Hypertensive Crisis
Target organ damage (TOD): refers to damage occurring in organs such as the brain, heart, kidneys, and eyes as a result of uncontrolled hypertension. These organs have a rich blood supply and damage to the blood vessels supplying these organs can lead to disease in these organs.Chronic elevated blood pressure can lead to an enlarged heart (cardiomegaly), kidney failure, brain or neurological damage, and changes in a part of the eye known as the retina.
A hypertensive crisis is defined as a sudden increase in blood pressure that at the time of presentation in a clinic or hospital is associated with target organ damage (referred to as an hypertensive emergency) or with no target organ damage (a hypertensive urgency).
A hypertensive crisis is a medical emergency that requires immediate treatment. The condition affects 1% of hypertensive individuals and may account for > 20% of emergency room visits.
The most critical factor determining the urgency of treatment is recognizing the deterioration of a vital target organ function (i.e. hypertensive emergency) in this setting, the blood pressure is best lowered over several minutes to limit or reverse target organ damage. The patient with hypertensive emergency is best monitored in a hospital setting preferably in an intensive care unit.
Examples of target organ damage seen in hypertensive emergency include hypertensive encephalopathy, intracranial hemorrhage, acute myocardial infarction, acute left ventricular failure with pulmonary edema, acute aortic dissection, acute renal failure and ecclampsia.
In a hypertensive emergency, the blood pressure is usually very high (>180/90mmhg).However it is important to note that it is the clinical status of the affected individual and NOT the degree of blood pressure elevation that defines hypertensive emergency. For example, a patient may present in a hospital with a blood pressure less than 180/90mmhg but with signs and symptoms of eclampsia.
The hypertensive urgency, on the other hand, is a less clearly defined condition in which severe uncontrolled blood pressure is not associated with any evidence of ongoing or imminent target organ dysfunction. Most of the patients presenting in hospital with hypertensive urgency are either inadequately treated for hypertension or do not take their drugs as recommended by a healthcare professional. In this setting, the blood pressure is lowered over a period of time, usually outside a hospital setting, from 4 hours to 24 hours as the patients involved are at low risk of developing complications of hypertension.
Hypertensive emergencies usually start with a sudden rise in blood pressure to a level which exceeds the normal resting blood pressure of a patient. In individuals with normal and elevated blood pressures, blood flow to target organs is maintained across a wide range of blood pressures by autoregulatory mechanisms. The sudden rise in blood pressure and hyperperfusion (increased blood flow) of target organs in hypertensive emergency overwhelms the compensatory or autoregulatory mechanisms resulting in target organ damage.
The exact pathophysiology surrounding the failure of autoregulatory mechanisms in hypertensive emergencies is poorly understood but perhaps involves a part of blood vessels known as the endothelium, as well as the generation of a prothrombotic state.
CAUSES OF HYPERTENSIVE EMERGENCY
Medical conditions associated with the development of Hypertensive Emergency include:
- Essential hypertension
- Kidney disease
- Chronic pyelonephritis
- Acute glomerulonephritis
- Systemic lupus erythematosus
- Renal artery stenosis
- Renovascular disease
- Chronic renal failure
- End stage renal disease
- Endocrine
- Glucocorticoid excess
- Pheochromocytoma
- Aldosterone secreting tumors
- Primary aldosteronism
- Renin secreting tumors
- Pregnancy
- Preecclampsia/Ecclampsia
- Drugs
- Abrupt withdrawal of centrally acting anti- hypertensive drugs such as Clonidine and Alpha Methyldopa
- Phencyclidine/cocaine intoxication
- Ingestion of tyramine containing foods in a patient on a monoamine oxidase inhibitor such as selegiline, phenelzine, and tranylcypromine.
- Central nervous system disorders
- Acute head injury
- Stoke
- Intracranial hemorrhage.
MAKING A DIAGNOSIS
The correct differentiation between the two forms of hypertensive crisis often poses a challenge to health care professionals. Making a diagnosis of hypertensive crisis requires a thorough history, a complete physical examination, laboratory studies and electrocardiography/echocardiography to determine the presence and severity of target organ damage.
A brief history should address the duration, type, and severity of hypertension, the type of medication taken (prescription and non prescription medication), compliance to medication and the use of illicit drugs. Historical evidence suggestive of renal, neurologic, and cardiovascular damage including chest pain (myocardial infarction), shortness of breath (pulmonary edema secondary to left ventricular failure), and neurologic symptoms such as headaches, seizures and blurring of vision, should be noted.
