| Hypertensive emergency | |
|---|---|
| Other names | Malignant hypertension, hypertensive crises |
 | |
| CT scan depicting intracranial hemorrhage, a possible complication of hypertensive emergency. Patients with spontaneous intracranial hemorrhage present with newfound headache and neurologic deficits. | |
| Specialty | Cardiology,Emergency medicine |
Ahypertensive emergency is veryhigh blood pressure with potentially life-threatening symptoms and signs of acute damage to one or moreorgan systems (especially brain, eyes, heart, aorta, or kidneys). It is different from ahypertensive urgency by this additional evidence for impending irreversiblehypertension-mediated organ damage (HMOD).Blood pressure is often above 200/120 mmHg, however there are no universally acceptedcutoff values.[1][2][3]
Symptoms may include headache,nausea, orvomiting. Chest pain may occur due to increased workload on the heart resulting ininadequate delivery of oxygen to meet the heart muscle's metabolic needs. The kidneys may be affected, resulting inblood orprotein in the urine, andacute kidney failure. People can havedecreased urine production,fluid retention, and confusion.[citation needed]
Other signs and symptoms can include:[4]
The most common presentations of hypertensive emergencies arecerebral infarction (24.5%),pulmonary edema (22.5%),hypertensive encephalopathy (16.3%), andcongestive heart failure (12%).[5] Less common presentations include intracranial bleeding, aortic dissection, andpre-eclampsia or eclampsia.[6]
Massive, rapid elevations in blood pressure can trigger any of these symptoms, and warrant further work-up by physicians. Physical exam would include measurement of blood pressure in both arms. Laboratory tests to be conducted include urine toxicology, blood glucose, a basic metabolic panel evaluating kidney function, or a complete metabolic panel evaluating liver function, EKG, chest x-rays, and pregnancy screening.[7]
The eyes may showbleeding in the retina, anexudate,cotton-wool spots, scattered splinter hemorrhages, or swelling of the optic disc calledpapilledema.[citation needed]
Many factors and causes are contributory in hypertensive crises. The most common cause is patients with diagnosed, chronic hypertension who have discontinued anti hypertensive medications.[8]
Other common causes of hypertensive crises are autonomic hyperactivity such aspheochromocytoma, collagen-vascular diseases, drug use particularly stimulants,cocaine andamphetamines and theirsubstituted analogues,monoamine oxidase inhibitors or food-drug interactions, spinal cord disorders,glomerulonephritis, head trauma,neoplasias,preeclampsia andeclampsia,hyperthyroidism and renovascular hypertension.[7][8] People withdrawing from medications such as clonidine or beta-blockers have been frequently found to develop hypertensive crises.[9] It is important to note that these conditions exist outside of hypertensive emergency, in that patients diagnosed with these conditions are at increased risk of hypertensive emergencies or end organ failure.[citation needed]
The pathophysiology of hypertensive emergency is not well understood. Failure of normal autoregulation and an abrupt rise in systemic vascular resistance are typical initial components of the disease process.[6]
Hypertensive emergency pathophysiology includes:[citation needed]
The resultingischemia prompts further release of vasoactive substances including prostaglandins,free radicals, and thrombotic/mitotic growth factors, completing a vicious cycle of inflammatory changes.[6] If the process is not stopped,homeostatic failure begins, leading to loss ofcerebral and local autoregulation, organ system ischemia and dysfunction, andmyocardial infarction. Single-organ involvement is found in approximately 83% of hypertensive emergency patients, two-organ involvement in about 14% of patients, andmulti-organ failure (failure of at least 3 organ systems) in about 3% of patients.[citation needed]
In the brain,hypertensive encephalopathy - characterized by hypertension, altered mental status, andswelling of the optic disc - is a manifestation of the dysfunction of cerebral autoregulation. Cerebral autoregulation is the ability of theblood vessels in the brain to maintain a constantblood flow. People with chronic hypertension can tolerate higher arterial pressure before their autoregulation system is disrupted. Hypertensives also have an increased cerebrovascular resistance which puts them at greater risk of developing cerebral ischemia if the blood flow decreases into a normotensive range. On the other hand, sudden or rapid rises in blood pressure may cause hyperperfusion and increased cerebral blood flow, causing increased intracranial pressure and cerebral edema, with increased risk ofintracranial bleeding.[7]
