cardiovascular physiology-for anesthesia

cardiovascular physiology for anesthesia - blood pressure control- cardiac output- heart rate- systemic vascular resistence

1. Cardiovascular Physiology

2. Lecture Outline
•Functional Anatomy of the Heart
•Myocardial Physiology
•Cardiac Cycle
•Cardiac Output Controls & Blood Pressure
•central venous pressyre
•pulmonary artery wedge pressure
•capillary dynamics

3. Lecture Outline
Functional Anatomy of the Heart
•Myocardial Physiology
•Cardiac Cycle
•Cardiac Output Controls & Blood Pressure
•central venous pressyre
•pulmonary artery wedge pressure
•capillary dynamics

4. Functional Anatomy of the Heart
Chambers
•4 chambers
–2 Atria
–2 Ventricles
•2 systems
–Pulmonary
–Systemic

5. Functional Anatomy of the Heart
Valves
•Function is to prevent backflow
–Atrioventricular Valves
•Prevent backflow to the atria
•Prolapse is prevented by the chordae
tendinae
–Tensioned by the papillary muscles
–Semilunar Valves
•Prevent backflow into ventricles

6. Functional Anatomy of the Heart
Intrinsic Conduction System
•Consists of
“pacemaker” cells
and conduction
pathways
–Coordinate the
contraction of the
atria and
ventricles

9. Lecture Outline
•Cardiovascular System Function
•Functional Anatomy of the Heart
•Myocardial Physiology
–Autorhythmic Cells (Pacemaker cells)
–Contractile cells
•Cardiac Cycle
•Cardiac Output Controls & Blood Pressure

10. Myocardial Physiology
Autorhythmic Cells (Pacemaker Cells)
•Characteristics of
Pacemaker Cells
–Smaller than
contractile cells
–Don’t contain many
myofibrils
–No organized
sarcomere structure
•do not contribute to
the contractile force
of the heart
normal contractile
myocardial cell
conduction myofibers
SA node cell
AV node cells

11. Properties of Cardiac Muscle Fibers
1.Autorhythmicity:The ability to initiate a heart
beat continuously and regularly without external
stimulation
2.Excitability: The ability to respond to a
stimulus of adequate strength and duration (i.e.
threshold or more) by generating a propagated
action potential
3.Conductivity: The ability to conduct excitation
through the cardiac tissue
4.Contractility:The ability to contract in
response to stimulation
11

12. Myocardial Physiology
Autorhythmic Cells (Pacemaker Cells)
•Characteristics of Pacemaker Cells
–Unstable membrane potential
•“bottoms out” at -60mV
•“drifts upward” to -40mV, forming a pacemaker potential
–Myogenic
•The upward “drift” allows the membrane to reach threshold
potential (-40mV) by itself
•This is due to
1. Slow leakage of K
+
out & faster leakage Na
+
in
»Causes slow depolarization
»Occurs through I
fchannels (f=funny) that open at negative
membrane potentials and start closing as membrane
approaches threshold potential
2. Ca
2+
channels opening as membrane approaches threshold
»At threshold additional Ca
2+
ion channels open causing more
rapid depolarization
»These deactivate shortly after and
3. Slow K
+
channels open as membrane depolarizes causing an
efflux of K
+
and a repolarization of membrane

13. Myocardial Physiology
Autorhythmic Cells (Pacemaker Cells)
•Characteristics of Pacemaker Cells

14. Myocardial Physiology
Autorhythmic Cells (Pacemaker Cells)
•Altering Activity of Pacemaker Cells
–Sympathetic activity
•NE and E increase I
fchannel activity
–Binds to β
1adrenergic receptors which activate cAMP and
increase I
fchannel open time
–Causes more rapid pacemaker potential and faster rate of
action potentials
Sympathetic Activity Summary:
increased chronotropic effects
heart rate
increased dromotropic effects
conduction of APs
increased inotropic effects
contractility

15. Myocardial Physiology
Autorhythmic Cells (Pacemaker Cells)
•Altering Activity of Pacemaker Cells
–Parasympathetic activity
•ACh binds to muscarinic receptors
–Increases K
+
permeability and decreases Ca
2+
permeability
= hyperpolarizing the membrane
»Longer time to threshold = slower rate of action
potentials
Parasympathetic Activity
Summary:
decreased chronotropic effects
heart rate
decreased dromotropic effects
conduction of APs
decreased inotropic effects
contractility

17. Myocardial Physiology
Contractile Cells
•Special aspects
–Intercalated discs
•Highly convoluted and interdigitated
junctions
–Joint adjacent cells with
»Desmosomes & fascia adherens
–Allow for synticial activity
»With gap junctions
–More mitochondria than skeletal muscle
–Less sarcoplasmic reticulum
•Ca
2+
also influxes from ECF reducing
storage need
–Larger t-tubules
•Internally branching
–Myocardial contractions are graded!

