Hypertension is described as either primary hypertension or secondary hypertension.
Primary hypertension (previously called essential hypertension) refers to the elevated blood pressure that doesn’t arise from a specific disease process. The exact cause isn’t fully understood, and there are multiple factors which appear to play a role in its development. Regardless, their is a ‘resetting’ of the homeostasis mechanisms for blood pressure control to a higher value. This higher value is then maintained by the normal homeostasis mechanisms (e.g. renin-angiotensin-aldosterone system).
Secondary hypertension refers to the elevated blood pressure that occurs in response to an specific disease process. This accounts for only 5% of the cases of hypertension. The causes can be divided into:
Renal - the most common
Renovascular disease
Diabetic nephropathy
Polycystic kidney disease
Glomerulonephritis
Systemic sclerosis
Endocrine
Cushing’s syndrome
Conn’s syndrome
Pheochromocytoma
Thyroid disease
Hyperparathyroidism
Acromegaly
Drugs
Cocaine
Alcohol misuse
Amphetamines
Combined oral contraceptive pill
Other
Pregnancy
Coarctation of the aorta
Obstructive sleep apnoea
The specific severity of the hypertension has also been defined by NICE. Although it is recognised that BP values are part of a skewed spectrum, these categories help assess the risks associated with them. Stage 1 - >140/90 mmHg (or home reading >135/85) Stage 2 - >160/100 mmHg (or home reading > 150/95) Severe - >180/110 mmHg
Of note, the American Heart Association/American College of Cardiology has also suggested the expansion of the definition to describe patients with a BP reading of 120/80-140/90 mmHg as also representing a hypertensive state. This new lower definition will notably increase the number of people labelled as having the condition, but represents the increasing awareness that even modest elevations carry an increased risk.
Risk Factors
Recognised risk factors for developing primary hypertension include. Non-modifiable:
Increasing age
Family history
Ethnicity
Modifiable:
Overweight
Inactivity
Alcohol excess
Excess dietary salt intake
Epidemiology
The prevalence of hypertension increases with age. Around 25% of all adults in the UK have hypertension. In adults over the age of 66%, this has increased to over ⅔ The condition seems to be more prevalent in men below the age of 65, becoming more prevalent in women after this age.
After smoking, hypertension is the biggest risk factor for premature death. A significant number of people have undetected or undertreated hypertension.
Complications
The adverse effects of untreated hypertension are widespread. Much of the effects relate to the end-organ damage occurring from the prolonged exposure to the elevated blood pressure, particularly to the endothelium. There is clearly a spectrum of adverse effects.
Cardiovascular
Left ventricular hypertrophy
Diastolic dysfunction
Ischaemic heart disease
Peripheral vascular disease
Heart failure
Renal
Glomerular injury
Renal tubular ischaemia
ESRF
CNS
Cerebrovascular accident
Impaired cognition
Hypertensive encephalopathy
Hypertensive retinopathy
Assessment
Measurement Hypertension is almost always asymptomatic (unless presenting in the form of an acute complication or malignant/accelerated form). As such, it will usually be detected incidentally. However, much of the primary prevention approach involves screening for hypertension.
Measurement of BP is more challenging than often realised, with a number of factors that impact on its reliability. The patient must be:
Sitting
Relaxed and not talking
Arm/cuff at heart level
Free of tight clothing
If there is an irregular heartbeat, the measurement must be done manually. Measurement of BP in both arms may be appropriate initially.
In patients with elevated BP in the community setting, ambulatory BP monitoring is recommended, to provide a more reliable assessment of the actual values.
History/Examination A full history is important to assess for the possibility of secondary hypertension, and sequelae of the hypertension itself.
Symptomatic hypertension (palpitations, feeling about to die) is worrying for a pheochromocytoma.
Lifestyle factors (obesity, poor diet, poor exercise) may be contributory factors.
Endocrine disease may be the cause (any features of thyroid disease/adrenal disease).
Drugs may be a contributing factor
Investigations Other that the initial measurement of blood pressure, these are again primarily to identify possible causes of secondary hypertension, and features of end organ damage:
Specific investigations for secondary causes are unlikely to be needed in many cases, but include:
TFTs
Cortisol/suppression test
Renin/aldosterone
Plasma metanephrines
MRI renal arteries
Management
Management of hypertension is focused on reducing the long-term cardiovascular risk (In some cases of severe accelerated hypertension it is more focused on short term avoidance of complications, but that is a different clinical scenario). As such, the management includes a holistic approach to the overall cardiovascular risk.
Non-medical A number of these will be considered as potentially helping with both BP control, and overall CVD risk:
Weight loss
Dietary advice
Reducing salt intake
Reducing alcohol consumption
General healthy eating advice
Smoking cessation
Increased exercise
Medical treatment Medical treatment will generally be started in patients with:
Severe hypertension (straight away)
Stage 2 hypertension
Stage 1 hypertension + end organ damage
The goal of medical therapy is a targeted reduction in BP values:
<140/90 mmHg in patients under 80
<150/90 mmHg in patients over 80
The SPRINT trial suggests that even more aggressive treatment with lower targets (<120 SBP) produced even better outcome but with higher adverse effects.
A step-wise approach of agents is advocated: Step 1
If <55 years old or non-black:
ACE inhibitor or Angiotensin II receptor blocker (ARB) (A)
Beta blocker if this not tolerated (but less good) (B)
If >55 years old or of black African or Caribbean family origin
Calcium channel blocker (CCB) (C)
Thiazide like diuretic (D)
This was previously easily remembered as the ABCD options, but as noted, B is not a first line therapy.
