Controlled hypotension is also known as deliberate or induced hypotension. It is an anesthetic technique (first described in 1917 by Dr. Cushing) that is implemented to reduce bleeding and the need for blood transfusions, as well as provide a "bloodless" surgical field in certain scenarios.
It is specifically mentioned in the ASA's Practice Guidelines for Perioperative Blood Transfusion and Adjuvant Therapies.
Deliberate hypotension is achieved by utilizing one (or a combination of) drugs and/or volatile agents to deliberately lower a surgical patient's BP. Agents are titrated to achieve one of the following endpoints:
Reduction in the baseline mean arterial pressure (MAP) of 30%
Goal MAP of 5065 mm Hg
Reduction in the systolic arterial pressure to 8090 mm Hg (1) [A].
Physiology Principles
Controlled hypotension is postulated to reduce blood loss by decreasing arterial and venous bleeding. It is most commonly utilized in orthopedic, neurosurgical, plastics, and vascular cases to improve surgical visualization, reduce operative time, and total blood loss.
BP can be measured by either a noninvasive BP cuff or invasive arterial catheter (allows beat-to-beat monitoring).
Reductions in BP and MAP to the above-specified range can be achieved by reducing cardiac output, preload, and/or afterload.
There are several drugs and techniques that can be utilized; they are categorized as primary, secondary, or both.
Primary methods can be used alone; they include regional anesthesia, volatile agents, sodium nitroprusside, remifentanil, nitroglycerin, trimethaphan, alprostadil, and adenosine.
Secondary methods are used adjunctively to limit the dosages needed or attenuate adverse effects of other drugs or techniques. They include ACE inhibitors (captopril), clonidine, dexmedeto-midine, opioids, and propofol (1) [A].
"Both" describes agents that can be used alone or in combination and include beta-blockers (labetalol, esmolol, propranolol), calcium-channel blockers (verapamil, diltiazem, nicardipine), and fenoldopam.
Hemodynamics. Vasodilators can decrease afterload and improve left ventricular function as well as decrease cardiac work and oxygen consumption. Additionally improved LV ejection can reduce the LVEDV/LVEDP and possibly improve coronary perfusion (however, this must be balanced against decreased diastolic blood pressure; see below).
Anatomy
BP measurements are typically performed in the upper extremities utilizing either a NIBP cuff or an arterial line.
The NIBP cuff can be used in the lower extremities. The arterial catheter is usually placed in a radial artery but other options exist such as ulnar, femoral, and dorsalis pedis sites. However, systolic BP readings in the leg can run 1020% higher than the brachial artery pressures.
Physiology/Pathophysiology
Although there are potential benefits, the anaesthetist needs to weigh them against the risks in each individual patient.
General risks include impaired perfusion and hypoxia of vital organs and microcirculatory dysregulation. This is often difficult to discern as adequate oxygen delivery is an ever-moving target that is altered by BP, hemoglobin content, oxygen saturation, tissue extraction, and utilization.
Cerebrum. CPP = MAP - ICP; where CPP is cerebral perfusion pressure, ICP is intracranial pressure.
Myocardium. No ideal number exists in regard to optimal cardiac perfusion pressures. Coronary perfusion is equal to the diastolic blood pressure minus the left ventricular end diastolic pressure.
Controlled hypotension can decrease the DBP but can also decrease afterload and myocardial oxygen consumption.
As discussed above, LVEDV/LVEDP may be decreased and can offset decreases in coronary perfusion pressure as well.
Additionally, because the LV is only perfused during diastole, the heart rate also becomes an important factor.
Renal concerns
Studies in patients with no preexisting renal disease have demonstrated that autoregulation generally remains intact with a MAP between 80 and 180 mm Hg
More recent information suggests that the kidneys do not seem to incur damage with MAPs of 5060 mm Hg
Renal compensatory mechanisms appear to be well preserved at MAPs to 60 mm Hg for >200 minutes (2) [B]
One study showed that MAPs of 50 mm Hg for approximately 120 minutes resulted in decreased urine flow rate, effective renal blood flow, osmolar clearance, and endogenous creatinine clearance; however, all parameters returned to normal after cessation of anesthesia (3) [B].
Hepatic concerns. The extent of autoregulation is unknown. Studies in patients with no preexisting hepatic disease have suggested that MAPs between 50 and 60 mm Hg did not appear to result in ischemia or affect autoregulation. Liver enzymes do not typically increase, and when they are elevated they returned to normal after 14 days (4) [B].
