Chapter 20: The Heart

BIO 211 LectureInstructor: Dr. Gollwitzer

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• Today in class we will discuss:– The heart and the heartbeat• The 2 types of cardiocytes (heart muscle cells) involved

– The structure and characteristics of contractile cells– Structures of cardiac muscle tissue– The events of an action potential (AP) in cardiac

muscle• AP of cardiac muscle compared to skeletal muscle

– The role of calcium (Ca2+) ions in the contractile process

– The components and functions of the conducting system of the heart

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Heart• Main function is to:– Receive blood from veins at low pressure, – Pump it through arteries at pressure high enough

to get it through blood vessels and– Back to heart again

• Heartbeat = single contraction of the heart

• Entire heart contracts in specific sequence so that blood flows in right direction at right time– First the atria– Then the ventricles

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Heart and the Heartbeat• Contraction of atria first and then ventricles

occurs because contractions of individual cardiac muscle cells that make up heart chambers occur in a specific sequence

• Involves 2 types of cardiac muscle cells– Contractile cells• Produce contractions that move blood through heart

– Conducting system cells• Control and coordinate contractile cells• Control and coordinate heartbeat

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Contractile Cells

• Cardiocytes • 99% of muscle cells in heart• Make up most of atria and ventricle walls

(myocardium)• Form branched network

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Cardiac Muscle Tissue• Myofibrils striations– Thin filaments (actin)– Thick filaments (myosin)

• Intercalated discs– Region in muscle tissue where membranes of

adjacent cardiac muscle cells are interconnected– Transfer force of contraction from cell to cell– Have 2 types of cell junctions• Gap junctions

– Allow ions and small molecules to move easily between cells

– Form direct electrical connection between cardiocytes• Desmosomes

– Interlock adjacent cardiac cells together to prevent cells from separating during contraction

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Fig. 10-3 7

Fig. 20-5 8

Review: Action Potential in a Neuron

Table 12-38th Edition 9

Contraction of Cardiac Muscle

• Action potential (AP)– = Electrical impulse conducted by muscle fiber– Leads to appearance of Ca2+ among myofibrils

• Ca2+ binds to troponin (muscle protein) on actin (thin filaments)– Initiates contraction

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Origin of AP in Cardiac Muscle

• Resting membrane potential of ventricular contractile cell = -90 mV

• Stimulus = excitation of cardiac muscle cell• Membrane of muscle cell brought to

threshold (-75 mV)– Usually reached next to intercalated disc– AP begins

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Fig. 20-15a

Action Potential in Cardiac Muscle

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Action Potential in Cardiac Muscle• Proceeds in 3 steps

– Depolarization • Voltage-regulated fast Na+ channels open, Na+ rushes into cell• Na+ channels close when transmembrane potential reaches +30 mV

– Plateau• As Na+ channels close, voltage-regulated slow Ca2+ channels open, Ca2+

enters cell• Provides 20% of Ca2+ required for contraction; 80% from SR• Transmembrane potential remains at 0 mV for extended period of time

(during Ca2+ entry)• Ends with closure of slow Ca2+ channels

– Repolarization• As Ca2+ channels close, slow K+ channels open• K+ leaves cells• Restores resting potential to -90mV

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Refractory Period• = Time after action potential begins when muscle will

not respond normally to a second stimulus• Absolute refractory period– Time after AP when membrane absolutely cannot respond

because Na+ channels opened/closed– Long in length– Lasts thru plateau and initial part of repolarization (approx.

200 msec)

• Relative refractory period– = time following absolute refractory period when muscle

can respond to stronger-than-normal stimulus– Shorter than absolute refractory period– Lasts thru repolarization (approx. 50 msec)

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Action Potentials in Cardiac and Skeletal Muscle

Figure 20–15a, b 15

Conducting System• Cardiac muscle contracts on its own – Autorhythmicity or automaticity– vs. neural/hormonal stimulation for skeletal

muscle• System of specialized cardiac muscle cells– Initiate and distribute electrical impulses that

stimulate contractions

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Conducting System• 3 Components to cardiac conduction

(nodal) system– Sinoatrial (SA) node– Atrioventricular (AV) node – Conducting cells• From SA node to

– Atrial myocardium– AV node along internodal pathways

• From AV node to ventricular myocardium

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Figure 20-11a The Conducting System of the Heart

AV bundle

Components of the conductingsystem

Purkinjefibers

Bundlebranches

Atrioventricular(AV) node

Internodalpathways

Sinoatrial(SA) node

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Sinoatrial (SA) Node• In posterior wall of R atrium near entrance to superior

vena cava• Contains cardiac pacemaker cells– Originate/generate action potential– Reach threshold first– Establish heart rate

