Download Pulmonary and Systemic Circuits Path of Blood Flow Heart Anatomy

3/22/2013
Pulmonary and
Systemic Circuits
• Heart: double pumps
– pulmonary circuit
• short, low-pressure
circulation
– systemic circuit
• long, high-friction
circulation
• Trace the flow of blood
to & away from the heart
Path of Blood Flow
P:4–6X
Heart Anatomy
• Atria: Receiving Chambers
– R. atrium
• Vena cava & Coronary sinus
– L atrium
• Pulmonary veins
• Ventricles: Discharging
Chambers
– Papillary muscles
– Chordae tendinae
– R. ventricle
• Pulmonary trunk
– L. ventricle
• aorta
Heart valves
• Open and close in response to pressure
changes
• atrioventricular (AV) valves: Tricuspid & mitral
– Open: P.atrium > P.ventricle
– Close: ___________
• semilunar (SL) valves: aortic & pulmonary
– Open: P.ventricle > P.great vessels
– Close: ___________
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Cardiac Muscle Fibers
Anatomy of Cardiac Muscle
• striated, short, branched, 1 central nucleus
• T tubules: wide, less numerous
• large mitochondria
– 25–35% of cell volume
– Aerobic respiration
Anatomy of Cardiac Muscle
• Intercalated discs
– Desmosomes: anchoring cells
– Gap junctions: electrically couple adjacent cells
• Allows heart to be functional syncytium (single
coordinated unit)
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Similarities between skeletal and
cardiac muscles
Skeletal muscle
Cardiac muscle
1) Depolarization (-90mV => +30mV)
•Opening VG fast Na+ channels
2) Depolarization waves travel down T-tubules
•Ca2+ release
3) Excitation contraction coupling
Differences between skeletal and
cardiac muscles
Source of
stimulation
Contraction
Contraction
duration
absolute
refractory
period
Skeletal muscle
Cardiac muscle
Somatic nervous
system
Motor unit
contraction
15-100ms
Auto-rhythmic
Brief: 1-2ms
All cardiomyocytes contract
as unit, or none do
200ms
•blood ejection from heart
Long: 250ms
•Prevents tetanic
contractions
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Differences between skeletal and
cardiac muscles
Skeletal muscle
Cardiac muscle
Ca2+ source
Sarcoplasmic
reticulum
Extracellular Ca2+ - 20%
•Depolarization: slow Ca2+
channels in sarcolemma
SR – 80%
Action
potential
Depolarization
Brief: 1-2ms
Long: 200ms
•Due to plateau phase
•Fast VG Na+ channels
•Slow Ca2+ channels
•Inactivation Ca2+ channels
•Opening VG K+ channels
Repolarization
Fast VG Na+
channels
Opening VG K+
channels
Cardiac Contractile Cells:
Excitation-Contraction Coupling
• Excitation – Contraction
– T-tubules
• ↑Ca2+ : PLATEAU PHASE
• Ca2+-induced Ca2+ release
• Relaxation
Action Potential of contractile
muscle cells
Setting the Basic Rhythm
• Intrinsic cardiac conduction system
• Network of autorhythmic cells
• gap junctions
– Allow coordinated heartbeat -- synchrony
– SR: Ca2+
– Plasma membrane
• 3Na+/1Ca2+-antiport
• 3Na+/2K+-ATPase
– Digitalis (Digoxin)
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APs Initiation by Pacemaker Cells
APs Initiation by Pacemaker Cells
• unstable RMPs (pacemaker potentials or
prepotentials)
– gradual depolarization
• Open slow Na+ channels
• Close K+ channels
• At threshold: Depolarization
– Open Ca2+ channels
• Repolarization
– Close Ca2+ channels
– Open K+ channels
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Conduction System
Extrinsic Innervation of the Heart
• cardiac centers in
medulla oblongata
– Cardioacceleratory
center
• Sympathetic
– Cardioinhibitory center
• Parasympathetic
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Heart Sounds
• lub-dup
– LUB: louder, longer
• P.ventricle > P.atria
• Ventricular systole begins
– DUP: Short, sharp
• Ventricular diastole
begins
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Cardiac Cycle
• Mechanical Events occurring during one
complete heartbeat
– 2 phases
• Systole = contractile phase of cardiac cycle
• Diastole = relaxation phase of cardiac cycle
– Series of pressure and blood volume changes
during 1 heartbeat
• Heart murmurs
– incompetent or stenotic
valves
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Ventricular filling Phase of Cardiac Cycle
• AV valves – open; semilunar valves - closed
– passively flows into ventricles -- 80% of blood
• pressure low
– Atrial systole -- 20%
• End diastolic volume (EDV): volume of blood
in ventricle at end of ventricular diastole
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Ventricular systole Phase of Cardiac Cycle
• Ventricles contract (while Atria relax)
– ventricular pressure: AV valves – closed;
semilunar valves - open
– Isovolumetric contraction phase: Volume 
– ejection phase: volume 
