Hypertensive crisis includes hypertensive emergencies and urgencies. Usually develops in patients with previous history of elevated BP but may arise in those who were previously normotensive. The severity of hypertensive crisis correlates with the rapidity of rise in BP.
Urgencies: SBP >180 mm Hg and/or DBP: >120 mm Hg without target organ damage.
Emergencies: Include
Hypertensive emergencies include accelerated HTN, typically defined as SBP >210 and DBP >130 mmHg, with acute and ongoing target organ damage to the kidneys, heart, vascular system, brains, or eyes. It is associated with HA, blurred vision, or focal neurologic symptoms.
Malignant hypertension is marked hypertension with retinal hemorrhages, exudates, or papilledema. There may also be renal involvement, called malignant nephrosclerosis. Although papilledema had been thought to represent a more severe lesion, it does not appear to connote a worse prognosis than hemorrhages and exudates alone (so-called accelerated hypertension). Thus, treatment is the same whether or not papilledema is present.
Hypertensive encephalopathy refers to the presence of signs of cerebral edema caused by breakthrough hyperperfusion from severe and sudden rises in blood pressure.
Isolated systolic HTN, defined as SBP >140 mm Hg and normal DBP, occurs frequently in elderly (>50-yo), and increases with age.
HTN - Manifestations of TOD
Large vessels: aneurysmal dilatation, accelerated atherosclerosis, aortic dissection
Cardiac:
Acute - Pulmonary edema, myocardial infarction.
Chronic - Clinical evidence of CAD, LVH by ECG or echocardiogram
Cerebrovascular:
Acute - ICH, coma, sz, mental status changes, TIA, stroke.
Chronic - TIA, stroke
Renal:
Acute - Hematuria, azotemia.
Chronic - Sr. creatinine >1.5 mg/dL, proteinuria >1+ on dipstick
Retinopathy:
Acute - Papilledema, hemorrhages.
Chronic - H'ges, exudates, AV nicking
Pre-eclampsia, eclampsia
Epidemiology:
60.5 million U.S adults. For non-hypertensive individuals 55 to 65 years of age, the lifetime risk of developing hypertension as 90%.
Data derived from the Framingham study have shown that hypertensive patients are 4 x increase risk of CVA, and 5 x increased risk and CHF when compared to some normal population.
BP control rates remain poor with only 34% of treated hypertensive patients below their goal the level.
Etiology:
Primary or essential hypertension (90%)
Secondary hypertension
renal parenchymal disease
renovascular disease
pheochormocytoma
Cushing's syndrome
Primary hyperaldosteronism
coarctation of aorta
OSA
Autosomal dominant or autosomal recessive diseases of the adrenal-renal axis that result in salt retention.
Cocaine, stimulants
Drug withdrawal (alcohol)
Rebound HTN: sudden withdrawal of anti-HTN medications (clonidine, alpha-adrenergic antagonists)
Volume overload, inadequate pain control
Risk factors
BP increases with age.
Overweight/obesity
Increased directories sodium intake
Decreased physical activity
Increased alcohol consumption
Lower dietary intake of fruits, vegetables, and potassium
Orders:
Cardiac monitored/Telemetry bed
Vitals, q30 min, then q2-4h after BP stable
Neurochecks
Clear liq diet, cardiac diet
Heplock
O2 at 2 L via n.c, keep SpO2 >92%
Strict bed rest with bedside commode
Labs/Dxtic: CBC with peripheral smear, CMP, LFT, UA, UDS, TSH, troponin q8h x 2, CPK-MB q6h x 4, fasting lipids, serum drug screen, uric acid, myoglobin, CXR (PA-Lat), 2-D echo, CT-heat, ECG.
If ICH suspected CT - head and LP
If renal a. stenosis, renal U/S
24-h, catecholamines, 24-h urine metanephrine and VMA, Renin level, aldosterone level, funduscopy.
