Human Anatomy and Human Anatomy and Physiology Physiology

Cardiovascular System: The Heart: Part B

Heart B ObjectivesHeart B Objectives1. Describe the components of

heart’s intrinsic conduction system

2. Draw and label a normal electrocardiogram tracing

3. Name some abnormalities detected on ECG tracing

4. Describe normal heart sounds5. Name and explain the effects of

common factors that regulate stroke volume and heart rate

What do you Remember What do you Remember about Physiological roles of about Physiological roles of Calcium?Calcium?

Bones: Structure of bone matrix◦ Osteoblasts/ osteoclasts◦ PTH/ to some extent calcitonin

Muscle contraction◦ Excitation-contraction coupling

Role in blood clottingRole in cell stimulation as second messengerNerve impulse

◦ Neurotransmitter release via gated Ca+2 channels

◦ For depolarization in some special senses

Figure 17.12

Absoluterefractoryperiod

Tensiondevelopment(contraction)

Plateau

Actionpotential

Time (ms)

1

2

3

Depolarization isdue to Na+ influx throughfast voltage-gated Na+

channels. A positivefeedback cycle rapidlyopens many Na+

channels, reversing themembrane potential.Channel inactivation endsthis phase.

Plateau phase isdue to Ca2+ influx throughslow Ca2+ channels. Thiskeeps the cell depolarizedbecause few K+ channelsare open.

Repolarization is due to Ca2+ channels inactivating and K+

channels opening. This allows K+ efflux, which brings the membranepotential back to itsresting voltage.

1

2

3

Tensi

on (

g)

Mem

bra

ne p

ote

nti

al (m

V)

Energy Requirements of Energy Requirements of Cardiac MuscleCardiac Muscle

1. More mitochondria2. Aerobic respiration

Means it must get oxygen

3. Any energy sourceglucoselipids/ fatty acidsproteins lactic acid

ISCHEMIC

Figure 17.13

1 2 3 Pacemaker potentialThis slow depolarization is due to both opening of Na+

channels and closing of K+

channels. Notice that the membrane potential is never a flat line.

Depolarization The action potential begins when the pacemaker potential reaches threshold. Depolarization is due to Ca2+

influx through Ca2+ channels.

Repolarization is due to Ca2+ channels inactivating and K+ channels opening. This allows K+ efflux, which brings the membrane potential back to its most negative voltage.

Actionpotential

Threshold

Pacemakerpotential

1 1

2 2

3

AutorhythmicAutorhythmic Cells Cells ReviewReview

Have unstable resting potentials (pacemaker potentials or prepotentials) due to open slow Na+ channels

At threshold, Ca2+ channels open Explosive Ca2+ influx produces the

rising phase of the action potentialRepolarization results from

inactivation of Ca2+ channels and opening of voltage-gated K+ channels

Remember our neurons and skeletal muscles can stay at a resting membrane potential

Heart Physiology: Electrical Heart Physiology: Electrical EventsEventsThe cardiac muscle does not depend

on the nervous system to contractSetting the basic heart contraction

rhythm depends on:◦Presence of gap junctions◦Intrinsic cardiac conduction system:

A network of noncontractile (autorhythmic) cells that initiate and distribute impulses to coordinate the depolarization and contraction of the heart

Autorhythmic cardiac cellsAutorhythmic cardiac cellsNot all cardiac muscle cells are

autorhythmic…only a small percentageLocated throughout heart to set up a

stimulation sequenceSinatrial node → atrioventricular node →

atrioventricular bundle → right and left bundle branches

→Purkinje fibers in ventricular

walls

Figure 17.14a

(a) Anatomy of the intrinsic conduction system showing the sequence of electrical excitation

Internodal pathway

Superior vena cavaRight atrium

Left atrium

Purkinje fibers

Inter-ventricularseptum

1 The sinoatrial (SA) node (pacemaker)generates impulses.

2 The impulsespause (0.1 s) at theatrioventricular(AV) node. The atrioventricular(AV) bundleconnects the atriato the ventricles.4 The bundle branches conduct the impulses through the interventricular septum.

