E N D
1. Anatomy & PhysiologyBio 2402 Lecture Instructor: Daryl Beatty
Day 4 Class 4
The Heart, Part 2
2. Review: Cardiac Cycle
Beginning of control system
3. Review of Cardiac Blood Flow Be able to trace flow, from start to finish Questions:
How do the valves work
Name the parts & vessels
Questions:
How do the valves work
Name the parts & vessels
4. Sequence of blood flow Right atrium ? tricuspid valve ? right ventricle
Right ventricle ? pulmonary semilunar valve ? pulmonary arteries ? lungs
Lungs ? pulmonary veins ? left atrium
Left atrium ? bicuspid valve ? left ventricle
Left ventricle ? aortic semilunar valve ? aorta
Aorta ? systemic circulation
5. Two systems: Pulmonary
Systemic
6. Review of Cardiac Blood Flow Function of chordae tendineae and papillary muscles?
What opens and closes the valves? Questions:
How do the valves work
Name the parts & vessels
Questions:
How do the valves work
Name the parts & vessels
7. New section for today
8. Control system - Autorhythmic Fibers See figure 18.14 on page 694
These fibers have an unstable resting potential due to Na+ & Ca++ leakage in.
9. Control system - Autorhythmic Fibers See figure 18.14 on page 694
These fibers have an unstable resting potential due to Na+ & Ca++ leakage in.
10. Control system - role of instability of RMP Sinoatrial node (SA)
Inherent rate of 100 BPM
Sinus Rhythm Hearts pacemaker
Location: Upper RA
Fastest cells in system
11. Atrial (Bainbridge) Reflex Atrial (Bainbridge) reflex a sympathetic reflex initiated by increased blood in the atria
Causes stimulation of the SA node
Stimulates baroreceptors in the atria, causing increased SNS (Sympathetic Nervous System) stimulation
12. Control system - Atrioventricular Node (AV)
13. Control system - Atrioventricular Node (AV)
Impulse is delayed here 0.1 second (Why?)
14. Control system - Atrioventricular bundle (Bundle of His)
15. Control system - Atrioventricular bundle (Bundle of His)
The only electrical connection between atria and ventricles
Rapidly conducts through Right Bundle branch, (RBB), Left Bundle Branch (LBB) and Purkinje fibers
16. Control system - Right Bundle branch, (RBB), - stimulates septal cells
Left Bundle Branch (LBB) septal cells
Purkinje fibers- most important, stimulates most of the ventricular walls, and first stimulates the papillary muscles (why?)
17. Control system - Time required: 220 ms from SA node to complete depolarization.
Longer time indicates conduction defect
18. Intrinsic Conduction System Autorhythmic cells:
Initiate action potentials
Have unstable resting potentials called pacemaker potentials
Use calcium influx (rather than sodium) for rising phase of the action potential
19. Pacemaker and Action Potentials of the Heart
20. Sequence of Excitation Sinoatrial (SA) node generates impulses about 75 times/minute
Atrioventricular (AV) node delays the impulse approximately 0.1 second
Impulse passes from atria to ventricles via the atrioventricular bundle (bundle of His)
21. Sequence of Excitation AV bundle splits into two pathways in the interventricular septum (bundle branches)
Bundle branches carry the impulse toward the apex of the heart
Purkinje fibers carry the impulse to the heart apex and ventricular walls
22. Cardiac Intrinsic Conduction
23. Heart Excitation Related to ECG
24. Heart Excitation Related to ECG
25. Heart Excitation Related to ECG
26. Heart Excitation Related to ECG
27. Heart Excitation Related to ECG
28. Extrinsic Innervation Heart is stimulated by the sympathetic cardioacceleratory center
Heart is inhibited by the parasympathetic cardioinhibitory center
29. ECG What it means Electrical activity is recorded by electrocardiogram (ECG)
P wave corresponds to depolarization of SA node
QRS complex corresponds to ventricular depolarization
T wave corresponds to ventricular repolarization
Atrial repolarization record is masked by the larger QRS complex
SEE IP 9 Intrinsic Conduction System pages 3-6
30. ECG
31. Heart Sounds - valves Heart sounds (lub-dup) are associated with closing of heart valves
First sound occurs as AV (Tricuspid and Mitral) valves close and signifies beginning of systole
Second sound occurs when SL (Pulmonary & Aortic) valves close at the beginning of ventricular diastole
32. Cardiac Cycle Cardiac cycle refers to all events associated with blood flow through the heart
Systole contraction of heart muscle
Diastole relaxation of heart muscle
33. Phases of Cardiac Cycle Ventricular filling mid-to-late diastole
Heart blood pressure is low as blood enters atria and flows into ventricles
AV valves are open, then atrial systole occurs
34. Phases of Cardiac Cycle Ventricular systole
Atria relax
Rising ventricular pressure results in closing of AV valves
Isovolumetric contraction phase
Ventricular ejection phase opens semilunar valves
