This document discusses cardiovascular physiology including the structure and function of the heart, regulation of the cardiovascular system, blood flow through the pulmonary and systemic circulations, factors that influence cardiac output and stroke volume, and regulation of the systemic vasculature. Key points include: - The cardiovascular system consists of the heart, blood vessels, and mechanisms that regulate blood circulation and pressure. - Cardiac output is determined by stroke volume and heart rate. Stroke volume depends on preload, afterload, and contractility. - The pulmonary circulation has low pressure and resistance while the systemic circulation has higher pressure and resistance. - Autonomic nervous system and chemical factors regulate heart rate and contractility. Venous return and vascular

1. cardiovascular physiology for
anesthesia

2. CARDIOVASCULAR SYSTEM
HEART
(PUMP)
VESSELS
(DISTRIBUTION SYSTEM)
REGULATION
AUTOREGULATION
NEURAL
HORMONAL
RENAL-BODY FLUID
CONTROL SYSTEM

3. PULMONARY
CIRCULATION
1. LOW RESISTANCE
2. LOW PRESSURE
(25/10 mmHg)
SYSTEMIC
CIRCULATION
1. HIGH RESISTANCE
2. HIGH PRESSURE
(120/80 mmHg)
PARALLEL
SUBCIRCUITS
UNIDIRECTIONAL
FLOW

4. VEINS
CAPACITY
VESSELS
HEART
80 mmHg 120 mmHg
SYSTOLE
DIASTOLE
ARTERIES (LOW COMPLIANCE)
CAPILLARIES

5. Na+
K+Na+
K+
-70 mV
RESTING
THRESHOLD
-0
Gradually
increasing PNa
AUTOMATICITY
Th e normal ventricular cell resting membrane
potential is –80 to –90 mV. As with other
excitable
tissues (nerve and skeletal muscle

6. PURKINJE FIBERS
BUNDLE
BRANCHES
Sino-atrial
(SA) node
Atrio-ventricular (AV) node
PACEMAKERS (in order of
their inherent rhythm
•Sino-atrial (SA) node
•Atrio-ventricular (AV) node
•Bundle of His
•Bundle branches
•Purkinje fibers

7. Extrinsic Innervationof the Heart
• Heart is stimulated by
the sympathetic
cardioacceleratorycardi
oacceleratorycenter
center
• Heart is inhibited by
the parasympathetic
cardioinhibitorycardioi
nhibitorycentercenter

11. Cardiac Output is the product of Stroke Volume
(SV) and Heart Rate (HR).
Stroke volume is determined by three factors:
preload, afterload and contractility

12. Normal Cardiac Output
•Normal resting cardiac output:
- Stroke volume of 70 ml
- Heart rate of 72 beats/minute
- Cardiac output ~ 5 litres/minute
•During exercise, cardiac output may increase
to > 20 liters/minutes
•You should be able to get stroke volume and
heart rate from volume-‐pressure curves and
ECG recordings, respectively

13. What are the Main Determinants of
Cardiac Performance?
• Preload
• Afterload
• Contractility
• Heart Rate
• Synergy of Contraction

14. Preload
• The force which fills the heart
• The extent of filling of the
heart
• Different definitions exist
– End-diastolic pressure
– End-diastolic volume
– Wall stress in diastole
Preload is the initial fibre length.
Preload is the load on myocardial
fibers just prior to contraction.
Therefore volume and
pressure are used as
surrogate markers of
preload.

16. The Frank Starling Curve
•  preload →  stroke
volume (SV)
• Only occurs up to a
certain point, then SV
and CO (cardiac
output) falls
From Ashley & Niebauer. Cardiology Explained

17. Afterload
• The forces needed to push blood
forward
• The pressure the ventricle ejects
against
• Definitions
– Wall stress in systole
– End-systolic pressure
• ↑afterload → ↓SV
Afterload is the tension which needs to be
generated in cardiac muscle before
shortening will occur In its simplest terms
afterload is thought of as
the impedence to flow from the ventricle
during systole. As such mean arterial
pressure may be used as an estimate.
More accurate still it to consider the
relationship
between mean pressure and mean flow
represented by systemic vascular
resistance (or PVR on the right).