3

The Purkinje fibersdepolarize the contractilecells of both ventricles.

5

Heart Physiology: Sequence Heart Physiology: Sequence of Excitationof Excitation1. Sinoatrial (SA) node

◦ Known as the Heart Pacemaker◦ Located in right atrial wall just inferior

to entrance of superior vena cava◦ Generates impulses about 75

times/minute ◦ Depolarizes faster than any other part

of the myocardium◦ SA node characteristic rhythm is called

the sinus rhythm and determines the heart rate

Heart Physiology: Sequence Heart Physiology: Sequence of Excitationof Excitation2. Atrioventricular (AV) node

◦ Located on inferior portion of interatrial septum, immediately above tricuspid valve

◦ Smaller diameter fibers; fewer gap junctions

◦ Delays impulses approximately 0.1 second

This allows the atria to respond and complete their contraction before the ventricles contract

◦ Would naturally depolarizes 50 times per minute in absence of SA node input

Heart Physiology: Sequence Heart Physiology: Sequence of Excitationof Excitation3. Atrioventricular (AV) bundle

This is also called the bundle of His◦ In the superior part of the

interventricular septum◦ The atria and ventricles are not

connected by gap junctions so…this is the

◦ Only electrical connection between the atria and ventricles

Heart Physiology: Sequence Heart Physiology: Sequence of Excitationof Excitation4. Right and left bundle branches

◦ Two pathways in the interventricular septum that carry the impulses toward the apex of the heart

Heart Physiology: Sequence Heart Physiology: Sequence of Excitationof Excitation

5. Purkinje fibers◦ Complete the pathway into the apex and

turn superiorly up the ventricular walls◦ Bulk of depolarization along Purkinje

fibers or cell to cell transmission via gap junctions

◦ Because left ventricle is so much larger than right, Purkinje network more elaborate on left

◦ AV bundle and Purkinje fibers naturally depolarize only 30 times per minute in absence of AV node input

Figure 17.14a

(a) Anatomy of the intrinsic conduction system showing the sequence of electrical excitation

Internodal pathway

Superior vena cavaRight atrium

Left atrium

Purkinje fibers

Inter-ventricularseptum

1 The sinoatrial (SA) node (pacemaker)generates impulses.

2 The impulsespause (0.1 s) at theatrioventricular(AV) node. The atrioventricular(AV) bundleconnects the atriato the ventricles.4 The bundle branches conduct the impulses through the interventricular septum.

3

The Purkinje fibersdepolarize the contractilecells of both ventricles.

5

Summary of Intrinsic Summary of Intrinsic Conduction SystemConduction SystemTotal time between initiation of

impulse by SA node and depolarization of last ventricular muscle cell◦.22 seconds in a healthy heart

Ventricular contraction ◦almost immediately follows ventricular

depolarization wave◦a “wringing” motion from apex toward

atria.◦Ejects blood in ventricles into large

arteries

Homeostatic ImbalancesHomeostatic ImbalancesDefects in the intrinsic conduction system

1. Arrhythmias: irregular heart rhythms2. Uncoordinated atrial and ventricular

contractions3. Fibrillation

rapid, irregular contractions; useless for pumping bloodHeart must be defibrillated quickly to prevent death

4. Ectopic focusAbnormal pacemaker or AV node takes over (40-60 bpm)

5. ExtrasystoleSmall region of heart becomes overexcited (caffeine,

nicotine) and adds extra contraction

6. Heart blockAny damage to AV node so ventricles don’t get pacing

impulse

Extrinsic Innervation of the Extrinsic Innervation of the HeartHeart

Heartbeat is modified by the ANS Cardiac centers are located in the

medulla oblongata◦Cardioacceleratory center innervates

SA and AV nodes, heart muscle, and coronary arteries through sympathetic neurons Increases both rate and force of heartbeat

◦Cardioinhibitory center inhibits SA and AV nodes through parasympathetic fibers in the vagus nerves Slows heart beat

Figure 17.15

Thoracic spinal cord

The vagus nerve (parasympathetic) decreases heart rate.