In the heart, increasedarterial stiffness, increasedsystolic blood pressure, and widened pulse pressures, all resulting from chronic hypertension, can cause significant damage. Coronary perfusion pressures are decreased by these factors, which also increase myocardial oxygen consumption, possibly leading to leftventricular hypertrophy. As the left ventricle becomes unable to compensate for an acute rise in systemic vascular resistance, left ventricular failure and pulmonary edema or myocardial ischemia may occur.[6]
In the kidneys, chronic hypertension has a great impact on the kidney vasculature, leading to pathologic changes in the small arteries of thekidney. Affected arteries develop endothelial dysfunction and impairment of normalvasodilation, which alter kidney autoregulation. When the kidneys' autoregulatory system is disrupted, theintraglomerular pressure starts to vary directly with the systemic arterial pressure, thus offering no protection to the kidney during blood pressure fluctuations. Therenin-aldosterone-angiotensin system can be activated, leading to further vasoconstriction and damage. During a hypertensive crisis, this can lead to acute kidney ischemia, with hypoperfusion, involvement of other organs, and subsequent dysfunction. After an acute event, this endothelial dysfunction has persisted for years.[6]
The term hypertensive emergency is primarily used as a specific term for a hypertensive crisis with a diastolic blood pressure greater than or equal to 120 mmHg or systolic blood pressure greater than or equal to 180 mmHg.[10] Hypertensive emergency differs from hypertensive urgency in that, in the former, there is evidence of acute organ damage.[10] Both of these definitions had collectively been known as malignant hypertension, although this medical term is replaced.[citation needed]
In the pregnant patient, the definition of hypertensive emergency (likely secondary to pre-eclampsia or eclampsia) is only a blood pressure exceeding 160 mmHg systolic blood pressure or 110 mmHg diastolic blood pressure.[11]
In a hypertensive emergency, treatment should first be to stabilize the patient's airway, breathing, and circulation perACLS guidelines. Patients should have their blood pressure slowly lowered over a period of minutes to hours with anantihypertensive agent. Documented goals for blood pressure include a reduction in themean arterial pressure by less than or equal to 25% within the first 8 hours of emergency.[7] If blood pressure is lowered aggressively, patients are at increased risk of complications including stroke, blindness, or kidney failure.[6] Several classes of anti hypertensive agents are recommended, with the choice depending on the cause of the hypertensive crisis, the severity of the elevation in blood pressure, and the patient's baseline blood pressure prior to a hypertensive emergency. Physicians will attempt to identify a cause of the patient's hypertension, including chest radiograph, serum laboratory studies evaluating kidney function, urinalysis, as that will alter the treatment approach for a more patient-directed regimen.[citation needed]
Hypertensive emergencies differ from hypertensive urgency in that they are treated parenterally, whereas in urgency it is recommended to use oral anti hypertensives to reduce the risk of hypotensive complications or ischemia.[6] Parenteral agents are classified into beta-blockers, calcium channel blockers, systemic vasodilators, or other (fenoldopam, phentolamine, clonidine). Medications includelabetalol,nicardipine,hydralazine,sodium nitroprusside,esmolol,nifedipine,minoxidil,isradipine,clonidine, andchlorpromazine. These medications work through a variety of mechanisms. Labetalol is a beta-blocker with mild alpha antagonism, decreasing the ability of catecholamine activity to increase systemic vascular resistance, while also decreasing heart rate and myocardial oxygen demand. Nicardipine, Nifedipine, and Isradipine are calcium channel blockers that work to decrease systemic vascular resistance and subsequently lower blood pressure. Hydralazine and Sodium nitroprusside are systemic vasodilators, thereby reducing afterload, however can be found to have reflex tachycardia, making them likely second or third line choices. Sodium nitroprusside was previously the first-line choice due to its rapid onset, although now it is less commonly used due to side effects, drastic drops in blood pressure, and cyanide toxicity. Sodium nitroprusside is also contraindicated in patients with myocardial infarction, due to coronary steal.[9] It is again important that the blood pressure is lowered slowly. The initial goal in hypertensive emergencies is to reduce the pressure by no more than 25% the mean arterial pressure. Excessive reduction in blood pressure can precipitate coronary, cerebral, or kidneyischemia and, possibly, infarction.[citation needed]
