HYPERTENSION: GENERAL, AND ANESTHESIA

MANAGEMENTABAYNEH BELIHU

AKSUM UNIVERESITYFEB 2016

“A man is as old as his arteries”

Hypertension

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

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

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.

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)

SIGNIFICANCE OF THE TOPIC FOR ANESTHETISTS 4Among 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)

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.)

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

IMPORTANCE OF KNOWING COMMON ANTIHYPERTENSIVE DRUGS 2And 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.

A little bit on physiology …

Renalfunction

Bloodvolume

Venoustone

Venousreturn

Heartrate

Nervouscontrol

Muscularresponsiveness

Myocardialcontractility

Strokevolume

Cardiacoutput

CNSfactors Renin

release

Angiontensin II formation

Intrinsic vascularresponsiveness

Peripheralresistance

Nervouscontrol

Renalfunction

MAP

Factors that Govern the Mean Arterial Pressure

Mean Arterial Pressure

MAP = CO X

CO = HR SV

PVR Myogenic tone Vascular

responsiveness Nervous control Vasoactive

metabolites Endothelial factors Circulating hormones

X

SNS Venous

tone

BVContactility

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 TPR2. Therefore, they are the targets of antihypertensive therapy.

Response mediated by the RAAS & sympathetic system on BP

SO WHAT IS HYPERTENSION?

Hypertension is defined as SBP >140 mmHg, DBP>90 mmHg, or taking antihypertensive medication.

VI JNC, 1997

JNC 8 HAS ALSO ARRIVED

http://jama.jamanetwork.com/article.aspx?articleid=1791497

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

GOAL OF THE REVISIONA.To identify individuals at any BP level who have

a reasonable likelihood of future CV events.OR

B.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

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 "

STAGES OF HYPERTENSION

HF Angina Post-MI Extensive CAD DM CRF Recurrent stroke prevention

CLASSIFICATION FOR ADULTS

Adapted from: Archives Int. Med. 157:2413-2446 (1997)

Category Systolic (mm Hg)

Diastolic (mm Hg)

Optimal BP < 120 And < 80Normal BP < 130 And < 85High-normal BP 130 – 139 Or 85 - 89Stage 1 (mild) 140 – 159 Or 90 - 99Stage 2 (moderate)

160 – 179 Or 100 - 109

Stage 3 (severe) ≥180 or ≥110

TYPES OFHYPERTENSION

ESSENTIAL SECONDARY

DISORDER OF UNKNOWN ORIGIN AFFECTING THE BP REGULATION

SECONDARY TO OTHER DISEASE PROCESSES

ENVIRONMENTAL FACTORS

STRESS Na+/ INTAKE OBESITY SMOKING

**********************************************************************************

DISEASES ATTRIBUTABLE TO HTN

HYPERTENSION

Gangrene of the Lower Extremities

Heart Failure

Left Ventricular

HypertrophyMyocardial Infarction

Coronary Heart Disease

Aortic Aneurym

Blindness

Chronic Kidney Failure

Stroke PreeclampsiaEclampsia

Cerebral Hemorrhage

Hypertensive encephalopathy

Adapted from Dustan HP et al. Arch Intern Med. 1996; 156: 1926-1935

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

TREATMENT – WHY? 2

IV. Pre-existing hypertension, particularly if

untreated, increases the likelihood of

intraop hypertension and of complications

(Prys-Roberts et al)

Pertinent complications of untreated HTN

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.

NON PHARMACOLOGICAL TREATMENT 1

Avoid harmful habits ,smoking ,alcoholReduce salt and high fat diets

Loose weight , if obeseRegular exercise

DASH

NON PHARMACOLOGIC TREATMENT 2MODIFICATION APPROX. SBP

REDUCTIONWeight reduction 5 – 20 mm of hg /10 kg

lostAdopt 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

PHARMACOLOGIC TREATMENT 1

PHARMACOLOGIC TREATMENT 2Drug therapy reduces: The progression of hypertension, and The incidence of:

strokeCHFCAD, and Renal damage with reversal of

pathophysiologic changes , such as LVH and altered CAR.

PHARMACOLOGIC TREATMENT 3

Most patients with mild hypertension

require only single-drug therapy, thiazide

diuretic, ACEI, ARB, ßAB, or CCB.

