cardiovascular3
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Transcript cardiovascular3
Abstracts and Test 2
• Earning up to 5 points for Test # 2 based
on topics of Frog Heart Lab:
– Regulation of pacemaker cells by
temperature, hormones, neurotransmitters,
antagonists
– Heart block: 1st, 2nd, and 3rd degree
– The conducting system
– Strategies for prolonging survival of in vitro
organs
Cardiac Cycle Animation
1QQ #24 for 10:30
Write each letter and circle the letter of correct statements.
a) Heart murmurs are caused by the closure of heart
valves.
b) The first heart sound is produced by the closure of
the atrioventricular valves.
c) Blood is about 65% plasma.
d) Pacemaker cells produce action potentials that last
about 200-300 milliseconds.
e) Chordae tendonae and papillary muscles prevent
eversion of the semilunar valves.
1QQ #24 for 11:30
Write each letter and circle the letter of correct statements.
a) The buffy coat is thicker in a person with an infection.
b) The first heart sound is produced by the closure of
the atrioventricular valves.
c) Blood is about 45% plasma.
d) Pacemaker cells produce action potentials that last
about 200-300 milliseconds.
e) The tricuspid valve is situated between the right
ventricle and the pulmonary artery.
S8
F=Q=ΔP/R
Flow = Pressure gradient/Resistance
from Ohm’s Law (V=IR)
44
RR==8Lη/πr
8Lη/πr
Q= ΔP πr4
8Lη
Poiseulle’s equation
Double radius … 16x flow
Half radius….1/16th flow
S1
Cardiac Output = Heart Rate X Stroke Volume
What regulates
heart rate?
What regulates
Stroke Volume?
CO = HR x SV
5L/min = 72 beat/min x 70 ml/beat
The Cardiac Cycle animation
S4
Figure 12.11
S5
SA node cells do not
have stable resting
membrane potential,
spontaneously
produce AP, are
Pacemaker cells
S 15
Figure 12.22
Intrinsic Rate = 100 beat/min
2 effects of Parasymp:
hyperpolarization &
slower depolarization
S6
NE
Beta-adrenergic receptors
Effect of “Beta blockers”
Recall: CO = HR x SV
EPI
ACh
mAChR
Effect of atropine
S7
What prevents the AP from being
conducted from ventricles to atria?
Fibrous connective tissue between atria and ventricles prevents the
conduction of action potential. Only route is via AV node, bundle of His,
bundle branches, Purkinje fibers, and to ventriclular myofibers.
S8
“Sis-toe-lee”
1st Heart Sound =
Closure of
Atrioventricular
(AV) valves at
beginning of
Ventricular
Systole
“die-ass-toe-lee”
2nd Heart Sound =
Closure of Semilunar
valves at beginning
of Ventricular
Diastole
S9
Figure 12.20
Systolic
Diastolic
Atrial Fibrillation
Stroke Volume
Ejection Fraction = SV/EDV
Ventricular
Fibrillation &
Defibrillation
Animation
S 10
Events are same for Cardiac Cycle for Right Side
of Heart; only difference is lower systolic pressures
in right atrium and right ventricle.
S1
So far, we’ve dealt with the factors that
control Cardiac Output by changing
heart rate.
3
CO = HR x SV
2
+ sympathetic
- parasympathetic
1
5L/min = 72 beat/min x 70 ml/beat
35L/min = ? beat/min x ? ml/beat
The Cardiac Cycle animation
S2
Figure 12.20
Stroke Volume
Animation
S3
Frank-Starling Law of the Heart
Does not depend on hormones or nerves
Assures that the heart adjusts its output based on VENOUS RETURN
Ventricular Function Curve
Ways to enhance
Venous Return:
1) muscle contractions
2) “respiratory pump”
3) venoconstriction
FS LoH = SV is proportional to EDV
↑VR→ ↑EDV → ↑SV
Respiratory pump
Mechanical pump for bedridden patients
Muscle pump
S4
Length-tension “curve” for Cardiac muscle
Fig. 09.21
High EDV
Low EDV
Overinflation of
ventricles leads to less
effective pumping
S5
Overinflation of
ventricles results in
reduction in stroke
volume
Treatments?
…..diuretics
S6
NE from Symp
postganglionics
& EPI from
Adrenal medulla
Contractility
Increase Ejection Fraction
Note: cardiac myofibers
NOT innervated by
parasympathetic division
S7
3 Effects of
Sympathetic
Stimulation
1: Increase rate of contraction
2: Increase peak tension
3: Decrease twitch duration
Why should the
contraction be
shorter?
S8
Summary: Control of Stroke Volume
FS LoH
• End diastolic volume (preload)
• Contractility (strength of ventricular
contraction due to adrenergic stimulation)
• Pressure in arteries that must be
overcome = Afterload
Afterload is analogous to trying to pump more air into a tire that is already fully inflated
(heart contracting to overcome diastolic pressure.)
S9
High blood pressure increases the workload of the heart….. Cardiac
hypertrophy….increase chance of irregular conduction of AP through heart
Hypertrophic cardiomyopathy
S 11
Factors that control Cardiac Output by
changing heart rate and stroke volume.
Afterload (MAP)
CO = HR x SV
+ sympathetic
- parasympathetic
VR and EDV
(FSLoH)
Contractility
(catecholamines)
5L/min = 72 beat/min x 70 ml/beat
35L/min = ? beat/min x ? ml/beat