Regulation Of Blood Pressure

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Regulation Of Blood Pressure : 

Regulation Of Blood Pressure Moderator: Prof. P.K. Gupta Speaker: Dr.Chandrasekhar

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The use of any anaesthetic,no matter how “trivial,”is an absolute indication for arterial blood pressure measurement.

Objectives: : 

Objectives: History Definition of Blood Pressure. JNC-7 Classification of Blood Pressure. Various method used for measurements of Blood Pressure. Physiological regulation of Blood Pressure both at tissue and central level. Pharmacology of selected agents used to treat hypertension and hypotension.

History: : 

History: The sphygmomanometer was invented by Samuel Siegfried, Karl Ritter, Von Basch in1880. In 1896, Italian pediatrician Riva-Rocci introduced it for BP measurement. In 1905 Korotkoff describe the auscultatory technique to measure both systolic & diastolic BP. The automated NIBP measurement by Oscillometry first described by Von Recklinghausen in 1931

Definitions: : 

Definitions: Blood pressure refers to the force exerted by circulating blood per unit surface area on the walls of blood vessels. The pressure of the circulating blood decreases as blood moves through arteries, arterioles, capillaries, and veins; the term blood pressure generally refers to arterial blood pressure, i.e., the pressure in the larger arteries.

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Systolic pressure(SBP) is defined as the peak pressure generated during systolic contraction. Diastolic pressure(DBP) is the lowest pressure during diastolic relaxation. Pulse pressure(PP) is the difference between the systolic and diastolic pressure. Mean arterial presssure (MAP) is average pressure throughout the cardiac cycle. (SBP)+2(DBP) MAP= 3

Technique for measurement of BP: : 

Technique for measurement of BP: Usually we measure two types of Blood Pressure I,e NIBP and IBP. NIBP: it can be measured by following ; Palpation: Inflating the cuff to a limit ,deflating it by 2mg per beat and measuring the cuff pressure at which arterial pulse begins gives the can’t measure DBP. Auscultation:Deflating the cuff from a limit ,appearance of korotkoff indicates SBP and muffling denotes can’t detect the “Auscultatory gap”.

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Oscillometry: It based on on change in the magnitude of is very sensitive to movement and also can’t measure BP during Shock. Doppler: It measure BP by determining the flow distal to the artery. Previosly doppler only measure SBP but now use of piezoelectric crystal in doppler can detect both SBP & DBP. Arterial Tonometry, Arterial volume clamp method are other types of continuous beat to beat NIBP measure.

Complication: : 

Complication: Pain and discomfort. Petechiae and ecchymoses Limb edema Venous stasis and Thrombophlebitis Peripheral Neuropathy Compartment syndrome

Invasive Blood Pressure (IBP): : 

Invasive Blood Pressure (IBP): It is a method of measuring blood pressure internally by using a sensitive IV catheter inserted into an superficial artery . This provides a more accurate reading of the patent's current blood pressure. Indication: Procedure where continuous BP monitoring required. Failure of NIBP measurement. Repeated blood sampling.

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4. Planned Pharmacological or mechanical cardiovascular manipulation. IBP is avoided in the absence of collateral circulation which to be elicited by doing Allen test. In the wave form the SBP,DBP,MAP is determined by the upstroke, down stroke and area under the pressure curve respectively. Complications include distal ischemia, bleeding, embolisation,infection and fistula formation.

JNC7 Classification of High Blood Pressure for Adults Aged 18 Years and Older* : 

JNC7 Classification of High Blood Pressure for Adults Aged 18 Years and Older* *based on the average of 2 or more properly measured, seated, BP readings on each of 2 or more office visits.

Physiological regulation of Blood Pressure: : 

Physiological regulation of Blood Pressure: It occur both at tissue level (local Regulation) and at systemic level (systemic Regulation) LOCAL REGULATION: Capacity of tissue to regulate its own blood flow is called as Autoregulation. It is well developed in kidney and also seen in brain,liver,heart,intestine and skeletal muscle.