• Abnormal function– Tachycardia = heart rate faster than normal

(>100 bpm)– Bradycardia = heart rate slower than normal

(<50 bpm)• Connected to AV node by internodal pathways in atrial

walls19

Atrioventricular Node

• Larger than SA node• In floor of R atrium near opening of coronary

sinus

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Conducting Cells• Smaller than contractile cells• Connect SA and AV nodes• Distribute contractile stimulus throughout

myocardium– Atrial conducting cells• In internodal pathways in atrial walls• Distribute contractile stimulus to atrial muscle cells as

impulse travels from SA node to AV node– Ventricular conducting cells• In IV septum• In AV bundle (bundle of His), L & R bundle branches and

Purkinje fibers that distribute stimulus to ventricular myocardium

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Path of an Impulse from Initiation at SA Node to AV node

• As AP passes from SA to AV node, conducting cells pass stimulus to contractile cells of both atria

• AP then spreads across entire atria via cell-to-cell contact

• Rate of propagation slows as impulse leaves internodal pathway– Nodal cells smaller in diameter than conducting cells– Connections between nodal cells less efficient

• Results in delay at AV node– Important because atria must contract before ventricles

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Fig. 20-13, Step 1 23

Fig. 20-13, Step 2 24

Fig. 20-13, Step 3, 25

AV Bundle, Bundle Branches, and Purkinje Fibers

• Connection between AV node and AV bundle (aka Bundle of His) is only electrical connection between atria and ventricles– Fibrous skeleton around valves “insulates” other AV connections

• When impulse enters AV bundle, it:– Travels to the interventricular septum– Enters the R and L bundle branches

• Both bundle branches extend toward the apex of the heart and fan out deep into the endocardial surface

• As branches diverge, they conduct impulse to:– Purkinje fibers– Papillary muscles of right ventricle

• Purkinje fibers radiate from apex to base– Contraction of ventricles occurs as a wave that begins at the apex and

spreads toward the base

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Fig. 20-13, Step 4 27

Fig. 20-13, Step 5 28

Summary of Cardiac Conduction

• Before each heart beat (contraction)– Action potential initiated spontaneously at SA

node – Wave of depolarization radiates from SA node– Spreads through contractile cells of atrial

myocardium– To AV node– Travels down IV septum to apex– Turns and spreads through contractile cells of

ventricular myocardium to the base

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• Today in class we will discuss:– The electrocardiogram• Important features of an electrocardiogram recording• The electrical events associated with an electrocardiogram

– The cardiac cycle• The events that occur during the cardiac cycle• How different heart sounds are related to specific events in

the cardiac cycle• Cardiac arrhythmias

– Cardiac output and describe factors that influence it– Age related changes in the heart

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Figure 20-13a An Electrocardiogram

Electrode placement forrecording a standard ECG.

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Electrocardiogram (ECG, EKG)• = Record of electrical events in heart• Associated with conduction/propagation of

heart beat– Strong enough to be detected on body surface

• Can monitor electrical activity of heart by comparing info from electrodes at specific body locations

• ECGs reveal abnormal patterns of impulse conduction– When portion of heart is damaged, those cells

no longer conduct AP

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Figure 20-13b An Electrocardiogram

800 msec

SQ

QRS interval(ventricles depolarize)

Millivolts

R

P–R segmentT wave

(ventricles repolarize)

R

P wave(atria

depolarize)S–T

segment

S–Tinterval

Q–Tinterval

P–Rinterval

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Electrocardiogram• Important features of an ECG– P wave = atrial depolarization

• Small wave• Atria start contracting about 100 msec after start of Pwave

– QRS complex = ventricular depolarization and atrial repolarization• Strong signal because ventricular muscle more massive

than atrial muscle• Complex because also includes atrial repolarization• Ventricles start contracting shortly after peak of R wave

– T wave = ventricular repolarization• Small, like P wave

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ECG Analysis• Measure:– Size of voltage changes: usually focused on

amount of depolarization occurring during P wave and QRS complex• Small P wave = mass of heart muscle decreased• Large QRS = heart has become enlarged• Small T wave = affected by anything that slows

ventricular repolarization– e.g., starvation, low cardiac energy reserves, coronary

ischemia, abnormal ion concentration

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ECG Analysis• Measure:– Duration and temporal relationships of various

components– Reported as intervals• P-R interval

– = From start of P wave to start of QRS complex– Extension may indicate damage to atrial conducting pathways

or AV node

• Q-T interval– = From end of P-R interval to end of T wave– Extension may indicate conduction problems, coronary

ischemia, myocardial damage, congenital heart defect

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Cardiac Arrhythmias

• = Abnormal patterns of electrical activity• Normal if transient• Clinical problems may develop and reduce

pumping efficiency of heart• May indicate:– Damage to myocardium– Injury to pacemaker or conducting pathways– Exposure to drugs– Variation in electrolyte concentration

