Chapter 20 – The Heart

The Heart
 Apex  Pointed Portion
o Midclavicular line of 5th intercostal
o Inferior Left Anterior
 Base  Broad and Wide Area
o Blood Vessels are attached
o Superior Right Posterior
 Pericardium  Enclosed covering of the heart
o Pericardial Sac
 Located in the mediastinum  Central Thoracic Cavity
o 2/3rd to the left
o Heart is found in the Pericardial Region
o Heart is surrounded by plural cavities on both sides
 Placed in a downward angle
o Anteriorly to the Left

Pericardium
 Covering on top of the heart
 Fibrous Pericardium  Outer layer
o Dense Irregular Connective Tissue
 Double lining found between outer and inner cavities
 Parietal Pericardium  Outer segment of pericardial sac
o Mesothelium
 Visceral Serious Pericardium Covers the heart itself
 Serious Components  Closed cavities
o Not open to exterior
 Pericardial Fluid Fills Pericardial Sac
o In between Visceral and Parietal Layers

Pericardium Function
 Anchors and Protects Heart
 Separates heart from surroundings
 Prevents Inflation
 Facilitates movement of heart

Clinical Situations
 Pericarditis  Rubbing of Parietal and Visceral Layer
 Pericardial Effusion  Excessive Fluid (Chronic)
o Pressure on heart and prevents blood from entering
 Pericardial Tamponed  Too much fluid (Acute)
o Blood can seep through and increase pressure on heart (Lethal)
Superficial Anatomy
 Sulcus  Depressions found on the heart
 Coronary Sulcus  Separates Right Atrium and Right Ventricle
o Base of Heart
 Interventricular Sulcus  Separate Left and Right Ventricles
o Anterior and Posterior Portions
 Landmarks for Intraventricular Septum
 Important blood vessels found inside
 Components of the Heart Wall
o Epicardium  Outer Wall (Visceral)
o Myocardium  Muscle
 Cardiac Muscle
o Endocardium  Inner heart
 Endothelium

Internal Anatomy
 Interatrial Septum  Separates Atrium
o Atria  Superior and Thin
 Interventricular Septum  Separates Ventricles
o Ventricles  Inferior and Thick
 Septum prevent blood from mixing between chambers

Chambers of the Heart

 Atria receive blood
o Right  Body
o Left  Lungs
 Ventricles pump blood
o Right  Lungs
 Pulmonary Hypertension can cause hypertrophy
 Ventricle becomes over worked
o Left  Body
 Most muscle because has to cover most area
 More force required to cover more area

Right Atrium
 Function  Receives blood from the body
 Superior Vena Cava  From Head
 Inferior Vena Cava  From Body
 Coronary Sinus  Drainage of blood from heart
o Empties heart’s blood into Right Atrium
 Foramen Ovale  Opening between atria found in babies (Placenta)
o Closes after the baby is born
o Pressure difference causes hole to close  Fossa Ovalis
Ductus Arteriosus
 Ductus Arteriosus  Connection between Pulmonary Artery and Aorta
o Blood travels from right ventricle to Aorta
o Skips left atrium as blood from lungs is not needed

Right Ventricle
 Blood passes from Left Ventricle to Right Ventricle
 Inferior to Right Atrium
 Tricuspid Valve  Allows blood to flow from RA  RV
o Tricuspid  3 Flaps
o Prevents backflow of blood
o Blood flows in one direction
o Incompetent Tricuspid Valve  Leaky Valve
 Blood flows back into RA
o Valvar Stenosis  Narrowing of Valve
 Increase of pressure in RA
 Can cause systemic swelling (Reduced Blood)
 Chorda Tendinae  Fingerlike Fibers in Tricuspid Valve
o Supports valve from not opening backwards
o Pressure in ventricles allows blood to flow from RA
 Opens the Valve and Chorda Tendinae
 Systole  Contraction
o Backflow is prevented
 Diastole  Relaxation
 Trabeculae Carnae  Raised muscles inside
o Unevenness  Prevents sticking of blood
 Pulmonary Valve  Guards blood flow to the lungs
o Semilunar Valve
o Valve is subdivided into Pulmonary Trunk
 Divided into Left and Right Pulmonary Arteries

