Cardiovascular physiology

1. BASIC CARDIOVASCULAR
PHYSIOLOGY
UCHENNA IFEANYI NWAGHA

2. INTRODUCTION
• The circulatory system consists of the heart, the
blood vessels, (arteries, arterioles, and blood)
and its purpose is to transport oxygen and
nutrients to tissues in the body, and to carry away
the by products of metabolism.
• Basically, events of the CVS consists of electrical
events which involves generation and
transmission of cardiac impulse.
• Mechanical event involves cardiac contractility
which leads to the pumping of blood to the
vessels and distribution to the tissues .

3. Electrical properties of the heart
Electrical properties of myocardium
• The resting membrane potential of individual cardiac muscle is – 90
MV.
This negativity is due to;
• a).Unequal distribution of ions between the ECF and ICF.
• b). Differential permeability e.g. K+ is (100x) more permeable than
Na;thus more positive K+ diffuses out of the cell along
concentration gradient than Na+ diffusing inside.
• c).The presence of organic negatively charged impermeable intra
cellular anions
• d).Na -K Atpase activity ensures the pumping of into the cell of, 2K+
as against the 3Na+ that is pumped out.

4. Electrical properties of the heart
Action potential
• The action potential in cardiac muscle is same as
that of other excitable tissue but with prolonged
duration of 300 MS compared to 2-4 MS in other
tissues.
Phases of AP
• Phase 0; Rapid depolarization occurs with Na+
influx associated with overshoot.
• Phase 1;Initial rapid repolarization ,closure of Na+
Phase 0 and 1 corresponds to QRS complex of
ECG.

5. Electrical properties of the heart
• Phase 2;Plateau phase is due to slow Ca+ influx
( ST segment of ECG).
• Phase 3;Rapid repolarisation due to closure of
Ca+ channels & opening of K+ leading to , K+
efflux( T wave of ECG).
• Phase 4;Closure of K+ channels and
restoration of the original membrane
potential by Na-K Atpase.

6. Electrical properties of the heart
Refractory period of the heart (Why the heart
cannot be tetanised).
• At phases 0,1,2 and part of 3 before,
repolarization reaches threshold potential, the
heart is absolutely refractory .
• Thus no stimulus no matter how intense can
evoke a response.
• Since systole ends in phase 3,the contractile
respond is over while the heart is still absolutely
refractory meaning that the heart cannot be
tetanised like skeletal muscle.

7. Electrical properties of the heart
• This is a safety mechanism as tetanic
contractions cannot pump blood.
• As repolarisation progresses beyond threshold
potential to resting membrane potential, only
very strong stimulus can evoke a
respond,(relative refractory period)
• Immediately following the (RRP) is a period of
super normal excitability ;when a weak
stimulus can evoke a response.

8. Cardiac action potential
Cardiac action potential

9. Electrical properties of the heart
Cardiac Automaticity and Rhythmicity.
• The heart has inherent rhythmicity due to presence of
specialized tissue which spontaneously depolarize and
trigger action potential.
These include;
SA node: Is the pace maker located at the endocardial surface
of the right atrium. It has the highest rate of spontaneous
depolarization of 72 times per minute.
• Consists of three cells ;1)P cells- generate cardiac impulse,
2) transitional cells -conduct impulse to AV node, and 3)
collagen fibers.

10. Electrical properties of the heart
Internodal fibers.
Three special fibers conduct impulse from SA
node to AV node.
1). Anterior fibers (Bachman).
2). Middle fibers (Wenckebach).
3).Posterior fibers (Thorel).

11. Electrical properties of the heart
Atrioventricular Node (A-V.Node)
. Located on the endocardial surface of the posterior and right border
of interatrial septum, near coronary sinus. Rate of spontaneous
discharge is 40 times per minute.
Bundle of His
• Named after German physician William His (1863-1934).
• Originates from AV Node and divides into two branches(right and
left) and terminates as Purkinje fibers.(Named after a Czech Jan
Evangelista Purkinje(1787-1869).
• These fibers penetrate the endocardium of corresponding
ventricles.
• Left bundle branches divides into anterior and posterior branches.
• Inherent rhythm of bundle of His is 20 times per minute.

12. Electrical properties of the heart
Generation and Propagation of Cardiac Impulse.
• The RMP in SA & AV node is –60mv thus a lower threshold potential of-
40mv is needed to generate action potential.
• This RMP is unstable and spontaneously depolarises and triggers off
action potential.
• This spontaneous depolarization generates the pacemaker potential.
• Depolarisation is due to calcium influx, while repolarizstion is due to K
efflux.
• Action potential in the SA node has no rapid upstroke and no plateau.
Rate of conduction at various stages are different
Atria ,ventricle and, bundle of his conduct at 1m/s.
• SA and AV node conduct at 0.05m/s
• Purkinge fibers conduct at 4m/s.

