Cardiovascular System components

Copyright © 2010 Pearson Education, Inc.

Cardiovascular System components

• The heart

• Blood vessels

• Blood

Copyright © 2010 Pearson Education, Inc. Figure 18.5

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

HeartLeft ventricleRight atrium

Right ventricle

Venae cavae



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


Coverings of the Heart: Anatomy• The heart is enclosed in a double-walled sac called the

pericardium. • Superficial fibrous pericardium

• Protects, anchors, and prevents overfilling• The outer parietal pericardium consists of a tough fibrous

layer of dense connective tissue. • The inner thin, smooth, moist serous layer turns in at the base of

the heart, forming the visceral pericardium/epicardium covering the heart surface.

• Between the parietal and visceral pericardia is a space called the pericardial cavity.

• It contains pericardial fluid that lubricates the membranes and allows the heart to beat almost without friction.


Layers of the Heart Wall myocardium

• Spiral bundles of cardiac muscle cells to allow “twisting” when contracting

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

• Supply structural support for the heart

• Anchors cardiocytes and give them something to pull against

• Limits spread of action potentials to specific paths


Heart Chambers

Atrium – singleAtria - pleural

Ventricle/s

http://mtsu32.mtsu.edu:11259/heart3.jpg


Atria of the Heart

• Atria are the receiving chambers of the heart – entering veins

• Blood enters right atria from superior and inferior venae cavae and coronary sinus

• Blood enters left atria from pulmonary veins• Each atrium has a auricle that increase atrial volume

• Separated internally by the interatrial septum• Coronary sulcus (atrioventricular groove) encircles

the junction of the atria and ventricles• Pectinate muscles mark the anterior atrial wall


Ventricles of the Heart

• Ventricles are the discharging chambers of the heart

• Right ventricle pumps blood into the pulmonary trunk

• Left ventricle pumps blood into the aorta

• Papillary muscles that attached to the valves

Copyright © 2010 Pearson Education, Inc.Figure 18.4e


Heart Valves

• Heart valves ensure unidirectional blood flow through the heart (prevent backflow)

• Atrioventricular (AV) valves lie between the atria and the ventricles

• AV valves prevent backflow into the atria when ventricles contract

• Chordae tendineae anchor AV valves to papillary muscles• Semilunar valves prevent backflow of blood into the ventricles

• Aortic semilunar valve lies between the left ventricle and the aorta

• Pulmonary semilunar valve lies between the right ventricle and pulmonary trunk


Heart Sounds

• Two sounds (lub-dup) 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 problems


Heart valves problems

• Valvular heart disease (VHD)• When valve function has deteriorated to where heart

cannot maintain adequate blood flow

• Can be due to:

• Congenital (present at birth) malformations

• Heart swelling (carditis)

• In severe cases, replacement with a prosthetic valve may be necessary

• Bioprosthetic valves come from pigs or cows


Vessels that Supply/Drain the Heart - coronary circulation

Figure 18.7


Risk factors that can lead to heart diseases

• Coronary artery disease• High blood pressure• Diabetes• Smoking• High cholesterol• Obesity• Excessive alcohol use• Drug abuse• Stress• Family history of heart disease• Advancing age


Arteriosclerosis and coronary artery disease

• Arteriosclerosis (arterio-, artery + sclerosis, hardness)

• Thickening or toughening of artery walls

• Related complications account for about half of all U.S. deaths


Arteriosclerosis and coronary artery disease

• Atherosclerosis (athero-, fatty degeneration)

• Formation of lipid deposits

• Most common form of arteriosclerosis

• Often associated with elevated cholesterol

• May form fatty tissue mass (plaque) in vessel that restricts blood flow

• Most common in older men

• Treatment can be removing damaged vessel or compressing plaque with balloon angioplasty


Heart Disease - Coronary Artery Disease (CAD)• Areas of partial or complete blockage of coronary

circulation

• Reduction in blood flow to heart muscle produces a corresponding reduction in cardiac performance

• Reduced circulatory supply causes coronary ischemia• One of the first symptoms of CAD is commonly

angina pectoris – pain in the middle of the chest, left neck, left shoulder, or left arm


Myocardial infarction (MI), or heart attack

• Part of the coronary circulation becomes blocked, and cardiac muscle cells die from lack of oxygen

• The death of affected tissue creates a nonfunctional area known as an infarct

• Heart attacks most commonly result from severe coronary artery disease (CAD)


Myocardial infarction (MI), or heart attack

• Consequences depend on the site and nature of the circulatory blockage

• If it occurs near the start of one of the coronary arteries: • The damage will be widespread and the heart may

stop beating• If the blockage involves one of the smaller arterial

branches:• The individual may survive the immediate crisis but

may have many complications such as reduced contractility and cardiac arrhythmias


