Copyright © 2010 Pearson Education, Inc. Chapter 18: THE HEART

Copyright © 2010 Pearson Education, Inc.

Chapter 18: THE HEART


Heart Anatomy

•Approximately the size of a fist

•Location

• In the mediastinum between second rib and fifth intercostal space

• On the superior surface of diaphragm

• Two-thirds to the left of the midsternal line

• Anterior to the vertebral column, posterior to the sternum

•Enclosed in pericardium, a double-walled sac

Copyright © 2010 Pearson Education, Inc. Figure 18.1a

Point ofmaximalintensity(PMI)

Diaphragm

(a)

Sternum

2nd rib

Midsternal line

Copyright © 2010 Pearson Education, Inc. Figure 18.1c

(c)

Superiorvena cava

Left lung

AortaParietalpleura (cut)

Pericardium(cut)

Pulmonarytrunk

Diaphragm

Apex ofheart


Pericardium

•3 layers

1. Fibrous pericardium (superficial)

2. Serous pericardium (2 layers)

• Parietal layer

• Visceral layer

• lines the internal surface of the fibrous pericardium

3. Visceral layer (epicardium) on external surface of the heart


Pericardium: Layer Functions

• Fibrous layer

•Protects, anchors, and prevents overfilling

• Serous parietal layer

• lines the internal surface of the fibrous pericardium

•Parietal means relating to or forming the wall of a body part, organ, or cavity

• Serous visceral layer

•on external surface of the heart, known as the epicardium

•Visceral means organs


Percardium: Layer Functions

•The parietal and visceral serous pericardium form a sac or cushion of space around the heart

•This sac is called the pericardial cavity

•Filled with fluid

•Purpose = decrease friction


Figure 18.2

Fibrous pericardium

Parietal layer ofserous pericardiumPericardial cavity

Epicardium(visceral layerof serouspericardium)Myocardium

Endocardium

Pulmonarytrunk

Heart chamber

Heartwall

Pericardium

Myocardium


Layers of the Heart Wall

1. Epicardium—visceral layer of the serous pericardium



2. Myocardium

• Myo = muscle

• Spiral bundles of cardiac muscle cells

• Fibrous skeleton of the heart: crisscrossing, interlacing layer of connective tissue

• Anchors cardiac muscle fibers

• Supports great vessels and valves

• Limits spread of action potentials to specific paths



3. Endocardium is continuous with endothelial lining of blood vessels


Figure 18.2

Fibrous pericardium

Parietal layer ofserous pericardiumPericardial cavity

Epicardium(visceral layerof serouspericardium)Myocardium

Endocardium

Pulmonarytrunk

Heart chamber

Heartwall

Pericardium

Myocardium

Copyright © 2010 Pearson Education, Inc. Figure 18.3

Cardiacmusclebundles


Chambers

•Four chambers

• Two atria (receiving chambers) and two ventricles (discharging chambers)

•Left and right atrium, left and right ventricle

•Coronary sulcus (atrioventricular groove, AV groove) encircles the junction of the atria and ventricles

•Sulcus = deep, narrow groove

•Auricles (ears) increase atrial volume


Chambers

•Two ventricles (discharging chambers)

• Separated by the interventricular septum

• Pumping chambers

•R ventricle pumps blood into the lungs

•L ventricle pumps blood into the body

• Inter = between

• Intra = within


A note on vessels

•Direction of blood flow

•Artery = Away from the heart

• Vein = to the heart

• This is important to remember when looking at the heart; arteries do not always carry oxygenated blood and veins do not always carry deoxygenated blood

•i.e., pulmonary artery carries deoxygenated blood

•Pulmonary veins carry oxygenated blood

Copyright © 2010 Pearson Education, Inc. Figure 18.4b

(b) Anterior view

Brachiocephalic trunk

Superior vena cava

Right pulmonaryarteryAscending aortaPulmonary trunk

Right pulmonaryveins

Right atrium

Right coronary artery(in coronary sulcus)

Right ventricle

Inferior vena cava

Left common carotidarteryLeft subclavian artery

Left pulmonary artery

Left pulmonary veins

Left coronary artery(in coronary sulcus)

