HYPERTENSION INTRODUCTION Hypertension is one of the most common medical problems that affects approximately 1 billion individuals worldwide. Hypertension also results in significant morbidities despite the availability of antihypertensive medications. Severe hypertension usually develops in individuals with chronic hypertension but may also occur in individuals with no previous elevation of blood pressure. Patients with severe hypertension may present to their primary care physician with relatively mild symptoms or to the emergency department or intensive care unit (ICU) with life-threatening complications. Severe hypertension may be the cause of critical illness, complicate the course of another critical illness, or have little impact on the primary critical illness. In general, elevations of blood pressure, either acute or chronic, can be particularly detrimental in a critically ill patient. Some patients can be managed in the outpatient setting but others require hospitalisation on the general ward, an intermediate care unit, or the ICU. Appropriate evaluation and management of patients with severe hypertension is important because inadequate therapy as well as overaggressive therapy can result in adverse consequences. This module will address the evaluation and therapy of acute severe hypertension rather than chronic management of hypertension. T HINK Try to remember the circumstances where you have encountered patients with severe elevation of blood pressure and whether the patients had chronic hypertension. References that provide additional information on hypertension in the critically ill are listed below. Both articles review causes of hypertensive emergencies and the management of specific clinical conditions associated with severe hypertension. More information on the use and pharmacology of drugs used to treat severe hypertension is detailed. 1/ CLINICAL EVALUATION OF THE HYPERTENSIVE PATIENT Chronic or acute increases in blood pressure are a common finding in the general population as we in critically ill patients. It is important for the physician to determine the accuracy of the blood pressu measurement and its clinical significance. The impact of an elevated blood pressure may be more difficult to assess in a critically ill patient due to concomitant diseases and therapeutic interventions such as mechanical ventilation, or sedation. Categories of hypertension The Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure in the USA classified hypertension in adults aged 18 years and older into stages based on the severity of blood pressure elevation. This classification may be helpful in the evaluation and management of patients with chronic hypertension, but is less helpful for acutely ill patients with sev elevations of blood pressure. It does, however, emphasize the importance of even slight elevations blood pressure. Stage Blood Pressure Systolic (mmHg) Diastolic (mmHg) Prehypertension 120-139 or 80-89 1 140-159 or 90-99 2 ≥160 or ≥100 Severe hypertension that is potentially life-threatening is referred to as a hypertensive crisis. Severe hypertension is further characterised into hypertensive emergencies or hypertensive urgencies. Hypertensive emergency refers to severe hypertension that is associated with new or progressive end-organ damage (primarily brain, heart and kidney). In these clinical situations, blood pressure should be reduced immediately (within minutes or a few hours depending on the clinical circumstances) to prevent or minimise organ dysfunction (see table below). Hypertensive urgency refers to severe hypertension without evidence of new or worsening endorgan injury (see table below). Blood pressure can be lowered less rapidly in these conditions. T HINK Classification of blood pressure in ambulatory adults The finding of new or progressive end-organ injury is key to distinguishing a hypertensive emergency from an urgency Consider how elevations of blood pressure lead to organ dysfunction. Useful information may be found in the following reference. Patients with severe hypertension who are asymptomatic and have no endorgan injury do not require urgent lowering of blood pressure. In most cases, institution or modification of an antihypertensive regimen is indicated. Classification of hypertensive crises When knowledge of prior end-organ dysfunction is unavailable, differentiating hypertensive emergencies from urgencies may be difficult. Accelerated hypertension is a term used to describe a hypertensive urgency characterised by the presence of retinal haemorrhages and exudates without papilloedema. The term malignant hypertension is best avoided since it has been used in a confusin manner to describe either pathological, fundoscopic or clinical findings. Document the number of patients in your ICU over the next several months who have severe elevations of blood pressure and classify them as hypertensive emergencies, hypertensive urgencies, or chronic hypertension. Determine whic type of severe hypertension is most common in your patient population N OTE There is not a specific blood pressure level that differentiates a hypertensiveemergency from a less urgent situation. The degree of blood pressure elevation does not necessarily correlate with the severity of end-orga injury. The rate at which blood pressure rises and the prior level of blood pressure are more important than the absolute level. Most hypertensive emergencies are associated with a diastolic blood pressure greater than 120 mmHg, but a previously normotensive patient may experience end-organ injury with a diastolic blood pressure of 100 to 110 mmHg. Conversely, patients with chronic elevations of blood pressure may be asymptomatic with diastolic blood pressures greater than 120 mmHg. What types of patients are likely to have hypertensive emergencies with lower diastolic blood pressures? Explain what pathophysiological factors play a role in the development of severe hypertension? Measurement of blood pressure Since potentially life-threatening conditions due to severe hypertension are first recognised by an elevated blood pressure, it is imperative that blood pressure is correctly measured. A standardised approach with properly calibrated equipment should be utilised when obtaining a manual blood pressure reading. The patient should be sitting or supine with the arm at heart level. The width of the bladder inside the cuff should be 40% of the circumference of the upper arm and the length should encircle 80% of the arm circumference. A cuff that is too small or wrapped too loosely on the arm may result in falsely elevated blood pressure measurements. A stethoscope is placed over the antecubital fossa and the blood pressure cuff inflated to a level at which the radial pulse disappears. The first appearance of repetitive sounds as the pressure is slowly released in the cuff is the systolic pressure (phase 1) and the disappearance of repetitive sound signals the diastolic pressure (phase 5). In circumstances where the sounds are difficult to auscultate, it is usually possible to obtain a systolic pressure by palpation of the radial pulse and its disappearance. If severely elevated, blood pressure should be measured in both upper extremities to assess for One of the most common errors in measuring blood pressure is using a cuff that is too small for the patient's arm size discrepancies suggesting aortic dissection. The reference below provides detailed standards for measuring blood pressure accurately with a sphygmomanometer device. Automated blood pressure devices using auscultatory or oscillometric techniques are frequently use to obtain intermittent blood pressure measurements. Oscillometric devices derive the diastolic press from the systolic pressure and the mean arterial pressure. Although the arm is the preferred site for cuff, the calf, thigh, or forearm can also be used. The cuff should not be placed on an extremity bein used for intravenous infusion or that has circulatory compromise. Inflation of the cuff will also transiently interfere with pulse oximetry readings from the same extremity. New noninvasive monitoring technologies being developed that measure beat by beat blood pressu are currently undergoing validation. Further information can be found in the PACT modules on Haemodynamic monitoring and Health Technology Assessment. Automatic blood pressure devices are less accurate in clinical situations that are commonly encountered