Cardioinhibitory center

Cardio-acceleratorycenter

Sympathetic cardiacnerves increase heart rateand force of contraction.

Medulla oblongata

Sympathetic trunk ganglion

Dorsal motor nucleus of vagus

Sympathetic trunk

AV node

SA nodeParasympathetic fibersSympathetic fibersInterneurons

Salivaryglands

Eye

Skin*

Heart

Lungs

Liverand gall-bladder

Genitals

Pancreas

Eye

Lungs

Bladder

Liver andgall-bladder

Pancreas

Stomach

Cervical

Sympatheticganglia

Cranial

Lumbar

Thoracic

Genitals

Heart

Salivaryglands

Stomach

Bladder

Adrenalgland

Parasympathetic Sympathetic

Sacral

Brainstem

L1

T1

Figure 14.3

Figure 17.16

Sinoatrialnode

Atrioventricularnode

Atrialdepolarization

QRS complex

Ventriculardepolarization

Ventricularrepolarization

P-QInterval

S-TSegment

Q-TInterval

Electrocardiogram (ECG) Electrokardiogram (EKG)

EKG leadsEKG leads

Remember:An EKG/ ECG is a COMPOSITEof all action potentials generated at a given time

Figure 17.16

Sinoatrialnode

Atrioventricularnode

Atrialdepolarization

QRS complex

Ventriculardepolarization

Ventricularrepolarization

P-QInterval

S-TSegment

Q-TInterval

ElectrocardiographyElectrocardiography Electrocardiogram (ECG or EKG): a

composite of all the action potentials generated by nodal and contractile cells at a given time

Three waves1. P wave: depolarization of SA node

Atria contracts .1second after P wave starts

2. QRS complex: ventricular depolarization

Ventricles contract after QRS starts

3. T wave: ventricular repolarizationAtrial reopolarization is masked by large QRS

Figure 17.17

Atrial depolarization, initiatedby the SA node, causes theP wave.

P

R

T

QS

SA node

AV node

With atrial depolarizationcomplete, the impulse isdelayed at the AV node.

Ventricular depolarizationbegins at apex, causing theQRS complex. Atrialrepolarization occurs.

P

R

T

QS

P

R

T

QS

Ventricular depolarizationis complete.

Ventricular repolarizationbegins at apex, causing theT wave.

Ventricular repolarizationis complete.

P

R

T

QS

P

R

T

QS

P

R

T

QS

Depolarization Repolarization

1

2

3

4

5

6

Figure 17.16

Sinoatrialnode

Atrioventricularnode

Atrialdepolarization

QRS complex

Ventriculardepolarization

Ventricularrepolarization

P-QInterval

S-TSegment

Q-TInterval

Figure 17.18

(a) Normal sinus rhythm.

(c) Second-degree heart block. Some P waves are not conducted through the AV node; hence more P than QRS waves are seen. In this tracing, the ratio of P waves to QRS waves is mostly 2:1.

(d) Ventricular fibrillation. These chaotic, grossly irregular ECG deflections are seen in acute heart attack and electrical shock.

(b) Junctional rhythm. The SA node is nonfunctional, P waves are absent, and heart is paced by the AV node at 40 - 60 beats/min.

Reading Heart Rate from Reading Heart Rate from EKGEKG

Each little square is 25mm/sec

Multiply by 60 sec/min

Divide by the number of squares from R to R peak

Alternative method: Count number of

QRS complexes in 6 sec

Multiply by x10

One more methodOne more method

Entire strip is 6 seconds: Entire strip is 6 seconds: This heart rate is __ beats/ This heart rate is __ beats/ min?min?