Left ventricle

Great cardiac vein

Apex

Aortic arch

Auricle ofleft atrium

Copyright © 2010 Pearson Education, Inc. Figure 18.4d

(d) Posterior surface view

Aorta

Left pulmonaryartery

Left pulmonaryveinsAuricle of leftatriumLeft atrium

Great cardiacvein

Posterior veinof left ventricle

Left ventricle

Apex

Superior vena cava

Right pulmonary artery

Right pulmonary veins

Right atrium

Inferior vena cava


Coronary sinus

Posteriorinterventricularartery (in posteriorinterventricular sulcus)Middle cardiac veinRight ventricle


Atria: The Receiving Chambers

•Walls are ridged by pectinate muscles

•Vessels entering right atrium

• Superior vena cava

• Inferior vena cava

•Coronary sinus

•Vessels entering left atrium

•Right and left pulmonary veins


Ventricles: The Discharging Chambers

•Walls are ridged by trabeculae carneae

•Papillary muscles project into the ventricular cavities (anchor valves)

•Vessel leaving the right ventricle

• Pulmonary trunk

•Vessel leaving the left ventricle

• Aorta

Copyright © 2010 Pearson Education, Inc. Figure 18.4e

Aorta

Left pulmonaryarteryLeft atriumLeft pulmonaryveins

Mitral (bicuspid)valve

Aortic valve

Pulmonary valveLeft ventriclePapillary muscleInterventricularseptumEpicardiumMyocardiumEndocardium

(e) Frontal section

Superior vena cava

Right pulmonaryarteryPulmonary trunk

Right atrium


Tricuspid valveRight ventricleChordae tendineae

Trabeculae carneae

Inferior vena cava


Pathway of Blood Through the Heart

•The heart is two side-by-side pumps

•Right side is the pump for the pulmonary circuit

•Vessels that carry blood to and from the lungs

• Left side is the pump for the systemic circuit

•Vessels that carry the blood to and from all body tissues


Oxygen-rich,CO2-poor bloodOxygen-poor,CO2-rich blood

Capillary bedsof lungs wheregas exchangeoccurs

Capillary beds of allbody tissues wheregas exchange occurs

Pulmonary veinsPulmonary arteries

PulmonaryCircuit

SystemicCircuit

Aorta and branches

Left atrium

Heart

Left ventricleRight atrium

Right ventricle

Venae cavae



•Right atrium

•Right ventricle

•Pulmonary trunk

•Pulmonary arteries

•Lungs

•Pulmonary veins

•Left atrium

•Left ventricle

•Aorta

•Systemic circulation



•Pulmonary circuit is a short, low-pressure circulation

•Systemic circuit blood encounters much resistance in the long pathways

•As a result, the left ventricle has a much thicker wall (stronger muscle)


Rightventricle

Leftventricle

Interventricularseptum


Heart Valves


Heart Valves

•Ensure unidirectional blood flow through the heart

•Atrioventricular (AV) valves (balloons)

• Prevent backflow into the atria when ventricles contract

• Tricuspid valve (right)

•Between R atrium and R ventricle

• Mitral valve (left)

•Between L atrium and L ventricle

•Chordae tendineae anchor AV valve cusps to papillary muscles


Heart Valves

•Semilunar (SL) valves (cups)

• Prevent backflow into the ventricles when ventricles relax

• Pulmonary valve

•between R ventricle and pulmonary trunk

• Aortic valve

•Between L ventricle and aorta

Copyright © 2010 Pearson Education, Inc. Figure 18.4e

Aorta

Left pulmonaryarteryLeft atriumLeft pulmonaryveins

Mitral (bicuspid)valve

Aortic valve

Pulmonary valveLeft ventriclePapillary muscleInterventricularseptumEpicardiumMyocardiumEndocardium

(e) Frontal section

Superior vena cava

Right pulmonaryarteryPulmonary trunk

Right atrium


Tricuspid valveRight ventricleChordae tendineae

Trabeculae carneae

Inferior vena cava


Blood flow through the heart with valves

•Right atrium tricuspid valve

•right ventricle pulmonary semilunar valve

•pulmonary trunk pulmonary arteries

•Lungs pulmonary veins

•left atrium (mitral) bicuspid valve

•left ventricle aortic semilunar valve

• aorta systemic circulation


Pulmonary valveAortic valveArea of cutaway

Mitral valveTricuspid valve

Myocardium

Tricuspid(right atrioventricular)valveMitral(left atrioventricular)valveAorticvalve