in the critically ill patient such as shock, mechanica ventilation and arrhythmias. If an abnormal reading is obtained, the position of the cuff and the function of the device should be assessed. The most accurate measurement of blood pressure is obtained by use of an appropriately calibrated intra-arterial catheter that allows continuous blood pressure measurements. Intra-arterial monitoring may be indicated for patients with hypertensive emergencies who require use of potent antihypertensive agents and close monitoring of blood pressure variation. In your ICU, compare blood pressures obtained by intra-arterial pressure monitoring and blood pressures obtained in the same patient by a manual or automated blood pressure device. Note discrepancies of systolic and diastolic pressures in patients with stable and unstable haemodynamics and in younger and older patients. Determine if the mean arterial pressures are similar with different devices. N OTE Pain, anxiety, stress of hospitalisation and cold can result in elevations of bloo pressure. These factors should be treated or corrected before considering use of antihypertensive medications. Clinical assessment of the patient The history and physical examination should be targeted to detect abnormalities in those organ systems most affected by elevations of blood pressure, in particular: the neurological, cardiovascula and renal systems. This evaluation will provide the necessary information to identify the clinical syndrome associated with the hypertensive crisis (see table ). In many circumstances, however, definitive diagnosis will require additional laboratory or imaging studies. Assessing neurological end-organ damage Neurological symptoms may be subtle or overt. Neurological involvement is suggested by complaints of headache, nausea, vomiting, visual disturbances, confusion, lethargy, seizures and focal neurological deficits. Subtle abnormalities of mental status may require confirmation from friends or family members. A rapid yet detailed neurological examination should be undertaken to assess mental status, the presence of focal motor or sensory deficits, and presence of cerebellar dysfunction. The examination should include a thorough inspection of the optic fundi for evidence of cotton wool exudates or flame-shaped haemorrhages as well as papilloedema. See the website below for more information. A fundoscopic examination is required as part of the assessment for neurological end-organ injury Lumbar puncture, if there is no cerebral oedema present, and toxicologic screens may be further required. See the PACT module on Altered consciousness for more information on lumbar puncture Neuroimaging (computed tomography or magnetic resonance imaging, see the PACT module on Clinical imaging) is mandatory for the diagnosis of acute intracranial events. A non-contrast CT s should be obtained initially to evaluate for the presence of intraparenchymal or subarachnoid blood. Typical hypertensive bleeds occur in the basal ganglia/hypothalamic regions and cerebellum (see th images below). A CT scan may initially be normal in acute thrombotic stroke. A normal CT scan or t presence of cerebral oedema may be compatible with hypertensive encephalopathy. CT scans showing hypertensive bleeds How is hypertensive encephalopathy diagnosed? N OTE It is crucial to rapidly distinguish hypertensive encephalopathy from other intracranial catastrophes because immediate blood pressure reduction is mandatory for hypertensive encephalopathy whereas it may worsen neurological deficits in stroke and intracranial haemorrhage. Using neuroimaging, a syndrome of reversible posterior leukoencephalopathy has been recently described in association with hypertensive encephalopathy and preeclampsia/eclampsia. It is also associated with immunosuppressive and cytotoxic therapy, erythropoietin use, and other conditions This syndrome is potentially fully reversible. You can read more about it in the following reference Assessing cardiovascular end-organ damage Symptoms suggesting involvement of the cardiovascular system due to severe hypertension include anginal chest pain, dyspnoea, or severe tearing chest pain associated with acute aortic dissection. Physical examination may reveal jugular venous distension, a third or fourth heart sound, tachycard or pulmonary rales. Physical findings that may suggest acute aortic dissection include pulse deficits the extremities, a new murmur of aortic valve insufficiency, and signs of left pleural effusion. An electrocardiogram and chest radiograph should be obtained in patients with severe hypertension who are suspected to have an acute coronary syndrome, left ventricular dysfunction causing pulmonary oedema or acute aortic dissection as the end-organ injury. Myocardial infarction may be apparent from ST-segment elevation on the electrocardiogram and/or confirmed by elevation of markers of myocardial injury such as CPK-MB or troponins. See the PACT module on Acute brain ischaemia. An electrocardiogram may reveal evidence of myocardial ischaemia or infarct Diagnosis of other acute coronary syndromes may depend on the clinical history and electrocardiographic findings such as ST-segment depressions or T-wave inversions. Left ventricular dysfunction associated with severe hypertension may be due to systolic or diastolic abnormalities. What clinical and ancillary test findings may be helpful in distinguishing between systolic and diastolic dysfunction? Echocardiography is useful to assess left ventricular function and to identify left ventricular hypertrop or dilation. Right heart catheterisation may differentiate haemodynamic pulmonary oedema from oth forms of bilateral pulmonary infiltrates (e.g. acute respiratory distress syndrome, severe bilateral pneumonia) but it is usually not needed in hypertensive emergencies. N OTE Echocardiography may show normal systolic function during hypertensive pulmonary oedema, since the majority of episodes are due to exacerbation of diastolic dysfunction. The clinical study cited below shows that left ventricular ejection fraction was normal in most patients, and similar during an episode of hypertensive pulmonary oedema and after treatment, when the blood pressure has been controlled. If acute aortic dissection is suspected, a definitive diagnostic test should be obtained and the choice will depend on availability of imaging procedures and patient factors. Recommended imaging studies are aortography, transoesophageal echocardiography (TOE), computed tomography scans or magnetic resonance imaging. Additional information on aortic dissection can be found in the review by Khan and Nair. If the patient is already in the ICU on a ventilator and there is good local expertise with echocardiography, TOE – if not contraindicated – can be diagnostic in dissection of the thoracic aorta. It is crucial to distinguish between aortic dissection and myocardial infarction quickly to avoid delay in proper treatment and to ensure that thrombolytic and anticoagulant therapy are not given to the patient with a dissection. Assessing renal end-organ damage The renal system is difficult to assess by history and physical examination in the setting of severe hypertension. Patients may present with non-specific symptoms of weakness, pretibial oedema, oliguria, polyuria, nocturia, or haematuria. Physical examination may rarely pick up the presence of bladder distension or polycystic kidneys in some individuals. Laboratory evaluation includes full blood count, measurement of blood urea nitrogen, creatinine, an electrolytes. The peripheral blood smear may reveal signs of microangiopathic haemolysis (schistocytes and other fragmented red cells). Urine analysis must be obtained to detect proteinuria haematuria, and the presence of cellular casts. Renal and urinary tract ultrasound is useful to detec obstructive acute renal failure. If acute glomerulonephritis is suspected, a renal biopsy should be performed soon after blood pressure control to confirm diagnosis and initiate appropriate therapy. See the PACT modules on Oliguria and anuria and Acute renal failure N OTE There is a higher than expected prevalence of secondary hypertension (such a renal artery stenosis, acute glomerulonephritis, Cushing's syndrome, phaeochromocytoma) among patients who present with a hypertensive crisis. Most authorities recommend screening for secondary causes of hypertension after initiation of antihypertensive treatment. In the acute setting, however, it is not useful to request costly laboratory or imaging studies to detect secondary hypertension. Kidney can be easily seen using an echo. Other assessments A urine toxicologic screen may be indicated in some patients with severe hypertension. Observe the clinical course of the next patients with drug or toxin-induced hypertensive crisis. What were the products suspected or identified? How did their care differ from patients with hypertensive crises due to other causes? 