CARDIOVASCULAR

PHYSIOLOGY &
ANESTHETIC IMPORTANCE

BY Moderator
DR Dhanesh B M DR CHAITHANYA
POSTGRADUATE SENIOR RESIDENT
DNB ANAESTHESIA , D.H BALLARI DEPT. OF ANAESTHESIA ,DH BALLARI
 INTRODUCTION
• Anesthesiologists must have a thorough understanding of cardiovascular
physiology
• Anesthetic successes and failures are directly related to skill of the
practitioner in manipulating cvs physiology.
• physiology of the heart and systemic circulation and the
pathophysiology of heart failure , anaesthetic drugs
• circulatory system consists of heart, blood vessels, and blood.
• function is to provide oxygen and nutrients to tissues and to carry away
waste products of metabolism.
• heart propels blood through two vascular systems arranged in series: low-
pressure pulmonary circulation, high-pressure systemic circulation,
• heart can be functionally divided into right and left pumps, each
consisting of an atrium and a ventricle
• normal pumping action of the heart is the result of a complex
series of electrical and mechanical events
• normal absence of direct connections between the atria and
ventricles except through the atrioventricular (AV) node delays
ventricular depolarization, enabling the atria to prime the
ventricles
CONTD..
• At rest, myocardial cell membrane is nominally permeable to K+
• RMP represents the balance between two opposing forces: movement of K+ down its
concentration gradient and electrical attraction of the negatively charged intracellular
space for the positively charged K+ 
• normal ventricular cell RMP is –80 to –90 mV
• spike in cardiac action potentials is followed by a plateau phase that lasts 0.2 to 0.3 s
• AP for skeletal muscle and nerves is exclusively d/t opening of voltage-gated sodium
channels, in cardiac muscle -initiated by voltage-gated Na+ channels (the spike) and
maintained by voltage-gated CA2+ channels
• In pacemaker cells depolarization is initiated by voltage-gated calcium channels  
• Following depolarization, the cells are typically refractory
to subsequent normal depolarizing stimuli until “phase 4.”
k/a absolute refractory period(ARP)
• relative refractory period is time beyond ARP in which a maximal
stimulus, but not a stimulus of normal intensity, will produce
a depolarization
• cardiac impulse originates in the sinoatrial (SA) node, a group of
pacemaker cells in the sulcus terminalis, located posteriorly at the junction
of RA and SVC
• hyperpolarization-activated cyclic nucleotide–gated (HCN) channels
results in a less negative RMP (–50 to –60 mV )
•  three important consequences : constant inactivation of voltage- gated
sodium channels, an action potential , regular spontaneous depolarizations
• impulse generated at the SA node is normally rapidly conducted across the
atria and to the AV node
• normally slower rate of spontaneous depolarization in AV junctional areas
(40–60 times/min) allows the faster SA node to control heart rate  
• Impulses from the SA node normally reach the AV node after about 0.04 s, but
leave after another 0.11 s. >> Bundle of His–Purkinje fibers >>ventricles
• requires less than 0.2 s to depolarize the entire heart. 
• inhaled anesthetics depress SA node automaticity, have modest effects on AV
node: occurrence of junctional tachycardia when anticholinergic is
administered for sinus bradycardia
• arrhythmogenic properties : potentiation of catecholamines, especially with
halothane.
• Opioids: fentanyl, sufentanil, can depress cardiac conduction ,
time of AV node conduction , prolonging the duration of the Purkinje fiber AP
• Local anesthetics :at low blood concentrations can be therapeutic. depress
conduction
• Bupivacaine dissociates from them more slowly: cause profound sinus
bradycardia and sinus node arrest and malignant ventricular arrhythmias ,depress
left ventricular contractility
• calcium channel blockers block Ca2+ influx through L-type,
employed perioperatively as antihypertensives and as antiarrhythmics.
• Dystrophin connects actin to the cell membrane .Cell shortening occurs when the
actin and myosin interact and slide over one another
• interaction is normally prevented : troponin and tropomyosin; troponin is
composed of three subunits (troponin I, troponin C, and troponin T)
• increase in intracellular Ca2+ concentration promotes contraction as Ca2+ ions
bind troponin C 
• active sites on actin that allow interaction with myosin bridges 
• myosin functions as a magnesium-dependent ATPase
• Relaxation occurs as Ca2+ is actively pumped back into the sarcoplasmic
reticulum by a Ca2+–Mg2+-ATPase
INTRACELLULAR SIGNALLING CASCADE WITHIN CARDIOMYOCYTES
• Sympathetic stimulation increases the force of contraction by raising
intracellular Ca2+ concentration via a β1 -(cAMP) through the action of a
stimulatory G protein
• Phosphodiesterase inhibitors, such as milrinone, produce similar effects by
preventing the breakdown of intracellular cAMP
• Digitalis glycosides increase intracellular Ca2+ conc. through inhibition of Na+–
K+-ATPase
• Glucagon enhances contractility by increasing intracellular cAMP
• levosimendan is a calcium sensitizer that enhances contractility by binding to
troponin C.
• Parasympathetic: Acetylcholine acts on specific cardiac muscarinic receptors (M2) to produce
negative chronotropic, dromotropic, and inotropic effects
• sympathetic fibers originate in the thoracic spinal cord (T1–T4) and travel to the heart initially
through the cervical (stellate) ganglia
• Norepinephrine release at the heart causes positive chronotropic, dromotropic, and inotropic
effects primarily through activation of β1-adrenergic receptors
• Beta-2 are normally fewer. Relative fraction of β2- to β1-adrenergic receptors increases in heart
failure
• innervation has an apparent sidedness: right sympathetic and right vagus nerves primarily
affect the SA node, whereas the left sympathetic and vagus nerves principally affect the AV
node
Cardiac cycle: systole and diastole : 0.8sec(0.3+0.5)
Events: starts with venous return
EVENTS IN CARDIAC CYCLE
HEART REASON
SOUND
S1 CLOSURE OF A-V VALVES

