a chapter from the general human anatomy and physiology course taught to pharmacy students.It discusses details and lecture notes about the chapter.

1. The Heart
… Farah El Soheil

2. Cardiac muscle fibers:
● Auto rhythmic fibers
● Contractile fibers
… Farah El Soheil

3. Cardiac cells comparing to other cells
● Uninucleated
● Has intercalated disc which is a thickening of the sarcolemma conecting
cardiac fibers with one another and it's made up of :
– Desmosome : hold fibers together
– Gap junction : for conduction of muscle action potential b/w fibers
● Larger and more numerous mitochondria
● Same arrangement of actin and myosin as in skeletal muscle.
● Wider t-tubules but less abundant
● Smaller SR
… Farah El Soheil

4. The conduction system: autorythmic
fibers
● The source of rhythmical electric activity of the
heart is the auto-rhythmic fibers that repeatedly
generate AP necessary for contraction. They're
self excitable. They stimulate the heart
● Function :
– Pacemaker : excitation of heart by “AP”
– Conducting system : provide a path for cardiac
excitation so the heart contract in a coordinated
manner
… Farah El Soheil

5. The conducting system
● Excitation starts in SA node ( sinoatrial node) of the right atria that
repeatedly depolarize to threshold “ pacemaker pot “ so AP is triggered
and pass to both atria via the gap junctions so both atria contract
● AP in atrial fibers move to AV node (inter-atrial system) where
conduction slows which provides time fr blood emptying
● AP then pass from AV node to AV bundle “ bundle of HIS” where AP
conduct from atria to ventricle then to bundle branches : interventricular
septum the purkinji conduct AP to ventricles which contract as a result
NB: SA has the fastest rate of AP conduction so AP is reached before it's generated which set rhythm of heart “
pacemaker”
… Farah El Soheil

6. ● Note :
hormones ( epinephrine) And ANS set the
frequency and the force of heart beat not
rhythm which is regulated by pacemaker cells
… Farah El Soheil

7. Coronary circulation
● Coronary arteries branch from aorta ( blood
flows through the arteries during heart
relaxation due to high pressure in aorta that
propel blood from coronary artery to capillary
then to coronary veins.
– Left : supplies ventricles and left atrium ( LAD is a
branch of the left coronary artery
– Right: supplies right atrium.

8. Coronary circulation
● Coronary vein : major vein is the coronary sinus
( vascular sinus) that has no smooth muscle so
can't dilate or constrict.
PS: Valves open or close in response pressure and they prevent backflow.

9. Heart sounds
● S1 : lubb : closure of AV valve ( at the
beginning of ventricle systole)
● S2 : dupp : closure of SL valve ( at the
beginning of ventricle diastole)
● S3: ventricular filling
● S4:atrial systole.

10. Regulation of heart rate
● 1) ANS (autonomic) : by CV center of medulla that
receive nerve impulses from proprioreceptor”that monitor
position of body”, chemoreceptor “ that monitor
hormones and chemicals of the blood”, baroreceptor* “
that monitor the stretching of blood vessels caused by
pressure of blood flow”). Those direct either increase or
decrease in frequency of AP in sympathetic or
parasympathetic states respectively.
*present in aorta and carotid.
… Farah El Soheil

11. Sympathetic state
● Epinephrine hormone
– Speeds the rate of pacemaker potential in SA and AV nodes so
the heart rate (HR) increase
– Increase the calcium entry in contractile fibers so contraction
increase
● Effect: increase in HR leads to decrease in preload ( blood
present before contraction ) so the stroke volume (SV)
decrease (directly proportional to preload). However,
increased HR has a greater effect than decreased preload
so contraction increase.
… Farah El Soheil

12. parasympathetic state
● Acetylcholine (Ach) : decease pacemaker
potential in SA and AV nodes.
… Farah El Soheil

13. ● 2) chemical :
– Hormones : epinephrine and NE ( by adrenal medulla) and
thyroid hormones increase contraction and HR.
– Cations:
● Difference in ions important for AP production
● Increase in Na+ block Ca2+ entry so contraction decrease.
● Increase in K+ decrease AP production
● Increase of Ca2+ in interstitial fluid leads to increase n HR and
contraction.
… Farah El Soheil

14. ● 3) other factors:
– Increase in temperature : increase SA impulse
which leads to increase in HR
– decrease in temperature leads to decrease in
metabolism which leads to increase in ability to
withstand decreased blood flow
… Farah El Soheil

15. Regulation of SV
● Preload :
– Caused by EDV ( ventricular filling during diastole)
that's increased by venous return or increase in
duration of ventricle diastole( I.e.: decreased HR)
– stretch of heart before it contracts
– Increase in HR leads to decreased duration
,decreased venous return and decreased EDV
eventually.
… Farah El Soheil