Pulmonaryvalve

(b)



Myocardium

Tricuspid(right atrioventricular)valve

(a)

Mitral(left atrioventricular)valveAortic valve

Pulmonaryvalve

Fibrousskeleton

Anterior




Myocardium

Tricuspid(right atrioventricular)valveMitral(left atrioventricular)valveAorticvalve

Pulmonaryvalve

(b)

Copyright © 2010 Pearson Education, Inc. Figure 18.8c

Pulmonaryvalve

AorticvalveArea ofcutawayMitralvalve

Tricuspidvalve

Chordae tendineaeattached to tricuspid valve flap

Papillarymuscle

(c)


PulmonaryvalveAortic valveArea of cutawayMitral valveTricuspidvalve

Mitral valve

Chordaetendineae

Interventricularseptum

Myocardiumof left ventricle

Opening of inferiorvena cava

Tricuspid valve

Papillarymuscles

Myocardiumof rightventricle

(d)


Physiology of Blood Flow through the

Heart


1 Blood returning to theheart fills atria, puttingpressure againstatrioventricular valves;atrioventricular valves areforced open.

1 Ventricles contract, forcingblood against atrioventricularvalve cusps.

2 As ventricles fill,atrioventricular valve flapshang limply into ventricles.

2 Atrioventricular valvesclose.

3 Atria contract, forcingadditional blood into ventricles.

3 Papillary musclescontract and chordaetendineae tighten,preventing valve flapsfrom everting into atria.

(a) AV valves open; atrial pressure greater than ventricular pressure

(b) AV valves closed; atrial pressure less than ventricular pressure

Direction ofblood flow

Atrium

Ventricle

Cusp ofatrioventricularvalve (open)

Chordaetendineae

Papillarymuscle

Atrium

Blood inventricle

Cusps ofatrioventricularvalve (closed)


As ventriclescontract andintraventricularpressure rises,blood is pushed upagainst semilunarvalves, forcing themopen.

As ventricles relaxand intraventricularpressure falls, bloodflows back fromarteries, filling thecusps of semilunarvalves and forcingthem to close.

(a) Semilunar valves open

(b) Semilunar valves closed

Aorta

Pulmonarytrunk


Heart Sounds

•AV valves closing (tricuspid and mitral) = lub

•Semilunar valves closing (pulmonic, aortic) = dub


Coronary Circulation



•The functional blood supply to the heart muscle itself

•Arterial supply varies considerably and contains many anastomoses (junctions) among branches



•Arteries

•Right and left coronary (in atrioventricular groove)

•Veins

• Small cardiac, anterior cardiac, and great cardiac veins, coronary sinus

•Coronary sinus is where dexoygenated blood from coronary circulation pools and is returned to venous circulation via the inferior vena cava


Rightventricle

Rightcoronaryartery

Rightatrium

Posteriorinterventricularartery

Anteriorinterventricularartery

Circumflexartery

Leftcoronaryartery

Aorta

Anastomosis(junction ofvessels)

Leftventricle

Superiorvena cava

(a) The major coronary arteries

Left atrium

Pulmonarytrunk


Superiorvena cava

Anteriorcardiacveins

Greatcardiacvein

Coronarysinus

(b) The major cardiac veins


(d) Posterior surface view

Aorta

Left pulmonaryartery

Left pulmonaryveinsAuricle of leftatriumLeft atrium

Great cardiacvein

Posterior veinof left ventricle

Left ventricle

Apex

Superior vena cava

Right pulmonary artery

Right pulmonary veins

Right atrium

Inferior vena cava


Coronary sinus

Posteriorinterventricularartery (in posteriorinterventricular sulcus)Middle cardiac veinRight ventricle


Homeostatic Imbalances

•Angina pectoris

• Thoracic pain caused by a fleeting deficiency in blood delivery to the myocardium

•Cells are weakened

•Myocardial infarction (heart attack)

• Prolonged coronary blockage

• Areas of cell death are repaired with noncontractile scar tissue


Histology of Cardiac Muscle


Microscopic Anatomy of Cardiac Muscle

•Cardiac muscle cells are striated, short, fat, branched, and interconnected

•Connective tissue matrix (endomysium) connects to the fibrous skeleton

•T tubules are wide but less numerous

•SR (sarcoplasmic reticulum) is simpler than in skeletal muscle

• SR stores Ca++, which plays an important part in cardiac cell APs and contraction