GI/DVT prophylaxis
Constipation and cough prophylaxis to prevent ICH.
Consult: cardiology, nephrology
Nursing: I/O, urine output, daily wts, stool guaiac.
Avoid ASA, Plavix, caffeine-containing products
Tx
Treat the patient, not the BP reading. Acute lowering of the BP of asymptomatic patients with long-standing hypertension can be dangerous.
Hypertensive emergencies require an ICU setting.
Goal is to lower the MAP by no more than to 10-15% first 1-2 hours; not more than 20-25% in 24 hrs to minimize end-organ damage. BP lowered to approximately 160/100 - 110 mm Hg. Rapid BP reduction below this level may precipitate renal, coronary, or cerebral ischemia. If the patient is stable and tolerates a BP of 160/100 - 110 mm Hg, further reduction to near normal BP levels can be attempted over 24 - 28 hours. In patients with ischemic stroke, normal BP should not be achieved. SBP should be lowered to less than 120 mm Hg in the patient with aortic dissection.
Blood pressure should be lowered with nonvasodilating IV drugs such as nicardipine, labetalol, or esmolol.
If SBP is 200 mm Hg or MAP is 150 mm Hg, then consider:
Aggressive reduction of BP with continuous intravenous infusion, with frequent BP monitoring every 5 min.
If SBP is 180 mm Hg or MAP is 130 mm Hg and there is the possibility of elevated ICP, then consider monitoring ICP and reducing BP using intermittent or continuous intravenous medications while maintaining a cerebral perfusion pressure 60 mm Hg.
If SBP is 180 mm Hg or MAP is 130 mm Hg and there is not evidence of elevated ICP, then consider a modest reduction of BP (eg, MAP of 110 mm Hg or target BP of 160/90 mm Hg) using intermittent orcontinuous intravenous medications to control BP and clinically reexamine the patient every 15 min.
How fast should blood pressure be lowered?
Results of small studies suggest that rapidly lowering MAP by approximately 15% does not lower cerebral blood flow, whereas reductions of 20% can do so. Therefore, if BP-lowering is considered, current guidelines suggest cautious lowering of BP by no more that 20% in the first 24 hours.
What Antihypertensive Agents:
IV nicardipine, labetolol, esmolol, enalapril
Others- Nitroglycerin, nitroprusside, hydralazine can increase ICP
HTN urgency. BP should be lowered gradually over a period of 12 to 24 hours, but not to a normal level (target level, approximately 160/110 mm Hg).
The clinical status of the patient, not the degree of BP elevation, defines an emergency in certain cases. For example, in a patient with acute aortic dissection who presents to the ED with a BP of 160/110 mm Hg, the SBP must be lowered to less than 120 mm Hg within 20 minutes. The rapid reduction reduces shear stress, thus limiting further dissection of the aorta.
if no renal failure, can use Vasotec 1.25 mg IV X 1
Enalaprilat IV. Time frame 2-3 hrs
0.625 - 5mg IVP q6 hrs. 1.25 mg of enalaprilat = 5 mg of enalapril PO. Adverse effects: angioedmea, hypotension, renal failure.
Labetolol IV. Give 20 mg IVP recheck BP q10 min.
Give 40 mg IVP recheck BP q10 min
Give 80 mg IVP. Can give upto 300 mg.
Onset 5 - 10 min, duration: 2 - 6 h.
Infusion 0.5 - 2 mg/min
Not recommended in asthma, COPD, CHF, heart block, bradycardia, scalp tingling, cardiogenic shock.
Esmolol IV. Onset 1 - 2 min; duration: 10 - 30 min.
Dose: 250 - 500 mcg/kg x 1 min, then 50 - 100 mcg/kg/min. Titrate to desired BP.
Used in ICU and ER.
Max: 300 mcg/kg/min.
Adverse effects include athma, first degree heart block, CHF, hypotension, nausea.
