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 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.

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- 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

(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

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 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.

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

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 of aorta

(arteriosclerosis; aortic rigidity)

2. Increased stroke volume : AR, thyrotoxicosis,

fever, AV fistula, PDA

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

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 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.

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 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

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

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 -

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

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

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 laryngoescopyesmolol 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, pheoch-romocytoma

• 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

EMERGENCE • Avoid pain, hypoxia, coughing • Patient should be returned to ward when

haemodynamically stable

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 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

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

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.