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PART 3

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CARDIAC REFLEXES

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Baroreceptor Reflex (Carotid Sinus Reflex) Chemoreceptor Reflex Bainbridge Reflex Bezold-Jarisch Reflex Valsalva Maneuver Cushing Reflex Oculocardiac Reflex

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Cardiac reflexes are fast-acting reflex loopsbetween the heart and central nervoussystem (CNS) that contribute toregulation of cardiac function andmaintenance of physiologic homeostasis.Specific cardiac receptors elicit theirphysiologic responses by various pathways.Cardiac receptors are linked to the CNS bymyelinated or unmyelinated afferentfibers that travel along the vagus nerve.

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Cardiac receptors can be found in the atria, ventricles, pericardium, and coronary arteries. Extra cardiac receptors are located in thegreat vessels and carotid artery.

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Sympathetic and parasympathetic nerveinput is processed in the CNS. Aftercentral processing, efferent fibers to theheart or the systemic circulation willprovoke a particular reaction. Theresponse of the cardiovascular system toefferent stimulation varies with age andduration of the underlying condition thatelicited the reflex in the first instance.

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CAROTID BODY AORTIC BODY Cells respond to changes in pH status and

blood oxygen tension. In acidosis, PaO2 less than 50 mmHg

chemo receptors send their impulses sinusnerve of Hering, ( a branch ofGlossopharyngeal nerve) chemo

sensitive area in medulla.

Chemosensitive cells

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This area gets responded and stimulatesVentilatory drive. In addition, activation of the

parasympathetic system ensues and leadsto an reduction in Heart Rate andmyocardial contractility.

In the case of persistent hypoxia, the CNSwill be directly stimulated, with a resultantincrease in sympathetic activity.

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Provoked by pressure over globe Traction over extra ocular muscles Stretch receptors Extra Ocular

muscles short and long ciliary nervesciliary ganglion ophthalmic division of

trigeminal nerve gasserian ganglionincreased parasympathetic toneBRADY CARDIA .(ATROPINE- GLYCO)

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CHEMO & MECHANORECEPTORS

Within the LV Wall in response to annoxious stimuli

HYPOTENSION BRADYCARDIA CORONARY ART. DILATATION

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Implicated in the physiologic response to arange of Cardiovascular conditions such asmyocardial ischemia or infarction,

thrombolysis, or revascularization and

syncope. Endogenous ANP - BNP may modulate

the Bezold-Jarisch reflex. So less

pronounced in atrial fibrillation andcardiac hypertrophy patients.

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CARDIAC OUTPUT BLOOD PRESSUREdecreased after this maneuver. Thedecrease will be sensed by Baroreceptorsand reflexively will result in an increase inHR and myocardial contractility, through

Sympathetic stimulation.

Increased intrathoracic pressure

Increased central venous pressure

DECREASED VENOUS RETURN

Forced expiration against the closed glottis will result in

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When glottis opens, venous returnincreases and causes the heart to respondby vigorous contraction and an increase in

blood pressure. This increase in blood pressure will in turn

be sensed by Baroreceptors, thereby

stimulating the Parasympathetic efferentpathways to the heart.

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Increased Intra Cranial PressureISCHAEMIA ( ischaemia in medullaryvasomotor center induces initial activation

of the SNS). Such activation will lead to an increase in

heart rate, blood pressure, and myocardial

contractility in an effort to improvecerebral perfusion. As a result of highvascular tone REFLEX BRADYCARDIA

mediated by baroceptors will ensue.

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-------atria

-------conducting tissues M2 RECEPTORS negative CHRONOTROPIC DROMOTROPIC IONOTROPIC LUSITROPIC

BATHMOTROPIC

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In contrast to the Para Sympathetic N SSympathetic fibers are more distributed

evenly in the Heart. They originate from T1 T4 (CARDIAC

ACCELERATORY FIBERS ) STELLATE

GANGLION HEART.