18. Myocardial Physiology
Contractile Cells
•Special aspects
–The action potential of a contractile cell
•Ca
2+
plays a major role again
•Action potential is longer in duration than a “normal” action
potential due to Ca
2+
entry
•Phases
4 –resting membrane potential @ -90mV
0 –depolarization
»Due to gap junctions or conduction fiber action
»Voltage gated Na
+
channels open… close at 20mV
1 –temporary repolarization
»Open K
+
channels allow some K
+
to leave the cell
2 –plateau phase
»Voltage gated Ca
2+
channels are fully open (started during initial
depolarization)
3 –repolarization
»Ca2+ channels close and K+ permeability increases as slower
activated K+ channels open, causing a quick repolarization
–What is the significance of the plateau phase?

19. Myocardial Physiology
Contractile Cells
•Skeletal Action Potential vs Contractile
Myocardial Action Potential

20. Myocardial Physiology
Contractile Cells
•Plateau phase prevents summation due to
the elongated refractory period
•No summation capacity = no tetanus
–Which would be fatal

21. Summary of Action Potentials
Skeletal Muscle vs Cardiac Muscle

22. Myocardial Physiology
Contractile Cells
•Initiation
–Action potential via pacemaker cells to
conduction fibers
•Excitation-Contraction Coupling
1. Starts with CICR (Ca
2+
induced Ca
2+
release)
•AP spreads along sarcolemma
•T-tubules contain voltage gated L-type Ca
2+
channels which open upon depolarization
•Ca
2+
entrance into myocardial cell and
opens RyR (ryanodine receptors) Ca
2+
release channels
•Release of Ca
2+
from SR causes a Ca
2+
“spark”
•Multiple sparks form a Ca
2+
signal
Spark Gif

23. Myocardial Physiology
Contractile Cells
•Excitation-Contraction Coupling cont…
2.Ca
2+
signal (Ca
2+
from SR and ECF) binds to troponin to initiate
myosin head attachment to actin
•Contraction
–Same as skeletal muscle, but…
–Strength of contraction varies
•Sarcomeres are not “all or none” as it is in skeletal muscle
–The response is graded!
»Low levels of cytosolic Ca
2+
will not activate as many
myosin/actin interactions and the opposite is true
•Length tension relationships exist
–Strongest contraction generated
when stretched between 80 &
100% of maximum (physiological
range)
–What causes stretching?
»The filling of chambers
with blood

24. Myocardial Physiology
Contractile Cells
•Relaxation
–Ca
2+
is transported back
into the SR and
–Ca
2+
is transported out of
the cell by a facilitated
Na
+
/Ca
2+
exchanger (NCX)
–As ICF Ca
2+
levels drop,
interactions between
myosin/actin are stopped
–Sarcomere lengthens

25. Lecture Outline
Functional Anatomy of the Heart
•Myocardial Physiology
–Autorhythmic Cells (Pacemaker cells)
–Contractile cells
•Cardiac Cycle
•Cardiac Output Controls & Blood Pressure
•central venous pressyre
•pulmonary artery wedge pressure
•capillary dynamics

26. Cardiac Cycle
Coordinating the activity
•Cardiac cycle is the sequence of events as
blood enters the atria, leaves the
ventricles and then starts over
•Synchronizing this is the Intrinsic Electrical
Conduction System
•Influencing the rate (chronotropy &
dromotropy) is done by the sympathetic
and parasympathetic divisions of the ANS

27. Cardiac Cycle
Coordinating the activity
•Electrical Conduction Pathway
–Initiated by the Sino-Atrial node (SA node) which is myogenic at
70-80 action potentials/minute
–Depolarization is spread through the atria via gap junctions and
internodal pathways to the Atrio-Ventricular node (AV node)
•The fibrous connective tissue matrix of the heart prevents further
spread of APs to the ventricles
•A slight delay at the AV node occurs
–Due to slower formation of action potentials
–Allows further emptying of the atria
–Action potentials travel down the Atrioventricular bundle (Bundle
of His) which splits into left and right atrioventricular bundles
(bundle branches) and then into the conduction myofibers
(Purkinje cells)
•Purkinje cells are larger in diameter & conduct impulse very rapidly
–Causes the cells at the apex to contract nearly simultaneously
»Good for ventricular ejection

28. Cardiac Cycle
Coordinating the activity
•Electrical
Conduction
Pathway

29. Cardiac Cycle
Coordinating the activity
•The electrical system gives rise to
electrical changes
(depolarization/repolarization) that is
transmitted through isotonic body fluids
and is recordable
–The ECG!
•A recording of electrical activity
•Can be mapped to the cardiac cycle