Heart SoundsHeart SoundsTwo sounds (lub-dub) associated with

closing of heart valves◦First sound occurs as AV valves close and

signifies beginning of systole◦Second sound occurs when SL valves close

at the beginning of ventricular diastole Heart murmurs: abnormal heart sounds

most often indicative of valve problemsBecause mitral (left AV) valve closes

slightly before tricuspid valve (rt AV), the aortic SL generally snaps shut just before the pulmonary valve…so technically can auscultate 4 sounds

Figure 17.19

Tricuspid valve sounds typically heard in right sternal margin of 5th intercostal space

Aortic valve sounds heard in 2nd intercostal space atright sternal margin

Pulmonary valvesounds heard in 2ndintercostal space at leftsternal margin

Mitral valve soundsheard over heart apex(in 5th intercostal space)in line with middle ofclavicle

Mechanical Events: The Mechanical Events: The Cardiac CycleCardiac Cycle

Cardiac cycle: all events associated with blood flow through the heart during one complete heartbeat◦Systole—contraction ◦Diastole—relaxation

Always follow the electrical events seen in the ECG

Marked by a succession of pressure and blood volume changes

Figure 17.20

1 2a 2b 3

Atrioventricular valves

Aortic and pulmonary valves

Open OpenClosed

Closed ClosedOpen

Phase

ESV

Left atriumRight atrium

Left ventricle

Right ventricle

Ventricularfilling

Atrialcontraction

Ventricular filling(mid-to-late diastole)

Ventricular systole(atria in diastole)

Isovolumetriccontraction phase

Ventricularejection phase

Early diastole

Isovolumetricrelaxation

Ventricularfilling

11 2a 2b 3

Electrocardiogram

Left heart

P

1st 2nd

QRSP

Heart sounds

Atrial systole

Dicrotic notch

Left ventricle

Left atrium

EDV

SV

Aorta

T

Ventr

icula

rvolu

me (

ml)

Pre

ssu

re (

mm

Hg

)

Phases of the Cardiac Phases of the Cardiac CycleCycle1. Ventricular filling—takes place in

mid-to-late diastole◦ AV valves are open ◦ 80% of blood passively flows into

ventricles◦ Atrial systole occurs, delivering the

remaining 20% Follows depolarization of P wave Sudden slight rise in atrial pressure

◦ End diastolic volume (EDV): volume of blood in each ventricle at the end of ventricular diastole

Phases of the Cardiac Phases of the Cardiac CycleCycle

2. Ventricular systole◦ Atria relax and ventricles begin to contract ◦ Rising ventricular pressure results in

closing of AV valves◦ Isovolumetric contraction phase (all valves

are closed)◦ In ejection phase, ventricular pressure

exceeds pressure in the large arteries, forcing the SL valves open

◦ At this point blood pressure in aorta reaches 120 mm Hg

◦ End systolic volume (ESV): volume of blood remaining in each ventricle

Phases of the Cardiac Phases of the Cardiac CycleCycle

3. Isovolumetric relaxation occurs in early diastole

◦ Follows T wave◦ Ventricles relax because blood in their

chambers (called end systolic volume or ESV) is no longer compressed

◦ Backflow of blood in aorta and pulmonary trunk closes SL valves and causes dicrotic notch (brief rise in aortic pressure)

◦ Here ventricles are totally closed chambers again

Figure 17.20

1 2a 2b 3

Atrioventricular valves

Aortic and pulmonary valves

Open OpenClosed

Closed ClosedOpen

Phase

ESV

Left atriumRight atrium

Left ventricle

Right ventricle

Ventricularfilling

Atrialcontraction

Ventricular filling(mid-to-late diastole)

Ventricular systole(atria in diastole)

Isovolumetriccontraction phase

Ventricularejection phase

Early diastole

Isovolumetricrelaxation

Ventricularfilling

11 2a 2b 3

Electrocardiogram

Left heart

P

1st 2nd

QRSP

Heart sounds

Atrial systole

Dicrotic notch

Left ventricle

Left atrium

EDV

SV

Aorta

T

Ventr

icula

rvolu

me (

ml)