PHARMACOLOGIC TREATMENT 4

A. Primary (essential hypertension) vs. secondary (10-15%)

E.g.pheochromocytoma, renal artery constriction, Cushing’s syndromeB. Diagnosis (based on 3 separate office visits) and

severityC. Individualization (age, gender, ethnicity) and

complianceD. Pre-existing risk factors and medical conditionsE. Smoking, Hyperlipidemia, DM, CHF, Asthma,

current medicationF. Monotherapy vs. Polypharmacy

Factors to consider

CLASSES OF DRUGS AND TARGET SITESDRUGS Targets Diuretics Agents acting on ANS Direct VasodilatorsCCB RAAS blockers

Blood Volume Cardiac Output Resistance of Vessel Arterioles RAAS Neuroregulation

Sites of action of antihypertensives

Mechanisms of action of antihypertensives

DIURETICS 1Bumetanide, furosemide, hydrochlorothiazide, spironolactone, triamterene

Act by decreasing blood volume and CO

Decrease PVR during chronic therapy

Drugs of choice in elderly hypertensive

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.

DIURETICS 3:NEPHRON ANATOMY & SITE OF ACTION

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.

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.

DIURETICS 7K-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.

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

SYMPATHOPLEGIC AGENTS1. 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)

CENTRALLY-ACTING ANTIHYPERTENSIVE AGENTS

Clonidine

reduces sympathetic and increases PS tone, leading to BP lowering and bradycardia.

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.

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.

CAUTION!

Abrupt withdrawal may induce

hypertensive crisis

Do not give to patients who are at risk of

mental depression, or are taking tricyclic

antidepressants

METHYLDOPAA prodrug that exerts its antihypertensive

action via an active metabolite

MECHANISM OF ACTIONThe 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.

THERAPEUTIC USEDoes 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.

DRUGS THAT ACT ON PNS1. β-blockers Propranolol, metoprolol, nadolol,carteolol,

atenolol, betaxolol,bisoprolol,pindolol, acebutolol, penbutolol, labetalol, carvedilol.

MECHANISM OF ACTION1. Reduces CO

2. Inhibits renin release and AT-II and aldosterone

production, and lower peripheral resistance

3. May decrease adrenergic outflow from the CNS

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

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

METOPROLOL

Much less β2-antagonistic than propranolol, thus can be used in patients who also suffer from asthma, DM, or peripheral vascular diseases.

PINDOLOL, ACEBUTOLOL, PENBUTOLOLAntagonistic effect is combined with partial

agonistic effect on β2-AR.

Particularly for patients with cardiac failure, bradyarrhythmias, or peripheral vascular disease

LABETALOL, CARVEDILOLGiven 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

-1 BLOCKERS

Prazosin, tetrazosin, doxazosin,

phentolamine, phenoxybenzamine.

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.

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

DIRECT VASODILATORS

Hydralazine, minoxidil, sodium NP,

diazoxide

MECHANISM OF ACTION

Relax smooth muscle (SM) of

arterioles (and sometimes veins),

thereby reduce SVR.

THERAPEUTIC USEHydralazine

Dilates arterioles but not veins.

Effect does not last long when used alone; but combination therapy can be very effective for even severe hypertension.

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

SODIUM NITROPRUSSIDEParenterally administered (IV) Powerful vasodilator hypertensive

emergenciesWorks by increasing intracellular cGMP and

dilates both arterial and venous vessels In patients with cardiac failure because CO

increases due to afterload reductionEffects last only <10 minutes after

discontinuation

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).

CALCIUM CHANNEL BLOCKERSverapamil, 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.

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.

ACEICaptopril, enalapril (lisinopril is a lysine-derivative), benazepril, fosinopril, moexipril, quinapril and ramipril

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).

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

MECHANISM OF ACTION 3

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

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).

ANGIOTENSIN-II ANTAGONISTSLosartan, valsartan, candesartan, irbesartan, telmisartan, eprosartan, and zolasartan. Saralasin- orally ineffective and requires continuous

IV infusion.

Saralasin has partial agonist activity, and is not currently in use for hypertension treatment.

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.

THERAPEUTIC USE

losartan has the advantage of not causing

cough and angioedema, which are effects

of bradykinin.

ADVERSE EFFECTS AND TOXICITY

Similar to those of ACEIs

Fetotoxic and should not be used for

treating hypertension in pregnant

women.

