Chapter 20 THE CARDIOVASCULAR SYSTEM: THE HEART

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Chapter 20THE CARDIOVASCULAR SYSTEM THE HEART

• Lecture Outline

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INTRODUCTION

• The cardiovascular system consists of the blood,
  heart, and blood vessels.
• The heart is the pump that circulates the blood
  through an estimated 60,000 miles of blood
  vessels.
• The study of the normal heart and diseases
  associated with it is known as cardiology.

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Chapter 20 The Cardiovascular System The Heart

• Heart pumps over 1 million gallons per year.
• Over 60,000 miles of blood vessels

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ANATOMY OF THE HEART
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ANATOMY OF THE HEART
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Location of the heart

• The heart is situated between the lungs in the
  mediastinum with about two-thirds of its mass to
  the left of the midline (Figure 20.1).
• Because the heart lies between two rigid
  structures, the vertebral column and the sternum,
  external compression on the chest can be used to
  force blood out of the heart and into the
  circulation. (Clinical Application)

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Heart Location

• Heart is located in the mediastinum
• area from the sternum to the vertebral column and
  between the lungs

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Heart Orientation

• Apex - directed anteriorly, inferiorly and to the
  left
• Base - directed posteriorly, superiorly and to
  the right
• Anterior surface - deep to the sternum and ribs
• Inferior surface - rests on the diaphragm
• Right border - faces right lung
• Left border (pulmonary border) - faces left lung

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Heart Orientation

• Heart has 2 surfaces anterior and inferior,
  and 2 borders right and left

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Surface Projection of the Heart

• Superior right point at the superior border of
  the 3rd right costal cartilage
• Superior left point at the inferior border of the
  2nd left costal cartilage 3cm to the left of
  midline
• Inferior left point at the 5th intercostal space,
  9 cm from the midline
• Inferior right point at superior border of the
  6th right costal cartilage, 3 cm from the midline

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Pericardium

• The heart is enclosed and held in place by the
  pericardium.
• The pericardium consists of an outer fibrous
  pericardium and an inner serous pericardium
  (epicardium. (Figure 20.2a).
• The serous pericardium is composed of a parietal
  layer and a visceral layer.
• Between the parietal and visceral layers of the
  serous pericardium is the pericardial cavity, a
  potential space filled with pericardial fluid
  that reduces friction between the two membranes.
• An inflammation of the pericardium is known as
  pericarditis. Associated bleeding into the
  pericardial cavity compresses the heart (cardiac
  tamponade) and is potentially lethal (Clinical
  Application).

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Pericardium

• Fibrous pericardium
• dense irregular CT
• protects and anchors the heart, prevents
  overstretching
• Serous pericardium
• thin delicate membrane
• contains
• parietal layer-outer layer
• pericardial cavity with pericardial fluid
• visceral layer (epicardium)

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Layers of the Heart Wall

• The wall of the heart has three layers
  epicardium, myocardium, and endocardium (Figure
  20.2a).
• The epicardium consists of mesothelium and
  connective tissue, the myocardium is composed of
  cardiac muscle, and the endocardium consists of
  endothelium and connective tissue (Figure 20.2c).
• Myocarditis is an inflammation of the myocardium.
• Endocarditis in an inflammation of the
  endocardium. It usually involves the heart
  valves.

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Layers of Heart Wall

• Epicardium
• visceral layer of serous pericardium
• Myocardium
• cardiac muscle layer is the bulk of the heart
• Endocardium
• chamber lining valves

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Muscle Bundles of the Myocardium

• Cardiac muscle fibers swirl diagonally around the
  heart in interlacing bundles

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Chambers and Sulci of the Heart (Figure 20.3).

