1. Chapter 20 - The Heart

2. Location and Size of Heart
Located in thoracic cavity in mediastinum
About same size as closed fist
base is the wider anterior portion
apex is tip or point

3. Pericardium: Heart Covering

4. Fibrous Pericardium Rests on and is attached to diaphragm
Tough, inelastic sac of fibrous connective tissue
Continuous with blood vessels entering, leaving heart at base
Protects, anchors heart, prevents overstretching

5. Parietal (Outer) Serous Pericardium
Thin layer adhered to inside of fibrous pericardium
Secretes serous (watery) lubricating fluid

6. Pericardial Cavity Contains pericardial (serous) fluid
lubricates surface of parietal and visceral serous pericardium
decreases friction

7. Visceral (Inner) Serous Pericardium
Adheres to Heart
Forms epicardium
Secretes watery (serous) lubricating fluid

8. Pericardium

9. Homeostatic Imbalances
Pericarditis
inflammation of pericardium
painful, rubbing of tissues
can damage myocardium
Cardiac tamponade
a buildup of pericardial fluid
bleeding into pericardial cavity
may result in cardiac failure

10. Heart wall - Three layers
Epicardium (outer)
visceral layer of pericardium
thin, transparent
smooth, slippery
Myocardium (middle) - cardiac muscle
Endocardium (inner)
endothelium over connective tissue
smooth lining for inside of heart, valves
continuous w/ endothelium of vessels

11. Chambers of the Heart External landmarks
coronary sulcus separates atria/ventricles
anterior/posterior interventricular sulcus separates right/left ventricles

12. Internally - 4 compartments
R/L atrium w/ auricles
R/L ventricles
Interatrial septum separates atria
Interventricular septum separates ventricles

13. Ventricular thickness varies depending on function
Right – pumps to lungs (pulmonary circulation)
Left – pumps to the body (systemic circulation)

14. Valves of the Heart
Function to prevent backflow of blood into/through heart
Open, close in response to changes in pressure in heart
Four valves

15. Valve Structure Dense connective tissue covered by endocardium
AV valves
chordae tendineae - thin fibrous cords
connect valves to papillary muscles

16. Valve Function Opening and closing a passive process
when pressure low, valves open, flow occurs
with ventricular contraction, pressure increases
papillary muscles contract, prevent valves from pushing back into atria

17. Atrioventricular (AV) valves
Separate atria, ventricles
tricuspid valve - right
bicuspid (mitral) valve - left

18. Semilunar valves
In arteries that exit heart to prevent blood from re-entering heart
pulmonary semilunar valves
aortic semilunar valves
Pathologies
incompetent – do not close
stenosis – stiff and do not close

19. Blood Flow Through Heart
Right atrium (RA) - receives deoxygenated blood from three sources
superior vena cava (SVC)
inferior vena cava (IVC)
coronary sinus

20. Pulmonary trunk - from RV branches into pulmonary arteries (PA)
Right ventricle (RV)
receives blood from RA
pumps to lungs
Pulmonary trunk - from RV branches into pulmonary arteries (PA)
Pulmonary arteries
from heart to lungs for gas exchange
right and left branches for each lung
blood gives up CO2 and picks up O2
Pulmonary veins (PV) - oxygenated blood from lungs to heart

21. Pulmonary Circulation

22. Left atria Left ventricle (LV) receives blood from PV
pumps to left ventricle
Left ventricle (LV)
sends blood to body via ascending aorta
aortic arch
curls over heart
three branches off of it that feed superior portion of body
thoracic aorta
abdominal aorta

25. Myocardial Blood Supply
Myocardium has own blood supply
coronary vessels
diffusion into tissue impossible due to thickness
much overlap of vessels and anastomoses (art-art connections)
Heart can survive on 10-15% of normal arterial blood flow

26. 4/13/2017
Arteries
left coronary artery divides into anterior interventricular artery and circumflex arteries
anterior interventricular artery supplies walls of both ventricles and septum
circumflex supplies LV and LA
right coronary artery small branches to RA, divides into posterior interventricular and marginal artery
posterior interventricular supplies walls of both ventricles
marginal branch supplies RV

27. Coronary veins blood into muscle then drains into coronary sinus
supplied by great cardiac vein (drains anterior of heart) and middle cardiac vein (drains posterior)

28. Coronary Circulation Pathologies
Faulty coronary circulation due to:
blood clots
fatty atherosclerotic plaques
smooth muscle spasms in coronary arteries
Problems
ischemia
hypoxia

29. Pathologies (cont.) Angina pectoris - "strangled chest"
pain w/ myocardial ischemia - referred pain!
tight/squeezing sensation in chest
labored breathing, weakness, dizziness, perspiration, foreboding
often during exertion - climbing stairs, etc
silent myocardial ischemia

30. Pathologies (cont.) Myocardial infarction (MI) - heart attack
thrombus/embolus in coronary artery
tissue distal to blockage dies
if survival, muscle replaced by scar tissue
Long term results
size of infarct, position
pumping efficiency?
conduction efficiency, heart rhythm