Autoregulation of arterioles (in the absence of external stimuli) : 

Autoregulation of arterioles (in the absence of external stimuli) Myogenic mechanism( response to mechanical stimulus): - VSM fibre contract when it streched and relaxes when pressure in the vessel increases. -Net effect: maintenance of near constant blood flow for a particular metabolic level.

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Metabolic mechanism: Accumulation of metabolites like Lactate, Phosphate, histamine, C02, H+,NO, K+ and adenosine (Specially in skeletal muscle. Decrease in O2, and Ph, causes vasodilatation in arteriole and increases the blood flow to the tissue Whereas increased O2,TXA2,Endothelin,substance-P, serotonin causes vasoconstriction

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Substances that mediate vascular smooth muscle relaxation

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Substances causing contraction in vascular smooth muscle

Systemic Regulation: : 

Systemic Regulation: Neural Control: Other than venules and capillaries all vascular system are innervated. Both cholinergic and adrenergic nerve plexuses lies on adventia and extend branches to the surface of VSM,only the neurotransmitters reach the inner part of VSM by diffusion and exert there effect. There is no tone in cholinergic system,but the vasoconstrictor fibers are tonically active so sympathectomy causes vasodilatation in most of vessels

Vasomotor Control: : 

Vasomotor Control: In CNS the control of Blood Pressure is exerted by groups of neurons in Medulla, collectively called as Vasomotor area. Impulse from this area both by sympathetic system and vagal discharge regulate the HR, stroke volume and vessel diameter.

Baroreceptors: : 

Baroreceptors: These are the stretch receptors present in the wall of blood vessel (carotid Sinus and Aortic Arch) and Heart (Rt &Lft atria at the junction of SVC and Pulm vein). These receptors are located in the adventitia ,consist of extensively branched,knobby,coiled, interwined ends of myelinated nerve fibre. In chronic Hypertension these receptors reset to maintain an elevated blood pressure.

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pain RAS c1

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These receptors works more effectively in MAP between 80 – 160 mm of Hg. Carotid sinus receptors are physiologically more important than Aortic arch recepters. Atrial Baroreceptors are of 2 types- type-A- Active during systole. type-B- Active during diastole. Atrial stretch receptors also respond to hypovolemia by increasing the secretion of AVP,Renin and Aldosterone.

Effect of Chemoreceptor on Vasomotor centre : 

Effect of Chemoreceptor on Vasomotor centre The cardiovascular response to chemoreceptors stimulation causes peripheral vasoconstriction and Bradycardia. In some hypotensive patient Chemoreceptor stimulation lead to production of “Meyer waves”, I,e. slow regular oscillation in arterial BP that occur at a rate of once in every 20-40 sec. In any case of increased ICT causes local hypoxia stimulation of vasomotor centre increased BP baroreceptors stimulation HR decreases (Cushing Reflex)

Hormonal Control: : 

Hormonal Control: Hormones responsible for BP: 1.KININS: Both bradykinin & lysyl-bradykinin relaxes VSM via NO and BP. These are mostly active in exocrine gland like sweat gland,salivary gland ,pancreas and increase the blood flow during active secretion.

Atrial Natriuretic Peptide(ANP): : 

Atrial Natriuretic Peptide(ANP): This hormone is stored and secreted by muscle of Atrium and to some extent ventricle and its secretion is stimulated by ECF volume and ingestion of Na+. Act by- Dilating afferent arteriole and relaxing mesangial cells GFR. Inhibiting Na+ reabsorption in renal tubule. Relaxing the VSM of arteriole and venule. It is also responsible for “ Escape Phenomenon” (Prolong exposure to mineralocorticoids don’t able to produce edema in normal individual due to the antagonist action of ANP)

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VIP AND HISTAMINE: These act through H1 receptors and increase the NO formation there by relaxes VSM. ADRENOMEDULLIN: This inhibits Aldosterone secretion in salt depleted individual and NO production the BP.

