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