1. Chapter 20
The Heart 1 1

2. Circulatory System: The Heart
cardiology – the scientific study of the heart and the treatment of its disorders
cardiovascular system
heart and blood vessels
circulatory system
heart, blood vessels, and the blood
major divisions of circulatory system
pulmonary circuit - right side of heart
carries blood to lungs for gas exchange and back to heart
systemic circuit - left side of heart
supplies oxygenated blood to all tissues of the body and returns it to the heart

3. Position, Size, and Shape
Heart lies in mediastinum (a central compartment of the thoracic cavity made of loose connective tissue) between lungs; 2/3 of its mass is to the left of the midline
Size: equivalent to a person’s closed fist.
Shape: cone-shaped, pointed apex inferior; flat base is superior.
Heart protected on the anterior side by the sternum; on the posterior side by the vertebrae
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Aorta
Pulmonary
trunk
Base of
heart
Apex
of heart
Diaphragm
(c)

4. SULCI - GROOVES on surface of heart containing blood vessels and fat
coronary sulcus
Separates the atria from the ventricles
anterior interventricular sulcus
marks the boundary between ventricles anteriorly
posterior interventricular sulcus
marks the boundary between ventricles posteriorly

5. Protective layers of the heart
Pericardium – 2 layered sac surrounds and protects the heart from external jerk or shock.
Fibrous pericardium dense irregular connective tissue, protects and anchors the heart to diaphragm and mediastinum; prevents overstretching
Serous pericardium
Parietal pericardium
Visceral pericardium (epicardium) covers the heart surface and becomes part of the heart wall
Pericardial cavity lies between the parietal and visceral layers of the serous pericardium; filled with pericardial fluid that reduces friction between the two membranes.
pericarditis. inflammation of the pericardium
cardiac tamponade buildup of fluid in the pericardial cavity
pericarditis: inflammation of the pericardium
cardiac tamponade: buildup of fluid in the pericardial cavity- resulting in slow or rapid compression of the heart.

6. Pericardium

7. Heart Wall Epicardium (visceral pericardium)
visceral serous membrane covering heart; adipose in thick layer in some places
Contain coronary blood vessels
Myocardium
cardiac muscle layer
Endocardium
covers the valve surfaces and continuous with endothelium of blood vessels

8. Structure of CARDIAC MUSCLE
Cardiocytes – small, striated, short, thick, branched cells, one centrally located nucleus, involuntary control
Abundant mitochondria, extensive blood supply
intercalated discs - join cardiocytes end to end
interdigitating folds –End of cells folded like the bottom of an egg carton. Produces interlocking and increased surface contact area.
mechanical junctions tightly join cardiocytes to prevent heart cells from pulling apart during contraction
fascia adherens –ribbon like structures that stabilizes non-epithelial tissue; actin of the thin myofilaments is anchored to the plasma membrane
desmosomes – prevents cardiocytes from being pulled apart
gap junctions allow ions to flow between cells –produces electrical stimulation to neighboring cells
Propagate action potentials
repair of damage of cardiac muscle is almost entirely by fibrosis (scarring)

10. http://droualb. faculty. mjc

11. 4 CHAMBERS
2 upper atria
2 lower ventricles

12. Right and Left Atrium
Pectinate muscles internal ridges of myocardium in right atrium and right auricle. Increase force of contraction w/o increasing heart mass
Interatrial septum separates right and left atrium
Auricle flap like extension increases surface area.
RIGHT ATRIUM
Receives blood from 3 veins: superior / inferior vena cava, coronary sinus
Blood flows through the right atrioventricular valve (AV valve) or the tricuspid valve) into the right ventricle.
Each valve consists of 2-3 fibrous flaps of tissue called cusps.
LEFT ATRIUM
Forms MOST of the base (top) of the heart
Receives blood FROM LUNGS via 4 pulmonary veins (2 right / 2 left) Remember blood always returns to the heart via veins
Blood flows through the left atrioventricular valve (AV valve) or the bicuspid valve (has 2 cusps) into the left ventricle.
This valve is also known as the mitral valve.

