This document outlines a presentation on hypertension given at Aksum University in February 2016. It discusses the significance of hypertension for anesthetists, including how familiarity with antihypertensive drugs is important. It also notes that hypertension commonly occurs during anesthesia and its recognition depends on correctly functioning monitors. The document provides definitions of hypertension and outlines its classification, as well as general management approaches including non-pharmacological and pharmacological treatment. It discusses various drug classes used to treat hypertension and their mechanisms of action.

1. ABAYNEH BELIHU
AKSUM UNIVERESITY
FEB 2016

2. “
”
Hypertension

3. OUTLINES
 RAS physiology
 Definition and classification of hypertension
 Overview of general management
 Non pharmacologic
 Pharmacologic
 Drug interaction
 Anesthesia management
 Preoperative hypertension
 Intraoperative hypertension
 Intraoperative monitoring
 Postoperative hypertension

4. SIGNIFICANCE OF THE TOPIC FOR
ANESTHETISTS 1
 Familiarity with the names and MOA of
antihtensive agents is important for anesthetists.
 The interaction of anesthesia drugs and
adjuvants with antihypertensive agents should be
born in mind

5. SIGNIFICANCE OF THE TOPIC
FOR ANESTHETISTS 2
 Hypertension occurs commonly during anaesthesia and is
usually promptly and appropriately treated.
 Its recognition is dependent on correctly functioning and
calibrated monitors.

6. SIGNIFICANCE OF THE TOPIC
FOR ANESTHETISTS 3
 Intraop hypertension is common and has many causes.
 However, when it is
 Severe
 No cause is evident or
 Fails to respond to routine measures, it has the potential to
cause morbidity and even mortality in susceptible patients.
(Reich et al)

7. SIGNIFICANCE OF THE TOPIC
FOR ANESTHETISTS 4
Among 4000 clients there were 252 in which hypertension was
mentioned,
 11 dealt with hypertension occurring only in recovery,
 10 reported hypertension 2⁰ laryngoscopy and ETI, and
 3 involved as a consequence of poorly controlled preoperative
HTN. (A D Paix et al)

8. SIGNIFICANCE OF THE TOPIC
FOR ANESTHETISTS 5
 Major morbidity occurred in six patients and consisted of
two reports each of MI, pulmonary oedema and awareness
under general anaesthesia.
 Hypertension and tachycardia under anaesthesia have been
shown to be independent risk factors for poor outcomes,
particularly after long procedures.(Reich DL et al.)

9. IMPORTANCE OF KNOWING COMMON
ANTIHYPERTENSIVE DRUGS 1
Because Antihypertensive drugs result in:
1. ↓peripheral vascular tone…interfere with circulatory
homeostasis
2. Difficulty compensation for stresses: Blood loss,
∆posture, IPPV.
3. Bad reaction to drugs such as thiopentone which can
cause a fall in BP.
4. Electrolyte imbalance related to Prolonged diuretic
therapy
9

10. IMPORTANCE OF KNOWING COMMON
ANTIHYPERTENSIVE DRUGS 2
And thus……
Electrolyte profile must be checked pre-operatively (esp. K+).
Antihtnsive drugs have to be continued till morning of surgery.
If heavy bleeding is expected, Enalapril has to be discontinued.
Patients on loop diuretics has to have e¯ determined.

12. Renal
function
Blood
volume
Venous
tone
Venous
return
Heart
rate
Nervous
control
Muscular
responsiveness
Myocardial
contractility
Stroke
volume
Cardiac
output
CNS
factors
Renin
release
Angiontensin II
formation
Intrinsic vascular
responsiveness
Peripheral
resistance
Nervous
control
Renal
function
MAP
Factors that Govern
the Mean Arterial Pressure

13. Mean Arterial Pressure
MAP = CO
X
CO = HR SV
PVR
Myogenic tone
Vascular responsiveness
Nervous control
Vasoactive metabolites
Endothelial factors
Circulating hormones
XSNS
Venous
tone
BV
Contactility

14. Mechanisms Controlling CO and TPR
Artery Vein
2. Hormonal
 Renal
Ang II
 Adrenal
CA
Aldosterone
3. Local Factors
Endothelial agents
ABG Concn
1. Neural
 SymNS
 PSNS
CRITICAL POINTS!
1. These organ systems and mechanisms control physical factors of CO and TPR
2. Therefore, they are the targets of antihypertensive therapy.