S2 CLOSURE OF SEMILUNAR VALVES

S3 VIBRATIONS IN RAPID FILLING OF

VENTRICLE EARLY IN DIASTOLE
S4 VIBRATIONS DURING ATRIAL
SYSTOLE LATE IN DIASTOLE
HEART SOUND PATHOLOGY

S3 1.Children , young
adults (upto 40yr),
2. high ouput states-
anemia, fever,
pregnancy
3.patho: LVF, MR,
S4 AS, HYPERTROPHIC
CARDIOMYOPATHY
 ARTERIAL WAVEFORM
•.
WATER HAMMER PULSE/ COLLAPSING PULSE : sudden upstroke f/b
sudden downstroke, seen in AR
 JUGULAR VENOUS
PULSE
• 1.positive waves :
• a wave- atrial contraction ( atrial systole)
• c wave- during isovolumetric contraction of ventricles, which pushes the TV
into the RA
• v wave- during isovolumetric relaxation of ventricles, marks venous return
into the RA and pressure raises, when AV valves are not yet open
• 2. Negative waves:
• X descent- occurs during ventricular ejection phase when papillary muscle
contracts and pull down TV valve
• Y descent- during rapid passive filling phase, AV valves are open blood flows
from RA to RV and pressure drops
 CARDIAC REFLEXES
• fast-acting reflex loops between heart and CNS that contribute to regulation of
cardiac function and maintenance of physiologic homeostasis.
1. Baroreceptor Reflex (Carotid Sinus Reflex) :
• responsible for the maintenance of arterial blood pressure.
• capable of regulating arterial pressure around a preset value through a negative-
feedback loop
• capable of establishing a set point for arterial BP when the preset value has been
reset because of chronic hypertension.
• circumferential and longitudinal stretch receptors located in the carotid sinus and
aortic arch.
• The nucleus solitarius, located in the cardiovascular center of the medulla,
receives impulses from these through glossopharyngeal and vagus nerves.
• cardiovascular center in the medulla consists of two functionally different
areas; the area responsible for increasing BP is laterally and rostrally located,
whereas the area responsible for lowering arterial blood pressure is
centrally and caudally located.
• The latter area also integrates impulses from the hypothalamus and the
limbic system
• receptors are activated if SBP is greater than 170 mm Hg. The response of
depressor system: decreased sympathetic activity, leading to a
• decrease in cardiac contractility, heart rate, and vascular tone. And
activation of the parasympathetic system further decreases the HR and
contractility. Reverse effects are elicited with hypotension
• beneficial role during acute blood loss and shock. This reflex loses its
functional capacity when arterial blood pressure is less than 50 mm Hg.
• Hormonal status and therefore sex differences may alter baroreceptor
responses.
• volatile anesthetics (halothane) inhibit HR component of this reflex.
Concomitant use of CCBs, ACE inhibitors, or phosphodiesterase inhibitors
will lessen the cardiovascular response of raising BP through this
• Patients with chronic hypertension exhibit perioperative circulatory
instability as a result of a decrease in their baroreceptor reflex response.
2. CHEMORECEPTOR REFLEX
• Receptors are located in the carotid bodies and aortic body.
• respond to changes in pH status and blood O2 tension.
• PaO2 of less than 50 mm Hg or in conditions of acidosis, the
chemoreceptors send their impulses along the sinus nerve of Hering (a
branch of IX CN) and Xth CN to the chemosensitive area of the medulla.
• This area responds by stimulating respiratory centers and thereby
increasing ventilatory drive.
• activation of PNS ensues and leads to a reduction in HR and contractility.
In case of persistent hypoxia, the CNS will be directly stimulated, with a
resultant increase in sympathetic activity.
3.Bainbridge Reflex
• stretch receptors located in the RA wall and the cavoatrial junction.
• An increase in RA filling pressure sends vagal afferent signals to the
cardiovascular center in the medulla. These afferent signals inhibit
PNS activity, increasing the HR.
• Acceleration of HR also results from a direct effect on the SA node by
stretching the atrium.
• The changes in heart rate are dependent on the underlying heart rate
before stimulation.
4.Bezold-Jarisch Reflex