Pre

ssu

re (

mm

Hg

)

Summary of Cardiac CycleSummary of Cardiac CycleBlood flow through the heart is

controlled by pressure changesBlood flows down a pressure gradient

through any available openingRight and left side essentially same

except for the actual pressure◦Pulmonary circulation is low-pressure

typical systolic and diastolic pressures for pulmonary artery: 24 and 8 mm Hg respectively

◦Systemic circulation must be high pressure Systolic/ diastolic aortic pressure: 120 and 80

mg Hg

Cardiac Output (CO)Cardiac Output (CO)Volume of blood pumped by each

ventricle in one minuteCO = heart rate (HR) x stroke

volume (SV)◦HR = number of beats per minute◦SV = volume of blood pumped out by a

ventricle with each beat

75bpm x 70mL/beat = 5.25 L/ min

Average adult blood volume: 5 L

Cardiac Output (CO)Cardiac Output (CO)◦CO at rest (ml/min) = HR (75 beats/min) SV (70 ml/beat)

= 5.25 L/min◦Cardiac reserve: difference between

resting and maximal CO◦In nonathletic people, the cardiac reserve

is typically 4-5 times the resting cardiac output which is about 20-25 L/ min

◦Maximal CO may reach 35 L/min in trained athletes, which is 7 times the resting CO

Figure 17.22

Venousreturn

Contractility Sympatheticactivity

Parasympatheticactivity

EDV(preload)

Strokevolume

Heartrate

Cardiacoutput

ESV

Exercise (byskeletal muscle andrespiratory pumps;

see Chapter 19)

Heart rate(allows more

time forventricular

filling)

Bloodborneepinephrine,

thyroxine,excess Ca2+

Exercise,fright, anxiety

Initial stimulus

Result

Physiological response

Regulation of Stroke Regulation of Stroke VolumeVolume

SV = EDV (end diastolic volume) – ESVEDV= end diastolic volumeESV=

◦Volume of blood in ventricles and end of filling

◦Sometimes called afterload

Three main factors affect SV◦Preload◦Contractility◦Afterload

Regulation of Stroke Regulation of Stroke VolumeVolumePreload: degree of stretch of cardiac

muscle cells before they contract (Frank-Starling law of the heart)◦ Cardiac muscle exhibits a length-tension

relationship◦ At rest, cardiac muscle cells are shorter

than optimal length◦ Slow heartbeat and exercise increase

venous return ◦ Increased venous return distends

(stretches) the ventricles and increases contraction force

Figure 17.21

Norepinephrine Adenylate cyclase

Ca2+ uptake pump

Ca2+

channel

1-Adrenergicreceptor G protein (Gs)

Ca2+

Sarcoplasmicreticulum (SR)

Activeproteinkinase A

Extracellular fluid

Cytoplasm

Phosphorylates SR Ca2+

pumps, speeding Ca2+

removal and relaxation

Phosphorylates SR Ca2+ channels, increasing intracellular Ca2+

release

Phosphorylatesplasma membraneCa2+ channels,increasing extra-cellular Ca2+ entry

Inactive proteinkinase A

Ca2+

Ca2+Enhancedactin-myosininteraction

Cardiac muscleforce and velocity

ATP is convertedto cAMP

bindsto

SR Ca2+

channel

GDP

Troponin

a

b c

Regulation of Stroke Regulation of Stroke VolumeVolumeContractility: contractile strength at a given

muscle length, independent of muscle stretch and EDV

increase contractility◦ Increased Ca2+ influx into cytoplasm due to

sympathetic stimulation◦ Hormones (thyroxine, glucagon, and

epinephrine)◦ Factors that increase contractility are called

positive inotropic agents (ino= muscle, fiber)Negative inotropic agents decrease

contractility◦ Acidosis◦ Increased extracellular K+

◦ Calcium channel blockers

Regulation of Stroke Regulation of Stroke VolumeVolume

Afterload: pressure that must be overcome for ventricles to eject blood

In most people, afterload is not a major determinant of stroke volume because afterload is relatively constant

Hypertension increases afterload, ◦reducing the ability of ventricles to eject

blood,◦resulting in increased ESV and reduced SV

Regulation of Heart RateRegulation of Heart RateA healthy cardiovascular system

results in relatively constant stroke volume.