15. Response mediated by the RAAS &
sympathetic system on BP

16. SO WHAT IS HYPERTENSION?
Hypertension is defined as SBP >140 mmHg,
DBP>90 mmHg, or taking antihypertensive
medication.
VI JNC, 1997

17. JNC 8 HAS ALSO ARRIVED
http://jama.jamanetwork.com/article.aspx?articl
eid=1791497

18. 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

19. GOAL OF THE REVISION
A.To identify individuals at any BP level who have a
reasonable likelihood of future CV events.
OR
A.To identify people with low BP levels as having
Stage 1 hypertension if they also exhibit early
signs of vascular damage, thus prompting HCPs to
offer treatment to this at-risk group

20. 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 "

21. STAGES OF HYPERTENSION
HF
Angina
Post-MI
Extensive CAD
DM
CRF
Recurrent stroke prevention

22. CLASSIFICATION FOR ADULTS
Adapted from: Archives Int. Med. 157:2413-2446 (1997)
Category Systolic (mm Hg) Diastolic (mm Hg)
Optimal BP < 120 And < 80
Normal BP < 130 And < 85
High-normal BP 130 – 139 Or 85 - 89
Stage 1 (mild) 140 – 159 Or 90 - 99
Stage 2 (moderate) 160 – 179 Or 100 - 109
Stage 3 (severe) ≥180 or ≥110

23. TYPES OF
HYPERTENSION
ESSENTIAL SECONDARY
DISORDER OF UNKNOWN ORIGIN
AFFECTING THE BP REGULATION
SECONDARY TO
OTHER DISEASE PROCESSES
ENVIRONMENTAL
FACTORS
STRESS Na+/ INTAKE OBESITY SMOKING
**********************************************************************************

24. DISEASES ATTRIBUTABLE TO HTN
HYPERTENSION
Gangreneof the Lower
Extremities
Heart Failure Left Ventricular
Hypertrophy Myocardial Infarction
CoronaryHeart DiseaseAorticAneurym
Blindness
ChronicKidney
Failure
Stroke Preeclampsia
Eclampsia
CerebralHemorrhage
Hypertensive encephalopathy
AdaptedfromDustanHPetal.ArchInternMed. 1996;156:1926-1935

25. 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

26. TREATMENT – WHY? 2
IV.Pre-existing hypertension, particularly if
untreated, increases the likelihood of intraop
hypertension and of complications (Prys-Roberts et al)

27. Pertinent complications of untreated HTN

28. 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.

29. NON PHARMACOLOGICAL TREATMENT 1
Avoid harmful habits ,smoking ,alcohol
Reduce salt and high fat diets
Loose weight , if obese
Regular exercise
DASH

30. NON PHARMACOLOGIC TREATMENT 2
MODIFICATION APPROX. SBP
REDUCTION
Weight reduction 5 – 20 mm of hg /10 kg lost
Adopt DASH eating plan 8 – 14 mm of hg
Dietary sodium reduction 2 – 8 mm of hg
Physical activity 4 – 9 mm of hg
Moderation of alcohol consumption 2 – 4 mm of hg

31. PHARMACOLOGIC TREATMENT 1

32. PHARMACOLOGIC TREATMENT 2
Drug therapy reduces:
 The progression of hypertension, and
 The incidence of:
 stroke
 CHF
 CAD, and
 Renal damage with reversal of pathophysiologic
changes , such as LVH and altered CAR.

33. PHARMACOLOGIC TREATMENT 3
 Most patients with mild hypertension
require only single-drug therapy, thiazide
diuretic, ACEI, ARB, ßAB, or CCB.

