chapter 9 the cardiovascular system
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Chapter 9 The Cardiovascular System. Learning Objectives. 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. - PowerPoint PPT PresentationTRANSCRIPT
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Chapter 9
The Cardiovascular System
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Learning Objectives
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.)
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
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.)
Pericardium Double walled sac enclosing heart
Pericarduim’s structure 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
Pericardial fluid Thin layer of fluid separating parietal & visceral
pericardium Helps minimize friction during contraction &
expansion Pericardial effusion
Abnormal amount of accumulated fluid between layers
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The Heart
Cardiac tamponade Large pericardial effusion may affect pumping
function Can cause serious drop in blood flow to body
• May ultimately lead to shock & death
Pericarditis 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.)
Heart wall is composed of 3 layers: 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 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
AV valves lie between atria & ventricles 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
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) Pulmonary valve lies between right ventricle &
pulmonary artery Aortic valve lies between left ventricle & aorta
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Semilunar Valves (cont.)
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
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.)
Right & left coronary arteries arise under aortic valve cusps 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)
Positioned underneath aortic semilunar valves
LCA branches into: 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.)
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)
RCA proceeds around right side of heart between right atrium & right ventricle 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
Myocardial Ischemia Partial obstruction of coronary artery Decreasing oxygen supply to tissue a.k.a. Angina Pectoris
Myocardial Infarction (MI) Sometimes called “infarct” Complete obstruction of coronary artery Causes death of heart tissue
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Coronary Veins Collect venous blood after passing through myocardial
capillary bed Veins closely parallel coronary arteries
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 Normal anatomic shunt = 2-3% of total cardiac output
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Properties of Heart Muscle
Heart’s ability to pump depends on: Initiating & conducting electrical impulses Synchronous myocardial contraction
Made possible by key properties of myocardial tissue 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 featurecannot go into tetany
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Properties of Heart Muscle (cont.)
Refractory period 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
Composed of 2 major subdivisions: Systemic vasculature Pulmonary vasculature
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: 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.)
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 3 components:
Arterial system (conductance vessels)• Large elastic low resistance arteries• Small muscular arterioles (resistance vessels)
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
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
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)/COWhere: MAP = mean aortic pressure
RAP = right atrial pressure or CVP
CO = cardiac output
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Pulmonary Vascular Resistance (PVR)
PVR: sum of all opposing forces to blood flow through pulmonary circulation
PVR then calculated as is SVR (ΔP/flow)
PVR = (MPAP – LAP)/COWhere: MPAP = mean pulmonary artery pressure
LAP = left atrial pressure or wedge pressure
CO = cardiac output
PVR: normally much lower than SVR as pulmonary system is low pressure, low resistance
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Determinants of Blood Pressure (BP)
Normal CV function maintains blood flow throughout body
Under changing conditions, need constant BP
MAP = CO × SVR
And
MAP = Volume/Capacity To maintain BP, capacity must vary inversely
with CO or volume
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Determinants BP(cont.)
Normal adult: MAP values range: 80 to 100 mm Hg
If MAP falls significantly below 60 mm Hg Perfusion to brain & kidneys is severely
compromised Organ failure may occur in minutes
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Control of Cardiovascular System
The heart works as a demand pump 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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Cardiac Output (CO) & its Regulation
CO = total amount of blood pumped by heart per minute
CO = Heart rate (HR) × stroke volume (SV) Normal CO = 5 L/min End Diastolic Volume (EDV): blood left in atria
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CO & its Regulation (cont.)
End Systolic Volume (ESV): blood left in ventricles HR is primarily determined by CNS
• CO is directly related to HR HR > 160180 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 Preload essentially equals venous return
Amount of volume & pressure at end diastole (EDV, EDP) stretches myocardium
• Greater the stretch, the stronger the contraction Frank-Starling Law
Normal EDV is ~110120 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.) Afterload: resistance against which ventricles
pump, so more afterload makes it harder for ventricles to eject SV 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.)
Afterload represents sum of all external factors opposing ventricular ejection Tension in ventricular wall Peripheral resistance or impedance
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Stroke Volume & Contractility Contractility: amount of force myocardium
produces at any EDV Increased contractility results in greater EF for any
EDV• Called positive inotropism
If afterload & contractility increase together, SV is maintained
Positive inotropes Drugs that increase contractility of heart muscle
Negative inotropes 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. decrease the force of contractions
B. increase the force of contractions
C. not affect the force of contractions
D. intermittently increase & decrease the force of contractions
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Cardiovascular Control Mechanisms
Integration of local & central mechanisms to ensure all tissues have enough blood flow Normally, local control is primary determinant With large changes in demand, central control
becomes primary Central control in medulla has areas for:
Vasoconstrictionincreases adrenergic output Vasodepressorinhibits vasoconstrictor center Cardioacceleratoryincreases heart rate Cardioinhibitorydecrease 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. Vasoconstriction
B. increased heart rate
C. decreased heart rate
D. inhibition of the vasoconstrictor center
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Peripheral Receptors: Baroreceptors
Baroreceptors respond to pressure changes: First set: Arch of aorta & carotid sinus
• Monitor arterial pressures generated by left ventricle. Second set: Atrial walls, large thoracic & pulmonary
veinslow-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
Located in aortic arch & carotid sinus Respond to changes in blood chemistry
Decreased PaO2 provides strong stimulus
Low pH & high PaCO2
Major CV response to increased output is vasoconstriction & increased heart rate Occurs only when CV system is overtaxed:
generally little effect
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Response to Changes in Volume
Best noted under abnormal conditions Hemorrhage sets up this sequelae:
• 10% blood volume loss decreases CVP
• 50% decrease in baroreceptor discharge ⇑ 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 Figure 9-14 provides visual summary of
mechanical, electrical, & auditory events during cardiac cycle
A. Timing of cardiac eventsB. Simultaneous pressures created throughout CV systemC. Electrical activity D. Heart sounds corresponding to cardiac cycleE. 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.)