ANAESTHETIC MANAGEMENT IN HYPERTENSIVE PATIENTS

DR.DEEPAK SOLANKI M.D.ANAESTHESIA dr.dsolanki@gmail.com

Blood pressure : Pressure exerted by the blood column on the lateral walls of the arteries. Factors affecting arterial B.P.: Age Sex Habitus Climate Diurnal variation Exercise, emotions, meals, heredity, gravity, posture and regional variation.

Determinants of blood pressure : 1. Cardiac output 2. Peripheral resistance Peripheral resistance Viscosity of blood Peripheral resistance 1/ Velocity of blood

Measurement of blood pressure

Non invasive method Invasive methods

By mercury Aneroid Sphygmomanometer meter Palpatory method

Electronic BP Meter

Auscultatory Oscillatory method method Kortkoffs sound

Note: Resting adults : DBP Disappearance of Kortkoffs sound Adults after exercise children, pregnancy hyperthyroidism DBP Muffling Keep the arm at the level of the heart Appropriate cuff size.

Regulation of blood pressure

Various interconnected mechanism work together to maintain normal MAP 1. Rapidly acting mechanisms Acts within seconds to minutes Loose their capacity after few hours Circulatory reflexes Main center is VMC

Receptors

Operates

Stimulation

Afferents

Cent-re Efferent

Effects

(a) Baroreceptor reflex Stretch receptor 60-20 mmHg Distension - Carotid sinus & of MAP aortic arch - atria IX & X nerve VMC Sympathetic and vagus Vasodilation Venodilatation BP HR

(b) Chemoreceptor reflex Carotid & aortic 40-100 bodies mmHg of MAP PCO2/H+ / Sinus nerve pH VMC Sympathetic and vagus Peripheral vasoconstriction BP HR

(c) Bezold Jarisch/Coronary chemoreflex Left ventricle MI Substance from Vagus infracted tissue Seratonin, capsasin etc Apnoea f/b rapid breathing BP HR

(d) Pulmonary chemoreflex Juxtracapillary in Hyperwalls of alveoli inflation of lug (e) Somatosympathetic reflex Muscles Exercise surgery Pain Somatic nerve VMC Sympathetic nerve BP Seratonin, capsacin etc. - do -

(f) Cushings reflex VMC ICT Hypoxia Hypercapnia Direct stimulation sympdischarge BP HR (reflexly)

(g) Bain Bridge reflex Increased venous return Increase heart rate

2. Moderately acting mechanisms Hormones : Epinephrine, Nor epinephrine, AVP, angiotensin I, histamine, ANP, VIP, Endothelin products: Endothelin-1, NO, kinins, TxA2 3. Long term regulatory mechanisms Slow to begin Comes to equilibrium in 3-10 days 1. Direct mechanism: by kidneys call as renal fluid mechanism 2. Indirect mechanism: aldosterone and renin angiotensin system.

Hypertension
An adult is considered to manifest hypertension when SBP/DBP are 140/90 mmHg or more on at least 2 occasions measured at least 1-2 weeks apart. For anaesthetists: on the basis of 2/3 readings taken over a period of hours.

Classification of hypertension
JNC VI classification:
Category Optimal Normal High normal Hypertension Stage 1 Stage 2 Stage 3 140-159 160-179 > 180 90-99 100-109 > 110 SAP (mmHg) < 120 120-129 130-139 DAP (mmHg) < 80 80-84 85-89

Note: Where patients SBP and DBP falls into 2 different categories, the higher category is selected.

