1. Aims Introduction to the heart.
Lecture #16 Handout
Aims
Introduction to the heart.
Heart contraction and electrical conduction.
Readings; Sherwood, Chapter 9

2. Cardiovascular Physiology
Lecture #16 Handout
Cardiovascular Physiology
Cardiac Muscle
Myocytes (cardiac muscle cells)
Myocytes are connected to each other via __Intercalated Disks__
Composed of Desmosomes and Gap Junctions
Allow waves of action potentials to spread from one cell to the next (Syncytium).
Cardiac muscle: Involuntary striated muscle
Intercalated disks: hold cells together; gap junctions allow cells to directly communicate; electrical synapse between muscle cells
Syncytium: just like smooth muscle; all cells contract at same time
Sherwood’s Human Physiology 9-8 (9-6 6th Edition)

3. Human Heart Anatomy Sherwood’s Human Physiology 9-5 (9-4 6th Edition)
Lecture #16 Handout
Human Heart Anatomy
Know from other courses
Sherwood’s Human Physiology 9-5 (9-4 6th Edition)

4. Lecture #16 Handout
Valve Physiology
Valves are mechanical devices and function in response to blood flow.
They function on the principle that they stay open as long as the blood pressure is greater in the emptying chamber.
They close as soon as the blood pressure is greater in the filling chamber, thus blood flow is unidirectional. P1 P2
Primarily function in response to pressure
One-way valves P1 P2
Sherwood’s Human Physiology 9-4 (9-3 6th Edition)

5. Ion Concentrations Inside a cell K+ Outside a cell Na + Ca + Cl-
Lecture #16 Handout
Ion Concentrations
Inside a cell K+
Outside a cell
Na +
Ca +
Cl-
Same ionic players
Guyton’s Textbook of Medical Physiology 4-1

6. Cell Membrane Transport
Lecture #16 Handout
Cell Membrane Transport
Passive
Simple diffusion
Facilitated diffusion
Active (needs energy)
All happens in cardiac muscles cells too
Guyton’s Textbook of Medical Physiology 4-2

7. Two Types of Cardiac Cells
Lecture #16 Handout
Two Types of Cardiac Cells
Autorhythmic Cells
__non-contractile_________
Initiate and conduct action potentials responsible for contraction.
Located in the SA node, AV node, Bundle of His, Purkinje fibers.
Contractile Cells
99% of the cardiac muscle cells
Autorhythmic: similar to pacemaker cells (non-contractile)
Contractile cells: same basic thick and thin filaments structures in skeletal muscle (troponin T,I,C)

8. Specialized Conduction System
Lecture #16 Handout
Specialized Conduction System
Sinoatrial (SA) node.
_Pacemaker____
Cells exhibit autorhythmicity.
SA node: top of right atria; sets pace of the heart; beats are nice continuous and even
Sherwood’s Human Physiology 9-11 (9-8 6th Edition)

9. Specialized Conduction System
Lecture #16 Handout
Specialized Conduction System
Atrioventricular (AV) node
Delays electrical signal due to a decreased number of gap junctions.
AV node: at junction of atria and ventricle
Non-contractile cells have gap junctions too
AV nodal cells have fewer  delay contraction of ventricle from atria
Need that delay so that Atria and Ventricle are not contracting at the same time
Sherwood’s Human Physiology 9-11 (9-8 6th Edition)

10. Conduction Delay Atrioventricular fibrous tissue Acts as an insulator
Lecture #16 Handout
Conduction Delay
Atrioventricular fibrous tissue
Acts as an insulator
Takes 0.03s from SA node to AV node
0.12 before crossing into ventricle
Into Bundle of His .16s from when SA node fired
Delay makes sure the atria contract first
Guyton’s Textbook of Medical Physiology 10-3

11. Specialized Conduction System
Lecture #16 Handout
Specialized Conduction System
Atrioventricular (AV) bundle or Bundle of His.
Transmits electrical signal down to the ventricles.
Purkinje fibers
Send action potential through ventricles.
Has increased number of gap junctions.
AV bundle turns into all the Purkinje fibers
Sherwood’s Human Physiology 9-11 (9-8 6th Edition)

