This course is designed to give and overview of the care and management of the patient who suffered a hypertensive intracerebral hemorrhage. Focus will be placed on the pathphysiologic changes as well as the risk factors, causes (focusing on hypertension) and diagnosis of a hemorrhagic stroke. Medical management (including pharmaceutical therapy) will also be presented. Patient education regarding prevention of secondary stroke, rehabilitation and nursing care and management (with suggested NANDA nursing diagnosis) will be the final focus of this course.

 

Upon completion of this course the student will be able to:

Non-traumatic or spontaneous intracerebral hemorrhage (ICH) occurs when a diseased blood vessel within the brain bursts, allowing blood to leak inside of the brain (the name means within the cerebrum or brain). The sudden increase in pressure within the brain can cause damage to the brain cells surrounding the blood. If the amount of blood increases rapidly, the sudden build up in pressure can lead to unconsciousness or even death. Intracerebral hemorrhage usually occurs in selected parts of the brain including the basal ganglia, cerebellum, brainstem or cortex.

 

The most common cause of ICH is high blood pressure (hypertension). Since high blood pressure by itself often causes no symptoms, many people with intracranial hemorrhage are not aware that they have high blood pressure or need to seek treatment. Treating hypertension initially could cut the annual number of “bleeding strokes” (in the U.S) by about one quarter.

 

Intracerebral hemorrhage secondary to pathologic changes initiated by chronic hypertension is responsible for approximately 75% of all cases of primary ICH. 27% of adult Americans have hypertension (which is defined as an SBP of 140 mmHg or higher and a DBP of 90 mmHg or higher). An additional 31% of Americans have pre-hypertension which is defined as an SBP of 120-139 mmHg and a DBP of 80-89 mmHg. In addition to hypertension; all of the following are also considered to be causes for ICH:

 

High blood pressure adds to the workload of the heart and arteries by causing the heart to pump harder and the arteries carrying blood to work under a much greater pressure. If high blood pressure goes undiagnosed for a long period of time the heart and arteries become affected and in turn affect other major organs of the body. There is an increased risk of stroke, congestive heart failure, kidney failure and heart attack in patients who have hypertension. When other contributing factors are present such as obesity, smoking, high cholesterol and diabetes; the risk of stroke increases by several times.

 

Symptoms depend on the location of the bleed and the damage that the brain has sustained. Most symptoms develop suddenly, without warning and often during physical activity. There is often a rapid loss of function(s) on one side of the body. The following are considered to be symptoms of a stroke and require immediate intervention:

Neurological exam may indicate increased intracerebral pressure such as swelling of the optic nerve or changes in eye movement. Localized abnormalities in the brain function are detected by observing abnormal reflexes or movement.

 

The specific pattern of function change may indicate the location of the problem within the brain. For conclusive diagnosis a brain CT or MRI is necessary.

 

The diagnostic CT of choice is one without contrast. The valuable information gathered from a non contrast head CT includes the size, location, presence of blood (either intraventricular, subarachnoid or Subdural), provides information to determine whether the stroke is hemorrhagic or non hemorrhagic, and can reveal any underlying structural abnormalities.

 

Rapid recognition and diagnosis of an ICH is essential because the disease process can rapidly progress in the first several hours. The classic clinical presentation of ICH includes the onset of a sudden focal neurological deficit (while the patient is active) which progresses over minutes (and sometimes hours).

 

Although ICH and ischemic stroke patients often present with similar symptoms the patient with and ICH has a greater risk of quickly deteriorating and has a greater need for quick intensive treatment.

 

In order to diagnose the hemorrhage as hypertensive in nature, there must be some evidence of high blood pressure (or a documented history). Upon admission to the hospital patient’s will often continued to exhibit other tell tail signs of hypertension as well such as kidney dysfunction or broken blood vessels in the eyes. Other tests to determine the amount and cause of bleeding should include the following:

 

IV Bolus Dose – 5 mg to 20 mg Q 15 min

 

Continuous Infusion Rate – 2 mg/min (max dose of 300 mg/d)

 

Nerves that are part of the adrenergic nervous system travel to most arteries where they release an adrenergic chemical known as norepinephrine. Norepinephrine attaches to the muscles of the arteries and causes the muscle to contract which narrows the artery and increases the blood pressure. Labetalol blocks these adrenergic nervous system receptors sites inhibiting this process. This blocking of the receptors allows the muscle to relax, allows the artery to expand and results in a fall in blood pressure.

