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Anatomy and Physiology
Reference: Pathophysiology by Kathryn McCance
Mindy Milton, MPA, PA-C
July 13, 2010
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2. Objectives
Brief review of the structure of the heart and
vascular system
Blood flow through the heart and body
Chambers
Valves
Pulmonary circulation
Systemic circulation
Coronary circulation
Electrical conduction through the heart
Specialized cells
Automaticity
Rhythmicity
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3. Objectives
Cardiac Action Potential
Four phases 0-4
ECG
Cardiac cycle
Diastole
Systole
Cardiac Workload
Cardiac Output
ANS, Hormones
Frank-Starling Law
LaPlace’s Law
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4. Objectives
Cardiac Workload
Preload - blood coming back to the heart.
Afterload
Structure of blood vessels
Blood flow
Capillary exchange
Blood pressure
C.O.
Stroke Volume
PVR
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5. Cardiovascular System
Heart is a four chambered pump
Blood vessels are the tubes
Purpose is life – supplies oxygen and nutrients
to every cell and clears C02 and wastes
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6. Cardiac Muscle
Cell
Bundles of myofibrils
Junctions – intercalated discs
Rapid syncytial contraction
Sacromere – functional unit
Z line to Z line
Actin and myosine bands
Optimum length 2.2 – 2.4 µm
T-tubules
Communicates with ECF
Majority of Ca++
Sarcoplasm Reticulum
Ca++ storage
Mitrochondria
Energy = ATP
Aerobic respiration
Oxygen
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7. Myocardial Cells
Nearly identical to skeletal muscle cells
Intercalated disks - desmosomes,
Actin, myosin, and the troponin-tropomyosin
complex
troponin - tested for
Troponin T, I, and C with MI
Myocardial metabolism
Myocardial oxygen consumption
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9. Circulatory System
Heart
Right heart
Pumps blood through the lungs (pulmonary
circulation)
Left heart
Pumps blood through the systemic circulation
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10. Circulatory System
Heart
Mediastinum
Heart wall
Pericardium
Parietal and visceral
Pericardial cavity and fluid
Myocardium
Endocardium
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11. The Heart Wall
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12. The Chambers of the Heart
Right atrium
Left atrium
Right ventricle
Left ventricle
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13. The Chambers of the Heart
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15. The Valves of the Heart
Atrioventricular valves
Tricuspid valve
Bicuspid valve (Mitral)
Semilunar valves
Pulmonic semilunar valve
Aortic semilunar valve
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16. The Valves of the Heart
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17. The Great Vessels
Superior and inferior venae cavae
Aorta
Pulmonary artery (trunk)
Right and left pulmonary arteries
Blood from right ventricle
Pulmonary veins
Four, two from left and right lung fields
Blood enters left atrium
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18. Blood Flow
Cardiac cycle
Diastole - 70 % of the blood comes in passively. Then last filling from atrial kick.
Systole
Phases of the cardiac cycle
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19. Phases of the cardiac cycle
1 – Systole with isovolumetric contraction
AV closed and SL not open yet
Increased intraventricular pressure
Blood volume unchanged
2 – LV pressure > aortic pressure
SL open and blood ejected
Rapid ventricle pressure and volume decrease
3 – Diastole with isovolumetric relaxation
SL close and AV not open yet
Decreased intraventricular pressure
Blood volume unchanged
4- LV pressure < LA pressure
AV open and ventricle fills
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20. Blood Flow
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22. The Coronary Vessels
Right coronary artery (RCA)
Conus
Right marginal branch
Posterior descending branch
Left coronary artery (LCA)
Left anterior descending artery (LAD)
Circumflex artery (LCX)
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23. The Coronary Vessels
Collateral arteries
Coronary capillaries
Coronary veins
Coronary sinus
Great cardiac vein
Posterior vein of the left ventricle
Coronary lymphatic vessels
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25. Structures That Control Heart
Action
Cardiac action potentials
Conduction system
Sinoatrial node (SA) - 60-100
Intranodal pathways
DELAY
Atrioventricular node (AV)
Bundle of His (AV bundle)
Right and left bundle branches
Purkinje fibers
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27. Structures That Control Heart
Action
Cardiac excitation
Propagation of cardiac action potentials
Depolarization – Na and Ca
Repolarization - K
Electocardiogram
Automaticity
Spontaneous depolarization = no stimulus
SA node, AV node, ventricles
Rhythmicity
Regular AP generation by conduction system
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28. Cardiac Action Potential
Four phases
Resting phase (4) cell membrane is relatively
impermeable to sodium. Electrical differences are
maintained by NA and K pump
Phase 0: rapid depolarization with increase permeability
to NA with increasing positive potential
Phase 1: Rapid decrease in Na movement
Phase 2: increased calcium movement
Phase 3: rapid repolarization with movement of K out of
the cell
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30. Comparison of Action Potential
Skeletal AP
Skeletal force
Cardiac AP
Allows ventricle filling
Cardiac force
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33. ECG Tracing
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34. Cardiac Cycle
Concepts:
Systole: contraction phase of the heart
Diastole: relaxation and filling phase of the heart
Blood moves from areas of higher to lower pressure
Valves between cardiac chambers also respond to pressure
changes
Heart rate will impact the length of each phase of the
cardiac cycle. (Increased heart rate all phases will be
shortened
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36. Cardiac Cycle
Systole
Aortic and pulmonic
valves are open
Contraction phase of the
heart
Responsible for stroke
volume
Stroke volume 70-80 cc
with residual volume of
50-60cc
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37. Cardiac Cycle
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41. Cardiac Workload
Frank-Starling Law of the heart
Increased stretch, increase force of contraction
The amount of blood in the ventricle at end of
diastole (EDV) is directly related to the
contraction force of the next systole assuming
function of heart remains constant
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42. Cardiac Workload
Laplace’s Law
Amount of ventricle wall tension to produce a
certain pressure depends on size/radius of
chamber and wall thickness.
