Trinity CVS lecture 2

Cardiac Cycle
All events associated with the flow of blood
through the heart during one complete
heart beat
Approx 0.83sec if heart rate is 72 bpm
Cardiac Cycle
2 Periods
4 Phases
Diastole/Systole
Ventricular filling
Isovolumetric contraction
Ventricular ejection
Isovolumetric relaxation
Wiggers Diagram
Pressure/volume relationships
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2 Main Periods of the Cardiac Cycle
Systole
Ventricles contract
AV valves close
SL valves open
Blood flow into arteries
Diastole
Ventricles relax
SL valves shut
AV valves open
Blood flows into ventricles
Phases of the Cardiac Cycle
Ventricular filling
Pressure atria > Pressure ventricles
AV valves open, SL valves still closed
Passive Phase-Blood flows from atria to
ventricles
Active phase- Atria contract
Isovolumetric ventricular contraction
Ventricle contracting
Ventricle pressure> atrial pressure
AV snap shut, SL valves already closed
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Phases of the Cardiac Cycle
Ventricular ejection
Pressure ventricles > pressure arteries
Semilunar valves open, AV valves closed
Blood flows into arteries
Isovolumetric ventricular relaxation
Ventricle relaxes
Aortic pressure > ventricular pressure
AV and semilunar valves closed
Cardiac Cycle
Wiggers diagram
ECG
Aortic pressure
Left ventricular
pressure
Left atrial pressure
Left ventricular
volume
Heart sounds
Sherwood, Figure 9-21, pg. 302
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Electrical
events
P-wave precedes
atrial contraction
QRS complex
precedes ventricular
contraction
T-wave precedes
ventricular
relaxation
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Ventricular pressure during cardiac cycle
Large variation
in ventricular
pressure to
allow for:
opening of
valves
pressure in
atria and
arteries
Copyright © 2005 Pearson Education, Inc.,
Publishing as Benjamin Cummings
4
Atrial Pressure Changes
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Education, Inc., Publishing
as Benjamin Cummings
Normal value for 80mmHg < aortic BP > 120mmHg
Pulse pressure = systolic - diastolic = approx 40mmHg
Mean Arterial pressure = 1/3 systolic + 2/3 diastolic = approx
93mmHg
Copyright © 2005 Pearson Education, Inc., Publishing as Benjamin Cummings
Aortic pressure during cardiac cycle
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Ventricular Volume & Stroke Volume
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Publishing as Benjamin Cummings
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5
4
2
3
EDV = end diastolic volume
ESV = end systolic volume
SV = volume of blood ejected by the ventricle each beat
SV = EDV - ESV
Heart Sounds
Sounds occur during turbulent blood flow when valves close
Copyright © 2005 Pearson Education, Inc., Publishing as Benjamin Cummings
First sound = soft lubb
2nd sound = louder dubb
AV valves close
Semilunar valves close
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Cardiac Output
Volume of blood pumped out by each
ventricle in one minute
CO= HR X SV
Average CO = 5 liters/min at rest
Extrinsic & Intrinsic regulation of CO
Extrinsic- neural (ANS) and hormonal
(epinephrine)
Intrinsic - local
Control of Heart Rate
Parasympathetic
Sympathetic
Decreases heart rate
Increases heart rate
Increases force of
contraction
Endocrine
Catecholamines:
Epinephrine and
Norepinphrine
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Control of Heart Rate
SA node
Intrinsic firing rate = 100 impulses/min
At rest (↑ vagal activity inhibits SA node)
Average HR = 70 beats/min
Achieved via :Parasympathetic (vagus) cholinergic
input, ↑ K+ permeability
→hyperpolarisation and slower drift to threshold
= Inherent SA node pacemaker activity
= Parasympathetic stimulation of SA node
Control of Heart Rate cont.
Initial increases in HR to 100-110 beats/min
Achieved via inhibition of parasympathetic tone (vagal
withdrawal)
HR > 110 beats/min
Achieved via sympathetic stimulation of:
SA node: ↓ K+ permeability: depolarizing effect & faster drift
to threshold
= SA node pacemaker activity
= Sympathetic stimulation of SA node
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Limitations to CO imposed by HR:
AV node conduction
Decremental conduction
Fewer gap junctions
Ventricular refractory period
Safety mechanism
0.25 to 0.3s
Control of Stroke Volume
Intrinsic Control
Extrinsic Control
End-diastolic volume (Frank Starling law)
Sympathetic stimulation
Ventricular contractility
Afterload
Sherwood, Fig. 9-20, p. 328
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Sherwood, 5th edition, fig 9.22, pg. 323
Preload: Frank Starling law of the heart
Venous return
Blood returning to the right atrium
via the great veins
Factors that affect venous return include:
Posture
Skeletal muscle pump
Respiratory/abdominal pump
Venous tone
Atrial pressure gradient
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Contractility
Sympathetic stimulation and epinephrine- input to
ventricular muscle:
Act via β1 adrenoceptors
Increases Ca2+ entry into cells
→ enhances excitation-contraction coupling
→ greater contractile force of ventricular myocytes
Increased SV
Sherwood 4th edition, fig 9.22, pg 304
Limitations to Preload:
Ventricular Filling Time
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Limitations to Preload:
Compliance
Rigidity
Limitations to SV imposed by:
Ventricular afterload
Increased afterload:
Chronic high blood pressure
or stenotic valve
Exercise -transient
Compensation:
Hypertrophy
May lead to pathological changes in heart structure
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Murmurs: ? increased afterload
Abnormal sound heard before, between, or after
the lubb-dubb of the first and second heart sounds
Caused by turbulent blood flow around the valves
Sherwood Fig. 9-5, p. 304
Murmurs: Stenotic Valve
Mitral stenosis
Left atrium needs
to generate more
pressure
Aortic stenosis
Left ventricle
needs to generate
more pressure
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Murmurs: Insufficient valve
Mitral regurgitation- ↑ left ventricular work
Aortic regurgitation- ↑ left ventricular work
http://www.ctsnet.org/graphics/experts/Adult/mckellar/figure_3.gif
Limitations to Stroke Volume:
Ventricular Contraction Duration
If contraction too short SV may be decreased
Dependent on venous return
Copyright © 2005 Pearson Education, Inc., Publishing as Benjamin Cummings
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Summary: Control of Cardiac Output
Summary
Blood flow is controlled by pressure changes
Wiggers diagram
Cardiac output = Heart rate x Stroke Volume
Heart rate- increased by sympathetic activity and
epinephrine. Decreased by parasympathetic activity.
Stroke volume- increased by increased venous return
and increased sympathetic nerve activity
Limitations of Cardiac Output
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