13. Right auricle
Left auricle
Pectinate muscles
internal ridges of myocardium in right atrium and both left and right auricles. Increase force of contraction w/o increasing heart mass

14. Right and Left Ventricle
Inside ventricles are raised bundles of cardiac muscle called trabeculae carneae
cone shaped traberculae carnae are called papillary muscles.
Chordae tendineae cords connect cusps of the AV valves to the papillary muscles
Interventricular septum: partitions the right and left ventricles
RIGHT VENTRICLE
Blood flows from the right ventricle into the pulmonary trunk (pulmonary artery) through the pulmonary semilunar valve.
LEFT VENTRICLE
The aortic semilunar valve allows the passage of blood from ventricle to the ascending aorta
just above valve are openings to the coronary arteries
Myocardium much thicker in the left ventricle - produces greater force for blood ejection to systemic tissues

15. NOTE: difference in myocardium thickness between left and right ventricles

17. Fibrous cardiac skeleton collagenous and elastic fiber provides
Heart Valves
Fibrous cardiac skeleton collagenous and elastic fiber provides
support structure
attachment for cardiac muscle
anchor for valve tissue
electrically insulate ventricular cells from atrial cells
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Left AV
(bicuspid) valve
Right AV
(tricuspid) valve
Fibrous
skeleton
Openings to
coronary arteries
Aortic
valve
Pulmonary
valve
(a) 17

18. Valve Action
The heart valves open and close passively because of pressure differences on either side of the valve. When pressure is greater BEHIND the valve (Ex: as blood fills atria), the cusps are blown open and the blood flows through the valve; when pressure is greater in FRONT of the valve (ventricles are full and press against the AV valves), the cusps snap shut and blood flow is stopped (from atria). The motion of a heart valve is analogous to the motion of the front door of your house. The door, which only opens in one direction, opens and closes due to pressure on the door.
Ventricle value action: Electrical stimulation signal from SA node in right atrium reaches papillary muscles on the floor of the ventricles before the myocardium muscle fibers.
Causes tension that pulls the chordae tendinae and they tighten pulling the AV valves shut as blood in ventricles surges against valves closing them.

19. Atrioventricular and Semilunar Valves
Values ensure a one-way flow of blood thru the heart; open and close in response to pressure changes as the heart contracts and relaxes.
AV Valves
When atria contract, the ventricular pressure is lower than atrial pressure
cusps OPEN chordae tendineae slack; papillary muscles relaxed
When ventricles initiate contraction:
AV cusps CLOSED, chordae tendinae are pulled taut and papillary muscles contract to pull cords and prevent cusps from slipping inside out
AV valves close preventing backflow of blood into atria
Semilunar Valves
SL valves open with ventricular contraction allow blood to flow into pulmonary trunk and aorta. Pressure inside ventricles overpowers the pressure inside the aorta and pulmonary trunk.
SL valves close with ventricular relaxation prevents blood from returning to ventricles. Pressure inside aorta and pulmonary trunk higher, closing the values.

20. AV and SL Values

21. Valve Disorders
Stenosis - narrowing of a heart valve which restricts blood flow.
Rheumatic Fever- inflammatory disease that occurs following a Streptococcus pyogenes infection (usually in the throat).
The immune system stimulates antibodies to attack the infection. Inadvertently, the antibodies also attack the heart tissue damaging the heart valves. The damaged valves can lead to heart failure.
Mitral valve prolapse- bulge too far into the left atrium during contraction
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.
Not all murmurs are abnormal or symptomatic, but most indicate a valve disorder. Sounds are thought to be produced by regurgitation through valves

22. Heart Sounds
The sound of a heartbeat comes primarily from the turbulence in blood flow caused by the closure of the valves.
Listening to sounds within the body is called auscultation, usually done with a stethoscope.
First heart sound S1 (lubb) created by blood turbulence associated with the closing of the ATRIOVENTRICULAR valves
The second heart sound S2 (dupp) represents the closing of the SEMILUNAR valves close to the end of the ventricular systole.