35. Phases of Cardiac Cycle Isovolumetric relaxation early diastole
Ventricles relax
Backflow of blood in aorta and pulmonary trunk closes semilunar valves
Dicrotic notch brief rise in aortic pressure caused by backflow of blood rebounding off semilunar valves
SEE IP9 Cardiac Cycle pages 3-19
36. Cardiac Output (CO) and Reserve CO is the amount of blood pumped by each ventricle in one minute
CO is the product of heart rate (HR) and stroke volume (SV)
HR is the number of heart beats per minute
SV is the amount of blood pumped out by a ventricle with each beat
Cardiac reserve is the difference between resting and maximal CO
37. Cardiac Output (CO) - Example CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)
CO = 5250 ml/min (5.25 L/min)
38. Stroke Volume SV = end diastolic volume (EDV) minus end systolic volume (ESV)
EDV = amount of blood collected in a ventricle during diastole
ESV = amount of blood remaining in a ventricle after contraction
39. What affects Stroke Volume? Preload amount ventricles are stretched by contained blood
Contractility cardiac cell contractile force due to factors other than EDV
Afterload back pressure exerted by blood in the large arteries leaving the heart
40. Frank-Starling Law of the Heart Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume
Slow heartbeat and exercise increase venous return to the heart, increasing SV
Blood loss and extremely rapid heartbeat decrease SV
41. Preload and Afterload
42. Chemical Regulation of Heart The hormones epinephrine and thyroxine increase heart rate
Intra- and extracellular ion concentrations (Ca++, K+, Na+) must be maintained for normal heart function
SEE IP9 Cardiac Output pages 3-9
43. Regulation of Heart Rate: Autonomic Nervous System Sympathetic nervous system (SNS) stimulation is activated by stress, anxiety, excitement, or exercise
Parasympathetic nervous system (PNS) stimulation is mediated by acetylcholine and opposes the SNS
PNS dominates the autonomic stimulation, slowing heart rate and causing vagal tone
44. Heart Contractilityand Norepinephrine Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP second-messenger system
45. Extrinsic Factors Influencing Stroke Volume Agents/factors that decrease contractility include:
Acidosis
Increased extracellular K+
Calcium channel blockers
46. Extrinsic Factors Influencing Stroke Volume Contractility is the increase in contractile strength, independent of stretch and EDV (End Diastolic Volume)
Increase in contractility comes from:
Increased sympathetic stimuli
Certain hormones
Ca2+ and some drugs
47. Cardiac Output The big picture
All factors:
Key: Be able to identify whether a factor influences SV or HR, and which direction
48. Control system - Clinical Applications Arrhythmias
Uncoordinated atrial and ventricular contractions
49. Control system - Clinical Applications Ectopic Foci Depolarization (beat) originates someplace other than SA node.
May be triggered by high caffeine or nicotine
Most common cause is low oxygen to a region of the heart
Premature Ventricular contractions (PVCs) most serious.
50. Control system - Clinical Applications Ventricular Tachycardia rapid rate stimulated by ventricular ectopic foci.
51. Control system - Clinical Applications Ventricular Fibrillation
This is the quivering of muscle uncoordinated
No pumping is occurring
Use of defibrillator is indicated here
52. Control system - Clinical Applications Congestive Heart Failure
Walls thinning, loss of strength
May be on either side (r or l)
If on left, fluid builds up in lungs (why?)
Treatment:
Digitalis (From poisonous Foxglove family of plants) slows the rate, but increases strength (contractility)
53. Clinical:What is a Heart attack? (Page 692 Btm Left)
Ishemia results in:
anaerobic metabolism - lactic acid formation:
Rising acidity hinders ATP & cannot pump out Ca++, then:
Gap junctions close - cells electrically isolated, and:
If ischemic area is large, pumping action impaired.
54. Clinical Application CHFCongestive Heart Failure Congestive heart failure (CHF) is caused by:
Coronary atherosclerosis
Persistent high blood pressure
Multiple myocardial infarcts
Dilated cardiomyopathy (DCM)
55. Age-Related Changes Affecting the Heart Sclerosis and thickening of valve flaps
Decline in cardiac reserve (max HR)
Fibrosis of cardiac muscle (normal)
Atherosclerosis (You are as old as your arteries)
56. Developmental Aspects of the Heart Contraction detectable at 23 days
57. Developmental Aspects of the Heart Contraction detectable at 23 days
4 chambers by day 25
58. Fetal Heart Development Fetal heart structures that bypass pulmonary circulation
Foramen ovale connects the two atria
Ductus arteriosus connects pulmonary trunk and the aorta
59. Congenital Heart Defects