• Asystole = flatline

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Figure 20–119th Edition

Cardiac Cycle

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Cardiac Cycle• = Period between start of one heartbeat and

beginning of next– Includes electrical events and associated blood

flow– Lasts approx. 0.8 sec in resting adult (72/min)

• Involves alternating periods of contraction and relaxation of atria and ventricles

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Cardiac Cycle• Systole = contraction (squeezing) of chambers– Pressure in chambers rises (systolic pressure)– In RV=30 mm Hg (only pumps blood through pulmonary circuit)– In LV=120 mm Hg (pumps blood through systemic circuit)– Pushes blood into adjacent chamber or arterial trunks

• Diastole = relaxation (dilation) of chambers– Pressure in chambers drops– Chambers fill with blood and prepare for next cardiac cycle

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Cardiac Cycle• Blood flows from one chamber to another only

if pressure in first exceeds that of second– Controlled by timing of contractions– Directed by 1-way valves

• Phases of cardiac cycle– Atrial systole– Atrial diastole– Ventricular systole – Ventricular diastole

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Figure 20-16a Phases of the Cardiac Cycle

Cardiaccycle

100 msec

0msec800

msec

Atrial systole begins:Atrial contraction forces a small amount of

additional blood into relaxed ventricles.

Start

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Figure 20-16b Phases of the Cardiac Cycle

Cardiaccycle

100 msec

Atrial systole ends,atrial diastole

begins

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Figure 20-16c Phases of the Cardiac Cycle

Cardiaccycle

Ventricular systole—first phase: Ventricularcontraction pushes AVvalves closed but does

not create enoughpressure to opensemilunar valves.

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Figure 20-16d Phases of the Cardiac Cycle

Cardiaccycle

370msec

Ventricular systole—second phase: As

ventricular pressure risesand exceeds pressure

in the arteries, thesemilunar valvesopen and blood

is ejected.45

Figure 20-16e Phases of the Cardiac Cycle

Cardiaccycle

370msec

Ventricular diastole—early:As ventricles relax, pressure in

ventricles drops; blood flows backagainst cusps of semilunar valves

and forces them closed. Bloodflows into the relaxed atria.

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Figure 20-16f Phases of the Cardiac Cycle

Cardiaccycle

Ventriculardiastole—late:

All chambers arerelaxed.

Ventricles fillpassively.

800msec

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Cardiac Cycle• People can usually survive with severe atrial

damage– Because atrial systole makes relatively minor

contribution to ventricular volume• Damage to one or both ventricles leads to heart

failure– Lack of adequate blood flow to peripheral

tissues/organs• Although both atria and ventricles undergo

systole and diastole, terms usually refer to ventricular contraction and relaxation

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Heart Sounds

• Closing of valves and rushing of blood through heart characteristic heart sounds heard during auscultation with stethoscope– AV valves close = “lubb” (S1)– Semilunar valves close = “dubb” (S2)– S3 and S4 are sounds of blood flowing through

heart

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Figure 20-18 Heart Sounds

Semilunarvalves close

AV valvesopen

AV valvesclose

“Dubb”“Lubb”

The relationship between heart sounds and key events in thecardiac cycle

Heart sounds

Pre

ssur

e(m

m H

g)

Aorticvalve

Pulmonaryvalve

Valve locationSounds heard

LeftAV

valve

RightAV

valve

Placements of a stethoscope forlistening to the different soundsproduced by individual valves

Valve locationSounds heard

Valve locationSounds heard

Valve locationSounds heard

Aorta

Semilunarvalves open

Leftventricle

Leftatrium

S1

S4S4

S2S3

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Figure 20-17 Pressure and Volume Relationships in the Cardiac Cycle

QRScomplex

Electro-cardiogram

(ECG)

ONE CARDIAC CYCLE

TP

ATRIALSYSTOLE

ATRIAL DIASTOLEATRIALSYSTOLE

ATRIALDIASTOLE

VENTRICULARDIASTOLE

VENTRICULARSYSTOLE

VENTRICULAR DIASTOLE

QRScomplex

P

AV valves open; passive ventricularfilling occurs.

Isovolumetric relaxation occurs.

Semilunar valves close.

Ventricular ejection occurs.

Isovolumetric ventricular contraction.

Atrial systole ends; AV valves close.

Atria eject blood into ventricles.

Atrial contraction begins.

