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Chapter 18
The Cardiovascular System: The Heart
The Heart: Size, Location and Orientation:
The heart is a pump that weighs less than a pound.
Did you know that the average heart beats more than 100,000 times a day?
In the next 24 hours, yours will pump nearly 2,000 gallons of blood, two-and-a-half ounces at a time.
By the time you're 70, it will have contracted 2.5 billion times and pumped 50 million gallons, in a feat
of unrelenting endurance that puts other muscles to shame.
Location: Mediastinum
Rests on superior surface of diaphragm, a bit to the left
Base point of attachment for great vessels (left atrium mostly)
Apex is inferior (pointy end)
Point of maximal intensity (PMI): between 6th and 5th ribs just below left nipple, you can feel your
heart beat easily
Coverings of the heart:
Fibrous Pericardium: tough dense CT
a. Protection
b. Anchors heart to surrounding structures
c. Prevents overfilling
Serous Pericardium:
a. Parietal layer Pericardial cavity is between these layers where
b. Visceral layer there is a thin film of pericardial fluid
Pericardial sac includes:
1. fibrous pericardium
2. parietal pericardium
Homeostatic Imbalances:
Pericarditis: inflammation of the pericardium
Cardiac tamponade: large amounts of fluid accumulates in pericardial cavity hindering the heart beat
cause: inflammation, infection, injury
Layers of Heart Wall:
Epicardium: visceral pericardium
Myocardium: middle layer composed mostly of muscle (bulk of heart)
Fibrous skeleton of the heart: dense network of CT that reinforces heart muscle
1. Prevents vessels & valves from becoming stretched out
2. Non-conductive: Prevents spread of action potentials to ventricles prematurely.
3. Gives something for the cardiac cells to pull against when contracting
Endocardium: endothelium (Keeps platelets from sticking!)
Three Layers of Heart wall are:
1. Lines all of interior
1. Epicardium
2. Covers fibrous skeleton of valves
2. Myocardium
3. Continuous with endothelium of blood vessels
3. Endocardium
Arrangement of muscle fibers:
Shows the spiral and circular arrangement of cardiac muscle bundles. Cells connect to each other this
way so that the whole heart is interconnected.
Chambers and Associated Vessels of the Heart:
Atria: receives incoming blood
Ventricles: outgoing blood
Interatrial septum: separates atria
Interventricular septum: separates ventricles
Heart Markings:
1. Atrioventricular groove (coronary sulcus) encircles junction of atria and ventricles like a crown
2. Anterior interventricular sulcus
Continuous depression that marks the position of the
Posterior interventricular sulcus
interventricular septum
The anterior interventricular artery would be lying in the interventricular sulcus.
This marks where the interventricular septum is.
Most of each atrium is on the posterior side of the heart, so only a small portion is visible from the
anterior side.
Pectinate muscles: bundles of muscle tissue make walls look as if raked by a comb on the anterior walls
the of atria. (See picture)
Crista terminalis – C shaped ridge that separates the anterior and posterior walls of the atrium
Atria: Receiving Chambers
Auricle: (ear) protruding appendages of atria (anterior view)
only distinguishing surface feature
Increases volume of atrium a bit.
Internal parts:
1. Smooth walled posterior
Atria:
2. Ridged anterior wall – pectinate muscles Small size and thin walled – must
3. Crista terminalis
pump blood only to next door
4. Fossa ovalis
ventricles
Blood enters right atrium from:
1. Superior vena cava
2. Inferior vena cava veins carrying deoxygenated blood
3. Coronary sinus
Blood enters left atrium from:
Pulmonary veins
Carry oxygenated blood
All arteries carry oxygenated blood (except pulmonary arteries) All veins carry
deoxygenated blood (except pulmonary veins)
Ventricles
Much larger chambers with thicker walls than atria to pump blood with more force.
Left chamber is much thicker than the right
Right – (sends blood only to lungs)
Left – (sends blood throughout body)
Trabeculae carnea – irregular ridges of muscle marking internal walls “cross bars of flesh”
Papillary muscles – valve function
Attach to chordae tendineae, which attach to cusps of AV valve. Function: to keep cusps
of
valves from being blown backward into atria with the force of increased pressure when
ventricles
contract.