12. Lecture #16 Handout
Pacemaker Potential
Decreased K+ efflux and constant Na+ influx via leak channels.
Resulting in a higher resting potential.
Slow Ca++ inward permeability via transient voltage-gated Ca++ channel.
In nodal cells (SA node, AV node, Bundle of His, Purkinje fibers) all have pacemaker potential, but a bit different
Different from muscle cells = Non-contractile; their own autorhythmicity determined by different ion fluxes
Resting membrane potential is roughly -60mV whereas muscle cells are at -80 to -90; due to less K+ leak channels in these nodal cells so not as much K efflux out of the cell; NA+ influx as usual; not balanced = higher resting membrane potential
Transient voltage-gated Ca++ channel (aka T-type): opens to allow Ca to slowly flow in from ECF which depolarize the cell even more -
- Responsible for
Sherwood’s Human Physiology 9-10 (9-7 6th Edition)

13. Lecture #16 Handout
Pacemaker Potential
Ca++ inward permeability via longer lasting voltage-gated Ca++ channel.
Resulting in __faster depolarization___
Not Na+ influx; all Ca++ from pacemaker potential to depolarizing; no Na+gated channels in pacemaker cells
Not many Na+ leak channels, but still have K+gated votage channels
Sherwood’s Human Physiology 9-10 (9-7 6th Edition)

14. Pacemaker Potential K+ outward permeability via voltage-gated channel.
Lecture #16 Handout
Pacemaker Potential
K+ outward permeability via voltage-gated channel.
Resulting in repolarization
K+ responsible for repolarizing
Sherwood’s Human Physiology 9-10 (9-7 6th Edition)

15. Pacemakers SA node (normal pacemaker) Ectopic Pacemakers AV node
Lecture #16 Handout
Pacemakers
SA node (normal pacemaker)
70-80 action potentials per minute.
Ectopic Pacemakers
AV node
40-60 action potentials per minute.
Bundle of His and purkinje fibers
20-40 action potentials per minute.
SA node is fastest; sets the pace
If SA node knocked out, the other cells could act as pacemaker of the heart; less action potentials per minute; HR decreases

16. Pacemakers Sherwood’s Human Physiology 9-12 5th Edition only
Lecture #16 Handout
Pacemakers
Due to slower rate of depolarization from t-type calcium channel
Sherwood’s Human Physiology th Edition only

17. Abnormal Conduction Pathway
Lecture #16 Handout
Abnormal Conduction Pathway
Normal
-SA node sets the pace
SA Node non-functional
-AV node sets the pace at a slower rate
AV Node non-functional
-Atria contract at SA node rate while ventricles contract at Purkinje fiber rate (much slower)
-Complete heart block that requires an artificial pacemaker.
Purkinje fiber is hyper-excitable
- Called an ectopic focus that causes a premature beat.
If SA node is knocked out: AV node takes over – it can depolarize atria AND ventricles
If knock out AV node, but SA node intact: we lose connection between atria and ventricle; contraction at two different rates = complete heart block; pacemaker sets rates of ventricles to that of atria
Purkinje fiber hyper-excitable: an extra beat somewhere
Guyton’s Textbook of Medical Physiology Sherwood’s Human Physiology 9-15

18. Abnormal Conduction Pathway
Lecture #16 Handout
Abnormal Conduction Pathway
If SA node is knocked out: AV node takes over – it can depolarize atria AND ventricles
If knock out AV node, but SA node intact: we lose connection between atria and ventricle; contraction at two different rates = complete heart block; pacemaker sets rates of ventricles to that of atria
Purkinje fiber hyper-excitable: an extra beat somewhere
Guyton’s Textbook of Medical Physiology Sherwood’s Human Physiology 9-15

19. Cardiac Muscle Cell Action Potential
Lecture #16 Handout
Cardiac Muscle Cell Action Potential
Depolarization
Na+ inward
Plateau
Ca++ inward
Repolarization
K+ outward
Looks similar to skeletal muscle, except that:
-- Resting membrane potential is -90mV; much more hyperpolarized than nodal cells (-60mV)
-- Depolarization of muscle cells is due to influx of Na+; in nodal cells it is due to Ca++
-- Plateau phase: slow ca++ influx through L-type calcium channel; hold it at a stable membrane potential
Sherwood’s Human Physiology 9-15 (9-11 6th Edition)

