Short-Term Regulation of Arterial Pressure PDF

SHORT - TERM REGULATION OF ARTERIAL PRESSURE NRAN 80413 SPRING 2024 RON ANDERSON, M.D. 1 INTEGRATION OF MULTIPLE SYSTEMS Rapid (seconds – minutes) – Baroreceptor reflexes – Chemoreceptor reflexes – CNS ischemic response Intermediate (minutes – hours) – Renin-angiotensin system – Vascular stress-rela...

SHORT - TERM REGULATION OF ARTERIAL PRESSURE NRAN 80413 SPRING 2024 RON ANDERSON, M.D. 1 INTEGRATION OF MULTIPLE SYSTEMS Rapid (seconds – minutes) – Baroreceptor reflexes – Chemoreceptor reflexes – CNS ischemic response Intermediate (minutes – hours) – Renin-angiotensin system – Vascular stress-relaxation – Capillary fluid shift Long-term – Renal body fluid mechanisms GUYTON 2 NERVOUS CONTROL OF THE CIRCULATION Plays a key role in: Redistribution of blood flow to various tissues throughout the body Variations in cardiac rate and contractility Producing rapid changes in systemic blood pressure 3 CARDIOVASCULAR EFFECTS OF ANS SYMPATHETIC Heart rate Contractility Peripheral vascular resistance Venous tone Stimulation of renin release PARASYMPATHETIC Heart rate Limited effect on contractility 4 LIPPINCOTT SYMPATHETIC OUTFLOW MILLER 6 AUTONOMIC NERVOUS SYSTEM ANATOMY 7 GUYTON AUTONOMIC INNERVATION OF THE HEART Parasympathetic – Fibers primarily distributed to SA node and AV node and to a lesser extent to the atria – Little or no parasympathetic distribution to ventricles – Primary PNS effect is therefore chronotropic with little effect on contractility Sympathetic – Fibers distributed to SA node, AV node, atria, and ventricles via the stellate ganglia Right stellate primarily to anterior epicardial surface and interventricular septum – stimulation primarily increases heart rate Left stellate distributes to posterior and lateral surfaces of ventricles – stimulation increases contractility and MAP without change in HR – Pretty good evidence for SNS regulation of small coronary resistance and larger conductance vessels 8 AUTONOMIC INNERVATION OF THE HEART GUYTON 9 CNS VASOMOTOR CENTER Located in the medulla and caudal 1/3 of pons Transmits parasympathetic impulses to heart via CN X Transmits impulses via the spinal cord to heart and blood vessels Receives input from periphery as well as higher nervous centers, e.g. hypothalamus and parts of the cerebral cortex 10 GUYTON CNS VASOMOTOR CENTER Vasoconstrictor Area – Excite preganglionic sympathetic vasoconstrictor fibers Vasodilator Area – Inhibits activity of the vasoconstrictor area Sensory Area – Receives input from CNs IX and X. Sends output to both the vasoconstrictor and vasodilator areas 11 LEVY SYMPATHETIC VASOCONSTRICTOR TONE Continuous slow firing of impulses from the vasoconstrictor area Results in partial contraction of the blood vessels Allows modulation up or down 12 GUYTON CARDIAVASCULAR INTEGRATION VASOCONSTRICTION - MECHANISM Release of norepinephrine from postganglionic sympathetic nerves causing: Activation of alpha adrenergic receptors on vascular smooth muscle AND: Sympathetic stimulation of adrenal medulla, resulting in release of norepinephrine and epinephrine into the circulation 14 SYMPATHETIC (thoracolumbar) α α1 SUBTYPES α2 α1A α1B α1D MECHANIS M EFFECTS cAMP cAMP β β3 D1 IP3, DAG INHIBIT ADENYLYL CYCLASE / EFFECT VASC SM. MUSCLE VASOCONSTRICTION ENDINGS MODULATE PUPILLARY DILATOR MYDRIASIS NT RELEASE PROSTATE CONTRACTION HEART FORCE OF CONTRACTION AGONIST ANTAGONIST β 1 PNENYLEPHRINE BROMOCRYPTINE LOCATION EFFECT D2 D3 D4 D5 G-PROTEIN COUPLED ACTIVATE ADENYLYL CYCLASE/ cAMP α2 LOCATION EFFECT PRAZOSIN EFFECT RATE FORCE OF CONTRACTION AGONIST β2 α2A α2B α2C α1 HEART LIPOLYSIS β1 D ANTAGONIST