Cardiac Anatomy and an Introduction to the Vascular System
| previous topic | next topic | syllabus | home page | BME Home Page | search the web | e-mail Doug |
As usual, all of this is in outline format with hypertext, so if you want to review the specifics, or if you have any questions on a specific topic, click the hypertext for that topic.
Today's topic:
Many of these topics are incomplete. They should be completed when the extra credit projects are turned in.
These are Dr. Schechtman's very own notes for this lecture.
I hope you find them helpful.
1
Cardiac Anatomy
And Introduction to the Circulation System
Weight ~300g
Chambers
Atria Thin walled, low pressure; not for pumping, but
for storing
Ventricles Right ventricle much thinner-walled than left,
since pulmonary circulation under 1/7 the
pressure of systemic circulation
Valves--allow one-way flow of blood
Atrioventricular (AV) valves
Tricuspid valve separates the right atrium and ventricle
Mitral valve separates the left atrium and ventricle
Chordae tendinae araising from the papillary muscles of
each ventricle, attach to the edges of the valves to
prevent inversion
Semilunar valves
Between right ventricle and pulmonary artery
Between left ventricle and aorta
Prevent reflux of blood into ventricles during diastole
Backflow feeds coronary arteries
Pericardium
Contains a small amount of fluid for lubrication
Tough, noncompliant, prevents overdistension of chambers
Heart can function normally without it
Gradually stretches with cardiac hypertrophy
Fused to diaphragm
Flow pattern
Inferior and Superior Vena Cava
Right heart
Pulmonary Artery (carries unoxygenated
blood
Pulmonary Veins (carry oxygenated blood
Left heart
Aorta
Heart sounds
Onset of systole--loudest, oscillation of blood in ventricles and
vibration of the walls
Closure of semilunar valves
Second sound often split (Aortic valve, then Pulmonary)
Coronary veins and arteries
Prone to the accumulation of fatty deposits, which limits coronary
blood flow--coronary artery disease
Repair with coronary bypass or balloon angioplasty
During ventricular systole:
The septum and the free wall of the left ventrical become thicker and move
closer to each other
Contraction of the pappilary muscles during systole prevent the AV valves
from being forced into the atria
At he end of ejection, a volume of blood approx equal to that ejected
during systole remains in the ventricular cavities--residual
volume. Average ejection fraction: ~67%.
In heart failure, the residual volume greatly exceeds stroke volume
Blood returns to the atria during ventricular systole
During ventricular diastole:
Rapid filling phase--The major part of ventricular filling occurs
immediately on opening of the AV valves
Elastic recoil of ventricles following contraction sucks blood in
Diastasis--Rapid filling phase is followed by a phase of slow filling
(diastasis), during which blood returning from the periphery flows
into the right ventricle and blood from the lungs into the left ventricle
During Atrial Systole:
Onset of atrial systole occurs soon after the beginning of the P wave of
the EKG, and completes the filling of the ventricles
Because there are no valves at the junctions of the venae cavae and the
right atrium or of the pulmonay veins and left atrium, atrial contraction
can force blood in both directions, but inertia of the inflowing blood
keeps backflow to a minimum
Atrial contraction is not essential for ventricular filling, as can be
observed in atrial fibrilation. At slow heart rates atrial
contraction contributes little. However, during tachycardia, diastasis is
abbreviated (and during extreme tachycardia even the rapid filling
phase may be encroached upon) atrial contraction is important to
propelling blood into the ventricles in minimal time.
Ventricular systole occupies ~30% of cycle time at rest. When HR speeds
up as during exercise systole shortens somewhat, but diastole
shortens most. This is a rate limiting factor. If diastole decreases
enough, you will not get adequate ventricular filling.
Resting systole .3 sec
diastole .6 sec
Near Max systole .2 sec
diastole .1 sec
Cardiac Output = Heart Rate X Stroke Volume
Starling's Law--If more blood flows into the heart, it doesn't accumulate
there, but the heart works harder to get it out
If more blood enters the heart, stroke volume increases
Stroke volume = End Diastolic Volume - End Systolic Volume
Greater expansion of the ventricle results in more forceful
contraction
Were it not for this fact, the extra blood would stay in the
venticle, and accumulate over time
Such an increase in heart size is caused by an increase in venous
pressure, i.e., lie down and blood from the lower extremities is
suddenly transferred to the thorax.
Only operates within a limited range of diastolic filling; at very
high levels of diastolic filling, contraction becomes
weaker
Therefore, it is important for central venous pressure to remain
within a limited range for normal function of the heart.
The ventricle must fill enough to produce adequate force in systole, but
not too much, or
contractile force decreases.
Over distention plays a role in congestive heart failure.
Especially as the heart weakens, the optimal range of
venous pressures narrows. If venous pressure is above the optimal limit,
contractile force (and stroke volume) is reduced, so venous
pressure increases further
Introduction to the vascular system
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
| previous topic | next topic | syllabus | home | BME | search the web | e-mail Doug |
| 1 | 2 | 3 | 4 | 5 | 6 | 7 | 8 | 9 | 10 | 11 | 12 | 13 | 14 | 15 | Exam #1 |
| 17 | 18 | 19 | 20 | 21 | 22 | 23 | 24 | 25 | 26 | Exam #2 |
| 28 | 29 | 30 | 31 | 32 | 33 | 34 | 35 | 36 | 37 | 38 | 39 | 40 | 41 | 42 | Exam #3 |