JNCDET VII classification Category Normal Pre Hypertensive Hypertensive Stage 1 Stage 2 SAP (mmHg) < 120 120-139 140-159 > 160 DAP (mmHg) < 80 80-89 90-99 > 100

Terminologies used for hypertension

1.Isolated systolic hypertension: SBP > 140 mmHg, DBP < 90 mmHg, elderly 2.Essential hypertension : No cause found 3.Secondary hypertension 4.Accelerated hypertension : Markedly elevated (recent over previous episodes) associated with retinal damage. But without papilledema. 5.Malignant hypertension: Markedly elevated hypertension (diastolic > 140 mmHg) + retinopathy + hypertensive encephalopathy. 6.Complicated hypertension : Hypertension + end organ damage 7.White coat hypertension

Classification of hypertension according to etiology

1. Primary/essential/idiopathic hypertension : 95% of all cases No cause found Possible factors : Multifactorial genetic defects Environmental : salt intake, obesity, smoking, alcohol, tobacco, occupation, large family size, inadequate intake of K and Ca. Generalized cell membrane defect

Increased sympathetic activity Sleep disorders Hypercholesterolemia, diabetes, insulin resistance Increased renin secretion Deficiency of vasodilators such as PG, NO 2. Secondary hypertension < 5% of all the cases Etiology is present

Types
(A) Systolic and diastolic hypertension with increased PVR. (1) Renal Renal vascular disease e.g. renal artery stenosis. Renal parenchymal diseases e.g. GN (acute/chronic), pyelonephritis Renal transplantation Renin secreting tumors Other e.g. PCK, diabetic nephropathy, arterial nephrosclerosis.

(2) Endocrine Cushings syndrome (excessive glucocorticoid) Congenital adrenal hyperplasia Conns syndrome (primary hyperaldosteronism) Pheochromocytoma Myxedema Acromegaly (3) Neurogenic Psychogenic Spinal cord injuries GBS Dysautonomia Increased ICT Diencephalic syndrome.

(4) Drugs OCP Glucocorticoids Mineralocorticoids Cyclosporine Tyramine Sympathomimetics (5) Miscellaneous Toxemia of pregnancy Coarctation of aorta PAN Hypercalcemia Increased intravascular volume Acute intermittent porphyria

(B) Systolic hypertension with wide pulse pressure 1.Decreased compliance (arteriosclerosis; aortic rigidity) of aorta

2.Increased stroke volume : AR, thyrotoxicosis, fever, AV fistula, PDA

PATHOPHYSIOLOGY OF ESSENTIAL HYPERTENSION

1. CVS
systemic BP after load acceleration of

atheromatous

Concentric LVH

Endomyocardial plaque

fibrosis
Myocardial O2 requirement Coronary insufficiency myocardial compliance CO

Infarction dysrrythmia

CCF Pulmonary oedema

2. Peripheral blood vessels Arterial and arteriolar wall thickening Decreased internal diametre Vascular contraction leads to abnormally large increase in BP Vascular relaxation leads to greater than expected decrease in BP. Relative hypovolumia ( intravascular volume) Rehydration following relaxation causes rebound hypertension.

3. Nervous system Cerebral haemorrhage Encephalopathy Atherosclerosis in cerebral blood vessels Cerebra infarcts TIA Chronic hypertension causes a shift to the right in cerebral and renal autoregulation Decrease in cerebral blood flow and cerebral ischaemia occurs at higher BP than in normal patients. Clinical pearls: 1.25% decrease in MAP reaches the lower limit of autoregulation. 2.A 55% decrease in MAP reaches symptomatic brain hypoperfusion.

4.

Fundus changes: Retinal exudates + papilloedema

haemorrhages,

5. Renal system: Arteriosclerotic lesions of the arterioles and glomerulus Decrease GFR and tubular dysfunction Proteinuria and microscopic hematuria Adversely affects renal autoregulation End organ damage to kidneys. Prerenal hypoperfusion due to sudden and sustained decreased in BP.