cAMP cAMP cAMP D1 LOCATION EFFECT PLATELETS AGGREGATION ANS TERMINALS AGONIST EFFECT RENAL SM. MUSCLE LOCATION DILATION NERVE CONSTRICTION LIPOLYSIS ANTAGONIST AGONIST β2YOHIMBINE LOCATION SMOOTH MUSCLE FENOLDOPAM EFFECT RELAXATION (RESP, VASC, UTERINE) LIVER SKELETAL MUSCLE AGONIST D2 NT RELEASE VASC SM. MUSCLE FAT CELLS CLONIDINE LOCATION cAMP GLYCOGENOLYSIS K+ UPTAKE ANTAGONIST AGONIST β3 LOCATION FAT CELLS HIGHER CONTROL OF THE VASOMOTOR CENTER Excitatory or inhibitory impulses arising from higher nervous centers act on the vasomotor center to modulate it’s activity, including: – Reticular substance of the pons, mesoncephalon, and diencephalon – Hypothalamus – Multiple areas of the cerebral cortex 16 VASODILATION - MECHANISM Impulses arising oin the motor cortex Modulated by the anterior hypothalamus Believed to be mediated by epinephrine released from vasodilator fibers activating skeletal muscle beta receptors Effect is relatively minor May allow an anticipatory increase in muscle blood flow prior to local metabolic control May contribute to vasovagal syncope 17 GUYTON RAPID CONTROL OF BLOOD PRESSURE Rapid increase in blood pressure (5-10 seconds) depends on multiple mechanisms: – Arteriolar constriction leading to increased peripheral resistance – Venous constriction leading to increased preload and stretch – Sympathetic stimulation of heart rate and contractility – Inhibition of parasympathetic vagal outflow 18 BLOOD PRESSURE MODULATION DURING EXERCISE Typically 30-40% increase with heavy exercise Due to: – Activation of the RAS resulting in stimulation of the vasoconstrictor and cardioacceleratory areas – You also see: Vasodilation following increase in local metabolism 19 REFLEX CONTROL OF ARTERIAL PRESSURE Baroreceptor Mechanisms Carotid Aortic Chemoreceptors Low Pressure Receptors Atrial Pulmonary Arterial Volume Reflex Bainbridge Reflex CNS Ischemic Response Response to Valsava Maneuver Oculocardiac Reflex 20 BARORECEPTOR REFLEXES Baroreceptors – Stretch receptors – Widespread distribution throughout large cervical and thoracic arteries – Highest concentrations at the carotid bifurcation and aortic arch – Operate by modulating frequency of firing 21 BARORECEPTOR RESPONSE Carotid Sinus – Via Hering’s nerve to glossopharyngeal – Begins firing at ~ 50 mm Hg Aortic Arch – Via vagus nerve – Operates in a range ~ 30mmHg higher than the carotid sinus receptors Greatest change in impulse frequency within the range of normal BP Extremely rapid response Greater response to a rapidly changing BP GUYTON 22 BARORECEPTOR REFLEXES GUYTON 23 LEVY BARORECEPTOR REFLEXES Mechanism – Activation of the stretch receptors results in: – Inhibition of the vasoconstrictor center – Increased vagal outflow – Resulting in: – Arteriolar and venous dilation – Decreased contractility and heart rate 24 GUYTON TESTS OF AUTONOMIC DYSFUNCTION CLINICAL EXAMINATION TECHNIQUE NORMAL VALUE HR RESPONSE TO VALSALVA The seated subject blows into a mouthpiece(maintaining a pressure of 40 mm Hg) for 15 seconds. The Valsalva ratio is the longest R-R interval(which comes shortly after the release )to the shortest R-R interval (which occurred during the maneuver). RATIO OF >1.21 HR RESPONSE TO STANDING HR is measured as the subject moves from a resting supine position to standing. Normal tachycardic response is maximal around the 15th beat after standing. A relative bradycardia follows that is most marked around the 30th beat after standing. The response is the ratio of the longest R-R interval around the 30th beat to the shortest R-R interval around the 15th beat. RATIO OF >1.04 HR RESPONSE TO DEEP BREATHING The subject takes 