K (hypokalemia) Arrhythmia, cardiac arrest HR, SV
? Temperature ? HR HR
24Life-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
25Review
- 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 hearts ability to conduct
impulses, heart enlargement, and myocardial
damage - Depolarization -gt contraction, repolarization -gt
relaxation
26Review
- 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
27Review
- 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
28Review
- 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
29Review
- Regulation of Cardiac Output
- Heart Rate
- Autonomic tone
- Hormones
- Venous return
- Stroke Volume
- Autonomic tone
- Hormones
- Venous return
- Afterload