3. Transport and distribute essential substances
to the tissues.
Remove metabolic byproducts.
Adjustment of oxygen and nutrient supply in
different physiologic states.
Regulation of body temperature.
Humoral communication.
4. 67% IN THE SYST. VEINS/VENULES
5% IN THE SYSTEMIC CAPILLARIES
11% IN THE SYSTEMIC ARTERIES
5% IN PULMONARY VEINS
3% IN PULMONARY ARTERIES
4% IN PULMONARY CAPILLARIES
5% IN HEART ATRIA/VENTRICLES
10. The intrinsic conduction system of the
heart Sinoatrial (SA) node
- impulse spreads through atria
-100 b.min-1
Atrioventricular (AV) node
- impulse delayed for 0.1sec
internodal
pathway
Ventricular contraction - time
course approx 0.22 secs
*Contraction of the atria*
Bundle of His -
branches -
Purkinje fibers
• A wringing effect starts at the apex following the same pathway as
wave of excitation atria ejecting some blood superiorly
11. Normal pacemaker of the heart
Self excitatory nature
• less negative Er
• leaky membrane to Na+/Ca++
• only slow Ca++/Na+ channels operational
• spontaneously depolarizes at fastest rate
Overdrive suppression
• contracts feebly
12. Delays the wave of depolarization from
entering the ventricle
• Allows the atria to contract slightly ahead of the
ventricles (.1 sec. delay)
Slow conduction velocity due to small
diameter fibers
In absence of SA node, AV node may act
as pacemaker but at a slower rate
13. Sympathetic nerves (release noradrenaline):
Left nerves supply atrial and ventricular muscle
Right nerves supply pacemaker and conduction
system
Effects:
Positive inotropic effect - increase contractility of
muscle
Positive chronotropic effect – increase in rate of
rise of pacemaker potential
Shorten conduction delay in AV node and increase
rate of relaxation
14. Parasympathetic innervation to the heart is
carried by the vagal nerves
These have their effects by releasing
acetylcholine (ACh)
Vagal stimulation produces bradycardia via 2
effects:
• 1. Rate of upward drift of the pacemaker potential is
slowed
• 2. Initial pacemaker potential becomes more negative
(hyperpolarised)
15.
16. Blood flow
left ventricle = 80/ml/min/100g
right ventricle = 40 ml/min/100g
atria = 20 ml/min/100g
*Flow can increase 4-fold
Capillary density - all capillaries open
Very high O2 extraction: (A-V)02 = 14
ml 02/dl
VO2 = 12 ml/min/100g ----> very high
17. to cardiac work
• influenced by
a) systolic pressure
b) heart rate
c) stroke volume
• increases achieved primarily by hyperemia
• 40% due to oxidation of carbohydrates, 60% fatty
acids
18. contraction (systole) leads to compression of
intramural vessels and reduction in flow
pressure inside left ventricle can exceed aortic
pressure during systole
vessel compression greatest in endocardium,
decreases toward epicardium
O2 demand and flow/g is greatest in
endocardium
LV coronary flow decreases as HR increases
since diastole shorter
20. Tachycardia: HR
time in systole
metabolic activity
vessel compression
vasodilation
Bradycardia: HR
time in systole vessel compression
metabolic activity vasoconstriction
21. Tissue oxygenation is major regulator
of vascular tone (adenosine, tiss pO2)
Essentially all capillaries are open to
flow (O2 diffusion distance)
Flow regulation occurs at arterioles
VO2 limited by blood flow (max O2
extraction)
22. AUTOREGULATION OF CBF - extremely good over wide
pressure range (50-150 mm Hg)
REACTIVE HYPEREMIA - peak flow reached after only 15
second occlusion
FUNCTIONAL HYPEREMIA - very tight coupling between
02 demand (V02) and 02 delivery (blood flow)
HYPOXEMIC HYPEREMIA - very sensitive to changes in
arterial oxygen saturation
METABOLIC MECHANISMS ( eg, adenosine) account for
above
IntrinsicVasoregulation-CoronaryCirculation
23. in coronary arteries, -adrenergic
receptors mediate vasoconstriction while
-adrenergic mediate vasodilation
sympathetic stimulation elicits vasodilation
because increases in contractility and HR
elevate VO2 metabolic vasodilation
parasympathetic stimulation elicits small
increment in CBF
24. Continuous capillaries - all perfused;
large surface area for exchange
Most exchange occurs during diastole
(when blood flow is greatest)
Tissue pressure = 15 mm Hg during diastole
Tissue pressure rises with ventricular
pressure during systole; greatest increase