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ADRENOCEPTORS

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BETA ADRENOCEPTOR

SIGNALLING SYSTEM

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CONTROL

OFCARDIO VASCULAR

SYSTEM

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Parasympathetic System Slow heart rate Reduce cardiac output

Sympathetic System Increase heart rate Increase force of contraction Increase cardiac output

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Neurotransmitter isNoradrenalin which haspositive effects on

Inotropic Lusitropic Chronotropic Dromotropic

AT EXERCISE

Predominantly in

Ventricles

Direct Inhibitory affect onAtria, and negativemodulatory affect onVentricles.

M1 -- M2 -- M3 -- M4---M5 (M3 coronary)

M2 CARDIAC Reduce SA AV node

Atria directly then Ventr. AT REST

Predominantly in Atria

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Angiotensin II, the effect hormone in therenin-angiotensin system, is alsoproduced by cardiomyocytes.

AT1

AT2 two types are present. AT1 are predominant stimulation causes

positive chronotropic inotropic effects

AT2 are in Foetus

anti proliferative . Role of AT 2 in adult not precisely

known.

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Increased stretch of the myocardium releases A N P ATRIA

B N P VENTRICLES Both represent part of the cardiac endocrineresponse to hemodynamic changes caused bypressure or volume overload. Also participate

in organogenesis of the embryo heart and cvs In patients in CCF both ANP, BNP

Predictors of mortality.

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ANATOMY & PHYSIOLOGY

OF CORONARYCIRCULATION

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ANATOMYANATOMY

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Entire heart is supplied only by two Blood flows from outside to inside of

Ht Coronary perfusion is very much

unique in that ---it is notcontinuous, rather intermittent Gets filled up during Diastole.

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RIGHT CORONARY

LEFT CORONARY

CONUS ACUTE MARGINAL POSTERIOR DESCENDING ARTER

LCMA LCX LAD OM PL OM 1 2

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RIGHT CORONARYRIGHT ATRIUM

RIGHTS VENTRICLEINFERIOR WALL OF LT. VENTRICLEPDA -- SUP & POST INT VENTRSEPTUM ------ 85 % cases

RIGHT DOMINANT CIRCULATION

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LEFT ATRIUMLEFT VENTRICLEMOST OF THE INT VENTR SEPTUMPDA POST SEPTUM INF WALL

-----in 15 % of cases

LEFT CORONARY

LEFT DOMINANT CIRCULATION

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Average blood flow is approximately 250ml/min at rest

It regulates own blood flow closelybetween 50 to 120 mm Hg, beyond whichit becomes much pressure-dependent.

Both alpha 1 beta-2 receptors present incoronary arteries but are very weak.

Hypoxia causes adenosine mediated vaso-dilatation.

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It is unique it is INTERMITTENT notcontinuous fills during DIASTOLE.

LEFT VENTRICLE during diastole RIGHT VENTRICLE during dia + syst. CORONARY PERFUSION

PRESSURE = DIA.PRESSURE LVEDPDiastolic Pre. Is more important thanMAP

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Most important determinant is Myocardial Oxygen demand

Other tissues O2 extraction 25 % Myocardium extraction - 65 % DISTRIBUTION : Basal requirements : 20 % Electrical activity : 1 % Volume work : 15 % Pressure work : 64 %

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C a Bl d Fl d i g

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Coronary Blood Flow duringCARDIAC CYCLE

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Most VOLATILE ANAESTHETIC agentsare CORONARY VASODILATORS

HALOTHANE -- large coronaries ISOFLURANE -- smaller coronaries DESFLURANE -- autonomic mediated SEVOFLURANE no such dilatation

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In the setting of Ischemia and infarction --Volatile agents exert beneficial effects They reduce myocardial O2 requirements

and protective against reperfusion injury

Volatile anesthetics enhance recovery ofthe stunned myocardium. They decreasemyocardial contractility, they canpotentially be beneficial in patients withCCF, because they decrease preload andafterload.

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