Hypertension in anaesthesia: Preoperative preparation is the key

When ever I inform my consultant anaesthetist about a patient in preanaesthetic checkup, his first question is, what is the blood pressure now? 

I often ask myself does the measured blood pressure in the preanaesthic check up really gives the whole picture?

I’m going to answer this issue in the following paragraphs.

Nevertheless Hypertension is a great burden for the perioperative management. In Bangladesh the prevalence of hypertension is 20% among adult population.


So we should be very vigilant regarding the preoperative assessment. Most of these patient experiences some degree of perioperative morbidity. Due to unavailability of proper postoperative care unit, people often asks a simple but burning question. 

Is my patient safe here to perform the surgery? 

Most of the time you ask them to keep faith in the Creator. It's obvious. But there are still something we've to do and we can do. 

Most of the patient with hypertension usually remains asymptomatic in preanesthetic checkup. Identification of the duration and severity of hypertension is important. 

We often ask some questions when facing these kind of patients.

  • Are you suffering from high blood pressure? If yes, how long you're suffering from high blood pressure?
  • Is your blood pressure controlled over the time period?
  • When you last checked your blood pressure?
  • Do you regularly take antihypertensives?
  • Which medications are you taking?
  • What was your previous medication? How was the response? Any side effects?
  • How long you are taking these medications?
  • Any adverse effects of current antihypertensive drug therapy?
  • Do you have other diseases?
  • Do you any other symptoms?
  • Did you experience any weight change?
  • Are you suffering from diabetes, dyslipidaemia?
  • Do you've any history of hospital admissions?
  • How much physical activity do you perform?
  • Do you smoke or take non-steroidal anti-inflammatory drugs (NSAIDs), oral contraceptives, steroids, herbal medications, sympathomimetics, hormonal therapy?
These questions usually tell us a lot. One of deficiency in our patient management is that we don't measure the blood pressure properly. In the next section I will enumerate the ideal blood pressure measurement procedure.

Beside asking the above questionnaire, the history and sign-symptoms of end organ damage should be evaluated. This is by far very important to exclude or to take necessary steps in the preoperative period to minimise perioperative complications.

Patients should be questioned  regarding:
  • Angina, myocardial infraction, heart failure, arrhythmia 
  • Exercise tolerance
  • Shortness of breath (particularly at night)
  • Dependent  edema
  • Postural lightheadedness  
  • Syncope
  • Episodic visual disturbances 
  • Episodic neurological symptoms
  • Claudication
  • Sexual dysfunction
It takes time to evaluate all of these. But these questionnaire will help you to make a proper planning for the patient. 

As 80 - 95% hypertensions are essential, we sometimes miss to feature out those 5 - 20% secondary causes. This step is very necessary because your diagnosis can make a big difference here.

This is a mnemonic of secondary hypertension: CHAPS

In an elaborate view secondary hypertension may be due to:

Source:  Harrison's Principles of Internal Medicine, 20e

In preanaesthetic checkup diagnosis of secondary hypertension is not entertaining  but there are plenty of clues to identify the secondary causes. 

If you find any sign or symptoms of secondary hypertension then you can make a decision for referral or make a plan regarding perioperative management. 

So the causes of secondary hypertension are as follow:

There are some clinical pattern of hypertension:
  • Vasoconsctricted hypertension - characterised by diastolic hypertension with raised systemic vascular resistance and normal or decreased cardiac output and heart rate.
e.g. chronic renovascular disease 

  • Hyperdynamic hypertension - characterised by systolic hypertension, widen pulse pressure, increased heart rate, cardiac output.
e.g. aortic regurgitation, thyrotoxicosis, fever, arteriovenous fistula, patent ductus arteriosus. 

  • Isolated systolic and pulse pressure hypertension - it represents arterial stiffening (decrease vascular compliance). This results inability to absorb pulsatile load, causing systolic pressure to rise. Due to stiffening, the propagated and reflected pulse wave augments systolic pressure and increases afterload but there is loss of diastolic augmentation. 
e.g. atherosclerosis

BP measurement

The measurement and recording of BP is one of the most frequent clinical observations, but the impact of technique on the reliability and reproducibility of observations is often overlooked. 