Hormones responsible for BP: : 

Hormones responsible for BP: EPINEPHRINE & NOREPINEPHRINE: Act through alpha and beta receptors to cause vasoconstriction and CO BP. VASOPRESSIN(ADH): It secreted from supraoptic nucleus of hypothalamus and BP by- V1A- mediated direct vasoconstriction. V1B-mediated ACTH secretion from pitutary. V2 – stimulation Sequestration of ‘Aquaporins water moves from lumen to interstitum urine become hypertonic and water conserved.

Renin- Ang-Aldosterone System : 

Renin- Ang-Aldosterone System This system plays an important role for intermediate regulation of BP JG Apparatus: Includes JG cells ,macula densa cells and Lacis cells. Renin secreted mainly by JG cells and to some extent by Lacis cells.

Factors affecting Renin secretion: : 

Factors affecting Renin secretion: Stimulatory: Increased sympathetic activity via renal nerve. Increased circulating catecholamines. Prostaglandins. Inhibitory: Increased Na+ and Cl- delivery to macula densa. Increased afferent arteriolar pressure. Angiotensin-II. Vasopressin

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Vasoconstriction NE

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- - Spironolactone Amiloride (-)

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Goldblatt hypertension or renal hypertension: Constiction of one renal artery or atheromatous occlusion of a renal artery causes stimulation of Renin secretion and leading to sustained hypertension. Kidney also have a important role for long term BP control by altering Na+ and water retention.

Pharmacological agents used for controlling BP: DRUGS FOR HYPERTENSION: : 

Pharmacological agents used for controlling BP: DRUGS FOR HYPERTENSION: DIURETICS: By excretion of Na and reducing the plasma volume and CO BP. Thiazide: Thiazide, Hydrochlorothiazide,Cholorthalidone,Indapamide High Ceiling: Furesamide,Bumetanide K+ Sparing: Spironolactone,Amiloride ACE Inhibitors: Enalapril,Captopril,Lisinopril AT-1 Antagonist(ARB): Losartan,Candesartan,Irbesartan Alfa Receptors Blockers: BP by the alfa mediated peripheral vasoconstriction. Alfa-1 & Alfa-2 Blockers: Phenoxybenzamine,Phentolamine Alfa-1 Blockers: Prazosin,Doxazosin,Terazosin Beta Receptors Blockers: BP by HR and CO. Propranolol,Nadolol,Esmolol,Atenolol

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Both Alfa & Beta Blockers: Labetalol,Carvedilol,Dilevalol Centrally acting Alfa-2 Agonist: Stimulation of Alfa-2 receptors presynaptically in CNS the Sympathetic discharge. Clonidine, Methyldopa. Vasodilators: Arteriolar: Hydralazine, Minoxidil Diazoxide. Venous: NTG, Other Nitrates. Both Arteriolar and Venous: SNP, ACE Inhibitos,ARBs Ca+ Channel Blockers: Verapamil,Diltiazem,Nifedipine, Nitrendipine Endothelin Receptors Antagonist: BP by antagonising the action of Endothelin,most potent vasoconstictor . ET-A and ET-B Antagonist: Bosentan. ET-A Antagonist: Sitaxsentan. Dopaminergic Agonist: BP by stimulating DA1 receptors which causes renal and splanchnic vasodilation and natriuresis by inhibiting the Na reabsorption at PCT. Fenoldopam. Others: Nesiritide,Reserpine, Guanethidine


SODIUM NITROPRUSSIDE It is a directly acting vasodilator causes relaxation of both artery & vein. Action is due to release of NO . SNP is rapidly degraded by non enzymatic processes in RBC and plasma to release CN, NO and methaemoglobin Speed of onset and duration of action : 60-120 sec Infusion at a rate of 0.3-10 g/kg/min Protected form light as photodegradation of SNP well liberate CN and increased risk of toxicity . 50mg 18mg