2/ EMERGENCY MEASURES AND INITIAL TREATMENT If untreated, hypertensive emergencies are associated with a high mortality and morbidity, depending on the severity of the associated organ damage. Since the advent of effective antihypertensive drug therapy, the prognosis of patients with hypertensive crisis has improved dramatically. However, serious and avoidable sequelae may occur if blood pressure is reduced too quickly and/or too much. Hence, the goal of antihypertensive therapy is to decrease blood pressure while maintaining organ perfusion and avoiding complications. The intensivist may be involved in making the initial decisions on management of patients when the hypertensive crisis occurs in the ICU or they may be called on to continue care that was initiated in the emergency department, operating suite or other hospital location. Both situations require prudent choices in management. The following steps are helpful in addressing critical decisions that need to be made for patients with severe elevations of blood pressure. They are to be considered successively. Should the blood pressure be lowered acutely? End-organ damage is present. This is a hypertensive emergency. Admit the patient to an intensive care unit or other available monitored bed, monitor blood pressure, and use parenteral agent(s) (see Task 3 and Task 4 ) to lower blood pressure to safer levels (not necessarily normal levels) within several minutes or hours. No end-organ damage is present (or unchanged from baseline). This could be a hypertensive urgency (see above). Admit the patient to a short-stay unit or the general ward, monitor blood pressure using non-invasive devices, and use oral therapy (see Task 3 and Task 4 ) to lower blood pressure to safer levels over several The most important management decision is to determine if the blood pressure needs to be lowered T HINK hours to 24 hours. The level of care is often dependent on the nature of coexisting conditions. Asymptomatic patients with severe hypertension usually do not require immediate reduction of blood pressure. An appropriate antihypertensive regimen should be instituted and adequate follow-up arranged. Since many potent antihypertensive drugs are available, the challenge is 'when' to reduce blood pressure rather than 'how'. As for many other medical situations, the principle, 'first do no harm', is to be applied. How much should the blood pressure be lowered? No clinical study has been designed to examine the optimal target blood pressure for each clinical condition associated with a hypertensive emergency or urgency. In hypertensive emergencies, a reasonable goal is to reduce mean arterial blood pressure by 20 to 25% or to reduce diastolic blood pressure to 100-110 mmHg over minutes to hours. If the patient's baseline blood pressure is known, that information should also be taken into account when choosing a target blood pressure. In aortic dissection, the target blood pressure could be as low as a systolic blood pressure ≤ 110 mmHg. Blood pressure should be lowered to a safer, but not usually a normal level In most situations, the blood pressure is not lowered to a normal range because hypoperfusion of vital organs may result. The vascular autoregulatory mechanisms in individuals with chronic hypertension have adapted to higher levels of blood pressure. An example is the autoregulation of cerebral blood flow in normotensive individuals compared to hypertensive patients (see figure below). The autoregulatory curve is shifted to higher pressures in hypertensive patients. A normal mean arterial blood pressure in a hypertensive patient may be below the lower limit of their ability to maintain cerebral blood flow and result in cerebral ischaemia. Similar autoregulation occurs in the myocardial and renal vasculature. Which medication should be used to lower blood pressure? More options are now available to lower blood pressure in hypertensive emergencies and the choice medication can be individualised depending on patient characteristics and the clinical situation. Coexisting patient conditions may determine whether some drugs are desirable. The available facili and personnel may also influence the drug choice especially if frequent monitoring is not available. course, the pharmacodynamics and pharmacokinetics of antihypertensive drugs play a role in all of these considerations. The drugs available to treat hypertensive crises are discussed in Task 3 . T HINK Consider which patient conditions would influence the use of certain parenteral antihypertensive drugs. 3/ PHARMACOTHERAPY OF HYPERTENSIVE CRISES The aim of drug therapy in patients with hypertensive emergencies is to reduce blood pressure in a controlled, predictable, and safe way. Depending on the nature of the end-organ damage, a particular therapeutic strategy may be more or less appropriate. This section reviews the pharmacology of drugs used to treat hypertensive crises and Task 4 addresses drug options for specific clinical conditions. N OTE All agents used to treat hypertensive emergencies can result in excessive decreases in blood pressure The availability of individual drugs will vary from country to country. What are the ideal characteristics of an agent for treatment of a hypertensive emergency? T HINK Observe in your unit the drug(s) used for specific hypertensive emergencies. Was the drug choice based on its pharmacodynamic properties, on the haemodynamic profile of the patient or on the underlying disease? Treating hypertensive emergencies Intravenous medications should be chosen for the treatment of true hypertensive emergencies. In general, a single agent is preferable to using multiple agents. Pharmacodynamic characteristics of parenteral antihypertensive drugs Drug Route Nitroprusside i.v. infusion 0.25-10 mcg/kg/min Immediate 1-2 min i.v. bolus 3-5 min 3-6 h Labetalol Dosage Start 10-20 mg up to 80 mg every 10 min Onset Duration i.v. infusion 0.5-2 mg/min Nitroglycerin i.v. infusion 5-300 mcg/min 1-2 min 1-3 min Nicardipine i.v. infusion 5-15 mg/h 5-10 min 15-40 min i.v. loading 1-2 min 20-30 min 1 mg/kg for 1 min Esmolol i.v. infusion 150-300 mcg/kg/min Urapidil i.v. infusion 15-120 mg/h 2 min 2-3 h Enalaprilat i.v. bolus 0.625-1.25 mg every 6 h 10-15 min 6-8 h Hydralazine i.v. bolus 5-20 mg every 20-60 min 10-30 min 3-6 h Fenoldopam i.v. infusion 0.1-1.6 mcg/kg/min 15 min 30-60 min Phentolamine i.v. bolus 1-2 min 10-30 min Clevidipine i.v. infusion 1-16 mg/h 2-4 min 5-15 min 5-10 mg every 10 min A separate line should be used for the infusion of antihypertensive agents to avoid flushing the line while giving another medication. Diazoxide, a potent arteriolar dilator, and trimethaphan camsylate, a ganglionic blocker, are now obsolete because of frequent adverse effects and the advent of better intravenous agents. Sodium nitroprusside Nitroprusside is the prototype of a shortacting easy-to-titrate arteriolar and venous vasodilator. It has been used effectively in all conditions associated with hypertensive emergencies. The most common adverse effect is arterial hypotension. Excessive drops in blood pressure can be detected by intra-arterial monitoring and are managed by reducing the dosage and administering fluids if needed. Other adverse effects include reflex tachycardia and cyanide or thiocyanate toxicity. These drugs are not grouped by class since there are no well defined pharmacological classes among these agents Explain which clinical conditions may increase the risk of cyanide or thiocyanate toxicity? Cyanide toxicity is best prevented by avoiding administration of large dosages for prolonged periods time (e.g. dosages greater than 3 mcg/kg/min for more than 72 hours), especially in patients with re or hepatic dysfunction. The maximum administration rate of 10 mcg/kg/min should not be maintaine for more than 10 minutes. In some centres, cyanide levels are monitored and sodium thiosulphate o hydroxocobalamin are