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    by: Jitendra

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    1 : ANAESTHESIA FOR THE PATIENT WITH HYPERTENSION AND HYPERTENSIVE HEART DISEASES Presented by - jitendra Kumar pal Moderator – Dr V. Dhama
    2 : DEFINITION of blood pressure blood pressure is pressure exerted by circulating blood upon the wall of blood vessels. During each heart beat , BP varies between a maximum (systolic) and a minimum (diastolic) BP.
    3 : BLOOD PRESSURE CLASSIFICATION(JNC 7)
    4 : IN PAEDIATRICS AGE GROUP In children's and adolescents HTn is generally defined as systolic and/ or diastolic BP consistently >95th percentile for age, gender and height. BP between the 90th and 95th percentile are considered prehypertensive and are an indication for lifestyle intervention.
    5 : AETIOLOGY OF HYPERTENSION Primary HTn – 95% of cases also termed as “ESSENTIAL” or “IDIOPATHIC” Secondary HTn – about 5% of cases -Renal or renovascular ds. – parenchymal ds. , renal cyst, renal tumors, obstructive uropathy , arteriosclerotic , fibromuscular dysplasia.
    6 : . Endocrine disease – Phaeochromocytoma Cushing syndrome Conn’s syndrome Acromegaly Hypo and hyperthyroidism Hypercalcaemia
    7 : . Coarctation of aorta Neurogenic – Psychogenic Familial dysautonomia Acute porphyries lead poisoning Acute spinal cord section
    8 : . Iatrogenic – Hormonal/OCPs NSAIDs Erythropoietin Cocaine Decongestant Miscellaneous- Pregnancy induced HTn Sleep apnea
    9 : SYSTOLIC HT WITH WIDE PULSE PRESSURE Decreased vascular compliance (arteriosclerosis) Increased cardiac output aortic regurgitation thyrotoxicisis hyperkinetic heart syndrome fever arteriovenous fistula patent ductus arteriosus
    10 : PATHOPHYSIOLOGY OF PRIMARY HT The hemodynamic hallmark of HTn is persistently increased SVR. Water and sodium(Na) retention: -A high Na intake may activate a number of pressure mechanism and causes water retention. Altered renin – angiotensin mechanism: -High plasma renin activity result in increased conversion of angiotensinogen to angiotensin causing arteriolar constriction , vascular hypertrophy and aldosterone secretion.
    11 : . Stress and increased SNS activity: -Arterial pressure is influenced by factor such as anger, fear and pain. -physiologic responses to stress , which are normally protective , may persist to a pathologic degree , resulting in prolonged increase in SNS activity. -Increased SNS stimulation produces increased vasoconstriction, increased HR, and increased renin release.
    12 : . Insulin resistance and hyperinsulinemia: -Abnormalities of glucose , insulin , and lipoprotein metabolism are common in primary HTn. Endothelial cell dysfunction: -Some hypertensive people have a reduced vasodilator response to nitric oxide(NO).NO , an endothelium derived relaxing factor help to maintain low arterial tone at rest , inhibit growth of smooth muscle layer, and inhibit platelet aggregation. Endothelin produces pronounced and prolong vasoconstriction
    13 : FACTORS CONTROLLIG BP CO =MAP/R so MAP = CO* R If R is constant , CO controls MAP CO is dependent on blood volume, Vascular Resistance, heart muscle and résistance(R) Resistance: 1 . Size of lumen R 2 . Blood viscosity SVR: Total peripheral resistance of Arterioles,Capilaries and venules.only if arterioles are controlled it will have major effect on SVR . Vasomotor center are main regulator of SVR.
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    16 : NEURAL REGULATION OF BP Baroreceptors are important pressure sensitive sensory neurons that monitor stretching of the wall of blood vessel and atria. -The cardiac sinus reflex is concerned with maintaining normal BP in brain and is initiated by baroreceptors in the wall of carotid sinus. -the aortic reflex is concerned with general systemic BP and is initiated by baroreceptors in the wall of arch of aorta. If BP falls , the baroreceptors reflex accelerate heart rate , increase force of contraction , and promote vasoconstriction.
    17 : CHEMORECEPTOR REFLEX Carotid body and Aortic bodies -detect change in blood level of O2,CO2, and H+. -Causes stimulation of cardiovascular center -increase sympathetic stimulation to arterioles & veins. -vasoconstriction & increase BP.