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CVS : Produces direct venous and arterial vasodilation. Though by reducing the venous return it seems to decrease the CO, by reflex sympathetic stimulation CO. It also produces coronary steal phenomenon. RESPIRATION: Inhibit HPV, increases shunt fraction, V/Q mismatch and increases dead space CNS : Cerebral vasodilator, increase CBF, and ICT So SNP should not be commenced until dura is opened. TOXICITY: should be suspected if there is resistance to high infusion rate or Previously responsive Pt becomes unresponsive , Finding of metabolic acidosis, Increased mixed venous O2 saturation. USE: Various hypertensive emergencies- Aortic surgeries, Embolectomy, Pheochromocytoma


NITROGLYCERINE It principally dilate venous capacitace vessel by same mechanism I,e by producing NO. But the production of NO is not spontaneous, require the presence of thiol group containing compounds like glutathione. By decreasing the venous return it also the CO. It also increases the blood flow to the ischemic region of heart. It ICT and decrease the CPP but less than SNP. Tolerance to NTG develop on continuous administration more than 24 hr( due to depletion of thiol containing group like glutathione).So there should be a free interval of at least 6 hr after every 14-16 hr of infusion. It can be given as infusion at -5mcg/min It also available to use as sublingual tablets,transdermal patch,NTG spray. used in Acute coronary syndrome,Hypertensive emergencies and cardiac failure


CLONIDINE It is a centrally acting selective alpha-2A agonist whose stimulation the sympathetic discharge. Clonidine on higher dose stimulate alpha-2B receptor and BP( therapuetic window phenomenon ). On addition it has analgesic property when given intrathecaly ,anti shivering & sedative action. It is active orally ,Dose-100-200mcg OD/BD. Clonidine withdrawl causes rebaound hypertension mostly by catecholamines and the sensitivity of receptors, can be treated with phentolamine or labetalol.


LABETALOL It is a alpha-1,beta-1and beta-2 receptor antagonist-decreasing both systolic and diastolic BP. The major advantage is that it don't causes tachycardia and don't crosses the placenta, so used for hypertension during pregnancy. Also used in clonidine withdrawal and pheocromocytoma. Side effect includes orthostatic hypotension,bronchospasm. ESMOLOL It is a ultra short acting beta-1 antagonist decreses BP and HR. Renin activity decreases, so hypotension is more sustained Dose- 0.5mg/kg loading dose followed by 0.05 mg/kg/min infusion. Used to decrease HR and BP in various cardiac surgery.


DRUGS USED IN HYPOTENSION: DOPAMINE: It act via-- D1 receptor Renal & Mesenteric vasodilation. -- Beta-1 receptor in heart +ve chronotrophic and ionotrophic effect. -- Alfa-1 receptors peripheral vasoconstriction. Administration of renal dose- a controversy: Now the renal dose of dopamine not recommended for prevention or reversal of Acute renal failure. Dose: 3-10 mcg/kg/min.

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It should never be administered along with alkaline fluid in which catecholamines get inactivated. It should be diluted with 5%DS and preferably given through central lines. Peripheral infusion of dopamine for long time causes extravasations of dopamine and produce ischemic limb necrosis. Tachycardia is a significant adverse effect so should be avoided in Vent. Tachyarrhythmias.


DOBUTAMINE: It is a potent beta-1 agonist SBP and weak beta-2 agonist DBP( MAP is almost not altered) At a dose > 5 mcg/kg/min its levorotatory isomer stimulate alfa-1 receptor and prevent further fall of BP. Dose: 3-15 mcg/kg/min Usually used with dopamine in heart failure


NOREPINEPHRINE: It stimulate all alfa and beta receptor (except beta-2) and increases the systemic vascular resistance. Though it has beta-1 agonist action SVR mediated baroreflex the CO. Chronic infusion of NE some times causes Hypotension and it is due to metabolic acidosis occurring due to prolonge vasoconstriction. Dose 0.3-1.2 mcg/kg/min Used in resistant hypotension not responding to other vasoconstrictor.


