10.1. Acute blood pressure management in hypertensive emergencies
10.1.1. Definition and characteristics of hypertensive emergencies
Hypertensive emergency is defined as BP of ≥180/110 mmHg (see Figure 10) associated with acute HMOD, often in the presence of symptoms. Hypertensive emergencies are potentially life-threatening and require immediate and careful intervention to reduce BP, often with i.v. therapy.
Symptoms of hypertensive emergency depend on the organs affected but may include headache, visual disturbances, chest pain, shortness of breath, dizziness, and other neurological deficits. In patients with hypertensive encephalopathy, somnolence, lethargy, tonic–clonic seizures, and cortical blindness may precede a loss of consciousness; however, focal neurological lesions are rare and should raise the suspicion of stroke.
As outlined in Section 7, we define HMOD among patients with chronically elevated BP or hypertension as the presence of specific cardiac, vascular, and renal alterations.31,159 However, in the setting of hypertensive emergency, more acute manifestations of organ damage are relevant for management.
Acute manifestations of organ damage include:
Patients with severe acute hypertension associated with other clinical conditions likely to require urgent reduction in BP, e.g. acute onset of aortic dissection, myocardial ischaemia, eclampsia, or heart failure.
Malignant hypertension, defined as extreme BP elevations and acute microvascular damage (microangiopathy) affecting various organs.947 The hallmark of this condition is small-artery fibrinoid necrosis in the kidneys, retina, and brain. The acute microangiopathy is typically characterized clinically by retinopathy (flame haemorrhages, cotton wool spots, and/or papilloedema). Other manifestations of microangiopathy include disseminated intravascular coagulation, encephalopathy (in about 15% of cases), acute heart failure, and acute deterioration in renal function.
Patients with sudden severe hypertension due to phaeochromocytoma, which can result in severe acute organ damage.
The term ‘hypertension urgency’ describes severe hypertension in patients without clinical evidence of acute organ damage. While these patients require BP reduction, they do not usually require admission to hospital, and BP reduction is best achieved with oral medication according to the drug treatment algorithm presented in Section 8. However, these patients may require more urgent outpatient review to ensure that their BP is controlled.
Acute and severe increases in BP can sometimes be precipitated by sympathomimetics such as methamphetamine or cocaine, when caution around beta-blocker use is also needed. Many patients in an emergency department with acute pain or distress may have acutely elevated BP that will normalize when the pain and distress are relieved, rather than requiring any specific intervention to lower BP.
A diagnostic work-up is necessary for patients with a suspected hypertensive emergency (see Supplementary data online, Table S12).
10.1.2. Acute management of hypertensive emergencies
Key considerations in defining treatment are:
Establishing the affected target organ(s) and whether they require any specific interventions other than BP lowering.
Determining whether there is a precipitating cause for the acute rise in BP and/or another concomitant health condition present that might affect the treatment plan (e.g. pregnancy).
The recommended timing and magnitude of BP lowering required for safe BP reduction.
These considerations will inform the type of BP-lowering treatment required. Regarding BP-lowering drugs, i.v. treatment using a short half-life drug is typically ideal to allow careful titration of the BP response to treatment. This requires a higher dependency clinical area with facilities for continuous or near-continuous haemodynamic monitoring. Recommended drug treatments for specific hypertensive emergencies are provided in the Supplementary data online, Table S13.
Rapid and uncontrolled or excessive BP lowering is not recommended in hypertensive emergency as this can lead to further complications. Although i.v. drug administration is recommended for most hypertensive emergencies, oral therapy with ACE inhibitors, ARBs, or beta-blockers (shorter-acting formulations like captopril or metoprolol) can also be effective. However, low initial doses should be used because these patients can be very sensitive to these agents, and treatment should take place in hospital. Further comprehensive details on the clinical management of hypertensive emergencies are available elsewhere.242
10.1.3. Prognosis and follow-up
The survival of patients with hypertensive emergencies has improved over the past few decades, but these patients remain at high risk and should be screened for secondary hypertension.
10.2. Acute blood pressure management in acute intracerebral haemorrhage
In acute intracerebral haemorrhage, an increased BP is common and is associated with a greater risk of haematoma expansion and death, and a worse prognosis for neurological recovery. In trials testing immediate BP lowering (within <6 h) to a systolic target of <140 mmHg, the achieved systolic BP in the intervention group was typically 140–160 mmHg and was reported to reduce the risk of haematoma expansion.948,949 Excessive acute drops in systolic BP (>70 mmHg) may be associated with acute renal injury and early neurological deterioration and should be avoided.950,951
10.3. Acute blood pressure management in acute ischaemic stroke
The beneficial effects of BP reduction in acute ischaemic stroke remain unclear. In patients not receiving i.v. thrombolysis or mechanical thrombectomy, there is no evidence for actively lowering BP unless it is extremely high (e.g. >220/120 mmHg). If BP is extremely high, an initial moderate relative reduction of 10%–15% over a period of hours may be considered.952 The reason for a more conservative approach to acute BP management is that cerebral autoregulation may be impaired in acute stroke, and maintaining cerebral perfusion relies on systemic BP.
