This document discusses hypotensive anesthesia techniques. It begins with the aims of deliberate hypotension during surgery, which are to provide an adequate surgical field, decrease blood loss in vascular areas, and avoid the need for blood transfusions. It then covers the physiology of blood flow regulation in vital organs like the brain, heart, kidneys, and liver that must be considered. Various pharmacological agents and mechanical techniques for reducing blood pressure are outlined. Strict patient selection, monitoring, fluid management and postoperative care are emphasized for safely using hypotensive anesthesia.

1. Hypotensive techniques
Dr. Radhwan Hazem Alkhashab
Consultant anesthesia & ICU
2020

2. Introduction
 Deliberate hypotensive technique is important
during many surgical procedures. One of them
are ENT surgery

3. Aims of hypotension
1. Provide adequate surgical field for better
outcome.
2. decrease the blood loss in highly vascular
area.
3. Avoid the needed for intraoperative blood
transfusion which may associated with many
complications.

4. Historical facts
 Deliberate hypotension was first introduced in
1917 in order to provide a bloodless field for
neurosurgery.
 In 1948, high spinal anaesthesia was use to
induce hypotension and create a dry field.
 In 1951 the high epidural block was introduced
 In 1962, sodium nitroprusside was first used
to induce hypotension during anaesthesia.

5. Definition
 The level required to produce the effect but at
the same time is limited by safety.
Generally, it is taken that a MAP as low as 50
mmHg or a 30% drop in MAP is safe for an
ASA 1 subject.
 Chronic hypertensive patient who may not
tolerate a drop of more than 25 % of the MAP

6.  It is recommended that hypotensive
anesthesia be adjusted in relation to the
patient's preoperative blood pressure rather
than to a specific target pressure and be
limited to that level necessary to reduce
bleeding in the surgical field and in duration
to that part of the surgical procedure
deemed to benefit by it.

7.  A mean arterial blood pressure (MAP)
30% below a patient's usual MAP, with a
minimum MAP of 50 mm Hg in ASA Class I
patients and a MAP not less than 80 mm
Hg in the elderly, is suggested to be
clinically acceptable.

8. The physiology of these 3 systems needs to be
examined separately to determine which is the
critical “weak link” i.e. the system that sets the
“minimal permissible pressure”.
Flow is a function of both MAP and autoregulation
in the cerebral, myocardial and renal beds

9. Indications
1. Expected major blood loss
2. Orthopedic surgeries :scoliosis, revision hip surgery,
pelvic malignancies.
3. Major vessel surgery.
4. Neurosurgical : reconstructive spinal surgery, Complex
neuro surgery ,Intracranial , spinal meningioma, AV
malformations ,Pituitary surgeries.
5. Microsurgery : Plastic, Middle ear, FESS .
6. Ophthalmic : Intra ocular surgery ,Choroid ,Vitrectomy.

10. Indications shortly (SPINE)
 S = SPINAL .
 P= PITUITARY, PELVIC, PLASTIC .
 I = INTRACRANIAL, INTRAOCULAR .
 N =NEURO, NEUROVASCULAR .
 E = EAR, ENDOSCOPIC SINUS.

11. Techniques which reduce blood loss
but not deliberate hypotension
 Local with adrenaline
 Tourniquet .
 IPPV .
 PEEP .
 Position .
 Spinal & Epidural.

12. Keep MAP at 55 to 60 mm Hg • WHY ?
Auto regulation of Coronary and cerebral
blood flow stops at MAP at 50 to 55 mm Hg

13. Organs capable of autoregulation are able to
maintain their perfusion over a wide range of
pressure changes.
This critical pressure varies from vessel to vessel,
organ to organ, and probably from individual to
individual.

14. CEREBRAL CIRCULATION
Autoregulation
Normal cerebral blood flow is maintained at
45-50mls/100g/min
MAP range of 50-150mmHg

15. Autoregulation & CBF

16. Factors influencing CBF
1. PaCO2:-
For every 1mmHg increase in PaCO2 there is an
increase in CBF in the order of 1ml/100g/min

17. 2. PaO2-
1. Changes in pao2 also alters CBF
2. 100% O2 administration in hyperbaric
produce toxic effects on cerebral function
and
3. Reduces CBF by 1/5
4. Administration 100% O2 during induced
hypotension not beneficial

18. 3. Volatiles agents:
 Volatile anaesthetics attenuate or abolish the
autoregulation of cerebral blood flow in a dose
dependent manner in the following order :
 Halothane > enflurane > isoflurane

19. 4. TEMPERATURE:
 Cerebral blood flow changes 5-7% per degree
celcius change in temperature.
 Hypothermia causes cerebral vasoconstriction
whereas an increase in body temperature causes
cerebral vasodilation.
5. VASODILATORS
Vasodilators such as nitroprusside and
nitroglycerine attenuate the autoregulation of
CBF in a similar manner to that of volatile
agents.