Weakened heart or temporary stressors can affect stoke volume and cardiac output◦Positive chronotropic factors increase

heart rate◦Negative chronotropic factors

decrease heart rate

Figure 17.22

Venousreturn

Contractility Sympatheticactivity

Parasympatheticactivity

EDV(preload)

Strokevolume

Heartrate

Cardiacoutput

ESV

Exercise (byskeletal muscle andrespiratory pumps;

see Chapter 19)

Heart rate(allows more

time forventricular

filling)

Bloodborneepinephrine,

thyroxine,excess Ca2+

Exercise,fright, anxiety

Initial stimulus

Result

Physiological response

Autonomic Nervous System Autonomic Nervous System RegulationRegulationSympathetic nervous system is

activated by emotional or physical stressors◦Norepinephrine causes the

pacemaker to fire more rapidly (and at the same time increases contractility)

◦Enhances Ca2+ movements in contractile cells

Autonomic Nervous System Autonomic Nervous System RegulationRegulation

Parasympathetic nervous system opposes sympathetic effects ◦Acetylcholine hyperpolarizes pacemaker

cells by opening K+ channelsThe heart at rest exhibits vagal tone

(parasympathetic) as the dominant influence on SA node

Because vagal innervation of the ventricles is sparse, parasympathetic activity has little or no effect on cardiac contractility

Autonomic Nervous System Autonomic Nervous System RegulationRegulationAtrial (Bainbridge) reflex: a

sympathetic reflex initiated by increased venous return◦Stretch of the atrial walls stimulates

the SA node◦Also stimulates atrial stretch

receptors activating sympathetic reflexes

Chemical Regulation of Heart Chemical Regulation of Heart Rate Rate 1. Hormones

◦ Epinephrine from adrenal medulla enhances heart rate and contractility

◦ Thyroxine increases heart rate and enhances the effects of norepinephrine and epinephrine

2. Intra- and extracellular ion concentrations (e.g., Ca2+ and K+) must be maintained for normal heart function

Other Factors that Influence Other Factors that Influence Heart RateHeart RateAge

◦Resting heart rate fastest in fetus, gradually declines throughout life

Gender◦Faster in females (72-80 bpm) than

males (64-72bpm)Exercise

◦Increases heart rate while exercising, but resting heart rate is lower in physically fit

Body temperature◦Heat increases heart rate by enhancing

metabolic rate of cardiac cells/ cold decreases

Homeostatic ImbalancesHomeostatic ImbalancesTachycardia: abnormally fast heart rate

(>100 bpm)◦May result from elevated body temperature,

stress, certain drugs, or heart disease◦ If persistent, may lead to fibrillation

Bradycardia: heart rate slower than 60 bpm◦May result from low body temperature,

certain drugs, or heart disease◦May be desirable result of endurance training◦May result in grossly inadequate blood

circulation particularly in poorly conditioned people

Congestive Heart Failure Congestive Heart Failure (CHF)(CHF)

Progressive condition where the CO is so low that blood circulation is inadequate to meet tissue needs

Caused by◦Coronary atherosclerosis

Clogging of coronary vessels with fatty buildup◦Persistent high blood pressure

Aortic diastolic pressure over 90 mm Hg◦Multiple myocardial infarcts

Depresses pumping efficiency because of dead heart cells

◦Dilated cardiomyopathy (DCM) Ventricles stretch and become flabby