19. Contractility
• The ability of the heart to contract with a given force
and rate
– Represented by dP/dV (or elastance, E)
– Independent of afterload and preload
Determined by
conditions within
the myocyte
 Degree of binding
between actin and
myosin
 Calcium is critical
is defined as the intrinsic ability of the
myocardial bre to shorten independent of
preload and
afterload. The intracellular mechanism that is
responsible for all factors which increase
contractility is increased intracellular calcium.
Measurement of contractility is difficult.
dp/dtmax refers the the maximum rate of
change in pressure in the left ventricle during
isovolumetric contraction. A more forceful
contraction would be associated with a
greater rise in pressure and for this reason
this is often used as a marker of contractility.

20. • Sympathetic stimulation
– Release norepinephrine from symp. postganglionic fiber
– Also, EP and NE from adrenal medulla
– Have positive ionotropic effect
– Ventricles contract more forcefully, increasing SV, increasing
ejection fraction and decreasing ESV
• Parasympathetic stimulation via Vagus Nerve -CNX
– Releases ACh
– Has a negative inotropic effect
• Hyperpolarization and inhibition
– Force of contractions is reduced, ejection fraction decreased
Effects of Autonomic Activity on
Contractility

21. Extrinsic Control of Contractility
• Contractility:
– Strength of contraction at
any given fiber length.
• Sympathoadrenal
system:
– NE and Epi produce an
increase in contractile
strength.
• + inotropic effect:
– More Ca2+ available
to sarcomeres.
• Parasympathetic
stimulation:
– Does not directly
influence contraction
strength.
Figure 14.2

22. Heart Rate and Stroke Volume
• HR influences SV
– ↑ HR leads to ↓ SV
– ↑ HR decreases
diastolic filling time
• ↓ Preload
• ↓ EDV
CO = HR × SV

23. Heart Rate and Cardiac Output
• Increasing HR only
increases CO to a
certain point
• Increasing HR also
increases force of
contraction slightly
Normal intrinsic heart rate = 118 beats/min
− (0.57 × age)

24. Synergy of Contraction
• AV synchrony
– Requires functional AV
node and His-Purkinje
– Atrial kick contributes up
to 20% of CO
• Intra- (or inter-)
ventricular synergy
– Requires functional
bundle branches (Purkinje
fibers)
– Bundle branch block
– Ectopic beats

25. Extrinsic Factors Influencing Stroke
Volume
• Contractility is the increase in contractile strength, independent of stretch
and EDV
• Referred to as extrinsic since the influencing factor is from some external
source
• Increase in contractility comes from:
– Increased sympathetic stimuli
– Certain hormones
– Ca2+ and some drugs
• Agents/factors that decrease contractility include:
– Acidosis
– Increased extracellular K+
– Calcium channel blockers

26. Normal Volume of Blood in Ventricles
•After atrial contraction, 110-120 ml in each
ventricle (end-diastolic volume)
•Contraction ejects ~70 ml (stroke volume
output)
•Thus, 40-50 ml remain in each ventricle (End‐
systolic volume)
•The fraction ejected is then ~60% (ejection
fraction)

27. Cardiac Output and Venous Return
•Cardiac output is the quantity of blood
pumped into the aorta each minute.
Cardiac output = stroke volume x heart rate
•Venous return is the quantity of blood flowing
from the veins to the right atrium.
•Except for temporary moments, the cardiac
output should equal the venous return

28. Cardiac Output
• Stroke Volume = the vol of blood pumped by
either the right or left ventricle during 1
ventricular contraction.
SV = EDV – ESV
70 = 125 – 55
CO = SV x HR
5,250 = 70 ml/beat x 75 beats/min
CO = 5.25 L/min

29. Cardiac Output
• Other chemicals can affect contractility:
- Positive inotropic agents: glucagon, epinephrine,
thyroxine, digitalis.
- Negative inotropic agents: acidoses, rising K+, Ca2+
channel blockers.
Afterload: Back pressure exerted by arterial blood.
Regulation of Heart Rate
• Autonomic nervous system
• Chemical Regulation: Hormones (e.g., epinephrine, thyroxine)
and ions.

