logging in or signing up hypertention & anesthesia ussavaraprasad Download Post to : URL : Related Presentations : Let's Connect Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Copy embed code: Embed: Flash iPad Dynamic Copy Does not support media & animations Automatically changes to Flash or non-Flash embed WordPress Embed Customize Embed URL: Copy Thumbnail: Copy The presentation is successfully added In Your Favorites. Views: 6569 Category: Education License: All Rights Reserved Like it (3) Dislike it (0) Added: July 20, 2008 This Presentation is Public Favorites: 9 Presentation Description essesment of hypertensive case,evaluation, pre o.p preparation and management of anesthesia during surgery. Comments Posting comment... Premium member Presentation Transcript HYPERTENTION AND ANESTHESIA : HYPERTENTION AND ANESTHESIA Dr.U.S.S.A.Varaprasad MD Professor of Anesthesia S M C / G G H Vijayawada How to remain without tension ? : How to remain without tension ? ACCEPTED NORMALS : ACCEPTED NORMALS ADOLESCENT 100 / 75 mmHg CHILDHOOD 85 / 55 INFANT 70 / 45 Systolic Hypertension is marker of Macro-Vascular Disease large Arterial stiffening. ( atherosclerosis ) Diastolic Hypertension is consequence of Micro-Vascular Disease involving arterioles of < 1mm size ( arteriosclerosis ) Categories of Hypertension : Categories of Hypertension CATEGORY SYSTOLIC DIASTOLIC High normal 130-139 85-89 HYPERTENTION: Stage – 1 140-159 90-99 Stage - 2 160-179 100-109 Stage - 3 > 180 > 110 I S H > 140 < 90 P P H ( pulse pressure > 65 mmHg ) Evaluating Circulation : Evaluating Circulation Measuring blood pressure with sphygmomanometer Korotkoff sounds are heard while taking pressure, absence of sounds taken for diastolic pressure. In case of pregnancy and continued sounds muffling is taken as diastolic pressure. Cuff with should be 40% of a r m circumference, the drop of pressure should be 2mm per second Normal ratio is 3:2:1 -- systolic/diastolic/pulse pressure Factors controlling B P : Factors controlling B P C O = M A P / R so M A P = C O * R If R is constant , C O controls M A P C O is dependent on Bl. Volume, VR, heart muscle and Resistance ( R ) RESISTANCE : 1. Size of Lumen R @ 1/d4 2. Blood Viscosity 3. Length of the Vessels S V R : Total peripheral Resistance of Arterioles, capillaries and venules. Only if Arterioles are controlled it will have major effect on SVR. Vasomotor center in is main regulator of SVR. Factors controlling MAP : Factors controlling MAP Hormonal Regulation of Blood Pressure : Hormonal Regulation of Blood Pressure Renin-angiotensin-aldosterone system decrease in BP or decreased blood flow to kidney release of renin / results in formation angiotensin II systemic vasoconstriction causes release aldosterone (H2O & Na+ reabsorption) Epinephrine & norepinephrine increases heart rate & force of contraction causes vasoconstriction in skin & abdominal organs vasodilation in cardiac & skeletal muscle ADH causes vasoconstriction ANP (atrial natriuretic peptide) lowers BP causes vasodilation & loss of salt and water in the urine Neural Regulation of Blood Pressure : Neural Regulation of Blood Pressure Baroreceptors are important pressure-sensitive sensory neurons that monitor stretching of the walls of blood vessels and the atria. The cardiac sinus reflex is concerned with maintaining normal blood pressure in the brain and is initiated by baroreceptors in the wall of the carotid sinus (Figure 21.13). The aortic reflex is concerned with general systemic blood pressure and is initiated by baroreceptors in the wall of the arch of the aorta or attached to the arch. If blood pressure falls, the baroreceptor reflexes accelerate heart rate, increase force of contraction, and promote vasoconstriction (Figure 21.14). Chemoreceptor Reflexes : Chemoreceptor Reflexes Carotid bodies and aortic bodies detect changes in blood levels of O2, CO2, and H+ (hypoxia, hypercapnia or acidosis ) causes stimulation of cardiovascular center increases sympathetic stimulation to arterioles & veins vasoconstriction and increase in blood pressure Local Regulation of Blood Pressure : Local Regulation of Blood Pressure The ability of a tissue to automatically adjust its own blood flow to match its metabolic demand for supply of O2 and nutrients and removal of wastes is called autoregulation. Local factors cause changes in each capillary bed important for tissues that have major increases in activity (brain, cardiac & skeletal muscle) Local changes in response to physical changes warming & decrease in vascular stretching promotes vasodilation Vasoactive substances released from cells alter vessel diameter (K+, H+, lactic acid, nitric oxide) systemic vessels dilate