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hypertension anesthesia, general management. antihypertensive pharmacology

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hypertension anesthesia, general management. antihypertensive pharmacology

  1. 1. ABAYNEH BELIHU AKSUM UNIVERESITY FEB 2016
  2. 2. “ ” Hypertension
  3. 3. OUTLINES  RAS physiology  Definition and classification of hypertension  Overview of general management  Non pharmacologic  Pharmacologic  Drug interaction  Anesthesia management  Preoperative hypertension  Intraoperative hypertension  Intraoperative monitoring  Postoperative hypertension
  4. 4. SIGNIFICANCE OF THE TOPIC FOR ANESTHETISTS 1  Familiarity with the names and MOA of antihtensive agents is important for anesthetists.  The interaction of anesthesia drugs and adjuvants with antihypertensive agents should be born in mind
  5. 5. SIGNIFICANCE OF THE TOPIC FOR ANESTHETISTS 2  Hypertension occurs commonly during anaesthesia and is usually promptly and appropriately treated.  Its recognition is dependent on correctly functioning and calibrated monitors.
  6. 6. SIGNIFICANCE OF THE TOPIC FOR ANESTHETISTS 3  Intraop hypertension is common and has many causes.  However, when it is  Severe  No cause is evident or  Fails to respond to routine measures, it has the potential to cause morbidity and even mortality in susceptible patients. (Reich et al)
  7. 7. SIGNIFICANCE OF THE TOPIC FOR ANESTHETISTS 4 Among 4000 clients there were 252 in which hypertension was mentioned,  11 dealt with hypertension occurring only in recovery,  10 reported hypertension 2⁰ laryngoscopy and ETI, and  3 involved as a consequence of poorly controlled preoperative HTN. (A D Paix et al)
  8. 8. SIGNIFICANCE OF THE TOPIC FOR ANESTHETISTS 5  Major morbidity occurred in six patients and consisted of two reports each of MI, pulmonary oedema and awareness under general anaesthesia.  Hypertension and tachycardia under anaesthesia have been shown to be independent risk factors for poor outcomes, particularly after long procedures.(Reich DL et al.)
  9. 9. IMPORTANCE OF KNOWING COMMON ANTIHYPERTENSIVE DRUGS 1 Because Antihypertensive drugs result in: 1. ↓peripheral vascular tone…interfere with circulatory homeostasis 2. Difficulty compensation for stresses: Blood loss, ∆posture, IPPV. 3. Bad reaction to drugs such as thiopentone which can cause a fall in BP. 4. Electrolyte imbalance related to Prolonged diuretic therapy 9
  10. 10. IMPORTANCE OF KNOWING COMMON ANTIHYPERTENSIVE DRUGS 2 And thus…… Electrolyte profile must be checked pre-operatively (esp. K+). Antihtnsive drugs have to be continued till morning of surgery. If heavy bleeding is expected, Enalapril has to be discontinued. Patients on loop diuretics has to have e¯ determined.
  11. 11. Renal function Blood volume Venous tone Venous return Heart rate Nervous control Muscular responsiveness Myocardial contractility Stroke volume Cardiac output CNS factors Renin release Angiontensin II formation Intrinsic vascular responsiveness Peripheral resistance Nervous control Renal function MAP Factors that Govern the Mean Arterial Pressure
  12. 12. Mean Arterial Pressure MAP = CO X CO = HR SV PVR Myogenic tone Vascular responsiveness Nervous control Vasoactive metabolites Endothelial factors Circulating hormones XSNS Venous tone BV Contactility
  13. 13. Mechanisms Controlling CO and TPR Artery Vein 2. Hormonal  Renal Ang II  Adrenal CA Aldosterone 3. Local Factors Endothelial agents ABG Concn 1. Neural  SymNS  PSNS CRITICAL POINTS! 1. These organ systems and mechanisms control physical factors of CO and TPR 2. Therefore, they are the targets of antihypertensive therapy.