is in endocardium
25. Syncytium = many acting as one
Due to presence of intercalated discs
• low resistance pathways connecting cardiac cells
end to end
• presence of gap junctions
27. STRUCTURE OF A MYOCARDIAL CELL
Mitochondria Sarcolemma
T-tubule
SR
Fibrils
28. In response to action potentials, the levels of
calcium within cardiac muscle rises
Some Ca2+ binds to troponin C, which exists on the
thin actin filaments
This exposes binding sites on the actin filaments
The thick myosin filaments have heads that can flip
These heads (powered by ATP) attach to the actin
binding sites
Myosin heads flip, and the myosin and actin
filaments slide over one another = contraction
29. Link between electrical excitation and
muscle contraction is calcium ions
AP causes sarcoplasmic [Ca2+] to rise from
0.1 M to 2 M in 10msec
Some Ca2+ binds to troponin C to activate
contraction proteins
Intact cell level of free Ca2+ during
excitation is 1-10 M
Typical concn of 2 M only gives partial
activation
If [Ca2+] increased (e.g. by adrenaline), get
more activation, and more contraction
30. Under normal conditions, not all of the contractile
cross-bridges are activated
Can activate more by:
• (a) the length-tension relationship or
• (b) chemically-induced rises in Ca2+ (e.g.
noradrenaline from sympathetic nerves, or
circulating adrenaline)
31. Inotropic = strengthening
Catecholamines increase the amount of Ca2+
stored in the SR (a rise in the Ca2+ current
during the plateau of the AP)
Uptake back into the SR is also upregulated,
meaning the muscle relaxes faster, and
preserves the diastolic filling period
Three mechanisms regulate contractile force:
• The size of the Ca2+ current
• Affinity of contractile proteins for Ca2+ (depends on
stretch)
• Degree of actin-myosin overlap (also depends on
stretch)
32. A small population of heart cells have
the ability to spontaneously depolarize –
autorhythmic.
The most important group of such cells
makes up the sinoatrial node (SA node).
• SA functions as our pacemaker..
33. The cells of the SA node do not maintain a
“normal” resting potential because Ca++ is
constantly leaking into the cell through slow
calcium channels = pacemaker potential.
The potential starts at ~ -60 mV and
gradually depolarizes to ~ -40 mV, which
triggers the opening of fast calcium channels
and maybe voltage-gated Na+ channels.
The membrane potential rapidly shoots up to
~ +20 mV = depolarization..
36. Repolarization begins when K+ voltage-gated
gates open and K+ rushes out of the cell.
A new pacemaker potential begins when the
potential reaches ~ -60 mV.
Adjacent myocardial cells begin depolarizing
because of the influx of cations (probably
Ca++) through the gap junctions.
At threshold, Na+ gates open and Na+ rushes
into the cell.
The membrane is depolarized to ~ +15 mV.
37. Unlike noncardiac cells, repolarization
does not begin immediately.
Instead the potential difference is
maintained for ~ 200 – 300 ms by the slow
diffusion of Ca++ into the cell which
balances the outward diffusion of K+. This
is the plateau phase.
Once the cell has slowly repolarized to
threshold, K+ gates open and the cell is
quickly repolarized to resting potential of ~
-90 mV..
38.
39. This wave of depolarization spreads
throughout the atrial myocardium but cannot
reach the ventricular myocardium because
of the fibrous skeleton.
The only electrical connection between the
myocardia is in the AV node to AV bundle to
bundle of His to Purkinje fibers.
The specialized cells in the AV bundle
conduct the impulse very slowly.
This time delay allows the atria to complete
systole before the ventricles begin systole..
40. The electrical activity occurring in the
heart can be monitored with the ECG
(EKG).
Each cardiac cycle produces three distinct
waves; P, QRS, and T.
The waves represent changes in potential
between two different regions of the
surface of the heart.
The waves do not represent APs in
individual cardiac cells nor do they
represent the flow of blood through the
heart..
41. The impulse then travels to the AV
bundle, located in the superior
interventricular septum.
The AV bundle then splits into left and
right bundle branches, which continue
as Purkinje fibers.
Conduction System Animation..