Left Atrium
 Pulmonary veins bring blood back to heart
 Fossa Ovalis is present
o Prevents blood from going back to Right Atrium
 Bicuspid Valve  Blood passes to Left Ventricle
o Mitral Valve
o Chordae Tendinae are present
Left Ventricle
 Holds same volume as right ventricle
 Thicker than RV
o Pumps through a greater area
 Size of Ventricle is the same
 Interventricular Septum  Partition between 2 Ventricles
 Aortic Semilunar Valve  Blood exits Systemically
 Ascending Aorta  Carries blood upward
o Aortic Arch Bends Aorta downward
 Descending Aorta  Carries blood downward

The Heart Valves

 Classified by location and shape
 AV Valve (Atrioventricular)
o Tricuspid  RA to RV
o Bicuspid  LA to LV
o Prevents backflow
 Blood pressure closes valves during contraction
o Chordae Tendinae prevent backflow
 SV Valve (Semilunar)
o Named by structure they are in front of
 Pulmonary  RV to Lung
 Aortic  LV to Body
o 3 Flaps but no Chorda Tendinae
 As they close, the flaps support each other
o Incompetence/Stenosis  Heart efficiency is
destroyed

Cardiac Skeleton
 Connective tissue that is supporting the valves (4 Rings)
o Stiffen and supports valves
 Electrically separates Atria from ventricles
o Cardiac muscles are linked electrically and send stimulus to entire heart
o Insulating Layer
 Prevents haphazard activation
 Allows origin and insertion points for cardiac muscles
 Acts as the “Bone”

Coronary Circulation
 Blood supply of the muscle tissue of the heart
o Coronary Arteries and Cardiac Veins
 Cardiac muscle is very thick so own blood supply is needed
 Artery is Away and Vein is Towards
Right Coronary Artery
 Branches off of Aorta
o Near Aortic Semilunar Valve
 Ventricles Contract  Blood enters circulation of body
o Internal Heart blood flow will stop
o Muscle wall squeezes
 Constrict the Coronary Artery and stop blood flow
o Aortic Semilunar Valve is open
 Flaps cover the opening of Coronary Artery
 Heart Relaxes  Coronary Flow

Right Coronary Artery Pathway

 Branches off Ascending Aorta
o Travels along Coronary Sulcus between RA and RV
o Wraps around Coronary Sulcus and goes Posterior
 Branches Form
o Right Marginal Artery  Large branch on border
o Posterior Interventricular Artery  Terminal Branch
 Supplies blood to RA, RV, LV
o Nourishes SA and AV Nodes
 Action Potential
o Proper nutrition is supplied to blood through Coronary Artery

Left Coronary Artery

 Shorter artery
 Most is hidden
 Supplies blood to LA, LV, and Interventricular Septum

Left Coronary Artery Pathway

 Branches left of Ascending Aorta
o Goes to Left Ventricle
o Wraps behind the Pulmonary Trunk
 Divides into smaller branches
o Anterior Interventricular Artery
o Circumflex Artery
 Wraps around left side and goes to posterior

Clinical Situation
 Bypass Surgery  Obstruction of Coronary Arteries
o Stents
o Blood Vessels
Cardiac Veins
 Drains blood back into the heart
 Great Cardiac Vein
o On left side of heart
 Gets larger and wraps around to right side
o Drains blood from Anterior Interventricular Vein to Coronary Sinus
 Anterior Cardiac Vein
o Drains blood into right atrium
 Posterior/Middle/Small Cardiac Vein
o Drains to either Great Cardiac Vein or Coronary Sinus (To Right Atrium)

Flow of Blood
 Superior/Inferior Vena Cava
 Right Atrium
o Tricuspid Valve
 Right Ventricle
o Pulmonary Semilunar Valves
 Pulmonary Trunk
 Pulmonary Artery
 Lungs
 Pulmonary Vein
 Left Atrium
o Bicuspid Valve
 Left Ventricle
o Aortic Semilunar Valve
 Aorta
o Coronary Arteries
o Heart Tissue
o Cardiac Veins and Coronary Sinus
 Body

Cardiac Muscle Tissue

 Myocytes
 Intercalated Discs
o Interlinks between muscle cells
 Junctions present
o Gap Junctions and Desmosomes
 Desmosomes hold cells together via ECM
 Heart generates tension so support is needed
 Gap Junctions allow Ion movement for Action Potential
 No Neuromuscular Junction
o One side of heart can activate other side
 Cardiac Muscle is also called Functional Syncytium
Cardiac Muscle Characteristics
 Small
 Single and Central Nucleus
 Intercalation between cells
 T – Tubules present at Z Disc
o 1 per Sarcomere
 No Triads