co-administered to prevent or treat cyanide toxicity. Haemodialysis is effectiv removing thiocyanate. What are the clinical signs of cyanide and thiocyanate toxicity? Although sodium nitroprusside has been reported to increase intracranial pressure, the associated f in systemic vascular resistance seems to offset this effect. Nitroprusside may increase mortality whe infused in the early hours after acute myocardial infarction. Intrapulmonary shunting may result in a decrease in oxygenation. Labetalol hydrochloride Labetalol is a non-selective β-adrenergic blocker with associated α-block activity, in a 7 to 1 ratio in intravenous formulation. It reduces systemic vascular resistance with mild reduction in heart rate and maintains cardiac output. Labetalol can be given intravenously (bolus or infusion) or orally. It is useful in most hypertensive emergencies, especially those associated with hi levels of circulating catecholamines. It is also effective in preeclampsia/eclampsia, by decreasing bl pressure while maintaining placental perfusion. As a β-blocker, labetalol is contraindicated in patien with active obstructive pulmonary diseases or second or third degree heart block, and should be use with caution in patients with decompensated systolic heart failure. Side effects are minor and includ nausea, vomiting, paresthesias and headache. Nitroglycerin Nitroglycerin is a venous and coronary artery dilator although higher doses can also dilate systemic arteries. Intravenous nitroglycerin is ideally indicated in hypertensive patients with ac coronary syndromes and has also been used for perioperative hypertension. Side effects include headache, nausea, bradycardia, hypotension, and rarely methaemoglobinaemia. Prolonged use ma induce tachyphylaxis. Nicardipine hydrochloride Nicardipine is a dihydropyridine calcium channel antagonist with system and coronary artery vasodilating effects. It can be administered intravenously for hypertensive emergencies and has minimal or no negative inotropic effects or atrioventricular conduction effects. Nicardipine is widely used for control of perioperative hypertension, and is also effective and safe in other forms of severe hypertension including preeclampsia/eclampsia. Lower doses may be appropriate in older patients or patients with liver disease who may have decreased hepatic metabolism. Side effects include headache, flushing, hypotension, nausea, vomiting and tachycardi (although there is usually minimal, if any, increase in heart rate in adult patients). Esmolol hydrochloride Esmolol is a short-acting cardioselective β-adrenergic blocker that is mainl used to control perioperative hypertension and tachycardia. It has no vasodilatory effects and lower blood pressure by decreasing heart rate and myocardial contractility. Side effects and contraindicati are those of β-blockers. If it is the only agent used and concurrent longer acting drugs are not initiat a prolonged infusion of esmolol, especially in high dose, is a relatively expensive means of blood pressure control. Phentolamine mesylate Phentolamine is a peripheral α-adrenergic blocker indicated for the management of hypertensive emergencies associated with catecholamine excess such as phaeochromocytoma, monoamine oxidase inhibitor interaction, antihypertensive withdrawal syndrom and cocaine abuse. This agent may cause tachycardia, hypotension, headache, vomiting, flushing a angina. N OTE Catecholamine storm is uncommon and can be effectively controlled by other agents such as labetalol, nitroprusside, or reinstitution of the previous antihypertensive regimen (especially clonidine). In the ICU patient, typically with unresponsive, intermittent (bursts of) hypertension, one should suspect the potential presence of pheochromocytoma, consider phentolamine, or alternative vasodilator, treatment acutely and be prompted to investigate formally for phaeochromocytoma. Urapidil Urapidil is a peripheral α1-adrenergic blocker with additional central 5-hydroxytryptamin A1 receptor agonist activity that has been found to be effective in severe hypertension, including perioperative hypertension. Its main advantage is that reflex tachycardia does not occur as a result reduced sympathetic outflow. It is not available in the USA. A test dose of 40-50 mg in an adult is useful and may discriminate whether urapidil will be effective in lowering blood pressure. Enalaprilat Enalaprilat is the intravenous formulation and the active metabolite of the orally active angiotensin-converting enzyme inhibitor enalapril. It reduces blood pressure by dilating arterial and venous vessels. The long duration of action, variable response and limited experience do not make agent an ideal drug for hypertensive emergencies. Moreover, angiotensin-converting enzyme inhibi are contraindicated during pregnancy, in patients with renal impairment especially with stenosis of renal arteries as the cause of hypertension. Adverse effects are hypotension (especially in sodium o volume-depleted patients), angio-oedema, renal dysfunction and hyperkalaemia. Hydralazine hydrochloride Hydralazine is a direct arteriolar dilator that may be given intravenously and orally. It is more difficult to manage than other intravenous agents because of the variable magnitude and duration of response. Its remaining parenteral indication is preeclampsia and eclamp because it improves placental blood flow. Even for this indication, labetalol and calcium antagonists seem preferable because maternal and perinatal side effects are less common. Since hydralazine increases heart rate, cardiac output and myocardial oxygen consumption, it should not be used in patients with myocardial ischaemia or aortic dissection. Fenoldopam mesylate Fenoldopam is a short-acting peripheral postsynaptic dopamine-1-receptor agonist approved for inhospital, short-term management of severe hypertension. Its antihypertensiv action is due to a combination of arterial vasodilatation, renal vasodilatation and natriuresis. It has n toxic metabolites. Fenoldopam and nitroprusside are equally effective in the treatment of severe hypertension, so that fenoldopam may be an alternative to nitroprusside. Fenoldopam may be particularly useful in severely hypertensive patients with impaired renal function or congestive heart failure. Adverse effects include headache, flushing, hypotension, dose-related tachycardia, decreas serum potassium and increased intraocular pressure. It is not available in the European community. learn more about this drug, read the following review article. Clevidipine Clevidipine is a short-acting intravenous dihydropyridine calcium channel antagonist recently approved for treatment of severe hypertension in the USA. This agent is an arteriolar vasodilator resulting in decreased blood pressure with little change in heart rate or cardiac output. Favourable characteristics include rapid hydrolysis by blood and tissue esterases to an inactive metabolite, a short duration of effect (1-3 min), and metabolism unaffected by renal or hepatic functi Intrapulmonary shunt fraction is increased and associated with a decrease in PaO2. Clinical trials reported in the references below suggest that clevidipine may be an option for blood pressure contr the perioperative period. Hypotension and reflex tachycardia have been described. What is the intravascular volume status of patients with hypertensive crises? Treating hypertensive urgencies Hypertensive urgencies do not require acute lowering of blood pressure. In most cases, oral medication appropriate for the chronic underlying disease processes can be initiated. There is no evidence to suggest that immediate lowering of blood pressure improves any outcome measure but considerable adverse effects can be precipitated by inappropriate rapid reductions in blood pressure. The decision to treat the blood pressure with an oral agent in the hospital or to institute a therapeutic regimen as an outpatient should take into consideration comorbid conditions, the potential for progression to a hypertensive emergency, and the ability to obtain timely follow-up. Most patients with hypertensive urgencies will not require intensive care. Oral agents for hypertensive urgencies Labetalol See . Oral labetalol has been used effectively to lower blood pressure in non-emergency conditions. This drug may be particularly helpful in patients with tachycardia. Clonidine Clonidine is a central α2-adrenergic agonist that