44. SINGLE VENTRICULAR ACTION POTENTIAL
ECG
P
Q S
T
R
1 mV
Repolarization of ventricles
Depolarization of ventricles
Depolarization of atria
ENDOCARDIAL FIBER
EPICARDIAL FIBER
ATRIAL
FIBER
45. SINGLE VENTRICULAR ACTION POTENTIAL
ECG
P
Q S
T
R
1 mV
Repolarization of ventricles
Depolarization of ventricles
Depolarization of atria
ENDOCARDIAL FIBER
EPICARDIAL FIBER
ATRIAL
FIBER
49. Cardiac Cycle
All events which occur between two consecutive
heartbeats.
Systole: simultaneous contraction of the two
ventricles creating pressure to pump blood to the
lungs and body.
Diastole: resting phase immediately after systole
and lasts about 0.5s assuming one complete
cycle takes 0.8s.
52. Volume of blood
pumped/min. by each
ventricle.
• Pumping ability of the
heart is a function of
the beats/ min. and
the volume of blood
ejected per beat.
CO = SV x HR
• Total blood volume
averages about 5.5
liters.
Each ventricle pumps
the equivalent of the
total blood volume
each min. (resting
conditions).
53. The total amount of blood pumped by the left
ventricle in one minute (Q)
Q = SV x HR
Average cardiac output at rest is 5-6 litres,
during exercise it can exceed 30 litres in a
trained endurance athlete.
54. Without neuronal influences, the
heart beats according to the
rhythm set by SA node.
Regulation of HR (chronotropic
effect):
• May be + or – effect.
Autonomic control:
• Sympathetic and parasympathetic
nerve fibers to the heart modify the
rate of spontaneous depolarization.
• Innervate the SA node.
NE and Epi stimulate opening of
Na+/Ca2+ channel.
ACH promotes opening of K+ channel.
Major means by which cardiac rate
is regulated.
Cardiac control center (medulla):
• Coordinates activity of
autonomic innervation.
55. Blood ejected from left ventricle - not all blood is
ejected, the amount of blood remaining is called
end-systolic volume.
Stroke Volume = end-
diastolic volume - end-systolic volume
56. Stroke volume is regulated by 3
variables:
• EDV:
Volume of blood in the ventricles at the end of
diastole.
• Total peripheral resistance (TPR):
Frictional resistance or impedance to blood flow in
the arteries.
• Contractility:
Strength of ventricular contraction.
57. Workload on the heart prior to contraction
(preload).
• SV directly proportional to preload.
Increase in EDV results in an increase in SV.
• SV directly proportional to contractility.
Strength of contraction varies directly with
EDV.
Ejection fraction:
• SV/ EDV.
Normally is 60%.
Clinical diagnostic tool.
58. Total Peripheral Resistance:
• Impedance to the ejection of blood from ventricle.
• Afterload.
In order to eject blood, pressure generated in the ventricle
must be greater than pressure in the arteries.
• Pressure in arteries before ventricle contracts is a
function of TPR.
SV inversely proportional to TPR.
• Greater the TPR, the lower the SV.
59. Relationship between
EDV, contraction
strength, and SV.
Intrinsic mechanism:
• Varying degree of
stretching of
myocardium by EDV.
• As EDV increases:
Myocardium is
increasingly
stretched.
Contracts more
forcefully.
60. As the ventricles
fill, the
myocardium
stretches; This
increases the
number of
interaction
between actin
and myosin.
Allows more
force to develop.
Explains how the
heart can adjust
to rise in TPR.
61. Contractility:
• Strength of contraction
at any given fiber
length.
Depends upon
sympathoadrenal
system:
• NE and Epi produce an
increase in contractile
strength.
+ inotropic effect:
More Ca2+ available to
sarcomeres.
62. Parasympathetic
stimulation:
- chronotropic effect.
Does not directly
influence contraction
strength.
CO affected 2
ways:
• + inotropic effect
on contractility.
• + chronotropic
effect on HR.
63. Return of blood to the
heart via veins.
Venous pressure is
driving force for return
of blood to the heart.
Veins have thinner
walls, thus higher
compliance.
• Capacitance vessels.
2/3 blood volume is
in veins.
EDV, SV, and CO are
controlled by factors
which affect venous
return.
70. CARDIAC OUTPUT (Q) =
VO2
[O2]a - [O2]v
250 ml/min
20 ml% - 15 ml%
=
= 5 L/min
.
Q = HR x SV
.
SV =
Q
HR
.
=
5 L/min
70 beats/min
= 0.0714 L or 71.4 ml
CARDIAC INDEX = Q
m2 body surface
area
.
