Transcript Chapter_009

Chapter 9
The Cardiovascular System
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Learning Objectives
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Describe the anatomy of the heart and vascular
systems.
State the key characteristics of cardiac tissue.
Calculate systemic vascular resistance given mean
arterial pressure, central venous pressure, and
cardiac output.
Describe how local and central control mechanisms
regulate the heart and vascular systems.
Describe how the cardiovascular system
coordinates its functions under normal and
abnormal conditions.
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Learning Objectives (cont.)
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Calculate cardiac output given stroke volume
and heart rate.
Calculate ejection fraction given stroke
volume and end-diastolic volume.
Identify how the electrical and mechanical
events of the heart relate to a normal cardiac
cycle.
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Functional Anatomy
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Heart is hollow, four chambered, muscular,
roughly fist-sized
Lies just behind the sternum, two thirds lie to
left, between the second through the sixth ribs
Heart apex at fifth intercostal space
Surface grooves (sulci) mark the boundaries of
the heart chambers
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Functional Anatomy (cont.)
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Pericardium
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Double walled sac enclosing heart
Pericarduim’s structure
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Outer fibrous layer: Tough connective tissue,
loose-fitting, inelastic sac surrounding heart
 Inner serous layer: thinner, more delicate
 Serous pericardium: Consisting of two layers:
• Parietal layer: Inner lining of fibrous pericardium
• Visceral layer (epicardium): covering outer surface of
heart & great vessels
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Functional Anatomy (cont.)
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The Heart
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Pericardial fluid
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Thin layer of fluid separating parietal & visceral
pericardium
Helps minimize friction during contraction &
expansion
Pericardial effusion
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Abnormal amount of accumulated fluid between
layers
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The Heart
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Cardiac tamponade
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Large pericardial effusion may affect pumping
function
Can cause serious drop in blood flow to body
• May ultimately lead to shock & death
Pericarditis
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Inflammation of pericardium
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What is the function of the pericardial fluid ?
A. helps minimize friction during heart contraction
& expansion
B. provide protection against trauma
C. mark the boundaries of the chambers of the
heart
D. prevents atrial backflow during ventricular
contraction
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The Heart (cont.)
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Heart wall is composed of 3 layers:
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Outer: epicardium
Middle: myocardium comprises bulk of heart & is
composed of muscle tissue
Inner: Endocardium
• Forms thin continuous tissue with blood vessels
Heart forms 4 muscular chambers
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Upper chambers, right & left atria
Lower chambers are right & left ventricles
• Responsible for forward movement of blood
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The Heart (cont.)
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Atrioventricular Valves
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AV valves lie between atria & ventricles
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Tricuspid valve is at right atrium exit
Mitral valve at left atrium exit
Ventricular contraction forces valves closed,
preventing backflow of blood into atria
Lower ends of valves anchor to ventricular
papillary muscles by chordae tendineae
• Papillary contraction during systole pulls on chordae,
preventing valve reversing into atria
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Atrioventricular Valves (cont.)
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What is the role of ventricular contraction ?
A. relaxes chordae tendineae, preventing valves
reversing into atria
B. to rest the heart muscle
C. to forward movement of blood
D. prevents atrial blood backflow
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Semilunar Valves
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Consist of 3 half-moon shaped cusps
Separates ventricles from their arterial outflow
tracts, pulmonary artery & Aorta
Situated at ventricle exits to outflow tracks
(arterial trunks)
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Pulmonary valve lies between right ventricle &
pulmonary artery
Aortic valve lies between left ventricle & aorta
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Semilunar Valves (cont.)
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Systole: (cardiac contraction) valves open,
allowing ventricular ejection into arteries
(pulmonary artery and aorta)
Diastole: valves close preventing back flow of
blood into ventricles
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Coronary Circulation
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Heart’s high metabolic demands require an
extensive circulatory system
The heart requires more blood flow per gram
of tissue weight than any other organ besides
kidneys
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Coronary Circulation (cont.)
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Right & left coronary arteries arise under
aortic valve cusps
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Coronary artery pressure becomes higher than
aortic pressure during systole
Prevents flow of blood into coronaries
Diastole is when coronary blood flow occurs thus,
diastolic pressure is very important
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Left Coronary Artery (LCA)
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Positioned underneath aortic semilunar
valves
LCA branches into:
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Left anterior descending (LAD): courses between
left & right ventricles
Circumflex: courses around left side of heart
between left atrium & left ventricle
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LCA (cont.)
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LCA provides blood to left atrium, left
ventricle, majority of interventricular septum,
half of interatrial septum, & part of right atrium
See Figure 9-4 & Table 9-1
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LCA (cont.)
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Right Coronary Artery (RCA)
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RCA proceeds around right side of heart
between right atrium & right ventricle
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Many small branches as RCA moves around right
ventricle
RCA ends in its posterior descending (RPD)
branch, which courses between right & left
ventricles.