Time (msec)

End-systolicvolume

Strokevolume

End-diastolicvolume

Lef

tve

ntr

icu

lar

volu

me

(mL

)

Pre

ssur

e(m

m H

g)

Aortic valvecloses

Aortic valveopens

Aorta

Dicroticnotch

Leftventricle

Left atriumLeft AV

valve opensLeft AV

valve closes

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Cardiodynamics

• Stroke volume (SV)– = Amount of blood ejected by ventricle during

single beat

• Cardiac output (CO)– = Amount of blood pumped by L ventricle

/minute– CO = SV (stroke volume) x HR– e.g. 80 mL/heartbeat x 72 beats/min = 5,760

mL/min (approx. 1.5 gallons!)– Adjusted by change in SV or HR

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Figure 20-20 Factors Affecting Cardiac Output

End-systolicvolume

End-diastolicvolume

HormonesAutonomicinnervation

STROKE VOLUME (SV) = EDV – ESVHEART RATE (HR)

CARDIAC OUTPUT (CO) = HR SV

Factors AffectingHeart Rate (HR)

Factors AffectingStroke Volume (SV)

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Factors Affecting Heart Rate• Autonomic innervation (by ANS)– To SA and AV nodes and atrial muscle cells

• Sympathetic accelerates HR• Parasympathetic slows HR

– Controlled by cardiac centers in medulla oblongata• Monitor chemoreceptors and baroreceptors• e.g. when walls of right atrium stretch b/c of increased venous

return, atrial (Bainbridge) reflex triggered increased sympathetic activity increased heart rate

• Hormones– Thyroid hormone and epinephrine/norepinephrine increase

heart rate– Stimulate SA node

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Cardiovascular Pathology

• Valvular heart disease– = When valve deteriorates and can’t maintain

adequate blood flow– Cause• Congenital malformations• Carditis (inflammation of the heart)

– Rheumatic fever

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Cardiovascular Pathology

• Mitral valve prolapse– Cusps do not close properly• Abnormally long or short chordae tendineae• Malfunctioning papillary muscles

– Regurgitation occurs• Detected by auscultation as a heart murmur (rushing,

gurgling sound)

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Cardiovascular Pathology• Coronary artery disease (CAD)– = Areas of partial or complete blockage of coronary circulation

(usually arteries) coronary ischemia (reduced blood supply to heart)

– Causes• Formation of fatty plaque in wall of vessel• Thrombus (clot)• Spasm of smooth muscle in walls of vessel

– Symptoms• Early: angina pectori (chest pain)• Exertion or emotional stress pressure, chest constriction, pain radiating

from sternal area to arms, back, and neck– Treatment

• Diet, exercise, no smoking• Medication• Balloon angioplasty• Coronary artery bypass graft (CABG), e.g., quadruple bypass)

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Cardiovascular Pathology• Myocardial infarction (MI) (heart attack)– Coronary circulation becomes blocked (occluded)– “Coronary thrombosis” if blockage due to thrombus at

plaque in coronary artery– Result

• Cardiac muscle cells die from lack of O2• Tissue degenerate creating “infarct” (nonfunctional area)

– Consequences: Depend on site and nature of blockage• If near start of coronary artery widespread damage, often fatal• If in smaller arterial branch, may survive with complications

– 25% mortality prior to medical assistance– If >50 y.o. = 65% die within 1 hour after initial infarct

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Damaged Cells vs. Normal Cells• Cells more dependent on anaerobic metabolism

to meet energy needs (due to lack of O2)• Accumulate large numbers of enzymes for

anaerobic metabolism (in cytoplasm)• As cell membranes deteriorate, enzymes enter

surrounding intercellular fluids and circulatory system– Measurable and diagnostic

• LDH = lactate dehydrogenase• CPK or CK = creatine phosphokinase• CK-MB = special creatine phosphokinase found only in

cardiac muscle

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Abnormal Conditions Affecting Cardiac Output

• Abnormal Ca– Hypocalcemia • Contractions weaken and may cease

– Hypercalcemia• Cardiac muscle cells very excitable• Have powerful, prolonged contractions• Extreme case: heart goes into extended state of

contraction that is usually fatal

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Abnormal Conditions Affecting Cardiac Output

• Abnormal K– Hypokalemia• Cells less responsive to stimulation and heart rate

decreases• Blood pressure falls• Heart eventually stops

– Hyperkalemia• Muscle cells depolarize, repolarization inhibited• Contractions weak and irregular• In severe cases, heart stops

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Abnormal Conditions Affecting Cardiac Output

• Abnormal body temperature– Reduced body temperature• Slows rate of depolarization at SA node, lowers

heart rate, reduces strength of cardiac contractions• In open heart surgery, heart chilled until it stops

beating

– Elevated body temperature• Accelerates heart rate and contractile force• Pounding and racing heart during high fever

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Age-related Changes

• Reduction in maximum cardiac output• Changed activity of nodal and conducting cells• Reduced elasticity• Progressive atherosclerosis that restricts

coronary circulation• Replacement of damaged cardiac muscle cells

by scar tissue

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