•Numerous large mitochondria

•Multiple nuclei per cell


Microscopic Anatomy of Cardiac Muscle

•Intercalated discs: junctions between cells anchor cardiac cells, cause heart to beat as a functional syncytium (as a group)

•Desmosomes prevent cells from separating during contraction

•Gap junctions allow ions to pass; electrically couple adjacent cells


Nucleus

DesmosomesGap junctions

Intercalated discs Cardiac muscle cell

(a)


Nucleus

Nucleus

I bandA band

Cardiacmuscle cell

Sarcolemma

Z disc

Mitochondrion

Mitochondrion

T tubule

Sarcoplasmicreticulum

I band

Intercalateddisc

(b)


Physiology of Cardiac Muscle Contraction


Cardiac Muscle Cells


Cardiac Muscle Contraction

1. Depolarization opens voltage-gated fast Na+ channels in the sarcolemma

1. Reversal of membrane potential from –90 mV to +30 mV

2. Slow Ca2+ channels open (delayed), about 20% of Ca2+ enters cell this way

1. Depolarization wave in T tubules causes the SR to release Ca2+; 80% of Ca2+ released thru SR

2. Ca2+ surge prolongs the depolarization phase (plateau)

3. K+ channels open and Ca2+ channels close, repolarizing the membrane

1. Ca2+ is pumped back into the SR and ECF


Cardiac Muscle Contraction

•Because of influx of Ca2+ from slow Ca2+ channels and the SR, the duration of the AP and the contractile phase is much greater in cardiac muscle than in skeletal muscle

• Skeletal muscle

•AP is 1-2ms

•Contraction is 15-100ms

• Cardiac muscle

•AP is 200ms

•Contraction is 200ms


Cardiac AP and Ca++ Channel

Ca++ Channel Open


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

Tension (g)

Membrane potential (mV)


Cardiac Muscle Physiology

EPI

EPIB-1

Adrenergicreceptor

Beta blockers

Ca++

CA++ Channels CA++

Influx

Adenylate cyclase

Cyclase-a

ATP

cAMP

Prot. Kinase

Prot.Kinase-a

“Phosphorylation”

Tension Generation

Cross Bridge Formation

CA++

Channel Blockers


Heart Conduction System


Heart Physiology: Electrical Events

•Intrinsic cardiac conduction system

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

•The independent but coordinated activity of the heart is a function of

•Gap junctions

• Intrinsic conducting system


Cardiac Pacemaker Cells



•Found in SA node, AV node, AV bundle, R and L bundle branches, Purkinje fibers; part of conduction system of the heart

•Autorhythmic cells (1% of cardiac muscle cells)

•Have unstable RMP (resting membrane potential)

• Cells continously depolarize because they drift toward threshold

•Depolarization of the heart is rhythmic and spontaneous

•Gap junctions ensure the heart contracts as a unit



•Unstable resting potentials = pacemaker potential

• Pacemaker potential is due to slow Na+ channels and closing of K+ channels

1.Slow Na+ channels leak positive ions into the cell, causing the RMP to creep up

2.At threshold, Ca2+ channels open

• Explosive Ca2+ influx produces the rising phase of the action potential (not Na+)

• Repolarization results from inactivation of Ca2+ channels and opening of voltage-gated K+ channels


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


Heart Physiology: Sequence of Excitation

1. Sinoatrial (SA) node (pacemaker)

• Generates impulses about 75 times/minute (sinus rhythm)

• Depolarizes faster than any other part of the myocardium

• Atrial contraction



2. Atrioventricular (AV) node

• Smaller diameter fibers; fewer gap junctions

• Delays impulses approximately 0.1 second

• Want a delay between contract of atria and ventricles

• Depolarizes 50 times per minute in absence of SA node input



3. Atrioventricular (AV) bundle (bundle of His)

• Only electrical connection between the atria and ventricles



4. Right and left bundle branches

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



5. Purkinje fibers

• Complete the pathway into the apex and ventricular walls

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


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

Superior vena cavaRight atrium

Left atrium

Purkinje fibers

Inter-ventricularseptum

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

2 The atrioventricular(AV) node.

The atrioventricular(AV) bundle

4

The bundle branches

3

The Purkinje fibers5



• Defects in the intrinsic conduction system may result in

1. Arrhythmias: irregular heart rhythms

2. Uncoordinated atrial and ventricular contractions

3. Fibrillation: rapid, irregular contractions; useless for pumping blood because atria, and more importantly ventricles, are not getting filled with blood