23. Blood Circulation Two closed circuits Systemic circulation
left side of heart pumps blood through body
Receives oxygenated blood FROM the lungs and distributes it to body cells
left ventricle  aorta  arteries  arterioles  capillaries  gas and nutrient exchange  venules  veins  right atrium
Pulmonary circulation
right side of heart pumps deoxygenated blood TO LUNGS for oxygenation.
right ventricle  pulmonary trunk  pulmonary arteries  lungs  exchange of gases  pulmonary veins  left atrium

24. Blood Circulation

25. Blood Circulation Coronary Circulation
delivers oxygenated blood and nutrients to the heart and removes carbon dioxide and wastes from the myocardium.
Left Coronary Artery blood to: left ventricle; left atrium; interventricular septum. Located above SL valve.
Right Coronary Artery blood to: right atrium; portions of both ventricles; cells of sinoatrial (SA) and AV nodes. Located above SL value
Route:
Left Ventricle  Aorta  left and right coronary arteries  supply blood to the atrium and the ventricles  large coronary sinus  right atrium.
Sinus - large vein without smooth muscle layer
Anastomoses provides alternate backup routes for blood to flow if one vessel is blocked or compromised.

26. Blood Flow Right atrium pumps deoxygenated blood
 Thru AV (tricuspid) Valve
 To right ventricle which pumps blood
 Thru pulmonary semilunar valve
 Into the pulmonary trunk
 Which divides into a right and left pulmonary artery
 Which carry deoxygenated blood to the lungs
 Gas exchange occurs
 Oxygenated blood returns via pulmonary veins (2 from left/2 from right
 Into the left atrium
 Thru the AV (bicuspid) valve
 Into the left ventricle pumps blood
 Thru the aortic semilunar valve
 Into the aorta
 In the ascending aorta which branches into 2 coronary arteries to heart
 Then the aorta arch with 3 branches to upper regions of the body
 Then to descending aorta with branches to lower regions of the body
 Where blood drops off oxygen and picks up carbon dioxide
 Returning the deoxygenated blood back to the atrium via
Superior vena cava –upper body; inferior vena cava-lower; coronary sinus-heart = TAKES APPROXIMATELY ONE MINUTE!!!!
Blood Flow

27. Specialized Anatomy of Fetal Heart Circulation
Foramen ovale
an opening through interatrial septum in the right atrium
Connects the two atria
Seals off at birth, forming fossa ovalis
Fossa ovalis
Ductus arteriosus – is a blood vessel CONNECTING the pulmonary artery (pulmonary trunk) to the proximal descending aorta. It allows most of the blood from the right ventricle to bypass the fetus's fluid-filled non-functioning lungs. O2 for the fetus is provided by the placenta. Closes at birth and becomes the nonfunctional ligamentum arteriosum.

28. Clinical Problems CONGESTIVE HEART FAILURE (CHF)
results from the FAILURE of EITHER ventricle to eject blood effectively
usually due to a heart weakened by myocardial infarction, chronic hypertension, valve insufficiency, or congenital defects in heart structure.
left ventricular failure – blood backs up into the LUNGS causing pulmonary edema
shortness of breath or sense of suffocation
right ventricular failure – blood backs up in the VENA CAVA causing SYSTEMIC or generalized edema
enlargement of the liver, ascites (pooling of fluid in abdominal cavity), distension of jugular veins, swelling of the fingers, ankles, and feet
eventually leads to total heart failure