  14. 14. Response mediated by the RAAS & sympathetic system on BP
  15. 15. SO WHAT IS HYPERTENSION? Hypertension is defined as SBP >140 mmHg, DBP>90 mmHg, or taking antihypertensive medication. VI JNC, 1997
  16. 16. JNC 8 HAS ALSO ARRIVED http://jama.jamanetwork.com/article.aspx?articl eid=1791497
  17. 17. PROPOSED DEFINITION OF WG- ASH, 2005  Writing Group of American Society of Hypertension (WG-ASH)  Based on the view of hypertension as a complex CV disorder rather than as just BP values.  Incorporates the presence or absence of  Risk factors,  Early disease markers, and  Target-organ damage
  18. 18. GOAL OF THE REVISION A.To identify individuals at any BP level who have a reasonable likelihood of future CV events. OR A.To identify people with low BP levels as having Stage 1 hypertension if they also exhibit early signs of vascular damage, thus prompting HCPs to offer treatment to this at-risk group
  19. 19. Their explanation is that… “Physician, responding to a patient's elevated BP in isolation represents only a partial understanding of hypertension rather is associated with many measurable CV indicators beyond BP "
  20. 20. STAGES OF HYPERTENSION HF Angina Post-MI Extensive CAD DM CRF Recurrent stroke prevention
  21. 21. CLASSIFICATION FOR ADULTS Adapted from: Archives Int. Med. 157:2413-2446 (1997) Category Systolic (mm Hg) Diastolic (mm Hg) Optimal BP < 120 And < 80 Normal BP < 130 And < 85 High-normal BP 130 – 139 Or 85 - 89 Stage 1 (mild) 140 – 159 Or 90 - 99 Stage 2 (moderate) 160 – 179 Or 100 - 109 Stage 3 (severe) ≥180 or ≥110
  22. 22. TYPES OF HYPERTENSION ESSENTIAL SECONDARY DISORDER OF UNKNOWN ORIGIN AFFECTING THE BP REGULATION SECONDARY TO OTHER DISEASE PROCESSES ENVIRONMENTAL FACTORS STRESS Na+/ INTAKE OBESITY SMOKING **********************************************************************************
  23. 23. DISEASES ATTRIBUTABLE TO HTN HYPERTENSION Gangreneof the Lower Extremities Heart Failure Left Ventricular Hypertrophy Myocardial Infarction CoronaryHeart DiseaseAorticAneurym Blindness ChronicKidney Failure Stroke Preeclampsia Eclampsia CerebralHemorrhage Hypertensive encephalopathy AdaptedfromDustanHPetal.ArchInternMed. 1996;156:1926-1935
  24. 24. TREATMENT – WHY? 1 Symptomatic treatment is mandatory because it can result in: I. Damage to the vascular epithelium, paving the path for atherosclerosis (IHD, CVA) II. Nephropathy due to high intra-glomerular pressure III. Increased load on heart due to high BP CHF
  25. 25. TREATMENT – WHY? 2 IV.Pre-existing hypertension, particularly if untreated, increases the likelihood of intraop hypertension and of complications (Prys-Roberts et al)
  26. 26. Pertinent complications of untreated HTN
  27. 27. GOALS OF THERAPY A. Reduce Cardiac and renal morbidity and mortality. B. Treat to <140/90 mmHg or BP <130/80 mmHg in patients with DM or chronic kidney disease. C. Achieve SBP goal especially in persons > 50 yr.
  28. 28. NON PHARMACOLOGICAL TREATMENT 1 Avoid harmful habits ,smoking ,alcohol Reduce salt and high fat diets Loose weight , if obese Regular exercise DASH
  29. 29. NON PHARMACOLOGIC TREATMENT 2 MODIFICATION APPROX. SBP REDUCTION Weight reduction 5 – 20 mm of hg /10 kg lost Adopt DASH eating plan 8 – 14 mm of hg Dietary sodium reduction 2 – 8 mm of hg Physical activity 4 – 9 mm of hg Moderation of alcohol consumption 2 – 4 mm of hg
  30. 30. PHARMACOLOGIC TREATMENT 1
  31. 31. PHARMACOLOGIC TREATMENT 2 Drug therapy reduces:  The progression of hypertension, and  The incidence of:  stroke  CHF  CAD, and  Renal damage with reversal of pathophysiologic changes , such as LVH and altered CAR.
  32. 32. PHARMACOLOGIC TREATMENT 3  Most patients with mild hypertension require only single-drug therapy, thiazide diuretic, ACEI, ARB, ßAB, or CCB.
  33. 33. PHARMACOLOGIC TREATMENT 4 A. Primary (essential hypertension) vs. secondary (10-15%) E.g.pheochromocytoma, renal artery constriction, Cushing’s syndrome B. Diagnosis (based on 3 separate office visits) and severity C. Individualization (age, gender, ethnicity) and compliance D. Pre-existing risk factors and medical conditions E. Smoking, Hyperlipidemia, DM, CHF, Asthma, current medication F. Monotherapy vs. Polypharmacy Factors to consider
  34. 34. CLASSES OF DRUGS AND TARGET SITES DRUGS Targets  Diuretics  Agents acting on ANS  Direct Vasodilators CCB  RAAS blockers  Blood Volume  Cardiac Output  Resistance of Vessel  Arterioles  RAAS  Neuroregulation
  35. 35. Sites of action of antihypertensives
  36. 36. Mechanisms of action of antihypertensives
  37. 37. DIURETICS 1 Bumetanide, furosemide, hydrochlorothiazide, spironolactone, triamterene  Act by decreasing blood volume and CO  Decrease PVR during chronic therapy  Drugs of choice in elderly hypertensive
  38. 38. DIURETICS 2: MECHANISM OF ACTION  Lower BP by depleting body Na+ stores.  Effects take 2 stages: 1. Reduction of TBV and therefore CO; initially causes increase of PVR, and 2. When CO returns to normal level (usu. 6-8 wks), PVR declines.