LOGICAL COMBINATIONSDiuretic b-

blocker CCB ACEI a-blocker

Diuretic          -   ü          -   ü   üb-blocker   ü          -   ü*          -   ü

CCB          -   ü*          -   ü   üACEI   ü          -   ü          -   ü

a-blocker   ü   ü   ü   ü          -* VERAPAMIL + BETA-BLOCKER = ABSOLUTE CONTRA-INDICATION

HYPERTENSIVE EMERGENCY & PARENTRAL DRUGSH/ encephalopathy Nitroprusside,nicardipine,labetalol,Malignant HTn Labetalol, nicardipine,NP,enalaprilat

stroke Nicardipin,labetalol,nitroprusside MI/unstable angina Nitroglycerin,nicardipine,labetalol,

esmololAcute LVF Nitroglycerin,enalaprilat,loop diureticAortic dissection Nitroprusside, esmolol, labetalol Adrenergic crisis Phentolamine, nitroprussidePostoperative HTn Nitroglycerin,NP,labetalol,nicardipinePreeclampsia/ Ec Hydralazine,labetalol,nicardipine

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).

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.

RECOMMENDATION 3A diuretic with adrenergic blockade or CCB

alone for elderly patients.

Patients with moderate to severe HTN require a second or third drug.

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.

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

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.

THE THREE FACTORS1. 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.

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.

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

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.

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.)

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.

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.

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.

ADRENERGIC NEURON INHIBITORS 1Reserpine, 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.

ADRENERGIC NEURON INHIBITORS 2Debrisoquine, 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.

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.

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.

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).

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.

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.

ANAESTHESIA MANAGEMENT

OF

HYPERTENSIVE PATIENTS

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

GOALS OF ANESTHESIA MANAGEMENT A. Preoperative consideration and evaluation

B. Perioperative risk reduction

C. Premedication

D. Balanced anesthesia

E. Proper monitoring

F. Parenteral medications

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.

PERIOPERATIVE RISK REDUCTION 3• Effective control of blood pressure• Anti Hypertensive drug therapy• Hydration• Choice of anesthetic agent• Adequate analgesia• Miscellaneous

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.

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 treatreschedule once the BP is controlled for 4-6

weeks

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 planConsider preop Rx with

oral ßAB e.g. atenolol, OR alpha-2-agonist, e.g. clonidine

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.

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

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.

PREOPERATIVELY… 2Transient 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

INTRAOPERATIVE HYPERTENSION: ETIOLOGY

A. Intubation hypertensionB. Inadequate anesthesiaC. HypercapniaD. HypoxemiaE. Pharmacological adjuvantsF. PhaeochromocytomaG. Surgical proceduresH. Bladder distensionI. Extubation hypertension

INTUBATION HYPERTENSION Laryngoscopy & intubation are known

causes of hypertension.

Severe if laryngoscopy is prolonged

Can be minimized by pre administration of lignocaine.

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.

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

HYPOXEMIA

Hypoxia increases CO

In severe hypoxia the SBP is raised

Severe systolic hypertension is a very late sign

and indicate complete circulatory collapse.

PHARMACOLOGICAL ADJUVANTS

Inotropic & vasoconstrictor agents

IV administration of adrenaline containing local

anesthetic

Nasal packing

Medication errors

SURGICAL PROCEDURES

Aortic cross clamping

Aortic valve replacement

Carotid endarterectomy

PDA ligation

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

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

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.

INDUCTION 2 Attenuate hypertensive response before

intubation by;deepening anesthesia with potent

VAA opioid lidocaine 1.5 mg/kg IV OR

intratracheallyAchieving ßAB with

esmolol;propranolol or labetalol Using topical airway anesthesia

INDUCTION 3Induction agentspropofol , 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.

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

MUSCLE RELAXATION Any NMBA can be used except pancuronium.

Hypotension following tubocurarine ,

metocurine, atracurium or mivacurium may

be accentuated in hypertensives

MONITORING 1Most 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.

MONITORING 2ECG monitoring should focus on detecting

signs of ischemia

UOP in patient with renal impairment or if duration of surgery is >2 hr.

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.

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.

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

POSTOP HYPERTENSION 3A "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.

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.

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.

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.

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.

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.

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;95:273–74. Archives Int. Med. 157:2413-2446 (1997) Dustan HP et al. Arch Intern Med. 1996; 156:

1926-19355. 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. Dustan HP et al. Arch Intern Med. 1996; 156: 1926-1935