31. Cardiac Cycle
Phases
•Systole = period of contraction
•Diastole = period of relaxation
•Cardiac Cycle is alternating periods of systole and
diastole
•Phases of the cardiac cycle
1. Rest
•Both atria and ventricles in diastole
•Blood is filling both atria and ventricles due to low pressure
conditions
2. Atrial Systole
•Completes ventricular filling
3. Isovolumetric Ventricular Contraction
•Increased pressure in the ventricles causes the AV valves to
close… why?
–Creates the first heart sound (lub)
•Atria go back to diastole
•No blood flow as semilunar valves are closed as well

32. Cardiac Cycle
Phases
•Phases of the cardiac cycle
4. Ventricular Ejection
•Intraventricular pressure overcomes aortic pressure
–Semilunar valves open
–Blood is ejected
5. Isovolumetric Ventricular Relaxation
•Intraventricular pressure drops below aortic pressure
–Semilunar valves close = second heart sound (dup)
•Pressure still hasn’t dropped enough to open AV valves so
volume remains same (isovolumetric)
Back to Atrial & Ventricular Diastole

33. Cardiac Cycle
Phases

34. Cardiac Cycle
Blood Volumes & Pressure

36. Cardiac Cycle
Putting it all together!

37. Lecture Outline
Functional Anatomy of the Heart
•Myocardial Physiology
•Cardiac Cycle
•Cardiac Output Controls & Blood
Pressure
•central venous pressyre
•pulmonary artery wedge pressure
•capillary dynamics
•fluid therapy

38. The volume of blood pumped by each ventricle per minuteis
called cardiac output
Cardiac output = Stroke Volume X Heart Rate
Normal value = 5 Liters /Minute
Cardiac output = Stroke Volume X Heart Rate
The factors which regulate stroke volume and Heart rate are
basically regulating Cardiac output
Volume of blood ejected by each ventricle in single systole;
Normal Value = 70 ml/beat
Normal intrinsic heart rate = 118 beats/min
− (0.57 ×age)
Stroke Volume = End diastolic Volume –End Systolic
Volume
So stroke volume is mainly controlled by
EDV
ESV

39. •VENOUS RETURN : What ever blood volume returns to
the heart, same is pumped forward through the Frank’s
Starlings Law. According to this law 13-15 liters of blood
volume can be pumped out without cardiac stimulation.
•DURATION OF DIASTOLE OR FILLING TIME:
ventricular filling occurs during diastole, so there must be
adequate ventricular filling time.
•DISTENSIBILITY OF THE VENTRICLES : Normally
ventricles are distensible to accommodate adequate
blood volume. Infarction decreases the distensibility
which decreases the EDV.
•ATRIAL CONTRACTION : There must be adequate atrial
contraction to have adequate EDV. If atrial function is not
adequate then EDV will decrease.

40. Factors Regulating EDV
•VENOUS RETURN: What ever blood volume
returns to the heart, same is pumped forward
through the Frank’s Starlings Law. According to this
law 13-15 liters of blood volume can be pumped
out without cardiac stimulation.
•DURATION OF DIASTOLE OR FILLING TIME:
ventricular filling occurs during diastole, so there
must be adequate ventricular filling time.
•DISTENSIBILITY OF THE VENTRICLES: Normally
ventricles are distensible to accommodate
adequate blood volume. Infarction decreases the
distensibilitywhich decreases the EDV.
•ATRIAL CONTRACTION: There must be adequate
atrial contraction to have adequate EDV. If atrial
function is not adequate then EDV will decrease.

41. Factors Regulating ESV
•E.S.V is basically CONTROLLED BY MYOCARDIAL
CONTRACTION
•FORCE OF MYOCARDIAL CONTRACTION: It depends upon the
initial length of muscle fibers according to frank’s starlings law.
•PRELOAD: The effect of EDV on initial length is called preload. So
EDV also effects the ESV.
•AFTER LOAD: Force of contraction is also dependant upon the
resistance against which the ventricles have to pump
•CONDITION OF THE MYOCARDIUM : It also effects the force of
contraction.
•AUTONOMIC NERVES : Sympathetic stimulation increases and
parasympathetic stimulation decreases force of contraction
•HORMONES: Catecholamines, thyroxine, glucagon,
digitalis, calcium, increased temp, caffeine,
theophylineincrease the force.
•Force decreases by hypoxia, acidosis, barniturates,
procainamideand quinidinedecrease the force of
contraction.