13. Electrical properties of the heart
Significance of nodal delay and rapid Purkinje
transmission
• Slow conduction in SA Node prevents re-entry of
impulses from atria to pacemaker.
• Since the AV node/ bundle of His are the only channels
by which impulses travel from atria to ventricles, AV
nodal delay occurs to enable the atria contract and
empty its content before ventricular contraction.
• The rapid conduction of purkinge fiber enable impulses
to reach all the large ventricular mass immediately at
same time.

14. Electrical properties of the heart
Measurement of electrical activity of the heart.
• The electrical activity can be picked up from the surface of
the body, magnified and displayed on the oscilloscope or
recorded with an electronic recorder on a moving chart as
an electrocardiogram (ECG).
• This is possible because the tissues of the body and body
fluids (water and electrolytes conduct electricity.
Basic information obtains from ECG. Include;
• Origin and rate of cardiac excitation.
• Cardiac arrhythmias (disorders of either of sinus origin or
ectopic origin).
• State of myocardium and conducting tissues.

15. Mechanical properties of the heart
• Excitation of the cell membrane of myocytes lead
to contraction .
• In skeleton muscle, this involves release of ca
from the sarcoplasmic reticulum into the cytosol
but in cardiac muscle, where powerful
contractions are needed ,ca in addition comes
from the ECF,binds to troponin thus exposing the
myosin binding sites of actin. Sliding of the two
filaments lead to contraction.
• Several factors affect the nature of contractile
responses of the heart.

16. Mechanical properties of the heart
Staircase Phenomenon (treppe).
• Stimulation of the heart with increasing frequency
after allowing full relaxation in each case leads to a
stepwise increase in strength of contraction.
• However as the frequency of stimulation continues to
increase, contractions become weaker or may even
disappear.
• This is because these stimulations now come before
full relaxation of the cardiac muscle.
• Thus tachycardia can increase contractility but in excess
reduces contractility and causes cardiac arrest .

17. Mechanical properties of the heart
Frank-Starlings law ;
Tension developed in cardiac muscle fiber depends on the
resting length of the fiber, thus tension increases as the
end diastolic volume increases up to a maximum
length.
Effects of ions on Cardiac Function;
Potassium; increase in ECF lowers RMP. Although this makes
membrane move excitable ,it reduces the rate of rise of AP
,which in turn reduces conductivity, slowing the heart and
any further increase may stop the head at diastole.
• Reduction in intracellular Na or K , increase force of
contraction.

18. Mechanical properties of the heart
Calcium
• High Ca in ECF decreases excitability of cell
membrane of myocardium but increases vigor
of contraction and heart may stop at systole
(Calcium rigor).
• Low Ca causes transient rise in excitability
followed by complete loss of propagated
response leading to flaccidity of the heart.

19. Cardiac cycle
• The pumping of blood by the heart requires
the following two mechanisms to be efficient:
• 1).Alternate periods of relaxation and
contraction of the atria and ventricles .
• 2).Coordinated opening and closing of the
heart valves for unidirectional flow of blood.
• Basically, the cardiac cycle is divided into 2
phases: ventricular diastole and ventricular
systole.

20. Cardiac Cycle;
• A Cardiac cycle begins with spontaneous discharge of SA Node,
• Then atrial depolarization and contraction ,ventricular
depolarization and contraction, atrial repolarization and relaxation,
ventricular repolarization and relaxation.
• Then followed by a pause (during which the heart continue to fill
with blood )before the SA Node discharges again .
• By tradition a cardiac cycle is described as beginning of one
ventricular systole to another; RR interval in ECG.
The cardiac cycle thus describes both the electrical and mechanical
event that affect cardiac function .

21. Cardiac Cycle;
Mechanical event of cardiac cycle
Ventricular systole
• P wave of atrial depolarization leads to atrial contraction
which completes ventricular filing .
• As soon as ventricles begin to contract, ventricular pressure
rises more than the atrial pressure and the AV valves close;
the mitral before tricuspid.
• Pressure then build s up in the ventricles with both
semilunar and AV valves closed (Isovolumetric contraction)
• As soon intraventricular pressure exceed pressure in large
arteries, semilunar valves open and blood is ejected
initially rapidly and then slowly.

22. Cardiac Cycle;
Ventricular Diastole
• Begin towards the end of the T wave in the ECG.
• Divided into 3 phases
Early Diastole
• Two components
In the 1st phase, the ventricles are still fully contracted but no ejection of
blood occurs; the pressure is gradually falling.
Sudden relaxation of ventricle with rapid fall in pressure below the pressure
in large arteries leads to closure of semilunar valves(aortic before
pulmonary (splitting of 2nd heart sound) .
This period of relaxation with both the semilunar and AV valves closed is
called isovolumteric relaxation .
Note that throughout the period of systole and early diastole atrial filling has
been occurring reaching a peak pressure known as the v-wave.