20. SA node potentials vs. cardiac cell potentials
Lecture #16 Handout
SA node potentials vs. cardiac cell potentials
Nodal contraction vs. Cardiac muscle
-- resting membrane potential
-- “overlap quite nicely”
SA node has a higher resting potential than other cardiac muscle cells.
Guyton’s Textbook of Medical Physiology 10-2

21. Lecture #16 Handout
ECC in Cardiac Muscle
The majority of Ca++ required for contraction comes from the sarcoplasmic reticulum and not the ECF.
Excitation Contraction Coupling
Primary source of Ca++ is sarcoplasmic reticulum
Sherwood’s Human Physiology 9-16 (9-12 6th Edition)

22. Refractory Period
Lecture #16 Handout
Long refractory period important because it makes tetanus impossible.
Plateau phase: action potential lasts almost as long as contractile response; we can’t have another action potential until after contractile response
Good thing for heart to not be able to tetanus; it would contract and not pump as it should
Frequency summation: no relaxation so no time for blood to fill back up
Plateau “safety valve” for having tetanus in cardiac muscle cells
Sherwood’s Human Physiology 9-17 (9-12 6th Edition)

23. Requirements for Efficient Cardiac Contraction
Lecture #16 Handout
Requirements for Efficient Cardiac Contraction
Atrial excitation and contraction need to be complete before ventricular contraction occurs.
Excitation of cardiac muscle fibers should be coordinated so that each chamber contracts as a unit.
Pair of atria and pair of ventricles should be coordinated so that both members of the pair contract simultaneously.
2. Need functional syncitium so all contracting at same time

24. What is an Electrocardiogram (ECG or EKG)?
It is not a direct recording of the actual electrical activity of the heart.
It measures the portion of the electrical activity of the heart that is transduced in the body fluids and reaches the body surface.
It is a complex recording that represents the overall activity throughout the heart during depolarization and repolarization.
Not a single cell measurement

25. ECG 6 body & 6 chest leads for a total of 12 leads
Lecture #16 Handout
ECG
Not important to know all this
6 body & 6 chest leads for a total of 12 leads
Sherwood’s Human Physiology 9-18 (9-14 6th Edition)

26. ECG P wave- atrial depolarization PR segment- AV nodal delay
Lecture #16 Handout
ECG
P wave- atrial depolarization
PR segment- AV nodal delay
QRS complex- ventricular depolarization and atrial repolarization
ST segment- ventricular contraction and emptying
T wave- ventricular repolarization
TP interval- ventricular filling
QRS complex: atrial repolarization at the same time but not measuring that; electrical activity is so low it doesn’t affect graph
Sherwood’s Human Physiology 9-19 (9-15 6th Edition)

27. Abnormal ECG Rate Abnormalities Rhythm Abnormalities (Arrhythmias)
Lecture #16 Handout
Abnormal ECG
Rate Abnormalities
Tachycardia (>100 beats/min.)
Rhythm Abnormalities (Arrhythmias)
Extrasystole (premature beat)
Ventricular fibrillation
Atrial fibrillation
Complete Block
Cardiac Myopathies
Myocardial Infarction
-- Extrasystole: extra beat (ectopic focus of purkinje fibers)
-- Ventricular fibrillation: not complete depolarization so not contracting; minor fluttering, but not complete; not pumping any blood
-- Atrial fibrillation (not shown): not good P waves; not pushing blood into ventricles
-- Heart block (knock out AV node): two rates; multiple P waves between QRS complex
Cardiac myopathies
-- Myocardial Infarction (heart attack)
Sherwood’s Human Physiology 9-20 (9-16 6th Edition)

28. Next Time Cardiac Cycle Cardiac regulation
Lecture #16 Handout
Next Time
Cardiac Cycle
Cardiac regulation
Extrinsic vs. intrinsic
Reading; Sherwood, Chapter 9
Clicker Question:

29. Objectives Describe the structure and function of cardiac myocytes.
Describe the anatomy of the heart and how blood flows through it.
Describe cardiac contraction
Conduction (normal and abnormal)
Pacemakers
Action potentials
Refractory period
Describe the ECG.
P Wave, QRS Complex, T Wave, Abnormal ECG