decreases sympathetic outflow, and hence systemic vascular resistance and heart rate. It is an alternative to oral β-blockers or labetalol if contraindications to these agents are present. It is available as a parenteral agent in Europe. Administration of clonidine is particularly helpful in patients with severe hypertension due to discontinuation of chronic clonidine therapy or withdrawal states. Side effects are dry mouth, bradycardia and orthostatic hypotension. Sedation may occur that can interfere with neurological evaluation in patients with cerebral disease. Captopril Captopril, an angiotensin-converting enzyme (ACE) inhibitor, has been used successfully in hypertensive urgencies. Other ACE inhibitors have also been administered with similar efficacy. Adverse effects are first-dose hypotension in patients with sodium or volume depletion or acute renal failure in patients with bilateral renal artery stenosis. Therefore, captopril should not be used when renal artery stenoses are suspected. Nifedipine Oral, sublingual or bite-and-swallow fast-acting nifedipine has been widely used to rapidly reduce blood pressure in acute hypertension in the past. However, the inability to control the rate or magnitude of decrease in blood pressure has been associated with serious adverse effects, including death, making this agent unacceptable for this purpose. In hypertensive urgencies tha require immediate oral antihypertensive treatment, an adequate dose of a longacting agent should be provided. The following position paper gives welldocumented arguments against the use of short-acting nifedipine. 4/ MANAGEMENT OF SPECIFIC CONDITIONS Hypertensive emergencies encompass a wide variety of clinical conditions and several drugs are now available for use in these situations. The clinician should take into account the specific aetiology of the severe hypertension, co-existing patient conditions, and the pharmacology of agents when selecting a drug for use. The antihypertensive drug should be tailored to the patient's needs and underlying disease Hypertensive encephalopathy In hypertensive encephalopathy, the lowering of blood pressure is therapeutic as well as diagnostic. If the mental status does not improve within a few hours of lowering the blood pressure, other diagnoses should be considered. Historically, nitroprusside has been the most commonly used agent in this clinical situation. Alternative drugs that are easy to administer include labetalol and fenoldopam. Nitroglycerin and nicardipine may also be effective but clinical experience in hypertensive encephalopathy is limited. Drugs that cause sedation such as clonidine should not be used in order to avoid confusion with the neurological assessment. Acute intracranial events Little prospective evidence exists for lowering the blood pressure or the extent of blood pressure reduction in the setting of traumatic injury, intracranial haemorrhage and thrombotic stroke. It is often difficult to determine if elevated blood pressure caused the intracranial injury or the primary intracranial injury caused the elevated blood pressure. Severe elevations of blood pressure may cause further damage leading to increased or new haemorrhage, extension of infarct, or cerebral oedema. However, injured areas may lose the ability to autoregulate cerebral blood flow and become dependent on blood pressure for collateral flow. Lowering the blood pressure could lead to inadequate cerebral perfusion and further ischaemia. Elevated blood pressure in the setting of an acute intracranial injury is often transient so a period of observation may be warranted. If moderate hypertension is present, an oral agent can be instituted with control of blood pressure achieved over several days. Severe sustained hypertension should be treated with a parenteral medication that can be easily titrated. A recent pilot study referenced below found that acute lowering of blood pressure in patients with thrombotic or haemorrhagic stroke was safe and may potentially improve mortality. This trial suggests that further evaluation in larger studies is warranted. Several clinical trials of intensive blood pressure control in intracerebral haemorrhage may provide more specific guidance in the future. You can read more about the Antihypertensive Treatment in Acute Cerebral Hemorrhage (ATACH) study and the Second Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage (INTERACT2) study at the following websites: N OTE During the acute phase of stroke, the increase in blood pressure is regarded as a compensatory mechanism to maintain cerebral perfusion pressure in face of an increased intracranial pressure (cerebral perfusion pressure = mean arterial pressure minus intracranial pressure). Therefore, antihypertensive treatment should be initiated only if blood pressure is markedly elevated: Recommended thresholds for antihypertensive therapy in stroke Recommended approach to hypertension in acute ischaemic stroke Threshold for lowering BP Eligible for thrombolysis or other acute reperfusion intervention Systolic BP >185 mmHg or diastolic BP >110 mmHg (I BP does not decline, do not administer thrombolytic) During or after treatment with thrombolysis Systolic BP >180 mmHg or diastolic BP >105 mmHg or other acute reperfusion intervention No thrombolysis or acute reperfusion intervention Systolic BP >220 mmHg or diastolic BP>120 mmHg (Lower BP by ~15% in first 24 h) BP = blood pressure. Suggested guidelines for treating elevated blood pressure in spontaneous intracranial haemorrhage Systolic BP>200 mmHg or mean BP>150 mmHg Consider aggressive reduction of BP with IV infusion Systolic BP>180 mmHg or mean BP>130 mmHg with suspicion or evidence of elevated ICP Consider ICP monitoring and reducing BP with intermittent or continuous IV medications to maintain cerebral perfusion pressure >60-80 mmHg Systolic BP>180 mmHg or mean BP>130 mmHg without suspicion or evidence of elevated ICP Consider modest reduction of BP (target mean BP 110 or BP 160/90 mmHg) with intermittent or continuous IV medications Mean BP = Diastolic BP + 1/3 (Systolic BP − Diastolic BP). BP = blood pressure. ICP = intracranial pressure. These consensus recommendations are found in the following guidelines. Further information on stroke can be found in the PACT module on Acute brain ischaemia . Drugs that may be considered include labetalol, nicardipine, nitroprusside, and nitroglycerin. Fenoldopam has not been systematically evaluated in intracranial injury. The effects of these agents on autoregulation, intracranial pressure, and cerebral blood flow must be considered. If the neurological status deteriorates while blood pressure is being lowered, therapy should be altered to allow the blood pressure to increase. N OTE Both high and low blood pressure have been found to be independent prognostic factors for poor outcome in acute stroke in the following report. Direct vasodilators such as nitroprusside and nitroglycerin may increase cerebral blood volume and intracranial pressure while decreasing mean arterial pressure. These effects may compromise cerebral perfusion, particularly in patients with increased intracranial pressure. If the patient's baseline neurological examination makes observation of further deterioration difficult or if neurological examinations cannot be performed frequently, drugs other than direct vasodilators are more appropriate. Labetalol does not appear to increase intracranial pressure and requires less intensive monitoring. Nicardipine causes cerebral vasodilatation and associated increased intracranial pressure and offers little advantage over direct vasodilators. A further discussion of the pharmacologic effects of these agents in intracranial injury can be found in the following reference. In the setting of subarachnoid haemorrhage, it may be prudent to treat severe hypertension until the aneurysm is effectively managed. Nimodipine is routinely used in this clinical situation and its effects on blood pressure must be considered before instituting any additional antihypertensive agents. Some centres use the maintenance or induction of hypertension to treat or prevent cerebral vasospasm in patients with subarachnoid haemorrhage. You can see further images of intracerebral haemorrhages in Task 1 . You can also find some further information about subarachnoid haemorrhage in the PACT module on Acute brain ischaemia and on Traumatic brain injury . CT scan of basal