•Defective SA node may result in

• Ectopic focus: abnormal pacemaker takes over

• If AV node takes over, there will be a junctional rhythm (40–60 bpm)

•Defective AV node may result in

• Partial or total heart block

• Few or no impulses from SA node reach the ventricles


Electrocardiography


Electrocardiography

• Electrocardiogram (ECG or EKG): a composite of all the action potentials generated by nodal and contractile cells at a given time

• Three waves

1. P wave: depolarization of SA node

2. QRS complex: ventricular depolarization

3. T wave: ventricular repolarization


Sinoatrialnode

Atrioventricularnode

Atrialdepolarization

QRS complex

Ventriculardepolarization

Ventricularrepolarization

P-QInterval

S-TSegment

Q-TInterval

Copyright © 2010 Pearson Education, Inc. Figure 18.17, step 1

Atrial depolarization, initiated bythe SA node, causes the P wave.

P

R

T

QS

SA node Depolarization

Repolarization

1



P

R

T

QS

SA node

AV node

With atrial depolarization complete,the impulse is delayed at the AV node.

P

R

T

QS

Depolarization

Repolarization

1

2



P

R

T

QS

SA node

AV node

With atrial depolarization complete,the impulse is delayed at the AV node.

Ventricular depolarization beginsat apex, causing the QRS complex.Atrial repolarization occurs.

P

R

T

QS

P

R

T

QS

Depolarization

Repolarization

1

2

3


Ventricular depolarization iscomplete.

P

R

T

QS

Depolarization

Repolarization

4



Ventricular repolarization beginsat apex, causing the T wave.

P

R

T

QS

P

R

T

QS

Depolarization

Repolarization

4

5



Ventricular repolarization beginsat apex, causing the T wave.

Ventricular repolarization iscomplete.

P

R

T

QS

P

R

T

QS

P

R

T

QS

Depolarization

Repolarization

4

5

6


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


(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.


Mechanical Events of the Cardiac Cycle


Mechanical Events: The Cardiac Cycle

•Cardiac cycle: all events associated with blood flow through the heart during one complete heartbeat

• Systole—contraction

•Diastole—relaxation

•Normal heart rate (HR) = 60-100 bpm


Heart Sounds

•Two 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 semilunar valves close at the beginning of ventricular diastole

•Heart murmurs: abnormal heart sounds most often indicative of valve problems


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


Cardiac Cycle: A Note on Pressure

•REMEMBER:

•Blood will always flow from high pressure to low pressure


Phases of the Cardiac Cycle

1. 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%

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



2. Ventricular systole

• 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

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



3. Isovolumetric relaxation occurs in early diastole

• Ventricles relax

• Backflow of blood in aorta and pulmonary trunk closes semilunar valves and causes brief rise in aortic pressure


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

Ventricular

volume (ml)

Pressure (mm Hg)


Cardiac Output (CO)

•Volume of blood pumped by each ventricle in one minute

•CO = 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


Regulation of Stroke Volume

•SV = EDV – ESV

•Three main factors affect SV

• Preload

•Contractility

• Afterload



•Preload: 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 (as opposed to skeletal muscle fibers which are kept near optimal length)

• This degree of stretch produces more contractile force

• Increased venous return distends (stretches) the ventricles and increases contraction force

• Higher preload = higher SV



•Contractility: contractile strength at a given muscle length, independent of muscle stretch and EDV

• Contractility rises when more Ca2+ is released into the ICF via the SR

•Positive inotropic agents increase contractility

• Ino = muscle, fiber

• Ca2+, hormones (thyroxine, glucagon, and epinephrine)

•Negative inotropic agents decrease contractility

• Acidosis (increased H+)

• Increased extracellular K+

• Calcium channel blockers



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

• The back pressure that arterial blood exerts on the aortic (80mg) and pulmonary (10mg) valves