Cardiac Physiology
 Conducting System
o Controls and Coordinates Heartbeat
o Generates and transmits Action Potential to parts of the heart
 Contractile System
o Produces contractions that propel blood
o Most abundant

Conducting System
 Specialized Cardiac Cells
o Send impulses to stimulate contractions
o Allows for cells to contract themselves
 Automaticity
o Action potential flows automatically without outside influence

Prepotential
 Also called Pacemaker Potential
o Depolarization to reach Threshold
 Conducting system is made up of Auto-rhythmic Cells
 Resting Potential  -60
o Not Stable
 Leakier sodium channels are in play
 Higher influx = Better Depolarization
 Threshold (-40)  Electrically gated Calcium Channels open
o Rush of Calcium brings positive charge
 Pacemaker Action Potential is due to Calcium
 Prepotential in muscle cells was graded potential
o Cardiac Muscles  Depolarization via Sodium
 Repolarization (0)  Potassium leaks out
o Repolarizes and cycle repeats
Action Potential Manipulation
 Action Potential Rate can cause repolarization to change
o Faster Threshold = Faster Heartbeat
 Drugs
 Lower threshold to -50 instead of -40
 Increase threshold to slow heart
 Calcium Blockers = Limit Depolarization
 Different parts of conducting system depolarize at different rates
o Fastest node will control rest of system
o External stimulus effects heart rate
 Keeps synchronized depolarization
 SA Node is the natural pacemaker
o Backups are in place if it fails

Contractile Cells
 Purkinje Fibers link 2 systems together
 Electrical stimulus is sent to contractile cells
o Sarcomere contracts
o Different contraction rate than skeletal muscles

Contractile Pathway
 SA Node sends signal of depolarization
o Action Potential Occurs
 Rapid Depolarization Resting Potential is -90
o Depolarizes to +30 during Action Potential
 Plateau  Calcium enters and Potassium leaves
o No net change
o Graph remains still
o Absolute Refractory
 Repolarization  Calcium closes and Potassium opens
o Slight Hyperpolarization
o Relative Refractory

Timing of Refractory
 30x Longer in Cardiac Muscles
 Skeletal Muscles  AP and Refractory occur before muscle can contract
o Tough to generate new AP
o Can stimulate muscle over and over again to alter rate
 Cardiac Muscles need to rest
o To fill with blood and keep constant rate
 Heart contraction occurs within refractory period
o Prevent Tetany
Structure of Conducting System
 SA Node  Right Atrium
o Near Superior Vena Cava
 AV Node  Between Interatrial Septum and Right Atrium Floor
o By the Right Ventricle
 Internodal Pathway  Between Left and Right Atrium
 Cardiac Skeleton  Electrically isolates chambers of heart
o Atria activation prevents ventricle activation
 Bundle of His (AV Bundle)  Electrical Pathway between Atria
and Ventricle
o Only way AP is transmitted
o Wolf Parkinson  Several Pathways Open
 Bundle of His divides at Interventricular Septum
o Bundle Branches (Left and Right)
o Left  Divided into Anterior and Posterior Divisions
 Purkinje Fibers  Apex of heart and termination of conducting system
o Fine Fibers

Transmission of Impulse
 Begins at SA node
o Natural Pacemaker
 Spreads towards the Atria and then through AV node
o Then travels through Bundles of His
 Travels through Bundle Branches
o Into Ventricles
 Ends at Purkinje Fibers
o Mechanical transmission becomes electrical

Heart Rate
 SA Node generates 80-100 AP/Minute
o Depolarization rate slows down as you travel through heart
o Controls how fast other cells depolarize
 Transmission goes through AV Node (40-60)
o Heart rates decreases if AV node is damaged
 If Atria is damaged, heart still pumps
o Ventricles still receive stimulus to pump blood
 Parasympathetic NS helps slow down heart rate
Abnormal Pacemaker
 Normal heart rate  72 beats per minute
 Vagus Nerve (X) suppresses full heart rate
o Heart Rate can be 100 without Vagul Influence
 Bradycardia  Less than 60 BPM
 Tachycardia  Over 100 BPM
 Etopic Pacemaker  Anything that is not SA Node
o Abnormal Cells
 Pacemaker influences EKG
o Shows if SA Node is working