• responds to noxious ventricular stimuli sensed by chemoreceptors and

mechanoreceptors within LV wall . The receptors communicate along unmyelinated
vagal afferent type C fibers.
• Inducing triad of hypotension, bradycardia, and coronary artery dilatation.
• reflexively increase parasympathetic tone. Because it invokes bradycardia, is thought
of as a cardioprotective reflex.
• physiologic response to a range of CVS conditions such as myocardial ischemia or
infarction, thrombolysis, or revascularization and syncope.
• Natriuretic peptide receptors stimulated by endogenous ANP or BNP may modulate
this reflex.
• Thus this reflex may be less pronounced in patients with cardiac hypertrophy or atrial
fibrillation
5.Valsalva Maneuver

• Forced expiration against a closed glottis. Produces increased intrathoracic

pressure, increased central venous pressure, and decreased venous return.
Cardiac output and blood pressure will be decreased .
• This decrease will be sensed by baroreceptors and will reflexively result in an
increase in HR and myocardial contractility through sympathetic stimulation.
• When the glottis opens, venous return increases and causes the heart to
respond by vigorous contraction and an increase in blood pressure.
• This increase in arterial blood pressure will, again be sensed by
baroreceptors, thereby stimulating the parasympathetic efferent pathways
to the heart.
6.Cushing Reflex
• is a result of cerebral ischemia caused by increased ICP.
• Cerebral ischemia at the medullary vasomotor center induces initial
activation of the sympathetic nervous system.
• Such activation will lead to an increase in heart rate, arterial blood
pressure, and myocardial contractility in an effort to improve cerebral
perfusion.
• As a result of the high vascular tone, reflex bradycardia mediated by
baroreceptors will ensue.
7.Oculocardiac Reflex