• End systolic volume (ESV): volume of blood
remaining in each ventricle after systole
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Isovolumetric relaxation Phase of Cardiac Cycle
Wigger’s Diagram: Summary of events during cardiac cycle
Left heart
QRS
P
EKG
• Ventricles relax
T
1st
Heart sounds
– Isovolumetric: volume 
– AV valves: closed
– Semilunar valves: closed
P
2nd
Dicrotic notch
120
80
Aorta
Pressure
(mm Hg)
Left ventricle
40
• atria relaxed
Atrial systole
Left atrium
0
120
EDV
Ventricular
volume (ml)
– Atrial filling
SV
50
ESV
Atrioventricular valves
Aortic and pulmonary valves
Phase
Closed
Open
2b
2a
1
Open
Closed
3
1
Ventricular
Isovolumetric
contraction phase ejection phase
2a
2b
Ventricular filling
(mid-to-late diastole)
Ventricular systole
(atria in diastole)
Atrial
contraction
Ventricular
filling
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Open
Closed
1
Isovolumetric
relaxation
3
Ventricular
filling
Early diastole
Pressure
EKG vs. Heart Sounds
Ventricular
ejection
Isovolumetric
contraction
Ventricular volume
Isovolumetric
relaxation
Cardiac Output (CO)
• Cardiac output varies to
meet metabolic demands
– CO = HR × SV
– At rest
• CO = HR (75 beats/min)  SV
(70 mL/beat)
– CO = 5.25 L/min
• HR
– (+) - chronotropic factors:
HR
– (-) - chronotropic factors:
HR
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Stroke Volume
• SV = EDV – ESV =
• factors affect SV
Frank Starling’s Law of the Heart
•The heart pumps all the blood that returns to it
•MAP = CO x TPR
Residual
– Preload = degree of stretch (tension) of cardiac
muscle cells before they contract (Frank-Starling
law of heart)
Stroke volume
•End-diastolic volume (EDV)
contraction
EDV
SV
•  Venous return =>  EDV (preload)
• Slow HR => ventricular filling (filling time) =>  EDV
– Afterload = pressure ventricles must overcome to
eject blood (resistance)
• Loss of arterial elasticity => Afterload
• Afterload => SV & ESV
Larger
EDV
Stronger
contraction
Larger
SV
– Contractility
Contractility
Atrial (Bainbridge) reflex
• Contractility: the amount of force produced
at a given preload
• sympathetic reflex initiated
– by venous return => atrial filling
• Stretch of atrial walls stimulates SA node   HR
– ONLY sympathetic
– NO parasympathetic influence
• Increased by Positive inotropic agents
– stimulates atrial stretch receptors, activating
sympathetic reflexes
– Thyroxine, glucagon, epinephrine, digitalis, high
extracellular Ca2+
• Decreased by negative inotropic agents
– Acidosis, increased extracellular K+, calcium
channel blockers
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Figure 18.22 Factors involved in determining cardiac output.
Exercise (by
sympathetic activity,
skeletal muscle and
respiratory pumps;
see Chapter 19)
Heart rate
(allows more
time for
ventricular
filling)
Exercise,
fright, anxiety
epinephrine,
thyroxine,
excess Ca2+
Principles of Blood Pressure and
Flow
• Blood Flow= pressure/ resistance
– pressure gradient: driving force for blood flow
Venous
return
Sympathetic
activity
Contractility
EDV
(preload)
Parasympathetic
activity
• Large gradient: from aorta to capillaries
– At aorta: 2.5 cm diameter and 100 mm Hg pressure
– At capillaries: 8 µm diameter and 25 mm Hg pressure
ESV
– Resistance opposes flow
Initial stimulus
Physiological response
Result
Stroke
volume
Heart
rate
Cardiac
output
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Blood pressure
and flow
Changes in
• vessel diameter
• blood pressure
• velocity of blood flow
• Arterial pressure is
variable
– Example: 120/90
• systolic pressure
• diastolic pressure
– Pulse pressure (difference
between systolic and
diastolic)
• Example: 120 – 90 = 30 mm
Hg
• Mean arterial pressure
(MAP)
Mean arterial pressure
• the average arterial pressure during a single
cardiac cycle
– perfusion pressure = driving force that pushes
blood through the systemic circuit
• MAP = 1/3(PSyst) + 2/3(PDiast)
• MAP = CO x TPR
– Total peripheral resistance: the force that
opposes the flow of blood
Peripheral resistance
• Resistance opposes
flow (R=8nl/πr4)
• Vasomotor
– vessel radius: principal
method of blood flow
control
– blood in direct contact
w/ vessel wall
Congestive heart failure
(CHF)
– Progressive condition; CO is so low that blood
circulation inadequate to meet tissue needs
– Pulmonary congestion
• LH failure  blood backs up in lungs
– Peripheral congestion
• RH failure  blood pools in body organs  edema
– Failure of either side ultimately weakens other
– Treat by removing fluid, reducing afterload,
increasing contractility
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