Region VIII
Continuing Education
Acute Hypertension
Differential Diagnosis
And
Management
April 2007
Objectives
- Discuss probable causes for a patient that presents with hypertension in the field
- Discuss findings in the patient’s history, physical and EMS-related diagnostics that will lead to various causes of hypertension
- Describe the most appropriate BLS/ALS EMS treatment based on the prehospital patient impression of hypertension
- List the most important ions involved in myocardial action potential and their primary function in this process
- Describe the most commonly used cardiac drugs in terms of therapeutic effects and dosages, routes of administration, side effects and toxic effects
- Identify the characteristics of the patient population at risk for developing a hypertensive emergency
- Identify the progressive vascular changes associated with sustained hypertension
- Describe clinical features of the patient in a hypertensive emergency
- From the priority of clinical problems identified, state the management responsibilities for the patient with a hypertensive emergency
- Correlate abnormal findings with clinical interpretation of the patient with a hypertensive emergency
The situation
You are called to the home of a 52-year-old gentleman, approximately 220 pounds, complaining of nausea and vomiting, weakness and headache. Onset about 1 hour ago. Vital signs are B/P 210/140, pulse 92, strong and regular, respiratory rate, 20 and labored. Lungs are clear, there is no peripheral edema or JVD, skin is warm, dry and flushed. The patient’s medications include Vasotec and Hydrodiuril. The pupils are equal and reactive. His social history includes 2-3 beers and a pack of cigarettes per day. He also states that he is under a lot of pressure at work for project deadlines and he is “on-the-go” constantly. Fast food is a “way of life”.
The definitions
Blood pressure: The pressure exerted on the walls of the arteries by the blood flowing through them.
Systolic blood pressure: The amount of pressure exerted on the walls of the arteries during the contraction and ejection of blood from the left ventricle.
Diastolic blood pressure: The amount of pressure on the artery walls while the ventricle is at rest and not contracting. (12)
There are varying degrees of hypertension, based on severity and longevity.
50% of Americans over 65 are clinically diagnosed with hypertension: >140/90 mmHg.
Men with B/P >165/95 have twice the risk of mortality (1) than with blood pressure that is controlled.
Hypertension is defined by: (2)
Stage I: Systolic 140-159 or diastolic 90-99 mmHg
Stage II: Systolic 160-179 or diastolic 100-109 mmHg
Stage III: Systolic >180 or diastolic >110
Bledsoe refers to a hypertensive emergency as one that is characterized by a rapid increase in diastolic pressure (usually > 130 mmHg) and is accompanied by restlessness, confusion, blurred vision, nausea and vomiting. Clinical hypertension is defined as a blood pressure > 140/90 mmHg.
A systolic of >169 mmHg or diastolic >109 mmHg in pregnancy is considered an emergency requiring immediate attention. (2)
Causes of Hypertension
There are two forms of hypertension to consider; essential (primary) and secondary hypertension. Essential hypertension accounts for about 95% of the cases and effects about 75 million Americans. (8)
Essential hypertension is the term used when no specific medical cause can be found to explain a patient's condition. Secondary hypertension means that the high blood pressure is a result of (i.e. secondary to) another condition, such as kidney disease or certain tumors. (10)
Environment and genetics are highly indicated as contributing factors.
