Review of HTN emergencies commonly seen in ICU

1. Hypertensive Emergencies
Sushilkumar S. Gupta (M.D.)

2. Definition:
ASYMPTOMATIC HTN: Most patients with significantly elevated blood pressure (systolic pressure
≥180 and/or diastolic pressure ≥120 mmHg) have no acute, end-organ injury (so called severe asymptomatic
hypertension)
ACCELERATED HYPERTENSION: recent significant increase over baseline blood pressure that is associated with
target organ damage. This is usually vascular damage on fundoscopic examination, such as flame-shaped hemorrhages
or soft exudates, but without papilledema.
HYPERTENSIVE URGENCY: the BP is a potential risk but has not yet caused acute end-organ damage. These
patients require BP control over several days to weeks.
HYPERTENSIVE EMERGENCY: also called hypertensive crisis, is severe hypertension with acute impairment of
an organ system (e.g., central nervous system [CNS], cardiovascular, renal). In these conditions, the blood pressure
(BP) should be lowered aggressively over minutes to hours.

3. EPIDEMIOLOGY:
• In the US: More than 60 million Americans, about 25-30% of the population, have hypertension. Of these
individuals, 70% have mild disease, 20% moderate, and 10% severe hypertension (diastolic BP [DBP] >110 mm Hg).
• Approximately 1-2% develop a hypertensive emergency with end-organ damage.
• Mortality/Morbidity: Morbidity and mortality depend on the extent of end-organ damage on presentation and
the degree to which BP is controlled subsequently.
• BP control may prevent progression to end-organ impairment.
• 1 yr mortality in untreated pts >90%, while 5 yr survival of all presentations is 74%.
• Race: African Americans have a higher incidence of hypertensive emergencies than Caucasians.
• Sex: Males are at greater risk of hypertensive emergencies than females.
• Age: Most commonly in middle-aged people. Peak age:40-50yrs.
• Of these HTN emergencies, eclampsia was the least common, whereas cerebral infarction and acute pulmonary
edema were the most common.

4. ETIOLOGY:
Essential hypertension : Inadequate blood pressure control and noncompliance are common
precipitants
Renovascular
Eclampsia/pre-eclampsia
Acute glomerulonephritis
Pheochromocytoma
Anti-hypertensive withdrawal syndromes
Head injuries and CNS trauma
Renin-secreting tumors
Drug-induced hypertension
Burns
Vasculitis
TTP
Idiopathic hypertension
Post-op hypertension
Coarctation of aorta

7. CEREBRAL AUTOREGULATION:
The CNS is affected as the elevated BP overwhelms the normal cerebral autoregulation.
It is the most sensitive vascular bed.
Under normal circumstances, with an increase in BP, cerebral arterioles vasoconstrict and cerebral blood flow (CBF)
remains constant.
During a hypertensive emergency, the elevated BP overwhelms arteriolar control over vasoconstriction and
autoregulation of CBF.
This results in transudate leak across capillaries and continued arteriolar damage.
Subsequent fibrinoid necrosis causes normal autoregulatory mechanisms to fail, leading to clinically apparent
papilledema, the sine qua non of malignant hypertension.
The end result of loss of autoregulation is hypertensive encephalopathy.

8. RENAL SYSTEM:
The renal system is impaired when high BP leads to arteriosclerosis, fibrinoid necrosis, and an overall impairment of
renal protective autoregulation mechanisms.
This may manifest as worsening renal function, hematuria, red blood cell (RBC) cast formation, and/or proteinuria.
CARDIOVASCULAR SYSTEM:
The cardiovascular system is affected as increased cardiac workload leads to cardiac failure; this is accompanied by
pulmonary edema, myocardial ischemia, or myocardial infarction in an acute phase and LVH and CAD as chronic
manifestations.
VASCULAR SYSTEM:
Aneurysm, accelerated atherosclerosis and aortic dissection.

9. SIGNS & SYMPTOMS:
• Acute head injury or trauma
●Generalized neurologic symptoms, such as agitation, delirium, stupor, seizures, or visual disturbances
●Focal neurologic symptoms that could be due to an ischemic or hemorrhagic stroke
●Fresh flame hemorrhages, exudates (cotton-wool spots), or papilledema when direct funduscopy is performed, as
these are consistent with grade III or IV hypertensive retinopathy and can rarely be associated with hypertensive
encephalopathy
●Nausea and vomiting, which may be a sign of increased intracranial pressure
●Chest discomfort, which may be due to myocardial ischemia or aortic dissection
●Acute, severe back pain, which might be due to heart failure
●Dyspnea, which may be due to pulmonary edema
●Pregnancy, as such patients with severe hypertension could have preeclampsia or develop eclampsia
●Use of drugs that can produce a hyperadrenergic state, such as cocaine, amphetamine(s), phencyclidine, or
monoamine oxidase inhibitors, or recent discontinuation of clonidineor other sympatholytic agents