29. Figure 19.21

30. Clinical Problems
Coronary Artery Disease (CAD) - partial or complete blockage of coronary circulation
Atherosclerosis -artery wall thickens as a result of the accumulation of fatty materials (plaque) producing a narrowing of vessels---results in artery spasm or clot
first symptoms of CAD is commonly angina pectoris (chest pain due to obstruction or spasm of the coronary arteries)
Angina pectoris – temporary ischemia (slow blood flow)
obstructing 75% or more of the blood flow to cardiac muscle- produces lack of blood and oxygen
When partially or fully blocked coronary artery constricts produces heaviness and pain. O2 deprived tissue shifts to anaerobic respiration resulting in lactic acid synthesis which stimulates pain receptors. The intermittent chest pain may radiate from the sternal area to the arms, back, and neck.
Arteriosclerosis hardening/loss of elasticity of medium or large arteries
Arteriolosclerosis hardening/loss of elasticity of arterioles

31. Clinical Problems Myocardial infarction (MI) (heart attack)
sudden death of a area of myocardium due to long-term obstruction of coronary circulation
interruption of blood supply due to a blood clot or fatty deposit- can result in death of cardiac cells within minutes
protection from MI is provided by arterial anastomoses alternative route of blood flow (collateral circulation) within the myocardium
MI responsible for about ½ of all deaths in the US
25% of MI patients die before obtaining medical assistance
65% of MI deaths under age 50 occur within an hour of infarction
Diagnosis:
1) ECG (EKG)
2) damaged myocardial cells release ENZYMES measured by blood tests.

32. Prevention and Treatment
> Medication –know for exam
beta blockers [blocks sympathetic response that increases heart rate- Ex: inhibit receptors for norepinephrine and epinephrine; used for secondary heart attack, stroke and hypertension]
ACE inhibitors [decrease BP; inhibit RAAS]
Aspirin -thins blood – prevents platelet aggregation
Heparin/Warfarin (Coumadin) blood thinners that interfere with chemical formation of clot
Nitroglycerin [nitric oxide- dilates arteries offsets angina increasing blood flow]
Calcium channel blockers [slows heart lowers electrical impulses, lowers BP]
> Coronary Artery Bypass Graft (CABG)
section of artery or vein (ex; great saphenous vein) used to create a detour around the obstructed portion of a coronary artery
procedures named by number of vessels repaired-single, double, triple, or quadruple coronary bypasses
> balloon angioplasty
> laser angioplasty
similar to balloon angioplasty uses laser tipped catheter instead of a balloon

33. Electrical Conduction System of the Heart.
NODE special tissue acts like muscle and nervous tissue.
A system of SPECIALIZED CARDIAC MUSCLE CELLS initiates and distributes electrical impulses that stimulate contraction.
Automaticity - heart cells act as both nervous and muscle tissue. Cardiac muscle contracts automatically and generate spontaneous action potential that goes through ENTIRE heart muscle.

34. The Beginning
The human heart begins to beat and pump blood through the embryo around day 22 of gestation.
The electric stimulus that triggers contractions in the myocardium arise spontaneously within the myocardium itself, and propagate from cell to cell. Input from the central nervous system can modify the heart rate (the frequency of heart beats), but it does not initiate beats.
The ability of cardiac myocytes to beat is an intrinsic property of these cells. It has been found that myocytes removed from the early heart and grown in culture will beat sporadically, and if they become connected to each other, will then begin to beat rhythmically, in unison.
As a functional organ, the heart begins to beat very early, even before it has assumed its final form.
Interestingly, the heart begins to beat even before structures such as valves and septa (singular: septum; the muscular walls that divide the chambers) have formed! The initial contractions are peristaltic--that is, they proceed in a wave-like fashion along the length of the heart.

35. Electrical Conduction System of Heart
SA (sinoatrial) node- pacemaker - cluster of cells in right atria wall
When nodal tissue contracts it generates nervous impulses that travels to BOTH atria simultaneously, then to the AV node.
Sets heart rhythm.
Right atria contracts slightly before left as it receives signal from the SA node first.
AV (atrioventricular) node- in atrial septum (alternative pacemaker)
Slows the transmission of the action potential; transmits signal to bundle of His
Fibrous skeleton helps to insulate and prevent currents from getting to the ventricles from other routes
Bundle of His (AV Bundle) -connection between atria and ventricles; continues to slow the action potential allowing more time for ventricles to fill with blood for ejection.
Right and Left Bundle Branches extend from the Bundle of His or AV bundle, and action potentials descend to the apex of the heart.
Purkinje fibers in right and left ventricles carry action potentials from the bundle branches to trigger muscle fibers in ventricles to contract.