  • Use a correctly calibrated and maintained machine (manual or automatic).
  • BP should be measured with the patient sitting quietly, not engaged in conversation, and with the arm supported at heart level with the hand relaxed. Remove tight clothing.
  • Because automated devices may not measure blood pressure accurately if there is pulse irregularity (for example, due to atrial fibrillation), palpate the radial or brachial pulse before measuring blood pressure. If pulse irregularity is present, measure blood pressure manually using direct auscultation over the brachial artery.
  • A cuff of appropriate size should be used.
  • Seated BP is adequate except in elderly patients or those with diabetes who may have orthostatic hypotension (standing BP is needed as well - after at least one minute's standing). If standing systolic blood pressure (SBP) is 20 mm Hg or lower than when seated, review medication, and measure all subsequent blood pressures with the person standing (consider specialist referral if postural hypotension symptoms persist).
  • Initially, measure BP in both arms; if there is a persistent difference of >15 mm Hg between arms then ensure subsequent blood pressures are taken in the arm with the higher reading.
  • If the BP is found to be elevated, a second reading should be taken with an interval of at least 1 min between readings. 
  • A third reading should be taken, if there is a significant difference between the first and second readings.

Use an automated machine or the following manual method (if the pulse is irregular (eg, in atrial fibrillation), always use the manual method):

    • Inflate the cuff whilst palpating the brachial artery, until the pulse disappears. This provides an estimate of systolic pressure.
    • Inflate the cuff until 30 mm Hg above systolic pressure, then place a stethoscope over the brachial artery. Deflate the cuff at 2 mm Hg per second.
    • Systolic pressure: the appearance of sustained repetitive tapping sounds (Korotkov I). Diastolic pressure: usually the disappearance of sounds (Korotkov V). However, in some individuals (eg, pregnant women) sounds are present until the zero point. In this case the muffling of sounds (Korotkov IV) should be used.
    • Record to the nearest 2 mm Hg.
    • If initial BP is ≥140/90 mm Hg, take a second or even a third reading and record the two lowest as the clinic BP.
These requirements for accurate measurement are often not met in a busy preassessment clinic or preoperative admission ward. 
  • If a patient presenting for surgery is found to have a markedly elevated BP, it is appropriate to move them to a quiet area and measure the BP again, ensuring that correct technique is used. This is an appropriate course of action in patients whose initial BP is >180/110 mm Hg, that is, above the threshold for severe hypertension.

BPs recorded in patients coming to hospital for elective surgery will often be above the values that would be recorded in the same patients in the community setting. 
  • It would not be appropriate to diagnose new or poorly controlled hypertension on the basis of readings taken immediately before surgery. However, if the patient has a consistently elevated BP, it is appropriate to refer the patient to their general practitioner for further measurements and every effort should be made to ensure that patients with pressures consistent with severe hypertension are followed up.

The above discussion applies to the patient sitting quietly. It is normal for the BP to increase on exercise, for example, during a preoperative cardiopulmonary exercise test; indeed, marked increases in pressure may be seen and the American Thoracic Society Guidelines suggest that an increase in systolic pressure up to 220 mm Hg may be considered a normal response. A decrease in BP on exercise would be considered abnormal and a possible indication of cardiac disease.

Diagnosis of hypertension:

When considering a diagnosis of hypertension, measure blood pressure in both arms:
  • If the difference in readings between arms is more than 15 mmHg, repeat the measurements.
  • If the difference in readings between arms remains more than 15 mmHg on the second measurement, measure subsequent blood pressures in the arm with the higher reading.
If blood pressure measured in the clinic is 140/90 mmHg or higher:
  • Take a second measurement during the consultation.
  • If the second measurement is substantially different from the first, take a third measurement.
Staging of hypertension:
  • Stage 1 hypertension - 
BP in surgery/clinic is ≥140/90 mm Hg 
ambulatory blood pressure monitoring (ABPM) or home blood pressure monitoring (HBPM) ranges from 135/85 mm Hg to 149/94 mm Hg.
  • Stage 2 hypertension - 
BP in surgery/clinic is ≥160/100 mm Hg but less than 180/120 mm Hg 
ABPM or HBPM is ≥150/95 mm Hg.
  • Stage 3 or severe or accelerated hypertension - 
systolic BP in surgery/clinic is 180 mm Hg or higher 
diastolic BP is 110 mm Hg or higher.
  • Masked hypertension - BP in surgery/clinic is less than 140/90 mm Hg but average ABPM or HBPM readings are higher.
  • White coat effect - a discrepancy of more than 20/10 mm Hg between clinic and average daytime ABPM or average HBPM blood pressure measurements at the time of diagnosis.

