CARDIAC REFLEXES ppt cardiac reflexes .pptx

CARDIAC REFLEXES

1. CARDIAC REFLEXES Presenter: Dr. Sushma Reddy (PG 1st Yr Anaesthesia) Moderator: Dr.Zohra Mehedi (Associate Professor) 6/24/2024 1

2. 6/24/2024 2

3. Contents : Introduction Cardiac receptors Types of reflexes Clinical significance of each reflex 6/24/2024 3

4. Introduction: Fast acting reflex loops between the heart and CNS that contribute to regulation of cardiac function and the maintenance of physiologic haemostasis Specific cardiac receptors elicit the physiologic responses by various pathways. 6/24/2024 4

5. Cardiac Receptors : Cardiac receptors are linked to CNS by myelinated or unmyelinated afferent fibers that travel along the vagus nerve . Cardiac receptors are in the atria, ventricles, pericardium, and coronary arteries . Extracardiac receptors are located in the great vessels and carotid artery. 6/24/2024 5

6. 6/24/2024 6

7. Autonomic control of the cardiovascular system is mediated through afferent and efferent pathways and neural networks involving the brainstem, spinal cord, peripheral ganglia, and the intrinsic cardiac nervous system (ICNS ).  The cardiovascular neuraxis can be considered in three different levels: Level 1 consists of the heart with its own ICNS, which is comprised of discrete ganglia found at the origin of the great vessels, and posteriorly along the atria and atrioventricular groove . Level 2 consists of intrathoracic components that regulate cardiac function including the middle cervical ganglia, stellate ganglia, and the T2–T4 portions of the paravertebral sympathetic chain. Level 3 can be considered as the dorsal root and nodose ganglia, which mediates the majority of afferent neurotransmission, as well as spinal cord, brainstem, and higher centers 6/24/2024 7

8. 6/24/2024 8

9. 6/24/2024 9

10. Types of Cardiac Reflexes 6/24/2024 10

11. Baroreceptor Reflex 6/24/2024 11

12. Baroreceptor Reflex Baroreceptors are stretch receptors found in the carotid body, aortic body and the wall of all large arteries of the neck and thorax. There are two types of baroreceptors: high-pressure arterial baroreceptors and low-pressure volume receptors, which are both stimulated by stretching of the vessel wall. Arterial baroreceptors are located within the carotid sinuses and the aortic arch. Low-pressure volume receptors, or cardiopulmonary receptors, are located within the atria, ventricles, and pulmonary vasculature. Respond progressively at 5 0-170 mm Hg . Respond more to a rapidly changing pressure than stationary pressure 6/24/2024 12

13. Baroreceptor Reflex Changes in arterial blood pressure are monitored by circumfrential and logitudinal stretch receptors located in the carotid sinus and aortic arch . The nucleus solitarius , located in the cardiovascular center of the medulla, recieves the impulse from these stretch receptors through afferent glossopharyngeal and va g us nerves. 6/24/2024 13

14. Baroreceptor Reflex The cardiovascular center in medulla consists of two functionally different areas; —LATERALLY & ROSTRALLY : This area is responsible for increasing blood pressure —CENTRALLY & CAUDALLY : This area is responsible for lowering arterial blood pressure. Typically , the stretch receptors are activated if systemic blood pressure is greater than 170 mmHg 6/24/2024 14

15. Mechanism of Baroreceptor Reflex: Nerve impulses from arterial baroreceptors are tonically active; increases in arterial blood pressure will result in an increased rate of impulse firing. Increased stimulation of the nucleus tractus solitarius by arterial baroreceptors results in increased inhibition of the tonically active sympathetic outflow to peripheral vasculature, resulting in vasodilation and decreased peripheral vascular resistance . The opposite is true of decreases in mean arterial pressure, resulting in decreased nerve firing and reduced stimulation of the nucleus tractus solitarius , thereby attenuating inhibition and increasing sympathetic outflow to peripheral vasculature and vasoconstriction. 6/24/2024 15

16. 6/24/2024 16

17. 6/24/2024 17

18. Anaesthetic Implications : I t plays important role during acute blood loss and shock. However, the reflex arch looses its functional capacity when arterial blood pressure is less than 50mmmofHg Hormonal status and sex di fference may alter the baroreceptor reflex. 6/24/2024 18