36. Fibrous skeleton

37. Cardiac Conduction System
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 1
SA node fires. 2
Excitation spreads through
atrial myocardium.
Right atrium 1 2
Sinoatrial node
(pacemaker)
Left
atrium 3
AV node fires. 2
Purkinje
fibers
Atrioventricular
node 3 4
Excitation spreads down AV
bundle.
Bundle
branches
Atrioventricular
bundle 5
Purkinje fibers distribute
excitation through
ventricular myocardium. 4 5
GOOD ANIMATION
Purkinje fibers

38. Receives impulse from SA Node
Begins atrial activation
Receives impulse from SA Node
Delays impulse

40. Conduction System of Heart
Heart contractions do not require nervous system intervention. Signals from the autonomic nervous system and hormones, such as epinephrine, MODIFY the heartbeat (rate and strength of contraction), but they do not ESTABLISH the fundamental rhythm.
Cycle of events in heart
SYSTOLE – “START” of atrial or ventricular CONTRACTION DIASTOLE – “DONE” with contraction atrial or ventricular = relaxation
Sinus rhythm - normal heartbeat; SA node triggers; 60 – 100 bpm
adult at rest is 70 to 80 bpm (vagal tone)
Parasympathetic stimulation slows heart rate
Ectopic focus – another area of heart fires BEFORE SA node
Premature ventricular contraction (PVC) initiated by the Purkinje fibers–extra heartbeat can be caused by hypoxia (low oxygen), electrolyte imbalance, or caffeine, nicotine, and other drugs. Produces insufficient blood ejection from ventricles; may be perceived as a "skipped beat" or felt as palpitations in the chest.
Nodal rhythm – if SA node is damaged, heart rate is set by AV node, 40 to 60 bpm (action potentials per minute)
Intrinsic ventricular rhythm – if BOTH SA and AV nodes are not functioning, rate set at 20 to 40 bpm
If occurs would require artificial pacemaker to sustain brain function

41. REVIEW Muscle Physiology - Membrane Potential
Membrane potentials result from a separation of positive (+) and negative (-) charges (ions) across the membrane
Voltage is a difference in electrical potential between the opposite sides of a plasma membrane. Voltage drives an electric current (the flow of electrons or electrical charge).
Action potentials are generated by the movement of ions through membrane ion channels in muscle cells. This shift from a negative to a positive internal cellular environment allows for the transmission of electrical impulses

42. REVIEW Muscle Physiology - Membrane Potential
When the muscle cell is not in a state of contracting it is said to be in a resting state, the INSIDE of the cell is more NEGATIVE than the OUTSIDE. Membrane is polarized. Each cell has an “at rest” potential to transmit an electrical current. This potential varies in different types of muscle cells.
For a muscle cell to contract, the negative (-) value inside the cell must become more positive (+). This is called depolarization.
Ion channels in the membrane open and positively charged ions move from the extracellular fluid into the interior of the cell
Positively charge channels close to prevent release of positive ions.
The change in electrical voltage generates electrical impulses that move along the surface of the membrane, alerting mechanisms inside the cell to produce a contraction.
Following the contraction, the ion channels that opened or closed to increase the positive value inside the cell CLOSE and the cell begins to resume a more negative value. This is a state of repolarization or relaxing.