20. 6. POSITIONING:
 Elevation of the head during hypotensive
anaesthesia can aggrevate the decrease in
cerebral perfusion pressure.
 The perfusion pressure decreases by 2mmHg
for every 2.5cm the head is raised above the
point of monitoring

21. CORONARY CIRCULATION
 Coronary blood flow is dependent upon the
aortic diastolic blood pressure and the coronary
vascular resistance.
 Control of coronary blood flow is autoregulated
predominantly by means of alteration in coronary
vascular resistance that are made to meet
myocardial oxygen demand.
 Any increase in myocardial oxygen demand
requires a parallel increase in coronary artery
blood flow.

22. Hypotensive anaesthesia may substantially:
1. Decrease coronary blood flow.
2. Decreases myocardial oxygen demand
3. Due to reduction in afterload or preload
4. Patients with CAD may have areas of
myocardium that are entirely dependent
upon
pressure to supply adequate blood flow.
5. Use of vasodilators in these patients may
induce
a steal phenomenon.
6. Significant intraoperative risk of myocardial
infarction.

23. RENAL CIRCULATION
 Autoregulation over the range 80-180
mmHg
 MAP less than 75 mmHg leads to
decrease in GFR
 Opioids and inhalational agents stimulate
ADH

24. HEPATIC CIRCULATION
Liver is not an autoregulated organ. decrease in
arterial pressure will lead to a decrease in liver
blood flow.
An increase in PaCO2 or a decrease in PaO2 will
lead to a catecholamine response which causes
splanchnic vasoconstriction and therefore a
decrease in liver blood flow.
Hypocapnia produced incidentally by
hyperventialtion during IPPV leads to a decrease
in liver blood flow as a result of the mechanical
effects.
Liver blood flow may be altered directly by the
effects of anaesthetic agents on splanchnic blood
flow.

25. RESPIRATORY SYSTEM
• During controlled hypotensive anaesthesia the
following occurs:
• Pulmonary blood flow gravitates to the dependent
areas of the lungs.
• The use of vasodilators to induce hypotension
inhibits the hypoxic pulmonary vasoconstriction
response thereby increasing intra-pulmonary shunt.
• All these factors result in hypercarbia, an
increase in arterial-end tidal CO2 gradient and
hypoxaemia

26. Contraindications of
techniques

27. 1. Anaethetist factors:
 Lack of understanding of the technique.
 Lack of technical experience.
 Inability to monitor the patient adequately

28. 2. Patient factors
 Cardiac disease .
 Diabetes .
 Severe Anemia.
 Hepatic disease.
 Cerebrovascular disease.
 Renal disease.
 Respiratory insufficiency.
 Severe systemic hypertension.
 Intolerance to drugs used for
hypotensive anaesthesia
 Pregnancy.
 Glaucoma.

29. Techniques
MAP = CO x SYSTEMIC VASCULAR RESISTANCE
The key equation in the provision of hypotensive
anaesthesia .
MAP can be manipulated by reducing either SVR
or Cardiac output or both.

30. METHODS TO REDUCE CARDIAC OUTPUT

31. METHODS TO REDUCE PERIPHERAL
VASCULAR RESISTANCE

32. Pharmacologic technique
 Ideal agent
 Ease of administration
 Predictable & dose-dependent effect
 Rapid onset/offset
 Quick elimination without the production
of toxic metabolites
 Minimal effects on blood flow to vital
organs

33. Inhalational anesthetics
negative inotropic effect vasodilation
Advantage:
1. Provides surgical
anesthesia
2. Rapid onset/offset.
3. Easy to titrate
4. Cerebral protection
Disadvantage:
1. Decreases CO
2. Cerebral vasodilation
Isoflurane is ideal • 2 MAC • SVR decrease without myocardial
depression • Inh. of baroreceptor reflexes thro anaesthetic action
• Halo OK but think of brady and myocardial depression.

34. Nitrates drugs
Which includes :
1. Sodium nitroprusside (SNP).
2. Nitroglycerin (GTN).

35. Mechanism of action of
nitrate
Sodium nitroprusside and other nitrovasodilators
relax both arteriolar and venous smooth muscle.
Its primary mechanism of action is shared with
other nitrates (eg, hydralazine and nitroglycerin).
As these drugs are metabolized, they release
nitric oxide

36. Mechanism of action Cont.
 Nitric oxide, a naturally occurring potent
vasodilator released by endothelial cells
(endothelium-derived relaxing factor), plays an
important role in regulating vascular tone
throughout the body. Its ultrashort half-life (<5
s) provides sensitive endogenous control of
regional blood flow.
 Inhaled nitric oxide is a selective pulmonary
vasodilator that is beneficial and routinely used
in the treatment of reversible pulmonary
hypertension.