Electrocardiogram (ECG/EKG)
 Measures electrical stimulus of the heart
 Electrodes detect stimulus change of heart
o Values apply to adults
 Leads are done to measure heart activity
o 6 on lungs and 6 on heart
o Limbs
 Standard  1, 2, 3
 Augmented  aVL, aVR, aVF
o Chest
 V1 – V6
 Voltmeter detects change

Limb Leads
 Net Deflection determines ECG Graph
 Positions reflect you viewing the patient
 Lead 1  Right (+) and Left (-) Arm
o If wave depolarization goes to right arm, it gets deflected
o Amplitude of ECG varies depending on strength of deflection
o Across Heart
 Lead 2  Left arm (-) and Right leg (+)
o Follows heart axis
o Follows angle of the heart
o Detection of Rhythm
 Lead 3  Right arm (-) and Right Leg (+)
 Augmented angles fill gaps between limbs
o Body (-) and Limbs (+)
 aVF  Augmented Voltage Foot
o Right foot suppresses static and measures frontal axis
 aVL  Augmented Voltage Left (Arm)
 aVR  Augmented Voltage Right (Arm)
Chest Leads
 Placed around heart
o Horizontal Readings
 V1 – V6 are placed around the chest
o V1  4th Intercostal Space of Right Sternum
o V2  4th Intercostal Space of Left Sternum
o V4  5th Intercostal of Midclavicular Line
o V3  Between V2 and V4
o V5  5th Intercostal in Armpit
o V6  Middle of Armpit
 Combine with Limb lead for complete heart image

ECG Reading
 Reflects Limb Lead 2 the most
 + and –  electrical waves
 Flats  No electrical change
 P Wave  Information of Atrial Depolarization
o Normal or Excessive Depolarization
o Usually SA Node
 Graph would change if it looked different
o Heart Block  Atria signal never reaches ventricle
 P-R Interval  Segment between P and R wave
o AV Node delays conductions from Atria to Ventricle
o Over conduction  Longer P-R Interval
o Defective AV Node  No QRS Complex
 No transmission of signal
 Ventricles will contract on their
own
 QRS Complex  Shows ventricular
depolarization
o Much Larger
o Hypertrophy  Excessive contraction
 Higher wave
 T Wave  Ventricular Repolarization
o Overshadows Atrial Repolarization
 Q-T Interval  From Q wave to T Wave
 Physical contraction of heart is seen by Echocardiogram
2 Phases of Cardiac Cycle
 Occurs in any of the 4 chambers
 1 Cycle  Systole + Diastole
o 1 Cycle per second
 Fast Heart Rate  Short Cycle
 Slow Heart Rate  Long Cycle
o Ventricles are usually chambers of interest

Phases of Cardiac Cycle

 Blood moves because pressure changes in heart
o High to Low
 Happens in Left and Right Side
 Late Ventricular Diastole  Ventricle is relaxed and
pressure is 0
o Atria is filled and has pressure of 7
o Right Ventricle has lowest pressure
 Blood travels there
o Tricuspid Valve (AV Valve) allows for blood to travel to ventricle
o Most blood (80%) is pushed by gravity
 Late Ventricular Diastole fulfils last 20%
 Ventricular Systole  Ventricular Pressure rises to 8
o Blood is present here
o Atria has decrease in pressure
 Pressure is lowest here
 Tricuspid Valve prevents backflow of blood
o All valves close and pressure in ventricle increases
o Volume remains stays same
 Pressure rises as blood fills
o Once pressure rises and is greater than Pulmonary Trunk/Aorta
 Blood is ejected  Ventricular Ejection
 Early/Mid Ventricular Diastole  Ventricles relax and pressure drops
o Semilunar Valves are closed so blood in Aorta/Pulmonary Trunk cannot push
back
o Isovolumetric Laxation  Decrease of pressure causes valves to be closed
o Atria fill with blood and their pressure increases
 AV valves open and blood will eventually rush into ventricles
 Relaxation is Longer than Contraction
 Peak Systole Pressure  120 mm Hg
 Peak Diastole Pressure  80 mm Hg
Sound of the Heart
 S1  Closing of AV Valves
o First sound of the heart
 S2  Closing of SV Valves
 Abnormal sounds can be heard
o Narrowing of valves
o Structural Abnormalities
 Different parts of the chest are linked to different sounds
o Sound and Flow move together
 Different Valves can be heard via stethoscope
o Aortic  2nd Intercostal Space on Right of Sternum
o Pulmonary  2nd Intercostal Space on Left of Sternum
o Tricuspid  5th Intercostal on Right of Sternum
o Bicuspid  5th Intercostal on Mid Clavicular Line