  • Hypertensive urgency - blood pressure >180/120 without end organ damage.
  • Hypertensive emergency - blood pressure >180/120 mmHg with the sign symptoms of end organ damage (encephalopathy, papilledema). 

Preoperative decision making:

It's little bit tricky. No guideline still published any clearcut opinion. But most agree upon certain issues:  

  • Elevated blood pressure without any other risk factors in asymptomatic patient doesn't support to delay surgery for cardiac evaluation.
  • Decision to delay surgery for persistent rise of diastolic blood pressure >110 mmHg should be made if the benefit of delaying surgery exceeds the risk. 
  • Decision of delaying surgery is based on severity of hypertension and coexisting morbidity - myocardial infraction, heart failure, cerebrovascular or renal complications.

Perioperative risk associated with hypertension:

Preexisting hypertension can induce a variety of cardiovascular responses that potentially increase the risk of surgery, including 

  • Diastolic dysfunction from left ventricular hypertrophy
  • Systolic dysfunction leading to congestive heart failure
  • Renal impairment
  • Cerebrovascular and coronary occlusive disease

The level of risk is dependent upon the severity of hypertension.

It is still unclear whether postponing surgery to achieve blood pressure control will lead to reduced cardiac risk. The American College of Cardiology/American Heart Association (ACC/AHA) guidelines list uncontrolled hypertension as a "minor" risk factor for perioperative cardiovascular events.

Severe hypertension — An early study found that patients with untreated severe hypertension (mean systolic and diastolic pressures of 211 and 105 mmHg, respectively) had exaggerated hypotensive responses to the induction of anesthesia and marked hypertensive responses to noxious stimuli. 


Patients with well-controlled hypertension responded similarly to normotensive subjects. Other studies have found that a diastolic pressure over 110 mmHg immediately before surgery is associated with a number of complications including dysrhythmias, myocardial ischemia and infarction, neurologic complications, and renal failure.


Mild to moderate hypertension — elective surgery in patients with hypertension does not need to be delayed as long as the diastolic blood pressure is less than 110 mmHg and intraoperative and postoperative blood pressures are carefully monitored to prevent hypertensive or hypotensive episodes. On the other hand, when hypertension has caused end-organ disease such as congestive heart failure and renal insufficiency, the probability of adverse cardiac outcome in the perioperative period increases significantly.

The impact of systolic hypertension on operative risk is less clear. One study of patients undergoing carotid endarterectomy found that a systolic pressure greater than 200 mmHg was associated with an increased risk of postoperative hypertension and neurologic deficits.

Secondary hypertension — Patients with suspected secondary hypertension should ideally undergo a diagnostic evaluation prior to elective surgery. However, most patients are not at increased perioperative risk as long as the hypertension is not severe and serum electrolytes and renal function are normal. An important exception is the patient with pheochromocytoma, in whom operative mortality may be as high as 80 percent in unsuspected cases.