44. The electrical current released during an action potential opens calcium channels that enable the binding of contractile proteins to produce contractions

47. Cardiac Conduction System
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 1
SA node fires. 2
Excitation spreads through
atrial myocardium.
Right atrium 1 2
Sinoatrial node
(pacemaker)
Left
atrium 3
AV node fires. 2
Purkinje
fibers
Atrioventricular
node 3 4
Excitation spreads down AV
bundle.
Bundle
branches
Atrioventricular
bundle 5
Purkinje fibers distribute
excitation through
ventricular myocardium. 4 5
Purkinje fibers

48. Pacemaker Physiology – Atria Action Potential
The resting membrane potential of a SA node cardiac muscle CELL, is less constant than a skeletal muscle cell, due primarily to the increased permeability ("leakiness") of its cell membrane to Na+ and K+ ions; as a result:
SA node cardiac muscle cells depolarize more easily.
SA node CELLS’ resting potential start at -60 mV and drifts upward (to a more positive value) from a SLOW inflow of Na+ and no compensating outflow of K+ (K+ channels are closed)
This gradual depolarization is called pacemaker potential
When potential reaches threshold of -40 mV, voltage-gated FAST Ca2+ and Na+ channels open; Ca2+ and Na+ flow in rapidly
depolarization occurs - peaking (maximum + value) at 0 mV
At 0 mV “K+” channels open and K+ exits the cell triggering repolarization
Each depolarization of the SA node produces one heartbeat
at rest, fires every 0.8 seconds or 75 bpm
Signal travels 1 m/sec thru atrial myocardium reaches AV node in approximately 50m/sec

49. Graph Depiction of Atria Potentials
Animation: Atria

50. Ventricular Filling from Atria
The ventricles RECEIVE blood from the atrium both PASSIVELY and as a result of ATRIAL CONTRACTIONS.
The first one third (1/3) occurs quite rapidly (passive)
The second one third (1/3) is somewhat slower (passive)
The final third (1/3) completes the filling process and is the RESULT of atrial systole (contraction)
Animation:

51. Myocardium Conduction-AV Node
An impulse in a ventricular contractile muscle fiber is characterized by RAPID depolarization, plateau, and repolarization.
AV node delays cardiac impulses from SA node to allow atria to contract and EMPTY
Signal slows at AV node DUE to
1) less numbers of cardiocytes
2) less gap junctions
3) cardiocytes have a stable resting membrane potential
4) depolarize only when stimulated
Depolarization
Ventricular cardiac cell resting membrane potential is - 90mv
Na+ channels open and depolarize the membrane.
This triggers a positive feedback that initiates the opening of more Na+ channels resulting in a RAPID ALMOST VERTICAL RISING membrane voltage. Peaks at 30+ mV. Na+ channels then close.

52. Cardiac Conduction System
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 1
SA node fires. 2
Excitation spreads through
atrial myocardium.
Right atrium 1 2
Sinoatrial node
(pacemaker)
Left
atrium 3
AV node fires. 2
Purkinje
fibers
Atrioventricular
node 3 4
Excitation spreads down AV
bundle.
Bundle
branches
Atrioventricular
bundle 5
Purkinje fibers distribute
excitation through
ventricular myocardium. 4 5
Purkinje fibers

53. Graph Depiction of Ventricular Action Potential
Na+ channels close
Ca2+ channels open

54. Myocardium Conduction-AV Node
Plateau phase – result of Ca2+ inflow
Period of prolonged, sustained depolarization ( msec) allows for the greater ejection of blood from the ventricles
Na+ channels close but slow Ca2+ channels open, Ca2+ enter from OUTSIDE the cell and binds to Ca2+ channels on sarcoplasmic reticulum releasing more Ca2+ ; cardiac muscle tissue very sensitive to extracellular calcium concentrations
Ca2+ binds to troponin to allow for actin-myosin cross-bridge formation & muscle contraction.
The plateau declines slightly due to leaky potassium (K+) channels but most K+ channels remain closed sustaining the depolarization.
Repolarization
Ca+2 channels CLOSE and K+ channels OPEN allowing K+ to rapidly LEAVE the cell restoring resting membrane potential -90mv.
Refractory period
the time interval when a second contraction cannot be triggered
Prevents wave summation and tetanus which would stop the pumping actions of the heart and decrease amount of blood ejected from ventricles.

