Transcript Electrical conduction in the Heart

Cardiac Cycle-Chapter 9
• Beginning of one heart beat to
the next.
– Includes a cycle of
contraction and relaxation
• Systole: contraction
• Diastole: relaxation (filling)
• Blood will only move from one
chamber to the next if the
pressure in the first chamber
exceeds the second!
• Timing is EVERYTHING!
Principles of Pressure and Flow
• Measurement:
compared to force
generated by column
of mercury (mmHg) –
sphygmomanometer
• Change in pressure
gradient creates a
change in volume
(Boyle’s law)
• Opposing pressures in
atria/ventricles/ large
arteries
Phases of Cardiac Cycle-step by step800mSec- only 370mSec for Systoles
•
Quiescent period/ Diastasis–
430mSec
– all chambers relaxed
– AV valves open
– blood flowing into ventricles
•
Atrial systole- 100mSec
– SA node fires, atria depolarize
– P wave appears on ECG
– atria contract, force additional
blood into ventricles
– ventricles now contain enddiastolic volume (EDV) of
about 120 ml of blood
– Heart sound 4 occurs
P
Isovolumic Contraction of
Ventricles
• Atria repolarize and relax
• Ventricles depolarize
• QRS complex appears in
ECG
• Ventricles contract
• Rising pressure closes AV
valves
• Heart sound S1 occurs
• No ejection of blood yet (no
change in volume)
Ventricular Ejection
• Rising pressure opens
semilunar valves
• Stroke volume: amount
ejected, ~ 70 ml
• Rapid and reduced ejection
phases
• SV/EDV= ejection fraction,
– at rest ~ 60%
– during vigorous exercise as
high as 90%
– diseased heart < 50%
• End-systolic volume: amount
left in heart (50ml)
• Ventricular systole lasts
270mSec
Isovolumic Relaxation of
Ventricles
• T wave appears in ECG
• Ventricles repolarize and
relax (begin to expand)
• Semilunar valves close
• AV valves remain closed
• Ventricles expand but do not
fill
• Heart sound S2 occurs
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ycle__quiz_2_.html
Ventricular Filling
• AV valves open
• Ventricles fill with
blood - 3 phases
– rapid ventricular filling
- high pressure
– diastasis - sustained
lower pressure
– filling completed by
atrial systole
• Heart sound S3 may
occur
Cardiac Cycle (cont’d)
4th
Heart sounds are from turbulent blood!
Figure 9-5; Guyton & Hall
Cardiac Output (CO)
• Amount ejected by a ventricle in
1 minute
• CO = HR x SV
• Resting values, usually about 4
to 6L/min
• Vigorous exercise  CO to 21
L/min for fit person and up to 35
L/min for world class athlete
• Cardiac reserve: difference
between maximum and resting
CO
Volumes and Fraction
•
•
•
•
End diastolic volume
= 120 ml
End systolic volume
= 50 ml
Ejection volume (stroke volume) = 70 ml
Ejection fraction = 70ml/120ml = 58%
(normally 60%)
• If heart rate (HR) is 70 beats/minute, what is
cardiac output?
• Cardiac output
= HR * stroke volume
= 70/min. * 70 ml
=
Factors that Affect Stroke volume
• EDV- dependent on filling time
(diastole) and venous return
– Skeletal pumping
– Respiratory pumping
• ESV– Preload- degree of stretching
• Frank-Starling Principle: more in,
more out
– Contractility of the ventricle
• Availability of calcium; positive and
negative inotropy
– Afterload- amount of tension ventricle
must exert to eject; affected by
peripheral vasculature; if greater ESV
then there was less stroke volume
Frank-Starling Mechanism
• Within physiological limits the heart pumps all the blood
that comes to it without excessive
damming in the
veins.
• Length-tension relationship of cardiocytes.
• Extra stretch on cardiac myocytes makes actin
and
myosin filaments interdigitate to a more optimal degree
for force generation.
Autonomic Effects on Heart
•
•
Sympathetic stimulation
causes increased HR +
increased contractility
with HR = 180-200 and
C.O. = 15-20 L/min.
Parasympathetic
stimulation decreases
HR markedly and
decreases cardiac
contractility slightly.
Vagal fibers go mainly to
atria.
Fast heart rate
(tachycardia) can
decrease C.O. because
there is not enough time
for heart to fill during
diastole.
Maximum
sympathetic stimulation
25
Cardiac Output (L/min)
•
20
sympathetic stimulation
15
No sympathetic and no parasympathetic
stimulation
10
(Parasympathetic
stimulation)
5
0
-4
0
+4
+8
Right Atrial Pressure (mmHg)
So What Happens to the Cycle
when the heart rate increases?
• All phases are
shortened
• Diastole pays the
biggest price!
• Reduced by almost 75%
at 200bpm
• What does that mean?
• Less Filling!
Factors Influencing CO
Figure 14-31: Factors that affect cardiac output
Drugs Affecting CO
• Atropine- parasympathetic
blocking (blocks muscarinic
AchR) agent, (+,+)
• Pilocarpine- drug that causes
cholinergic neurons to release
ACH. Since Ach decreases heart
rate, it causes (-, ) effect on
heart.
• Propranalol- Reversible,
competitive blocker of Beta1
receptor. So blocks
sympathetics effect of heart (-,-)
Decrease heart rate and force of
contraction, and lowers blood
pressure.
Drugs Affecting CO (2)
• Digoxin (shorter ½ life) or
Digitoxin- come from group of
drugs derived from digitalis.
Digitalis derived from foxglove
plant. It has a (-,+) effect, neg
chronotropic and positive
inotropic effect; slows heart rate
but increases force of contraction.
Is only drug with this effect on
heart.
– increases intracellular concentration
of Ca.
– increase force of contraction by
inhibiting Na+/K+ pump. So cells
start to accumulate Na.
– Disadvantage of using digitalis is that
it’s extremely toxic. The optimal dose
is very close to lethal dose- stops
heart
Q: How do cardiac glycosides
increase cardiac contractility?
• Glycosides (eg. digoxin) inhibit the Na/K ATPase…




increase intracellular Na+
decrease Na+ gradient
decrease Na+/Ca2+ counter-transport
increase intracellular Ca2+
Digoxin has been a
cornerstone for the treatment
of heart failure for decades
and is the only oral inotropic
support agent currently used
in clinical practice.
Na+
Na+
K+
Na+
Ca++