A hypertensive emergency is not based solely on an absolute level of blood pressure, but also on a patient's baseline blood pressure before the hypertensive crisis occurs. Individuals with a history ofchronic hypertension may not tolerate a "normal" blood pressure, and can therefore present symptomatically withhypotension, including fatigue, light-headedness, nausea, vomiting, or syncope.[citation needed]
| <1 hr | 25% reduction in the mean arterial pressure, diastolic blood pressure above 100 |
|---|---|
| 2-6 hr | Systolic BP < 160 mmHg or Diastolic BP <110 mmHg |
| 6-24 hr | monitor BP targets, ensure non-rapid drop in BPs below 160 SBP or 100 DBP |
| 1-2 d | if no end-organ damage, monitor out-patient and JNC8 Guidelines for maintaining BP control |
Severe hypertension is a serious and potentially life-threatening medical condition. It is estimated that people who do not receive appropriate treatment only live an average of about three years after the event.[11]
Themorbidity andmortality of hypertensive emergencies depend on the extent of end-organ dysfunction at the time of presentation and the degree to which blood pressure is controlled afterward. With good blood pressure control and medication compliance, the 5-year survival rate of patients with hypertensive crises approaches 55%.[1]
The risks of developing a life-threatening disease affecting the heart or brain increase as the blood flow increases. Commonly, ischemic heart attack and stroke are the causes that lead to death in patients with severe hypertension. It is estimated that for every 20 mm Hg systolic or 10 mm Hg diastolic increase in blood pressures above 115/75 mm Hg, the mortality rate for both ischemic heart disease, cancer and stroke doubles.[citation needed]
Consequences of hypertensive emergency result after prolonged elevations in blood pressure and associated end-organ dysfunction. Acute end-organ damage may occur, affecting the neurological, cardiovascular, kidney, or other organ systems. Some examples of neurological damage includehypertensive encephalopathy,cerebral vascular accident/cerebral infarction, subarachnoid hemorrhage, andintracranial bleeding. Cardiovascular system damage can includemyocardial ischemia/infarction, acute left ventricular dysfunction,acute pulmonary edema, andaortic dissection. Other end-organ damage can include acutekidney failure or insufficiency,retinopathy,eclampsia,lung cancer,brain cancer,leukemia andmicroangiopathic hemolytic anemia.[citation needed]
In 2000, it was estimated that 1 billion people worldwide have hypertension, making it the most prevalent condition in the world.[5] Approximately 60 million Americans have chronic hypertension, with 1% of these individuals having an episode of hypertensive urgency. In emergency departments and clinics around the U.S., the prevalence of hypertensive urgency is suspected to be between 3-5%.[9] 25% of hypertensive crises have been found to be hypertensive emergency versus urgency when presenting to the ER.[11]
Risk factors for hypertensive emergency include age, obesity, noncompliance to anti hypertensive medications, female sex, Caucasian race, preexisting diabetes or coronary artery disease, mental illness, and sedentary lifestyle.[5] Several studies have concluded thatAfrican Americans have a greater incidence of hypertension and a greater morbidity and mortality from hypertensive disease thannon-Hispanic whites, however hypertensive crises have a greater incidence in Caucasians.[12] Although severe hypertension is more common in theelderly, it may occur in children (though very rarely), likely due to metabolic or hormonal dysfunction. In 2014, a systematic review identified women as having slightly higher increased risks of developing hypertensive crises than do men.[5]
With the usage of anti hypertensives, the rates of hypertensive emergencies has declined from 7% to 1% of patients with hypertensive urgency.[5]
16% of patients presenting with hypertensive emergency can have no known history of hypertension.[6]
A summary of recommendations from the selected guidelines is presented in Table 2.
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