• Four chambers
• 2 upper atria
• 2 lower ventricles
• Sulci - grooves on surface of heart containing
  coronary blood vessels and fat
• coronary sulcus
• encircles heart and marks the boundary between
  the atria and the ventricles
• anterior interventricular sulcus
• marks the boundary between the ventricles
  anteriorly
• posterior interventricular sulcus
• marks the boundary between the ventricles
  posteriorly

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Chambers and Sulci
Anterior View
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Chambers and Sulci
Posterior View
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Right Atrium

• Receives blood from 3 sources
• superior vena cava, inferior vena cava and
  coronary sinus
• Interatrial septum partitions the atria
• Fossa ovalis is a remnant of the fetal foramen
  ovale
• Tricuspid valve
• Blood flows through into right ventricle
• has three cusps composed of dense CT covered by
  endocardium

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Right Ventricle

• Forms most of anterior surface of heart
• Papillary muscles are cone shaped trabeculae
  carneae (raised bundles of cardiac muscle)
• Chordae tendineae cords between valve cusps and
  papillary muscles
• Interventricular septum partitions ventricles
• Pulmonary semilunar valve blood flows into
  pulmonary trunk

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Left Atrium

• Forms most of the base of the heart
• Receives blood from lungs - 4 pulmonary veins (2
  right 2 left)
• Bicuspid valve blood passes through into left
  ventricle
• has two cusps
• to remember names of this valve, try the
  pneumonic LAMB
• Left Atrioventricular, Mitral, or Bicuspid valve

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Left Ventricle

• Forms the apex of heart
• Chordae tendineae anchor bicuspid valve to
  papillary muscles (also has trabeculae carneae
  like right ventricle)
• Aortic semilunar valve
• blood passes through valve into the ascending
  aorta
• just above valve are the openings to the coronary
  arteries

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Myocardial Thickness and Function

• The thickness of the myocardium of the four
  chambers varies according to the function of each
  chamber.
• The atria walls are thin because they deliver
  blood to the ventricles.
• The ventricle walls are thicker because they pump
  blood greater distances (Figure 20.4a).
• The right ventricle walls are thinner than the
  left because they pump blood into the lungs,
  which are nearby and offer very little resistance
  to blood flow.
• The left ventricle walls are thicker because they
  pump blood through the body where the resistance
  to blood flow is greater.

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Myocardial Thickness and Function

• Thickness of myocardium varies according to the
  function of the chamber
• Atria are thin walled, deliver blood to adjacent
  ventricles

• Ventricle walls are much thicker and stronger
• right ventricle supplies blood to the lungs
  (little flow resistance)
• left ventricle wall is the thickest to supply
  systemic circulation

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Thickness of Cardiac Walls
Myocardium of left ventricle is much thicker than
the right.
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HEART VALVES AND CIRCULATION OF BLOOD

• Valves open and close in response to pressure
  changes as the heart contracts and relaxes.

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Fibrous Skeleton of Heart

• (Figure 20.5). Dense CT rings surround the valves
  of the heart, fuse and merge with the
  interventricular septum
• Support structure for heart valves
• Insertion point for cardiac muscle bundles
• Electrical insulator between atria and ventricles
• prevents direct propagation of APs to ventricles

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Atrioventricular Valves Open

• A-V valves open and allow blood to flow from
  atria into ventricles when ventricular pressure
  is lower than atrial pressure
• occurs when ventricles are relaxed, chordae
  tendineae are slack and papillary muscles are
  relaxed

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Atrioventricular Valves Close

• A-V valves close preventing backflow of blood
  into atria
• occurs when ventricles contract, pushing valve
  cusps closed, chordae tendinae are pulled taut
  and papillary muscles contract to pull cords and
  prevent cusps from everting

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Semilunar Valves

• SL valves open with ventricular contraction
• allow blood to flow into pulmonary trunk and
  aorta
• SL valves close with ventricular relaxation
• prevents blood from returning to ventricles,
  blood fills valve cusps, tightly closing the SL
  valves

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Heart valve disorders

• Stenosis is a narrowing of a heart valve which
  restricts blood flow.
• Insufficiency or incompetence is a failure of a
  valve to close completely.
• Stenosed valves may be repaired by balloon
  valvuloplasty, surgical repair, or valve
  replacement.