23. The cardiac Cycle
The cardiac Cycle

24. Cardiac physiologic anatomy
Cardiac physiologic anatomy

25. Cardiac Cycle;
Mid Diastole
• The pressure in atria then exceeds that in
ventricle ,AV valve opens and ventricular filling
occurs initially rapidly and the slowly
,constituting(70-80% of ventricular filling)
Late Diastole
• Responsible for 20-30 percent of ventricular
filling
• causes atrial contraction (a-wave in atrial
pressure curve).

26. Cardiac cycle
Heart sounds.
• 1st sound is due to - closure of AV value (beginning of systole)
• 2nd sound is due to closure of semilunar valve (beginning of
ventricular diastole ).
• 3rd heart sound is due to rapid flow of blood from atria to
ventricles .
• 4th heart sound is due to atrial contraction.
• 1st and 2nd sound can be heard clinically with the stethoscope while
the 3rd and 4th is by using a phonocardiogram .The 3rd can be heard
children.

27. Cardiac cycle
Clinical Importance of the heart sound.
• Ventricular depolarisation starts from left septum thus mitral valve
closes before tricuspid valve.
• Inspiration increase venous return to right heart causing further
delay in closure of tricuspid valve and completion of right
ventricular ejection thus aortic value closes before tricuspid valve.
• In mitral stenosis,mitral valves are thickened and cannot open
properly ,thus 1st heart sound (closure of mitral) is loud. Ventricular
filling through an improperly open valve produces the mid diastolic
murmur. In incompetence, valves do not close tightly leading to
back flow of the blood during systole-systolic murmur.

28. Cardiac cycle
Pressure changes during the cardiac cycle
• Most of the work of the heart is completed when
ventricular pressure exists. The greater the ventricular
pressure, the greater the workload of the heart.
Increases in BP dramatically increase the workload of
the heart.
• Arterial BP is the pressure that is exerted against the
walls of the vascular system. BP is determined by
cardiac output and peripheral resistance. Cardiac
output is a function of stroke volume and heart rate.

29. Cardiac cycle
• The difference between systolic and diastolic
pressure is called the pulse pressure. The
average pressure during a cardiac cycle is
called the mean arterial pressure (MAP).
• MAP determines the rate of blood flow
through the systemic circulation.
• During rest, MAP = diastolic BP + (0.33 X pulse
pressure). For example, MAP = 80 + (0.33 X
[120-80]), MAP = 93 mm Hg.

30. Regulation of cardiovascular function
Coordinated control of the heart
• The heart has the ability to generate its own
electrical activity, which is known as intrinsic
rhythm.
• In the healthy heart, contraction is initiated in the
sinoatrial (SA) node, which is often called the
heart's pacemaker.
• If the SA node cannot set the rate, then other
tissues in the heart are able to generate an
electrical potential and establish a HR.

31. Regulation of cardiovascular function
Control of cardiac output (HR)
• The parasympathetic nervous system and the
sympathetic nervous system affect a person's HR.
• Parasympathetic nervous system: The vagus
nerve originates in the medulla and innervates
the SA and AV nodes. The nerve releases ACh as
the neurotransmitter. The response is a decrease
in SA node and AV node activity, which causes a
decrease in HR.

32. Regulation of cardiovascular
function
• Sympathetic nervous system: The nerves arise
from the spinal cord and innervate the SA
node and ventricular muscle mass. The nerves
release nor epinephrine as the
neurotransmitter. The response is an increase
in HR and a force of contraction of the
ventricles.
• The heart is under tonic inhibition from the
vagus nerve and this predominates over tonic
excitation from the VMC

33. Regulation of cardiovascular function
Control of sympathetic and parasympathetic activity
• At rest, sympathetic and parasympathetic nervous stimulation are
in a balance.
• During exercise, parasympathetic stimulation decreases and
sympathetic stimulation increases. Several factors can alter
sympathetic nervous system input.
• A) Baroreceptors are groups of neurons located in the carotid
arteries, the arch of aorta, and the right atrium. These neurons
sense changes in pressure in the vascular system.
• An increase in BP results in an increase in parasympathetic activity
except during exercise, when the sympathetic activity overrides the
parasympathetic activity.

34. Regulation of cardiovascular
function
• Chemoreceptors are groups of neurons
located in the carotid and aortic bodies.
• These neurons sense changes in oxygen
concentration.
• When oxygen concentration in the blood is
decreased, parasympathetic activity
decreases and sympathetic activity increases.