In contrast, patients who are treated with i.v. thrombolysis or mechanical thrombectomy (or both) should have more proactive management of severe hypertension, because they have an increased risk of reperfusion injury and intracranial haemorrhage. In patients undergoing treatment with i.v. thrombolysis, BP should be lowered to <185/110 mmHg prior to thrombolysis and then maintained at <180/105 mmHg over the following 24 h.953 In patients undergoing treatment with mechanical thrombectomy (with or without i.v. thrombolysis) there is limited evidence from clinical trials, but BP should also be lowered to <180/105 mmHg prior to thrombectomy and maintained over the next 24 h.953,954 Therefore, patients with acute ischaemic stroke and a BP of <180/105 mmHg in the first 72 h after stroke do not seem to benefit from the introduction or reintroduction of BP-lowering medication.955 For stable patients who remain hypertensive (≥140/90 mmHg) ≥3 days after an acute ischaemic stroke, initiation or reintroduction of BP-lowering medication is recommended.
Recommendation Table 32
Recommendations for acutely managing blood pressure in patients with intracerebral haemorrhage or acute ischaemic stroke
10.4. Acute blood pressure management in pre-eclampsia and severe hypertension in pregnancy
10.4.1. Pre-eclampsia
Pre-eclampsia is discussed in Section 9. Here we focus on its management in the acute setting. Pre-eclampsia is cured by delivery. Most international societies, including the ESC, recommend an intensive approach to BP lowering in pre-eclampsia.89,964,965 In women with pre-eclampsia and severe hypertension, immediately reducing systolic BP to <160 mmHg and diastolic BP to <105 mmHg using i.v. labetalol or nicardipine (with administration of magnesium sulfate if appropriate and consideration of delivery if appropriate) was recommended in the 2018 ESC/ESH Guidelines on the management of arterial hypertension and the 2022 ESC Guidelines for management of cardiovascular disease in pregnancy.1,89 The objective of treatment is to lower BP within 150–180 min.
Magnesium sulfate [4 g i.v. over 5 min, then 1 g/h i.v.; or 5 g intramuscularly (i.m.) into each buttock, then 5 g i.m. every 4 h] is recommended for eclampsia treatment but also for women with pre-eclampsia who have severe hypertension and proteinuria or hypertension and neurological symptoms or signs.966 There is a risk of hypotension when magnesium is given concomitantly with nifedipine.967 If BP control is not achieved by 360 min despite two medications, consulting critical care is recommended for intensive care unit admission, stabilization, and delivery (if appropriate).966 Since plasma volume is reduced in pre-eclampsia, diuretic therapy should be avoided.
10.4.2. Severe acute hypertension in pregnancy
Severe hypertension in pregnancy (without pre-eclampsia) may necessitate acute BP-lowering therapies. Severe hypertension in pregnancy is defined in general as systolic BP of >160 mmHg and diastolic BP of >110 mmHg and is associated with adverse maternal and peri-natal outcomes independent of pre-eclampsia and potentially of the same magnitude as eclampsia itself.89,968
There are differences in rate of BP control between i.v. labetalol and i.v. hydralazine in severe hypertension in pregnancy.969 While evidence is conflicting,667,668 hydralazine may be associated with more peri-natal adverse events than other drugs.970 Nifedipine seems to provide lower BP with lower rates of neonatal complications than labetalol.971
Recommendations for acutely managing blood pressure in patients with severe hypertension in pregnancy and pre-eclampsia (see Evidence Table 46)
10.5. Peri-operative acute management of elevated blood pressure
Details are provided in the ESC Guidelines on cardiovascular assessment and management of patients undergoing non-cardiac surgery.972 Peri-operative hypertension, hypotension, and BP variability are associated with haemodynamic instability and poor clinical outcomes for patients undergoing surgery.973 Pre-operative risk assessment for BP management, therefore, should involve assessing for underlying end-organ damage and comorbidities.974 Postponing necessary non-cardiac surgery is not usually warranted for patients with minor or moderate elevations in BP, as they are not at higher CVD risk.130,975
Avoiding large fluctuations in BP in the peri-operative course is important, and planning a strategy for a patient should account for the baseline office BP.974–977
There is insufficient evidence for reduced or increased peri-operative BP targets compared to usual care BP targets to lower peri-operative events.978 No specific measure of BP appears better than any other for predicting risk of peri-operative events.975
10.5.1. Blood pressure-lowering drugs in the peri-operative phase
Routine initiation of a beta-blocker peri-operatively is not necessary.979
Pre-operative initiation of beta-blockers in advance of high-risk, non-cardiac surgery may be considered in patients who have known coronary artery disease or myocardial ischaemia980 or two or more significantly elevated clinical risk factors in order to reduce the incidence of peri-operative myocardial infarction.979 Peri-operative continuation of beta-blockers is recommended for patients currently taking beta-blockers.981
Some studies suggest that continued use of ACE inhibitors is associated with a higher risk of peri-operative hypotension and subsequent end-organ damage including kidney injury, myocardial infarction, and stroke.982 In the Prospective Randomized Evaluation of Preoperative Angiotensin-Converting Enzyme Inhibition (PREOP-ACEI) trial, transient pre-operative interruption of ACE inhibitor therapy was associated with a decreased risk of intra-operative hypotension.983 A subsequent systematic review also showed a decreased risk of intra-operative hypotension with withholding ACE inhibitors/ARBs before surgery, but no association with decreased mortality or CVD outcomes.984 On the other hand, vigilance is needed because withholding ACE inhibitors has also been shown to increase post-operative hypertension.985 In patients with heart failure, loop diuretics can be continued in patients prone to volume overload.986 CCBs are generally considered safe pre-operatively.
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