(See Picture)the
Pathway of Blood Through
Pulmonary circuit – short, low pressure circuit
Heart
Systemic circuit – long, high pressure circuit
S. Vena cava
I. Vena cava
Coronary sinus
Right atrium
Tricuspid
valve
Right
ventricle
Equal amounts of blood is pumped through
the
Pulmonary
pulmonary circuit as through the systemictrunk
circuit,
but still, ventricles have very unequal work loads.
Systemic
circulation
Pulmonary
arteries
aorta
Aortic
Semilunar
Valve
Pulmonary
Semilunar
valve
Left
ventricle
Mitral
valve
Left
atrium
Pulmonary
veins
lungs
Coronary Circulation:
Shortest route of circulation
in the body:
left coronary
artery
Left side of
heart
Aorta
Circumflex artery
Anterior
interventricular
artery
anastomoses
Right coronary
artery
Right side of
heart
Marginal artery
Posterior
interventricular
artery
After running through the capillary beds, the blood enters the veins which follow roughly the pattern of
the arteries to end up in the coronary sinus à right atrium of the heart.
Coronary Circulation
Capillary beds
Nutrient, gas and
waste exchange
Cardiac veins
Follow path of
cardiac arteries
Coronary sinus
Enlarged vessel
where veins joined
Right
atrium
1.
How do the tissues of the heart get nutrition and oxygen?
_____________________________
___________________________________________________________________________
2. Why can’t the blood moving through the inside of the heart give nutrition to all tissues of the
heart? _______________________________________________________________________
____________________________________________________________________________
Anastomoses:
1. Networks where arteries branch and then merge
2. Many exist in the heart
3. Provide collateral routes
4. Blockage of arteries leads to tissue death and heart attack
Blood is delivered through coronary arteries when heart is relaxed, but is stopped when the heart
contracts. Why? ________________________________________________________________
_____________________________________________________________________________
Homeostatic Imbalance
Angina Pectoris: (“choked chest)” thoracic pain from temporary deficiency of blood to myocardium.
(Stress induced spasms of coronary arteries.) Cells do not die.
Myocardial infarction: (MI) heart attack or coronary.
Cause: prolonged coronary blockage - (clot, piece of fatty tissue…)
Heart Valves:
Atrioventricular (AV) valves: Tricuspid valve and Bicuspid valve (mitral valve)
Semilunar (SL) valves: pulmonary SL valve and aortic SL valve
Function: prevent backflow of blood when ventricles contract
Describe how heart valves work to keep blood flowing in the correct direction. (See picture).
Atrioventricular valves:
1.
Blood returning to the heart fills the atria. Putting pressure against AV valves & forces
them open
2.
As ventricles fill, AV valves hang open.
3.
Atria contract forcing rest of blood into ventricles
4.
Ventricles contract forcing blood up against AV valve flaps, forcing them closed.
5.
Papillary muscles contract to make sure the AV valve flaps do not turn inside out into the
atria
Semilunar Valves
1.
As ventricles contract and intraventricular pressure rises, blood is pushed up against the
SL valves, forcing them to open.
2.
As ventricles relax, intraventricular pressure falls, blood falls back from arteries filling
cusps of SL valves, forcing them to close.
Homeostatic Imbalance of Heart Valves:
Leaky heart valves: heart can still function as long as impairment is not too great.
Incompetent valves: so much backflow occurs that the heart is only pumping the same blood over and
over and blood isn’t going anywhere.
Valvular stenosis: “narrowing”
Properties of Cardiac Muscle Fibers:
Cardiac Muscle:
1. Striated
2. Involuntary
3. Contracts by sliding filament mechanism
4. Cells are short and flat, branched and interconnected
5. Cells have one (or at most 2) nuclei
6. Intercellular spaces filled with loose CT matrix called endomycium containing numerous capillaries
7. Adjacent cell membranes interlock at junctions called intercalated discs
Endomycium: Loose CT that fills spaces between the cardiac cells and contains many capillaries
Intercalated discs: contain gap junctions so that cardiac cells can share materials allowing all the cells
in the area to contract at the same time - Functional syncytium.