10. DIAGNOSTIC TESTS:
• Electrocardiography
●Conventional chest radiography
●Urinalysis
●Serum electrolytes and serum creatinine
●Cardiac biomarkers (if an acute coronary syndrome is suspected)
●Computed tomography (CT) or magnetic resonance imaging (MRI) of the brain (if head injury, neurologic symptoms,
hypertensive retinopathy, nausea, or vomiting are present)
●Contrast-enhanced CT or MRI of the chest or transesophageal echocardiography (if aortic dissection is suspected,
although rapid blood pressure lowering need not be delayed in such patients while awaiting the results of imaging)

11. NEUROLOGIC EMERGENCIES:
Ischemic stroke – Patients with acute ischemic stroke-in-evolution are most often not given antihypertensive
drugs during the initial three days of hospitalization unless they are candidates for tissue plasminogen activator and
their initial blood pressure is ≥185/110 mmHg.
The blood pressure should be stabilized and maintained at or below 180/105 mmHg for at least 24 hours after
thrombolytic treatment.
Permissive HTN is recommended to keep the blood pressure is <220/120, if they are not candidates for reperfusion
therapy.
Recommendation to treat high blood pressure is only if the hypertension is extreme (systolic blood pressure >220
mmHg or diastolic blood pressure >120 mmHg), or if the patient has another clear indication (active ischemic
coronary disease, heart failure, aortic dissection, hypertensive encephalopathy, or pre-eclampsia/eclampsia).
When treatment is indicated, BP should be lowered cautiously by approximately 15 percent during the first 24 hours
after stroke onset.
Rationale: In patients with ischemic stroke, the perfusion pressure distal to the obstructed vessel is low, and the distal
vessels are dilated. Because of impaired cerebral autoregulation, blood flow in these dilated vessels is thought to be
dependent upon the systemic blood pressure.

13. • Hemorrhagic stroke – Management of blood pressure in patients with spontaneous intracerebral
hemorrhage and subarachnoid hemorrhage is complicated by competing risks (eg, reducing cerebral perfusion) and
benefits (eg, reducing further bleeding).
• Severe elevations in blood pressure may worsen ICH by representing a continued force for bleeding, causing
hemorrhage expansion and potentially worse outcomes.
• However, an increased MAP may be necessary to maintain cerebral perfusion in some patients, and lowering the
arterial pressure (eg, to a systolic blood pressure [SBP] below 130 mmHg) may cause ischemia and worsen
neurologic injury.
• Observational studies and INTERACT2 trail, 2 groups< 140 within 1 hr vs traditional management <180.
• Intensive blood pressure lowering was associated with improved measures of disability according to modified
Rankin scores, a secondary outcome measure. Adverse events were similar in the patient groups.
• Currently the guidelines recommend to keep the Bp <140mmhg.
• Intravenous labetalol, nicardipine, esmolol, hydralazine are most often used as first-line agents.
• Avoid nitroprusside as it can increase intracranial pressure.

14. • Head trauma:
• Head trauma with increased intracranial pressure can produce severe elevations in blood pressure.
• Hypertension is usually treated in this setting only if the cerebral perfusion pressure (mean arterial pressure minus
intracranial pressure) is >120 mmHg and the intracranial pressure is >20 mmHg.
• Hypertensive Encephalopathy:
• The signs and symptoms of hypertensive encephalopathy (eg, headache, confusion, nausea, vomiting) usually abate
after the blood pressure is lowered. In fact, hypertensive encephalopathy is most often a diagnosis of exclusion,
confirmed retrospectively when the mental status improves after the blood pressure is lowered into the
autoregulatory range.
• Patients with suspected hypertensive encephalopathy should have their blood pressure lowered by approximately 10
to 20 percent during the first hour of treatment. However, additional lowering should be gradual such that,
compared with the initial blood pressure upon presentation, the pressure is reduced by no more than 25 percent at
the end of the first day of treatment.
• Commonly used medications in this setting include clevidpine, nicardipine, fenoldopam, and nitroprusside(Avoid).
• PRES Syndrome: commonly seen with pregnancy, immunosuppressive agents (tacrolimus & cyclosporine)

15. CARDIAC EMERGENCIES:
• The most common cardiac emergencies associated with severely elevated blood pressure are acute left ventricular
dysfunction with pulmonary edema and acute coronary syndrome (including acute myocardial infarction).
• Acute heart failure – Patients with acute left ventricular dysfunction and pulmonary edema should usually receive
INTRAVENOUS loop diuretics.
• A vasodilator that is easy to titrate (sodium nitroprusside, NTG) is often added to reduce afterload. It si
contraindicated to use NTG drip in patients on sildenafil/tadalafil.
• Drugs that increase cardiac work ( hydralazine  Reflex tachycardia) or acutely decrease cardiac contractility
( labetalol or other beta blocker) should be avoided.
• The goal of these therapies is amelioration of volume excess and heart failure and improvement in pulmonary
edema, which can often be achieved with a 10 to 15 percent reduction in blood pressure.
• Therefore, Nicardipine drip is contraindicated as it contains significant volume, which may worsen the HF.