Risk factors
Things you can change (it’s
up to you)
|
· Exercise for cardiovascular fitness. Aerobic exercise is recommended for 20-30 minutes at lease 3 times per week. · Calcium (Hypocalcemia) has been implicated in HTN. · Magnesium: (Hypomagnesemia) may be linked to HTN. Foods that contain magnesium include low-fat dairy products and grains. · Potassium: (Hypokalemia) may have links to HTN. · Polyunsaturated fats may cause a reduction in blood pressure. (3) · Excessive weight: The greater the mass, the greater the demands on the cardiovascular system. (4) · Inactivity: Inactivity produces tendencies towards higher heart rates, meaning your heart has to work harder. · Sodium: Hypernatremia can cause fluid retention. (4) · Low potassium intake: Helps maintain a balance of sodium in the cells. (4) · Excessive alcohol consumption: Over time, heavy drinking can damage the myocardium, not to mention hepatic injury. · Stress: Chronic severe stress may lead to HTN. · Tobacco: Tobacco contains chemicals that can be harmful to the lining of arteries, contributing to narrowing. · Birth control pills · Pregnancy- May be transient.(3) |
FYI Alcohol:
Does it affect blood pressure? Excessive
alcohol use can raise your blood pressure to an unhealthy level. Heavy
drinkers who cut back to moderate drinking can lower their systolic blood
pressure by two to four points and their diastolic pressure by one to two
points. If
you have high blood pressure, avoid alcohol or drink it in moderation.
Moderate drinking is two drinks a day if you're a man younger than age 65 or
one drink a day if you're a woman or older than age 65. A drink is defined as
12 ounces of beer, 5 ounces of wine or 1 ounce of 100-proof whiskey. Keep
in mind that alcoholic drinks are often high in calories and may contribute
to unwanted weight gain. Also, alcohol can interfere with the effectiveness
of some blood pressure medications and increase their side effects. (4) |
Things you can’t change.
Heredity: Black males have a greater propensity for HTN than whites.
Heredity: HTN runs in families.
Age: The older we are, the greater the likelihood of HTN. (4)
Physiological make-up of our patient
A&P of the vascular system
|
|
|
A few Words About: Electrophysiology
There are 3 different types of cardiac muscle: atrial, ventricular and specialized excitatory and conductive fibers. The atrial and ventricular muscle is very similar, compared to skeletal muscle, but the atria and ventricles have specialized, high-speed conductors called intercalated discs. Because this high-speed network can speed messages so rapidly, all of the cells in the interconnected area contract at the same time.
In order for these cells to depolarize (fire or contract) ions have to change places from inside the cell to outside the cell (electrical potential). Sodium rapidly moves into the cell while potassium moves out. In addition to the sodium ions moving into the cell, calcium also migrates to the interior of the cell. This adds to the overall positive charge in the cell during depolarization. (What would a drug class like a calcium channel blocker do to conduction?) This message for depolarization is transmitted through the cardiac muscle via the intercalated discs so until the entire muscle has depolarized.
Once depolarization has taken place, the sodium-potassium pump fixes the ion movement during repolarization by pumping the sodium out and the potassium back in. This does take energy.
Pathophysiology of
Hypertension
The sympathetic nervous system tracks, mediated by the vasomotor center in the medulla, when stimulated, release acetylcholine which, in turn, causes the release of norepinephrine resulting in the constriction of the vessels. To that, add stimulation to the adrenal gland which secretes epinephrine causing vasoconstriction. Then, the adrenal cortex secretes cortisol (and other steroids) further enhancing vasoconstriction. This reduces the flow of blood to the kidneys triggering the release of renin. This leads to the formation of angiotensin, a potent vasoconstrictor, and this leads to the secretion of aldosterone which promotes the retention of water and sodium increasing intravascular volume. Can you say…hypertension!? (13)
Other important mechanisms include atherosclerosis and arteriosclerosis. Atherosclerosis is a disease process involving the mid and large-sized arteries. As lipids and cholesterol are deposited in the inner lining (tunica intima), damage to the middle layer (tunica media) also occurs. Additionally, calcium deposits can cause hemorrhages which can lead to scarring, fibrosis, larger plaque buildup and an aneurysm. As this process continues, the vessels loose elasticity, reducing the ability dilate or constrict. This loss of elasticity is called arteriosclerosis.
Pulmonary Hypertension
While the typical blood pressure is 120/80, the typical pulmonary blood pressure is 25/15. Should this pressure increase, vessel walls thicken and vascular injuries may begin to take place, causing difficulty with oxygen/carbon dioxide exchange. As this process continues, oxygen levels begin to fall and this contributes to vasoconstriction and increased pressures in the pulmonary vasculature. The right ventricle has to work harder and in time, the walls thicken and enlarge leading towards heart failure. In some patients, polycythemia develops, which results in thicker blood (viscosity) that can cause clumping or clotting. The result may be pulmonary embolus, stroke or AMI.