Physical examination:
  • General examination
    • Cushing syndrome: characteristic facies and habitus
    • Central obesity 
    • Hyperlipidaemia 
  • Pulse rate, rhythm, volume 
    • AF is common in dystolic dysfunction caused by left ventricular hypertrophy or the effect of CAD
    • Radio-femoral delay: coarctation of aorta 
  • Radio - radial or femoral pulse synchrony 
    • Coarctation of aorta 
  • Ophthalmoscopy 
  • Distended neck vein - JVP measurement 
  • Carotid briuts 
  • Abdominal auscultation for abdominal bruits 
    • Abdominal bruits: renal artery stenosis 
    • Enlarged kidney: polycystic kidney disease 
  • look for thyroid enlargement 

Preoperative investigations 

Some realities about end organ damage due to hypertension:

End organ damage due to hypertension is one of the major concern in perioperaive care. Complications of hypertension to vascular disease probably involve three interrelated processes: 

  • Pulsatile flow
  • Endothelial cell dysfunction and
  • Smooth muscle cell hypertrophy

These three interrelated processes are probably responsible for the arteriolar and arterial sclerosis that is the usual consequence of long-standing hypertension. 

Large vessels such as the aorta may be directly affected and be at risk for aneurysms and dissection. 

Both systolic hypertension and high pulse pressure are strongly associated with risk for perioperative cerebrovascular accidents and acute renal failure. The brain and the kidneys as well as the heart differ from most organs in that they receive large amount of blood flow and have very low resistance. As such, the pulsatile load (pulse pressure) tends to be very high. The pulsatile stress also can cause dislodgment of plaques from the aorta and its major branches, resulting in embolic stroke.

Relative or absolute hypotension is common in the perioperative period and may be associated with adverse outcome. Cardiovascular lability is more common in patients with hypertension and in hypertensive patients, the autoregulatory curve may be shifted to the right. The implication of this is that, in hypertensive patients, blood flow to organs such as the brain and the kidneys may be compromised by intraoperative reductions in BP that would not be a cause for concern in normotensive individuals. This supports a recommendation that avoiding intraoperative hypotension in patients with a history of hypertension may reduce the occurrence of adverse events and at the very least will do no harm.

The renal blood flow and GFR of cortical nephrons are autoregulated by changes in tone of afferent arterioles. Renal blood flow is more precisely regulated than GFR over the MAP range of 75–170 mmHg. 

Chronic hypertension leads to thickening of arteriole wall and narrowing of the lumen, a process called arteriolosclerosis. This results inadequate blood flow to the glomeruli and produce glomerular and interstitial ischemia. 

Glomerular injury may also be due to a consequence of direct damage to glomerular capillary due to glomerular hyper perfusion.

In progressive hypertension, the loss of auto regulation to renal blood flow at the afferent arterioles results in transmission of elevated pressure to the unprotected glomerulus. This cause hypertrophy and sclerosis. 

In progressive hypertension there is vicious cycle of renal damage and there is low blood pressure threshold for renal damage.

Clinically macroalbuminuria (urinary albumin/creatinine ratio >300 mg/g) or microalbuminuria (urinary albumin/creatinine ratio 30 - 300 mg/g) are the early marker of renal injury. 

As chronic renal insufficiency is a common sequela of hypertension, patients with hypertension should have a measurement of baseline serum creatinine. In the revised Cardiac Risk Index a preoperative serum creatinine level greater than 2.0 mg per dL (176.8 mmol per L) is one of six independent factors that predict increased cardiovascular risk.

It is to remembered that even short episodes of intraoperative MAP of <55 mmHg are associated with acute kidney injury and myocardial injury after a non-cardiac surgery. 

For chronically hypertensive patients with high baseline blood pressures (eg, MAP >100 mmHg), a MAP target of 65 mmHg may be too low. In a retrospective study of 57,315 patients undergoing noncardiac surgery, low MAP values <65 mmHg or MAP values <20 percent of the individual patient's baseline were associated with myocardial and kidney injury, and such injury was more likely in those with chronic hypertension.


In a trial of older adults with chronically elevated MAP (approximately 100 mmHg), maintaining an intraoperative MAP target of 80 to 95 mmHg produced a lower incidence of AKI compared with a lower target of 65 to 79 mmHg or a higher target of 96 to 110 mmHg (6.3 versus 13.5 and 12.9 percent, respectively).


Coronary auto-regulation is also affected by hypertension. Heart rate, systolic blood pressure and diastolic blood pressure all affect coronary blood flow. Increased level of these variables reduces coronary blood flow as coronary perfusion pressure raises.