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    19 : LOCAL REGULATION OF BP The ability of tissue to automatically adjust its own blood flow to match its metabolic demand or supply of O2 and nutrients and removal of wastes is called AUTOREGULATION.(90-220 mm of hg) Local factors causes change in capillary bed: -important for tissue that have major increases in activity(brain cardiac and skeletal muscle). Local changes in response to physical change: -warming and decreases in vascular stretching promotes vasodilatation Vasoactive substances released from cells alter vessel diameter. -systemic vessels dilate in response to low level of O2 -pulmonary vessels constrict in response to low level of O2
    20 : THE POSSIBILITY OF SECONDRY HTn Young age Family history of renal disease Evidence of renal disease Hypertension due to drugs Episode of sweating headache, anxiety (phaeochromocytoma) Episode of muscle weakness and tetany (hyperalosteronism)
    21 : TARGET ORGAN DAMAGE Heart: LVH/prior MI Prior coronary revascularization Heart Failure Brain: stroke or TIA Dementia CKD Peripheral arterial disease retinopathy
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    23 : APPROACH TO THE PATIENT History; duration previous therapy; response and side effect family history of HTn and CVD dietary & psychosocial history other risk factors evidence of secondary HTn evidence of target organ damage
    24 : . Physical examination pulse BP JVP
    25 : BP MEASUREMENT TECHNIQUES Non invasive & invasive NON INVASIVE- Condition of patient -posture For pt. >65 yrs., diabetic or receiving antihypertensive therapy, check for postural change by taking reading immediately 2 min after pt. stands Sitting pressure are usually adequate for routine follow up pt. should sit quietly with back supported for 5 min. and arm supported at level of heart
    26 : Circumstances No caffeine for preceding hr. No smoking for preceding 15 min. no exogenous adrenergic stimulants Home reading taken under varying circumstances & 24 hr. ambulatory recording may be preferable & more accurate in predicting subsequent CVD
    27 : EQUIPEMENT Cuff size the bladder should encircle & cover 2/3 0f length of arm ; if not, place the bladder over the brachial artery; if bladder is too small, spuriously high reading may result The equipment whether aneroid,mercury,or electronic- should be regularly inspected & validated. For infants use ultra sound equipement,e.g. Doppler method.
    28 : TECHNIQUE Initially take pressure in both arm if pressure differ use arm with higher pressure At least 2 measurement should be made 5 min apart and average is recorded For manual determination palpated radial pulse obliteration pressure should be used to estimate SBP- the cuff should then be inflated 20-30 mm of hg above this level for the auscultatory determination The cuff deflation rate should be 2 mm of hg/sec SBP is the point at which the first of two or more korotkoff sound heard(phase 1) The disappearance of korotkoff sound (phase v)is use to define DBP except in little children in whom phase 4(muffling )is use to define DBP
    29 : INVASIVE BP MEASUREMENT Arterial BP is most accurately measured invasively through an arterial line Invasive arterial BP measurement with intravascular cannula involves direct measurement of arterial pressure by placing cannula needle in an artery (usually radial,femoral,dorsalis pedis & femoral) Cannula must be connected with sterile fluid filled system which is connected to an electronic pressure transducer Advantage of this system is that BP is constantly monitored beat by beat
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    31 : White coat ht(wch) Doctor’s office measurement of BP is higher than their typical BP This type of error is called “white coat HT” This results from anxiety related to an examination by health care professional The misdiagnosis of HT for these pt. can result in needless & possibly harmful medication WCH can be reduced by automated BP measurement
    32 : LABORATORY TESTS & OTHER DIAGNOSTIC PROCEDURES Routine test ECG Microscopic Urinalysis, albumin excretion, serum BUN and/ or creatinine blood glucose & hematocrit Serum sodium , serum potassium ,calcium, ?TSH Lipid profile
    33 : SCREENING TEST FOR IDENTIFIABLE HTn.