Eclampsia/Preeclampsia
Preeclampsia is the
most common hypertensive disorder of pregnancy, occurring in approximately 5%
of all pregnancies. The highest incidence is seen in primigravidas over the age
of 35 or under the age of 20. Diabetes, multiple fetuses, edema, protein in the
urine and a history of preeclampsia increase the risk of developing
preeclampsia. It is classed as mild or severe. Severe may progress to seizures
(eclampsia). Preeclampsia may be defined as an increase in systolic blood
pressure of 30 mmHg and/or a diastolic increase of 15 mmHg over the patient’s
baseline. When the baseline is not known, a pressure > 140/90 is
considered hypertensive. It is typically seen in the last 10 weeks of pregnancy
to about 48 hours post partum.
The preeclamptic
patient is experiencing an intravascular volume depletion due to a shift in
fluid distribution to a third space. Due to this unusual shift, the mom-to-be
is at increased risk for cerebral hemorrhage, pulmonary embolism, abruptio placenta,
disseminated intravascular coagulopathy (DIC) and renal failure.
Some of the signs
and symptoms that may be present include headache, visual disturbances,
hyperactive reflexes and the development of pulmonary edema.
Blood pressure regulators/mechanisms
Blood pressure is mediated by interactions of the nervous system, hormonal and renal systems.
The primary mechanisms are the adrenergic nervous system (rapid acting) and the renin-angiotensin-aldosterone mechanism (long term). (6)
Many drugs can either induce or exacerbate hypertension.
- The sympathetic nervous system is affected by sympathomymetics like cocaine, amphetamine, ergotamine, estrogen, monoamine oxidase (MAO) inhibitors, and NSAIDs.
- The kidneys are affected by NSAIDs, estrogens, corticosteroids, cocaine and amphetamine.
- The renin-angiotensin II-aldosterone system is affected by estrogens, alcohol and glycyrrhizic acid (licorice).
- Arterioles are affected by alcohol, sympathomimetics, cocaine, amphetamine, and ergotamine.
For a discussion of preload, afterload, cardiac output and functional properties of the cardiac muscle, including Starling’s Law, see Region VIII February 2007 Continuing Education.
In the pregnant patient, indicators for abrupt systemic vascular resistance points towards humoral vasoconstrictors causing vascular injuries contributing to the deposits of platelets and fibrin, increasing pressure even more, and a malfunction in the auto regulation of blood pressure. (2)
Assessment
Get a history: SAMPLE, OPQRST, vitals and pain scale assessment. Any change in mental status, syncopal episode or dizziness should include a check on blood sugar. Some OTC medications can be contributing factors. Some of the offenders include cold remedies, decongestants, pain relievers as well as birth control pills and other prescribed drugs. Be aware of the recreational drugs like cocaine and amphetamines. (4) Lung sounds may be very important, especially if the patient is developing left heart failure.
Hypertension may produce symptoms ranging from none (“the
silent killer) to seizures and coma. In between, a patient may present with
headache, dizziness, or nosebleeds. In addition, the patient may complain of
nausea, vomiting, blurred vision and shortness of breath. The pregnant patient
may also present with edema of the hands and face as well as photosensitivity.
The skin ranges from normal to warm or cool, moist or dry, flushed or pale. Watch for pitting or non-pitting edema
and tinnitus. (1)
Be cautious with patients on herbal medications. Approximately half of Americans aged 65 and older take five or more medications, including prescription, herbal and over-the-counter drugs, on a regular basis.(11) Many individuals do not consider herbal products as medications and do not report their use. There can be serious interactions between prescribe medications and herbal preparations. These products are not tested by the Federal Drug Administration (FDA), consequently, the effectiveness, purity and usefulness of some of these are in question, especially when purity is involved.