Diastolic dysfunction is an early consequence of hypertension-related heart disease and is exacerbated by left ventricular hypertrophy and ischemia. The therapeutic window for fluid management in perioperative period  is notoriously small in patients with diastolic dysfunction and intraoperative fluid management should focus on minimising LV filling pressure while avoiding inadequate preload and its associated low-output state. 


For example, diastolic hypertension being a better predictor of coronary heart disease in younger patients, whereas systolic and pulse pressure hypertension being associated with greater risk of stroke, coronary heart disease, and mortality in persons older than 60 years.

In most adults this range is between mean arterial pressures of 50–60 mmHg and 150 mmHg. Blood flow control is lost when the perfusion pressure is outside the autoregulatory range; in this situation the cerebral blood flow is dependent on the mean arterial pressure. Pressures above the autoregulatory range cause increased cerebral perfusion and eventually vasogenic edema; pressures below the autoregulatory range cause cerebral hypoperfusion and ischemic injury.


In hypertensive patients, autoregulation of cerebral blood flow is reset to a higher range than normal, and although it protects the brain against sudden increases in pressure, it makes it more vulnerable to hypotension. Therefore, when BP is lowered acutely, hypertensive patients will show signs of cerebral ischemia at a higher level of BP than normotensive patients.


Hypertension may accelerate cognitive decline with age. Hypertension, particularly systolic, is a major risk factor for initial and recurrent stroke and for transient ischemia attacks caused by extracranial atherosclerosis.

Anesthesia: Consequences on Hemodynamics in Hypertensive Patient 

Cardiovascular system regulation depends on three systems: 

  • Sympathetic nervous system
  • Renin-angiotensin system (RAS)
  • Vasopressin

General anaesthesia interferes with both the sympathetic nervous system and the RAS. Similarly, epidural anaesthesia, beyond sympathetic blockade, suppresses renin release in response to arterial hypotension

The anaesthesia-induced reduction in sympathetic tone on the vascular capacitance results in a decreased effective intravascular volume, and angiotensin II may counterbalance this effect. Accordingly, blood pressure may decrease markedly during general anaesthesia when angiotensin II action is impeded by an angiotensin II competitive inhibitor

Yet, besides RAS and the sympathetic system, endogenous vasopressin may be involved in blood pressure regulation during anaesthesia through binding to receptors involved in vasoconstriction (V1a receptors)

During epidural anaesthesia and ACEI-induced inhibition of the RAS, the plasma vasopressin concentration increases significantly. Vasopressin may compensate both systems blockade through a mesenteric vasoconstriction with blood flow redistribution away from the mesenteric circulation towards shorter-time-constant circulatory territories, therefore increasing venous return indirectly. 

Each individual pressor system may therefore act as a compensatory mechanism whenever other systems are depressed. The RAS contribution to blood pressure support is crucial when the sympathetic nervous system is blocked by epidural or general anesthesia and when endogenous vasopressin is antagonised by a specific V1 receptor antagonist. The greatest and most significant decrease in blood pressure during anesthesia occurs with the combination of RAS blockade and a V1 receptor antagonist.


Anesthesia: Interaction between Anesthetics and Antihypertensive Drugs

Differences among anesthetics or anesthetic management are mainly related to the effects on the sympathetic nervous system, the worst tolerated occurring with fast and/or extended sympathetic blockade. 

However, propofol has specific impact on vascular reactivity. Several experimental studies have shown that propofol drastically reduced vascular response to norepinephrin, angiotensin II and vasopressin. Interestingly, these effects are amplified in hypertensive subjects. These specific effects may explain the description of the catecholamine-resistant hypotension, the so-called refractory hypotension, observed almost exclusively after anesthesia induction with propofol. 

Regarding the antihypertensive treatment, after 2 decades of concern with RAS antagonist and anesthesia interference, there is less evidence that the treatment can cause adverse effects that may justify treatment withdrawing before surgery. Indeed, refractory hypotension was thought to be related to the preoperative treatment with renin-angiotensin system antagonist but it can be related actually to the confounding effect of propofol on vessels. 


Antihypertensive drugs:



It is important to monitor serum potassium levels if the patient is treated with diuretics. 