TREATMENT OF HYPERTENSION
1. Life style modifications: Salt restriction Stop smoking Limit alcohol intake Reduce weight Relaxation Regular exercise

2. Pharmacological treatment
Site of action Drug & Dose Diuretics Renal tubule Thiazides O : 12.5-25 mg daily Mild hypertension GOUT, DM, Primary As adjunct aldosteronism, Elderly dyslipidemia heart failure Mild hypertension - do As adjunct Particularly with renal failure Hypokalemia Hyepruricemia Hypercalcemia Hypercholestrolemia Hyperglycemia Hypokalemia Hyepruricemia Hypocalcemia Hypercholestrolemia Hyperglycemia Hyperkalemia Diarrhea Gynecomastia Indications Contraindications Side effects

Loop diuretics O : 20-80 mg BD/TDS

Potassium Hypertension due Renal failure sparing to hyper mineraloSpironolactone corticoid O : 25 mg BD/QID Amiloride D : 5-10 mg OD

Anti-adrenergic agent Central Clonidine Renal disease D : 0.005-0.6 mg with hypertension OD Premedication Bradycardia Sedation Xerostomia Rebound hypertension Pheochromocytoma Hepatic disease Drowsiness Dry mouth Fatigue Positive coombs test

Methyl dopa Malignant D : 250-1000 mg hypertension BD D : IV 250-1000 mg every 4-6 hours Autonomic ganglia Trimethaphan D : IV 1-6 mg/ min - do -

DM Postural hypotension Coronary artery disease Constipation Visual symptoms

Nerve endings Guanethidine D: O 10-150 mg OD

Alpha receptors25

Prazosin Mild to moderate Caution in the elderly First dose syncope D : O 1-10 mg OD hypertension Orthostatic hyportension Prostatism Fluid retention Sedation Terazosin D: 1-20 mg OD - do - do - do -

Phentolamine PheochromoD: IV 30 mcg/ kg cytoma Beta receptors Propanolol D: O 10-20 mg BD/QID ; IV 1025 mcg/kg. Metaprolol Atenolol Esmolol D: bol. IV .2-.5mg/kg Alpha/Beta receptors

Severe CA disease

Tachycardia Dizziness Bradycardia Bronchospasm CHF Mask hypoglycemia

Mild to moderate CHF hypertension Heart block specially with DM hyperdynamic circulation

Labetalol - do D : IV 0.1-0.25 mg/kg D : O 100-600 mg BD Carvedilol

- do -

- do -

Vasodilators Vascular smooth muscle Hydralazine Malignant D : IV 10-50 mg hypertension every 6 hrs Minoxidil D : 2.5-40 mg BD Nitroprusside D : 0.5-8 g/ kg/min ACE inhibitors Captopril Enalpril Fisinopril Benazipril Severe hypertension Malignant hypertension Lupus Tachycardia Angina Lupus like syndrome Tachycardia Hair growth Pericardial effusions Diphoresis Nausea Cyanide toxocity

Severe CA disease

Mild to severe hypertension Heart failure LV dysfunction Diabetic retinopathy

Renal failure Pregnancy B/L Renal artery Stenosis

Cough Angioedema Hyperkalemia Loss of taste Proteinuria

Angiotensin receptor antagonist Losartan Valsartan Mild to severe hypertension Renal artery Stenosis Renal failure Pregnancy B/L Renal artery Stenosis Hyperkalemia Hypotension

Calcium channel blockers Vascular smooth muscle Verapamil Nifedipine Felodipine Mild to moderate hypertension Heart failure 2o or 3o block Hypercalemia Tachycardia GIT disturbances

ANAESTHETIC MANAGEMENT
For elective surgery DBP > 110 mmHg should not undergo elective surgery until there hypertension has been corrected over few days. For emergency surgery Treat pain and anxiety Reduce BP to around 160/100 mmHg Careful fluid replacement

PREOPERATIVE EVALUATION
Aims of preoperative evaluation: 1.To determine whether hypertension is primary or secondary 2.Evaluate end organ damage : LVH, CHF, angina, CVA, PVD, renal insufficiency 3.Determine adequacy of systemic blood pressure control 4.Review pharmacology of drugs

HISTORY AND EXAMINATION

(A) Whether hypertension is primary/secondary H/o repeated UTI : suggests renal origin H/o weight gain or emotional liability : cushings syndromes H/o weight loss with episodic headaches, palpitation, diaphoresis, postural dizziness : pheochromocytoma H/o polyuria, polydipsia, muscle weakness, hypokalemia: primary aldosteronism