•Hypertension increases afterload, resulting in increased ESV and reduced SV


Regulation of Heart Rate

•Positive chronotropic factors increase heart rate

•Chrono = time

•Negative chronotropic factors decrease heart rate

•Can be neural, chemical, or physical factors


Autonomic Nervous System Regulation



•Exerts the most important extrinsic controls affecting HR

•Sympathetic nervous system is activated by emotional or physical stressors

•Sympathetic nerves release norepinephrine which binds to β1 adrenergic receptors on the heart, causing the pacemaker to fire more rapidly

• It also increases contractility



•Parasympathetic nervous system opposes the sympathetic effects and reduces HR when a stressful situation has passe

•Parasympathetic-initiated cardiac responses are mediated by Acetylcholine (ACh)

• ACh hyperpolarizes the membranes by opening K+ channels



•At rest, the heart exhibits vagal tone

• At rest, both SNS and PNS send impulses to SA node, but the dominant influence is inhibitory (PNS)

•The heart rate is slower than if the vagus nerve was not innervating it


Thoracic spinal cord

The vagus nerve (parasympathetic) decreases heart rate.

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


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


Chemical Regulation of Heart Rate

1. Hormones

• Epinephrine from adrenal medulla increases HR and contractility

• Thyroxine increases HR 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

• Electrolyte imbalances pose serious danger to the heart


Other Factors that Influence Heart Rate

•Age

•Gender

•Exercise

•Body temperature



•Tachycardia: abnormally fast heart rate (>100 bpm)

• If persistent, may lead to fibrillation

•Bradycardia: heart rate slower than 60 bpm

•May result in grossly inadequate blood circulation

•May be desirable result of endurance training


Congestive Heart Failure (CHF)

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

•Caused by

•Coronary atherosclerosis

• Persistent high blood pressure

•Multiple myocardial infarcts

•Dilated cardiomyopathy (DCM)


Occurs inabout 1 in every500 births

Occurs inabout 1 in every 1500 births

Narrowedaorta

Occurs inabout 1 in every 2000births

Ventricular septal defect.The superior part of the inter-ventricular septum fails to form; thus, blood mixes between the two ventricles. More blood is shunted from left to right because the left ventricle is stronger.

(a) Coarctation of the aorta. A part of the aorta is narrowed,increasing the workload of the left ventricle.

(b) Tetralogy of Fallot. Multiple defects (tetra = four): (1) Pulmonary trunk too narrow and pulmonary valve stenosed, resulting in (2) hypertrophied right ventricle; (3) ventricular septal defect; (4) aorta opens from both ventricles.

(c)


QUESTIONS TO TEST WHAT YOU NOW KNOW!!!


The principle of complementary structure and function is evident when examining the coverings of the heart. In what way is this relationship evident?A. The pericardium surrounds the heart.

B. The epicardium and visceral layer of the pericardium are synonymous.

C. The pericardial cavity surrounds the heart.

D. The visceral and parietal membranes of the pericardium are smooth and slide past each other, providing a low-friction environment for heart movement.


Of the following layers of the heart wall, which consumes the most energy?

A. Epicardium

B. Myocardium

C. Endocardium

D. Visceral pericardium


Which of the following structures is an exception to the general principle surrounding blood vessel oxygenation levels?

A. Pulmonary artery

B. Aorta

C. Pulmonary veins

D. Both a and c


What purpose does the coronary circuit serve?

A. None; it is a vestigial set of vessels.

B. It delivers 1/20 of the body’s blood supply to the heart muscle itself.

C. It delivers blood to the anterior lung surface for gas exchange.

D. It feeds the anterior thoracic wall.


A heart murmur would be detected when blood is heard flowing from the ________ to the __________ through the ___________.

A. right atrium; right ventricle; tricuspid valve

B. right atrium; left atrium; tricuspid valve

C. left ventricle; left atrium; mitral valve

D. left atrium; left ventricle; mitral valve


The presence of intercalated discs between adjacent cardiac muscle cells causes the heart to behave as a _____________.

A. single chamber

B. contractile myofibril

C. desmosome

D. functional syncytium


Cardiac muscle cells have several similarities with skeletal muscle cells. Which of the following is not a similarity?

A. The cells are each innervated by a nerve ending.

B. The cells store calcium ions in the sarcoplasmic reticulum.

C. The cells contain sarcomeres.

D. The cells become depolarized when sodium ions enter the cytoplasm.


The plateau portion of the action potential in contractile cardiac muscle cells is due to:

A. an increased potassium permeability.

B. an influx of calcium ions.

C. an influx of sodium ions.

D. exit of calcium ions from the sarcoplasmic reticulum.


The stimulus for the heart’s rhythmic contractions comes from _________.