A physical exam should begin with an assessment of the blood pressure in both arms as well as in one or both lower limbs. In addition, blood pressure should be assessed in both the supine and sitting position to assess volume status. Further examination should include assessment of peripheral pulses, listening with a stethoscope for murmurs, and listening to the chest for signs of congestion. Thorough cardiovascular and neurological examinations are necessary to determine the presence of target organ damage as well as provide clues to the possible existence of a secondary form of hypertension. Examination of the eye using a fundoscope provides clues (retinopathy, papilloedema) to the presence of a hypertensive emergency.
Baseline laboratory investigations for patients in hypertensive crisis include a blood count with peripheral smear, serum electrolytes, blood urea nitrogen, and serum creatinine concentrations(to evaluate for renal impairment), as well as urinalysis (to determine the presence of casts which are suggestive of renal disease). Other diagnostic tests of importance include electrocardiography (may reveal evidence of a myocardial infarction, left ventricular hypertrophy) a chest radiograph (to evaluate for pulmonary congestion, aortic dissection) and a computed tomographic scan (mandatory in patients with neurologic symptoms).
TREATMENT OF HYPERTENSIVE CRISIS
The goal of treatment of hypertensive crisis is to achieve a progressive, controlled reduction in blood pressure.
A case of hypertensive urgency can be treated using oral antihypertensive agents usually in an out patient setting except in patients in whom follow may be difficult to achieve.
The initial goal of treatment of hypertensive urgency is to reduce the blood pressure to 160/110 mmhg over several hours to days using oral antihypertensive drugs. A rapid reduction in blood pressure should be avoided as it poses a risk to vital organ circulation.The oral antihypertensive agents employed in the management of hypertensive urgency include:
It is important to note that treatment with these agents should be initiated with very low doses. Doses can be increased as needed. Large starting doses should be avoided because of the risk for hypotensive complications.
A precise and rapid reduction in blood pressure is the primary goal in the treatment of hypertensive emergency.
The patient should be monitored in an intensive care unit (ICU) where suitable supervision and monitoring of blood pressure can be provided. Parenteral (intravenous/intramuscular) antihypertensive agents are the drugs of choice for the treatment of hypertensive emergency as rapid reduction of blood pressure is critical. Common parenteral drugs used for treatment of hypertensive emergencies include:
- Sodium nitroprusside- acts as a non-selective vasodilator and has a very rapid onset of action, effective within seconds following an infusion. It, however, has an offset of effect within 1-2 minutes and is rapidly degraded by light. Delivery sets for sodium nitroprusside must be light resistant to prevent degradation. It should be used with caution in patients with renal impairment as its use may result in thiocyanate and cyanide intoxication in these patients.
- Labetalol- can be administered as a bolus intravenous dose or as a slow continuous infusion. Its beta adrenergic receptor antagonistic effect results in decreased heart rate and decreased force of contraction of the heart while its alpha receptor blocking effect helps preserve renal blood flow despite systemic reductions in blood pressure. It is contraindicated in heart block greater than first degree.
- Nicardipine- in intravenous form has a rapid onset of action and is easily titratable. It is effective in a high percentage of hypertensive emergencies and its dosing is not dependent on body weight. It, however, has a long duration of action and over-titration can result in marked reduction in blood pressure (hypotension) and heart rate (bradycardia).
- Fenoldapam- is a vasodilator which binds to the dopamine-1 receptor site at therapeutic doses. It has been shown to be an effective parenteral antihypertensive agent in patients with severe hypertension and is particularly useful in hypertensive emergencies associated with significant renal impairment.
- Hydralazine- is a vasodilator and is considered safe in pregnancy. Its use as first line antihypertensive agent in pregnant women with preeclampsia has become limited in recent years although it significantly improves uterine blood flow on administration. It is contraindicated in individuals with coronary atherosclerosis as its use is associated with significant reflex tachycardia.
- Enalaprilat- is the active metabolite of the oral drug enalapril, an angiotensin converting enzyme inhibitor. It is available in intravenous form and is suitable for treating hypertensive emergencies associated with congestive heart failure. Its use is contraindicated in patients with renal artery stenosis and in the second or third trimesters of pregnancy.