• is provoked by pressure applied to the globe of the eye or traction on the

surrounding structures. Stretch receptors are located in the extraocular
muscles.
• will send afferent signals through the short- and long-ciliary nerves. The ciliary
nerves will merge with the ophthalmic division of the trigeminal nerve at the
ciliary ganglion. The trigeminal nerve will carry these impulses to the gasserian
ganglion,
• resulting in increased parasympathetic tone and subsequent bradycardia.
• The incidence of this reflex during ophthalmic surgery ranges from 30% to 90%.
• Administration of an antimuscarinic drug such as glycopyrrolate or atropine
reduces the incidence of bradycardia during eye surgery
• Systolic function involves ventricular ejection, whereas diastolic function is
related to ventricular filling
• systolic function is often equated with cardiac output, which can be defined as the
volume of blood pumped by the heart per minute. Because the two ventricles
function in series, their outputs are normally equal. Cardiac output (CO) is expressed by
the following equation
• CO = SV × HR
• where SV is the stroke volume (the volume pumped per contraction) and HR is heart
rate.
• To compensate for variations in body size, CO is often expressed in terms of total body
surface area:
 • CI= CO/BSA
1. where CI is the cardiac index and BSA is body surface area normally
2.5-4.2L/min/m2.
2. . Abnormalities in CI therefore usually reflect gross ventricular
impairment
3. more accurate assessment can be obtained in the absence of hypoxia
or severe anemia, measurement of mixed venous oxygen tension
(or saturation) provides an estimate of the adequacy of cardiac output
• Heart rate is an intrinsic function of the SA node . modified by
autonomic, humoral, and local factors
• normal intrinsic rate of the SA node in young adults is about 90 to
100 beats/min, but it decreases with age
• Normal intrinsic heart rate = 118 beats/min – (0.57 × Age)
• Enhanced vagal activity slows the heart
• sympathetic activity increases the heart rate
 2.STROKE VOLUME
• normally determined by three major factors: preload, afterload, and
contractility
• Preload is muscle length prior to contraction, whereas afterload is the
tension against which the muscle must contract. Contractility is an
intrinsic property of the muscle
 A. PRELOAD
• Ventricular preload is end-diastolic volume.
• Ventricular filling can be influenced by a variety of factors; most important is venous
return
• vascular capacity is normally its major determinant. Increases in metabolic activity
reduce vascular capacity, so that venous return to the heart and cardiac output increase as
the volume of venous capacitance vessels decreases
• relationship between cardiac output and left ventricular end-
diastolic volume was first described by Starling  
• cardiac output increases with increasing preload until
excessive end-diastolic volumes are reached 
• In the absence of significant pulmonary or right ventricular dysfunction,
venous return is also the major determinant of left ventricular preload
• Increases in heart rate are associated with proportionately greater
reductions in diastole than systole.
• Ventricular filling therefore progressively becomes impaired at increased
heart rates (>120 beats/min in adults).
• Absent (atrial fibrillation), ineffective (atrial flutter), or altered timing of
atrial contraction (low atrial or junctional rhythms)
DIASTOLIC FUNCTION & VENTRICULAR
COMPLIANCE
• Left ventricular end-diastolic
pressure (LVEDP) can be used as
a measure of preload
• the same LVEDP that corresponds
to a normal preload in a normal
patient may correspond to a
decreased preload in a patient
with impaired diastolic function.
• Factors affecting ventricular compliance can be separated into those related to
the rate of relaxation (early diastolic compliance) and passive stiffness of the
ventricles (late diastolic compliance)
• Hypertrophy (from hypertension or aortic valve stenosis), ischemia, and
asynchrony reduce early compliance
• hypertrophy and fibrosis reduce late compliance
• Extrinsic factors (such as pericardial disease, excessive distention of the
contralateral ventricle, increased airway or pleural pressure, tumors, and
surgical compression) can also reduce ventricular compliance.
• right ventricle is more compliant than the left
 B. AFTERLOAD
• Afterload for the intact heart is commonly equated with either ventricular wall tension
during systole
• If the ventricle is assumed to be spherical, ventricular wall tension can be expressed by
Laplace’s law
where P is intraventricular pressure,
R is the ventricular radius, and H is wall thickness.
• Systolic intraventricular pressure is dependent on
the force of ventricular contraction; the viscoelastic properties of the aorta and its proximal
branches, blood (viscosity and density); and systemic vascular resistance (SVR)
• Because viscoelastic properties are generally fixed in any given patient, left
ventricular afterload is usually equated clinically with SVR
MAP=mean arterial pressure in mm of Hg,
CVP=central venous pressure in mm Hg
• CO is cardiac output in L/min.
• Normal SVR is 900–1500 dyn · s cm–5.
• Some clinicians prefer to use CI instead of CO in calculating a systemic vascular
resistance index (SVRI), so that
• SVRI = SVR × BSA
• Right ventricular afterload is mainly dependent on pulmonary vascular resistance
(PVR) and is expressed by
PAP is mean pulmonary artery pressure
LAP is left atrial pressure.
• In practice, PCWP can be
substituted as an approximation for LAP
• Normal PVR is 50 to 150 dyn · s cm–5 >
• Cardiac output is inversely related to large changes in afterload
• right ventricle is more sensitive to changes in afterload
