hypertension
TRANSCRIPT
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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.
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Determinants of blood pressure :
1. Cardiac output
×
2. Peripheral resistance
Peripheral resistance Viscosity of blood
Peripheral resistance 1/ Velocity of blood
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Measurement of blood pressure
Non invasive Invasive methodsmethod
By mercury Aneroid Electronic BPSphygmomanometer meter Meter
Palpatory Auscultatory Oscillatory method method method
Kortkoffs soundNote: • 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.
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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
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Receptors Operates Stimulation Afferents Cent-re
Efferent Effects
(a) Baroreceptor reflex
Stretch receptor- Carotid sinus & aortic arch- atria
60-20 mmHg of MAP
Distension IX & X nerve
VMC Sympathetic and vagus
VasodilationVenodilatation BP HR
(b) Chemoreceptor reflex
Carotid & aortic bodies
40-100 mmHg of MAP
PCO2/H+ /
pH Sinus nerve VMC Sympathetic
and vagusPeripheral vasoconstriction BP HR
(c) Bezold Jarisch/Coronary chemoreflex
Left ventricle MI Substance from infracted tissueSeratonin, capsasin etc
Vagus Apnoea f/b rapid breathing BP HR
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(d) Pulmonary chemoreflex
Juxtracapillary in walls of alveoli
Hyper-inflation of lug
Seratonin, capsacin etc.
- do -
(e) Somatosympathetic reflex
Muscles Exercise surgery
Pain Somatic nerve
VMC Sympathetic nerve
BP
(f) Cushings reflex
VMC ICT Hypoxia Hypercapnia
Direct stimulation
symp-discharge
BP HR (reflexly)
(g) Bain Bridge reflex
Increased venous return Increase heart rate
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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.
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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.
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Classification of hypertension
JNC VI classification:Category SAP (mmHg) DAP (mmHg)
Optimal < 120 < 80
Normal 120-129 80-84
High normal 130-139 85-89
Hypertension
Stage 1 140-159 90-99
Stage 2 160-179 100-109
Stage 3 > 180 > 110
Note: Where patients SBP and DBP falls into 2 different categories, the higher category is selected.
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JNCDET VII classification
Category SAP (mmHg) DAP (mmHg)
Normal < 120 < 80
Pre Hypertensive 120-139 80-89
Hypertensive
Stage 1
Stage 2
140-159
> 160
90-99
> 100
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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
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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
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• 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
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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.
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(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.
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(4) Drugs• OCP• Glucocorticoids• Mineralocorticoids• Cyclosporine• Tyramine• Sympathomimetics
(5) Miscellaneous• Toxemia of pregnancy• Coarctation of aorta• PAN• Hypercalcemia• Increased intravascular volume• Acute intermittent porphyria
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(B) Systolic hypertension with wide pulse
pressure
1. Decreased compliance of aorta
(arteriosclerosis; aortic rigidity)
2. Increased stroke volume : AR, thyrotoxicosis,
fever, AV fistula, PDA
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PATHOPHYSIOLOGY OF ESSENTIAL HYPERTENSION
1. CVS
systemic BP
after load
acceleration ofatheromatous Concentric LVH Endomyocardial plaque fibrosis
Myocardial O2 requirement
Coronary insufficiency myocardial compliance
Infarction CCF COdysrrythmia
Pulmonary oedema
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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.
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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.
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4. Fundus changes: Retinal haemorrhages, exudates + papilloedema
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.
