Transcript NVCC Bio 212 - gserianne.com

Marieb’s Human
Anatomy and Physiology
Ninth Edition
Marieb w Hoehn
Chapter 18
Heart
Lecture 3
Lecture Overview
• Physiology of cardiac muscle contraction
• The electrocardiogram
• Cardiac Output
• Regulation of the cardiac cycle and cardiac
output
2
Comparison of Skeletal and Cardiac Muscle
Cardiac and skeletal
muscle differ in:
1. Nature of action
potential
Figure from: Martini,
Anatomy & Physiology,
Prentice Hall, 2001
2. Source of Ca2+
3. Duration of
contraction
Let’s look at this
more closely
3
The Cardiac Muscle Action Potential
Ca2+ ions enter from
1.
Extracellular fluid
(20%)
2.
Sarcoplasmic
reticulum (80%)
** Cardiac muscle is
very sensitive to
Ca2+ changes in
extracellular fluid
Figure from: Martini, Anatomy &
Physiology, Prentice Hall, 2001
Recall that tetanic contractions
usually cannot occur in a
normal cardiac muscle cell
4
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
Important points to remember:
- Depolarization precedes contraction
- Repolarization precedes relaxation
Three
waves per
heartbeat
P wave – atrial depolarization
QRS wave – ventricular depolarization
T wave – ventricular repolarization
5
Electrocardiogram
PR Interval: 0.12 – 0.20 sec
QT Interval: 0.20 – 0.40 sec
QRS Interval: < 0.10 sec
Figure from: Martini, Anatomy & Physiology, Prentice Hall, 2001
6
Review of Events of the Cardiac Cycle
Figure from: Martini, Anatomy
& Physiology, Prentice Hall,
2004
S2
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
12
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%)
13
Cardiac Output (CO)
• The volume of blood pumped by each
ventricle in one minute
CO
ml/min
=
heart rate (HR)
beats/min
x
stroke volume (SV)
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
14
Regulation of Cardiac Output
CO
=
heart rate (HR) x stroke volume (SV)
Figure from:
Martini, Anatomy &
Physiology, Prentice
Hall, 2001
• physical exercise
• body temperature
• concentration of various ions
SV = EDV – ESV
• calcium
• potassium
• parasympathetic impulses (vagus nerves) decrease heart action
• sympathetic impulses increase heart action; epinephrine
15
Regulation 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
16
Figure from: Hole’s Human A&P, 12th edition, 2010
Regulation of Cardiac Rate
Tachycardia > 100 bpm
Bradycardia < 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
17
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
18
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.
19
Factors Affecting Cardiac Output
Figure adapted from: Aaronson & Ward, The Cardiovascular System at a Glance, Blackwell Publishing, 2007
ANS
Parasympathetic
HR
Contractility
CO = HR x SV
SV
Sympathetic
ESV
Afterload
= EDV - ESV
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)
20
Regulation of Cardiac Output
Recall: SV = EDV - ESV
Figure from:
Martini, Anatomy &
Physiology, Prentice
Hall, 2001
CO
=
heart rate (HR) x stroke volume (SV)
21
Be sure to review, and be able to use, this summary chart
Summary of Factors Influencing Cardiac Output
Factor
Effect on HR and/or SV
Effect on Cardiac Output
DECREASE
 HR

 K+ (hyperkalemia)
 HR and SV (weak, irreg. beats)

 K+ (hypokalemia)
Irritability

 Ca2+ (hypocalcemia)
 SV (flaccidity)

Decreased temperature
 HR

Sympathetic activity
 HR and SV

Epinephrine
 HR and SV

Norepinephrine
 HR

Thyroid hormone
 HR

 SV (spastic contraction)

 HR

 HR and SV

Parasympathetic activity
(vagus nerves)
INCREASE
 Ca2+ (hypercalcemia)
Rising temperature
Increased venous return
22
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
24
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
25
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
26
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
27
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
28
Review
• Regulation of Cardiac Output
– Heart Rate
• Autonomic tone
• Hormones
• Venous return
– Stroke Volume
•
•
•
•
Autonomic tone
Hormones
Venous return
Afterload
29