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Valve Function Review
Which side is anterior surface?
What are the ventricles doing?
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Valve Function Review
Ventricles contract, blood pumped into aorta and
pulmonary trunk through SL valves
Atria contract, blood fills ventricles through
A-V valves
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Blood Circulation

• Two closed circuits, the systemic and pulmonic
• Systemic circulation
• left side of heart pumps blood through body
• left ventricle pumps oxygenated blood into aorta
• aorta branches into many arteries that travel to
  organs
• arteries branch into many arterioles in tissue
• arterioles branch into thin-walled capillaries
  for exchange of gases and nutrients
• deoxygenated blood begins its return in venules
• venules merge into veins and return to right
  atrium

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Blood Circulation (cont.)

• Pulmonary circulation
• right side of heart pumps deoxygenated blood to
  lungs
• right ventricle pumps blood to pulmonary trunk
• pulmonary trunk branches into pulmonary arteries
• pulmonary arteries carry blood to lungs for
  exchange of gases
• oxygenated blood returns to heart in pulmonary
  veins

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Blood Circulation

• Blood flow
• blue deoxygenated
• red oxygenated

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Coronary Circulation

• The flow of blood through the many vessels that
  flow through the myocardium of the heart is
  called the coronary (cardiac) circulation it
  delivers oxygenated blood and nutrients to and
  removes carbon dioxide and wastes from the
  myocardium (Figure 20.8b).
• When blockage of a coronary artery deprives the
  heart muscle of oxygen, reperfusion may damage
  the tissue further. This damage is due to free
  radicals. Drugs that lessen reperfusion damage
  after a heart attack are being developed .

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Coronary Circulation

• Coronary circulation is blood supply to the heart
• Heart as a very active muscle needs lots of O2
• When the heart relaxes high pressure of blood in
  aorta pushes blood into coronary vessels
• Many anastomoses
• connections between arteries supplying blood to
  the same region, provide alternate routes if one
  artery becomes occluded

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Coronary Arteries

• Branches off aorta above aortic semilunar valve
• Left coronary artery
• circumflex branch
• in coronary sulcus, supplies left atrium and left
  ventricle
• anterior interventricular art.
• supplies both ventricles
• Right coronary artery
• marginal branch
• in coronary sulcus, supplies right ventricle
• posterior interventricular art.
• supplies both ventricles

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Coronary Veins

• Collects wastes from cardiac muscle
• Drains into a large sinus on posterior surface of
  heart called the coronary sinus
• Coronary sinus empties into right atrium

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CARDIAC MUSCLE AND THE CARDIAC CONDUCTION SYSTEM
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Histology of Cardiac Muscle

• Compared to skeletal muscle fibers, cardiac
  muscle fibers are shorter in length, larger in
  diameter, and squarish rather than circular in
  transverse section (Figure 20.9).
• They also exhibit branching (Table 4.4B).
• Fibers within the networks are connected by
  intercalated discs, which consist of desmosomes
  and gap junctions
• Cardiac muscles have the same arrangement of
  actin and myosin, and the same bands, zones, and
  Z discs as skeletal muscles.
• They do have less sarcoplasmic reticulum than
  skeletal muscles and require Ca2 from
  extracellular fluid for contraction.

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Cardiac Muscle Histology

• Branching, intercalated discs with gap junctions,
  involuntary, striated, single central nucleus per
  cell

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Cardiac Myofibril
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Conduction System of Heart
Coordinates contraction of heart muscle.
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Myocardial ischemia and infarction

• Reduced blood flow through coronary arteris may
  cause ischemia. Ischemia cuases hypoxia and may
  weaken the myocardial cells. Ischemia is often
  manifested through angina pectoris.
• A complete obstruction of flow in a coronary
  artery may cause myocardial infarction (heart
  attack).
• Tissue distal to the obstruction dies and is
  replaced by scar tissur.
• Treatment may involve injection of thrombolytic
  agents, coronary angioplasty, or coronary artery
  bypass grafts.
• While it was long thought that cardiac muscle
  lacked stem cells, recent studies five evidence
  for replacement of heart cells. It appears that
  stem cells in the blood can migrate to the heart
  and differentiate into myocardial cells.