16. ● Contractility :
– Positive ionotropics increase Ca2+ entry during AP
ex: sympathetic and epinephrine and NE.
– Negative ionotropics as increase in K+ leads to
decrease in ca2+ inflow.
… Farah El Soheil

17. ● Afterload: the pressure to be overcame
– If : Pressure in ventricles > pressure in
artery(afterload) , the valve opens.
PS: HTN leads to narrowed arteries so afterload increase so SV decrease and blood
remains in ventricle

18. AP of contractile fibers
● Depolarization : due to opening of Na+
channels* ( due to depolarization to threshold
by neighboring fibers) and Na+ enters
* fast because they open directly in response to depolarization to threshold

19. ● Plateau:state of maintained depolarization due to
opening of slow Ca2+ channels in sarcolemma
and entry to cytosol. This inflow of Ca2+ causes
Ca2+ to exit from SR due to increase in CA2+ this
leads to contraction due to binding of Ca2+ to
troponin and the slide of actin across myosin and
the start of tension. Before plateau K+ in
sarcolemma opens so K+ leaves But the Ca2+
entry = K+ release so depolarization continues.

20. ● Repolarization : due to additional K+ channels
opening so K+ exits and the closure of Ca2+
channels in SR and sarcolemma

21. Refractory period
● It lasts longer than contraction so contraction
can't occur except after relaxation so no
tetanus occurs ( extended contraction) which is
good because pumping depends on alternating
contraction and relaxation so blood flows.

22. Energy used by cardiac cells
● Aerobic
● From oxidation of FA “mainly”, glucose, A.A.,
lactic acid “during exercise” ketone bodies and
creatinine phosphate.

23. Signs of infarction
● Creatinine kinase (CK) in blood where it should
be always inside muscles
● Enlarged Q wave

24. Electrocardiogram
● Sum of all AP generated by cardiac fibers per
beat
● Uses:
– Amplifies heart electrical signals
– Determine if conducting pathway is abnormal
● If heart is enlarged
– Enlarged P wave then the atrium is enlarged
– Enlarged R wave then the ventricles are enlarged

25. ● P wave: depolarization of the atria contractile fibers
( after p wave atria contracts)
● QRS wave : depolarization of cells of ventricles and
repolarization of atria( masked by QRS wave). After
this wave the ventricles contract.
● T wave: repolarization of the ventricles ( smaller and
wider than the QRS wave since repolarization is
slower than depolarization ) after repolarization atria
and venticles are relaxing.

26. Cardiac cycle
● In each side of the heart same volume of blood
is expelled but with different pressure ( it's
higher in left side)
● Each cycle takes 0.8 sec as a total when HR=
75 beat/ min

27. Cardiac cycle
● Atrial systole : and ventricular diastole (0.1 sec)
depolarization (dep.) in SA node followed by
dep. In atrial fibers then atrial systole
( contraction ) so blood is forced into ventricles
through opened AV valves (25ml) but there's
(105ml) already present so the end of
ventricular diastole ( relaxation) there's EDV=
130 ml as a total.

28. Cardiac cycle
● Ventricular systole : and atrial diastole (0.3 sec)
– Dep. In ventricle followed by ventricle systole so blood is
forced to AV valve which close ( prevent backflow ). SL and
AV valves are closed. Isovolumetric contraction state takes
place where :
● Fibers are contracting but not shortening “isometric cont.”
● Volume in ventricle is the same “ isovolumic”
– More contraction of ventricles so pressure increase. Once
p(ventricle)> p(artery) SL valve opens so SV= 70 ml of
blood is ejected
– At the end of contraction ESV=60 ml remaining in the
ventricles

29. Cardiac cycle
● Relaxation period : it's the variable period of the cycle
based on HR but mainly it's (0.4 sec)
● Ventricles and atria relax
● Repolarization of the ventricle (DIASTOLE) so
p( ventricle) decrease so blood flows from arteries back
to ventricles SL closes as a result and AV are already
closed. Hence there's a state of isovolumetric volume.
● More relaxation leads to p(ventricle)<p(atria) so AV
valve open and blood flows (45 ml) : ventricular filling so
ventricles are ¾ filled at end of relaxation.

30. AV valves
● Open : when ventricles are relaxed papillary
muscles are relaxed.
● Close: when ventricles contract so papillary
myscles contract

31. notes
● No valve between vein and heart but
contraction of atria close venous entry points.
● Fibrous skeleton of the heart :
– Prevent overstretching of valves
– Insulates atria from ventricles electrically.