30. Regulation of Stroke Volume
• SV: volume of blood pumped by a ventricle per beat
SV= end diastolic volume (EDV) minus end systolic volume
(ESV); SV = EDV - ESV
• EDV = end diastolic volume
– amount of blood in a ventricle at end of diastole
• ESV = end systolic volume
– amount of blood remaining in a ventricle after contraction
• Ejection Fraction - % of EDV that is pumped by the
ventricle; important clinical parameter
– Ejection fraction should be about 55-60% or higher

31. Factors Affecting Stroke Volume
• EDV - affected by
– Venous return - vol. of blood returning to heart
– Preload – amount ventricles are stretched by
blood (=EDV)
• ESV - affected by
– Contractility – myocardial contractile force due
to factors other than EDV
– Afterload – back pressure exerted by blood in
the large arteries leaving the heart

32. Wall Motion Abnormalities
Regional wall motion abnormalities cause a breakdown of the analogy between the
intact heart and skeletal muscle preparations.
Such abnormalities may be due to ischemia, scarring, hypertrophy, or altered
conduction.
When the ventricular cavity does not collapse symmetrically or fully, emptying
becomes impaired.
• Hypokinesis (decreased contraction),
• akinesis (failure to contract), and
• dyskinesis (paradoxic bulging) during systole reflect increasing degrees of
contraction abnormalities.
Although contractility may be normal or even enhanced in some areas,
abnormalities
in other areas of the ventricle can impair emptying and reduce stroke volume.
The severity of the impairment depends on the size and number of abnormally
contracting areas.

33. Valvular Dysfunction
Valvular dysfunction can involve any one of the four valves in the heart and can
include stenosis, regurgitation (incompetence), or both. Stenosis of an AV valve
(tricuspid or mitral) reduces stroke Volume primarily by decreasing ventricular
preload, whereas stenosis of a semilunar valve (pulmonary or aortic) reduces stroke
volume primarily by increasing ventricular afterload.
In contrast, valvular regurgitation can reduce stroke volume without changes in
preload, afterload, or contractility and without wall motion abnormalities.
The eff ective stroke volume is reduced by the regurgitant volume with every
contraction.
When an AV valve is incompetent, a significant part of the ventricular end-diastolic
volume can fl ow backward into the atrium during systole; the stroke volume is
reduced by the regurgitant volume.
Similarly, when a semilunar valve is incompetent, a fraction of end-diastolic volume
arises from backward flow into the ventricle during diastole.

34. Preload, afterload, heart rate in stenotic and
reguitation lesions

35. ASSESSMENT OF
VENTRICULAR FUNCTION
1. Ventricular Function Curves
2. Assessment of Systolic Function:
Ejection Fraction
3. Assessment of Diastolic Function

36. Plotting cardiac output or
stroke volume against
preload (End-diastolic
pressure)is useful in evaluating
pathological states and
understanding drug therapy.
A curve that show
the contractility change in an
intact heart.
Ventricular pressure–volume diagrams are
useful because they dissociate contractility
from both preload and afterload.
It depends on the Starling’s law
A shift to the left in a ventricular function
curve usually signifies an enhancement of
contractility, whereas a shift to the right
usually indicates an impairment of
contractility, and a consequent tendency
toward cardiac failure.
. Ventricular Function Curves

37. Assessment of Systolic Function
The change in ventricular pressure over time during systole (
dP/dt ) is defined by the first derivative of the ventricular
pressure curve and is often used as a measure of contractility.
Contractility is directly proportional to dP/dt
It can be measured by:
-echocardiography
- the initial rate of rise in arterial pressure (rough estimation)
The usefulness of dP/dt is also limited in that it may be affected
by preload, afterload, and heart rate.