16. Acute coronary syndrome:
• Severe hypertension associated with an acute coronary syndrome (including acute myocardial infarction) is
appropriately treated with intravenous NTG, clevidpine, nicardipine, or
• Intravenous metoprolol or esmolol (to reduce myocardial oxygen consumption, to reduce the underlying coronary
ischemia, and to improve prognosis).
• For STEMI patients, if fibrinolytic is indicated then BP should be maintained <180/110mmhg.
• Nitroprusside should be carefully used as it can cause Coronary steal syndrome.
• Acute MI are sometimes associated with Type A aortic dissection, most commonly the RCA infarction.

17. VASCULAR emergencies:

18. RENAL Emergencies:
• Severe hypertension may occasionally cause acute injury to the kidneys (acute hypertensive nephrosclerosis,
formerly called "malignant nephrosclerosis").
• UA show hematuria (usually microscopic hematuria, which is found in approximately 75 percent of patients with
hypertensive emergencies) and an elevated serum creatinine.
• Mucoid intimal thickening and luminal narrowing in a small muscular renal artery (arrow) in the early stages of
healing in acute hypertensive nephrosclerosis (formerly "malignant nephrosclerosis"). Similar changes can be seen
in other thrombotic microangiopaties, such as scleroderma and the hemolytic-uremic syndrome.

19. Scleroderma Renal Crisis:
• It occurs in 10-15% of patients, more commonly in Ds SSC, It occurs due to autoimmunity, vasculopathy and
fibrosis.
• Symptoms include, acute onset of accelerated HTN along with oliguria, MAHA, thrombocytopenia
• Rx  Captopril is the DOC.
HEMATOLOGIC emergencies:
• MAHA (mechanical trauma)  characterized by coinciding thrombocytopenia and increased LDH
• Rx  supportive treatment
SYMPATHETIC overactivity resulting in HTN emergencies:
• Ingestion of sympathomimetic agents ( tyramine-containing foods in patients who take chronic monoamine
oxidase inhibitors, amphetamine-like compounds, cocaine, etc) can precipitate severe hypertension and end-
organ damage. Such patients can be treated with intravenous phentolamine or, if phentolamine is
unavailable, labetalol or nitroprusside.

20. COCAINE abuse:
• Cocaine use is more frequently associated with acute rather than chronic cardiovascular illness.
• Pt frequently complaint of chest pain. In such patients, ACS (including myocardial ischemia and infarction), aortic
dissection and rupture, arrhythmias, myocarditis, and vasculitis need to be considered.
• The major cardiovascular effects of cocaine appear to be caused by the inhibition of norepinephrine reuptake into
the synaptic cleft by sympathetic neurons, which results in potentiation of the response to sympathetic stimulation
of innervated organs and to infused catecholamine.
• Cocaine also enhance the release of catecholamines from central and peripheral stores.
• BZD can be used to control BP, HR and achieve sedation.
• Oral Clonidine can be used to treat BP??
• BB should be avoided for BP control alone, if used for ACS/MI then labetalol or carvedilol in the presence of
Phentolamine, or if phentolamine is unavailable then use (vasodilators) NTG or nitroprusside

21. PHEOCHROMOCYTOMA:
• Combined alpha 14 days and beta-adrenergic 2-3 days blockade can be used pre-operatively to control blood
pressure and prevent intraoperative hypertensive crises.
• Studies have shown despite adequate premedication larger tumor size of > 4cm, prolonged anesthesia, and
increased level of preoperative urinary catecholamines and catecholamine metabolites.
• Acute HTN crisis can be managed with IV Sodium nitroprusside, Nicardipine and Phentolamine.
• Sodium Nitroprusside is an ideal vasodilator for intraoperative management of hypertensive episodes because of its
rapid onset of action and short duration of effect. It is administered as an intravenous infusion at 0.5 to
5.0 mcg/kg of body weight per minute and adjusted every few minutes for target blood pressure response; to keep
the steady-state thiocyanate concentration below 1 mmol/L, the rate of a prolonged infusion should be no more
than 3 mcg/kg per minute.
Hypertensive emergencies during pregnancy:
• As per ACOG 2015 guidelines, BP of 160/110mmhg or greater persisting for more than 15min.
• Methyldopa, hydralazine, and labetalol have been widely used in pregnant women with severe hypertension, which
is usually due to preeclampsia or exacerbation of preexistent hypertension. Fenoldopam, and nicardipine have also
been used.

22. Thank You!!!