19. Anaesthetic Implications : Volatile anaesthetics particularly Halothane inhibit the heart rate component of this reflex. Calcium channel blockers, ACE inhibitors, phosphodiestrase inhibitors will lessen the cardiovascular response of raising the blood pressure through the baroreceptor reflex. Patients with chronic hypertension often exhibit per operative circulatory instability as a r esult of decrease in their baroreceptor reflex 6/24/2024 19

20. Chemoreceptor Reflex 6/24/2024 20

21. Chemoreceptor Reflex Peripheral chemoreceptors are located in both the carotid body and the aortic body. They detect large changes in the partial pressure of oxygen (pO 2 ) as the arterial blood supply leaves the heart. When low levels of oxygen are detected, afferent impulses travel via the glossopharyngeal and   vagus  nerves to the medulla oblongata and the  pons in the brainstem. A number of responses are then coordinated which aim to restore pO 2 : The respiratory rate and tidal volume are increased to allow more oxygen to enter the lungs and subsequently diffuse into the blood Blood flow is directed towards the kidneys and the brain (as these organs are the most sensitive to hypoxia) Cardiac Output is increased to maintain blood flow, and therefore oxygen supply to the body’s tissues 6/24/2024 21

22. Chemoreceptor Reflex Central chemoreceptors are located in the medulla oblongata of the brainstem.  They detect changes in the arterial partial pressure of carbon dioxide (pCO 2 ).  When changes are detected, the receptors send impulses to the respiratory centres in the brainstem that initiate changes in ventilation to restore normal pCO 2. Detection of an increase in pCO 2  leads to an increase in ventilation. More CO 2  is exhaled, the pCO2 decreases and returns to normal. Detection of a decrease in pCO2 leads to a decrease in ventilation. Less CO 2  is retained in the lungs, the pCO2 increases and returns to normal. The mechanism behind how central chemoreceptors detect changes in arterial pCO 2  is more complex, and is related to changes in the pH of the Cerebral Spinal Fluid (CSF). 6/24/2024 22

23. Chemoreceptor Reflex pH Control The pH of the CSF is established by the ratio of  pCO 2  : [HCO 3 – ] . The HCO 3 –  levels remain relatively  constant . CO 2  freely diffuses across the  blood brain barrier,  from the arterial blood supply into the CSF. CO 2  reacts with H 2 O, producing  carbonic acid , which lowers the pH.   This means that the pH of the CSF is  inversely proportional  to the arterial pCO 2 . A small decrease in pCO 2 ­ leads to an increase in the pH of the CSF, which stimulates the respiratory centres to decrease ventilation. A small increase in pCO 2  leads to a decease in the pH of the CSF, which stimulates the respiratory centres to increase ventilation. However if pCO 2  levels stay abnormal for a longer period of time, e.g. three days or more,  choroid plexus  cells within the blood brain barrier allow HCO 3 –  ions to enter the CSF. Movement of HCO 3 –  ions alters the pH which in turn resets the pCO 2  to a different value.  This can be relevant in certain diseases, such as Chronic Obstructive Pulmonary Disease (COPD ). 6/24/2024 23

24. Chemoreceptor Reflex At an arterial partial 02 pressure of less than 50mmof Hg or in condition of acidosis, the chemoreceptors send their impulses along the sinus nerve of Henring and vagus nerve to chemosensitive area of medulla. This area responds by stimulating the respiratory center and there by increasing the ventilatory rate 6/24/2024 24

25. Chemoreceptor Reflex In addition, activation of the parasympathetic system, leads to a reduction in heart rate and myocardial contractility. In case of persistent hypoxia, the CNS will be directly stimulated, with a resultant increase in sympathetic activity. 6/24/2024 25

26. 6/24/2024 26

27. Anaesthetic Implications : 1. All anaesthetic drugs (except ketamine, ether and nitrous oxide) cause a dose- dependent reduction in ventilatory minute volume . This can be due to either a reduction in the respiratory rate (e.g. opioids), a reduction in the tidal volume (e.g. volatile anaesthetics both (e.g. propofol ). As alveolar ventilation decreases the PaCO2 increases . Hypercapnia causes vasodilation, tachycardia, arrhythmias, hypertension and in an awake patient, headache, confusion, tremor, sedation and eventually coma (CO2 narcosis ). All of these effects can be seen in the postoperative period 6/24/2024 27