Phentolamine. Dose: 5 - 10 mg/min, q5 - 15 minutes, onset: 1 - 2 min, duration: 10 - 30 min.
Adverse effects include flushing, HA, tachycardia
Furosemide, 20 - 40 mg x 5 min. Onset: 5 - 15 min, duration: 2 - 3 h.
Adverse effects: hypokalemia, volume depletion.
Nitroprusside. Few minutes. Used in Aortic dissection and encephalopathy.
0.25- 10mcg/kg/min.
Start at 3 mcg/kg/min, titrate to desired BP. Acts in sec. Last 3 - 5 min. Continuous drip.
If used >48 - 72hrs or in Pts with renal insufficiency may result in thiocyanate toxicity. Check Sr. thiocyanate after 48 - 72 h (should be kept <10 mg/dL). Hepatic dysfunction can result in accumulation of cyanide causing metabolic acidosis, dyspnea, vomiting, dizziness, ataxia, and syncope. HD or nitrities and sodium thiosulfate in cyandie toxicity. Used only in ICU.
(SE: paresthesiae, tinnitus, blurred vision, delirium or sz.)
* Do not give in CAD or advance renal or hepatic dz, pregnancy *. Give with BB (esmolol) in Pts with Ao. dissection.
NTG drip. Give in CAD, pulmonary edema, IHD, CABG. Reduces preload more than afterload, so don't give in Pts with Inferior wall MI or RV infarction (dependent on preload, rapid IVF). 0.25 - 5mcg/kg/min.
Nicardipine 5 mg/hr; increase by 1 - 2.5 mg/hr q15 min, max: 15 mg/hr. Onset: 1 - 5 min. Duration: 3 - 6 h.
Fenoldopam, 0.1 - 0.3 mcg/kg/min. Onset: 5 - 10 min, duration: 30 min. Increase by 0.1 mcg/kg/min q15 min to desired effect. Max dose: 1.6 mcg/kg/min Adverse effects: HA, nausea, tachycardia.
If Pt. in renal failure, can use
Hydralazine 10 - 20 mg IV q20 min x 2. Can cause reflex tachy (stress test). Do not give in CAD, or Aortic dissection. Give in pregnancy./
If beta-blocker is available, O.K to use.
Avoid centrally acting meds, in CNS symptoms, use BB.
Oral meds for HTN urgencies
Control BP with extra dose of current medication
Clonidine only if patient is already on Clonidine. Need time frame of 3 - 6 hrs. Pt. should be able to take PO.
Give Clonidine 0.2 mg PO x 1 and then 0.1 mg PO qh to a total dose of 0.8 mg. Onset: 30-60 min; duration: 6-8 hrs.
Catapres TTS patch, 0.1 - 0.3 mg/24h. Change qwk.
Catapres is known to cause hallucinations in elderly Pts, ESRD on HD.
Do not stop abruptly (rebound HTN). Wean Catapres as follows:
0.2 mg, q8h x 3 days
0.1 mg, q8h x 3 days
0.1 mg, q12h x 3 days, then
Stop.
Amlodipine, 5 - 10 mg.
Captopril, 12.5 - 25 mg
Labetalol, 200 - 400 mg
Nicardipine, 20 - 30 mg
Preferred IV therapy in hypertensive emergency
1% of all HTN patients will experience a HTN crisis in their lifetimes.
HTN crises accounts for 27.5% of all ED visits for medical urgencies - emergencies.
Pathophysiology: poorly understood. A sudden increase in BP accentuates shear stress in the vessel wall, leading to additional endothelial damage, further activation of the neurohormonal RAA, sympathetic nervous system, and vasopressin system, induction of oxidative stress, and inflammatory cytokines. The coagulation cascade is also activated by the resultant platelet aggregation and fibrin deposition. These changes lead to vasoconstriction, thrombosis, and fibrinoid necrosis and result in hypoperfusion and ischemia. Cerebral edema and HTN encephalopathy may result from impaired autoregulation of the brain. A sudden increase in BP causes forced vasodilatation of the cerebral vessel to accomodate hyperperfusion. The vasodilatation is initially segmental, giving the appearance of a sausage-string pattern on MRA or conventional angiography, but soon becomes diffuse. The endothelium becomes more dysfunctional than before, allowing plasma components to diffuse into the surrounding interstitium, leading to cerebral edema and, finally, HTN encephalopathy.