  39. 39. DIURETICS 3: NEPHRON ANATOMY & SITE OF ACTION
  40. 40. DIURETICS 4  Thiazides, such as HCT, act on DCT and inhibit Na+-Cl– symport  Counteract the Na+ & H2O retention effect of hydralazine (direct vasodilator), and thus suitable for combined use.  Thiazides are particularly useful for elderly patients, but not effective when kidney function is inadequate.
  41. 41. DIURETICS 6  Use carefully and monitor serum K+ level in patients with cardiac arrhythmias and when digitalis is in use.  Loop diuretics, such as furosemide and bumetanide, are more powerful than thiazides.  For severe HTN when direct vasodilators are administered and Na+ and H2O retention becomes a problem.  In patients with poor renal function and those not respond to thiazides.  Loop diuretics increase urine Ca2+ content.
  42. 42. DIURETICS 7 K-sparing diuretics include:  triamterene, amiloride (both Na+ channel inhibitors) and  spironolactone (aldosterone antagonist).  In patients given digitalis  Enhance natriuretic effects of others (e.g., thiazides) and counteract the K+ -depleting effect of these diuretics.
  43. 43. DIURETICS 7: ADVERSE EFFECTS AND TOXICITY (1)Depletion of K+(except K+-sparing) (2)Increase uric acid concn and precipitate gout (3)Increase serum lipid concen (not used in pts with hyperlipidemia or DM) Hypokalemia
  44. 44. SYMPATHOPLEGIC AGENTS 1. Centrally-acting adrenergic drugs (α2-agonists such as clonidine and α-methyldopa). 2. Drugs that act on PNS (β & α1-blockers; ganglion blocking agents; agents that block adrenergic NT synthesis and/or release)
  45. 45. CENTRALLY-ACTING ANTIHYPERTENSIVE AGENTS Clonidine reduces sympathetic and increases PS tone, leading to BP lowering and bradycardia.
  46. 46. MECHANISM OF ACTION Binds α2-AR with higher affinity than α1-AR  The α2-agonistic - BP-lowering effect due to negative feedback at the presynaptic neurons  When given IV induces a brief rise of BP, followed by prolonged hypotension.
  47. 47. THERAPEUTIC USE  Reduces CO due to HR and relaxation of capacitance vessels  For mild to moderate hypertension, often together with diuretics  Because it decreases renal vascular resistance, it maintains RBF and glomerular filtration.
  48. 48. CAUTION!  Abrupt withdrawal may induce hypertensive crisis  Do not give to patients who are at risk of mental depression, or are taking tricyclic antidepressants
  49. 49. METHYLDOPA A prodrug that exerts its antihypertensive action via an active metabolite
  50. 50. MECHANISM OF ACTION The metabolite, α-methyl-norepinephrine, is stored in neurosecretory vesicle in place of NE. When released, α-methyl-NE is a potent α-AR agonist and in PNS is a vasoconstrictor. Its CNS effect is mediated by α2-AR, resulting in reduced adrenergic outflow and an overall reduced TPR.
  51. 51. THERAPEUTIC USE Does not alter most of the CV reflexes CO and BF to vital organs are maintained Reduces renal vascular resistance and safer in patients with renal insufficiency Not used as first drug in monotherapy, but effective when used with diuretics.
  52. 52. DRUGS THAT ACT ON PNS 1. β-blockers  Propranolol, metoprolol, nadolol,carteolol, atenolol, betaxolol,bisoprolol,pindolol, acebutolol, penbutolol, labetalol, carvedilol.
  53. 53. MECHANISM OF ACTION 1. Reduces CO 2. Inhibits renin release and AT-II and aldosterone production, and lower peripheral resistance 3. May decrease adrenergic outflow from the CNS
  54. 54. THERAPEUTIC USE  Recommended as first-line  Commonly in combination with diuretics  More effective in white than black patients, and in young patients than elderly (due to high occurrence of chronic lung and heart diseases in the elderly).  Safe in patients with preexisting conditions such as previous MI, AP, Migraine Headache
  55. 55. PROPRANOLOL  Prototype β-blocker  Antagonizes β1 and β2 AR  Inhibits renin production (β1-antagonistic activity) and used in patients with high renin level  No prominent postural hypotension in mild to moderate hypertension patients
  56. 56. METOPROLOL  Much less β2-antagonistic than propranolol, thus can be used in patients who also suffer from asthma, DM, or peripheral vascular diseases.