28. Anaesthetic Implications : 2.Under normal conditions the PaCO2 of arterial blood is the predominant factor controlling ventilation . Any increase in PaCO2 is detected by peripheral (carotid bodies) and central (medullary) chemoreceptors. As a result there is a linear increase in ventilation of approximately 2 I/min for each 1 mmHg rise in PaCO2 . This ventilatory response to carbon dioxide is reduced by virtually all anaesthetic drugs (the main exception being ether) until excessively high concentrations are produced . As a result, anaesthetized patients become hypercapnic . 6/24/2024 28

29. Anaesthetic Implications : 3.In addition, anesthetics have two further undesirable effects on ventilation ; Firstly after a period of mechanical ventilation the threshold at which the PaCO2 stimulates the return of spontaneous ventilation is increased, thus delaying the return of spontaneous ventilation Secondly, the ventilatory response to acidosis is blunted, reducing a patient’s ability to compensate. 6/24/2024 29

30. Bain Bridge Reflex The Bainbridge reflex is a compensatory reflex resulting in an increase in heart rate following an increase in cardiac preload.  Scientist Sir Arthur Bainbridge first demonstrated this reflex in unconscious anesthetized dogs with the monitoring of venous pressure, pulse rate, and arterial pressure following administration of blood or saline. The reflex has become more widely known as the  “Atrial reflex." 6/24/2024 30

31. Mechanism of Bain Bridge Reflex: Stretch receptors present in the atria detect increases in central venous pressure (CVP) resulting from increased volume which increases the heart rate by a signaling mechanism with the brain .  The afferent limb of the reflex within this signal, when activated takes sensory information from the vagus nerve to medulla oblongata, and the efferent limb sends out inhibitory signals by reducing vagus nerve tone and increasing the sympathetic outflow. 6/24/2024 31

32. Bain Bridge Reflex Acceleration of heart rate also results from a direct effect on the SA node by the stretching the atrium . The changes in heart rate are dependent on the underlying heart rate before stimulation . Bainbridge Reflex is involved in Respiratory Sinus Arrhythmia. During inhalation intrathoracic pressure decreases. It triggers increased venous return which is registered by stretch receptors, which via Bainbridge Reflex increases the heart rate momentarily during inspiration . The Bainbridge reflex controls heart rate in response to blood volume. 6/24/2024 32

33. 6/24/2024 33

34. 6/24/2024 34

35. Anaesthetic Implications : The Bainbridge reflex and the baroreceptor act antagonistically to control heart rate . The baroreceptor reflex acts to decrease heart rate when blood pressure rises . When blood volume is increased, the Bainbridge reflex is dominant; when blood volume is decreased, the baroreceptor reflex is dominant 6/24/2024 35

36. Bezold-jarisch Reflex 6/24/2024 36

37. Bezold-jarisch Reflex It responds to ventricular stimuli sensed by the chemoreceptors and mechanoreceptors within the left ventricular wall by inducing the triad of - Hypotension - Bradycardia - Coronary artery dilatation The activated receptors communicate along unmyelinated vagal afferent type C Fibers BJR is cardio inhibitory response. 6/24/2024 37

38. 6/24/2024 38

39. 6/24/2024 39

40. Bezold-jarisch Reflex It produce increase in parasympathetic tone . Because it invokes bradycardia, the Bezold jarisch reflex is thought of as a cardioprotective Reflex The reflex has been implicated in physiologic response to a range of cardiovascular conditions such as Myocardial ischemia, thromboIysis,or revascularisation and syncope. Bezold Jarisch reflex may be less pronounced in patients with cardiac hypertrophy or atrial fibrillation . Bradycardia and Hypotension seen in Neuraxial Anaesthesia and Peripheral Nerve Blockade is claimed to be due to activation of the BJR. 6/24/2024 40

41. 6/24/2024 41

42. Valsalva Maneuver Valsalva maneuver is the performance of forced expiration against a closed glottis .  The key event occurring during the maneuver is increasing intrathoracic pressure leading to the reduction of preload to the heart. The reflex cardiovascular changes during and after the maneuver are because of reduced preload engaging baroreflex and other compensatory reflex mechanisms. 6/24/2024 42