Step 2
ACEi/ARB with CCB
ACEi/ARB with thiazide-like diuretic if CCB not tolerated or heart failure
Beta blocker with CCB if already started on beta blocker
Step 3
A + C + D
Step 4
Fourth agent
Specialist referral
Specific choices may be more suitable in the context of co-existing disease.
Anaesthetic Implications
Hypertension is very common, and it will be encountered frequently. This may be diagnosed, or may only be detected in the perioperative setting.
Much of the concern is about reducing the perioperative risk of these patients. Hypertension increases the risk of perioperative complications, particularly myocardial ischaemia. However, the stress of the perioperative period is also well recognised to elevate BP readings above the patient’s ‘normal’. As such, it is generally felt that the increased risk is only of particular concern if >180/110 mmHg. In these cases, a period of relaxation and remeasurement is most suitable initially, with the expectation of improvement. However, if the measurements remain severely elevated and there is concern that this is a genuine, long-standing severe hypertension, then postponement of elective surgery with referral to the patients GP for treatment/follow up is important, as these patients are at higher risk of perioperative complications. This is clearly a risk vs benefit decision in non-elective surgery.
The AAGBI guidance on the topic is very useful: http://onlinelibrary.wiley.com/doi/10.1111/anae.13348/full
Preoperative A full history and examination should be taken. Any associated comorbidities should be explored. Specific questioning into end organ damage may be suitable in some patients. Medication history is important to explore.
It is important that antihypertensive agents are continued perioperatively to reduce the risk of perioperative hypertensive episodes - particularly beta blockers and other cardioprotective medications. The exception to this are ACE inhibitors, which may contribute to significant intraoperative hypotension.
Intraoperative Patients with hypertension commonly demonstrate increased lability of BP under anaesthesia. It is common that the autoregulatory mechanisms for tissue perfusion are disturbed in hypertensive patients, and set at a higher level. As such, impaired perfusion is more likely to occur at higher levels than would be expected for non-hypertensive patients. Hypotension (even relative) should therefore be treated more aggressively, as it is associated with adverse outcomes in these patients. Hypotension is more likely in patients who are excessively ‘deep’ or volume depleted, so these factors must be taken into consideration.
Postoperative Patients should be monitored for an appropriate recovery period to ensure that there is no hypo or hypertension. Recommencement of normal antihypertensives should be when clinically suitable, balancing the risks of hyper and hypotension.
Hypertensive Crisis
A.K.A. Accelerated hypertension or hypertensive emergency or malignant hypertension. This refers to the acutely hypertensive state with significant short term complications arising from the elevated blood pressure.
The definitions have slight variation, but refer to clinical states where there has been an acute rise in BP to >180/110 mmHg. This can be subdivided into:
Hypertensive urgency - no evidence of end organ damage.
Hypertensive emergency - evidence of end organ damage.
Both need treatment, but hypertensive urgency allows this to be started more gradually.
Aetiology/Pathophysiology This is usually related to a secondary hypertension cause, but can occasionally occur in primary hypertension. The rapid rise in BP results in damage to the endothelial system and to many end organs, with risks of significant complications developing. The cause can be varied, and often unknown, but there is often a general increase in peripheral vascular resistance, with development of impaired vascular autoregulation, leading to tissue damage.
The end organ damage can include:
Heart/CVS
Myocardial ischaemia/infarction
Heart failure
Aortic dissection
Brain
Hypertensive encephalopathy
CVA
Kidneys
Presentation Can be asymptomatic. Symptoms may include:
Seizures
Headache
Chest pain
Shortness of breath
Visual disturbances
Nausea and vomiting
Acute neurological event (CVA)
Assessment The focus is looking for:
Causes of secondary hypertension
Features of end organ damage
A full history is important. A detailed drug history may also elicit a cause.
A detailed systematic review is needed. Specific features will include:
BP - lying and standing and in both arms (looking for coarctation)
Looking for signs of heart failure
Fundoscopy - looking for papilloedema, flame haemorrhages
Neurological examination - focal neurology or mental state change
Investigations will include:
FBC
U&E
LFTs
TFTs
Troponin
BNP
Urine dip - blood/protein
ECG - features of ischaemia
CXR - features of failure
Specific investigations for secondary cause may then be needed, as above. A CT aortogram will be needed if aortic dissection is considered.
Management The goal is reduction of BP over 24-48 hours. Due to the autoregulatory changes, too rapid a drop may result in ischaemia. As such, an arterial line may be indicated in severe cases, to allow cautious control. A target of a gradual reduction by 25% is useful.
In hypertensive urgency, it is likely that careful introduction of oral antihypertensives is possible. In hypertensive urgency, this is unlikely to provide adequate and safe reduction in blood pressure, so an intravenous infusion of antihypertensive agent is likely to be required initially, with introduction of oral agents.
Pharmacological options for IV treatment include:
Nicardipine
Labetalol
Nitroprusside
GTN
Magnesium (preeclampsia)
Phentolamine (pheochromocytoma)
Many patients will be intravascularly dry, and may require IV fluid to prevent a significant hypotension with the introduction of treatment.
Links & References
Nadella, V. et al. Hypertension: pathophysiology and perioperative implications. BJA Education. 2015. 15(6):275-279