55. Physiology of Contraction
Na+ gates open
2) Rapid depolarization
Na+ gates close-cell depolarizes
Slow Ca2+ channels open prolonging depolarization creates plateau
5) Ca2+ channels close, K+ channels open (repolarization)
Plateau is the ST segment
of the ECG –ventricle contraction and blood ejection.

56. Electrocardiogram---ECG or EKG
A recording of the electrical changes (“ACTION POTENTIAL”) that accompany each cardiac cycle (heartbeat)
Equipment detects and amplifies electrical changes on the skin when the heart muscle impulse is generated
ECG helps to determine abnormal conduction pathway; if the heart is enlarged or has damaged regions

57. Electrocardiogram---ECG or EKG
P wave
atrial depolarization
systole
P to Q interval
conduction time from SA node to AV node
QRS complex
Atrial repolarization
diastole
Ventricular depolarization ST
plateau period of sustained contraction
T wave
ventricular repolarization
ECG/EKG Good Animation
(3.34 min)

58. Normal Electrocardiogram (ECG)

59. Atria contract
Ventricles contract

61. Fibrillation

62. Cardiac Cycle
A cardiac cycle includes all the events occurring in a SINGLE heart beat (0.8 sec)
It consists of repetitive contraction (systole) and relaxation (diastole) of heart chambers
In a cardiac cycle the atria then the ventricles contract and relax forcing blood from areas of high pressure to areas of lower pressure

63. atrial depolarization begins
2) atrial depolarization complete (atria contracted)
ventricles begin to depolarize at apex; atria repolarize (atria relaxed)
ventricular depolarization complete (ventricles contracted)
ventricles begin to repolarize at apex
6) ventricular repolarization complete (ventricles relaxed)

64. Phases of Cardiac Cycle
Isovolumetric contraction
Blood enters atria flows to the ventricles via the opened tricuspid and mitral valves. Atrial contraction follows
As atria diastole ends, the ventricles BEGIN depolarizing- start contracting, the AV valves close, to prevent back flow to the atria; corresponds to the R peak or the QRS complex seen on an ECG
Aortic and pulmonary valves are also closed; no overall change in volume as all four valves are closed. The isovolumetric contraction lasts about 0.03 sec, enough time to build sufficiently high pressure to overcome aortic and the pulmonary trunk semilunar valves (blood in ventricles)
Relaxation period: isovolumetric relaxation Both atria and ventricles are relaxed. Pressure in the ventricles fall and the SL valves close. All four valves are closed (blood begins flowing into the atria). Pressure in the ventricles continues to fall, the AV valves open, and ventricular filling begins. It can be used as an indicator of diastolic dysfunction.

65. Phases of Cardiac Cycle
Ventricular Filling and Ejection
Pressure continues to rise as ventricle muscles decrease chamber volume size opening SL valves leading to ventricular ejection.
In cardiovascular physiology, end-diastolic volume (EDV) is the volume of blood in the right and/or left ventricle at end load or filling in (atrial diastole) or the amount of blood in the ventricles just before systole.
The amount of blood REMAINING in a ventricle AFTER it has contracted is End Systolic Volume (ESV)
Stroke volume (SV) is the volume of blood ejected by a ventricle with each heart beat. SV = EDV minus ESV
Ejection fraction - % of blood at EDV ejected during SV (SV/EDV)
A normal heart's ejection fraction may be between 55 and 70
Between 40 and 55 indicates damage, perhaps from a previous heart attack, but it may not indicate heart failure.
Under 40 may be evidence of heart failure or cardiomyopathy.
Examples:
EDV = amount of blood available prior to ejection = 150
ESV = amount of blood left in ventricle following contraction = 50
Amount of blood ejected (SV) = 100ml (150-50)
Ejection Factor: Divide SV by EDV EF= 100ml/150 ml= 67%