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Autorhythmic Cells The Conduction System

• Cardiac muscle cells are autorhythmic cells
  because they are self-excitable. They repeatedly
  generate spontaneous action potentials that then
  trigger heart contractions.
• These cells act as a pacemaker to set the rhythm
  for the entire heart.
• They form the conduction system, the route for
  propagating action potential through the heart
  muscle.

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Conduction System of Heart
Coordinates contraction of heart muscle.
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Conduction

• Components of this system are the sinoartrial
  (SA) node (pacemaker), atrioventricular (AV)
  node, atrioventricular bundle (bundle of His),
  right and left bundle branches, and the
  conduction myofibers (Purkinje fibers) (Figure
  20.10)
• Signals from the autonomic nervous system and
  hormones, such as epinephrine, do modify the
  heartbeat (in terms of rate and strength of
  contraction), but they do not establish the
  fundamental rhythm.

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Conduction System of Heart

• Autorhythmic Cells
• Cells fire spontaneously, act as pacemaker and
  form conduction system for the heart
• SA node
• cluster of cells in wall of Rt. Atria
• begins heart activity that spreads to both atria
• excitation spreads to AV node
• AV node
• in atrial septum, transmits signal to bundle of
  His
• AV bundle of His
• the connection between atria and ventricles
• divides into bundle branches purkinje fibers,
  large diameter fibers that conduct signals quickly

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Rhythm of Conduction System

• SA node fires spontaneously 90-100 times per
  minute
• AV node fires at 40-50 times per minute
• If both nodes are suppressed fibers in ventricles
  by themselves fire only 20-40 times per minute
• Artificial pacemaker needed if pace is too slow
• Extra beats forming at other sites are called
  ectopic pacemakers
• caffeine nicotine increase activity

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Timing of Atrial Ventricular Excitation

• SA node setting pace since is the fastest
• In 50 msec excitation spreads through both atria
  and down to AV node
• 100 msec delay at AV node due to smaller diameter
  fibers- allows atria to fully contract filling
  ventricles before ventricles contract
• In 50 msec excitation spreads through both
  ventricles simultaneously

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Abnormal Conduction

• Sick sinus syndrome describes an abnormally
  functioning SA node that initiates irregular
  heart beats.
• When abnormal pacing of the heart develops, heart
  rhythm can be restored by implanting an
  artificail pacemaker, a device that sends out
  small, regular currents to stimulate myocardial
  contraction..

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Action potential and contraction of contractile
fibers

• An impulse in a ventricular contractile fiber is
  characterized by rapid depolarization, plateau,
  and repolarization (Figure 20.11).
• The refractory period of a cardiac muscle fiber
  (the time interval when a second contraction
  cannot be triggered) is longer than the
  contraction itself (Figure 20.11). Therefore
  tetanus cannot occur in myocardial cells.

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Conduction System of the Heart
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Physiology of Contraction

• Depolarization, plateau, repolarization

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Depolarization Repolarization

• Depolarization
• Cardiac cell resting membrane potential is -90mv
• excitation spreads through gap junctions
• fast Na channels open for rapid depolarization
• Plateau phase
• 250 msec (only 1msec in neuron)
• slow Ca2 channels open, let Ca 2 enter from
  outside cell and from storage in sarcoplasmic
  reticulum, while K channels close
• Ca 2 binds to troponin to allow for actin-myosin
  cross-bridge formation tension development
• Repolarization
• Ca2 channels close and K channels open -90mv
  is restored as potassium leaves the cell
• Refractory period
• very long so heart can fill

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Action Potential in Cardiac Muscle
Changes in cell membrane permeability.
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ATP production in cardiac muscle

• Cardiac muscle relies on aerobic cellular
  respiration for ATP production.
• Cardiac muscle also produces some ATP from
  creatine phosphate
• The presence of creatine kinase (CK) in the blood
  indicates injury of cardiac muscle usually caused
  by a myocardial infarction.