Provides blood flow to most of right ventricle &
right atrium, including sinus node
See Figure 9-4 & Table 9-1
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Problems With Coronary Blood Flow
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Myocardial Ischemia
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Partial obstruction of coronary artery
Decreasing oxygen supply to tissue
a.k.a. Angina Pectoris
Myocardial Infarction (MI)
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Sometimes called “infarct”
Complete obstruction of coronary artery
Causes death of heart tissue
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Coronary Veins
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Collect venous blood after passing through myocardial
capillary bed
Veins closely parallel coronary arteries
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Great cardiac vein follows LAD
Small cardiac vein follows RCA
Left posterior vein follows circumflex
Middle vein follows RPD
These all come together to form coronary sinus, which empties
into right atrium
Thebesian veins drain some coronary venous blood into all heart
chambers
• Those draining into left atrium & left ventricle bypass lungs, creating
an anatomic shunt
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Normal anatomic shunt = 2-3% of total cardiac output
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Properties of Heart Muscle
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Heart’s ability to pump depends on:
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Initiating & conducting electrical impulses
Synchronous myocardial contraction
Made possible by key properties of myocardial
tissue
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Excitability: ability to respond to stimuli
Inherent rhythmicity: initiation of spontaneous
electrical impulse
Conductivity: spreads impulses quickly
Contractility: contraction in response to electrical
impulse
• Unique featurecannot go into tetany
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Properties of Heart Muscle (cont.)
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Refractory period
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Time period myocardium cannot be stimulated
Lasts 250 milliseconds; nearly as long as systole
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Properties of Heart Muscle (cont.)
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The Vascular System
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Composed of 2 major subdivisions:
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Systemic vasculature begins with aorta on left ventricle &
ends in right atrium
Pulmonary vasculature begins with pulmonary trunk out of
right ventricle & ends in left atrium
Systemic venous blood returns to right atrium via:
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Systemic vasculature
Pulmonary vasculature
Superior vena cava (SVC): drains upper extremities & head
Inferior vena cava (IVC): drains lower body
Blood flows through tricuspid valve into right ventricle
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The Vascular System (cont.)
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Pumped from right ventricle through pulmonary
valve into pulmonary artery, which carries it to
lungs (oxygenation)
Pulmonary arterial blood returns via pulmonary
veins to left atrium
From left atrium oxygenated blood flows through
mitral valve into left ventricle
Left ventricle pumps the blood out through aortic
valve into systemic circulation
Blood passes through systemic capillary beds
into systemic veins & back to SVC & IVC
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The Vascular System (cont.)
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Where does systemic vasculature begin & end?
A. begins in the right atrium & ends in the right
ventricle
B. begins in the aorta on the left ventricle & ends
in the right atrium.
C. begins in the pulmonary trunk out of the right
ventricle & ends in the left atrium.
D. begins the left atrium & ends in the inferior
vena cava
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Systemic Vasculature
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3 components:
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Arterial system (conductance vessels)
• Large elastic low resistance arteries
• Small muscular arterioles (resistance vessels)
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Major role in distribution & regulation of blood pressure
Like faucets, control local blood flow into capillaries
Capillary system, microcirculation (exchange vessels)
• Transfer of nutrients & waste products
Venous system (capacitance vessels)
• Reservoir for circulatory system
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Generally holds 3/4 of body’s blood volume
Conduct blood back to heart
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Systemic Vasculature (cont.)
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Vascular Resistance
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Sum of all opposing forces to blood flow through
systemic circulation is systemic vascular
resistance (SVR)
SVR = Change (Δ) in pressure from beginning to
end of system, divided by flow
SVR = (MAP – RAP)/CO
Where: MAP = mean aortic pressure
RAP = right atrial pressure or CVP
CO = cardiac output
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Pulmonary Vascular Resistance
(PVR)
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PVR: sum of all opposing forces to blood flow
through pulmonary circulation
PVR then calculated as is SVR (ΔP/flow)
PVR = (MPAP – LAP)/CO
Where: MPAP = mean pulmonary artery pressure
LAP = left atrial pressure or wedge pressure
CO = cardiac output
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PVR: normally much lower than SVR as
pulmonary system is low pressure, low
resistance
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Determinants of Blood Pressure (BP)
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Normal CV function maintains blood flow
throughout body
Under changing conditions, need constant BP
MAP = CO × SVR
And
MAP = Volume/Capacity
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To maintain BP, capacity must vary inversely
with CO or volume
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Determinants BP(cont.)