 

The most common side effects of Labetalol include:

Continuous Infusion Rate – 5 mg to 15 mg/hr

 

Nicardipine belongs to a class of medications called calcium channel blockers. These medications block to the transport of calcium into the smooth muscle cell that lines the arteries. Since calcium is important in the contraction of muscle, clocking calcium blockers allow the muscles surrounding the artery to relax which in turn causes a decrease in blood pressure and a decrease in the burden of the heart as it pumps blood to the body. This in turn decreases oxygen demand helps prevent angina in patients with coronary artery disease as well. Unlike other calcium channel blockers, Nicardipine has little effect on the heart muscle or in the electrical conduction system of the heart.

 

Nicardipine can sometimes cause and increase in the frequency or duration of angina (for reasons that are unclear). Excessively low blood pressure can occur in rare incidents (especially during initial initiation of this medication or during drug dose adjustments). These periods will require additional monitoring. Cimetidine (Tagamet) increases Nicardipine levels in the blood and therefore increases the effect of Nicardipine. Safe use of Nicardipine in children has not yet been established.

 

IV Bolus Dose – 250 mcg/kg IVP loading dose

 

Continuous Infusion Rate – 25 mcg to 300 mcg/kg/min

 

Esmolol is a cardio-selective beta 1 receptor with rapid onset, a very short duration of action and no significant intrinsic sympathomimetic or membrane stabilizing activity at therapeutic dosages. Esmolol decreases the force and rate of heart contractions by blocking beta-adrenergic receptors of the sympathetic nervous system (these receptors are found in the heart, lungs and other organs of the body). Esmolol prevents the action of two naturally occurring substance; epinephrine and norepinephrine.

 

Hypersensitivity to Esmolol may cause:

IV Bolus Dose – 1.25 mg to 5 mg IVP Q 6 hours (first test dose should be 0.625 mg due to the precipitous blood pressure lowering possibility).

 

Enalapril is an Angiotensin converting enzyme (ACE) inhibitor that is used in the treatment of hypertension and some types of chronic heart failure. ACE is an enzyme in the body that causes the formation of Angiotensin II. Angiotensin II causes the arteries of the body to narrow and thereby increases blood pressure. ACE inhibitors such as Enalapril lower blood pressure by preventing the formation of Angiotensin II thereby relaxing the arteries. ACE Inhibitors also improve the effectiveness of the heart in patients with heart failure by reducing the systemic blood pressure from which the heart must pump against.

 

Enalapril may increase potassium levels and cause Hyperkalemia. Patients receiving supplemental potassium or medications known to increase potassium levels (i.e. spironolactone), should have potassium levels closely monitored. Patients on diuretics and especially those in whom diuretic therapy was recently instituted may experience excessive reduction in blood pressure after initial initiation of Enalapril or Enalaprilat.

 

IV Bolus Dose – 5 mg to 20 mg IVP Q 30 minutes.

 

Continuous Infusion Rate – 1.5 to 5 mcg/kg/min

 

Hydralazine hydrochloride (1-hydrazinophthalazine monohydrochloride: Apresoline) is a vasodilator that is used to treat hypertension. Hydralzine works by relaxing blood vessels (arterioles more so than venules) and increasing the supply of blood and oxygen to the heart (which reduces the work load of the heart).

 

Profound hypotension can occur when Hydralazine is used with other anti-hypertensive medications (such as Diazoxide) and therefore require frequent and close blood pressure monitoring when being used together.  Beta blockers such as Metoprolol and Propranolol may have increased effects when used with Hydralazine. NSAIDS may decrease the hemodynamic effects of Hydralazine (avoid NSAID use when using Hydralzine whenever possible).

 

Continuous Infusion Rate – 0.1 to 10 mcg/kg/min

 

Nipride is a potent, rapid acting IV antihypertensive agent. The brief duration of the drugs action is due to its rapid biotransformation. The hypotensive effect is augmented by ganglionic blocking agents. Nipride causes peripheral vasodilation as a result of a direct action on the blood vessels, independent of autonomic innervation.

 

Uncommon symptoms include:

The hypotensive effect of Nipride is augmented by that of most other anti-hypertensive medications including; ganglionic blocking agents, negative inotropic agents and inhaled anesthetics.