The question of prehospital management of hypertension shouldn t raise your blood pressure. The answer is usually to do nothing. Believe it or not, acute hypertension never killed anyone.
We generally classify hypertension as benign or malignant. Benign hypertension indicates the presence of measurable hypertension without gross signs or symptoms. Measurable hypertension associated with signs or symptoms of "end-organ damage," such as heart failure, angina, stroke or renal failure is called malignant hypertension. Somewhere in between lie those patients whose hypertension has produced minimal symptoms, such as headache or nausea. We refer to these patients as exhibiting "accelerated hypertension" or a "hypertensive urgency" (as opposed to a "hypertensive emergency," which is synonymous with malignant hypertension). Note these definitions reflect clinical symptoms and not cause.
You may have heard the term "essential hypertension," which means the exact cause is unknown, or "renovascular hypertension," which means the elevated blood pressure is the result of blood vessels within the kidney narrowing. These are descriptions of cause, not of effect.
On a call, you may discover an elevated BP in patients with benign hypertension, but it s often not the reason they called 9-1-1. They may or may not be on chronic blood-pressure medication, but they have no headache, nausea, vomiting, chest pain, shortness of breath or focal neurologic complaints. The hypertension itself is not manifesting any acute clinical effect, so there is no urgent clinical need to lower it.
It s also important to remember that most patients with hypertension have been walking around with it for some time prior to the EMS call. If the patient has been doing well for months or years without symptoms, there is no reason to become acutely involved if they are still asymptomatic. The patients do need follow-up and chronic care with their own physician, but there is no "emergency condition" here.
Another reason to not acutely lower asymptomatic hypertension relates to the agents we might use in this endeavor. Medications used to lower blood pressure in the field include nitroglycerin (NTG), nifedipine, labetalol, sodium nitroprusside and hydralazine. Asymptomatic hypertension is a poor indication for nitroglycerin use. Side effects (such as headache) are relatively common, and the effect of NTG on blood pressure may be erratic and uncontrolled.
Nifedipine (Procardia) was used frequently in both the EMS and ED settings, but has rightfully fallen out of favor because it produced a rapid, uncontrolled fall in BP, resulting in cases of cerebral ischemia and stroke. (It s worth noting here that some older people with severe narrowing of the cerebral arteries may actually require a higher than "normal" systolic pressure to circulate blood to the brain.)
Labetalol, a beta-blocker, can also be useful, but requires IV administration and is contraindicated in patients with congestive heart failure, asthma and cardiac arrhythmias.
The ultimate way to control the fall in BP is with sodium nitroprusside (Nipride). However, nitroprusside is often difficult to use, requiring minute dosing. In addition, the bag containing the drug must be protected from light at all times. These considerations make it impractical in most EMS settings.
Hydralazine, a potent direct-acting vasodilator, may be used, but it also produces an uncontrolled BP fall. It is usually restricted to the treatment of eclampsia in pregnant women, where nitrate administration may adversely impact the ability of both maternal and fetal hemoglobin to carry oxygen.
The patient with malignant hypertension is a different story, because symptoms such as stroke, angina or heart failure do deserve acute, aggressive care. But in these cases, we re not treating the hypertension, we re treating its symptoms. If we treat the symptoms properly (with oxygen, aspirin, nitroglycerin and morphine sulfate for chest pain; oxygen, nitroglycerin, morphine sulfate and a diuretic for heart failure) the hypertension may go away as well.
Even if the elevated blood pressure persists, once you resolve the symptoms of end-organ malfunction, the patient is no longer exhibiting signs of malignant hypertension. Specific treatment of the BP alone is no longer indicated. In terms of the "in-betweeners" (those patients with mild symptoms, such as headache and nausea, but no chest pain or signs of failure), I think the risks of acutely lowering the BP in the field outweigh the benefits of simple transport and symptomatic care. Primum non nocere ("First, do no harm").
What about stroke? Blood pressure management in cases of cerebrovascular accident (CVA) is a point of concern, especially because we have no other prehospital therapies for stroke that might decrease the pressure. If the elevated blood pressure results in signs or symptoms of a stroke, shouldn t it be lowered?
There are two critical issues here. One is the fact that high blood pressure causes cerebral blood vessels to burst, resulting in acute hemorrhagic (and not ischemic) events. The difference is important because ischemic strokes do not cause cerebral edema (brain swelling) and increases in pressure inside the head. Conversely, a hemorrhagic stroke may increase intracranial pressure through both the mass effect of the spilled blood and swelling of the surrounding tissues.
In these cases, the patient may need a higher than normal pressure to "fight" the back pressure inside the head and get blood to the brain. The question is really how much higher is still OK? The recommendation that only patients with systolic BPs above 220-240 mmHg or diastolic values above 120-140 mmHg absolutely require emergent blood pressure reduction suggests a wide margin of error. There are no firm recommendations of how low the blood pressure should be, but, in my experience, most neurologists prefer that the systolic pressure not drop below 160 mmHg. As long as the patient is not exhibiting an acute progression of the stroke or signs of imminent brainstem herniation (seizures, unequal pupils or an acute fall in Glasgow Coma Score), I d let the BP ride. If it bothers you, contact your online medical control physician for advice.
While we re on the subject of stroke, let me put in a good word for the Los Angeles Prehospital Stroke Scale (LAPSS). In an effort to facilitate thrombolytic therapy, the new ACLS guidelines stress early recognition of stroke, early exclusion of other conditions that may mimic a CVA and transportation to a receiving facility with expertise in stroke management.
The LAPSS is the only scale developed for the EMS setting that has the benefit of a high sensitivity (the ability to tell if someone does have a "true" CVA), high specificity (the ability to tell if someone does not have a "true" CVA) and the ability to exclude other causes of focal neurologic symptoms. It s an excellent tool to raise an early-warning flag to the hospital, similar to prehospital ECG for acute myocardial infarction. A copy of the LAPSS is in the new ACLS 2000 Guidelines and on the Web (see www.fpnotebook.com/NEU72.htm). It takes a while to learn, but it s an indispensable weapon in the war to preserve the brain.