ganglia bleeding Acute coronary syndromes Sustained hypertension in patients with myocardial ischaemia should be treated to reduce myocardial oxygen demand. Despite an initial elevation of blood pressure in many patients, the blood pressure usually decreases without specific antihypertensive therapy within the first six hours of admission. The first priority in patients with myocardial ischaemia is to relieve pain with traditional medications such as nitroglycerin and morphine. An intravenous beta-blocker is also administered as part of standard care in most patients. If further interventions are needed for severe sustained hypertension, intravenous nitroglycerin in higher doses would address blood pressure as well as coronary vasodilatation. Labetalol is an alternative agent that benefits the patient for the β-blocking effects as well as the vasodilatation. Although nitroprusside has been used in this clinical setting, concerns have been raised about coronary artery steal resulting in decreased collateral flow to ischaemic areas and it is no longer used for this condition. Mild to moderate hypertension (less than 160/100 mmHg) can usually be treated with oral β-blockers and angiotensin-converting enzyme inhibitors. Both classes of drugs are routinely used in myocardial ischaemia to improve outcomes. Pure vasodilator agents such diazoxide and hydralazine should be avoided because of reflex tachycardia that could increase myocardial oxygen demand. Acute left ventricular dysfunction The clinician should consider whether the patient with pulmonary oedema secondary to acute left ventricular dysfunction has systolic or diastolic dysfunction. Systolic dysfunction with low cardiac output and dilated ventricles can be associated with hypertension resulting from catecholamine-induced peripheral vasoconstriction. Often, there is only a mild to moderate increase in the diastolic blood pressure. Additional clues include the lack of hypertensive retinopathy and the presence of marked cardiomegaly on chest radiograph. Hypertensive emergencies associated with diastolic dysfunction are more common. In these situations, the hypertrophied left ventricle has decreased compliance due to the acute elevation of blood pressure that results in inadequate diastolic filling. Elevations of diastolic blood pressure are often greater with diastolic dysfunction. Other clinical clues that suggest diastolic dysfunction are the presence of significant hypertensive retinopathy and left ventricular hypertrophy on electrocardiogram. Differentiation of the clinical situations may be difficult. Hypertensive emergencies with pulmonary oedema are most commonly due to left ventricular diastolic dysfunction Nitroprusside would be effective in systolic or diastolic dysfunction. If ischaemia is thought to play a role in the ventricular dysfunction, nitroglycerin may be an appropriate agent. Labetalol is an excellent drug to treat diastolic dysfunction in this setting and the decrease in heart rate facilitates left ventricular filling. Alternatives include fenoldopam and nicardipine. Intravenous diuretics may be considered in the patient with systolic dysfunction and evidence of volume overload (pulmonary rales, jugular venous distension, and peripheral oedema). Diuretics should be avoided initially in the setting of diastolic dysfunction in order to avoid excessive reduction of left ventricular filling pressures. Adequate preload is needed to optimise filling of the hypertrophied, non-compliant left ventricle. To view pathology specimens of dilated cardiomyopathy and left ventricular hypertrophy, click on image numbers 106 and 113 under systemic pathology/cardiovascular pathology/cardiomyopathies on the following website. Hypertension Acute aortic dissection MRI showing a type A acute aortic dissection Aortic dissection may occur either in the ascending aorta (proximal, type A), which requires surgery or in the descending aorta (distal, type B), which can initially be treated medically. The immediate goal in acute aortic dissection is to lower the blood pressure and reduce the shear force (from ejection of ventricular blood) on the aorta until definitive surgical or medical therapy can be instituted The blood pressure should be reduced to the lowest level that relieves pain and allows adequate organ perfusion. Usually, the goal is a systolic blood pressure of 100 to 110 mmHg. Therapy include a β-blocker usually associated with an easy-to-titrate vasodilator. A vasodilator should never be use alone, since it may worsen the shear force. Labetalol is a single agent that provides β-blockade and vasodilatation in this setting. Trimethaphan is rarely used because of adverse effects but it may be needed in patients who cannot tolerate β-blockers. Excess catecholamine states The treatment of choice for severe hypertension due to increased levels of catecholamines depends on the aetiology if known. Drug-induced hypertension due to cocaine and other illicit sympathomimetic agents is often transient and responds to sedation with benzodiazepines. If blood pressure elevations are severe and sustained, labetalol may be used. Alternative agents include nitroprusside and fenoldopam. Severe alcohol withdrawal associated with hypertension will also respond to benzodiazepines. Phentolamine has been the treatment of choice for phaeochromocytoma but other drugs such as labetalol and nitroprusside are also effective. In phaeochromocytoma, an α-blocker should always be used before a β-blocking agent. Intravascular volume should be optimised to attenuate vasoconstriction due to salt and water excretion. Explain what foods can precipitate severe hypertension through interaction with monoamine oxidase inhibitors? Severe preeclampsia/eclampsia Preeclampsia is diagnosed on the basis of pregnancy-induced hypertension (>140 mmHg systolic or >90 mmHg diastolic blood pressure, confirmed by two separate measurements, occurring after 20 weeks gestation in a woman who was normotensive before 20 weeks gestation) and proteinuria (500 mg/l protein in a random specimen or an excretion of 300 mg per 24 h). Peripheral oedema is often associated. The treatment of severe preeclampsia/eclampsia includes consideration of delivery of the fetus, seizure prophylaxis with magnesium sulphate, blood pressure control, and supportive measures. In this setting, the diastolic blood pressure should be reduced to 90 to 100 mmHg. However, precipitous drops in blood pressure should be avoided to prevent compromise of placental circulation. Hydralazine, labetalol, and nicardipine are commonly used and preserve myometrial blood flow. Nifedipine has also been used safely in this setting. In the pregnant patient, nitroprusside and angiotensin-converting enzyme inhibitors should be avoided due to adverse fetal effects. Additional information on the management of hypertension in pregnancy and severe preeclampsia/eclampsia can be found in the following references. Perioperative hypertension A preoperative history of hypertension and the type of surgery influence the incidence of perioperative hypertension. The decision to treat hypertension in the perioperative setting requires an assessment of the risk of myocardial ischaemia, haemorrhage, and disruption of vascular integrity. As previously mentioned, the impact of pain, anxiety and hypothermia on blood pressure must be addressed. The effects of analgesics, anaesthetic agents and shifts in intravascular volume on blood pressure must be taken into account before initiating additional therapy. Postoperative hypertension is usually self-limited (2-6 h) so short-acting titratable agents are preferred. Nitroprusside and nitroglycerin have been routinely used in the postoperative period. Additional agents that have been used effectively include labetalol, esmolol, nicardipine, urapidil, fenoldopam and clevidipine. N OTE A NECDOTE Although nitroglycerin and nitroprusside are commonly used, the choice of agent will be decided by the clinical circumstance, the experience of the clinician and local custom. Consider intravenous clonidine in difficult situations where supplementary analgesia and control of hypertension and agitation are required. In postoperative hypertension, the clinician must assess for precipitating factorssuch as pain, anxiety, altered blood gases (hypoxaemia, hypercapnia, acidosis), hypervolaemia, bladder distention, and hypothermia. These factors should be corrected before considering