Biomedical Engineering 403

Cardiac Anatomy and an Introduction to the Vascular System

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Reading for Today:

Chapters 1 and 3 in Berne & Levy .

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Howdy Folks!

This is what happened in class today (10-8-97).

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:

A General Introduction to the Class and some of the Basic Stuff Covered in it.

Consequently, we'll discuss:

Many of these topics are incomplete. They should be completed when the extra credit projects are turned in.

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Dr. Schechtman's Notes!

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


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A Copy of Today's Overhead Images:

Figure 1

Figure 1

Figure 2

Figure 2

Figure 3

Figure 3

Figure 4

Figure 4

Figure 5

Figure 5

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