5 L/min
1.6 m2=
= 3.1 L/min/m2
71. The pressure exerted by the blood on the
vessel walls
Expressed by two numbers - systolic and
diastolic
Systolic= highest pressure & corresponds to
ventricle contraction
Diastolic= lowest pressure & represents the
ventricle relaxing
72. Mean arterial pressure = the average
pressure exerted by the blood as it travels
through the arteries:
MAP = 1/3 pulse pressure + diastolic pressure
Generalised constriction of blood vessels
increases blood pressure whereas dilation
decreases blood pressure
Hypertension is a chronic elevation of blood
pressure above normal healthy values
73. Elevated body temperature
• HR increases about 10 beats for every degree F
elevation in body temperature
• Contractile strength will increase temporarily but
prolonged fever can decrease contractile strength
due to exhaustion of metabolic systems
Decreased body temperature
• decreased HR and strength
74. Pressure inside is 35 to 15 mmHg
5% of the blood is in capillaries
exchange of gases, nutrients, and wastes
flow is slow and continuous
76. VASOMOTION = Intermittent flow due to constriction-
relaxation cycles of precapillary shpincters
or arteriolar smooth muscle (5 - 10/min)
AUTOREGULATION OF VASOMOTION:
1. Oxygen Demand Theory (Nutrient Demand Theory)
O2 is needed to support contraction (closure)
2. Vasodilator Theory
Vasodilator substances produced (via O2)
e.g. Adenosine Heart
CO2 Brain
Lactate, H+, K+ Skeletal Muscle
3. Myogenic Activity
77. 3 central priorities of CVS:
1. adequate blood supply to brain & heart
2. “ “ “ to other organs
after brain & heart supply assured
3. control capillary pressure to maintain
tissue volume & composition of interstitial
fluid within reasonable ranges
78. Baroreceptors monitor BP – info from
baroreceptors + info from chemoreceptors
(monitoring CO2 & O2 concentrations & pH of
blood) is transmitted to brain – other sensory
receptors are involved in reflex effects on the
CVS including mechanoreceptors (respond to
mechanical distortion & pressure) &
thermoreceptors (responsive to temperature
changes) = all this info is integrated in a collection
of brain neurons called medullary CV center (at
the level of medulla/pons)
79. Medullary CV center receives info also from
medullary respiratory center, hypothalamus,
amygdala nucleus & cortex – output from
medullary CV center feeds into sym & para
autonomic motor neurons that innervated heart
& smooth muscle of arterioles & veins
Stim. of sympathetic nerves = increases rate &
force of heart contraction & causes
vasoconstriction = marked increase in arterial
BP & CO; in general, the reverse happens
when stim para nerves ending in reduction of
BP & CO
80. 2 functional regions with opposing effects on
BP:
1. stimulation of pressor center results in
sympathetic activation & rise in BP
2. stimulation of depressor center = in parasym.
activity & drop in BP fig 12-42 p. 513
Role played by baroceptors which are widely
distributed in arterial system show increased
rates of firing with increase in BP …
81. unmyelinated barorecptors (mammals, amphibians &
reptiles) respond only to pressures above normal
initiating reflexes that reduce arterial BP
myelinated baroreceptors (only mammals) respond
only to pressures below normal initiating reflexes
that raise BP - many baroreceptors are located in
carotid sinus & in mammals, carotid sinus is a
dilation of internal carotid artery at its origin =
buried in the thin walls are finely branched nerve
endings function as baroreceptors ( inc. in BP stretches
wall of carotid sinus causing an increase in discharge frequency)
82. arterial chemoreceptors located in carotid &
aortic bodies NB in ventilation (later) but also
have some effect on CVS = when blood
perfusing carotid & aortic bodies has high
levels of CO2 or low O2 & pH, arterial
chemoreceptors respond with increase in
discharge frequency which results in peripheral
vasoconstriction & slowing of HR if animal is
not breathing (e.g. submersion)
CO is reduced while birds & mammals are
diving
83. 1. atrial receptors (esp. mechanoreceptors in
atrial walls) &
2. ventricular receptors (nerve endings of both
myelinated {mechanoreceptive &
chemoreceptive} & unmyelinated sensory
afferent fibers imbedded in ventricles) =
together monitor venous pressure & HR to
ensure activity of heart is correlated with
blood inflow from venous system & blood
outflow into arterial system
84. Chronotropic (+ increases) (- decreases)
• Anything that affects heart rate
Dromotropic
• Anything that affects conduction velocity
Inotropic
• Anything that affects strength of contraction
eg. Caffeine would be a + chronotropic agent
(increases heart rate)