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Electrocardiogram

• Impulse conduction through the heart generates
  electrical currents that can be detected at the
  surface of the body. A recording of the
  electrical changes that accompany each cardiac
  cycle (heartbeat) is called an electrocardiogram
  (ECG or EKG).
• The ECG helps to determine if the conduction
  pathway is abnormal, if the heart is enlarged,
  and if certain regions are damaged.
• Figure 20.12 shows a typical ECG.

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Electrocardiogram---ECG or EKG

• EKG
• Action potentials of all active cells can be
  detected and recorded
• P wave
• atrial depolarization
• P to Q interval
• conduction time from atrial to ventricular
  excitation
• QRS complex
• ventricular depolarization
• T wave
• ventricular repolarization

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ECG

• In a typical Lead II record, three clearly
  visible waves accompany each heartbeat It
  consists of.
• P wave (atrial depolarization - spread of
  impulse from SA node over atria)
• QRS complex (ventricular depolarization - spread
  of impulse through ventricles)
• T wave (ventricular repolarization).
• Correlation of ECG waves with atrial and
  ventricular systole (Figure 20.13)

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ECG

• As atrial fibers depolarize, the P wave appears.
• After the P wave begins, the atria contract
  (atrial systole). Action potential slows at the
  AV node giving the atria time to contract.
• The action potential moves rapidly through the
  bundle branches, Purkinje fibers, and the
  ventricular myocardium producing the QRS complex.
• Ventricular contraction after the QRS comples and
  continues through the ST segment.
• Repolarization of the ventricles produces the T
  wave.
• Both atria and ventricles repolarize and the P
  wave appears.

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THE CARDIAC CYCLE

• A cardiac cycle consists of the systole
  (contraction) and diastole (relaxation) of both
  atria, rapidly followed by the systole and
  diastole of both ventricles.
• Pressure and volume changes during the cardiac
  cycle
• During a cardiac cycle atria and ventricles
  alternately contract and relax forcing blood from
  areas of high pressure to areas of lower
  pressure.
• Figure 20.14 shows the relation between the ECG
  and changes in atrial pressure, ventricular
  pressure, aortic pressure, and ventricular volume
  during the cardia cycle.

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One Cardiac Cycle - Vocabulary

• At 75 beats/min, one cycle requires 0.8 sec.
• systole (contraction) and diastole (relaxation)
  of both atria, plus the systole and diastole of
  both ventricles
• End diastolic volume (EDV)
• volume in ventricle at end of diastole, about
  130ml
• End systolic volume (ESV)
• volume in ventricle at end of systole, about 60ml
• Stroke volume (SV)
• the volume ejected per beat from each ventricle,
  about 70ml
• SV EDV - ESV

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Phases of Cardiac Cycle

• Isovolumetric relaxation
• brief period when volume in ventricles does not
  change--as ventricles relax, pressure drops and
  AV valves open
• Ventricular filling
• rapid ventricular fillingas blood flows from
  full atria
• diastasis as blood flows from atria in smaller
  volume
• atrial systole pushes final 20-25 ml blood into
  ventricle
• Ventricular systole
• ventricular systole
• isovolumetric contraction
• brief period, AV valves close before SL valves
  open
• ventricular ejection as SL valves open and blood
  is ejected

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Cardiac Cycle
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Atrial systole/ventricular diastole

• The atria contract, increasing pressure forces
  the AV valves to open.
• The amount of blood in the ventricle at the end
  of diastole is the End Diastolic Volume (EDV)
• Ventricular systole/atrial diastole
• Ventricles contract and increasing pressure
  forces the AV valves to close.
• AV and SL valves are all closed (isovolumetric
  contraction).
• Pressure continues to rise opening the SL valves
  leading to ventricular ejection.
• The amount of blood in the left ventrical at the
  end of systole is End Systolic Volume (ESV).
  Stroke volume (SV) is the volume of blood ejected
  from the left ventricle SV EDV-ESV.