• Cardiac output in patients with marked right or LV impairment is very sensitive to acute
increases in afterload
 C) CONTRACTILITY
• is the intrinsic ability of the myocardium dependent on the intracellular
Ca2+ conc
• Sympathetic nervous system is most imp. increase contractility
• contractility is depressed by hypoxia, acidosis, depletion of catecholamine
stores within the heart
• ischemia or infarction
• most anesthetics and antiarrhythmic agents are negative inotropes
D) WALL MOTION ABNORMALITIES
• Regional wall motion 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.
• can impair emptying and reduce stroke volume. The severity of the
impairment depends on the size and number of abnormally
contracting areas
 E) VALVULAR DYSFUNCTION
• can involve any one of the four valves in the heart
• can include stenosis, regurgitation (incompetence), or both.
• Stenosis of an AV valve (TV or mitral) reduces stroke volume by
decreasing ventricular preload, whereas stenosis of a semilunar valve
(pulmonary or aortic) reduces stroke volume by increasing ventricular
afterload
• When an AV valve is incompetent, part of the ventricular EDV can flow
backward into atrium during systole; the SV is reduced
• Similarly, when a semilunar valve is incompetent, a fraction of EDV
arises from backward flow into the ventricle during diastole.
ASSESSMENT OF VENTRICULAR
FUNCTION
• 1. Ventricular Function
Curves:
• Two points are identified on such diagrams: the endsystolic point
(ESP) and the end-diastolic point (EDP)
• ESP is reflective of systolic function, whereas EDP is reflective of
diastolic function. For any given contractile state, all ESPs are on the
same line
• 2. Assessment of Systolic Function
• The change in ventricular pressure over time during systole (dP/dt)
can be used as a measure of contractility.
• Contractility is directly proportional to dP/dt, but accurate
measurement of this value requires a high-fidelity (“Millar”)
ventricular catheter.
• Ventricular systolic function is routinely estimated using
echocardiography
 Ejection Fraction
• fraction of the end-diastolic ventricular volume ejected, is the most commonly
used clinical measurement of systolic function.
• EF= EDV-ESV
EDV
• EDV is left ventricular diastolic volume and ESV is end-systolic volume. Normal
EF is approximately 0.67 ± 0.08.
• Measurements can be made preoperatively from cardiac catheterization,
radionucleotide studies, or transthoracic (TTE) or transesophageal
echocardiography (TEE).
• DISADV: 1. when pulmonary vascular resistance increases, decreases in right
ventricular EF may reflect afterload rather than contractility
2. Left ventricular EF is not an accurate measure of ventricular
contractility in the presence of mitral insufficiency
• Myocardial deformation analysis : provides another measure to quantify
ventricular function
• Deformation of the heart occurs along three dimensions: circumferential, radial,
and longitudinal
• Strain is a measure of the change of length between two points. Using strain
analysis, echocardiography can determine the percent change in length at different
points of the myocardium
• −19% to −22% longitudinal strain is a normal range established for healthy patient
• Longitudinal strain is a negative change
because during systole the ventricle shortens,
resulting in L being less than L0
3. Assessment of Diastolic Function
• LV diastolic function can be assessed clinically by Doppler
echocardiography on a transthoracic or transesophageal examination.
• Flow velocities are measured across the mitral valve during diastole,
• Three parameters : based on isovolumetric relaxation time(IVRT), ratio of peak
early diastolic flow (E) to peak atrial systolic flow (A), and the deceleration time
(DT) of E (DTE)
• Tissue Doppler is frequently used to distinguish “pseudonormal” from normal
diastolic function.
• During systole the mitral annulus moves toward the apex of the heart, away from
the echocardiography probe in the esophagus. A negative deflection s’ wave is
generated,
• During diastolic filling the mitral annulus moves toward the
transesophageal echocardiography probe, producing a positive e’
wave.
• An e’ wave peak velocity of less than 8 cm/s is associated with
impaired diastolic function.
• An E/e' wave ratio that is greater than 15 is consistent with elevated
LV end-diastolic pressure
 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.
• Changes in systemic venous tone
allow VEINS to function as a
reservoir for blood
• Following significant blood or fluid
losses, shifts blood into other parts of the vascular system.
• Reduced venous tone following induction of anesthesia frequently results in
pooling of blood, reduced cardiac output, and hypotension
 AUTOREGULATION
• Most tissue beds regulate their own blood flow (autoregulation).
Arterioles
• generally dilate in response to reduced perfusion pressure or
increased tissue demand.
• These phenomena are likely due to both an intrinsic response of
vascular smooth muscle to stretch and the accumulation of
vasodilatory metabolic byproducts. The latter may include K+, H+,
CO2, adenosine, and lactate.
AUTONOMIC CONTROL OF THE
SYSTEMIC VASCULATURE
• primarily sympathetic. Outflow -all thoracic segments and the first two
lumbar segments.
• These fibers reach blood vessels via specific autonomic nerves or by
traveling along spinal nerves. principal function is to regulate vascular
tone.
• Sympathetic induced vasoconstriction (via α1-receptors) potent in
skeletal muscle, kidneys, gut, and skin; least in brain and heart.
• SNS maintains some tonic vasoconstriction on the vascular tree.
• Loss of this tone following induction of anesthesia or sympathectomy -
perioperative hypotension.
ARTERIAL BLOOD PRESSURE