Mechanism and Events of Contraction:
1. Means of stimulation: ~1% of cardiac muscle cells are self excitable (automaticity or autorhythmicity)
can initiate their own contraction and that of the rest of the heart
2. Organ vs. motor unit contraction: The heart contracts as a unit or not at all. How? _______
3. Length of absolute refractory period: 250ms in heart cells, but only 1-2ms in skeletal muscle cells.
Why? _____
4. Contractile muscle fibers require electrical stimulation to contract in much the same way as skeletal
muscles do (2401)
Energy Requirements:
Heart requires much energy and O2
Cannot operate anaerobically as can skeletal muscle for short periods
Can use any nutrient available - So, danger from lack of blood flow is the lack of O2
Homeostatic Imbalance of Blood Flow: Ischemia: lack of O2 to tissue cells
Heart Physiology:
The ability for the heart to contract is intrinsic
Does not rely on nervous system
But the rhythm cannot by modified without the NS
Without the NS heart will continue to beat
rhythmically (heart cells in a dish), but at a
different rate than what we may need
Setting the Basic Rhythm:
1. Gap junctions
2. “in-house” conduction system – 1% of heart is autorhythmic fibers
How does it work? See Pictures
1.
Autorhythmic cells of the SA node depolarize
2.
Signal is sent to all heart cells in the atria via their gap junctions so all cells contract at
the same time
3.
There is much CT (fibrous skeleton of the heart) between atria and ventricles blocking
the signal except for one path to the AV node
4.
5.
6.
7.
Autorhythmic cells of the AV node depolarize
Signal travels down the AV bundle à Bundle of His à Purkinje fibers
Signal is passed to all cells of the ventricles via their gap junctions
So, bottom of ventricles contract first pushing blood upward toward larger arteries.
Pace-makers:
Autorhythmic cells are set to depolarize
1. At SA node: ~ 75X/min
2. At AV node: ~ 50X/min
3. At AV bundle: ~ 30X/min
4 Purkinji fibers: ~ 30X/min
Fastest pace-maker sets the pace
If cells at the SA node become nonfunctional, the cells at the AV node sets the pace (next fastest)
Why? _________________________________________________________________________
Homeostatic Imbalances of Heart Rhythm
1. Arrythmias – irregular heart beat
2. Fibrillation – rapid, irregular, out of phase contraction
Like a “squirming bag of worms”.
3. Defective SA node
a. junctional rhythm - AV node becomes the pacemaker (at 50 beats/min –slow, but can maintain
circulation)
b. ectopic focus – abnormal pacemaker appears & takes over
causes: tumor, caffeine, nicotine
4. Heart Block – damaged AV node
Partial Heart Block: Transmission from AV node only sometimes gets through to the ventricles.
Total heart block:
Transmission from AV node does not get through at all
Ventricles beat at intrinsic pace (30X/min)
Too slow to maintain circulation
Treatment - _________________________________________________________
Modification of Base Rhythm
Sympathetic NS - accelerator
Parasympathetic NS – decelerator
Electrocardiography
Electrocardiograph: machine that amplifies electric currents generated & transmitted through the heart
Electrocardiogram: graphic recording of heart activity ECG or EKG
Deflection waves: Three distinguishable waves
1. P wave – Depolarization wave from SA node through atria preceding atrial contraction.
2. QRS wave – Ventricular depolarization wave preceding ventricular contraction
3. T wave – ventricular repolarization
Atrial repolarization takes place during ventricular excitation & is normally obscured by QRS wave
P-Q Interval: Time from the beginning of atrial excitation to the beginning of ventricular excitation
S-T Segment: AP is at plateau phase. Entire myocardium is depolarized
Q-T Interval: Period from beginning of ventricular depolarization through ventricular repolarization
Homeostatic Imbalance of Heart Sounds
Enlarged R-wave hints at enlarged ventricles
Flattened T-wave indicates cardiac ischemia
Prolonged Q-T interval reveals repolarization abnormality which increases risk of ventricular
arrhythmias
Heart Murmurs: backflow of blood through a valve that should be closed
Stenotic valve: high pitched sound or click when blood is trying to get through abnormally narrow
opening
Mechanical Events
Systole – heart is contracting
Diastole – heart is relaxing
Cardiac cycle – all events associated with blood flow through the heart during one complete heart beat
1. Ventricular filling
2. Ventricular systole
3. Isovolumetric relaxation
Quiescent period: time when entire heart is relaxed
1. Ventricular filling –
a. Heart is relaxed – blood has been pushed out
b. AV valves are open – blood enters atria and passes to ventricles; 70% of ventricular
filling
occurs this way
c. Atria contract – pushes remaining blood into ventricles
d. EDV – End Diastolic Volume (how much blood the ventricles can fill with.)