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43. Cardiac Workload
Afterload - systemic blood pressure.
PVR
Resistance to left ventricular ejection of blood
Heart rate
Neural control mechanisms
Thyroid Hormones
Increased HR will increase Oxygen demand.
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44. Structures That Control Heart
Action
Cardiac innervation
Sympathetic nerves
Parasympathetic nerves
Adrenergic receptor function
α- or β-adrenergic receptors
Norepinephrine or epinephrine
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46. Systemic Circulation
Macrocirculation
Arteries
High pressure
Elastin
Smooth muscle
Veins
Thin walled
Low pressure
valves
Microcirculation
Arterioles
Metarterioles – pre-capillary sphincter
Capillaries
Microcirc are the major
Hydrostatic and oncotic pressures contributors the the
Venules peripheral vascular
resistance
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47. Factors Affecting Blood Flow
Poiseuille law
Pressure
Force of walls exerted on a liquid per unit area
Resistance
Opposition to force
Diameter and length of the blood vessels
contribute to resistance
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48. Factors Affecting Blood Flow
Velocity
Laminar vs. turbulent flow
Vascular compliance
C=VP
If there is an increase in volume, there is a
compliance of the vessel to accommodate an
increase in pressure.
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50. Regulation of Blood Pressure
Arterial pressure
Mean arterial pressure (MAP)
MAP = DP + 1/3(SP-DP) --> 90. High is 120-60.
Effects of cardiac output (CO)
Effects of total peripheral resistance (TPR)
Effects of hormones and Peptides
Epinephrine and norepinephrine - constriction.
Antidiuretic hormone, renin-angiotensin-aldosterone
system, and
natriuretic peptides(opposite of Angiotensin II, Aldo)
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51. Regulation of Coronary Circulation
Coronary perfusion pressure (CPP)
Difference in the aorta pressure and the pressure
in the right atrium coronary vessels
Autoregulation
Metabolic overrides neurogenic
Systemic and coronary
Autonomic regulation
SNS/PNS
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52. Lymphatic System
Special vascular system that picks up excess
fluid and returns it to the bloodstream
Lymphatic fluid
Lymphatic veins and venules - pick up a lot of
fluid.
Right lymphatic duct
Thoracic duct
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54. Questions?
Thanks for your attention..
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Notas del editor \n More ATP needed for cardia than skeletal, b/c never sleeps. \n \n Force behind blood flow is pressure. FLow is passive \n \n \n \n \n \n \n \n \n \n all because of Pressure.\n \n \n More murmurs in diastlole than systale.\nOrder an echo.\n Gallum - blood hitting a non-compliant ventricle. \n \n Right output is the inflow of the left.\n \n Coronary circ is hier in diastole and lower in systole. \n \n \n \n \n pr interval represents the AV conduction --> important\n \n Look at this and understand. \nStep 1 - fast Na\nStep 2 - slow Ca\nStep 3 - K out. \n \n \n Leaky K channels. ?\n \n \n Kintuckee - S3 \nTennisee - S4 - blood hitting an uncompliant ventricel\n SV is for each contraction.\nCO is per minute.\n SV and Ejection Fraction.\nEDV and ESV\n \n \n NE --> increase HR and contractility\nNE on beta 1, \nNE on alpha cause constriction of the peripheral vessels. \n \n A big sloppy heart will have to generate more tension on the same amount of blood to generate the same pressure. \n \n Normally Parasym is the dominant neural control, stim beta 2 (1?)on heart, causing increased HR and contractility. \nSym NE and Epi\nEpi from adrenal goes on beta 2 on vessels causing dilation (coronary circ).\n \n \n Flow is = Pressure \n resistance\n \n \n \n Myoglobin, in the heart, allows heart to survive systole as circulation will only happen during diastole.\n \n \n \n