Myocardial infarction (MI), or heart attack• Pain does not always accompany a heart attack• therefore, the condition may go undiagnosed and may not be

treated before a fatal MI occurs• A myocardial infarction can usually be diagnosed with an

ECG and blood studies• Damaged myocardial cells release enzymes into the

circulation, and these elevated enzymes can be measured in diagnostic blood tests

• The enzymes include:• Cardiac troponin T, • Cardiac troponin I, • A special form of creatinine phosphokinase, CK-MB


CAD and Myocardial Infarction prognosis

• About 25% of MI patients die before obtaining medical assistance

• 65% of MI deaths among those under age 50 occur within an hour after the initial infarction


Treatment of CAD and Myocardial Infarction

• Risk Factor Modification

• Stop smoking

• High blood pressure treatment

• Dietary modification to lower cholesterol and promote weight loss

• Stress reduction

• Increased physical activity (where appropriate)


Treatment of CAD and Myocardial Infarction

• Drug Treatment

• Drugs that reduce coagulation and therefore the risk of thrombosis, such as aspirin and coumadin

• Drugs that block sympathetic stimulation (propranolol or metoprolol) – for hypertension

• Drugs that cause vasodilation, such as nitroglycerin

• Drugs that block calcium movement into the cardiac and vascular smooth muscle cells (calcium channel blockers)


Coronary Artery Bypass Surgery (CABG)

• In a coronary artery bypass graft, a small section is removed from either a small artery or a peripheral vein and is used to create a detour around the obstructed portion of a coronary artery


Pathway of Blood Through the Heart • The heart is two side-by-side pumps

• Equal volumes of blood are pumped to the pulmonary and systemic circuits

• Right side is the pump for the pulmonary circuit

• Vessels that carry blood to and from the lungs

• Pulmonary circuit is a short, low-pressure circulation

• Left side is the pump for the systemic circuit

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

• Systemic circuit blood encounters much resistance in the long pathways


Cardiovascular system – the heart


The cells of the heart• Two types of cardiac muscle cells that are involved in

a normal heartbeat:• Specialized muscle cells of the conducting system• Contractile cells

• The heart is an autonomic system that can work without neural stimuli – an intrinsic conduction system.

• The autonomic function of the heart results from:• The pacemaker function – Autorhythmic cells• The conductive system that transfer those impulses

throughout the heart


Properties of Cardiac Muscle

• Aerobic muscle

• No cell division after infancy - growth by hypertrophy

• 99% contractile cells (for pumping)

• 1% autorhythmic cells (set pace)


Intrinsic cardiac conduction system – autorhythmic cells

• Have unstable resting potentials/ pacemaker potentials

• constantly depolarized slowly towards AP

• At threshold, Ca2+ channels open

• Ca2+ influx produces the rising phase of the action potential

• 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


Autorhythmic Cells

Location Firing Rate at Rest

SA node 70–80 APs/min*

AV node 40–60 APs/min

Bundle of His 20–40 APs/min

Purkinje fibers 20–40 APs/min

• Cardiac cells are linked by gap junctions

• Fastest depolarizing cells control other cells

• Fastest cells = pacemaker = set rate for rest of heart* action potentials per minute


Autorythmic cells - ectopic pacemakers

• Autorythmic cells of the SA node (pacemaker) may be replaced by ectopic pacemakers

• Ectopic pacemakers – other parts in the heart that can induce beating

• The ectopic pacemakers may become dominant:

• If their rythmicity increased

• The pacemaker is inhibited/blocked

• The conduction system pathways are blocked• First to take over will be the AV node



Cardiac contractile cells

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

• Depolarization wave causes release Ca2+ that causes the cell contraction

• Depolarization wave also opens slow Ca2+ channels in the sarcolemma

• Ca2+ surge prolongs the depolarization phase (plateau)


Myocardial Contractile Cells

• Refractory period in skeletal muscle

Figure 14-14a


Myocardial Contractile Cells

• Refractory period in cardiac muscle

Figure 14-14c


Action Potentials

Table 14-3


Heart Physiology: Sequence of Excitation


Electrical Conduction in the Heart

Figure 14-18, steps 1–5

1

2

3

4

5

5

4

3

2

1

THE CONDUCTING SYSTEMOF THE HEART

SA node

AV node

Purkinjefibers

Bundlebranches

AV bundle

AV node

Internodalpathways

SA node

SA node depolarizes.

Electrical activity goesrapidly to AV node viainternodal pathways.

Depolarization spreadsmore slowly acrossatria. Conduction slowsthrough AV node.

Depolarization movesrapidly through ventricularconducting system to theapex of the heart.

Depolarization wavespreads upward fromthe apex.


