1. The Cardiovascular System: The Heart: Part B18
The Cardiovascular System: The Heart: Part B

2. Cardiac Cycle
Cardiac cycle - The period between the start of one heartbeat and the beginning of the next.
During the cycle, each of the four chambers goes through
Systole – contraction of heart muscle
Diastole – relaxation of heart muscle
An average heart beat (HR)/cardiac cycle is 75 bpm. That means that a cardiac cycle length is about 0.8 second.
Of that 0.1 second is the atrial contraction, 0.3 is the atrial relaxation and ventricular contraction.
The remaining 0.4 seconds are the ventricular relaxation
The cardiac cycle creates pressure gradient that maintains blood flow

3. Phases of the Cardiac Cycle and pressure gradient
80% of blood flows passively into the ventricles
Figure 20.16

4. The conductive system
The heart is an autonomic system that can work without neural stimuli – an intrinsic conduction system.
The autonomic function of the heart results from:
The pacemaker function – Autorhythmic cells
The conductive system that transfer those impulses throughout the heart

5. Conduction pathways in the heart
The upper part of the heart (the 2 atria) is insulated from the lower part
Sinoatrial (SA) node (pacemaker)
Generates impulses about 75 times/minute (sinus rhythm)
Depolarizes faster than any other part of the myocardium
Atrioventricular (AV) node
Smaller diameter fibers; fewer gap junctions
Delays impulses approximately 0.1 second
Depolarizes 50 times per minute in absence of SA node input

6. Heart Physiology: Sequence of Excitation
Atrioventricular (AV) bundle (bundle of His)
Only electrical connection between the atria and ventricles
Right and left bundle branches
Two pathways in the interventricular septum that carry the impulses toward the apex of the heart
Purkinje fibers
Complete the pathway into the apex and ventricular walls
AV bundle and Purkinje fibers depolarize only 30 times per minute in absence of AV node input

7. Electrocardiography (ECG or EKG)
Body fluids are good conductors which allows the record of the myocardial action potential extracellularly
EKG pairs of electrodes (leads) one serve as positive side of the lead and one as the negative
Potentials (voltage) are being measured between the 2 electrodes
EKG is the summed electrical potentials generated by all cells of the heart and gives electrical “view” of 3D object (different from one action potential)
EKG shows depolarization and repolarization

8. Electrocardiography EKG is made of waves and segments
Waves are deflections above or below baseline
Three waves
P wave: depolarization of SA node
QRS complex: ventricular depolarization (Atrial repolarization record is masked by the larger QRS complex)
T wave: ventricular repolarization
Segments are sections of baseline between waves

9. An Electrocardiogram
Figure 20.14b

10. Cardiac muscle contraction
Two types of cardiac muscle cells that are involved in a normal heartbeat:
Specialized muscle cells of the conducting system
Contractile cells

11. Cardiac muscle contraction – conductive cells
Conductive cells have unstable resting potentials/ pacemaker potentials
They constantly depolarized slowly towards AP
At threshold, Ca2+ channels open
Ca2+ influx produces the rising phase of the action potential
Repolarization results from inactivation of Ca2+ channels and opening of voltage-gated K+ channels

12. Cardiac muscle contraction - Contractile Cells
In cardiac muscle, slow calcium channels remain open longer (after sodium channels close), prolonging the depolarization of the cell.
As long as the action potential is in its plateau and calcium is entering the myocytes, the myocytes contract.
These plateaus are more pronounced in the ventricles.
Cardiac muscle has an absolute refractory period of 250 msec, compared with 1–2 msec in skeletal muscle.
The cardiac muscle must return completely to resting potential before it can be contracted again.
As a result, the heart can not go through tetanus contraction.

13. Action potential in contractile cardiac muscle cells

14. Extrinsic Innervation of the Heart
Heartbeat is modified by the ANS
Cardiac centers are located in the medulla oblongata
Cardioacceleratory center innervates SA and AV nodes, heart muscle, and coronary arteries through sympathetic neurons
Cardioinhibitory center inhibits SA and AV nodes through parasympathetic fibers in the vagus nerves

15. Homeostatic Imbalances
Defects in the intrinsic conduction system may result in
Arrhythmias: irregular heart rhythms
Uncoordinated atrial and ventricular contractions
Fibrillation: rapid, irregular contractions; useless for pumping blood

16. Homeostatic Imbalances
Defective SA node may result in
Ectopic focus: abnormal pacemaker takes over
If AV node takes over, there will be a junctional rhythm (40–60 bpm)
Defective AV node may result in
Partial or total heart block
Few or no impulses from SA node reach the ventricles

17. Heart Sounds
Two sounds (lub-dup) associated with closing of heart valves
First sound occurs as AV valves close and signifies beginning of systole
Second sound occurs when SL valves close at the beginning of ventricular diastole
Heart murmurs: abnormal heart sounds most often indicative of valve problems

18. Aortic valve sounds heard in 2nd intercostal space at
right sternal margin
Pulmonary valve
sounds heard in 2nd
intercostal space at left
sternal margin
Mitral valve sounds
heard over heart apex
(in 5th intercostal space)
in line with middle of
clavicle
Tricuspid valve sounds typically
heard in right sternal margin of
5th intercostal space
Figure 18.19

19. Cardiodynamics
Movements and forces generated during cardiac contractions
End-diastolic volume (EDV) – the amount of blood in each ventricle at the end of ventricular diastole (before contraction begins)
End-systolic volume (ESV) - the amount of blood remains in each ventricle at the end of ventricular systole