34. PHARMACOLOGIC TREATMENT 4
A. Primary (essential hypertension) vs. secondary (10-15%)
E.g.pheochromocytoma, renal artery constriction, Cushing’s syndrome
B. Diagnosis (based on 3 separate office visits) and severity
C. Individualization (age, gender, ethnicity) and compliance
D. Pre-existing risk factors and medical conditions
E. Smoking, Hyperlipidemia, DM, CHF, Asthma, current
medication
F. Monotherapy vs. Polypharmacy
Factors to consider

35. CLASSES OF DRUGS AND
TARGET SITES
DRUGS Targets
 Diuretics
 Agents acting on ANS
 Direct Vasodilators
CCB
 RAAS blockers
 Blood Volume
 Cardiac Output
 Resistance of Vessel
 Arterioles
 RAAS
 Neuroregulation

36. Sites of action of antihypertensives

37. Mechanisms of action of antihypertensives

38. DIURETICS 1
Bumetanide, furosemide, hydrochlorothiazide, spironolactone, triamterene
 Act by decreasing blood volume and CO
 Decrease PVR during chronic therapy
 Drugs of choice in elderly hypertensive

39. 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.

40. DIURETICS 3:
NEPHRON ANATOMY & SITE OF ACTION

41. 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.

42. 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.

43. DIURETICS 7
K-sparing diuretics include:
 triamterene, amiloride (both Na+ channel inhibitors) and
 spironolactone (aldosterone antagonist).
 In patients given digitalis
 Enhance natriuretic effects of others (e.g., thiazides) and
counteract the K+ -depleting effect of these diuretics.

44. 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

45. SYMPATHOPLEGIC AGENTS
1. Centrally-acting adrenergic drugs (α2-agonists
such as clonidine and α-methyldopa).
2. Drugs that act on PNS (β & α1-blockers;
ganglion blocking agents; agents that block
adrenergic NT synthesis and/or release)

46. CENTRALLY-ACTING
ANTIHYPERTENSIVE AGENTS
Clonidine
reduces sympathetic and increases PS tone,
leading to BP lowering and bradycardia.

47. 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.

48. 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.

49. CAUTION!
 Abrupt withdrawal may induce hypertensive crisis
 Do not give to patients who are at risk of mental
depression, or are taking tricyclic antidepressants

50. METHYLDOPA
A prodrug that exerts its antihypertensive action
via an active metabolite

51. MECHANISM OF ACTION
The metabolite, α-methyl-norepinephrine, is stored in
neurosecretory vesicle in place of NE.
When released, α-methyl-NE is a potent α-AR agonist and
in PNS is a vasoconstrictor.
Its CNS effect is mediated by α2-AR, resulting in reduced
adrenergic outflow and an overall reduced TPR.

52. THERAPEUTIC USE
Does not alter most of the CV reflexes
CO and BF to vital organs are maintained
Reduces renal vascular resistance and safer in patients
with renal insufficiency
Not used as first drug in monotherapy, but effective when
used with diuretics.

53. DRUGS THAT ACT ON PNS
1. β-blockers
 Propranolol, metoprolol, nadolol,carteolol, atenolol,
betaxolol,bisoprolol,pindolol, acebutolol, penbutolol,
labetalol, carvedilol.

54. MECHANISM OF ACTION
1. Reduces CO
2. Inhibits renin release and AT-II and aldosterone
production, and lower peripheral resistance
3. May decrease adrenergic outflow from the CNS

55. 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

56. 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

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

58. PINDOLOL, ACEBUTOLOL, PENBUTOLOL
 Antagonistic effect is combined with partial
agonistic effect on β2-AR.
 Particularly for patients with cardiac failure,
bradyarrhythmias, or peripheral vascular disease

59. LABETALOL, CARVEDILOL
 Given as racemic mixture of isomeric compounds
 Labetalol also has some β2-agonistic effects.
 Labetalol-Hypertensive emergencies (injection) or
hypertension resulting from pheochromocytoma
 Carvedilol- in patients with CHF

60. ∝-1 BLOCKERS
 Prazosin, tetrazosin, doxazosin, phentolamine,
phenoxybenzamine.