38. Ejection Fraction
What? The ventricular ejection
fraction (EF), the
fraction of the end-diastolic ventricular
volume
Ejected.
the most commonly used clinical measurement
of systolic function.
Normal EF is approximately 0.67±8
EDV is left ventricular diastolic
volume and ESV is end-systolic
volume.
Measurements can be made preoperatively from
•cardiac catheterization,
•radionucleotide studies, or
• transthoracic (TTE)
•or transesophageal echocardiography (TEE).
Pulmonary artery catheters with
fast-response thermistors allow
measurement of the right
ventricular EF.

39. Assessment of Diastolic Function
Left ventricular diastolic function can be assessed clinically by Doppler
echocardiography on a transthoracic or transesophageal.
Tissue Doppler is frequently used to distinguish “pseudonormal” from normal
diastolic function.
Tissue Doppler is also an excellent way to detect “conventional” diastolic
dysfunction.

40. Systemic Circulation
The systemic vasculature can be divided
Functionally into arteries, arterioles, capillaries,
and veins.
Arteries are the high-pressure conduits that
Supply the various organs.
Arterioles are the small vessels that directly
feed and control blood flow through each
capillary bed.
Capillaries are thin-walled vessels that allow the
exchange of nutrients between blood and
tissues.
Veins return blood from capillary beds to
the heart.
most of the blood volume is in the systemic
circulation—specifi cally, within systemic veins.
Changes in systemic venous tone allow these
vessels to function as a reservoir for blood.

41. Following significant blood or fluid losses,
a sympathetically mediated increase in venous
tone reduces the caliber of these vessels and shifts
Blood into other parts of the vascular system.
Conversely, venodilation allows these vessels to
accommodate increases in blood volume.
Sympathetic control of venous tone is an important
determinant of venous return to the heart.
Reduced venous tone following induction of anesthesia
frequently results in venous pooling of blood and
contributes to hypotension.

42. AUTOREGULATION
Most tissue beds regulate their own blood flow
(autoregulation).
Arterioles generally dilate in response to reduced
perfusion pressure or increased tissue demand.
Conversely, arterioles constrict in response to increased
pressure or reduced tissue demand.
These phenomena are likely due to both an intrinsic
response of vascular smooth muscle to stretch and the
accumulation of vasodilatory metabolic by-products.
The latter may include K + , H + , CO 2 , adenosine, and
lactate.

43. ENDOTHELIUM-DERIVED FACTORS
The vascular endothelium is metabolically active in elaborating or modifying
substances that directly or indirectly play a major role in controlling blood pressure and
flow.
These include:
 vasodilators (eg, nitric oxide, prostacyclin [PGI 2 ]),
 Vasoconstrictors (eg, endothelins, thromboxane A 2 ),
 Anticoagulants (eg, thrombomodulin, protein C),
 fibrinolytics (eg, tissue plasminogen activator), and
 factors that inhibit platelet aggregation (eg, nitric oxide and PGI 2 ).
Nitric oxide is synthesized from arginine by nitric oxide synthetase. This substance has a
number of functions In the circulation, it is a potent vasodilator. It binds guanylate cyclase,
increasing cGMP levels and producing vasodilation.
Endothelially derived vasoconstrictors (endothelins) are released in response to
thrombin and epinephrine.

44. AUTONOMIC CONTROL OF
THE SYSTEMIC VASCULATURE
Autonomic control of the vasculature is primarily sympathetic
Sympathetic fibers innervate all parts of the vasculature
except for capillaries. Their principal function is to regulate
vascular tone.
Variations of arterial vascular tone serve to regulate blood
pressure and the distribution of blood flow to the various
organs, whereas variations in venous tone alter vascular
capacity, venous pooling, and venous return to the heart.
Vascular tone and autonomic influences on the heart are
controlled by vasomotor centers in the reticular formation of
the medulla and lower pons.
The sympathetic system normally maintains some tonic vasoconstriction
on the vascular tree. Loss of this tone following induction of anesthesia or
sympathectomy frequently contributes to perioperative hypotension.