42. Factors Regulating Heart Rate
•In the body heart rate is
modified by nervous
mechanisms which
include the autonomic
nerves and vasomotor
centre. We can also
include the afferent
nerves which carry
impulses to vasomotor
centre.
•So heart rate is controlled
by
–Parasympathetic
nerves –Vagi

43. Effects of Parasympathetic stimulation
on Heart Rate
•Vagii.e. right vagusmailnlycontrols the SA node
and left vagusmainly controls the AV node.
•Vagalfibers arise form Dorsal nucleus of Vagus
and supply the atrialmuscle, SA NODE, AV NODE
PURKINGE FIBER but not ventricular muscle.
•PARASYMPATHETIC STIMULATION leads to :

44. Effects of Parasympathetic stimulation
on Heart Rate
•NEGATIVE CHRONOTROPIC EFFECT: decrease
frequency of heart beat
•NEGATIVE DROMOTROPIC EFFECT: Velocity of
conduction is slowed down. AV nodal delay is prolonged.
•NEGATIVE BATHMOTROPIC EFFECT: Decreased
excitability of heart.
•SLIGHT NEGATIVE IONOTROPIC EFFECT: decrease
force of contraction of heart.

45. Effects of Sympathetic stimulation on
Heart Rate
•Sympathetic nerves are called accelerator nerves.
•Effect of sympathetic is also continuous but not as
powerful as vagaltone.
•Preganglionicsympathetic fibers arise form T1 to T5.
These fibers go to the inferior cervical ganglion. And
then supply the heart.
•Sympathetic supply is mainly to ventricle musculature.
–POSITIVE IONOTROPIC EFFECT
–POSITIVE DROMTROPIC EFFECT
–POSITIVE BATHMOTROPIC EFFECT
–POSITIVE CHRONOTROPIC EFFECT

46. Vasomotor Centre
•The vasomotor center is a portion of the medulla
oblongata that regulates blood pressure and other
homeostatic processes.
•The actions of the sympathetic and parasympathetic
nerves is coordinated by vasomotor centre.
•The medial partof vasomotor centre is
cardioinhibitorythrough the vagisupplying the heart
•The lateral partis cardioacceleratorythrough the
sympathetic nerve supplying the heart.
•The vasomotor centre is affected by impulses from
different parts of the heart to modify the heart rate.

47. pulmonary artery catheter

59. Control of Arterial Blood
Pressure
A.Immediate Control
B. Intermediate Control
C. Long-Term Control

60. Immediate Control
Minute-to-minute control of blood pressure is primarily the
function of autonomic nervous system reflexes.
Changes in blood pressure are sensed both
centrally(in hypothalamic and brainstem areas)and
peripherallyby specialized sensors (baroreceptors).
Decreases in arterial blood pressure result in increased sympathetic tone,
increased adrenal secretion of epinephrine, and reduce vagalactivity. The
resulting systemic vasoconstriction, increased heart rate, and enhanced
cardiac contractility serve to increase blood pressure .
Peripheral baroreceptorsare located at the bifurcation of the common carotid
arteries and the aortic arch. Elevations in blood pressure increase baroreceptor
discharge,
inhibiting systemic vasoconstriction and enhancing vagaltone (baroreceptorreflex) .
Reductions in blood pressure decrease baroreceptordischarge, allowing
vasoconstriction and
reduction of vagaltone.
Carotid baroreceptorssend afferent signals to circulatory brainstem centers via
Hering’snerve
(a branch of the glossopharyngealnerve), whereas aortic baroreceptorafferent
signals travel
along the vagusnerve.

61. Of the two peripheral sensors, the carotid baroreceptoris
physiologically
more important and is primarily responsible for minimizing changes in
blood
pressure that are caused by acute events, such as a change in
posture.
Carotid baroreceptorssense MAP most effectively between pressures
of 80
and 160 mm Hg. Adaptation to acute changes in blood pressure occurs
over
the course of 1–2 days, rendering this reflex ineffective for longer term
blood
pressure control.
All volatile anesthetics depress the normal baroreceptorresponse, but
isofluraneand desfluraneseem to have less effect.
Cardiopulmonary stretch receptors located in the atria, left ventricle,
and
Pulmonary circulation can cause a similar effect.

62. B. Intermediate Control
In the course of a few minutes, sustained decreases in arterial pressure, together with enhanced
sympathetic outflow, activate the renin–angiotensin–aldosteronesystem, increase secretion of
argininevasopressin (AVP), and alter normal capillary fluid exchange.
Both angiotensinII and AVP are potent arteriolar vasoconstrictors. Their immediate action is to
increase SVR.
Sustained changes in arterial blood pressure can also alter fluid exchange in tissues by their
Secondary effects on capillary pressures.
Hypertension increases interstitial movement of intravascular fluid, whereas hypotension
increases reabsorptionof interstitial fluid. Such compensatory changes in intravascular volume
can reduce fluctuations in blood pressure, particularly in the absence of adequate renal function

63. C. Long-Term Control
The effects of slower renal mechanisms become
apparent within hours of sustained changes in
arterial pressure.
As a result, the kidneys alter total body sodium
and water balance to restore blood pressure to
normal.
Hypotension results in sodium (and water)
retention, whereas hypertensiongenerally
increases sodium excretion in normal
individuals.