EPHEDRINE: It exert its action by stimulating the release of epinephrine (indirect action) and acting on alfa and beta receptors(direct action). SBP & DBP,HR,CO are ,but blood flow to renal and splanchnic circulation . Second dose of ephedrine produces less effect due to tachyphylaxis (by persistent blockade of receptors) Dose: 10-25 mg i.v. Used in hypotension produced by regional anaesthesia and inhaled & i.v anaesthetics.


MEPHENTERMINE: Mechanism of action same as that of ephedrine. It is structurally closely related to methylamphetamine and also crosses BBB up to some extent which explains its modest CNS stimulation quality. Dose:10-20 mg i.v. Used to treat hypotension due to spinal anaesthesia and other hypotensive crisis


PHENYLEPHRINE: It is a synthetic catecholamine that stimulate principally alfa-1 receptor. It is particularly useful in pt with coronary artery disease because this drug, in contrast to other sympathomimetics the coronary perfusion without chronotropic effect. Systemic BP control is similar with both phenylephrine and ephedrine but phenylephrine is associated with a higher umbilical artery pH at delivery,so now phenylephrine is a prefered drug over ephedrine for t/t of hypotension during spinal anaesthesia in CS. Dose: 50-100 mcg i.v.or 180mcg/min & then 30-60 mcg/min.


DELIBERATE HYPOTENSION: ACTUALITY How do we call the situation in which : “a patient’s arterial blood pressure is intentionally lowered to facilitate a surgical procedure” ? (Elliot, 1999) Controlled hypotension ? Induced hypotention ? Hypotensive anesthesia ? Deliberate hypotension ? Permissive hypotension ? Controlled circulation ? WE Decide To Use The Term Deliberate Hypotension (DH)

DEFINITION:*Deliberate Hypotension (DH) is the reduction of systolic pressure during general anesthesia to 80-90 mm Hg or mean arterial pressure (MAP) to 50-65 mm Hg IN NORMOTENSIVE PATIENTS : 

DEFINITION:*Deliberate Hypotension (DH) is the reduction of systolic pressure during general anesthesia to 80-90 mm Hg or mean arterial pressure (MAP) to 50-65 mm Hg IN NORMOTENSIVE PATIENTS Decreased surgical blood loss Better exposure of and improved visibility of the surgical field More definite identification and resection of tumor margins Decreased operating time Decreased number of blood products transfused Decreased amount of suture and cauterized tissue within surgical wound PURPOSES:


INDICATIONS NEUROSURGERY: Clipping of cerebral Aneurysm Tumor resection AV malformation GYNECOLOGICAL: Radical pelvic procedure ORTHOPEDIC: Total Hip Replacement Spinal fusion ENT: Oral surgery Major Facial Reconstruction Head and Neck Tumor Resection


DIFFERENT TECHNIQUES USED FOR HYPOTENSIVE ANAESTHESIA Spinal and epidural anesthesia Volatile anesthetics Direct vasodilating drugs Alpha-adrenergic receptor blocking drugs Betha-adrenergic receptors blocking drugs Combined alpha and betha-adrenergic blocking drugs Calcium channel entry blocking drugs


CONTRAINDICATIONS OF DH Cerebrovascular disease, incl. TIA Spinal cord compression Cardiovascular diseases :MI Aortic stenosis Renal dysfunction Increased ICP Pregnancy Severe pulmonary disease Severe hypovolemia or anemia


COMPLICATIONS OF DH Secondary hemorrhage Renal insuffciency Thrombic phenomena (cerebral, coronary) Rebound hypertension Very severe and sustained hypotension, leading to cardiac arrest Increased ICP Short-term impaired memory


CONCLUSION DH is a double-edge sword In most cases helps reducing blood loss but the danger is there all the time It can transform an uneventful anesthesia into a very stormy one It demands a very strict selection of: patients drugs monitoring

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