HTN Pts in an emergency state present with TOD and patients with urgency do not have TOD.
TOD: cerebral infarction (24.5%), acute pulmonary edmea (22.5%), HTN encephalopathy (16.3%), acute heart failure (14.3%), acute MI or unstable angina (12%), aortic dissection (4.5%), and eclampsia (2%).
Symptoms and Evaluation
HTN Emergency
HTN Urgency
Pt present with severe headache, dyspnea, anxiety, or epistaxis.
Pt present with severe headache, nausea, vomiting, chest pain, dyspnea, neurologic deficit, and vertigo.
Diagnosis: Accurate non-invasive BP measurement, which should be obtained in a seated patient with along resting level with a heart. BP cuff encircling at least 80% of the arm. Two reading should be taken, separated by 2 minutes. SBP should be noted with the appearance of Korotkoff sounds (phase I) and DPB with the disappearance of sounds (phase V). In some patients, the Korotkoff sounds do not disappear and are present to 0 mm Hg. In this case, the initial muffling of Korotkoff sounds (phase IV) should be taken as the DPB. Hypertension should be confirmed in both arms, and the higher reading should be used.
History: HTN noncompliance with anti-HTN medications, diet, inadequately controlled HTN. Secondary causes of HTN. Medications that can raise BP (decongestants, OCP, appetite suppressants, NSAIDs, exogenous thyroid hormones, recent alcohol consumption, caffeine anabolic steroids, and illicit stimulants such as cocaine).
A diagnosis of secondary hypertension should be considered in the following situations:
Age at onset <30 or >60 years
Hypertension that is difficult to control after therapy has been initiated
Stable hypertension that becomes difficult to control
Clinical occurrence support hypertensive crisis
Hypokalemia or metabolic alkalosis that is not explained by diuretic therapy.
In patients who present with significant hypertension at a young age, a careful family history may give information of forms of hypertension that follow simple Mendelian inheritance.
Physical Exam: funduscopic to check for papilledema, retinopathy, cardiac including carotid bruits, S3, S4, murmurs, JVD, lung, and neurologic exams. Renal disease - enlarged or small kidneys, cushingoid features, and abdominal bruits. Overeweight/obesity, Ht. Wt. BMI, abdominal waist circumference.
DDx:
HTN part of withdrawal syndrome from drugs, including alcohol, cocaine and opioid analgesics.
Rebound hypertension in patients who abruptly discontinue BP medications, particularly Beta-adrenergic antagonists and central-alpha2-agonists.
Cocaine and other sympathomimetic drugs (amphetamine, phencyclidine) both in the setting of acute intoxication and abrupt discontinuation after chronic use. Phentolamine is effective in acute management, and sodium nitroprusside or NTG can be used as an alternative. Avoid BB due to risk of unopposed alpha-adrenergic activity, which can exacerbate HTN
HTN encephalopathy Fast Facts
This following information is from Becker K. Hypertensive Encephalopathy, Eclampsia, and Reversible Posterior Leukoencephalopathy. In: Becker K, editor. Critical Care Neurology. Continuum: Lifelong Learning in Neurol 2006;12(2):30-45.
1.) General Information
Reversible posterior leukoencephalopathy is a syndrome that is best defined by magnetic resonance imaging and is most commonly seen in patients with hypertensive encephalopathy and eclampsia. Hypertensive encephalopathy is a manifestation of hypertensive emergency. Hypertensive emergency is defined as a severe elevation in blood pressure that precipitates end organ damage. Examples of end organ damage include acute pulmonary edema, congestive heart failure, ischemic chest pain, retinopathy, papilledema, retinal hemorrhages, aortic dissection, and rapid deterioration in renal function as evidenced by rising creatinine and red cell casts in the urine.