43. Phases of Valsalva maneuver: T he Valsalva maneuver is divided into four phases . : Phase I, which corresponds to the onset of strain, is associated with a transient rise in blood pressure because of the emptying of some blood from the large veins and pulmonary circulation. Phase II follows this when positive intrathoracic pressure leads to a reduced venous return to the heart. Because of reduced venous return and thus reduced preload, stroke volume falls; this leads to a fall in blood pressure activating the baroreceptors in the carotid sinus and aortic arch. The vagal withdrawal followed by increased sympathetic discharge ensues, leading to marked tachycardia, increased cardiac output, and vasoconstriction, which leads to the recovery of blood pressure to normal values in healthy individuals. Phase III is the transient phase involving the release of strain which leads to a sudden dip in blood pressure. The release of positive pressure leads to expansion of the pulmonary vascular bed and reduces the left ventricular cross-sectional area resulting in a transient fall in blood pressure. Phase IV is the overshoot of the blood pressure above the baseline, which is because of the resumption of normal venous return to the heart stimulated by the sympathetic nervous system during Phase II. The overshoot of blood pressure leads to stimulation of baroreflex , leading to bradycardia and the return of blood pressure to the baseline 6/24/2024 43

44. 6/24/2024 44

45. Technique of of Valsalva Maneuver : The patient can perform the maneuver in the sitting, supine, or recumbent position. Some reports advocate a recumbent position, while others report an increased incidence of abnormal blood pressure responses in the supine position .  While different combinations of pressure and duration have been tried, an optimal combination for autonomic function assessment is 40 mm Hg for 15 seconds. Lower pressures may not be sufficient, while higher pressures suffer from poor reproducibility. 6/24/2024 45

46. Technique of of Valsalva Maneuver : Modified VM In order to increase the relaxation phase venous return and vagal stimulation, a modification to the standard VM has been described in the REVERT trial, which includes supine positioning with leg elevation immediately after the Valsalva strain. This is used for the emergency treatment of supraventricular tachycardias . Reverse VM The patient in a sitting position is asked to inhale against resistance for ten seconds while keeping the nose pinched and having the mouth closed tightly. This leads to increased vagal tone and decreased sympathetic activity, which in turn leads to bradycardia and arterial hypotension (the Bezold – Jarich reflex), causing supraventricular tachycardia to resolve in the next 15 seconds if effective. 6/24/2024 46

47. Contra indications of Valsalva Maneuver : Valsalva maneuver is relatively safe and can be performed in all patients . Side effects reported are rare. S ince there is a rise in intraocular and intra-abdominal pressure, the test must be avoided in patients with retinopathy and intraocular lens implantation. Valsalva retinopathy may result in susceptible patients .   Also , there are reports of syncope, chest pain, and arrhythmias due to the performance of VM. Therefore , caution is necessary for patients with pre-existing coronary artery disease, valvular disease, or congenital heart disease. 6/24/2024 47

48. Clinical Significance : Autonomic function assessment:   Valsalva maneuver is an integral part of the Ewing battery of tests used for the evaluation of cardiac autonomic neuropathy . Valsalva ratio, the ratio of the longest inter-beat (RR) interval after the expiratory strain and the shortest inter-beat interval during the strain, is an index of parasympathetic function. Also , determination of baroreflex sensitivity (BRS) can be performed using the Valsalva maneuver to assess the integrity of the baroreflex by estimating the slope of a regression plot between RR intervals and systolic blood pressure values during phases II and IV of the maneuver . Assessment of heart failure:   VM is useful for the assessment of heart failure. Patients with heart failure show an abnormal blood pressure overshoot in response to the Valsalva maneuver due to impaired ventricular function. 6/24/2024 48

49. Clinical Significance : Termination of Arrhythmias : VM is also useful for the termination of paroxysmal supraventricular tachycardia (PSVT) with variable success. Increased vagal activity, leading to increased refractoriness of atrioventricular (AV) nodal tissue interrupting re-entry, has been proposed as the mechanism for the termination of PSVT . Diagnosis of murmurs:   VM may be used to differentiate between different murmurs. Since the maneuver reduces preload and thus end-diastolic volume, it can help accentuate some murmurs while diminishing others . The murmur of aortic stenosis (AS) is reduced in intensity on the administration of VM because reduced end-diastolic volume (EDV) diminishes the blood available for ejection through the stenosed aortic orifice. Contrary to AS, the murmur of hypertrophic obstructive cardiomyopathy (HOCM) accentuates in response to VM because reduced EDV during VM leads to the worsening of the obstruction in hypertrophic obstructive cardiomyopathy . 6/24/2024 49

50. Clinical Significance : To detect bleeding points towards the end of thyroid surgery and for the diagnosis of varicocele . To assist in the radiological diagnosis of liver hemangiomas , venous disease and foramen ovale . To confirm hemostasis and absence of cerebrospinal fluid leak after neurosurgical procedures. To reduce venipuncture pain in pregnant women. 6/24/2024 50