• Systemic blood flow is pulsatile in large arteries because of the heart’s cyclic
activity
• largest pressure drop, nearly 50%, at 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:
MAP – CVP ≈ SVR × CO
• 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
• MAP=DBP+1/3PP PP=SBP-DBP
• PP is directly related to SV, but is inversely related to the compliance of the arterial
tree.
• Thus, decreases in PP may be due to a decrease in SV,an increase in SVR, or both.
• Increased PP increases shear stress on vessel walls, potentially leading to
atherosclerotic plaque rupture and thrombosis or rupture of aneurysms.
• in patients undergoing cardiac surgery -renal and neurological outcomes.
• Transmission of the arterial pressure wave faster than the actual movement of
blood
• PP is generally greater when measured in the femoral or dorsalis pedis arteries
than in the aorta
 Control of Arterial Blood Pressure
A. Immediate Control Minute-to-minute control
• primarily the function of ANS reflexes.
• sensed both centrally (in hypothalamic and brainstem areas) and peripherally by specialized
sensors (baroreceptors).
• Decreases in BP result in increased sympathetic tone, increased adrenal secretion of epinephrine,
and reduced vagal activity.
• resulting systemic vasoconstriction, increased HR, and enhanced cardiac contractility to increase
BP
• Peripheral baroreceptors are located at the bifurcation of the common carotid
arteries and the aortic arch.
• Elevations in BP 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
• sense MAP most effectively between 80 and 160 mm Hg. Adaptation
to acute changes in blood pressure occurs over the course of 1 to 2
days, rendering this reflex ineffective for longer term blood pressure
control.
• All volatile anesthetics depress
• B. Intermediate Control:
• course of a few minutes, sustained decreases in BP, with enhanced
sympathetic outflow, activate the renin–angiotensin–
aldosterone(RAS), increase secretion of arginine vasopressin (AVP),
and alter normal capillary fluid exchange.
• Hypertension increases interstitial movement of intravascular fluid,
whereas hypotension increases reabsorption of interstitial fluid
• 3.Long-Term Control
• slower renal mechanisms apparent within hours
• kidneys alter total body sodium and water balance to restore blood
pressure to normal.
• Hypotension results in sodium (and water) retention, whereas
hypertension increases sodium excretion in normal individuals
ANATOMY & PHYSIOLOGY OF THE
CORONARY CIRCULATION
• right and left coronary arteries, epicardial to endocardial vessels
• coronary sinus and the anterior cardiac veins.,small amount of blood
directly by thebesian veins.
• RCA supplies the right atrium, most of the RV , and a variable portion
of LV(inferior wall).
• In 85% of persons, the RCA gives rise to the posterior descending
artery (PDA), which supplies posterior interventricular septum and
inferior wall—a right dominant circulation; in the remaining 15% of
persons, the PDA is a branch of the LCA—a left dominant circulation.
• LCA normally supplies the left atrium and most of the
interventricular septum and left ventricle (septal, anterior, and lateral
walls).
• bifurcates into the left anterior descending artery (LAD) and the
circumflex artery (CX);
• the LAD supplies the septum and anterior wall and the CX supplies
the lateral wall.
• In a left dominant circulation, the CX wraps around the AV groove and
continues down as the PDA
• SA node : RCA (60%) or LAD (40%).
• AV node: RCA (85–90%) CX (10–15%);
• bundle of His: dual blood supply, PDA and LAD.
• The anterior papillary muscle of the mitral valve: dual blood
supply ,diagonal branches of the LAD and marginal branches of the
CX.
• posterior papillary : only by the PDA ,vulnerable to ischemic
dysfunction
2. Determinants of Coronary Perfusion
Coronary perfusion
• unique : intermittent rather than continuous
• During contraction, intramyocardial pressures in the LV approach
systemic arterial pressure. force of LV contraction almost completely
occludes the intramyocardial part of the coronaries.
• Coronary perfusion pressure(CPP) :determined by difference between
aortic pressure and ventricular pressure.
• LV is perfused almost entirely during diastole. In contrast, the RV is
perfused during both systole and diastole
• arterial diastolic pressure is more important than MAP
• Decreases in aortic pressure or
increases in ventricular end-diastolic
pressure can reduce coronary perfusion
pressure
• Increases in HR also decrease coronary
perfusion because of the disproportionately
greater reduction in diastolic time
Control of Coronary Blood Flow
• normally parallels myocardial metabolic demand. In the average adult man, apprx.
250 mL/min at rest.
• myocardium regulates own blood flow between perfusion pressures of 50 and 120