6 deep breaths in 1 minute. The maximum and minimum heart rates during each cycle are measured, and the mean of the differences during 3 successive breathing cycles is taken as the maximum - minimum heart rate. MEAN DIFFERENCE >15 BPM BP RESPONSE TO STANDING The subject moves from resting supine to standing, and the standing BP is subtracted from the supine BP. DIFFERENCE 16 mm HG PARASYMPATHETIC SYMPATHETIC BARORECEPTOR REFLEXES EVERS PRESSURE BUFFER SYSTEM Baroreceptor mechanism functions as a pressure buffer, maintaining the blood pressure within a narrower range. 27 PRESSURE BUFFER SYSTEM GUYTON 28 BARORECEPTORS AND LONG-TERM BLOOD PRESSURE CONTROL Likely of minor importance for long-term blood pressure control due to “resetting” of baroreceptors to new pressure “Resetting” begins within minutes and becomes complete over a period of 1-2 days May produce some long-term control through interaction with the renin-angiotensin-aldosterone system 29 CHEMORECEPTORS Located at: – Carotid bifurcation – carotid bodies – Aortic arch – aortic bodies Respond to: – Decreased oxygen – Increased CO2 – Increased H+ ion Transmission of impulses via: – Hering’s nerve – Glossopharyngeal – Vagus Produce: – Excitation of the vasomotor center – Increased respiratory drive 30 LOW-PRESSURE RECEPTORS (ATRIAL) Located in: – Atria – Pulmonary arteries Respond to: – Changes in volume 31 VOLUME REFLEX (ATRIAL) Atrial stretch due to increased blood volume produces: – Reflex dilation of renal afferent arterioles – Signaling to hypothalamus to decrease ADH secretion – Increased release of atrial natriuretic peptide 32 BAINBRIDGE REFLEX (ATRIAL) Increased right sided filling pressure produces two effects on heart rate: – Direct stretch of the SA node, resulting in up to a 15% increase in rate – Stretch receptors located in the right atrium and cavoatrial junction are stimulated Vagal afferent impulses travel to medulla with a subsequent : – Decrease in efferent parasympathetic activity – Increase in sympathetic activity Resulting in increased heart rate and contractility (up to 40 60% increase in rate) 33 CNS ISCHEMIC RESPONSE Dramatic increase in blood pressure in response to a decrease in blood flow to vasomotor center significant enough to impair removal of CO2 – Produces marked stimulation of the vasoconstrictor and cardioaccelerator neurons – May produce a sympathetic discharge severe enough to completely shut down some peripheral vessels 34 CUSHING REFLEX CNS Ischemic Response produced by CSF pressure approaching or exceeding arterial pressure and thereby compromising CNS blood flow. 35 GUYTON VALSALVA MANEUVER Forced expiration against a closed glottis results in: – Increased intrathoracic pressure – Increased CVP – Decreased venous return Cardiac output and blood pressure will fall Baroreflexes will increase heart rate and contractility When the valsalva is released the opposite will occur. 36 OCULOCARDIAC REFLEX Produced by: – Pressure on the globe – Traction on surrounding structures (muscles) Pathway: – Ciliary nerves trigeminal nerve Results in: – Increased parasympathetic outflow gasserian ganglion bradycardia Incidence: – 30-90% in some opthalmic surgery Management: – Reflex fatigues with repeated episodes – Antimuscarinics e.g. atropine or glycopyrrolate 37 ABDOMINAL COMPRESSION REFLEX Contraction of abdominal skeletal muscle following initiation of a baroreceptor or chemoreceptor reflex Compresses venous reservoirs increasing venous return and subsequently cardiac output and blood pressure 38 SOURCES Textbook of Medical Physiology- Guyton, Hall. 2021. 14th Edition Miller’s Anesthesia- Miller. 2020. 9th Edition 39