51. Cushing Reflex The Cushing reflex (vasopressor response, Cushing reaction, Cushing effect, and Cushing phenomenon) is a physiological nervous system response to acute elevations of intracranial pressure (ICP), resulting in Cushing’s triad of widened pulse pressure (increasing systolic, decreasing diastolic), bradycardia, and irregular respirations . The Cushing reflex was proposed in 1901 by Dr. Harvey Cushing. He believed that the dramatic increase in blood pressure was a reflex to brainstem ischemia seen in patients with increasing ICP from causes such as intracranial hemorrhage, a mass effect from a tumor, and cerebral edema, to name a few.  6/24/2024 51

52. Cushing Reflex With an acute intracranial pathology that causes a mass effect and increased resistance in intracranial vessels, the only way for the body to perfuse intracranial tissue is through elevating the MAP to restore baseline CPP. Dr . Cushing proposed that systemic vasoconstriction and subsequent rise in systemic blood pressure was a mechanism to overcome increased resistance in the brain, increase the CPP, and prevent further ischemia in the brain. 6/24/2024 52

53. Stages of Cushing Reflex : In the first stage of the Cushing reflex, blood pressure and heart rate rise in response to sympathetic activation to overcome increases in ICP .  This sympathetic response allows for brain perfusion as long as the ICP is not too high to overcome. For the brain to remain adequately perfused, mean arterial pressure (MAP) must be maintained higher than ICP. In the second stage of the Cushing reflex, hypertension continues to be present, but the patient becomes bradycardic rather than tachycardic . There are differing opinions on the mechanisms leading to this stage of the Cushing reflex. The prior thinking was that increased blood pressures lead to activation of baroreceptors in the aortic arch, triggering parasympathetic activation and resultant bradycardia. Tsai et al. proposed that chemoreceptors outside the brain do not participate in this stage, and bradycardia actually results from compression of the intracranial vagal nerve. 6/24/2024 53

54. 6/24/2024 54

55. Clinical Significance : As a result of the Cushing reflex, the Cushing triad is typically observed in the later stages of acute head injury . Although the reflex is a homeostatic response by the body in an attempt to rescue under-perfused brain tissues, the Cushing triad is, unfortunately, a late sign of increasing ICP and indicative that brainstem herniation is imminent . Patients who present to the emergency department with concerns for increased ICP and two of three signs of the Cushing reflex have been found to have almost two-fold higher mortality than patients with normal and stable vital signs . It is, therefore, important to recognize early signs of elevated ICP (e.g., a headache, nausea, vomiting, altered level of consciousness) to intervene as early as possible. Cushing reflex is most usually an irreversible condition with a terminal prognosis for the patient. Initial emergency treatments aim to lower the ICP rapidly and include: Elevation of the patient’s head 30 to 45 degrees, mannitol and/or furosemide, which act as an osmotic diuretic, induced hyperventilation, steroids, or cerebrospinal fluid drainage. 6/24/2024 55

56. 6/24/2024 56

57. Oculocardiac Reflex 6/24/2024 57

58. Oculocardiac Reflex The oculocardiac reflex (OCR), also known as the Aschner reflex or  trigeminovagal  reflex, was first described in 1908 as a heart rate reduction from direct pressure placed on the eyeball or periorbital structures.  Currently , this reflex is defined by a heart rate decrease greater than 20% following globe pressure or extraocular muscle traction. 6/24/2024 58

59. Oculocardiac Reflex The OCR most commonly results in sinus bradycardia, though associations with reduced arterial pressure, arrhythmia, asystole , and even cardiac arrest have been reported. Ophthalmologic procedures, specifically strabismus surgery, consistently trigger the OCR.  However , facial trauma, regional anesthetic nerve blocks, and mechanical stimulation may also activate this reflex . 6/24/2024 59

60. Oculocardiac Reflex The OCR's incidence is reported to be anywhere from 14% to 90% and decreases with age. Pediatric populations face the highest risk of OCR development due to their increased susceptibility. Young individuals are also particularly vulnerable to OCR's complications due to their heavy dependence on the heart rate for maintaining cardiac output. The OCR's varying occurrence and severity are linked to factors like hypoxia, hypercarbia , acidosis, and the anesthetic agent type employed during surgery 6/24/2024 60