Electrocardiography (ECG or EKG)

• Body fluids are good conductors which allows the record of the myocardial action potential extracellularly

• EKG pairs of electrodes (leads) one serve as positive side of the lead and one as the negative

• Potentials (voltage) are being measured between the 2 electrodes

• EKG is the summed electrical potentials generated by all cells of the heart and gives electrical “view” of 3D object (different from one action potential)

• EKG shows depolarization and repolarization


Electrical Activity of Heart

• P wave: atrial depolarization

• QRS complex: ventricular depolarization and atrial repolarization

• T wave: ventricular repolarization

• PQ segment: AV nodal delay

• QT segment: ventricular systole

• QT interval: ventricular diastole


Correlation between an ECG and electrical events in the heart


Electrical Activity

Figure 14-21 (9 of 9)

P

Q

R

T

S P

T wave:ventricularrepolarization

PQ or PR segment:conduction throughAV node and AVbundle

P wave: atrialdepolarization

ELECTRICALEVENTSOF THE

CARDIACCYCLE

Repolarization

START

P

Q

P

Q

R

P

Q

R

T

S

R waveP

Q

R

S

S wave

Q

R

P

Q wave

Ventricles contract

ST segment

The end

P

Atria contract

S


Homeostatic Imbalances

• Defects in the intrinsic conduction system may result in

1. Arrhythmias: irregular heart rhythms

2. Uncoordinated atrial and ventricular contractions (heart block)

3. Fibrillation: rapid, irregular contractions; useless for pumping blood

Copyright © 2010 Pearson Education, Inc. Figure 13.17 (1 of 4)

ECG Arrhythmias: Abnormal Rates

• Sinus rhythm = pace generated by SA node

• Abnormal rates shown

• Tachycardia = fast rhythm

• Bradycardia = slow rhythm



• 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


First and second degree Heart Block• Slowed/diminished conduction through AV node occurs in

varying degrees

• First degree block• Increases duration PQ segment

• Increases delay between atrial and ventricular contraction

• Second degree block • Lose 1-to-1 relationship between P wave and QRS

complex

• Lose 1-to-1 relationship between atrial and ventricular contraction


Third Degree Heart Block

Third degree block

• Loss of conduction through the AV node

• P wave becomes independent of QRS

• Atrial and ventricular contractions are independent

Copyright © 2010 Pearson Education, Inc. Figure 13.17 (4 of 4)

ECG Arrhythmias: Fibrillation

Ventricular Fibrillation

• Loss of coordination of electrical activity of heart

• Death can ensue within minutes unless corrected


Cardiac Cycle• Cardiac cycle - The period between the start of one heartbeat and the

beginning of the next.

• refers to all events associated with blood flow through the heart• During the cycle, each of the four chambers goes through

• Systole – contraction of heart muscle

• Diastole – relaxation of heart muscle

• An average heart beat (HR)/cardiac cycle is 75 bpm. That means that a cardiac cycle length is about 0.8 second.

• Of that 0.1 second is the atrial contraction, 0.3 is the atrial relaxation and ventricular contraction.

• The remaining 0.4 seconds are called the quiescent period which represent the ventricular relaxation


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


Phases of the Cardiac Cycle2. 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

• 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 SL valves and causes dicrotic notch (brief rise in aortic pressure)



Figure 20.16


Cardiodynamics

• Movements and forces generated during cardiac contractions

• End-diastolic volume (EDV) – the amount of blood in each ventricle at the end of ventricular diastole (before contraction begins)

• End-systolic volume (ESV) - the amount of blood remains in each ventricle at the end of ventricular systole


Cardiodynamics• Stroke volume (SV) – The amount of blood that leaves the

heart with each beat or ventricular contraction; EDV-ESV=SV

• Not all blood ejected

• Normal Adult 70 ml / beat• Ejection fraction – The percentage of end-diastole blood

actually ejected with each beat or ventricular contraction.

• Normal adult 55-70% (healthy heart)


• Cardiac output (CO) – the amount of blood pumped by each ventricle in one minute.

• Physiologically, CO is an indication of blood flow through peripheral tissues

• Cardiac output equals heart rate times stroke volume; Normal CO: Approximately 4-8 liters/minute

Stroke Volume and Cardiac Output

COCardiac output

(ml/min)=

HRHeart rate(beats/min)

X

SVStroke volume

(ml/beat)


1 2a 2b 3

Atrioventricular valvesAortic and pulmonary valves

Open OpenClosed

Closed ClosedOpenPhase

ESV

Left atriumRight atriumLeft ventricleRight 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

Vent

ricul

arvo

lum

e (m

l)Pr

essu

re (m

m H

g)


Factors Affecting Cardiac Output

Figure 20.20


Extrinsic Innervation of the Heart

• 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

• Cardioinhibitory center inhibits SA and AV nodes through parasympathetic fibers in the vagus nerves


• Effect inotropy – (from Greek, meaning fiber) effect on contractility of the heart

• Effect chronotropy – effect on HR

• Effect dromotropy – Derives from the Greek word "Dromos", meaning running.