(B) For associated complications H/o headache localized especially to occipital regions and occurring on waking up, dizziness, palpitation : severe hypertension Episodes of chest pain, dyspnoea, edema : Cardiac failure, angina Episodes of weakness/dizziness : TIA Episodes of epistaxis : vascular changes Episodes of haematuria: Renal vascular changes Severe sharp pain : dissection of aorta Fundus examination : Hypertensive retinopathy

Preoperative investigations
Always included: Full blood count, DLC Blood urea and creatinine Electrolyte Hb & haematocrit Microscopic urinalysis Blood glucose Lipid profile Chest X-ray 12 lead ECG Usually but not always included TSH Serum calcium and phosphate Echocardiogram

Special studies to screen for secondary hypertension

Renovascular disease : Renal scan, renal duplex, doppler flow studies, MRI angiosraphy Pheochromocytoma: 24 hours urine assay for creatinine, metanephrines and catecholamines Cushings syndrome: overnight dexamethasone suppression test, 24 hr urine cortisol and creatinine Primary aldosteronism: Plasma aldosterone : renin activity ratio.

Methods to reduce perioperative risks

1. Adequate perioperative BP control Continue all antihypertensives up to the day of surgery except diuretics. Delay elective surgery if SBP> 200mmHg or DBP > 120mmHg until lowered to 140/90 mmHg over several weeks. Acute control within hour is not advisable. 2. Measures to prevent hypertensives episodes Use of agents to attenuate hemodynamic responses to intubation incision and extubation. Opioids - fentanly, alfentanyl Antihypertensive - Esmolol, labetalol, clonidine, enalpril. Lignocaine I.V. & spray.

3. Hydration 4. Choice of agents with minimal hemodynamic effects Thiopentone over propofol Pethidine over morphine Vecuronium and cis atracurium over atracurium. 5. Analgesics

Monitoring Pulse BP invasive and non-invasive ECG CVP Urine output Invasive pulmonary artery catheter if LVF dysfunction TEE for LV function Premedication Sympathetic activation can cause BP to rise by 20-30 mmHg & HR by 15-20 BPM. Aims to avoid hypertension and hypotension, tachycardia Benzodiazepines : Lorazepam 2-4mg 2 hours prior to surgery. If possible avoid atropine

Induction
Intravenous agents Many inducing agents are vasodilators Avoid propofol and ketamine Use of opioids reduces dose of inducing agents. Thiopentone dose titrated against response

Intubation
Hypertensive response to laryngoescopy can be reduce by
Use of opioids : Alfentanil : 15-30 g/kg IV at the time of injection Remifentanil : 1 g/kg IV of inducing agent Fentanyl : 50-150 g/kg IV 3 mins before Sufentanyl : 30 g/kg IV induction Lignocaine - IV 1.5 mg/kg & spray Duration should not exceed 15 sec. If duration likely to exceed 15 sec. sodium nitropusside 1-2 g/kg IV before laryngoescopy esmolol 100-200 g/kg IV 15 sec. before induction

Maintenance
GOAL: Adjust the depth of anaesthesia to minimize wide fluctuations in blood pressure Alpine anaesthesia : Exhibit swings in arterial pressure (graphical presentation) Volatile agents : Cardiovascular depressant Poorly soluble desflurane and sevoflurane permit more rapid changes in alveolar concentration and hence depth. Opioids reduces the amount of volatile agents required N2O can be used safely

Intraoperative hypertension
Causes Poorly controlled preoperative hypertension Hypertension secondary to laryngoscopy and intubation Hypercapnia : Hypoventilation, depleted sodalime, CO2 during laparoscpy etc. Hypoxemia Inadequate regional anaesthesia/excessive surgical site stimulation or light anaesthesia. Drug related: inadverent infusion of vasopressors.