45. ARTERIAL BLOOD PRESSURE
Systemic blood flow is pulsatile in large arteries because of
the heart’s cyclic activity; by the time blood reaches the
systemic capillaries, flow is continuous(laminar).
The mean pressure falls to less than 20 mm Hg in the large
systemic veins that return blood to the heart. The largest
pressure drop, nearly 50%, is across the arterioles, and the
arterioles account for the majority of SVR.
MAP is proportionate to the product of
SVR . CO. This relationship is based on an
analogy to Ohm’s law, as applied to the
circulation:
Because CVP is normally very small compared with MAP, the former can usually be
ignored.
From this relationship, it is readily apparent that hypotension is the result of a
decrease in SVR, CO, or both: To maintain arterial blood pressure, a decrease
in either SVR or CO must be compensated by an increase in the other.

46. MAP can be measured as the integrated mean of the arterial pressure waveform.
Alternatively, MAP may be estimated by the following
formula:
pulse pressure is the difference between systolic and diastolic
blood pressure.
Arterial pulse pressure is directly related to stroke volume, but is
inversely proportional to the compliance of the arterial tree.
Thus, decreases in pulse pressure may be due to a decrease in
stroke volume, an increase in SVR, or both.
Increased pulse pressure increases shear stress on vessel walls,
potentially leading to atherosclerotic plaque rupture and
thrombosis or rupture of aneurysms.
Increased pulse pressure in patients undergoing cardiac surgery
has been associated with adverse renal and neurological
outcomes.

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

48. 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
peripherally by specialized sensors (baroreceptors).
Decreases in arterial blood pressure result in increased sympathetic tone,
increased adrenal secretion of epinephrine, and reduce vagal activity. The
resulting systemic vasoconstriction, increased heart rate, and enhanced
cardiac contractility serve to increase blood pressure .
Peripheral baroreceptors are 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 vagal tone (baroreceptor reflex) .
Reductions in blood pressure decrease baroreceptor discharge, allowing vasoconstriction and
reduction of vagal tone.
Carotid baroreceptors send afferent signals to circulatory brainstem centers via Hering’s nerve
(a branch of the glossopharyngeal nerve), whereas aortic baroreceptor afferent signals travel
along the vagus nerve.

49. Of the two peripheral sensors, the carotid baroreceptor is 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 baroreceptors sense 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 baroreceptor response, but
isoflurane and desflurane seem to have less effect.
Cardiopulmonary stretch receptors located in the atria, left ventricle, and
Pulmonary circulation can cause a similar effect.

50. B. Intermediate Control
In the course of a few minutes, sustained decreases in arterial pressure, together with enhanced
sympathetic outflow, activate the renin–angiotensin–aldosterone system, increase secretion of
arginine vasopressin (AVP), and alter normal capillary fluid exchange.
Both angiotensin II 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 reabsorption of interstitial fluid. Such compensatory changes in intravascular volume
can reduce fluctuations in blood pressure, particularly in the absence of adequate renal function

51. 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 hypertension generally increases sodium
excretion in normal individuals.

52. ANATOMY & PHYSIOLOGY OF
THE CORONARY CIRCULATION
1. Anatomy
2. Determinants of Coronary Perfusion
3. Myocardial Oxygen Balance
4.EFFECTS OF ANESTHETIC AGENTS

53. 1. Anatomy
The right and left coronary arteries.
Blood flows from epicardial to endocardial vessels.
After perfusing the myocardium, blood returns to the right
atrium via the coronary sinus and the anterior cardiac veins.
A small amount of blood returns directly into the chambers of
the heart by way of the thebesian veins.
The right coronary artery (RCA) normally supplies the right atrium,
most of the right ventricle, and a variable portion of the left
ventricle (inferior wall).
The left coronary artery normally supplies the left atrium and most of
the interventricular septum and left ventricle (septal, anterior, and
lateral walls).
After a short course, the left main coronary artery bifurcates into the
left anterior descending artery (LAD) and the circumfl ex artery (CX);
the LAD supplies the septum and anterior wall and the CX supplies the
lateral wall.