  57. 57. PINDOLOL, ACEBUTOLOL, PENBUTOLOL  Antagonistic effect is combined with partial agonistic effect on β2-AR.  Particularly for patients with cardiac failure, bradyarrhythmias, or peripheral vascular disease
  58. 58. LABETALOL, CARVEDILOL  Given as racemic mixture of isomeric compounds  Labetalol also has some β2-agonistic effects.  Labetalol-Hypertensive emergencies (injection) or hypertension resulting from pheochromocytoma  Carvedilol- in patients with CHF
  59. 59. ∝-1 BLOCKERS  Prazosin, tetrazosin, doxazosin, phentolamine, phenoxybenzamine.
  60. 60. MECHANISM OF ACTION:  Phentolamine is antagonist for both α1 and α2-AR.  Phenoxybenzamine- irreversible blocker for α1 and α2-AR  Blocking α1-AR leads to relaxation of both arterial and venous smooth muscles and thereby reduces PVR.
  61. 61. THERAPEUTIC USE  Prazosin- for mild to moderate hypertension  Combined use + propranolol or diuretics- additive effects  Long-term use is not likely to cause significant changes in CO and RBF.  Thus less likelihood to have tachycardia and increased renin release for long-term users  Phentolamine and phenoxybenzamine – for Pheochromocytoma
  62. 62. DIRECT VASODILATORS  Hydralazine, minoxidil, sodium NP, diazoxide
  63. 63. MECHANISM OF ACTION  Relax smooth muscle (SM) of arterioles (and sometimes veins), thereby reduce SVR.
  64. 64. THERAPEUTIC USE Hydralazine  Dilates arterioles but not veins.  Effect does not last long when used alone; but combination therapy can be very effective for even severe hypertension.
  65. 65. MINOXIDIL  Opens K+ channels in SM by its active metabolite, minoxidil sulfate, and stabilizes membrane at its resting potential  For patients with renal failure and severe hypertension, who do not respond well to hydralazine
  66. 66. SODIUM NITROPRUSSIDE  Parenterally administered (IV)  Powerful vasodilator hypertensive emergencies  Works by increasing intracellular cGMP and dilates both arterial and venous vessels  In patients with cardiac failure because CO increases due to afterload reduction  Effects last only <10 minutes after discontinuation
  67. 67. DIAZOXIDE  Stimulates opening of K+ channels and stabilizes membrane potential at resting level  A long-lasting antihypertesive agent (effective from 4-12 h, with half-life of 24 h).  For treating hypertensive emergencies (IV).
  68. 68. CALCIUM CHANNEL BLOCKERS  verapamil, diltiazem, dihydropyridine family (eg, nifedipine).  In addition to antianginal and antiarrhythmic effects, dilate peripheral arterioles and reduce BP by inhibiting calcium influx into arterial SM cells.  verapamil has more cardiac effect (decreasing CO) and nifedipine has more vasodilating effect.
  69. 69. ADVERSE EFFECTS AND TOXICITY  Cardiac: tachycardia, palpitation, angina.  Excessive hypotension- diazoxide.  Diazoxide also retains sodium and water.  Accumulation of cyanide, metabolic acidosis have been observed with patients using sodium nitroprusside.  Minoxidil causes hypertrichosis (hair growing), an effect now used for correction of baldness.
  70. 70. ACEI Captopril, enalapril (lisinopril is a lysine-derivative), benazepril, fosinopril,moexipril,quinaprilandramipril
  71. 71. MECHANISM OF ACTION 1 (1) Directly block the formation of AT-II, (2) At the same time increase bradykinin level. (3) The net results are reduced vasoconstriction, reduced Na+ and H2O retention, and increased vasodilation (through bradykinin).
  72. 72. MECHANISM OF ACTION 2  Captopril and other ACEIs are competitive inhibitors of ACE  Mimicking the structure of its substrate.  Captopril and lisinopril are active molecules  Others listed above are prodrugs that need to be converted to active metabolites (di acids) for functions
  73. 73. MECHANISM OF ACTION 3
  74. 74. THERAPEUTIC USE  Primarily when the first-line diuretics or β-blockers are ineffective or contraindicated.  Most effective in white and young; this d/ce diminishes when used together with diuretics  More effective in patients with higher renin level  Commonly in pts following MI, and in patients with CHF
  75. 75. ADVERSE EFFECTS AND TOXICITY  In hypovolemic patients, severe hypotension may occur after initial doses  Fetotoxic and should not be used in pregnant  Contraindication: spironolactone (K-sparing diuretics).