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TREATMENT OF HYPERTENSION
1. Life style modifications:• Salt restriction• Stop smoking• Limit alcohol intake• Reduce weight• Relaxation • Regular exercise
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2. Pharmacological treatment
Site of action
Drug & Dose Indications Contraindications Side effects
Diuretics
Renal tubule ThiazidesO : 12.5-25 mg daily
Mild hypertension As adjunctElderlyheart failure
GOUT, DM, Primary aldosteronism, dyslipidemia
HypokalemiaHyepruricemiaHypercalcemiaHypercholestrolemiaHyperglycemia
Loop diureticsO : 20-80 mg BD/TDS
Mild hypertensionAs adjunctParticularly with renal failure
- do - HypokalemiaHyepruricemiaHypocalcemiaHypercholestrolemiaHyperglycemia
Potassiumsparing SpironolactoneO : 25 mg BD/QIDAmilorideD : 5-10 mg OD
Hypertension due to hyper mineralo-corticoid
Renal failure HyperkalemiaDiarrheaGynecomastia
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Anti-adrenergic agent
Central ClonidineD : 0.005-0.6 mg OD
Renal disease with hypertension Premedication
Bradycardia Sedation XerostomiaRebound hypertension
Methyl dopaD : 250-1000
mg BDD : IV 250-1000
mg every 4-6 hours
Malignant hypertension
PheochromocytomaHepatic disease
Drowsiness Dry mouthFatiguePositive coombs test
Autonomic ganglia
TrimethaphanD : IV 1-6 mg/ min
- do - DMCoronary artery disease
Postural hypotension Constipation Visual symptoms
Nerve endings
GuanethidineD: O 10-150 mg OD
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Alpha receptors25
PrazosinD : O 1-10 mg OD
Mild to moderate hypertensionProstatism
Caution in the elderly First dose syncope Orthostatic hyportension Fluid retention Sedation
TerazosinD: 1-20 mg OD
- do - - do - - do -
PhentolamineD: IV 30 mcg/
kg
Pheochromo-cytoma
Severe CA disease TachycardiaDizziness
Beta receptors
Propanolol D: O 10-20 mg BD/QID ; IV 10-25 mcg/kg.MetaprololAtenololEsmolol D: bol. IV .2-.5mg/kg
Mild to moderate hypertension specially with hyperdynamic circulation
CHF Heart blockDM
Bradycardia BronchospasmCHFMask hypoglycemia
Alpha/Beta receptors
Labetalol D : IV 0.1-0.25 mg/kgD : O 100-600 mg BDCarvedilol
- do - - do - - do -
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Vasodilators
Vascular smooth muscle
Hydralazine D : IV 10-50 mg every 6 hrs
Malignant hypertension
Lupus TachycardiaAnginaLupus like syndrome
MinoxidilD : 2.5-40 mg BD
Severe hypertension
Severe CA disease Tachycardia Hair growth Pericardial effusions
NitroprussideD : 0.5-8 g/ kg/min
Malignant hypertension
DiphoresisNauseaCyanide toxocity
ACE inhibitors
Captopril EnalprilFisinoprilBenazipril
Mild to severe hypertension Heart failureLV dysfunctionDiabetic retinopathy
Renal failurePregnancy B/L Renal artery Stenosis
CoughAngioedemaHyperkalemiaLoss of tasteProteinuria
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Angiotensin receptor antagonist
Losartan Valsartan
Mild to severe hypertension Renal arteryStenosis
Renal failurePregnancy B/L Renal artery Stenosis
HyperkalemiaHypotension
Calcium channel blockers
Vascular smooth muscle
VerapamilNifedipineFelodipine
Mild to moderate hypertension
Heart failure 2o or 3o block
HypercalemiaTachycardia GIT disturbances
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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
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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
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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
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(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
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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
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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.
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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.
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3. Hydration
4. Choice of agents with minimal hemodynamic effects
• Thiopentone over propofol• Pethidine over morphine • Vecuronium and cis atracurium over atracurium.
5. Analgesics
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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
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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
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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 laryngoescopyesmolol 100-200 g/kg IV 15 sec. before induction
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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
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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.
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• Surgical causes: use of 10% phenylephrine drops in ophthalmic surgery
• Malignant hyperthermia, thyrotoxicosis, pheoch-romocytoma
• Distended bladder
Treatment • Correct the cause before treating blood
pressure with antihypertensives. • Increase the depth of anaesthesia
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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
EMERGENCE • Avoid pain, hypoxia, coughing • Patient should be returned to ward when
haemodynamically stable
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ACUTE POSTOPERATIVE HYPERTENSION
Causes: • Pain• Emergence excitement• Hypercarbia• Intolerance of endotracheal tube• Full bladder• Hypervolaemia• Hypothermia• Withdrawal of chronic therapy• After carotid endarterectomy
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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
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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
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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
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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
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Drug Dose Length of action
Nitropruside 0.25 mcg/kg/min IV 2-5 minutes
Nitroglycerin 5 mcg/min IV 3-10 minutes
Esmolol 250-500 mcg/min for 1 min, then 50-100 mcg/kg/min
10-20 minutes
Propranolol 1-4 mg IV 1-2 hours
Labetolol 10-200 mg IV (2 mg/min) 1-4 hours
Nicardipine 5-15 mg/hour IV 1-4 hours
Nifedipine 10 mg sublingual or oral 2-5 hours
Diazoxide 30 mg boluses IV (max 300 mg) 4-12 hours
Hydralazine 5-20 mg IV 4-12 hours
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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.
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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
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Various studies• 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.
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