37. Clinical Uses
Sodium nitroprusside is a potent and reliable
antihypertensive. It is usually diluted to a
concentration of 100 mcg/mL and administered as
a continuous intravenous infusion (0.5–10
mcg/kg/min). Its extremely rapid onset of action
(1–2 min) and fleeting duration of action allow
precise titration of arterial blood pressure. A bolus
of 1–2 mcg/kg minimizes blood pressure elevation
during laryngoscopy but can cause transient
hypotension in some patients.

38. CLINICAL USES CONT.
potency of this drug requires frequent blood
pressure measurements—or, preferably,
intraarterial monitoring—and the use of mechanical
infusion pumps. Solutions of sodium nitroprusside
must be protected from light because of
photodegradation

39. Sodium nitroprusside
Direct vasodilator (nitric oxide release)
Advantages
 Rapid onset/offset
 East to titrate
 Increases CO
Disadvantages
1) Cyanide/thiocyanate
toxicity
2) Increased ICP
3) Increased pulm. Shunt
4) Sympathetic stimulation
5) Rebound hypertension
6) Coronary steal
7) Tachycardia
Onset 30 sec, peak 2 min. • 1 to 1.5 mic /Kg /min • Toxicity due
to cyanide as metabolite – common after 8 mic /Kg /min •
Systemic and pulmonary vasodilation .

40. Nitroglycerin
Direct vasodilator (nitric oxide release)
Advantages
 Rapid onset/offset
 East to titrate
 Limited increase in heart rate
 No coronary steal
Disadvantages
 Lack of efficacy depending on
anesthetic technique
 Increased ICP
 Increased pulm. shunt
 Methemoglobinemia
 Inhibition of plt. aggregation
More effect on capacitance vessels • Better in IHD patients •
Action a little delayed : 2 -10 min. • Reflex tachycardia

41. Beta adrenergic antagonist
Advantage
 Rapid onset/offset
 Decreased myocardial O2
consumption
 No increase in ICP
 No increase in pulm. shunt
Disadvantage
 Decreased CO
 Heart block
 Bronchospasm
 Limited efficacy when used
alone
β-Blocker therapy should be maintained perioperatively in
patients who are being treated with β-blockers as a part of
their routine medical regimen

42. Calcium channel blocker -
vasodilation
Advantage
 Rapid onset
 Limited increase in HR
 Increase CO
 No effect on airway reactivity
 Increased GFR/urine output
Disadvantage
 Prolonged duration of action
 Increased ICP
 Increased pulm. shunt

43. DELIBERATE HYPOTENSION: NEW TECHNIQUES
 Use the natural hypotensive effects of anaesthetic drugs
with regard to the definition of the ideal hypotensive
agent.
 Remifentanil( 0.05-2 µg/kg/min) .
 Propofol (2-3 mg/kg)
 Sevoflurane(2-2.5 %)
 Clonidine IV (α2 agonist).

44. MECHANICAL MANOEUVERS TO
POTENTIATE
THE ACTION OF HYPOTENSIVE AGENTS

45. 1. Positioning:
 Position of the patient is criticalto ensure success
of the controlled hypotensive technique.
 Elevation of the site of operation allows easy
venous drainage from the site of surgery. This is
critical to ensure a bloodless field
 change in blood pressure is at a rate of
0.77mmHg per cm change in vertical height from
the heart.

46. 2. Positive airway pressure
 An attractive adjunct to hypotensive
anaesthesia is the use of positive pressure
ventilation
1. with high tidal volumes,
2. prolonged inspiratory times and
3. raising positive end expiratory pressure.

47. Anaesthetic management

48. Preoperative management
 Thorough knowledge by the anaesthetist.
 Proper patient evaluation and selection.
 HB of 10 g/dl.
 Arterial blood gas analysis sampling.
 Good level of anxiolytics ,analgesics .
 Vagolytic drugs should be avoided.

49. Intraoperative management
 Stress free induction.
 Enough peripheral venous access.

50. Monitoring
 HR,NIBP,SPO2,ETCO2
 Invasive blood pressure .
 ECG V5 lead with ST segment analysis.
 Central venous pressure.
 Urine output.
 Temperature.

51. Fluid therapy
 Proper fluid therapy is essential during hypotensive
anaesthesia.
 Preoperative fluid status must be assessed and corrected.
 At the same time maintenance volumes need to be
infused.
 Blood loss must be replaced with an equal amount of
colloid or three to four times the amount of crystalloid.
 If the blood loss exceeds a predetermined level (eg. 20-
25% of thepatient’s total blood volume ), a blood
transfusion is warranted

52. Postoperative management
 Rebound hypertension.
 Reactionary hemorrhage.

53. CONCLUSION
 advantage of miminimisng blood loss during
surgery thereby reducing blood transfusion
requirements.
 an improved surgical field results thereby
improving surgical technique and dissection and
reducing the need for electrocauterization.
 reduce post operative pain and sepsis.
 It is also a safe technique provided appropriate
patient evaluation and selection, proper
positioning and monitoring and adequate fluid
therapy .