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PART 3

CARDIAC

REFLEXES

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

Cardiac reflexes are fast-acting reflex loops between the heart and central nervous system (CNS) that contribute to regulation of cardiac function and maintenance of physiologic homeostasis. Specific cardiac receptors elicit their physiologic responses by various pathways. Cardiac receptors are linked to the CNS by myelinated or unmyelinated afferent fibers that travel along the vagus nerve.

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

Sympathetic and parasympathetic nerve input is processed in the CNS. After central processing, efferent fibers to the heart or the systemic circulation will provoke a particular reaction. The response of the cardiovascular system to efferent stimulation varies with age and duration of the underlying condition that elicited the reflex in the first instance.

CAROTID BODY Chemosensitive cells 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 sinus nerve of Hering, ( a branch of Glossopharyngeal nerve) chemo sensitive area in medulla.

This area gets responded and stimulates Ventilatory drive. In addition, activation of the parasympathetic system ensues and leads to an reduction in Heart Rate and myocardial contractility. In the case of persistent hypoxia, the CNS will be directly stimulated, with a resultant increase in sympathetic activity.

Provoked by pressure over globe Traction over extra ocular muscles Stretch receptors Extra Ocular muscles short and long ciliary nerves ciliary ganglion ophthalmic division of trigeminal nerve gasserian ganglion increased parasympathetic tone BRADY CARDIA .(ATROPINE- GLYCO)

CHEMO & MECHANORECEPTORS Within the LV Wall in response to an noxious stimuli HYPOTENSION BRADYCARDIA CORONARY ART. DILATATION

Implicated in the physiologic response to a range of Cardiovascular conditions such as myocardial ischemia or infarction, thrombolysis, or revascularization and syncope. Endogenous ANP - BNP may modulate the Bezold-Jarisch reflex. So less pronounced in atrial fibrillation and cardiac hypertrophy patients.

Forced expiration against the closed glottis will result in Increased intrathoracic pressure Increased central venous pressure DECREASED VENOUS RETURN

CARDIAC OUTPUT BLOOD PRESSURE decreased after this maneuver. The decrease will be sensed by Baroreceptors and reflexively will result in an increase in HR and myocardial contractility, through Sympathetic stimulation.

When glottis opens, venous return increases and causes the heart to respond by vigorous contraction and an increase in blood pressure. This increase in blood pressure will in turn be sensed by Baroreceptors, thereby stimulating the Parasympathetic efferent pathways to the heart.

Increased Intra Cranial Pressure ISCHAEMIA ( ischaemia in medullary vasomotor 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 improve cerebral perfusion. As a result of high vascular tone REFLEX BRADYCARDIA mediated by baroceptors will ensue.

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

In contrast to the Para Sympathetic N S Sympathetic fibers are more distributed evenly in the Heart. They originate from T1 T4 (CARDIAC ACCELERATORY FIBERS ) STELLATE GANGLION HEART.

ADRENOCEPTORS

BETA ADRENOCEPTOR SIGNALLING SYSTEM

CONTROL OF CARDIO VASCULAR SYSTEM

Parasympathetic System
Slow heart rate Reduce cardiac output

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

Neurotransmitter is Noradrenalin which has positive effects on Inotropic Lusitropic Chronotropic Dromotropic

AT EXERCISE
Predominantly in Ventricles

Direct Inhibitory affect on Atria, and negative modulatory affect on Ventricles. M1 -- M2 -- M3 -- M4--M5 (M3 coronary) M2 CARDIAC Reduce SA AV node Atria directly then Ventr. AT REST Predominantly in Atria

Angiotensin II, the effect hormone in the renin-angiotensin system, is also produced 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.

Increased stretch of the myocardium releases ANP ATRIA BNP VENTRICLES Both represent part of the cardiac endocrine response to hemodynamic changes caused by pressure or volume overload. Also participate in organogenesis of the embryo heart and cvs In patients in CCF both ANP, BNP Predictors of mortality.

ANATOMY & PHYSIOLOGY

OF CORONARY CIRCULATION

ANATOMY

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 not continuous, rather intermittent Gets filled up during Diastole.

RIGHT CORONARY
CONUS ACUTE MARGINAL POSTERIOR DESCENDING ARTER

LEFT
LCMA LCX

CORONARY
LAD OM PL OM 1 2

RIGHT CORONARY
RIGHT ATRIUM RIGHTS VENTRICLE INFERIOR WALL OF LT. VENTRICLE PDA -- SUP & POST INT VENTR SEPTUM ------ 85 % cases

RIGHT DOMINANT CIRCULATION

LEFT CORONARY
LEFT ATRIUM LEFT VENTRICLE MOST OF THE INT VENTR SEPTUM PDA POST SEPTUM INF WALL -----in 15 % of cases

LEFT

DOMINANT

CIRCULATION

Average blood flow is approximately 250 ml/min at rest It regulates own blood flow closely between 50 to 120 mm Hg, beyond which it becomes much pressure-dependent. Both alpha 1 beta-2 receptors present in coronary arteries but are very weak. Hypoxia causes adenosine mediated vasodilatation.

It is unique it is INTERMITTENT not continuous fills during DIASTOLE. LEFT VENTRICLE during diastole RIGHT VENTRICLE during dia + syst. CORONARY PERFUSION PRESSURE = DIA.PRESSURE LVEDP Diastolic Pre. Is more important than MAP

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 %

Coronary Blood Flow during CARDIAC CYCLE

Most VOLATILE ANAESTHETIC agents are CORONARY VASODILATORS HALOTHANE -- large coronaries ISOFLURANE -- smaller coronaries DESFLURANE -- autonomic mediated SEVOFLURANE no such dilatation

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 of the stunned myocardium. They decrease myocardial contractility, they can potentially be beneficial in patients with CCF, because they decrease preload and afterload.