In an outpatient setting, 1-time potassium lab values are practical. The measurement of a 24-hour urinary potassium excretion is appropriate for patients who are at high risk, for example, those patients with congestive heart failure. 


The early reduction in blood pressure with thiazide use is due to a reduction in blood volume, and chronic thiazide treatment results in blood pressure control through reduced vascular resistance despite return of fluid to pretreatment levels.

Thiazide diuretics may aggravate glucose control, especially in combination with β-blockers. 

In addition, thiazide diuretics appear to prolong neuromuscular blockade with nondepolarizing neuromuscular blockers. 

Diuretics can cause dehydration. In addition to natriuresis, the volume depletion occurs on a biochemical level is due to the loss of sodium from the body. The hyponatraemic state leads to decreased extracellular fluid osmotic pressure. This results in a shift of fluid into the cells and therefore causes a hypovolaemic state.

Many long-term hypertensive patients therefore have a masked state of hypovolemia. Prudent volume augmentation in ambulatory settings with a crystalloid solution prior to the induction of anaesthesia may help with masked hypovolaemia.

The volume status of a patient can be difficult to assess in the outpatient and ambulatory setting without laboratory values, yet indirect measures of volume status may include 

  • An observation of mucous membranes
  • Quality of peripheral pulses
  • Increasing resting heart rate accompanied by decreased blood pressures from normal
  • Orthostatic heart rate and blood pressure changes from positional changes
  • Urine specific gravity
  • Decreased urinary flow rates and output

During the postoperative period, fluids shift from the intravascular space to the third space and administration of diuretics may exacerbate the intravascular volume contraction. This may explain the significant increase in the risk of postoperative AKI with patients getting perioperative diuretics. 


If the patient is taking a diuretic for treatment of hypertension, consider holding the diuretic on the morning of surgery in order to avoid dehydration while the patient is NPO. However, if the patient has severe liver disease or congestive heart failure, it may be best to continue diuretic therapy. 


ACE inhibitors (ACEIs)

Because of an increased risk of refractory hypotension, ACEIs are typically held on the day of surgery if general anaesthesia or some type of deep sedation is planned, particularly during induction of general anaesthesia. 

Coriat and colleagues found that ACEIs were associated with hypotension in 100% of patients during induction versus approximately 20% in whom ACEIs were withheld on the morning of the surgical procedure. 


A recent large prospective cohort study found that patients who did not take ARBs or ACE inhibitors in the 24 hours before noncardiac surgery were less likely to suffer intraoperative hypotension and the primary composite outcome of all-cause death, stroke, or myocardial injury.


According to UpToDate, ACEI is usually withheld on the morning of surgery. However, when the indication is for heart failure or poorly controlled hypertension, ACEI is usually continued to avoid further exacerbation of these conditions. 


If the patient did take their usual dose of ACEI on the day of surgery, some sources suggest administering an intravenous bolus of 250 mL to 1 L of crystalloid solution prior to the induction of general anesthesia to decrease the severity of hypotension.

If traditional vasopressor options such as phenylephrine or ephedrine have been used without the desired clinical response for the treatment of hypotension, then further treatment options include vasopressin, epinephrine, and norepinephrine. 

ACEIs may generally be continued during the perioperative period if moderate sedation is planned.

As mentioned above, angioedema is a known adverse effect of ACEIs. It is important to make the distinction between the histamine-mediated edema that is often associated with urticaria or anaphylaxis and the bradykinin-mediated angioedema that is associated with ACEI use. Although the incidence of ACEI angioedema is low, some reported that 30% of angioedema cases that presented to the emergency department were due to ACEIs. Discontinuation of the ACEI, maintaining airway patency, and supportive therapies are the mainstay of treatment. Corticosteroids and antihistamines are typically given to rule out histamine-mediated angioedema and are usually ineffective in the bradykinin-mediated angioedema, as seen with ACEIs. 