Continuing with the assessment, look for neurological deficits. A GCS and a Cincinnati Stroke Scale would be in order.
Treatment
In a true hypertensive emergency, it is best to limit scene time as much as possible. The longer the patient is hypertensive, the greater the probability of end-organ damage along with potential hemorrhage. Place the patient in a position of comfort, unless contraindicated by trauma or stroke. ABCs! Provide airway and ventilatory support and oxygen as needed. Elevate the head of the cot 15-30º if not contraindicated. To help limit scene time, an IV may be attempted enroute to the hospital.
Speed is important, but not in all areas. How fast should the blood pressure be allowed to drop? If it drops too quickly in a hypertensive emergency, the result may include cerebral, myocardial and renal ischemia/infarction. (2) Marik suggests that a controlled drop in blood pressure for hypertensive urgencies (severely elevated B/P with no end-organ damage) may be treated over a 24-48 hour period and those with end-organ damage should have their blood pressure controlled within 30-60 minutes, but not down to the normal level.
For the preeclamptic patient, IMC, gentle handling, position in the left lateral recumbent position, start an IV (or saline lock). Keep stimulation to a minimum. Transport rapidly with reduced illumination and no lights/siren if possible. With excess stimulation, preeclampsia could become eclampsia characterized by generalized seizures. Magnesium sulfate may be administered and/or a benzodiazepine to control the seizures.
There are a number of medications that may be prescribed to control blood pressure definitively. Depending on the situation, they may be used alone or together.
Thiazide diuretics control the retention of sodium and water to reduce circulating volume. This control is provided by the kidneys.
Beta1 receptors, when stimulated, increases heart
rate, contractility and conduction. Beta2 receptors cause
bronchodilation when stimulated. Therefore, beta blockers are expected to reduce heart rate, contractility and
conduction, thereby reducing blood pressure. Selective beta1 blockers
will not cause bronchoconstriction.
Calcium channel blockers are similar to beta blockers but use a
different mechanism. Calcium channel blockers work by slowing conduction
through the AV node, thereby slowing heart rate. A word of caution for patients
that are on calcium channel blockers; they can be hypotensive and not be
tachycardic.
Angiotensin-converting enzyme (ACE)
inhibitors involve a chain
reaction. ACE
inhibitors block the
reaction ending in the production of angiotensin II, a vasoconstrictor.
Vasoconstriction increases peripheral resistance which increases afterload.
Angiotensin Receptor Blockers (ARB) block the actions of angiotensin II, as opposed to interrupting the chain reaction. This reduces peripheral resistance.
Medications to Lower Blood Pressure It is
important to have a general understanding of which medications are in what
class. This information is valuable especially when the patient may be a poor
historian and does not know why they are taking the pills. This gives you an
insight to the patient’s medical history.
The following depicts drug class, some “common” drugs in
that class, some side effects and actions.
|
Diuretics
|
Side Effects (Most Prevalent) And Actions (7) Diuretics Dizziness, vertigo, orthostatic hypotension, nausea, diarrhea, vomiting (N/V/D), anorexia, constipation, polyuria, nocturia, impotence Thiazide and thiazide-related diuretics inhibit
reabsorption of Na+ and Cl- in the distal renal
tubials. Potassium sparing
diuretics block the effect of aldosterone on the renal tubule causing a loss
of Na+ water and retention of potassium. Osmotic diuretics
pull fluid from the tissues. Bottom line: loss
of fluids and electrolytes. |
|
Beta blockers
|
Beta blockers Bradycardia, CHF, cardiac arrhythmias, sinoatrial or AV nodal block, tachycardia, GI pain, flatulence, constipation, N/V/D, impotence, decreased libido, fatigue, decreased exercise tolerance. Beta blockers competitively block beta-adrenergic receptors in the heart and juxtoglomerular apparatus. They decrease the influence of the sympathetic nervous system on these tissues, the excitability of the heart, cardiac workload, oxygen consumption, and the release of renin. Bottom line: they lower blood pressure. |
|
Calcium channel blockers
|
Calcium channel blockers Dizziness, light-headedness, headache, asthenia*, nervousness, peripheral edema, angina, bradycardia, AV block, nausea, diarrhea, constipation, nasal congestion, cough. Ca+ channel blockers and antianginal and
antihypertensive. By inhibiting the movement of calcium ions across the cell
membranes of cardiac and arterial muscle cells, the transmembrane calcium
flow results in the depression of impulse formation in specialized cardiac
pacemaker cells, slowing the velocity of conduction of the cardiac impulse,
depression of myocardial contractility and dilation of coronary arteries and
arterioles and peripheral arterioles. Bottom line:
decreased cardiac work and energy consumption and increased delivery of
oxygen to the myocardial cells.