2.) Symptoms and Signs
The onset of symptoms in hypertensive encephalopathy is usually subacute over several days and consists of diffuse cerebral symptoms (headache, nausea, vomiting, confusion, drowsiness, and seizures) with or without focal symptoms. Visual symptoms are particularly common with blurring, scotoma and field defects being the usual complaints. On exam patients may have focal signs, papilledema, or visual field defects associated with markedly elevated blood pressure. Hypertensive encephalopathy is usually accompanied by retinal arteriolar spasm, retinal hemorrhages, and cotton wool spots.
3.) Diagnosis
Imaging studies can help to corroborate the diagnosis of hypertensive encephalopathy. Lesions that are hyperintense on T2- and fluid-attenuated inversion recovery-weighted images and hypointense on T1-weighted images characterize the MRI findings. There is a predilection for involvement of the vertebrobasilar circulation, with the occipital lobes and posterior parietal lobes being preferentially involved. The lesions are usually bilateral and symmetrical and follow the gyri in a serpentine manner; both the white matter and gray matter are involved. The cerebellum and brain stem may also be affected. In addition to abnormalities in the posterior circulation, the deep white matter and basal ganglia may also be involved. The MRI findings are usually reversible with blood pressure control. It should be stressed, however, that imaging abnormalities may involve areas outside the posterior circulation and the gray matter; furthermore, they may not always be reversible.
4.) Treatment
The diagnosis of hypertensive encephalopathy requires that antihypertensive agents be administered emergently. On the other hand, hypertensive patients who are suffering an ischemic stroke should not have their blood pressure lowered unless they are to receive tissue plasminogen activator or signs of hypertensive end organ damage are present. The best agents to use and the degree to which the blood pressure should be acutely reduced depend upon several variables, including the patient's premorbid blood pressure, the duration of their hypertensive emergency, concomitant medical disease, and the extent of neurological involvement. The ideal drug should have a rapid and predictable onset of action and be easy to titrate. The choice of drug should be based on the patient's concomitant medical problems. Almost by definition, patients with hypertensive encephalopathy are at risk for developing increased ICP, which should be an important factor to consider when choosing the appropriate antihypertensive agent. Labetalol is the preferred agent for treating hypertension in patients with intracranial processes because of its favorable pharmacokinetics and lack of effect on intracranial vessels.
5.) Remember
• The diagnosis of hypertensive encephalopathy should be suspect if no signs of concomitant damage in other end organs are present.
• Immediate but gradual lowering of blood pressure (10% to 15% reduction in mean arterial pressure over the first 1 to 2 hours) is mandated in patients with hypertensive encephalopathy. Concomitant medical issues should guide drug selection.
• Patients with hypertensive encephalopathy and eclampsia develop reversible posterior leukoencephalopathy on magnetic resonance imaging. These abnormalities are generally diffusion negative but hyperintense on ADC mapping.
Individual patient considerations:
The elderly hypertensive patient: (older than 60 years) has increased vascular resistance, decreased plasma renin activity, and greater LVH than in younger patients. Diuretics > CCB > ACEI or ARBs.
Black hypertensive patient: Diuretics +/- CCB. ACEI, ARBs, and BB with diuretics.
Obese hypertensive patient: Weight reduction.
Diabetic hypertensive patient: ACEI or ARBs
Hypertensive with chronic kidney disease: Loop diuretics if Cr >2.5
Hypertensive patient with LVH: ACEI
Hypertensive patient with CAD: BB, ACEI in those with LVEF <40%.
Hypertensive patient with CHF: ACEI, ARBs, Nitrates + hydralazine.
Pregnancy and hypertension: Hydralazine and labetalol