• A dromotropic agent is one which affects the conduction speed in the AV node

• Sympathetic stimuli has a positive effect (increase) all

• Parasympathetic stimuli has a negative effect (decrease) all


Heart Rate — Determined by SA Node Firing Rate

• SA node intrinsic firing rate = 100/min

• No extrinsic control on heart, HR = 100

• SA node under control of ANS and hormones

• Rest: parasympathetic dominates, HR = 75

• Excitement: sympathetic takes over, HR increases


Autonomic Nervous System Regulation

• In healthy conditions, parasympathetic effects dominate and slows the rate of the pacemaker from 80-100 bpm to a 70-80 bpm.• The binding of Ach to muscarinic receptors (M2) inhibit NE

release (mechanism by which vagal stimulation override sympathetic stimulation)

• Sympathetic nervous system is activated by emotional or physical stressors• Norepinephrine causes the pacemaker to fire more rapidly (and

at the same time increases contractility) • Parasympathetic nervous system opposes sympathetic effects

• Acetylcholine hyperpolarizes pacemaker cells by opening K+ channels

• The heart at rest exhibits vagal tone (parasympathetic)


Sympathetic presynaptic nerve terminal

parasympathetic nerve terminal

a2

b2M2

a1b2b1

M2

NE

ACh

-

-

-

+ + +

+

NT-receptor interaction - heart


Autonomic Nervous System Regulation

• Atrial (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


Pacemaker Function

Figure 20.22


Chemical Regulation of Heart 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



• 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


Factors Affecting Stroke Volume

Figure 20.23


Regulation of Stroke Volume

• SV = EDV – ESV

• Three main factors affect SV

• Preload

• Contractility

• Afterload


Regulation of Stroke Volume• Preload• The amount of tension on a muscle before it begins to

contract. The preload of the heart is determined by the EDV.

• In general, the greater the EDV the larger is the stroke volume : EDV-ESV=SV

• These relationships is known as the Frank-Starling principle/Sterling’s law of the heart :• The force of cardiac muscle contraction is

proportional to its initial length• The greater the EDV the larger the preload


Preload and Stroke Volume

• Frank-Starling law states

• Stroke volume increase as EDV increases• EDV is affected by venous return

• Venous return is affected by

• Skeletal muscle pump

• Respiratory pump

• Sympathetic innervation


• Stroke volume is the difference between the EDV and ESV. Changes in either one can change the stroke volume and cardiac output:

• The EDV volume is affected by 2 factors:

• The filling time – duration of ventricular diastole; depends on HR – the faster the HR the shorter is the available filing time

• The venous return – changes in response to several changes: cardiac output, blood volume, peripheral circulation.

Factors Affecting stroke volume - Preload/EDV


Reminder - Length-tension relationship

• The force of muscle contraction depends on the length of the sarcomeres before the contraction begins

• On the molecular level, the length reflects the overlapping between thin and thick filaments

• The tension a muscle fiber can generate is directly proportional to the number of crossbridges formed between the filament



Preload = Contractility (to a point)


Diastolic filling increased

EDV increase (preload increased)

Cardiac muscle stretch increased

Force of contraction increased

Ejection volume increased


Regulation of Stroke Volume - Contractility

• Force of ventricular contraction (systole) regardless of EDV

• Positive inotropic agents increase contractility

• Increased Ca2+ influx due to sympathetic stimulation

• Hormones (thyroxine and epinephrine)

• Negative inotropic agents decrease contractility

• Increased extracellular K+ (hyperpolarization)

• Calcium channel blockers (decrease calcium influx)


Inotropic Effect

• The effect of norepinepherine on contractility of the heart

Figure 14-29


Regulation of Stroke Volume - Afterload

• The amount of resistance the ventricular wall must overcome to eject blood during systole (influenced by arterial pressure).

• The greater is the afterload, the longer is the period of isovolumetric contraction (ventricles are contracting but there is no blood flow), the shorter the duration of ventricular ejection and the larger the ESV – afterload increase – stroke volume decrease

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


Factors Influencing Stroke Volume


Regulation of Cardiac Output


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 (decreased blood supply and myocardial cell death)

• Dilated cardiomyopathy (DCM) – heart wall weakens and can not contract efficiently. Causes are unknown but sometimes associated with toxins (ex. Chemotherapy), viral infections, tachycardia and more

Documents

Cardiovascular System components