61. 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.

62. 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

63. DIRECT VASODILATORS
 Hydralazine, minoxidil, sodium NP, diazoxide

64. MECHANISM OF ACTION
 Relax smooth muscle (SM) of arterioles (and
sometimes veins), thereby reduce SVR.

65. THERAPEUTIC USE
Hydralazine
 Dilates arterioles but not veins.
 Effect does not last long when used alone; but
combination therapy can be very effective for
even severe hypertension.

66. 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

67. SODIUM NITROPRUSSIDE
 Parenterally administered (IV)
 Powerful vasodilator hypertensive emergencies
 Works by increasing intracellular cGMP and dilates
both arterial and venous vessels
 In patients with cardiac failure because CO
increases due to afterload reduction
 Effects last only <10 minutes after discontinuation

68. 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).

69. CALCIUM CHANNEL BLOCKERS
 verapamil, diltiazem, dihydropyridine family
(eg, nifedipine).
 In addition to antianginal and antiarrhythmic
effects, dilate peripheral arterioles and reduce BP
by inhibiting calcium influx into arterial SM cells.
 verapamil has more cardiac effect (decreasing CO)
and nifedipine has more vasodilating effect.

70. 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.

71. ACEI
Captopril, enalapril (lisinopril is a lysine-derivative), benazepril,
fosinopril,moexipril,quinaprilandramipril

72. 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).

73. 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

74. MECHANISM OF ACTION 3

75. 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

76. 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).

77. ANGIOTENSIN-II ANTAGONISTS
Losartan,valsartan,candesartan,irbesartan,telmisartan,eprosartan,andzolasartan.
 Saralasin- orally ineffective and requires
continuous IV infusion.
 Saralasin has partial agonist activity, and is not
currently in use for hypertension treatment.

78. 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.

79. THERAPEUTIC USE
 losartan has the advantage of not causing cough
and angioedema, which are effects of bradykinin.

80. ADVERSE EFFECTS AND
TOXICITY
 Similar to those of ACEIs
 Fetotoxic and should not be used for treating
hypertension in pregnant women.

81. LOGICAL COMBINATIONS
Diuretic
b-
blocker
CCB ACEI
a-
blocker
Diuretic -  -  
b-blocker  - * - 
CCB - * -  
ACEI  -  - 
a-blocker     -
* VERAPAMIL + BETA-BLOCKER = ABSOLUTE CONTRA-INDICATION

82. HYPERTENSIVE EMERGENCY & PARENTRAL DRUGS

83. 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).

84. 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.

85. RECOMMENDATION 3
 A diuretic with adrenergic blockade or CCB alone
for elderly patients.
 Patients with moderate to severe HTN require a
second or third drug.

86. 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.

87. 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

88. 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.

89. THE THREE FACTORS
1. Emphasis on early recognition and treatment of
hypertensives, with the result that more
patients are receiving antihypertensives.
2. Introduction of a wide variety of potent medications.
3. Most antihypertensive agents should be continued up to
and including the day of surgery and in some
instances should be administered during the
anaesthetic.

90. 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.

91. 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

92. 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.

93. 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.)

94. 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.

95. 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.

96. 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.

97. ADRENERGIC NEURON
INHIBITORS 1
 Reserpine, when used in large doses as a
major tranquilizer or as an antihypertensive,
has the potential to produce significant and
refractory hypotension during anaesthesia.
 However, in very small doses, and usually in
combination with other antihypertensive agents,
greatly reduces the potential for drug
interactions.

98. ADRENERGIC NEURON
INHIBITORS 2
 Debrisoquine, has MAO inhibitory effects.
 The product information for debrisoquine
contains: "To avoid the possibility of vascular
collapse, discontinue debrisoquine 24 hours prior
to elective surgery."
 Clinical experience suggests that debrisoquine
can be safely continued until time of surgery.

99. 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.

100. 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.

101. 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).

102. 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.

103. 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.