  76. 76. ANGIOTENSIN-II ANTAGONISTS Losartan,valsartan,candesartan,irbesartan,telmisartan,eprosartan,andzolasartan.  Saralasin- orally ineffective and requires continuous IV infusion.  Saralasin has partial agonist activity, and is not currently in use for hypertension treatment.
  77. 77. MECHANISM OF ACTION  Competitive inhibition of AT-II receptor (Type 1)  Effect is more specific on AT-II action, and less or none on bradykinin production or metabolism.
  78. 78. THERAPEUTIC USE  losartan has the advantage of not causing cough and angioedema, which are effects of bradykinin.
  79. 79. ADVERSE EFFECTS AND TOXICITY  Similar to those of ACEIs  Fetotoxic and should not be used for treating hypertension in pregnant women.
  80. 80. LOGICAL COMBINATIONS Diuretic b- blocker CCB ACEI a- blocker Diuretic -  -   b-blocker  - * -  CCB - * -   ACEI  -  -  a-blocker     - * VERAPAMIL + BETA-BLOCKER = ABSOLUTE CONTRA-INDICATION
  81. 81. HYPERTENSIVE EMERGENCY & PARENTRAL DRUGS
  82. 82. RECOMMENDATION 1  ACEI is considered an optimal first-line choice for patients with LVD or HF,  ACEI or ARB is considered an optimal initial single agent in the setting of hyperlipidemia, CRD, or DM (particularly with nephropathy).
  83. 83. RECOMMENDATION 2  ßB or, less commonly, CCB-as a first-line agent for patients with CAD.  ACEIs, ARBs, and ßAB - less effective than diuretics and CCB in black patients.
  84. 84. RECOMMENDATION 3  A diuretic with adrenergic blockade or CCB alone for elderly patients.  Patients with moderate to severe HTN require a second or third drug.
  85. 85. RECOMMENDATION 4  Diuretics often to supplement ßAB and ACEIs when single-drug therapy is ineffective.  ACEIs have been shown to prolong survival in CHF or LVD patients.  In addition, appear to preserve renal function in patients with DM or underlying renal disease.
  86. 86. RECOMMENDATION 5  The Joint National Committee on Hypertension (USA) recommends low doses of a thiazide diuretic for most patients.  However, concomitant illnesses should influence drug selection. -AP-D+BB+ACEI+CCB -DM-D+BB+ACEI+ARB+CCB -HF=D+BB+ACEI+ARB -PMI=BB+ACEI+ARb -CRD=ACEI+ARB
  87. 87. DRUG INTERACTIONS IN ANAESTHESIA: CHRONIC ANTIHYPERTENSIVE THERAPY Three factors have combined need for the anaesthetist to be aware of potential drug interactions involving chronic antihypertensive therapy.
  88. 88. THE THREE FACTORS 1. Emphasis on early recognition and treatment of hypertensives, with the result that more patients are receiving antihypertensives. 2. Introduction of a wide variety of potent medications. 3. Most antihypertensive agents should be continued up to and including the day of surgery and in some instances should be administered during the anaesthetic.
  89. 89. SPECTRUM OF DRUG THERAPY  Drugs employed range from the sedative/hypnotics and tranquilizers to agents with specific and direct cardiovascular activity.  Combination therapy, involving either drugs within the same therapeutic group or different groups has become common.
  90. 90. ANAESTHETIC IMPLICATIONS 1 Implications fall into two categories A. Interference with homeostatic mechanisms necessary to maintain perioperative CV stability B. Actual direct interactions or potential interactions
  91. 91. ANAESTHETIC IMPLICATIONS 2  Responses to:  CV depressant drugs  blood and fluid losses  positioning, and  PPV requires an intact SNS with a responsive heart and peripheral vasculature.
  92. 92. DIURETICS 1  The acute effects include a decrease in ECF and CO with an accompanying increase in SVR.  With time, and maintenance of a natiuresis, the BV returns normal and the remaining effect is decreased vascular resistance. (Prys-Roberts C.)
  93. 93. DIURETICS 2  With the exception of agents acting on the distal tubule, which have the potential to produce hyperkalemia, other diuretics tend to produce hypokalemia.  Chronic hypokelamia is normally well tolerated  Circumstances during anaesthesia and surgery may tend to superimpose an acute reduction in extracellular potassium.
  94. 94. DIURETICS 3  Such circumstances include the rapid intracellular shifts produced by respiratory alkalosis or glucose administration as well as acute loss of potassium from the body due to administration of diuretics such as mannitol or acetazolamide.