    34 : TREATMENT Goals of therapy Lifestyle modification Pharmacological treatment
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    36 : GOAL OF THERAPY Reduce CVD & renal morbidity & mortality Treat to BP <140/90 mm of hg or BP<130/80 mm of hg in pt. with diabetes or chr. Kidney ds. Achieve SBP goal especially in persons > or equal 50 yr. of age
    37 : LIFESTYLE MODIFICATION
    38 : Table 9. Lifestyle modifications to prevent and manage hypertension* Weight reduction Maintain normal body weight 5–20 mmHg/10kg92,93 (body mass index 18.5–24.9 kg/m2). Adopt DASH eating plan Consume a diet rich in fruits, 8–14 mmHg94,95 vegetables, and lowfat dairy products with a reduced content of saturated and total fat. Dietary sodium reduction Reduce dietary sodium intake to no 2–8 mmHg94-96 more than 100 mmol per day (2.4 g sodium or 6 g sodium chloride). Physical activity Engage in regular aerobic physical 4–9 mmHg97-98 activity such as brisk walking (at least 30 min per day, most days of the week). Moderation of alcohol Limit consumption to no more than 2–4 mmHg99 consumption 2 drinks (e.g., 24 oz beer, 10 oz wine, or 3 oz 80-proof whiskey) per day in most men, and to no more than 1 drink per day in women and lighter weight persons. Modification Recommendation Approximate SBP Reduction (Range)† DASH, Dietary Approaches to Stop Hypertension; SBP, systolic blood pressure
    39 : MANAGEMENT OF BP FOR ADULT
    40 : ORAL DRUGS USED IN TT OF HT
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    43 : IV DRUG DOSES OF ANTI HYPERTENSIVE IN HYPERTENSIVE EMERGENCY
    44 : HYPERTENSIVE EMERGENCY & PAENTRAL DRUGES
    45 : HYPERTENSIVE HEART DISEASES Left ventricular hypertrophy Heart failure Diastolic dysfunction CHF Atherosclerotic heart disease and micro vascular disease Cardiac arrhythmias
    46 : LEFT VENTRICULAR HYPERTROPHY(LVH) The common feature of all form of LVH is increased left ventricular mass LVH subclass can be can be characterized -by relative wall thickness -presence or absence of reduced contractility -end diastolic chamber size
    47 : PATHOPHYSIOLOGY OF LVH SYSTOLIC OVERLOAD is the expression of resistance to left ventricular systolic out flow and hence left ventricular systolic contraction LVH due to HTn. Is CONCENTRIC with circumferential hypertrophy of myofibrils Normal or increased contractility Increased relative wall thickness Normal or low end diastolic volumes Impaired relaxation “diastolic dysfunction”
    48 : SYMPTOMS & SING Dyspnea, fatigue, syncope , palpitation cardiomegaly, apical systolic thrill and heave; brisk cardiac upstroke, S4 common , systolic murmur that increases with valsava maneuver
    49 : INVESTIGATION & RISK Routine investigation X – ray chest- show cadiomegaly Echocardiography is much more sensitive than ECG for detection of LVH Individual with LVH are more than twice as like to suffer premature cardiovascular event or death.
    50 : ECG MANIFESTATION IN LVH (SYSTOLIC OVERLOAD) Abnormalities of QRS complex -increased magnitude of QRS deflexions -attenuation of small initial q wave in left oriented leads -An increase in left ventricular activation time -a small equiphasic rs complex in lead AVF -counter-clockwise electrical rotation
    51 : . Abnormalities of S-T segment and T wave T wave vector is directed away from left toward right T wave consequently be inverted in left oriented leads;V5 ,V6 standard lead 1 and AVL T wave is upright in right oriented lead ;V1, V2 and AVR The associated S-T segment in right oriented lead may be minimally elevated with slight upward concavity.
    52 : . Abnormalities of U wave compromised left ventricle may result in inverted U wave in left precordial leads it is not ,however ,specific for left ventricular systolic overload & is indeed more commonly associated with left ventricular diastolic overload
    53 : . Left atrial enlargement wide notched P wave in standard lead 1,prominent delayed deflexion of P wave in lead V1 constitute contributory or corroborative evidence of presence of potential LVH This is useful pointer to potential LVH in presence of LBBB
    54 : . Abnormalities of QRS & T wave axis long standing systemic HTn QRS axis is commonly directed to 0 degree whereas the T wave axis is commonly directed to +_ 180 degree
    55 : THE ROMHILT & ESTES POINT SCORE SYSTEM(FOR EVALUATION OF LVH) A score 5 or more indicate left ventricular hypertrophy
    56 : Anesthetic management of ht Aims – confirm diagnosis - effect of HT on organs( invx. ) - review of drug tt.(side effects) - anesthetic plan
    57 : Confirm diagnosis First confirm that the HT actually exist Pt. may be anxious , fearful , in pain or rushed during initial evaluation We determine this by putting the pt. at ease with reassurance and calm environment Reliving pain Allowing a period to pass then repeat BP measurement Long term BP may be determine by pt. medical record
    58 : Preoperative evaluation Determine of adequacy of BP control Hypertensive pt. should be made normotensive prior to elective surgery The incidence of hypotension and MI during maintenance of anesthesia is increased in pt. who are hypertensive prior to induction of anesthesia Intraoperative increases in BP commonly occurs in pt. with h/o HT; whether or not the BP is controlled preoperatively
    59 : . Co-existing HT may increases the incidence of postoperative reinfarction with h/o MI The pt. with anxiety related HT are likely to have exaggerated pressure response to direct laryngoscopy.