antihypertensive drug therapy. The resident was called to see a patient with hypertension the evening after a urological operation. On arrival, obvious dyspnoea and cyanosis were noted. Physica examination showed dullness to percussion and no air entry in the right lung. Chest radiograph revealed a massive right pleural effusion and malposition of the right jugular catheter. Arterial blood gases showed hypoxaemia and respiratory acidosis. Hypertension and respiratory failure resolved after pleural drainage and removal of th jugular catheter. Which types of surgery are most likely to be associated with perioperative hypertension? CONCLUSION Severe hypertension must be rapidly and appropriately evaluated to assess its clinical significance and to determine if treatment should be immediately instituted. An organised approach using the following questions can guide the clinician in decision-making. Should the blood pressure be lowered? Should the blood pressure be lowered acutely? How much should the blood pressure be lowered? Which medication should be used to lower the blood pressure? Hypertensive emergencies and hypertensive urgencies should be identified and an individualised plan developed that includes a goal for blood pressure reduction and selection of the best parenteral drug for the patient's clinical situation. PATIENT CHALLENGES In the Patient Challenges, you are given information about patients with acute care problems. As a case develops, you are asked to interpret the nature of the problems or make management decisions. You are presented with questions and materials designed to raise learning issues relevant to the subject. The learning issues link to the relevant sections in the Tasks. Two cases are presented here, a 62-year-old woman with diabetes and chronic hypertension, and a 68-year-old-man admitted to the emergency department for acute respiratory failure. Case 1 A 62-year-old woman with diabetes and chronic hypertension underwent elective coronary artery revascularisation for progressive unstable angina. She is known to have renal insufficiency with a creatinine of 210 µmol/l (2.4 mg/dl). Her medication prior to surgery included enalapril, hydrochlorothiazide, metformin, glyburide, atenolol, isosorbide dinitrate, and aspirin. The patient had taken her antihypertensive medications at 5.00 am, and her surgery was completed at 3.00 pm. General anaesthesia consisted of midazolam, fentanyl, vecuronium, and isoflurane. She is transferred to the ICU with heart rate 95 beats/min, respiratory rate 14 beats/min (on mechanical ventilation), blood pressure 140/88 mmHg by intra-arterial monitor, and temperature 36 °C. Thirty minutes later, the patient is noted to be agitated with blood pressure 168/94 mmHg and heart rate 104 beats/min. N OTE Pressure monitoring by intra-arterial catheter provides the most accurate measurement of blood pressure. Case 1 Screen 2 Is this patient experiencing a hypertensive emergency or hypertensive urgency? Give reasons fo your answer. Learning issues Evaluation of the hypertensive patient Definitions of hypertensive crises Perioperative hypertension What evaluations would be helpful to determine the significance of the elevated blood pressure? Learning issues Assessment of end-organ injury N OTE The operative record should be reviewed for blood loss, fluid balance, and administered medications. Case 1 Screen 3 The patient's lung examination is clear except for decreased breath sounds in the bases and no cardiac gallop is appreciated. Blood loss in the operating room was 500 ml and fluid balance was +2200 ml. Urine output in the previous hour was 60 ml. Blood pressure during surgery was well controlled with systolic pressures ranging from 110-120 mmHg. An electrocardiogram shows inverted T-waves in the inferior leads that were changed from the preoperative electrocardiogram. Her blood pressure remains at 158/96 mmHg. What additional factors must be considered before administering medication to lower blood pressure? Learning issues Perioperative hypertension Case 1 Screen 4 The patient is medicated with morphine 4 mg intravenously and lorazepam 1 mg intravenously. There is no evidence of excessive blood loss, hypoxia, hypercapnia or acidosis. Despite control of the agitation, the blood pressure remains elevated at 160/94 mmHg and the heart rate is 100-110 beats/min. Should a medication be administered to lower the blood pressure? Why? What medication characteristics are desirable when considering treatment of this patient's blood pressure? Learning issues Pharmacotherapy of hypertensive crises Treatment of specific clinical conditions Case 1 Screen 5 What options are there to lower this patient's blood pressure? Learning issues Initial treatment N OTE The effects of one agent on the blood pressure should be assessed before initiating another medication that affects blood pressure in order to prevent excessive decreases. Esmolol is administered as a continuous infusion to decrease the heart rate to 60-70 beats/min. The blood pressure subsequently is 150/90 mmHg. A nitroglycerin infusion is titrated to 50 micrograms/min with a reduction in blood pressure to 120/74 mmHg. Case 1 Screen 6 What is the optimum blood pressure for this patient? Four hours after nitroglycerin is initiated, the blood pressure decreases to 100/60 mmHg. Then, the nitroglycerin infusion is gradually decreased to allow the systolic blood pressure to rise to 110-120 mmHg. Within 30 minutes, the nitroglycerin infusion is discontinued. Analgesics are administered as needed and the patient is successfully extubated that evening. A follow-up electrocardiogram shows resolution of the inferior ischaemic changes. The following morning, oral antihypertensives are administered with reinstitution of β-blocker therapy. Case 2 A 68-year-old man is admitted to the emergency department for acute respiratory failure. He had experienced a similar episode two months ago, which came on abruptly and resolved rapidly. He has a history of long-standing, poorly controlled systemic hypertension, and revascularisation for femoralpopliteal artery disease. He is taking a diuretic (chlorthalidone 25 mg daily), a βblocker (atenolol 100 mg daily), a calcium antagonist (amlodipine 5 mg daily), and an antiplatelet agent (aspirin 75 mg daily), but admits poor compliance. The patient is cyanotic, pulse rate is 100 beats/min and systemic arterial pressure is 224/118 mmHg. Pulmonary rales are heard but there is no jugular venous distension or peripheral oedema of the lower extremities. Electrocardiogram shows left ventricular hypertrophy, an ischaemic pattern, but no evidence of an acute event. Serum creatinine is 140 µmol/l (1.6 mg/dl). Case 2 Screen 2 Is this a hypertensive emergency or hypertensive urgency? Why? Learning issues Evaluation of the hypertensive patient Cardiovascular end-organ damage N OTE Poor compliance to antihypertensive therapy and secondary hypertension are common causes of difficult blood pressure control. Together with antihypertensive treatment, other measures should be taken. What immediate actions should be taken? Learning issues Emergency measures Case 2 Screen 3 Pulse oximetry confirms severe arterial desaturation. The patient receives oxygen and an injection of nitroglycerin, and he is immediately transferred to your intensive care unit where continuous positive airway pressure is applied using a face mask. Blood pressure decreases to 196/112 mmHg. N OTE The application of continuous positive airway pressure may by itself reduce blood pressure, by improving arterial PO 2, which decreases sympathetic stimulation, and by increasing intrathoracic pressure, which reduces venous return. How much should the blood pressure be lowered? Learning issues Initial treatment Case 2 Screen 4 Explain what would be the appropriate antihypertensive drug therapy for this patient? Learning issues Pharmacotherapy of hypertensive crises Management of specific conditions N OTE In patients with left ventricular hypertrophy and diastolic dysfunction, overzealous reduction of filling pressures may compromise left ventricular volume, and hence cardiac output. Echocardiography or right heart catheterisation may help to evaluate filling of the left ventricle. Nitroglycerin and morphine are administered intravenously. Nitroglycerin is titrated so that blood pressure gradually decreases to 156/98 mmHg within the next 6 hours. Echocardiography shows left ventricular