mm Hg. Beyond this range, blood flow becomes increasingly pressure dependent.
• 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—
coronary vasodilation. Autonomic influences are generally weak.
• Sympathetic stimulation increases myocardial blood flow because of an increase in
metabolic demand and a predominance of β2-receptor activation. PNS- weakly
vasodilatory
3. Myocardial Oxygen Balance
• Myocardial oxygen demand -most imp. determinant of myocardial
blood flow.
• Relative contributions to oxygen requirements include basal
requirements (20%), electrical activity (1%), volume work (15%), and
pressure work (64%).
• The 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 flow
EFFECTS OF ANESTHETIC AGENTS
• volatile anesthetic agents are coronary vasodilators. Their effect on coronary
blood flow is variable : direct vasodilating properties, reduction of myocardial
metabolic requirements, effects on arterial BP.
• Volatile agents exert beneficial effects in experimental myocardial ischemia
and infarction.
• They reduce myocardial oxygen requirements and protect against reperfusion
injury; by activation of ATP-sensitive K+ (KATP) channels.
• volatile anesthetics enhance recovery of “stunned” myocardium
(hypocontractile, but recoverable, myocardium after ischemia).
• potentially beneficial in patients with heart failure because most of them
decrease preload and afterload.
The Pathophysiology of Heart Failure
• Systolic heart failure occurs when heart is unable to pump a sufficient amount of
blood to meet body’s metabolic requirements.
• Clinical manifestations (eg, fatigue, dyspnea, oxygen debt, acidosis), the damming-up
of blood behind the failing ventricle (dependent edema or pulmonary venous
congestion), or both.
• LV is most commonly the primary cause, often with secondary involvement of the
right ventricle.
• Isolated right ventricular failure can occur in disease of t lung parenchyma or
pulmonary vasculature.
• LVF is most commonly the result of myocardial dysfunction, usually from CAD, but
may also be of viral disease, toxins, untreated hypertension, valvular dysfunction,
arrhythmias, or pericardial disease.
• Failure of the heart to relax during diastole leads to elevated LV EDP,
which is transmitted to LA and pulmonary vasculature.
• Common causes : hypertension, coronary artery disease, hypertrophic
cardiomyopathy, valvular heart disease, and pericardial disease.
• In patient with systolic failure heart compensates by dilating, which
leads to an increase in EDV to preserve the SV.
• In patients with diastolic failure, poor ventricular relaxation leads to a
higher LVEDP
• diastolic dysfunction is diagnosed echocardiographically. Placing the
pulse wave Doppler sample at mitral valve during LV filling, will
produce the characteristic diastolic flow pattern
• In patients with normal diastolic function, the ratio between the peak
velocities of the early (E) and the atrial (A) waves is from 0.8 to 2.
• tissue Doppler: An e' wave less than 8 cm/s is consistent with diastolic
dysfunction.
• In the early stages of diastolic dysfunction, the primary abnormality is
impaired relaxation. reduced peak E wave velocity. The A wave velocity
is increased relative to the E wave, and the E/A ratio is reduced
• As diastolic dysfunction advances, the LA pressure increases, restoring the
gradient between the left atrium and left ventricle with an apparent
restoration of the normal E/A ratio. This pattern is characterized as
“pseudonormalized.”
• Using the E/A ratio alone cannot distinguish, Doppler patterns of pulmonary
venous flow CAN, tissue doppler too
• As diastolic dysfunction worsens further, a restrictive pattern is obtained.
LV is so stiff that pressure builds in LA, resulting in a dramatic peak of early
filling and a prominent, tall, narrow E wave.
• atrial contraction contributes little to filling, resulting in a diminished A wave
and an E/A ratio greater than2:1.
• CO may be reduced at rest with heart failure, but the key point is ;
heart is incapable of appropriately increasing CO and oxygen delivery
in response to demand.
• Inadequate oxygen delivery to tissues is reflected by a low mixed
venous oxygen tension and an increase in the arteriovenous oxygen
content difference.
• In compensated heart failure, the A-V difference may be normal at
rest, but it rapidly widens during stress or exercise.
COMPENSATORY MECHANISMS
• generally present in patients with heart failure include activation of
sympathetic NS and RAS and increased release of AVP.
• One result is increased preload (fluid retention).
• Although these mechanisms can initially compensate for mild to
moderate cardiac dysfunction, with increasing severity of dysfunction,
they may actually worsen the cardiac impairment.
• Many of the drug treatments of chronic heart failure serve to
counteract these mechanisms
 A.Increased Preload