61. Pathway of Oculocardiac Reflex The trigeminal or 5th cranial nerve (CN V) comprises the reflex's afferent or sensory limb. The vagus or 10th cranial nerve (CN X) constitutes the efferent OCR limb. Ocular and periorbital stretch receptors activate this pathway. The short and long ciliary nerves conduct impulses that carry the sensory message to the ciliary ganglion. The impulses are then transported via CN V's ophthalmic division to the Gasserian ganglion, followed by the trigeminal nucleus, where the afferent limb terminates in the central nervous system. The CNS processes the sensory input, facilitating communication between the trigeminal sensory nucleus and the vagus nerve's visceral motor nucleus. The outflow triggers the efferent limb, sending impulses from the brainstem to the myocardium, specifically the sinoatrial node, activating the vagal motor response.  Negative chronotropy consequently arises, causing bradycardia. 6/24/2024 61

62. Risk Factors : The OCR is often triggered by extraocular muscle traction, with the medial rectus muscle most commonly implicated . Additional stimuli linked to OCR activation include direct globe pressure, ocular manipulation, and ocular pain. Retrobulbar blocks, ocular hematomas, and facial or orbital trauma may also activate the reflex due to increased pressure.  However , the OCR is fatigable, decreasing in intensity with multiple, repeated stimuli 6/24/2024 62

63. Complications : The OCR's complications arise from vagal responses and may include the following: Sinus bradycardia Arrhythmia Reduced atrial pressure Ventricular tachycardia Ventricular fibrillation Multifocal premature ventricular contractions 6/24/2024 63

64. Complications : Ventricular bigeminy Asystole Cardiac arrest Dizziness Light headedness Nausea Weakness Prompt recognition and management are essential to avert significant morbidity and mortality. 6/24/2024 64

65. 6/24/2024 65

66. 6/24/2024 66 Pressure applied on globe or surrounding structures stretch receptors in extra ocular muscles send impulses through long and short ciliary nerves Ciliary nerves merges with ophthalmic division of trigeminal nerve at cilliary ganglion Gasserian ganglion Increased parasympathetic tone Bradycardia

67. Clinical Significance : Bradycardia is the OCR's most common manifestation, though it may deteriorate to potentially fatal arrhythmias, asystole , and cardiac arrest .  Apt et al (1973) and Espahbodi  et al (2015) reported OCR occurrence rates in patients undergoing ophthalmologic surgeries to be 67.9% and 63%, respectively.  OCR activation has also been linked to noncardiac manifestations, including hypotension, syncope, and gastrointestinal symptoms like nausea and vomiting due to the vagal motor response.  Vagal effects may influence postoperative nausea and vomiting severity.  Nausea and vomiting rates in pediatric patients can reach 85%  poststrabismus  surgery, making it a leading cause of inpatient admission after outpatient procedures 6/24/2024 67

68. How to deactivate the reflex ? Relieving eye or orbital pressure can deactivate the reflex. Proceeding  cautiously is essential after removing the source. However , stimulus withdrawal may be more challenging in uncontrolled situations like trauma.  Pharmacological management with cardiac monitoring may be necessary in instances where the OCR may develop. 6/24/2024 68

69. How to deactivate the reflex ? The occurrence of the reflex may be reduced by choosing the appropriate anesthetic, as some agents are associated with a greater risk of OCR activation than others. Studies indicate that pretreatment with intravenous anticholinergics like atropine or glycopyrrolate decreases OCR incidence. Atropine blocks peripheral cardiac muscarinic receptors, increasing sinoatrial node firing and atrioventricular node conduction and countering OCR's vagal outflow. Ketamine may also counteract vagal stimulation by enhancing sympathetic activity. Choi et al. reported lower OCR incidence with ketamine infusion than sevoflurane , halothane, and propofol . Espahbodi et al. (2015) found ketamine superior to atropine in OCR reduction. 6/24/2024 69

70. 6/24/2024 70

71. 6/24/2024 71

72. References : Textbook of Physiology, AK Jain, 10 th E d Ganong's Review of Medical Physiology. 24th Ed . Miller’s textbook of Anaesthesia, 9 th Edition. Morgan & Mikhail's Clinical Anesthesiology,5th ed. https ://partone.litfl.com/cardiac_reflexes.html https :// anaesthesianews.wordpress.com/2022/05/16/cardiac-reflexes Crisafulli A, Marongiu E, Ogoh S. Cardiovascular Reflexes Activity and Their Interaction during Exercise. Biomed Res Int. 2015;2015:394183. doi : 10.1155/2015/394183. Epub 2015 Oct 18. PMID: 26557662; PMCID: PMC4628760 6/24/2024 72

73. 6/24/2024 73