Patients with end-organ disease are at increased risk for ischemia or hypoperfusion
Cerebral disease
With chronic hypertension, the cerebral autoregulation curve is shifted to the right
One well-controlled study by Williams-Russo et al (5), however, demonstrated no long-term cognitive dysfunction in patients with end-organ disease (44% of 117 patients had baseline HTN) at MAPs between 45 and 55 mm Hg suggesting that at these pressures the metabolic requirements of the brain are met (4) [A]
Carotid stenosis results in maximal dilation distal to the lesion; thus, drops in BP cannot be compensated by further vasodilation to maintain flow
Cardiac disease
Chronic and significant hypertension alter the autoregulation range
Significant stenotic valve lesions have a fixed cardiac output and drops in SVR or the reflexive tachycardia that may occur with controlled hypotension are not well tolerated
Atherosclerotic vessels are perfusion-dependent; vessels are maximally vasodilated just distal to the lesion (similar to carotid stenosis)
Renal. Acute on chronic renal dysfunction can result from intraoperative hypoxia or hypotension.
Perioperative Relevance
The major indication for imposing controlled hypotension is to reduce bleeding:
Provides a favorable and clear surgical field and may increase the quality and speed of a surgical procedure (6) [B].
Decreases the need for blood product transfusion. This is generally welcomed secondary to the concerns of infection and adverse systemic reactions (7) [A].
Appropriate adjuncts should be implemented to aid in monitoring end-organ perfusion and function as well as volume status. They include, but are not limited to
Hemodynamic variables such as pulse pressure waveform variation in pulse oximetry and arterial line waveforms aid with assessing volume status
EKG rhythm analysis to asses myocardial perfusion and oxygenation
ETCO2 reduces from "dead space" pathophysiology (decreases in BP reduce alveolar perfusion and exhalation of CO2)
Urine output is an indicator of renal perfusion
BIS/EEG/SSEP/MEP monitoring to assess neural perfusion and oxygenation
Blood gas analysis (pH, CO2, HCO3, base deficit) can indicate metabolic acidosis from anaerobic metabolism (lactate production).
CVP trends can aid with volume assessment
Mixed venous O2 aids with assessing oxygen delivery and utilization at the tissue level.
Of note, none of these methods guarantee end-organ perfusion but are adjunctive to clinical impression.
Hemodynamics
The effect of controlled hypotension on HR, SVR, and ischemia varies based on the drug or drugs used to achieve the hypotensive state. The overriding concern is ischemia, and trying to gauge the level of hypotension that can safely be handled by patients with preexisting cardiac conditions is sometimes difficult. Patient-specific decisions are certainly warranted in this case.
Equations
BP = CO × HR; BP is blood pressure, CO is cardiac output, and HR is heart rate
Normal = 120/80 mm Hg
MAP = [(2 × DBP) + SBP]/3; where MAP is mean arterial pressure, DBP is diastolic blood pressure, and SBP is systolic blood pressure
Normal = 70110 mm Hg
CPP = MAP RAP (or ICP if greater); where CPP is cerebral perfusion pressure, MAP is mean arterial pressure, RAP is right atrial pressure, and ICP is intracranial pressure
Normal = between 7090 mm Hg
References⬆⬇
TobiasJD.Controlled hypotension in children: A critical review of available agents. Paediatric Drugs. 2003;4(7):439453.
ToivonenJ, KaukinenS, OikkonenM, et al.Effects of deliberate hypotension induced by labetalol on renal function. Eur J Anaesthesiol. 1991;8:1320.
LessardMR, TrepanierCA.Renal function and hemodynamics during prolonged isoflurane-induced hypotension in humans. Anesthesiology. 1991;74:860865.
FukusakiM, MiyakoM, HaraT, et al.Effects of controlled hypotension with sevoflurane anaesthesia on hepatic function of surgical patients. Eur Acad Anesthesiol. 1999;16:111116.
Williams-RussoP, SharrockNE, MattisS, et al.Randomized trial of hypotensive epidural anesthesia in older adults. Anesthesiology. 1991;91(4):926935.
EnderbyGEH.The advantages of controlled hypotension in surgery. Br Med Bull. 1958;14(1):4951.
ChoiWS, SammanN.Risks and benefits of deliberate hypotension in anaesthesia: A systematic review. Int J Oral Maxillofac Surg. 2008;37(8):687703.
Additional Reading⬆⬇
Textbook of Neuroanaesthesia and Critical Care. 1st Edition, 2000. Edited by Basil F.Matta, David K.Menon, and John M.Turner.
Goodman & Gilman's The Pharmacological Basis of Therapeutics. 21th Edition, 2011. Edited by LaurenceBrunton, BruceChabner, and BjornKnollman.
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