  95. 95. DRUGS INFLUENCING ADRENERGIC TRANSMISSION  In order to understand the actions and potential interactions of drugs within this classification, it is necessary to review the physiology of the sympathetic nervous system.
  96. 96. ADRENERGIC NEURON INHIBITORS 1  Reserpine, when used in large doses as a major tranquilizer or as an antihypertensive, has the potential to produce significant and refractory hypotension during anaesthesia.  However, in very small doses, and usually in combination with other antihypertensive agents, greatly reduces the potential for drug interactions.
  97. 97. ADRENERGIC NEURON INHIBITORS 2  Debrisoquine, has MAO inhibitory effects.  The product information for debrisoquine contains: "To avoid the possibility of vascular collapse, discontinue debrisoquine 24 hours prior to elective surgery."  Clinical experience suggests that debrisoquine can be safely continued until time of surgery.
  98. 98. ADRENERGIC NEURON INHIBITORS 3  Possibility of rebound HTN following abrupt withdrawal of clonidine.  This can be avoided by continuation of the agent up to the time of surgery and its early resumption  Or, alternately, substitution of another agent several days before surgery.
  99. 99. BETA ADRENERGIC RECEPTOR ANTAGONISTS 1  Potential of beta blockers (propanolol) to produce myocardial depression when used in combination with IAA  Slogoff S. et al concluded that BB should be continued up to the time of surgery and possibly during surgery and recommended the use of BB friendly IAA like isoflurane, enflurane, halothane in carefully adjusted, reduced doses.
  100. 100. BETA ADRENERGIC RECEPTOR ANTAGONISTS 12  Withdrawal syndrome associated with abrupt cessation of BB is in part related to the time course of elimination, the time available for adjustment and the induction of new beta receptors.  Therefore, most frequent in patients receiving agents with a short half-life (e.g., propranolol) and less common with agents with longer half-lives (e.g., nadolol).
  101. 101. VASODILATORS  This category includes:  drugs with direct muscle relaxing properties,  post- synaptic alpha 1 adrenergic antagonists, and  calcium channel blocking agents.  The greatest potential for drug interactions in anaesthesia appears to be associated with the CCB.  Although few clinical reports of such interactions have appeared, laboratory investigation has identified potential interactions with IAA, myocardial depressants, and NMBA.
  102. 102. TO CONCLUDE… 1. The perioperative period, and most particularly the anaesthetic itself, creates an interface b/n chronic and acute drug therapy. 2. As the primary managers of this interface, anaesthetists must be aware of the actions and interactions of varied and complex medications. 3. Antihypertensive agents present a significant potential for drug interactions during anesthesia. 4. With the exception of MAOI, antihypertensive should be continued up to the time of surgery 5. Safe anaesthetic management requires anticipation of drug interactions, recognition of their effects, and knowledge of appropriate corrective therapy.
  103. 103. ANAESTHESIA MANAGEMENT OF HYPERTENSIVE PATIENTS
  104. 104. WHY ANAESTHETIST CARE ABOUT HYPERTENSION? Because hypertension is common (from 1,001 patients undergoing non cardiac operations, preoperative evaluation detected 280 with current or past elevated BP (Goldman et al)) and results in: CVD End organ damage – Heart, Brain & Kidney Alteration in cerebral & renal blood flow
  105. 105. GOALS OF ANESTHESIA MANAGEMENT A. Preoperative consideration and evaluation B. Perioperative risk reduction C. Premedication D. Balanced anesthesia E. Proper monitoring F. Parenteral medications
  106. 106. PERIOPERATIVE RISK REDUCTION 2  Htn is a leading cause of death and disability in most Western societies and the most frequent preoperative abnormality in surgical patients  The presence of LVH in hypertensive patients may be an important predictor of cardiac mortality.  Increased cardiac mortality has also been reported in pts with carotid bruits—even in the absence of symptoms.
  107. 107. PERIOPERATIVE RISK REDUCTION 3 • Effective control of blood pressure • Anti Hypertensive drug therapy • Hydration • Choice of anesthetic agent • Adequate analgesia • Miscellaneous
  108. 108. PERIOPERATIVE RISK REDUCTION 4  Drug-controlled hypertension is not a contraindication  Medication should be maintained throughout the operative period as there is a risk of rebound hypertension causing a cerebrovascular accident.  Sustained rise in end diastollic pressure reduces the inflow of blood to the myocardium during diastole.