104. ANAESTHESIA MANAGEMENT
OF
HYPERTENSIVE PATIENTS

105. 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

106. GOALS OF ANESTHESIA
MANAGEMENT
A. Preoperative consideration and evaluation
B. Perioperative risk reduction
C. Premedication
D. Balanced anesthesia
E. Proper monitoring
F. Parenteral medications

107. 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.

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

109. 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.

110. PERIOPERATIVE RISK REDUCTION 5
 Untreated hypertension discovered at the preop anaesthetic
assessment necessitates a systematic approach
 The following algorithm is one possibility
 Three DBP readings are taken. If the average value is:
A. >120 mmHg:
cancel the operation.
Admit, investigate ,and treat
reschedule once the BP is controlled for 4-6 weeks

111. PERIOPERATIVE RISK REDUCTION 6
B. 105-115 mmHg with signs of end-organ damage:
follow the same course as for BP>120 mmHg
C. 105-115 mmHg without signs of end-organ damage:
Continue with operative plan
Consider preop Rx with
oral ßAB e.g. atenolol, OR
alpha-2-agonist, e.g. clonidine

112. 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.

113. 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

114. 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.

115. PREOPERATIVELY… 2
 Transient hypertension only on admission may not
need therapy but indicate a propensity to become
hypertensive during anesthesia and surgery
 Particularly for such patients, better to monitor
BP directly through an intra-arterial catheter

116. INTRAOPERATIVE HYPERTENSION:
ETIOLOGY
A. Intubation hypertension
B. Inadequate anesthesia
C. Hypercapnia
D. Hypoxemia
E. Pharmacological adjuvants
F. Phaeochromocytoma
G. Surgical procedures
H. Bladder distension
I. Extubation hypertension

117. INTUBATION HYPERTENSION
 Laryngoscopy & intubation are known causes of
hypertension.
 Severe if laryngoscopy is prolonged
 Can be minimized by pre administration of
lignocaine.

118. 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.

119. 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

120. HYPOXEMIA
 Hypoxia increases CO
 In severe hypoxia the SBP is raised
 Severe systolic hypertension is a very late sign
and indicate complete circulatory collapse.

121. PHARMACOLOGICAL ADJUVANTS
 Inotropic & vasoconstrictor agents
 IV administration of adrenaline containing local anesthetic
 Nasal packing
 Medication errors

122. SURGICAL PROCEDURES
 Aortic cross clamping
 Aortic valve replacement
 Carotid endarterectomy
 PDA ligation

123. 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

124. 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

125. 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.

126. INDUCTION 2
 Attenuate hypertensive response before intubation by;
 deepening anesthesia with potent VAA
 opioid
 lidocaine 1.5 mg/kg IV OR intratracheally
 Achieving ßAB with esmolol;propranolol or
labetalol
 Using topical airway anesthesia

127. INDUCTION 3
Induction agents
 propofol , barbiturates, benzodiazepines and
etomidates are equally safe for induction of GA in
hypertensive pt.
 ketamine may be used in hypertensive by blunting
its sympathetic stimulation activity by other
agents.

128. 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

129. MUSCLE RELAXATION
 Any NMBA can be used except pancuronium.
 Hypotension following tubocurarine , metocurine,
atracurium or mivacurium may be accentuated in
hypertensives

130. MONITORING 1
 Most hypertensive patients do not require any
special intraop monitors
 Invasive BP monitoring for patient with wide swing
in BP & for major surgical procedure associated
with rapid or marked change in cardiac pre & after
load.

131. MONITORING 2
 ECG monitoring should focus on detecting signs of
ischemia
 UOP in patient with renal impairment or if
duration of surgery is >2 hr.

132. 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.

133. 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.

134. 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

135. POSTOP HYPERTENSION 3
 A "stiff,“ often hypertrophied, ventricle resulting
from chronic hypertension may lead to intolerance
of tachycardia, often seen postop because of
inadequate ventricular filling time, resulting in
hypotension and inadequate CO.

136. 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.

137. 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.

138. 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.

139. 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.

140. 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.

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