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Relaxation period

• Both atria and ventricles are relaxed. Pressure
  in the ventricles fall and the SL valves close.
  Brief time all four valves are closed is the
  isovolumetric relaxation. Pressure in the
  ventricles continues to fall, the AV valves open,
  and ventricular filling begins.

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Ventricular Pressures

• Blood pressure in aorta is 120mm Hg
• Blood pressure in pulmonary trunk is 30mm Hg
• Differences in ventricle wall thickness allows
  heart to push the same amount of blood with more
  force from the left ventricle
• The volume of blood ejected from each ventricle
  is 70ml (stroke volume)
• Why do both stroke volumes need to be same?

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Auscultation

• The act of listening to sounds within the body is
  called auscultation, and it is usually done with
  a stethoscope. The sound of a heartbeat comes
  primarily from the turbulence in blood flow
  caused by the closure of the valves, not from the
  contraction of the heart muscle (Figure 20.15).
• The first heart sound (lubb) is created by blood
  turbulence associated with the closing of the
  atrioventricular valves soon after ventricular
  systole begins.
• The second heart sound (dupp) represents the
  closing of the semilunar valves close to the end
  of the ventricular systole.

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Heart Sounds
Where to listen on chest wall for heart sounds.
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Murmurs

• A heart murmur is an abnormal sound that consists
  of a flow noise that is heard before, between, or
  after the lubb-dupp or that may mask the normal
  sounds entirely.
• Some murmurs are caused by turbulent blood flow
  around valves due to abnormal anatomy or
  increased volume of flow.
• Not all murmurs are abnormal or symptomatic, but
  most indicate a valve disorder.

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CARDIAC OUTPUT

• Since the bodys need for oxygen varies with the
  level of activity, the hearts ability to
  discharge oxygen-carrying blood must also be
  variable. Body cells need specific amounts of
  blood each minute to maintain health and life.
• Cardiac output (CO) is the volume of blood
  ejected from the left ventricle (or the right
  ventricle) into the aorta (or pulmonary trunk)
  each minute.
• Cardiac output equals the stroke volume, the
  volume of blood ejected by the ventricle with
  each contraction, multiplied by the heart rate,
  the number of beats per minute. CO SV X HR
• Cardiac reserve is the ratio between the maximum
  cardiac output a person can achieve and the
  cardiac output at rest.

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Cardiac Output

• CO SV x HR
• at 70ml stroke volume 75 beat/min----5 and 1/4
  liters/min
• entire blood supply passes through circulatory
  system every minute
• Cardiac reserve is maximum output/output at rest
• average is 4-5x while athletes is 7-8x

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Influences on Stroke Volume

• Preload (affect of stretching)
• Frank-Starling Law of Heart
• more muscle is stretched, greater force of
  contraction
• more blood more force of contraction results
• Contractility
• autonomic nerves, hormones, Ca2 or K levels
• Afterload
• amount of pressure created by the blood in the
  way
• high blood pressure creates high afterload

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Stroke Volume and Heart Rate
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Preload Effect of Stretching

• According to the Frank-Starling law of the heart,
  a greater preload (stretch) on cardiac muscle
  fibers just before they contract increases their
  force of contraction during systole.
• Preload is proportional to EDV.
• EDV is determined by length of ventricular
  diastole and venous return.
• The Frank-Starling law of the heart equalizes the
  output of the right and left ventricles and keeps
  the same volume of blood flowing to both the
  systemic and pulmonary circulations.