35. Regulation of cardiovascular function
Control of cardiac output (SV)
• SV is controlled by end-diastolic volume, average aortic BP,
and the strength of ventricular contraction.
• End-diastolic volume: This is often referred to as the
preload. If the end-diastolic volume increases, the SV
increases. With an increased end-diastolic volume, a slight
stretching of the cardiac muscle fibers occurs, which
increases the force of contraction .
• Average aortic BP: This is often referred to as the after
load. The BP in the aorta represents a barrier to the blood
being ejected from the heart. The SV is inversely
proportional to the aortic BP. During exercise, the after load
is reduced, which allows for an increase in SV.

36. Regulation of cardiovascular function
• Strength of ventricular contraction: Epinephrine
and norepinephrine can increase the contractility
of the heart by increasing the calcium
concentration within the cardiac muscle fiber.
• Epinephrine and nor epinephrine allow for
greater calcium entry through the calcium
channels in cardiac muscle fiber membranes.
This allows for greater myosin and actin
interaction and an increase in force production.

37. Regulation of cardiovascular function
Control of cardiac output (venous return)
• Veno-constriction occurs as a response to sympathetic
nervous system stimulation. Sympathetic stimulation
constricts the veins that drain skeletal muscle. This
causes greater blood to flow back to the heart.
• The muscle pump is the rhythmic contraction and
relaxation of skeletal muscle that compresses the veins
and thus drains the skeletal muscle. This causes greater
blood flow back to the heart.
• The muscle pump is very important during both resting
and exercise conditions.

38. Regulation of cardiovascular function
Vasomotor center(vasomotor tone)
• Located in the reticular formation of the
medulla.
• Tonically discharges sympathetic impulses to
blood vessels.
• Receives input(excitatory or inhibitory )from
baroreceptors, chemoreceptors,respiratory
center, and higher centers.

39. Regulation of cardiovascular function
(E) Actions
• (a) Chronotropic action = heart rate
• - Tachycardia
• - Bradycardia.
• (b) Dromotropic action –increase or decrease in the
velocity of conduction.
• © Bathmotropic action,-increase or decrease in
cardiac
muscle excitability.
• (d) Ionotropic action – increase or decrease in force
of
• contraction.

40. Regulation of cardiovascular
function
Cardio-acceleratory centre located in the
medulla causes positivity of these actions via
the sympathetic nervous system while cadio-
inhibitory centre causes negative action via
the vagus.
• These cardiac centers work in collaboration
with vasomotor center that control blood
vessels in other to regulate mean arterial
blood pressure.

41. Regulation of cardiovascular function
Humoral factors that control CVS
• Catecholamine; vasoconstrictor and cardio accelerator
• Acetylcholine; vasodilator and cardio inhibitor
• Other
vasoconstrictors;angiotensin11,vasopressin,endothelins-
1,thromboxanes,serotonin.
• Other vasodilators; kinins, histamine, prostacyline, nitric
oxide.

42. Flow of blood in the vessels
Haemodynamics;
• The circulatory system is a closed-loop system, and flow
through the circulatory system is the result of pressure
differences between the 2 ends of the system, the left
ventricle (90 mm Hg) and the right atrium (approximately 0
mm Hg).
• Systemic blood flow affects haemodynamics.
• The control of blood flow during exercise is extremely
important to ensure that blood and oxygen are transported
to the tissues that need them most.
• Blood flow to tissues is dependent on the relationship
between BP and the resistance provided by the blood
vessels.

43. Flow of blood in the vessels
• Blood flow at rest is equal to the change in
pressure divided by the resistance of the
vessels (ie, BF = P/R, where BF is blood flow, P
is pressure, and R is resistance).
• The pressure change at rest in the
cardiovascular system is 93 mm Hg, as follows:
Mean aortic pressure = 93 mm Hg, mean right
atrial pressure = 0 mm Hg, and driving
pressure in the system = 93 mm Hg

44. Flow of blood in the vessels
•
Resistance is determined by the following formula:
Resistance = 8(length of tube X viscosity of blood)/ π radius4.This is
the Hagen-Poiseuilles formula.
Changing the radius of the vessels has the most profound effect on
blood flow.
• Doubling the radius of a blood vessel decreases resistance by a
factor of 16.
• Decreasing the radius of a blood vessel by half increases resistance
by a factor of 16.
• The arterioles have the most control over blood flow in the
systemic circulation.

45. Conclusion
• Cardiovascular complications during
anaesthesia are life threatening.
• It thus pertinent for the anaesthetist to
understand clearly cardiovascular function in
health and disease.
• So as to minimise an anaesthetic mortality
and morbidity.

46. Thank you
• Thank you