ARBs have no effect on bradykinin metabolism; therefore, their use is associated with significantly reduced incidence of cough and angioedema as compared with ACEIs. Because of this decreased incidence of angioedema, some patients are shifted toward ARB therapy from ACEI therapy. However, it is important to note that there is still a small angioedema risk involved. The current thinking among many anesthesiologists is that, similar to ACEIs, ARBs should be withheld on the day of surgery to avoid refractory hypotension during induction of general anesthesia. Heightened awareness of the possible refractory hypotension that can occur with ACEIs and ARBs and recognition of the need to treat with an adequate dose of vasopressin, epinephrine, or norepinephrine are required.

In addition to the refractory hypotension that can occur during induction, there have been incidents of rebound hypertension following the discontinuation of ARBs. The risks and benefits of continuing or withholding ARBs should be taken into consideration during any medication adjustment in the perioperative period.

Calcium channel blockers (CCBs)

β blockers


  • All “cardiac” or blood pressure drugs, EXCEPT ACE inhibitors, AT2 antagonists and diuretics (see below)
  • All epilepsy or Parkinsons drugs
  • All asthma drugs or inhalers
  • All tablets which reduce gastric acid (omeprazole, lansoprazole, ranitidine)
  • All thyroid drugs
  • All major and minor tranquilisers, which are taken regularly at home. Also anti depressants and nicotine patches.
  • All steroids taken regularly, including inhalers
  • All immunosuppressants and cancer drugs (eg. azathioprine, tamoxifen)
  • All analgesics can be given before surgery - EXCEPT NSAID’S (see below)

  • ACE inhibitors (ramipril, enalapril, perindopril, captopril)
  • Angiotensin 2 antagonists (candesartan, losartan)
Decision regarding these two drugs should be taken according above mentioned considerations.
  • All diuretics (frusemide, bumetanide, bendroflumethiazide, amiloride, spironolactone). The anaesthetist may request that these are given – this will be on an individual basis.
  • Diabetic treatment (alternative diabetic treatment must be arranged).
  • Aspirin, clopidogrel, dipyridamole, warfarin. These drugs must NOT be stopped in patients who have a coronary stent without prior discussion with an anaesthetist or cardiologist.
  • Drugs which are not essential in the short term. eg. vitamins, iron, laxatives, osteoporosis treatment, liquid antacid medicines, anti- histamines, herbal remedies or homeopathic medicines.
  • Lithium should be omitted.
  • Non steroidal anti inflammatory drugs , unless prescribed by an anaesthetist as a pre-med.

Lastly, my feelings is, the importance of blood pressure measurement is the first and most important clinical marker of the patient. My consultant is correct about the blood pressure but I should dig deep to find out more. 

The proper assessment of the hypertensive patients, a single work, can reduce a lot of postoperative mortality and morbidity in the country in the current setup.


  1. Excellent and informative write-up.

  2. Excellent work-and very detailed...covers almost all corners...please continue your effort as it will help and inspire our junior colleagues as well!!!

  3. There is quite a bit of information on hypertension presented that seen through the eye of a practicing anaesthesiologist. It cannot be called a casual dispatch as its loaded with upto date knowledge on this particular disorder. It’s only natural for the anaesthesiologist to consider hypertension as discuss worthy, for now a days patients are plentiful and rising. This is the side effect of the slowly but surely improving living standard of the people of this country. The write up has almost complete picture of hypertension and its implications in anaesthesia, something inadvertently overlooked by a busy clinician at times.
    While all the material is there for consideration and putting in practice, I personally feel that one perhaps can use the information to one’s better advantage if a flow chart/ algorithm could be provided for use in both pre-anaesthetic room and also in the operating room . Post-operative management also varies and that too should be protocolized. In fact the knowledge that we need to know is all described here, a user friendly stepwise “ to do” list would have completed the picture. To understand the disorder, exceptionally good diagrams and other images and tables have been used. Some of them lack the mention of source, which I think is necessary if these were not done by the author himself.
    The writer ought to be encouraged to do more of this kind.

    1. Thank you sir. Your kind words made my day.
      I tried to mention the sources. In some diagrams which are built by myself but didn't mention the source. I'm mentioning the sources of those diagrams as soon as possible.

      Regarding flow chart or protocol, I am really encouraged and will communicate with the senior anaesthesiologist consultants for further progress.

      Thank you sir.


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