• increase in ventricular volume serves to increase SV by moving the heart up the

Starling curve
• Even when EF is reduced, an increase in EDV can maintain a normal SV .
• Worsening venous congestion caused by the pooling of blood behind the failing
ventricle and excessive ventricular dilation can rapidly lead to clinical deterioration.
• LVF results in pulmonary vascular congestion and progressive transudation of fluid,
first into the pulmonary interstitium and then into alveoli (pulmonary edema).
• RVF leads to systemic venous hypertension,results in peripheral edema, hepatic
congestion and dysfunction, and ascites.
• Dilation of the annulus of mitral or tricuspid valves from ventricular dilation leads
to valvular regurgitation, further impairing ventricular output.
B.Increased Sympathetic Tone
• Sympathetic activation increases release of NE from nerve endings in
heart and secretion of E from the adrenal glands
• Although enhanced sympathetic outflow can initially maintain CO by
increasing HR and contractility, worsening ventricular function elicits
increasing degrees of vasoconstriction in an effort to maintain arterial
blood pressure.
• The associated increase in afterload, however, reduces cardiac output
and exacerbates the ventricular failure.
• Chronic sympathetic activation in patients with heart failure
eventually: decreases the response(receptor uncoupling), number of
receptors (downregulation), and cardiac catecholamine stores.
• the failing heart becomes increasingly dependent on circulating
catecholamines.
• Abrupt withdrawal in sympathetic outflow or decreases in circulating
catecholamine levels, such as can occur following induction of
anesthesia, may lead to acute cardiac decompensation.
• A reduced density of M2 receptors also decreases parasympathetic
influences on the heart.
• Sympathetic activation tends to redistribute systemic blood flow output
awayfrom the skin, gut, kidneys, and skeletal muscle to the heart and
brain.
• Decreased renal perfusion, with β1-adrenergic activity at the JG apparatus,
activates RAS, which leads to sodium retention and interstitial edema.
• vasoconstriction secondary to elevated angiotensin II levels LV afterload
and causes further deterioration of systolic function.
• accounts for the efficacy of ACE inhibitors and ARBs in heart failure.
Symptoms may also improve in some patients with careful, low-dose β-
adrenergic blockade
• Circulating AVP levels, often markedly increased in patients with
severe heart failure, will increase ventricular afterload and are
responsible for a defect in free water clearance that is commonly
associated with hyponatremia.
• Brain natriuretic peptide (BNP) is produced in the heart in response
to myocyte distention.
• Elevated BNP concentration (>500 pg/mL) indicates heart failure, and
measurement of BNP conc. can be used to distinguish between heart
failure and lung disease as a cause of dyspnea
C.Ventricular Hypertrophy
• Ventricular hypertrophy can occur with or without dilation, depending
on the type of stress imposed
• In the volume-overloaded ventricle, the problem is an increase in
diastolic wall stress.
• Sarcomeres replicate mainly in series, resulting in eccentric
hypertrophy.
• Although ventricular EF remains depressed, the increase in end-
diastolic volume can maintain normal at-rest stroke volume
• The problem in a pressure-overloaded ventricle is an increase in
systolic wall stress
• sarcomeres mainly replicate in parallel, resulting in concentric
hypertrophy: The hypertrophy is such that the ratio of myocardial wall
thickness to ventricular radius increases
• Ventricular hypertrophy, particularly that caused by pressure
overload, usually results in progressive diastolic dysfunction. The most
common reasons for isolated left ventricular hypertrophy are
hypertension and aortic stenosis.
 TAKE HOME MESSAGE
• Anethetist deals with CVS & RS in everyday life. Its important to understand the
physiology and its application for effective patient management
• Heart is distinct from skeletal muscle d/t automaticity, action potential dependent on
ca2+
• systolic function is ability to pump out blood to meet o2 requirements, diastolic
function is to relax to adapt blood with optimal pressure
• Baroreceptor is an effective compensatory mechanism in immediate control of BP in
acute blood loss, lost by anesthesia
• Myocardial oxygen supply& demand balance- most imp factor deciding ischemic
damage to heart
• Anesthesia impairs many compensatory mechanisms of body to adapt ,need to have
adequate understanding to manage optimally
 REFERENCES
• MILLER’S ANESTHESIA-9H EDN.
• MORGAN & MIKHAIL’S CLINICAL ANESTHESIOLOGY 6TH EDN
• Clinical Anesthesia-8TH EDN. By Paul G. Barash ET AL
• GUYTON & HALL TEXTBOOK OF MEDICAL PHYSIOLOGY-12TH EDN
• Hutchinson clinical methods 24th edn
• Textbook of medical physiology- Indu Khurana 2nd edn