    60 : Review drug treatment to control bp Review pharmacology & potential side effect of drug used for antihypertensive therapy many of these drug interfere with ANS function preoperatively this may manifest orthostatic hypotension During anesthesia exaggerated fluctuation in BP seen with blood loss, positive pressure ventilation or sudden change in body position this reflect impaired vascular compensation due to autonomic inhibitory effect
    61 : . Administration of vasopressure such as phenylephrine & ephedrine result in appropriate & predictable BP response in these pt. Bradycardia may be manifestation of selective alteration of SNS activity Exaggerated bradycardia could occur when drug that normally increases PNS (aticholinestrase )
    62 : . Decrease anesthetic requirement parallel the sedative effect produced by clonidine Hypokalemia(<3.5 meq/l) despite potassium supplementation is common in pt. with diuretics Hyperkalemia seen in pt. treated with ACEI
    63 : ACE INHIBITORS Risk of hemodynamic instability & hypotension will occur during anesthesia attenuating the vasoconstrictor effect of angiotensin on capacitance vessels this will result in - decreases venous return -decreases CO Maintenance of intravascular fluid volume is crucial during surgery Discus with seniors to continue or discontinue ACEI prior to surgery
    64 : Angiotensin receptor antagonists Effectively treat HT by preventing binding of angiotensin 2 to angiotensin receptors ARB increases potential of hypotension during anesthesia Hypotension require vasoconstrictor tt ;occur more often after induction of anesthesia Hypotension may be refractory to conventional vasoconstrictor(ephedrine & phenylephrine)necessitating use of vasopressin or analog ARB discontinue before day of surgery
    65 : End organ damage Should evaluate preoperatively Heart: LVH/prior MI Prior coronary revascularization Heart Failure Brain: stroke or TIA Dementia CKD Peripheral arterial disease Retinopathy
    66 : . Pt. exhibit sign of end organ damage postponement of elective procedure is justified if that end organ damage can be improved or if further evaluation of that damage could alter the anesthetic plan
    67 : Plan of anesthesia Plan for hypertensive pt. is to maintain an appropriate stable BP range Those with long standing or poorly controlled BP,however,have altered auto regulation of cerebral blood flow; higher than normal mean BP may be required to maintain adequate cerebral blood flow Arterial BP should generally be kept within 20% of preoperative level
    68 : premedication Premedication reduces preoperative anxiety & is highly desirable in hypertensive pt. Mild to moderate HT often resolve following administration of anxiolytic agent Preoperative antihypertensive agent should be continued, can given with small sip of water Central alpha 2 adrenergic agonist (clonidine 0.2 mg)can be useful adjuncts for premedication
    69 : Intraoperative management MONITORING Most hypertensive pt. do not require any special intraoperative monitors Invasive BP monitoring should reserved for pt. with wide swing in BP & for those undergoing major surgical procedure associated with rapid or marked change in cardiac pre & after load ECG monitoring should focus on detecting signs of ischemia Urine output with indwelling catheter in pt. with renal impairment or duration of surgery is >2 hr.
    70 : induction Induction & intubation are often period of hemodynamic instability for hypertensive pt. Many hypertensive pt. display an accentuated hypotensive response induction of anesthesia, followed by exaggerated hypertensive response to intubation The laryngoscopy, should short , smooth & gentle Intubation should performed under deep anesthesia
    71 : . Techniques may be used before intubation to attenuate hypertensive response; -deepening anesthesia with potent volatile agent -administering bolus of an opioid (fentanyl 2.5-5mmg/kg; alfentanyl 15-25 mmg/kg; sufentanyl o.25-0.5 mmg/kg ; or ramifentanyl 0.5-1mmg/kg) -administering lidocaine 1.5 mg/kg IV OR intratracheally Achieving beta adrenergic blocked with esmolol 0.3-1.5 mg/kg; propranolol 1-3 mg; or labetalol 5-10 mg Using topical airway anesthesia
    72 : . Induction agents propofol , barbiturates, benzodiazepines and etomidates are equally safe for induction of Gain hypertensive pt. ketamine may be use in hypertensive by blunting its sympathetic stimulation activity by other agents
    73 : . Maintenance agents anesthesia may be safely continued with volatile agent a balanced technique( opioids + nitrous oxide + muscle relaxant) by total intravenous anesthesia Opioids sufentanyl may provide greater autonomic suppression & control over BP
    74 : . Muscle relaxant any neuromuscular blocking agent can use except pancuronium hypotension following large doses of tubocurarine metocurine,atracurium or mivacurium may accentuated in hypertensive pt.