Surgical causes: use of 10% phenylephrine drops in ophthalmic surgery Malignant hyperthermia, thyrotoxicosis, pheochromocytoma Distended bladder Treatment Correct the cause before treating blood pressure with antihypertensives. Increase the depth of anaesthesia

Intraoperative hypotension
Causes Direct effect of anaesthetic agents Inhibition of the sympathetic nervous system Loss of the baroreceptor reflex Treatment Reduce the depth of anaesthesia Correct hypovolumia Small dose vasopressors Avoid pain, hypoxia, coughing Patient should be returned haemodynamically stable

EMERGENCE
to ward when

ACUTE POSTOPERATIVE HYPERTENSION Causes: Pain Emergence excitement Hypercarbia Intolerance of endotracheal tube Full bladder Hypervolaemia Hypothermia Withdrawal of chronic therapy After carotid endarterectomy

Risk associated Loss of vascular anastomosis Intracranial bleeding Myocardial ischaemia Treatment depends on The clinical situation Etiology Level of analgesia Degree of hypertension Drug used Labetalol 0.1-0.5 mg/kg IV every 10 min Hydralazine 2.5-10 mg IV every 10-20 min Nitroprusside 0.5-10 g/kg/min IV

HYPERTENSIVE EMERGENCIES
Common causes of hypertensive crisis Antihypertensive drug withdrawal (e.g. clonidine) Autonomic hyperactivity Collagen-vascular diseases Drugs (e.g., cocaine, amphetamines) Glomerulonephritis (acute) Head trauma Neoplasias (e.g., pheochromocytoma) Preeclampsia & eclampsia Removascular hypertension

Clinical manifestations: Hypertensive encephalopathy : Headache, altered consciousness and confusion, CVA, Fundus changes Acute aortic dissection Acute myocardial infarction Acute cerebral vascular accident Acute hypertensive renal injury : Renal failure with oliguria and/or hematuria. Acute congestive heart failure

Management
Key: prompt recognition and initiation of treatment Does the patient have any prior or current complaints and what medications, prescription has the patient taken. Palpation of pulses in all extremities Fundoscopic examination Routine investigations

Drug Nitropruside Nitroglycerin Esmolol Propranolol Labetolol Nicardipine Nifedipine Diazoxide Hydralazine

Dose 0.25 mcg/kg/min IV 5 mcg/min IV

Length of action 2-5 minutes 3-10 minutes

250-500 mcg/min for 1 min, then 50-100 10-20 minutes mcg/kg/min 1-4 mg IV 10-200 mg IV (2 mg/min) 5-15 mg/hour IV 10 mg sublingual or oral 30 mg boluses IV (max 300 mg) 5-20 mg IV 1-2 hours 1-4 hours 1-4 hours 2-5 hours 4-12 hours 4-12 hours

REGIONAL ANAESTHESIA
Hypertension is not a contraindication But spinal and epidural causes unpredictable and profound hypotension. Hypertensives may have LVH and deranged autoregulation, thus these organs will cope poorly with low perfusion pressure. Local blocks should always be considered.

JNCDET Guidelines for anaesthesia in hypertensive patients

Stage 1 hypertension : little or no increased risk of peri-operative cardiac morbidity, therefore, anaesthesia and surgery can proceed as planned. Stage 2 & Stage 3 : More of a delimma Balance has to be stuck Options available: to ignore the elevated arterial
BP to institute acute treatment to defer surgery for a period of

weeks

Prys-Roberts & colleagues: demonstrated an association between poorly controlled hypertension and intraoperative MI and arrythmias. Another prospective study: demonstrated an increasing incidence of postoperative myocardial ischaemia with increasing arterial pressure. Studies also demonstrate that very rapid control of blood pressure with drugs such as sublingual nifedipine is associated with morbidity and mortality. Charleson and colleagues: demonstrated that those with more than 1 hour of a decrease in MAP > 20 mmHg and those with > 15 mins of an increase in MAP > 20 mmHg were at greatest risk of complications. On the basis of these findings; best course for anaesthetists is to defer anaesthesia and surgery in patients with stage 3 hypertension to allow the arterial pressure to be treated.

Various studies

T H A N K S