* weakness |
|
Angiotensin-Converting Enzyme (ACE) inhibitors
|
ACE inhibitors Myocardial infarction, rash, GI irritation, aphthous ulcers*, cough. ACE inhibitors block the cascade of events when renin is released from the lungs. The progression is renin is used to convert angiotensin I into angiotensin II. Angiotensin II is a powerful vasoconstrictor. If this action is blocked, then the blood pressure may be lower. *painful ulcers usually affecting the oral mucosa |
|
Angiotensin-receptor blockers (ARBs).
|
Angiotensin-receptor blockers (ARBs). Fatigue, depression, abdominal pain, upper respiratory infection symptoms. A selective blockade of angiotensin II to effectively block the vasoconstriction effects of the renin-angiotensin system. |
|
Direct-acting vasodilators.
Centrally acting agents
Methyldopa (Aldomet®). |
Direct-acting vasodilators Headache,
palpitations, tachycardia, angina pectoris, anorexia, N/V/D, weakness,
orthostatic hypotension, hypotension, syncope. Direct
acts on vascular smooth muscle to cause vasodilation. |
|
Centrally acting agents
Methyldopa (Aldomet®). |
Centrally acting agents Drowsiness,
sedation, dizziness, dry mouth and constipation, headache, weakness,
bradycardia. Stimulates
CNS alpha2-adrenergic receptors inhibits sympathetic
cardioaccelerator and vasoconstrictor centers. |
|
Nitrates
|
Nitrates Be
very cautious regarding interactions between administering nitroglycerin and
other drugs. Specifically, sildenefil citrate (Viagra®,
Revatio®) which is used, not only for erectile dysfunction, but for pulmonary
hypertension. Tadalafil (Cialis®) and vardenafil
(Levitra®) are prescribed for erectile dysfunction. Side effects of these drugs
include headache, dizziness, rash and flushing. Do not use nitrates with these
drugs. Irreversible hypotension may result. |
Back to our 52-year-old gentleman. What can we derive from his history and exam?
1. 52 years old- As we age, the probability of our blood pressure increasing goes up too. Vessels become less compliant.
2. Nausea, vomiting, weakness- potential indicator of increased intracranial pressure (due to increased blood pressure). Other causes include meningitis, influenza, food poisoning and the side effects of many drugs (to name a few).
3. 220 pounds- the greater the body mass, the greater the demand for oxygen and nutrients and removal of unwanted substances. As the volume of circulating blood increases, so does blood pressure.
4. 210/140- definite indicator of high blood pressure. A good law to live by: If you use mechanical blood pressure devices, your first reading should always be manual for a baseline.
5. Lungs clear- probability of no left heart failure (yet).
6. No peripheral edema- good pertinent negative indicating a lack of support for concomitant heart failure.
7. Vasotec- ACE inhibitor suppressing Angiotensin II, thereby reducing peripheral resistance, an indicator of (treated) hypertension. (Knowing medications can help with the patient’s history.)
8. Hydrodiuril- diuretic indicating excessive fluid that can contribute to hypertension. (Knowing medications can help with the patient’s history.)
9. Excessive alcohol consumption- can lead to myocardial and renal damage.
10. Smoker- chemicals in tobacco can damage vessel lining reducing elasticity, impeding the ability to dilate and contributing to hypertension.