e. Atria relax
2. Ventricular systole – ventricles contract
a. Ventricular pressure rises
b. Isovolumetric contraction phase – all valves are closed
c. Ventricular ejection phase - ventricles contract, pressure pushes SL valves open
3. Isovolumetric relaxation: early diastole
a. Ventricles relax
b. SL valves close, AV valves open
c. ESV - End Systolic Volume (Blood remaining in ventricles after contraction
d. Interventricular pressure drops – SL valves close on backflow (rise in aortic pressure –
dicrotic notch – as
blood rebounds off of SL valves)
Important:
1. Blood flow through the heart is controlled entirely by pressure changes
2. Blood flows down a pressure gradient through any available opening
So, pressure changes reflect alternating contraction and relaxation and cause valves to open or close
keeping blood flowing in only one direction
Cardiac Output (CO)
Cardiac Output (CO): Amount of blood pumped by each ventricle in one minute
Stroke Volume (SV): Volume of blood pumped by each ventricle each beat
CO = HR X SV
CO increases if either HR increases or SV increases or both – but it is only effective as long as the heart
has time to fill between each beat. What is the effect of tachycardia on CO?
Cardiac reserve: difference between resting CO and maximum CO
In non-athletic people Cardiac Reserve is ~4-5X resting CO
In athletic people, cardiac reserve is ~7X resting CO
Regulation of Stroke Volume
SV = EDV - ESV
= 120mL/beat – 50mL/beat
= 70mL/ beat (normal resting)
The three most important things that affect Stroke Volume
1.
Preload – degree of stretch of heart muscle
2.
Contractility – amount of muscle contraction independent of muscle stretch and EDV
3.
Afterload – back pressure exerted by arterial blood (must be overcome for ventricles to
eject blood)
Regulation of Heart Rate
When SV declines (blood loss, weakend heart…) CO is maintained by increasing HR
Endocrine System
Positive chronotropic factors: anything that increase HR
Negative chronotropic factors: anything that decrease HR
Autonomic nervous system
Sympathetic division: increases HR
Parasympathetic division: decreases HR
Vagal tone: cardiac center in medulla oblongata sends inhibitory signals via the parasymapthetic fibers
of the vagal nerve to the SA node to keep the HR at ~75bpm
Baroreceptors: respond to changes in systemic blood pressure
This signal is sent to the brain (medulla) and it will adjust the HR and SV accordingly.
Atrial (Bainbridge) reflex: Sympathetic reflex
Initiated by increased venous return
and congestion in the atria.
Atrial walls stretch,
SA node and baroreceptors are stimulated by this,
which increases sympathetic stimulation
Chemical Regulation
1. Hormones: a. epinephrine (like NE): increases HR
b. thryoxine: slower, more sustained HR
2. Ions: delicate balance must be maintained
Electrolyte imbalance poses real danger to heart. Which ones?
_______________________
What does chronically high levels of thyroxine do to the heart?
______________________
Homeostatic Imbalance of Heart Rate
Hypocalcemia
Hypercalcemia
Hypernatrimia
Hyperkalemia
Hypokalemia
Other Factors Affecting the Heart Rate
1.
Body temperature: heat increases metabolic rate of cells
2.
Fever, exercise… HR increases
3.
Chill… HR decreases
4.
Gender: Females 72-80 Males 64-72
5.
Exercise: During exercise HR increases
6.
Age: Fetus 140-160
More Homeostatic Imbalances:
Of Heart
Cardiac
rate:
Output:
Tachycardia
Congestive
heart failure - Causes:
Bradycardia
1. Coronary atherosclerosis
2. Persistent high BP
3. Multiple myocardial infarcts
4. Dilated cardiomyopathy (DCM)
1. What happens if only the right side of the heart fails or becomes weakened? __________________
2. What happens if only the left side of the heart fails or becomes weakened? ___________________
3. If on side fails, then greater stress is placed on the other side. What is the likely result? _________
How would you treat these conditions? __________________________________________________
Congenital heart Defects
a. Ventricular septal defects: Oxygenated blood and deoxygenated blood are mixing
b. Coarctation of aorta: Narrowed valves or vessels that greatly increase work load on
c. Tetralogy of Fallot: multiple defects)
Maintaining a Healthy Heart
Regular exercise is the key
Going all week without exercising and then exercising vigorously does more damage than good
Inactivity
Smoking
Stress
Poor diet
Increases risk of heart damage more than age does.
Diet being the most risky behavior. Inactivity comes
in closely in second place.