  109. 109. PERIOPERATIVE RISK REDUCTION 5  Untreated hypertension discovered at the preop anaesthetic assessment necessitates a systematic approach  The following algorithm is one possibility  Three DBP readings are taken. If the average value is: A. >120 mmHg: cancel the operation. Admit, investigate ,and treat reschedule once the BP is controlled for 4-6 weeks
  110. 110. PERIOPERATIVE RISK REDUCTION 6 B. 105-115 mmHg with signs of end-organ damage: follow the same course as for BP>120 mmHg C. 105-115 mmHg without signs of end-organ damage: Continue with operative plan Consider preop Rx with oral ßAB e.g. atenolol, OR alpha-2-agonist, e.g. clonidine
  111. 111. FOR EXAMPLE…  A BP of 240/80 mmHg in an elderly patient may be due to arteriosclerosis.  It is important to avoid perioperative hypotension in these patients as they need an elevated BP to maintain tissue perfusion.
  112. 112. PERIOPERATIVE HYPERTENSION: PATHOPHYSIOLOGY:  Increase in SVR , increased preload  Rapid intravascular volume shifts  Renin angiotensin activation  Adrenergic stimulation (cardiac & neural)  Serotonergic overproduction  Baroreceptor denervation  Altered cardiac reflexes  Depth of anesthesia inadequate  Aortic Cross clamp
  113. 113. PREOPERATIVELY… 1  Assess BP & review the patient's medical records  Patients may be anxious, fearful, in pain, all of which can induce non hypertensive physiologic increase in BP  Put the patient at ease With reassurance and a calm environment, relieving pain if it exists, then repeating the BP measurement.  The basic principles of BP measurement, such as the use of a proper sized cuff, must not be forgotten.
  114. 114. PREOPERATIVELY… 2  Transient hypertension only on admission may not need therapy but indicate a propensity to become hypertensive during anesthesia and surgery  Particularly for such patients, better to monitor BP directly through an intra-arterial catheter
  115. 115. INTRAOPERATIVE HYPERTENSION: ETIOLOGY A. Intubation hypertension B. Inadequate anesthesia C. Hypercapnia D. Hypoxemia E. Pharmacological adjuvants F. Phaeochromocytoma G. Surgical procedures H. Bladder distension I. Extubation hypertension
  116. 116. INTUBATION HYPERTENSION  Laryngoscopy & intubation are known causes of hypertension.  Severe if laryngoscopy is prolonged  Can be minimized by pre administration of lignocaine.
  117. 117. INADEQUATE ANAESTHESIA  Stimulation during inadequate anaesthesia  The depth of anaesthesia can be monitored by BIS  Indicators: Tachycardia, sweating, grimacing, tears and movement  Beware of empty vaporizers.
  118. 118. HYPERCAPNIA  Increased sympathetic stimulation  Watch out for:  Inadequate tidal volume  Depleted soda lime  Disconnection of circuits  Inadequate fresh gas flow  Malignant hyperthermia and thyrotoxicosis  Exogenous administration during laproscopic procedures
  119. 119. HYPOXEMIA  Hypoxia increases CO  In severe hypoxia the SBP is raised  Severe systolic hypertension is a very late sign and indicate complete circulatory collapse.
  120. 120. PHARMACOLOGICAL ADJUVANTS  Inotropic & vasoconstrictor agents  IV administration of adrenaline containing local anesthetic  Nasal packing  Medication errors
  121. 121. SURGICAL PROCEDURES  Aortic cross clamping  Aortic valve replacement  Carotid endarterectomy  PDA ligation
  122. 122. PLAN OF ANESTHESIA  To maintain an appropriate stable BP range  Those with long standing or poorly controlled BP have altered cerebral autoregulation; higher than normal mean BP may be required to maintain adequate CBF  Arterial BP should generally be kept within 20% of preop level
  123. 123. PREMEDICATION  Premedication reduces preoperative anxiety & is highly desirable in hypertensives  Mild to moderate hypertension often resolve following administration of anxiolytic agent  Preop 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
  124. 124. INDUCTION 1  Induction & intubation are often period of hemodynamic instability for hypertensive patients.  Many hypertensive patients display an accentuated hypertensive response to induction of anesthesia, followed by exaggerated response to intubation  The laryngoscopy, should be short , smooth & gentle.  Intubation should be performed under deep anesthesia.
  125. 125. INDUCTION 2  Attenuate hypertensive response before intubation by;  deepening anesthesia with potent VAA  opioid  lidocaine 1.5 mg/kg IV OR intratracheally  Achieving ßAB with esmolol;propranolol or labetalol  Using topical airway anesthesia
  126. 126. INDUCTION 3 Induction agents  propofol , barbiturates, benzodiazepines and etomidates are equally safe for induction of GA in hypertensive pt.  ketamine may be used in hypertensive by blunting its sympathetic stimulation activity by other agents.