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Contractility

• Myocardial contractility, the strength of
  contraction at any given preload, is affected by
  positive and negative inotropic agents.
• Positive inotropic agents increase contractility
• Negative inotropic agents decrease contractility.
• For a constant preload, the stroke volume
  increases when positive inotropic agents are
  present and decreases when negative inotropic
  agents are present.

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Afterload

• The pressure that must be overcome before a
  semilunar valve can open is the afterload.
• In congestive heart failure, blood begins to
  remain in the ventricles increasing the preload
  and ultimately causing an overstretching of the
  heart and less forceful contraction
• Left ventricular failure results in pulmonary
  edema
• Right ventricular failure results in peripheral
  edema.

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Regulation of Heart Rate

• Cardiac output depends on heart rate as well as
  stroke volume. Changing heart rate is the bodys
  principal mechanism of short-term control over
  cardiac output and blood pressure. Several
  factors contribute to regulation of heart rate.

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Regulation of Heart Rate

• Nervous control from the cardiovascular center in
  the medulla
• Sympathetic impulses increase heart rate and
  force of contraction
• parasympathetic impulses decrease heart rate.
• Baroreceptors (pressure receptors) detect change
  in BP and send info to the cardiovascular center
• located in the arch of the aorta and carotid
  arteries
• Heart rate is also affected by hormones
• epinephrine, norepinephrine, thyroid hormones
• ions (Na, K, Ca2)
• age, gender, physical fitness, and temperature

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Regulation of Heart Rate
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Autonomic regulation of the heart

• Nervous control of the cardiovascular system
  stems from the cardiovascular center in the
  medulla oblongata (Figure 20.16).
• Proprioceptors, baroreceptors, and chemoreceptors
  monitor factors that influence the heart rate.
• Sympathetic impulses increase heart rate and
  force of contraction parasympathetic impulses
  decrease heart rate.

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Chemical regulation of heart rate

• Heart rate affected by hormones (epinephrine,
  norepinephrine, thyroid hormones).
• Cations (Na, K, Ca2) also affect heart rate.
• Other factors such as age, gender, physical
  fitness, and temperature also affect heart rate.
• Figure 20.16 summarizes the factors that can
  increase stoke volume and heart rate to cause an
  increase in cardiac output..

87
Risk Factors for Heart Disease

• Risk factors in heart disease
• high blood cholesterol level
• high blood pressure
• cigarette smoking
• obesity lack of regular exercise.
• Other factors include
• diabetes mellitus
• genetic predisposition
• male gender
• high blood levels of fibrinogen
• left ventricular hypertrophy

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Plasma Lipids and Heart Disease

• Risk factor for developing heart disease is high
  blood cholesterol level.
• promotes growth of fatty plaques
• Most lipids are transported as lipoproteins
• low-density lipoproteins (LDLs)
• high-density lipoproteins (HDLs)
• very low-density lipoproteins (VLDLs)
• HDLs remove excess cholesterol from circulation
• LDLs are associated with the formation of fatty
  plaques
• VLDLs contribute to increased fatty plaque
  formation
• There are two sources of cholesterol in the body
• in foods we ingest formed by liver

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Desirable Levels of Blood Cholesterol for Adults

• TC (total cholesterol) under 200 mg/dl
• LDL under 130 mg/dl
• HDL over 40 mg/dl
• Normally, triglycerides are in the range of
  10-190 mg/dl.
• Among the therapies used to reduce blood
  cholesterol level are exercise, diet, and drugs.

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EXERCISE AND THE HEART

• A persons cardiovascular fitness can be improved
  with regular exercise.
• Aerobic exercise (any activity that works large
  body muscles for at least 20 minutes, preferably
  3 5 times per week) increases cardiac output
  and elevates metabolic rate.
• Several weeks of training results in maximal
  cardiac output and oxygen delivery to tissues
• Regular exercise also decreases anxiety and
  depression, controls weight, and increases
  fibrinolytic activity.
• Sustained exercise increases oxygen demand in
  muscles
• As a heart fails, a persons mobility decreases.
  Heart transplants may help such individuals.
  Other possibilities include cardiac assist
  devices and surgical procedures. Table 20.1
  describes several devices and procedures.