A. intercalated discs

B. acetylcholine

C. a neuromuscular junction

D. a pacemaker potential


The major ionic change that initiates the rising phase of the autorhythmic cell action potential is __________.

A. potassium ion exit

B. sodium ion entry

C. calcium ion entry

D. calcium ion exit


For which type of heart condition might a doctor prescribe calcium channel blockers?

A. Depressed heart rate

B. Heart irritability

C. Heart murmur

D. Weak heart rate


In a normal heart, which of the following structures is responsible for setting the heart’s pace?

A. Sinoatrial node

B. Atrioventricular node

C. Atrioventricular bundle

D. Purkinje fibers


Predict the nature of an ECG recording when the atrioventricular node becomes the pacemaker.

A. There would continue to be a normal sinus rhythm.

B. The P wave would be much larger than normal.

C. The rhythm would be slower.

D. The T wave would be much smaller than normal.


The primary input to the heart by the cardioinhibitory center is primarily found in the ___________.

A. sinoatrial node and atrioventricular node

B. Purkinje fibers

C. the cardiac contractile fibers

D. bundle of His


The “lub-dup” heart sounds are produced by:A. the walls of the atria and ventricles slapping

together during a contraction.

B. the blood hitting the walls of the ventricles and arteries, respectively.

C. the closing of the atrioventricular valves (“lub”) and the closing of the semilunar valves (“dup”).

D. the closing of the semilunar valves (“lub”) and the closing of the atrioventricular valves (“dup”).


Atrial systole occurs _______ the firing of the sinoatrial node.

A. before

B. after

C. simultaneously with

D. alternately with


The majority (80%) of ventricular filling occurs ___________.

A. during late ventricular systole

B. passively through blood flow alone

C. with atrial systole

D. both a and b


In terms of blood flow, why is it important that atrial diastole occurs just as ventricular systole begins?A. Blood is continually propelled in a forward

motion down its pressure gradient.

B. The atria need that time to prepare for the next contraction.

C. Ventricular systole pulls the remaining 20% of blood volume from the atria.

D. Blood would flow too fast otherwise.


Cardiac output is determined by________.

A. heart rate

B. stroke volume

C. cardiac reserve

D. both a and b


Predict what would happen to the end systolic volume (ESV) if contraction force were to increase.

A. It would decrease.

B. It would increase.

C. It would remain constant.

D. ESV is not affected by contraction force.


The Frank-Starling law of the heart can be demonstrated when an individual takes a deep breath. This is because:A. the heart expands during inhalation.

B. the negative intrathoracic pressure induces a larger than normal venous return to the right atrium, thereby stretching the wall of the right ventricle.

C. sympathetic impulses are sent to the heart during inspiration.

D. both a and c occur.


Your heart seems to “pound” after you hear a sudden, loud noise. This increased contractility is:

A. because you were startled.

B. because when a gasp of surprise is emitted, the Frank-Starling law of the heart is evident.

C. due to norepinephrine causing threshold to be reached more quickly.

D. because acetylcholine release is inhibited.


Predict what happens to end diastolic volume when an increase in heart rate is not accompanied by an increase in contractility.

A. End diastolic volume is increased.

B. End diastolic volume is decreased.

C. End diastolic volume is unchanged.

D. End diastolic volume is not affected by heart rate.


What is the nature of acetylcholine’s inhibitory effect on heart rate?A. Acetylcholine induces depolarization in the

sinoatrial node.

B. Acetylcholine causes closing of sodium channels in the sinoatrial node.

C. Acetylcholine causes opening of fast calcium channels in contractile cells.

D. Acetylcholine causes opening of potassium channels in the sinoatrial node, thereby hyperpolarizing it.


Why is high blood pressure damaging to the heart?A. With high blood pressure, the blood is more

viscous and harder to pump.

B. The heart rate slows down to dangerously low levels if blood pressure is too high.

C. Due to increased afterload, the left ventricle must contract more forcefully to expel the same amount of blood.

D. Sodium concentration increases during high blood pressure and is toxic to the myocardium.

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Copyright © 2010 Pearson Education, Inc. Chapter 18: THE HEART