Chapter 9 The Cardiovascular System

Copyright © 2013, 2009, 2003, 1999, 1995, 1990, 1982, 1977, 1973, 1969 by Mosby, an imprint of Elsevier Inc.

Chapter 9

The Cardiovascular System

Copyright © 2013, 2009, 2003, 1999, 1995, 1990, 1982, 1977, 1973, 1969 by Mosby, an imprint of Elsevier Inc. 2

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.


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.


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


The Vascular System (cont.)


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


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


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


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


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


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


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


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


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


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


Stroke Volume and Contractility (cont.)


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


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)


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


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


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


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


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


Events of the Cardiac Cycle (cont.)

Documents

Chapter 9 The Cardiovascular System