Hypertension

• Essential (primary) hypertension - 95%


• Secondary hypertension - 5%
• Renal disease e.g. renal artery stenosis, other renal comorbidity
• Endocrine disease e.g. Conn's syndrome, phaeochromocytoma, Cushing's syndrome, hyperthyroidism, acromegaly
• Vascular disease e.g. coarctation of the aorta
• Drug-induced e.g. steroids, sympathomimetics
• Pregnancy-related e.g. pre-eclampsia

• Systolic BP rises continuously with age
• Diastolic BP plateaus in late-middle age, and then may decrease
• Pulse pressure therefore rises


• Pulse-pressure hypertension has gained prominence as a risk factor for MI/stroke
• The raised pulse pressure induces stress forces on the vascular tree and causes endothelial dysfunction and plaque rupture
• Dysfunction in the autonomic nervous system and RAAS is thought to play a key role

• Once hypertension is established, the baroreceptors 'reset' to the new level causing persistent hypertension
• Patients may therefore have exaggerated sympathetic responses to stressors and exogeneous vasopressors

• In some patients RAAS disorders contribute to hypertension
• Renin activity is normal or increased in 75% of hypertensive patients, even though it should be decreased due to negative feedback
• There may also be an impaired natriuretic response to volume excess


• Once hyperetnsion is established it becomes self-propagating due to:
• Baroreceptor resetting
• Vascular remodelling: luminal narrowing increases vascular resistance
• LV hypertrophy


• Chronic arterial hypertension produces end-organ damage, particularly cardiac, renal and cerebral (see next section)

• Chronic HTN causes arterial/arteriolar wall stress
• Endothelial dysfunction ensues and endogenous NO function is impaired
• This leads to:
• Atherosclerotic plaque formation
• Accelerated aneurysm formation


• The increased myocardial wall tension causes concentric LV hypertrophy
• Poorer diastolic relaxation leads to impaired diastolic blood flow and myocardia ischaemia
• This process is accelerated by atherosclerosis
• Eventually, LV failure occurs


Cardiovascular sequelae

LV hypertrophy

Diastolic dysfunction

LV failure

Atherosclerotic coronary artery disease

Coronary artery dissection

Aortic dissection

Aortic aneurysms

Rupture of clot/uncontrolled surgical bleeding

• Cerebrovascular atherosclerosis leads to shifting of the autoregulatory curve, predisposing to haemorrhagic and watershed strokes
• Carotid artery stenosis can lead to embolic events and global ischaemia from hypotension, predisposing to ischaemic and haemorrhagic strokes

• Atherosclerosis of the renal vasculature leads to ischaemia, with:
• Tubular injury
• Glomerular atrophy
• Nephropathy and renal failure
• Renovascular autoregulation is defective/shifts to a higher pressure, leading these patients to be more susceptible to hypotension

• Patients should receive lifestyle advice and treatment if they have a persistent blood pressure
• >135/85mmhg and co-existing disease e.g. diabetes mellitus, renal disease, cardiovascular disease, Q-risk >10%
• >160/100mmHg i.e. stage 2 disease


• Step 1
• If the patient is <55yrs or has T2DM then first line treatment is an ACE-I or ARB
• If the patient does not have T2DM and is >55yrs or of Afro-Caribbean family origin, then first line treatment is a calcium channel blocker


• Step 2
• 2^nd line therapy is either an ACE-I/ARB, calcium channel blocker or thiazide diuretic, depending on which drugs the patient is already on


• Step 3
• ACE-I/ARB and calcium channel blocker and thiazide diuretic


• Step 4
• K⁺ <4.5 → spironolactone
• K⁺ >4.5 → ɑ-blocker or β-blocker
• Seek expert help

• Hypertension is common among inpatients (up to 80%)
• Multiple trials demonstrate negative sequelae following inappropriately treating HTN in inpatients (e.g. JAMA [2019],  JAMA [2020] and Journal of HTN [2023])


Associations of inappropriately treating hypertension in inpatients

Excessive reductions in BP

Higher rates of AKI

Higher rates of myocardial injury

Higher rates of ischaemic neurovascular events

Drug-related adverse events

Intensification of outpatient anti-hypertensive regimens but no long-term improvements in BP control or cardiovascular event risk

Increased risk of re-admission or serious adverse event within 30 days

Longer duration of inpatient stay

• Establish diagnosis of hypertension and current treatment
• Confirm efficacy of treatment ± whether modification is required


• Establish presence of other commonly coalescing comorbidities e.g. diabetes mellitus

• Cardiovascular: ECG ± TTE
• Cerebrovascular e.g. previous TIA/stroke
• Renovascular
• U&E esp. if on diuretic therapy
• Urine dipstick for haematuria or proteinuria

• Continue all drugs up until morning of surgery except ACE-I
• ACE-I/ARB should be stopped at least 24hrs before surgery, as they are associated with refractory intra-operative hypertension
• The exception is in patients with established heart failure, where the benefit of continuing them may outweigh the risk


• Inappropriate cessation of β-blockade is associated with an increased risk of silent ischaemia


• Patients with hypertension are generally considered suitable to proceed with surgery if:
• In-hospital BP is <180/110mmHg, or
• Outpatient BP is <160/100mmHg, or
• The patient is already on maximal anti-hypertensive therapy, or
• The patient refuses (further) anti-hypertensive medication


• For patients undergoing urgent or emergent surgery, one generally proceeds irrespective of hypertension but uses techniques to minimise BP instability

• In general, the cardiovascular system is more 'sensitive':
• Labile blood pressure is more likely, especially in response to stimuli (intubation, surgical stimulus, extubation, post-operative pain)
• Exaggerated response to vasoactive medications
• Poor tolerance of large fluid shifts; maintain intravascular volume


• The organ sequelae of hypertension increase risks:
• Right shift in organ autoregulatory curves make key circulations susceptible to hypotension e.g. cerebral, renal, coronary
• Hypertrophied LV is at risk of subendocardial myocardial ischaemia if there is inadequate coronary perfusion pressure


Intra-operative management

Low threshold for invasive BP monitoring

Avoid tachycardia

Maintain BP within 20% of baseline throughout procedure

Uncontrolled hypertension is an anaesthetic emergency, and I would seek senior anaesthetic support as well as making a rapid but thorough assessment of the patient

• As ever, ask the surgeons to stop prodding and/or poking and make an A-E assessment

1. Maintain and if necessary secure the airway
2. Ensure adequate oxygenation and ventilation
3. Measure BP, HR, ECG inc. ensuring appropriate cuff size and transducer height
• Treat cause (see table above) e.g. increase depth of anaesthesia, administer analgesic
• Alternative pharmacotherapy based on cause e.g. magnesium, IV nitrate, ɑ-blocker, β-blocker, CCB, hydralazine
4. Ensure appropriate depth of anaesthesia and monitor for sequelae e.g. by checking pupillary responses

• Considerations include:
• Whether it's safe to proceed with surgery
• The need for investigations e.g. CTB, CT angiogram
• Whether planned post-operative location is suitable i.e. is HDU required

• Address factors which increase the risk of rebound hypertension: pain, hypoxia, hypercarbia, fluid overload or hypothermia
• Plan for reintroduction of anti-hypertensive therapy, often in a stepwise fashion
• Multimodal anti-emesis to enable patient to take their regular anti-hypertensives
• Consider HDU setting, although often unnecessary