Cardiodynamics
 Movement and force generated by Cardiac Contractions
o End – Diastolic Volume  Amount of Blood When fully Relaxed
o End – Systolic Volume  Amount of Blood when fully Contracted
o Strove Volume  EDV – ESV
 Amount of blood pushed out in 1 Cardiac Cycle
o Ejection Fraction  Percentage of blood pushed out
 Compared to what remains
 If EDV is 130, and ESV is 50, SV is 80
o 50 mL of blood has been pushed out

Cardiac Output
 Amount blood pumped out per minute
 CO = HR x SV
o 70 bpm x 80 mL = 5.6 L/min
o Beats per Minute x Contraction Cycles
 CO is proportional to HR and SV

What Influences Cardiac Output

 Heart Rate
o Nervous System
o Hormones
 Stroke Volume
o EDV
o ESV
Heart Rate Influences
 Autonomic Innervation
o Medulla Oblongata and Pons have neurons that effect several systems
 Cardioacceleratory Center raises HR (Sympathetic)
 Cardioinhibitory Center lowers HR (Parasympathetic)
o Input comes from Baroreceptors and Chemoreceptors
 In Brain and Circulatory System
 Carotid Artery and Carotid Sinus
 Monitors blood flow through the head
 Aorta monitors blood flowing through body
 Information is sent to Medulla and response is sent
o Autonomic Tone
 Suppression when sympathetic is not activated
 Monitor the heart via ACh and NE

Nervous System X Heart Rate

 Sympathetic  Releases NE and reduces threshold
o Heart beats faster due to channels opening up
o SA Node and AV Node are stimulated
 Cardiac Muscles
 Parasympathetic  Release of ACh increases threshold
o SA Node and AV Node are stimulated
 Cardiac Muscles are not effected

Heart Rate Influences

 Atrial Reflex (Bainbridge Reflex)
o Stretch receptors found in Atria
o Depends on how much blood enters
 More blood  More stretch  More stimulation
 Causes Cardioacceleratory Center to Activate
 Blood is contracted faster
o Sympathetic Response

Heart Rate Influences

 Hormonal Effect
o Catecholamine
 Released from Adrenal Medulla
 Increase Heart Rate
o Thyroid Hormones
 Rapid Heart Rate
 Hyperthyroidism  Increase HR = Increase CO
 Hypothyroidism  Decrease HR = Decrease CO
Stroke Volume Influences
 End-Diastolic Volume (EDV)  Proportional
o Amount of blood in ventricles after relaxation
 Increase EDV = Increase SV = Increase CO
o Filling Time  Time it takes to fill ventricle with blood
 Longer filling time = Increase EDV
o Venous Preload  Amount of blood entering ventricle
 Increase Preload = Increase SV
 Muscles Contract More
 Taking a deep breath

Clinical Situation
 Myocardial Infarction (Heart Attack)
o Reduce oxygen consumption so you slow down the heart
o Slow down the heart
 In theory  Cardiac Output is decreased
 Heart rate will go down
 Filling time will increase though
 Cardiac Output will be the same

Stroke Volume Influences

 End-Systolic Volume (ESV)
o Amount of blood in heart after contraction
o Preload  Amount of blood returning to heart in Diastole
 ESV increases due to Frank Starling Law
 Stretching Heart Muscles increases efficiency of contractions
 As heart stretches  ESV decreases  EDV increases
 Limitations to stretching
 Connective Tissue
 Cardiac Skeleton
 Pericardial Sac
o Contractility
 Influenced by Nervous System, Hormones, Drugs
 Causes an increase in Cardiac Activity  Increase EDV
 Beta and Calcium blockers
o Can manipulate ESV by influencing contractility
o Afterload  Resistance to outflow of blood
 Increases by factors that restrict blood flow
 Increase in afterload = decrease in stroke volume
 Blood is pushed with greater force
 Less Blood Present
Clinical Situation
 Aortic Stenosis  Aortic Narrowing
o Less volume to pump blood out of
 Hypertension
o Heart pumps against greater pressure
o Less blood is pushed out
o Raises ESV
 Hypertrophy of Heart
o Can damage ventricles

Other Influences
 Age
o Kids have slower heart rate
 Fitness
o Larger hearts for more fit people
 Gender

Cardiac Reserve
 Difference between resting and max cardiac output
 Smaller reserve when a person is not fit