  127. 127. MAINTENANCE  may be safely continued with VAA  a balanced technique( opioids + nitrous oxide + muscle relaxant)  TIVA  Opioids esp. sufentanyl may provide greater autonomic suppression & control over BP
  128. 128. MUSCLE RELAXATION  Any NMBA can be used except pancuronium.  Hypotension following tubocurarine , metocurine, atracurium or mivacurium may be accentuated in hypertensives
  129. 129. MONITORING 1  Most hypertensive patients do not require any special intraop monitors  Invasive BP monitoring for patient with wide swing in BP & for major surgical procedure associated with rapid or marked change in cardiac pre & after load.
  130. 130. MONITORING 2  ECG monitoring should focus on detecting signs of ischemia  UOP in patient with renal impairment or if duration of surgery is >2 hr.
  131. 131. VASOPRESSOR  If use is necessary direct acting agent (phenylephrine 25-50mmg) may be preferable to indirect acting agent  Small dose of ephedrine (5-10 mg) is more appropriate when vagal tone is high.
  132. 132. POSTOP HYPERTENSION 1  It is during the hours and first few days after an operation that most episodes of surgically related MI occur.  Several factors may contribute to this risk, including oxygenation problems, tachycardia, and altered thrombotic potential, but prominent is hypertension.
  133. 133. POSTOP HYPERTENSION 2  Hypertension directly raises the myocardial oxygen demand.  In the presence of CAD, this demand may not be able to be met.  Postop hypertension may also cause a ventricle With systolic dysfunction-for which chronic hypertension is a risk factor to fail
  134. 134. POSTOP HYPERTENSION 3  A "stiff,“ often hypertrophied, ventricle resulting from chronic hypertension may lead to intolerance of tachycardia, often seen postop because of inadequate ventricular filling time, resulting in hypotension and inadequate CO.
  135. 135. POSTOP HYPERTENSION 4  postop control of the BP using an intra-arterial catheter and evaluating the patient for possibly reversible contributing causes like pain and other discomfort, anxiety and fear, hypercarbia, and volume overload.
  136. 136. POSTOP HYPERTENSION 5  Newer approaches toward pain management, such as epidural narcotic infusion, may be useful in patients with postoperative pain.  If these factors are corrected as much as possible and the patient remains hypertensive, additional intervention will almost certainly achieve normotension.
  137. 137. CONCLUSION 1  In those instances where no obvious cause could be identified, it should be assumed to be due to a combination of light anaesthesia and/or excessive surgical stimulation and the patient depth of anaesthesia rapidly deepened.  This will constitute effective treatment for the great majority of cases of hypertension where the cause remains obscure.
  138. 138. CONCLUSION 2  A reliable and early diagnosis of hypertensioin is only possible with accurate, regularly repeated BP measurements.  Monitor accuracy is dependent on correct maintained calibration of the zero point and on linearity throughout the measurement range.  one further report of a sphygmomanometer cuff bladder herniation giving rise to an erroneously high blood pressure.
  139. 139. CONCLUSION 3  Finally, it is important that a full explanation of what happened be given to the patient  The event and the results of any tests should be documented in the anaesthetic record and that, if appropriate, the patient be given a letter to warn future anaesthetists.  If a particular precipitating event was significant or a particular action was useful in resolving the crisis, this should be clearly explained and documented.
  140. 140. REFERENCES 1. Reich DL, Bennett-Guerrero E, Bodian CA, et al. Intraoperative tachycardia and hypertension are independently associated with adverse outcome in noncardiac surgery of long duration.Anesth Analg2002;95:273–7. 2. A D Paix, W B Runciman, B F Horan, M J Chapman, M Currie. Crisis management during anaesthesia: hypertension 3. Reich DL, Bennett-Guerrero E, Bodian CA, et al. Anesth Analg 2002;95:273–7 4. Archives Int. Med. 157:2413-2446 (1997) Dustan HP et al. Arch Intern Med. 1996; 156: 1926- 1935 5. Prys-Roberts C. Chronic Antihypertensive Therapy. Chap 15, pp. 345-62 in: Kaplan JA, Editor. Cardiac Anesthesia, Volurne 2, Cardiovascular Pharmacology. Grune & Stratton, New York, 1983. 6. SlogoffS. Beta-adrenergic blockers. Chap 8, pp. 181-208./n:Kaplan JA, Editor. Cardi~tc Anesthesia, Volume 2, Cardiovascular Pharmacology. Grune & Stratton, New York, 1983) 7. Goldman L,Caldera DL,Nussbaum SR,et al: Multifactorial index of cardiac risk in non cardiac surgical procedures. NEnglJ Med1977;297:845-850 8. DustanHPet al.ArchInternMed. 1996;156:1926-1935

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