54. Intermittent rather than continuous
The force of left ventricular contraction almost
completely occludes the intramyocardial part of the
coronary arteries.
coronary perfusion pressure is usually determined by the
difference between aortic pressure and ventricular
pressure .
the left ventricle is perfused almost entirely during
diastole.
In contrast, the right ventricle is perfused during both systole
and diastole
2. Determinants of Coronary Perfusion

55. Decreases in aortic pressure or increases in ventricular
end-diastolic pressure can reduce coronary perfusion
pressure.
Increases in heart rate also decrease coronary perfusion
because of the disproportionately greater reduction in
diastolic time as heart rate increases .
Because it is subjected to the greatest intramural
pressures during systole, the endocardium tends to be
most vulnerable to ischemia during decreases in
coronary perfusion pressure.

56. Control of Coronary Blood Flow

57. In the average adult man,coronary blood flow is approximately 250 mL/min at rest.
Th e myocardium regulates its own blood flow closely between perfusion pressures of 50
and 120 mm Hg.
Beyond this range, blood flow becomes increasingly pressure dependent.
Under normal conditions, changes in blood flow are entirely due to variations in coronary
arterial tone (resistance) in response to metabolic demand.
Hypoxia—either directly, or indirectly through the release of adenosine—causes coronary
vasodilation.
Autonomic influences are generally weak. Both α 1 - and β 2 -adrenergic receptors are
present in the coronary arteries. The α 1 –receptors are primarily located on larger
epicardial vessels, whereas the β 2 -receptors are mainly found on the smaller
intramuscular and subendocardial vessels.
Sympathetic stimulation generally increases myocardial blood flow because of an increase
in metabolic demand and a predominance of β 2 –receptor activation.
Parasympathetic effects on the coronary vasculature are generally minor and weakly
vasodilatory.

58. 3. Myocardial Oxygen Balance
Myocardial oxygen demand is usually the most
important determinant of myocardial blood flow.
Relative contributions to oxygen requirements
include basal requirements (20%), electrical activity
(1%), volume work (15%), and pressure work(64%).
Th e myocardium usually extracts 65% of
the oxygen in arterial blood, compared with 25%
in most other tissues.
Coronary sinus oxygen saturation is usually 30%.
Therefore, the myocardium (unlike other tissues) cannot
compensate for reductions in blood fl ow by extracting more
oxygen from hemoglobin.
Any increases in myocardial metabolic
demand must be met by an increase in coronary
blood fl ow.
in myocardial oxygen demand and supply. Note
that the heart rate and, to a lesser extent, ventricularend-
diastolic pressure are important determinants
of both supply and demand.

59. EFFECTS OF ANESTHETIC
AGENTS
Most volatile anesthetic agents are coronary vasodilators.
Their effect on coronary blood flow is variable because of their direct vasodilating
properties, reduction of myocardial metabolic requirements (and secondary decrease
due to autoregulation), and effects on arterial blood pressure.
The mechanism is not clear, and these effects are unlikely to have any clinical
importance.
Halothane and isoflurane seem to have the greatest effect; the former primarily
affects large coronary vessels, whereas the latter affects mostly smaller vessels.
Vasodilation due to desflurane seems to be primarily autonomically mediated,
whereas sevoflurane seems to lack coronary vasodilating properties. Dose-
dependent
abolition of autoregulation may be greatest with isoflurane.
and afterload.

60. Volatile agents exert beneficial effects in experimental myocardial
ischemia and infarction.
They reduce myocardial oxygen requirements and protect against
reperfusion injury; these effects are mediated by activation of ATP-
sensitive K+ (K ATP ) channels.
Some evidence also suggests that volatile anesthetics enhance
recovery of the “stunned” myocardium (hypocontractile,
but recoverable, myocardium aft erischemia).
Moreover, although volatile anesthetics decrease myocardial
contractility, they can be potentially beneficial in patients with heart
failure because most of them decrease preload