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DEVELOPMENT OF THE HEART

• The heart develops from mesoderm before the end
  of the third week of gestation.
• The endothelial tubes develop into the
  four-chambered heart and great vessels of the
  heart (Figure 20.18).

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Developmental Anatomy of the Heart

• The heart develops from mesoderm before the end
  of the third week of gestation.
• The tubes develop into the four-chambered heart
  and great vessels of the heart.

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DISORDERS HOMEOSTATIC IMBALANCES
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Clinical Problems

• MI myocardial infarction
• death of area of heart muscle from lack of O2
• replaced with scar tissue
• results depend on size location of damage
• Blood clot
• use clot dissolving drugs streptokinase or t-PA
  heparin
• balloon angioplasty
• Angina pectoris----heart pain from ischemia of
  cardiac muscle

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CAD

• Coronary artery disease (CAD), or coronary heart
  disease (CHD), is a condition in which the heart
  muscle receives an inadequate amount of blood due
  to obstruction of its blood supply. It is the
  leading cause of death in the United States each
  year. The principal causes of obstruction include
  atherosclerosis, coronary artery spasm, or a clot
  in a coronary artery.
• Risk factors for development of CAD include high
  blood cholesterol levels, high blood pressure,
  cigarette smoking, obesity, diabetes, type A
  personality, and sedentary lifestyle.

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CAD

• Atherosclerosis is a process in which smooth
  muscle cells proliferate and fatty substances,
  especially cholesterol and triglycerides (neutral
  fats), accumulate in the walls of the
  medium-sized and large arteries in response to
  certain stimuli, such as endothelial damage
  (Figure 20.18).
• Diagnosis of CAD includes such procedures as
  cardiac catherization and cardiac angiography.
• Treatment options for CAD include drugs and
  coronary artery bypass grafting (Figure 20.19).

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Coronary Artery Disease

• Heart muscle receiving insufficient blood supply
• narrowing of vessels---atherosclerosis, artery
  spasm or clot
• atherosclerosis--smooth muscle fatty deposits
  in walls of arteries
• Treatment
• drugs, bypass graft, angioplasty, stent

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By-pass Graft
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Percutaneous Transluminal Coronary Angioplasty
Stent
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Congenital Heart Defects

• A congenital defect is a defect that exists at
  birth, and usually before birth.
• Congenital defects of the heart include
  coarctation of the aorta, patent ductus
  arteriosus, septal defects (interatrial or
  interventricular), valvular stenosis, and
  tetralogy of Fallot.
• Some congenital defects are not serious or remain
  asymptomatic others heal themselves.
• A few congenital defects are life threatening and
  must be corrected surgically. Fortunately,
  surgical techniques are highly refined for most
  of the defects listed.

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Arrythmia

• Arrhythmia (disrhythmia) is an irregularity in
  heart rhythm resulting from a defect in the
  conduction system of the heart.
• Categories are bradycardia, tachycardia, and
  fibrillation.
• Those that begin in the atria are
  supraventricular or atrial.
• Those that begin in the ventricle are ventricular.

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Congestive Heart Failure

• Congestive heart failure is a chronic or acute
  state that results when the heart is not capable
  of supplying the oxygen demands of the body.
• Causes of CHF
• coronary artery disease, hypertension, MI, valve
  disorders, congenital defects
• Left side heart failure
• less effective pump so more blood remains in
  ventricle
• heart is overstretched even more blood remains
• blood backs up into lungs as pulmonary edema
• suffocation lack of oxygen to the tissues
• Right side failure
• fluid builds up in tissues as peripheral edema

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• end