in response to low levels of O2 pulmonary vessels constrict in response to low levels of O2 Causes : Causes Essential : 90% Renal , Endocrine , Neurogenic Miscellaneous : increased intra vascular volume, P I H, Stress induced, Hypercalcaemia, Alcohol, and Drug use Vasoconstricted Hyp – medical patient with Diastolic bp & >S V R with normal or even low CO, HR Hyperdynamic Hyp – P O Surgical patient with acute systolic bp, widened PP, > CO,HR & SVR Essential hypertension : Essential hypertension Increased S V R with normal CO Marked increase in sympathetic response to stress, eg. Intubation Enhanced response to Vasoconstrictors and vasodilators, because of increased thickening of arterial wall and high ratio of wall thickness to internal diameter. Changes caused by long standing Hypertension : Changes caused by long standing Hypertension CARDIAC : L V H Angina / MI Arrhythmias Congestive failure EYE : fundus: hypertensive retinopathy & arteriosclerotic retinopathy RENAL : Nephropathy CEREBRAL : Stroke / Transient ischemic attacks Perioperative cardiac morbidity : Perioperative cardiac morbidity Mild to Moderate Hypertension does not increase the risk of major morbidity (Goldman et.al.) Hypertension may effect morbidity through the end organ damage, not as disease it self. LVF, may cause ischemia by imbalances in myocardial o2 demand and supply, regardless of coronary artery disease. I S H is identified as risk factor ( Aronson & Fontis ) . Treatment reduces risk of future stroke, renal failure and mortality. 10 mmHg raise in pulse pressure is associated with 20% more risk. Slide 20: In Hypertensive pts. Autoregulation of cerebral flow is set to higher range. But, it is more vulnerable to Hypotension. Chronic renal insufficiency is common sequela. An elevated serum creatinine > 3 mg/dl is one of risk factor for perioperative cadiovascular morbidity. Controlled hypotension : Controlled hypotension Is contra indicated in untreated patients Used with caution in treated patients Clinical guide is 25% decrease in MAP reaches lower limit of Auto regulation Systolic pressure of hypotension should not be lower than pts. usual diastolic pressure Non invasive Cerebral Oximetry (85% of Jvso2 + 15% of Spo2) usually unaltered in anesthesia,unless there is hypoperfusion Diastolic pres is imp particularly in coronary pts. During anesthesia usual emphasis is on Systolic pressure ( dangerous ) Anti Hypertesive Drugs : Anti Hypertesive Drugs DIURETICS : THIAZIDES, LOOPDIURETICS (eg. Furosemide ), K+ Sparing (spiranolactone, triamterene) They may cause: Hypokalemia,Hypomagnesimia, Hyperurecimia, hypercacemia,hyperlipidimia and hyperglycemia. ANTI ADRENERGIC AGENTS: Centrally acting drugs : Clonidine, Dexmeditomidine and Mivazerol (stimulation of alfa2 recep in vasomotor center – reduces sympathetic outflow) Slide 23: Alfa 1&2 blockers : phenoxybenzamine, phentolamine. Alfa 1 blockers : prazocin, doxazocin, these cause fall in peripheral resistance by both arteriolar & venous dilatation. Beta blockers :atenolol, metaprolol, propranolol, pidolol, esmolol. They act by decreasing HR, Contractility, CO and Renin levels. There is no reflex tachycardia or widening of pulse pressure. They also have anti arrhythmic activity. Slide 24: Alfa & Beta blocker : Labetolol Endothelin recptor blocker : Bosenton and sitaxsenton used mainly in pul. Hypertension Direct Vasodilators: Hydralazine, nitroprusside, nitroglycerene and ca+ channel blockers Dopaminergic agonists: DA 1 (fenoldopam – cause Vasodilatation, inhibit active Na+ transport leading to natriuresis. 0.05ug/kg/min.half life is 10 minutes.) DA 2 inhibit norepinephrine release and promote peripheral vasodilatation. Ca+ channel blockers : Ca+ channel blockers They cause mainly peripheral vaso dilatation. Renin, aldosterone secretion is also reduced. Verap diltiazem nifidip nicard HR Condu -- -- Vasodil ACE inhibitors : ACE inhibitors Captopril, Analapril, lisinopril, quinapril, ramipril. They inhibit inactive decapeptide angiotensin-1 to active octapeptide angiotensin-2. ( also decrease aldosterone ) Provide predominantly arterial vaso dilatation and became therapy for CHF by afterload reduction. Angiotensin receptor blockers: ( A R B ) In heart,kidney,bl.vess may be catalysed by other than conv.enzyme – Chymase, this is inhibited only by A R B. These are more effective in treating I S H and P P H. ACE inhibitors and Hypotension : ACE inhibitors and Hypotension In patients on chronic therapy with ACEinhibitors exagerated hypotensive response may occur at induction. Hypotension may be severe in neuroaxial blockade. Can be corrected by administration of alfa agonist. No. of studies shown improve in outcome in