    75 : . Vasopressure if use is necessary direct acting agent (phenylephrine 25-50mmg) may be preferable to indirect acting agent Small dose of ephedrine (5-10 mg) are more appropriate when vagal tone is high
    76 : CAUSEA OF INTRAOPERATIVE ht Pre existing undiagnosed HT uncontrolled HT withdrawal of antihypertensive
    77 : . Increased sympathetic tone inadequate analgesia inadequate anesthesia hypoxaemia airway manipulation hypercapnia
    78 : . Drug over dose vasoconstrictor inotropes ketamine ergometrine
    79 : . Others hypervolaemia aortic cross clamping phaeochromocytoma malignant hyperthermia
    80 : IV ANTIHYPERTENSIVE DRUG Sodium nitroprusside 0.25–10µg/kg/min IV infusion†(maximum dose for 10 min only) Use in most hypertensive emergencies Nausea, vomiting, agitation, muscle twitching, sweating, cutis anserina (if BP is reduced too rapidly), thiocyanate and cyanide toxicity Should be used cautiously in patients with high intracranial pressure or azotemia
    81 : . Nicardipine  5–15 mg/h IV Most hypertensive emergencies, except acute heart failure Tachycardia, headache, flushing, local phlebitis Should be used cautiously in patients with myocardial ischemia
    82 : . Fenoldopam 0.1–0.3 µg/kg/min IV infusion; maximum dose 1.6µg/kg/min Most hypertensive emergencies, except acute heart failure Tachycardia, headache, nausea, flushing, hypokalemia, elevation of intraocular pressure in patients with glaucoma Should be used cautiously in patients with myocardial ischemia
    83 : . Nitroglycerin 5–100 µg/min IV infusion† Headache, tachycardia, nausea, vomiting, apprehension, restlessness, muscular twitching, palpitations, methemoglobinemia, tolerance with prolonged use Myocardial ischemia, heart failure
    84 : . Enalaprilat 0.625–5 mg q 6 h IV Acute left ventricular failure Precipitous fall in BP in high- renin states, variable response Should be avoided in acute MI
    85 : . Hydralazine 10–40 mg IV 10–20 mg IM Tachycardia, flushing, headache, vomiting, aggravation of angina Eclampsia
    86 : . Labetalol  20 mg IV bolus over 2 min, followed q 10 min by 40 mg, then up to 3 doses of 80 mg; or 0.5–2 mg/min IV infusion Most hypertensive emergencies, except acute left ventricular failure Vomiting, scalp tingling, burning in throat, dizziness, nausea, heart block, orthostatic hypotension Should be avoided in patients with asthma
    87 : . Esmolol  250–500µg/kg/min for 1 min, then 50–100µg/kg/min for 4 min; may repeat sequence Hypotension, nausea Aortic dissection perioperative
    88 : . Phentolamine 5–15 mg IV Tachycardia, flushing, headache Catecholamine excess
    89 : Postoperative ht Post operative HT is common & typically occur within first 30 min. Noxious stimulation from incisional pain , intubation, or bladder distention is usually responsible May reflect sympathetic activity Neuroendocrine response to surgery or secondary to hypoxemia hypercapnia or metabolic acidosis Pt. with h/o HT
    90 : TREATMENT Mild HT generally dose not require tt. Marked HT can precipitate postoperative bleeding , MI, heart failure, intracranial hemorrhage BP >20-30% of pt. baseline or associated with adverse effect should be treated. Mild to moderate elevation is treated with iv BB,CCB or nitroglycerin Sublingual nifedipine & hydralazine are also effective
    91 : . Marked hypertension is treated with intra venous infusion of nitroprusside nitroglycerin nicardipine fenoldopam
    92 : Thank you

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