hypertrophy and normal systolic function. N OTE Many episodes of pulmonary oedema are due to exacerbation of diastolic dysfunction in hypertensive patients, who usually have left ventricular hypertrophy. Learning issues Acute left ventricular dysfunction For how long should intravenous therapy administered? Case 2 Screen 5 Arterial oxygenation improves rapidly, positive airway pressure is discontinued, and intravenous antihypertensives are shifted to orally administered agents (chlorthalidone, atenolol, amlodipine). Blood pressure remains around 150/90 mmHg and the patient is discharged from the intensive care unit to a general ward the day after admission. You could recommend further evaluation. What are your recommendations for the further management of this patient and why? Learning issues Secondary hypertension Further evaluation includes a magnetic resonance angiogram that shows bilateral atherosclerotic renal artery stenosis. After angioplasty and stenting of the affected arteries, blood pressure normalises on chlorthalidone and atenolol therapy, and the patient subsequently remains free of pulmonary oedema for four years. On reflection On reflection, many effective agents exist for the treatment of hypertensive crises, so that it is almo always possible to decrease blood pressure. The challenge is to reduce blood pressure without compromising organ perfusion. Unfortunately, no trial has definitively identified optimal blood pressu targets or rates of blood pressure lowering in hypertensive emergencies and urgencies. Clinical judgment and knowledge of the underlying pathophysiological process and autoregulation mechanisms will help the physician to avoid the adverse effects of antihypertensive therapy. Q1. Which of the following statements are correct regarding management of severe hypertension in a patient with a thrombotic stroke? A. Lowering the blood pressure may result in worsening of the neurological deficits True False B. Antihypertensive agents should only be initiated if thrombolytics are to be administered True False C. A period of observation of a severely elevated blood pressure may be appropriate before considering use of an antihypertensive agent True False D. Labetalol increases intracranial pressure and should be avoided True False Q2. A hypertensive patient presents to the emergency department with a suspected broken ankle. His blood pressure is 180/108 mmHg. Which of the following interventions should be done? A. Control the pain and ask for radiograph of the ankle True False B. Give nifedipine 5 mg sublingually True False C. Insert an intravenous line to be prepared for intravenous antihypertensive treatment as this is a hypertensive emergency True False D. Emphasize to the patient that he has to take his usual antihypertensive medications every day True False Q3. A 68-year-old hypertensive patient presents with acute crushing chest & interscapular pain. BP 172/100 mmHg. ECG and troponin levels do not suggest myocardial ischaemia. Which are indicated? A. Consider an intra-arterial catheter to monitor blood pressure and its response to therapy True False B. Give a fibrinolytic agent True False C. Reduce blood pressure progressively, first using an intravenous beta-blocker True False D. Administer intravenous hydralazine True False Q4. Which of the following intravenous drugs can be used to control blood pressure in a patient with preeclampsia and severe hypertension? A. Enalaprilat True False B. Labetalol True False C. Hydralazine True False D. Nicardipine True False Q5. Identify which of the following is a hypertensive emergency requiring intravenous therapy A. BP of 175/110 mmHg associated with acute pulmonary oedema True False B. BP of 185/105 mmHg associated with headache True False C. BP of 185/105 mmHg associated with an acute coronary syndrome True False D. BP over 220/120 mmHg in a patient with acute ischaemic stroke True False Q6. In an ischaemic stroke, guidelines for therapy are A. BP should be controlled to less than 220/120 mmHg if thrombolysis not indicated True False B. Aim of BP control therapy should be a 15% reduction (approx) in 24 hours True False C. BP should be controlled to less than 185/110 mmHg if thrombolysis indicated True False D. BP should be controlled to less than 180/105 mmHg after thrombolysis True False Q7. A hypertensive emergency is characterised by A. A diastolic BP > 130 mmHg True False B. A systolic BP > 250 mmHg True False C. Worsening signs and symptoms of end-organ damage True False D. Mean arterial BP > 180 mmHg True False Q8. Worsening of end-organ damage is a feared complication to any hypertensive crisis; the following are a list of often encountered end-organ damage in this context: A. Hypertensive encephalopathy True False B. Hypertensive retinopathy True False C. Acute coronary syndromes True False D. Acute polyneuropathy True False Hypertension Type A Q9 Which of the following is correct in regard to intravenous antihypertensive agents? A. Nitroglycerin is contraindicated in patients with renal failure B. Since labetalol combines α and β-blocking properties, it can be used safely in patients with chronic obstructive pulmonary disease C. Nicardipine is an agent of choice to control blood pressure after coronary artery bypass surgery D. Enalaprilat is an agent of choice for hypertensive emergencies E. Cyanide levels should be monitored systematically during nitroprusside infusion Hypertension Type A Q10 A. B. C. D. E. A 76-year-old male is admitted to the ICU for recovery after lung volume reduction surgery for severe emphysema. He is alert and his BP is 168/96 mmHg. All of the following are appropriate EXCEPT? A. Assess for pain B. Start an antihypertensive treatment with a β-blocker A. B. C. D. E. A. B. C. D. E. A. B. C. D. E. C. Reassess the patient later since there is no end-organ damage D. Fundoscopic examination is not indicated for the transient, postoperative, acute hypertensive episode E. Recommend the consultation of a hypertensive specialist once the patient is transferred to the ward if the blood pressure remains high Hypertension Type A Q11 Which of the following patients requires immediate lowering of blood pressure with a parenteral antihypertensive drug? A. A patient with chronic hypertension undergoing upper endoscopy whose medications were held; blood pressure 188/110 mmHg B. An agitated cocaine abuser; blood pressure 180/120 mmHg C. A patient with heart failure, dyspnoea, and rales; blood pressure 170/116 mmHg D. A chronic alcoholic with vomiting and tremulousness; blood pressure 160/102 mmHg E. A patient in pain in the recovery room following repair of an aortic aneurysm; blood pressure 150/100 mmHg Hypertension Type A Q12 Which of the following is correct in regard to measurement of blood pressure in severe hypertension? A. Automated oscillometric monitors are adequate for blood pressure measurement in the critically ill patient B. A blood pressure cuff that is too small for the patient may result in a falsely decreased blood pressure measurement C. Hypothermia causes hypotension; it does not increase blood pressure D. Intra-arterial pressure monitoring provides the most accurate blood pressure measurement E. A blood pressure cuff that is wrapped too loosely on the arm may result in a falsely low blood pressure Hypertension Type A Q13 In a hypertensive emergency patient (BP 200/110 mm Hg, HR 100/min) associated with acute coronary syndrome, the following are appropriate therapies EXCEPT A. IV cannulation, oxygen and IV morphine B. Intravenous beta blockade e.g. by esmolol infusion C. Intravenous titration of metoprolol 2-3mg boluses D. Labetalol by infusion E. Nifedipine by chewable capsule A. B. C. D. E. A. B. C. D. E. Hypertension Type A Q14 An acute hypertensive episode (190/110 mmHg), in a known hypertensive patient, is associated with acute congestive heart failure (HR 95/min). All of the following are true EXCEPT A. Is a medical emergency requiring IV antihypertensive therapy B. Is a medical urgency requiring oral antihypertensive therapy C. Could be appropriately treated with a labetalol infusion D. Requires caution with diuretics in case of diastolic dysfunction E. Is most likely due to diastolic dysfunction Hypertension Type A Q15 The following medications are frequently used to lower arterial BP in an emergency hypertensive crisis, EXCEPT A. Diazoxide B. Nitroglycerin C. Nicardipine D. Esmolol hydrochloride E. Fenoldopam A. B. C. D. E.