continuing anti hypertensives, rather discontinue. Preoperative evaluation : Preoperative evaluation Etiology, Severity, current therapy and the end organ damage. Mortality is high in renovascular hypertension Diuretics cause hypokalemia, hypomagnesim, so evaluate electrolytes. Presence of target organ damage in brain, heart, kidney shows long standing & poorly controlled hypertension. Presence of Asymptomatic carotid bruit increase the incidence of stoke. Pre op evaluation--2 : Pre op evaluation--2 E C G, Chest X-Ray, ECHO. L V H increase the risk of perioperative M I, regardless presence or absence of coronary artery disease. There is high correlation between L V H and ISH and PPH. Severe hypertension pts., are at increased risk for C H F and pul.edema. Cerebral: T I A and hypertensive retinopathy. For Renal : urinalysis, sr.creatinine, bl.urea. If chronic renal failure : hyperkelemia and elevated plasma volume are of concern. When to postpone surgery : When to postpone surgery Elective surgery is delayed in severe cases DIASTOLIC > 110 mmHg., I S H (systolic) > 200 Bring BP below 180 /110, If time permits allow 4-6 weeks and Aim at < 140 / 90 In moderate cases ( < 110 ) with end organ disease : normalize B P as much possible. Patients with mild to moderate disease are not at increased risk , unless they have other risks like coronary disease. (pathological changes are chronic in nature and unlikely to change with therapy) Discontinue medications ? : Discontinue medications ? Current opiniom favours continuation of anti hypertensives , especially beta blockers. Ca+ blockers, Ace inhibitors and Diuretics can be maintained. ACE therapy until the day of surgery may increase probability of hypotension at induction. (easily corrected by ephedrine) Withdrawal of clonidine is associated with rebound hypertension. K+ and Mg+ : K+ and Mg+ Hypokelemia ( 3.0 -3.5 mEq/L ) seen in thiazide therapy. Oral Supplemental K+ for one week, if renal function is not impaired. In emergency, give K+ i.v. not exceeding 0.5mEq / Kg / hr., Administration should be stopped during surgery and restarted p.o checking levels. Hypomagnesemia (<0.75 mEq /L ) can cause : coronary spasm, CHF, dysarrythmias, seizures, confusion and coma. Small i.v doses are used. Observe toxicity : lethargy, weakness and loss of deep tendon reflexes. Pt. With untreated hypertension of 170/100mmHg.would you pre treat preoperatively ? : Pt. With untreated hypertension of 170/100mmHg.would you pre treat preoperatively ? YES. Pre op administration of Clonidine, Beta blockers, ACE inhb has been advocated to reduce hemodynamic liability and MI. Clonidine (central alfa2 agonist) 5ug/Kg orally, 2 Hrs.before surgery, Reduce sympathetic outflow, < catochalamines, < aldosterone and renin activity. Small oral dose of Labetolol / Atenelol pre op Attenuated hemodynamic response and significantly reduced pri op MI ( 2% from 28%) Monitoring : Monitoring ECG : leads V5 and II with s-t analysis Continuous monitoring of BP : usually NIBP is sufficient. Intra arterial beat to beat can be done. Pul Art Cath : for those with CHF or MI useful in managing fluid replacement and ventricular function. Spo2 : peripheral blood flow and oxygen EtCo2 : maintain normocarbia Temparature GOALS OF ANESTHESIA : GOALS OF ANESTHESIA Prevent MI from Tachycardia, less commonly from hypo / hypertension CEREBRAL hypo perfusion, STROKE and encephalopathy ( hypertension ) RENAL FAILURE from hypo perfusion Attention to diastolic BP is imp. (unfortunate clinical practice hinges on systolic BP) paticularly in pts. with ISH / wide PP, where already lower diast pres can reduce further, leading to MI. GOALS… : GOALS… PTS. WITH WIDE PP HAVE INCREASED RISK OF THROMBOGENESIS ( Lee et.al.,) marked by elevated levels of D-dimer, Von willibrand, and platelet activation. Atherosclerotic Disease is common in pts., with ISH : basis for periop Stroke, MI, and Renal dysfunction. Careful Control of hemodynamic response to intubation, surgical incision and manupulation, emergence is essential. INTUBATION : INTUBATION Intubation is associated with tachycardia, hypertension and < EF . This is paricularly marked with coronary disease. This occurs 14 sec. after laryngoscopy and becomes maximum at 30 - 45 sec. PREVENTION: Fentanyl 7-8ug/Kg with pentothal/propofol Lidocaine 1.5mg/Kg, 2 mints before Esmolol 1-2mg/Kg, consistant, effective and short half life of 9 mints. Labetolol 0.2-0.4mg/Kg, minimal effect on HR due to alfa effect, half life is 5Hr., Nicadapine 0.015-0.03mg/Kg HYPOTENSION AFTER INDUCTION : HYPOTENSION AFTER INDUCTION COMBINATION OF VASODILATATION, HYPOVOLEMIA & CARDIAC DEPRESSION You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.