31. Pathologies (cont.) Treatment Reperfusion damage
clot-dissolving agents
angioplasty
Reperfusion damage
re-establishing blood flow may damage tissue
oxygen free radicals - electrically charged molecules w/ unpaired electron
radicals attack proteins (enzymes), neurotransmitters, nucleic acids, plasma membranes
further damage to previously undamaged tissue or already damaged tissue

32. Myocardium (Cardiac Muscle)
Cells are involuntary, striated, branched
Fibers connected to others by intercalated discs
gap junctions allow AP's to pass from fiber to fiber
desmosomes
“spot welds”
prevent cardiac fibers from separating

33. Intercalated Discs

34. Normal Action Potential
4/13/2017

35. Cardiac Muscle Action Potential

37. Long absolute refractory period

38. Pacemaker potentials
Leaky membranes
Spontaneously depolarize

39. Conduction System and Pacemakers
Autorhythmic cells
cardiac cells repeatedly fire spontaneous action potentials
autorhythmic cells: the conduction system
pacemakers
SA node
origin of cardiac excitation
fires /min
AV node
conduction system
AV bundle of His
R and L bundle branches
Purkinje fibers

40. Conduction System and Pacemakers
Arrhythmias
irregular rhythm
abnormal atrial and ventricular contractions
Fibrillation
rapid, out of phase contractions
squirming bag of worms
Ectopic pacemakers (ectopic focus)
abnormal pacemaker controlling the heart
SA node damage, caffeine, nicotine, electrolyte imbalances, hypoxia, toxic reactions to drugs
Heart block
AV node damage - severity determines outcome
may slow conduction or block it

41. Conduction System and Pacemakers
SA node damage (MI)
AV node can run things (40-50 bts/min)
if AV node out AV bundle, bundle branch/conduction fibers fire at bts/min
Artificial pacemakers - can be activity dependent

43. Atrial,Ventricular Excitation Timing
SA node to AV node - small delay
about 0.05 sec from SA to AV, 0.1 sec to get through AV node
conduction slows
allows atria time to finish contraction and better fill the ventricles
once to AV bundle, conduction rapid to rest of ventricle

44. Extrinsic Control of Heart Rate
Basic rhythm of heart set by pacemaker system
Central control from medulla
sympathetic input
parasympathetic input

45. Electrocardiogram Electrical activity of the heart P wave QRS complex
T wave

47. Cardiac Cycle Connection between electrical and mechanical events
Systole
Diastole
Isovolumetric contraction
Isovolumetric relaxation

48. Quiz!!!!! 1. Superior vena cava 2. Right atrium 3. Tricuspid valve
4. Right ventricle
5. Papillary muscle
6. Aorta (aortic arch)
7. Pulmonary trunk
8. Left atrium
9. Bicuspid valve
10. Interventricular septum

49. Cardiac Output Amount of blood pumped by each ventricle in 1 minute
CO = HR x SV HR
heart rate
70 bts/min SV
stroke volume
70 ml/min
CO  5 L/min (70 bts x 70 ml)

50. Regulation of Stroke Volume
SV = EDV – ESV
EDV
End Diastolic Volume
volume of blood in the heart after it fills (following diastole)
120 ml
ESV
End Systolic Volume
volume of blood in the heart after contraction (after systole)
50 ml
each beat ejects about 60% of blood in ventricle

51. Most important factors in regulating SV: preload, contractility and afterload
degree of stretch of cardiac muscle cells before contraction
determined by EDV
Contractility
increase in contractile strength separate from stretch and EDV
determined by changes in Ca++ availability
Afterload
pressure that must be overcome for ventricles to eject blood from heart
determined by TPR

52. Preload Muscle mechanics Cardiac muscle length-tension relationship?
fiber length determines # of cross bridges
cross bridge # determines force
increase/decrease fiber length increase/decrease force generation
Cardiac muscle
how is cardiac fiber length determined/regulated?
fiber length determined by filling of heart – EDV
factors that effect EDV (anything that effects blood return to heart) increase/decrease filling
increase/decrease SV

53. Preload – Frank-Starling Law of the Heart
length tension relationship of heart
length = EDV
tension = SV

54. Contractility
Increase in contractile strength separate from stretch and EDV
Do not change fiber length but increase contraction force?
what determines force?
how can we change this if we don’t change length?

55. Increase the number of cross bridges by increasing amount of Ca++ inside the cell – positive inotrope
Sympathetic nervous system opens channels to allow Ca++ to enter the cell

56. Increase force of contraction without changing fiber length

57. Afterload
Flow = P/R
If blood pressure is high (TPR), difficult for heart to eject blood
More blood remains in ventricle with each beat
Heart has to work harder to eject blood, change the length/tension of the heart

58. Regulation of Heart Rate
Intrinsic regulators
pacemakers
Bainbridge effect
increase in EDV increases HR
filling stretches SA node increasing depolarization and HR
Extrinsic regulators
autonomic nervous system
sympathetic
parasympathetic
hormones – epinephrine, thyroxine
ions – Na+, K+, Ca++
body temperature
age
gender
exercise