66. CARDIAC OUTPUT
Cardiac output (CO) is the volume of blood ejected from the ventricles into the aorta or pulmonary trunk in ONE MINUTE.
Cardiac output equals the stroke volume (the volume of blood ejected by the ventricles with each contraction) multiplied by the heart rate (the number of beats per minute).
CO = SV x HR
70 ml blood x 75 beats/min = 5250 ml divided by 1000 = 5.25 L/min
Entire blood supply of the body passes through the circulatory system every minute.
Cardiac reserve is the ratio between the maximum cardiac output a person can achieve and the cardiac output at rest.
Average is 4-5 times the normal output (5.25 L/min x 4 = 21 L/min)
Trained athlete’s cardiac reserve can be as much as 7-8 times the normal amount of blood sent through the circulatory system during intense exercise

67. EDV= amount available that ESV = amount remaining
SV= 70ml
EDV= amount available that ESV = amount remaining
can be ejected after contraction

68. Influences on Stroke Volume
PRELOAD – TENSION in heart muscle (affect of stretching)
the more EACH muscle fiber sarcomere is stretched, greater the contraction force; STRETCH RESULT OF GREATER BLOOD VOLUME
Ex: stretching a rubber band produces more tension
Preload is affected by venous blood pressure and the rate of venous return to the heart. More blood volume in ventricles - greater tension; greater force of contraction -more blood ejected
Higher volume = higher preload
Frank Starling Law - stroke volume (SV) proportional to EDV
Amount of blood ejected dependent on available blood in ventricles.
CONTRACTILITY–strength/force of contraction (how hard)
The more responsive cardiocytes are to stimulation the more force they can create; stimulation dependent on binding capacity of actin and myosin contractile proteins which is regulated by Ca Are all the fibers contracting together?
Affected by: autonomic nerves (sympathetic, parasympathetic), hormones, pharmaceutical drugs, Ca2+ or K+ levels
Positive inotropic agents increase force of contraction
Ca2+ prolongs plateau increases actin/myosin coupling
Negative inotropic agents decrease force of contraction
Ca2+ reduces strength of myocardium action potential

69. Influences on Stroke Volume
Afterload – Tension the ventricles produce to open the semilunar valves and eject blood
If pressure increases, afterload also increases.
It is the result of the pressure exerted in the aorta and pulmonary trunk.
The pressure in the ventricles must be greater than the aortic and pulmonary pressure to open the aortic and pulmonic SL valves. As afterload increases, cardiac output DECREASES.
The longer time it takes to open the valves the less time available for blood ejection during plateau; reducing blood output.
Limits stroke volume (SV) [ventricle output]
high BP creates high afterload decreasing ventricular ejection

70. Regulation of Heart Rate
Intrinsic regulation: normal natural characteristics inside the heart - Gap junctions, SA rhythmic cells
Chemoreceptors, proprioceptors, baroreceptors; Bainbridge reflex (causes increase in heart rate)
Cations (Na+, K+, Ca+2)
Cardiac centers of medulla oblongata control
Parasympathetic stimulation (slow as bpm)
Supplied by vagus nerve, DECREASES HEART RATE, acetylcholine is secreted and hyperpolarizes the heart
Sympathetic stimulation (high as bpm)
Cardiac nerves innervate the SA and AV nodes, coronary vessels and the atrial and ventricular myocardium. INCREASES HEART RATE and force of contraction. Epinephrine and norepinephrine released
Nicotine, caffeine, medications, stress, emotional excitement
Age, gender, physical fitness, temperature,

71. Clinical Problems
Congenital Heart Defect an abnormality or defect that exists AT or BEFORE birth.
Arrhythmia (dysrhythmia) is an irregularity in heart rhythm resulting from a defect in the conduction system of the heart.
Bradycardia- slow rate below 60 bpm
resting-sleep, well-conditioned hearts
Tachycardia – fast rate above 100 bpm
stress, anxiety, drugs, heart disease
Fibrillation – asynchronous contraction that can kill very easily- heart loses its rhythm- some parts of the atria and ventricle contract while others remain un-stimulated