20. Cardiodynamics Not all blood ejected Normal Adult 70 ml / beat
Stroke volume (SV) – The amount of blood that leaves the heart with each beat or ventricular contraction; EDV-ESV=SV
Not all blood ejected
Normal Adult 70 ml / beat
Ejection fraction – The percentage of end-diastole blood actually ejected with each beat or ventricular contraction.
Normal adult 55-70% (healthy heart)

21. Stroke Volume and Cardiac Output
Cardiac output (CO) – the amount of blood pumped by each ventricle in one minute.
Physiologically, CO is an indication of blood flow through peripheral tissues
Cardiac output equals heart rate times stroke volume; Normal CO: Approximately 4-8 liters/minute CO
Cardiac output
(ml/min) = HR
Heart rate
(beats/min) X SV
Stroke volume
(ml/beat)

22. Factors Affecting Cardiac Output
Figure 20.20

23. Effect inotropy – effect on contractility of the heart
Effect chronotropy – effect on HR
Effect dromotropy – effect on the conductive velocity
Sympathetic stimuli has a positive effect (increase) all
Parasympathetic stimuli has a negative effect (decrease) all

24. Autonomic Nervous System Regulation
In healthy conditions, parasympathetic effects dominate and slows the rate of the pacemaker from bpm to a bpm.
The binding of Ach to muscarinic receptors (M2) inhibit NE release (mechanism by which vagal stimulation override sympathetic stimulation)
Sympathetic nervous system is activated by emotional or physical stressors
Norepinephrine causes the pacemaker to fire more rapidly (and at the same time increases contractility)
Parasympathetic nervous system opposes sympathetic effects
Acetylcholine hyperpolarizes pacemaker cells by opening K+ channels
The heart at rest exhibits vagal tone (parasympathetic)

25. Autonomic Nervous System Regulation
Atrial (Bainbridge) reflex: a sympathetic reflex initiated by increased venous return
Stretch of the atrial walls stimulates the SA node
Also stimulates atrial stretch receptors activating sympathetic reflexes

26. Effects on SA node
The effect of the ANS on the heart is by changing the permeability of the conducting system cells.
Ach released by the parasympathetic neurons slow the depolarization rate and extend slightly the repolarization.
This decreases the HR
The NE released by the sympathetic neurons binds to beta–1 receptors, leading to the opening of calcium ion channels.
That increases the depolarization rate and shortens the repolarization period. Threshold is reached more quickly and HR increases

27. Chemical Regulation of Heart Rate
Hormones
Epinephrine from adrenal medulla enhances heart rate and contractility
Thyroxine increases heart rate and enhances the effects of norepinephrine and epinephrine
Intra- and extracellular ion concentrations (e.g., Ca2+ and K+) must be maintained for normal heart function

28. Homeostatic Imbalances
Tachycardia: abnormally fast heart rate (>100 bpm)
If persistent, may lead to fibrillation
Bradycardia: heart rate slower than 60 bpm
May result in grossly inadequate blood circulation
May be desirable result of endurance training

29. Factors Affecting Stroke Volume
Figure 20.23

30. Regulation of Stroke Volume
SV = EDV – ESV
Three main factors affect SV
Preload
Contractility
Afterload

31. Regulation of Stroke Volume
Preload
The amount of a muscle stretching before it begins to contract.
The preload of the heart is determined by the EDV.
In general, the greater the EDV the larger is the stroke volume : EDV-ESV=SV
These relationships is known as the Frank-Starling principle/Sterling’s law of the heart :
The force of cardiac muscle contraction is proportional to its initial length

32.  Preload =  Contractility (to a point)

33. Factors Affecting stroke volume - Preload/EDV
Stroke volume is the difference between the EDV and ESV. Changes in either one can change the stroke volume and cardiac output:
The EDV volume is affected by 2 factors:
The filling time – duration of ventricular diastole (assuming venous return is constant)
depends on HR – the faster the HR the shorter is the available filing time
The venous return – amount of blood returning to heart by the venae cavae or pulmonary veins each minute
changes in response blood volume (if blood volume decreases so will venous return), muscle contractions that press veins or changes in tissue activity.

34. EDV increase (preload increased)
Diastolic filling increased
EDV increase (preload increased)
Cardiac muscle stretch increased
Force of contraction increased
Ejection volume increased

35. Regulation of Stroke Volume
Contractility
Force of ventricular contraction (systole) regardless of EDV
Positive inotropic agents increase contractility
Increased Ca2+ influx due to sympathetic stimulation
Hormones (thyroxine and epinephrine)
Negative inotropic agents decrease contractility
Increased extracellular K+
Calcium channel blockers

36. Regulation of Stroke Volume
Afterload
The amount of tension the ventricle need to produce to open the semilunar valves and eject blood to arteries
influenced by arterial pressure.
The greater is the afterload, the longer is the period of isovolumetric contraction (ventricles are contracting but there is no blood flow), the shorter the duration of ventricular ejection and the larger the ESV – afterload increase – stroke volume decrease
Hypertension increases afterload, resulting in increased ESV and reduced SV

37. Congestive Heart Failure (CHF)
Progressive condition where the CO is so low that blood circulation is inadequate to meet tissue needs
Caused by
Coronary atherosclerosis
Persistent high blood pressure
Multiple myocardial infarcts (decreased blood supply and myocardial cell death)
Dilated cardiomyopathy (DCM) – heart wall weakens and can not contract efficiently. Causes are unknown but sometimes associated with toxins (ex. Chemotherapy), viral infections, tachycardia and more