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Normal adult: MAP values range:
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80 to 100 mm Hg
If MAP falls significantly below 60 mm Hg
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Perfusion to brain & kidneys is severely
compromised
 Organ failure may occur in minutes
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Control of Cardiovascular System
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The heart works as a demand pump
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CV system may alter capacity - how much blood it
holds
Decreased capacity results in greater venous
return & greater CO
CV system tells heart how much to pump
• Accomplished by local & central control mechanisms
Heart plays secondary role in regulating blood flow
Blood flow through large veins can also be
affected by abdominal & intrathoracic pressure
changes
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CO & its Regulation (cont.)
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End Systolic Volume (ESV): blood left in
ventricles
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HR is primarily determined by CNS
• CO is directly related to HR
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HR > 160180 is exception; too little time for filling results
in decreased EDV, EF, SV, &, thus, CO
SV is determined by
• Preload
• Afterload
• Contractility
SV = EDV-ESV
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CO & its Regulation (cont.)
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Stroke Volume & Preload
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Preload essentially equals venous return
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Amount of volume & pressure at end diastole
(EDV, EDP) stretches myocardium
• Greater the stretch, the stronger the contraction
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Frank-Starling Law
Normal EDV is ~110120 ml
Normal SV is ~70 ml
Ejection fraction (EF) = SV/EDV
• Normal ~65%
• If it falls to 30% range or below, patient’s exercise
tolerance becomes severely limited
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Stroke Volume & Preload (cont.)
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Stroke Volume & Preload (cont.)
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Afterload: resistance against which ventricles
pump, so more afterload makes it harder for
ventricles to eject SV
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RV afterload = PVR
 LV afterload = SVR
 All else constant, increase in vascular resistance
would decrease SV
• Usually does not occur as contractility increases to
maintain SV & thus CO
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Stroke Volume & Preload (cont.)
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Afterload represents sum of all external
factors opposing ventricular ejection
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Tension in ventricular wall
Peripheral resistance or impedance
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Stroke Volume & Contractility
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Contractility: amount of force myocardium
produces at any EDV
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If afterload & contractility increase together,
SV is maintained
Positive inotropes
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Increased contractility results in greater EF for any
EDV
• Called positive inotropism
Drugs that increase contractility of heart muscle
Negative inotropes
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Drugs decreasing contractility of heart muscle
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Stroke Volume and Contractility
(cont.)
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If a patient is given Dobutamine, a positive
inotropic drug, how is contraction of the heart
affected?
A.
B.
C.
D.
decrease the force of contractions
increase the force of contractions
not affect the force of contractions
intermittently increase & decrease the force of
contractions
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Cardiovascular Control Mechanisms
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Integration of local & central mechanisms to
ensure all tissues have enough blood flow
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Normally, local control is primary determinant
 With large changes in demand, central control
becomes primary
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Central control in medulla has areas for:
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Vasoconstrictionincreases adrenergic output
Vasodepressorinhibits vasoconstrictor center
Cardioacceleratoryincreases heart rate
Cardioinhibitorydecrease heart rate (by
increasing vagal stimulation to heart)
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Cardiovascular Control Mechanisms
(cont.)
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Stimulation of the cardioinhibitory area in the
medulla (brainstem) results in:
A.
B.
C.
D.
Vasoconstriction
increased heart rate
decreased heart rate
inhibition of the vasoconstrictor center
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Peripheral Receptors: Baroreceptors
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Baroreceptors respond to pressure changes:
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First set: Arch of aorta & carotid sinus
• Monitor arterial pressures generated by left ventricle.
Second set: Atrial walls, large thoracic & pulmonary
veinslow-pressure monitors
• Respond to volume changes
Baroreceptor output is directly proportional to vessel
stretch
• Negative feedback system: greater stretch causes venodilation
& decreased heart rate & contractility
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Peripheral Receptors:
Chemoreceptors
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Located in aortic arch & carotid sinus
Respond to changes in blood chemistry
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Decreased PaO2 provides strong stimulus
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Low pH & high PaCO2
Major CV response to increased output is
vasoconstriction & increased heart rate
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Occurs only when CV system is overtaxed:
generally little effect
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Response to Changes in Volume
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Best noted under abnormal conditions
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Hemorrhage sets up this sequelae:
• 10% blood volume loss decreases CVP
• 50% decrease in baroreceptor discharge
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⇑ Sympathetic discharge increases HR
• ADH begins to rise
• Normal BP is maintained
 Blood loss approaches 30%, BP starts to fall
• Aortic barorecptors now increase output
• If no further blood loss, BP still maintained
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Response to Changes in Volume
(cont.)
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Response to Changes in Volume
(cont.)
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Events of Cardiac Cycle
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Figure 9-14 provides visual summary of
mechanical, electrical, & auditory events
during cardiac cycle
A. Timing of cardiac events
B. Simultaneous pressures created throughout
CV system
C. Electrical activity
D. Heart sounds corresponding to cardiac cycle
E. Ventricular blood volume during cardiac cycle

Understanding cause & effect of each event
will help you attain mastery of cycle
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Events of the Cardiac Cycle (cont.)
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