Bear the following points in mind when managing a hypertensive patient in the ED:
• Most patients with hypertension are asymptomatic.
• Hypertension is an important risk factor for cardiovascular disease and stroke.
• Most patients found to be hypertensive in the ED do not require any immediate intervention or treatment, but do require careful follow-up — usually by their GP.
• Never intervene on the basis of a single raised BP measurement in the absence of any associated symptoms and signs.
Approach
Approach patients found to be hypertensive as follows:
• Those with no previous history of hypertension, and no other concerns or history of other conditions (eg diabetes, peripheral vascular disease, IHD, or stroke) — arrange follow-up and monitoring with GP.
• Those known to be hypertensive already on treatment — arrange follow-up and monitoring with GP.
• Those displaying evidence of end organ damage (eg LV hypertrophy, retinal changes, renal impairment) — refer to the medical team.
• Those with hypertension associated with pain, vasoconstriction (eg acute pulmonary oedema) or stroke — treat underlying cause where possible.
Do not intervene in stroke associated hypertension except under the direction of a neurologist or stroke specialist.
• Those with hypertension directly associated with symptoms or signs — contact the medical team and consider whether intervention is appropriate (see below).
Mild/moderate hypertension (diastolic 100–125mmHg) Ascertain if the patient has a past history of hypertension and is taking drug therapy for this. Examine for retinal changes and evidence of hypertensive encephalopathy. Investigate as appropriate (U&E, urinalysis, CXR, ECG).
Further management will depend upon the BP and the exact circum-stances. If the BP is moderately elevated (ie diastolic BP: 110–125mmHg) and the patient is symptomatic, refer to the medical team. If the patient is asymptomatic with normal examination and renal function, he/she may be suitable for GP follow up.
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HYPERTENSIVE PROBLEMS
Severe hypertension (diastolic > 125mmHg)
Patients with a diastolic BP > 125mmHg require urgent assessment. Search for evidence of hypertensive encephalopathy : headache, nausea, vomiting, confusion, retinal changes (haemorrhages, exudates, papilloedema), fi ts, focal neurological signs, d conscious level. Ask about recent drug ingestion (eg ecstasy or cocaine — b pp. 214 & 215).
Investigations
Insert an IV cannula and send blood for U&E, creatinine, and glucose. Obtain a CXR and ECG, and perform urinalysis. If there is d conscious level, focal signs, or other clinical suspicion that the hypertension may be secondary to stroke or intracranial haemorrhage, arrange an emergency CT scan.
Management
• Refer patients with a diastolic pressure > 125mmHg or evidence of hypertensive encephalopathy to the medical team. Resist commencing emergency treatment until consultation with an expert. There is a sig-nifi cant risk of complications (stroke or MI) if the BP is reduced rapidly.
It may be appropriate to commence oral antihypertensive therapy using a B-blocker (eg atenolol or labetalol) or calcium channel blocker (eg nifedipine).
• If treatment is appropriate, commence an IVI of sodium nitroprusside, labetalol or GTN with continuous BP monitoring via an arterial line and admit to high dependency unit (HDU) or ICU. Sodium nitroprusside has a very short half-life ( 8 1–2min) and acts as a vasodilator of both arterioles and veins. IV labetolol may be preferred if aortic dissection ( b p.92) or phaeochromocytoma are suspected.
• Beta-blockers are contraindicated in hypertension caused by cocaine, amphetamine or related sympathomimetic drugs ( b p.215), since B-blockade may cause unopposed A-adrenergic activity with paradox-ical hypertension and d coronary blood fl ow.
Hypertension in pregnancy
Hypertension may be part of pre-eclampsia or eclampsia (see b p.592).
Pre-eclampsia is diagnosed with 2 or more of: hypertension ( > 140/90), proteinuria and oedema. This can be associated with haemolysis, elevated liver function tests (LFTs), low platelets (HELLP syndrome).
Check urine for protein and check blood for FBC, LFT, platelets, and coagulation screen. Call for senior obstetric help. Eclampsia is diagnosed with the onset of grand mal seizures after 20 weeks gestation, and carries a signifi cant mortality rate.
Aortic dissection
Remember: hypertensive patients with sudden, severe chest, and/or back pain may have acute aortic dissection.
Pathology
Aortic dissection is longitudinal splitting of the muscular aortic media by a column of blood. The dissection may spread proximally (possibly resulting in aortic incompetence, coronary artery blockage, cardiac tamponade), distally (possibly involving the origin of various arteries), or rupture internally back into the aortic lumen, or externally (eg into the mediastinum, resulting in rapid exsanguination).
More than 70 % of patients have a history of hypertension. It occurs more frequently in those with bicuspid aortic valve, Marfan’s syndrome or Ehlers–Danlos syndrome. Up to 20 % follow recent cardiac surgery or recent angiography/angioplasty.
Dissection may be classifi ed Stanford type ‘A’ or ‘B’, according to whether the ascending aorta is involved or not, respectively. Overall mortality is 30 % (35 % type A and 15 % type B).
Type A Type B
Fig. 3.21
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AORTIC DISSECTION
History
Aortic dissection may mimic the presentation of an MI, requiring a high index of suspicion. It typically presents with abrupt onset sharp, tearing or ripping pain (maximal at onset) in anterior or posterior chest. Migration of the pain may refl ect extension of the dissection. Syncope occurs in 8 10 % of patients, sometimes in the absence of any pain. Occasionally, patients can present with neurological defi cit associated with chest pain.
Examination
The patient is usually apprehensive and distressed, with pain which is dif-fi cult to alleviate, even using IV opioid. Clues to the diagnosis include:
• An aortic regurgitation murmur (30 % ).
• Asymmetry or absence of peripheral pulses or a pulse defi cit (15–20 % ).
• Hypertension.
• Hypotension with features of tamponade or neurological signs in asso-ciation with pain (eg secondary to spinal/carotid artery involvement).
Investigations
• Send blood for U&E, glucose, FBC, coagulation, and cross-matching.
• Obtain an ECG and CXR.
Thoracic aortic dissection usually results in an abnormal CXR. One or more of the following changes may be seen:
• A widened or abnormal mediastinum (present in 875 % ).
• A ‘double knuckle’ aorta.
• Left pleural effusion ( 8 20 % ).
• Deviation of the trachea or nasogastric (NG) tube to the right.
• Separation of two parts of the wall of a calcifi ed aorta by > 5mm (the
‘calcium sign’).
The ECG may demonstrate MI, LVH. or ischaemia.
Note thatu 8 12 % of patients with aortic dissection have a normal CXR and 8 30 % have a normal ECG.
CT angiography or formal angiography will provide the defi nitive diagnosis.
In a haemodynamically unstable patient, trans-oesophageal echo in theatre may be the investigation of choice.
Management
On suspicion of aortic dissection:
• Provide O 2 by face mask as appropriate.
• Insert 2 large-bore (14G) IV cannulae and cross-match for 6U (inform blood bank of suspected diagnosis).
• Give IV morphine and titrate according to response ( ± anti-emetic).
• Call cardiothoracic team and cardiologist at an early stage.
• Insert an arterial line (preferably right radial artery) and discuss with specialist teams how to control the BP (eg labetalol infusion).
• Arrange further investigation based upon specialist advice and available resources (eg aortography, echocardiography, CT scan, MRI).
Type A dissections are usually treated surgically; type B lesions are usually treated medically.