11. Stress- high levels of stress can produce the release of catecholamines which can lead to an increase in blood pressure.
12. Fast food- has an increased salt content increasing fluid retention, increasing vascular load and blood pressure.
When we understand the indications of the pieces of the puzzle when we assess a patient’s history, we can have a much greater understanding of the “big picture”. This patient is experiencing a hypertensive crisis and needs his blood pressure brought down in a controlled manner.
Drug of the Month:
Glucagon
(GlucaGen™)
We are most familiar
with Glucagon as the medication that mobilizes hepatic glycogen and converts it
into glucose. We give it to the hypoglycemic individual that we can’t get an IV
on for Dextrose administration. We can give it IM. But what else can Glucagon
do? It has another important use. Read on.
Beta-blockers are used for treating hypertension, angina,
myocardial infarction, arrhythmias and heart failure.
Beta blockers
compete with catecholamines,
inhibiting their affects on the receptor sites and can slow the heart rate.
Glucagon, a beta blocker antagonist, can increase the heart rate. The actual
process is quite complicated, but suffice it to say that the conduction through
the AV node is accelerated so that the heart rate increases.
When a patient
overdoses (accidentally or intentionally) on beta- or calcium channel blockers,
the heart can slow to a life-threatening level. Glucagon, being a beta blocker
antagonist, can bring the rate up again, when given IV.
This is why Glucagon
may be used for beta- or calcium channel blockers. See Toxicological Emergences
SOP included in this packet.
|
DRUG
NAME |
ADULT
DOSE / ROUTE |
PEDIATRIC
DOSE / ROUTE |
ACTION |
INDICATIONS |
CONTR-INDICA-TIONS |
SIDE
EFFECTS |
|
Glucagon (Gluca-Gen™) |
Diabetic / Glucose Emergencies 1
mg IM |
0.5
mg IM |
Causes
a breakdown of stored glycogen into glucose. |
Hypoglycemic patient
without venous access. |
Hyper-sensitivity to
glucagons or proteins |
N&V, dizziness,
headache |
|
Beta / Calcium Channel Blocker OD 1
mg slow IV, may repeat x 1 |
0.5
mg IV/IO, may repeat x 1 |
Independent
of blockade, positive inotropic and chronotropic and improved AV conduction |
b or calcium channel blocker OD with symptomatic bradycardias including
AV blocks (dosage required usually exceeds that carried in field) |
Bonus Drug of the Month:
ALBUTEROL
It’s not true that everything that wheezes is helped by Albuterol. First off, what causes wheezing sounds? Wheezing is a whistling sound due to narrowing of the airways by edema, bronchoconstriction or foreign materials during inspiration and/or expiration. (1) As the smaller airways fill with fluid (pulmonary edema) they produce wheezing. Beta blockers may precipitate airway narrowing.
Albuterol is a beta2 selective adrenergic agonist. In low doses, it acts relatively selective on beta2 receptors and causes bronchodilation. At higher doses, the selectivity is lost and causes sympathomimetic cardiac effects. (7)
We know that asthma is a reversible, intermittent, obstructive airway disease. When the airways narrow due to contraction of muscles surrounding the bronchi, swelling of membranes lining the bronchi and mucus plugs, we often hear wheezing.
|
DRUG
NAME |
ADULT
DOSE / ROUTE |
PEDIATRIC
DOSE / ROUTE |
ACTION |
INDICA-TIONS |
CONTRA-INDICA-TIONS |
SIDE
EFFECTS |
|
Albuterol (Proventil™ Ventolin™) |
2.5
mg of 0.83% solution (3 ml) via nebulizer (6 LPM oxygen supply) until mist
stops (usually 5 – 15 min). |
Same
as adult. |
Beta2
stimulation causing selective bronchial smooth muscle relaxation /
broncho-dilation. |
Bronchospasm in patients
with reversible obstructive airway disease attacks of bronchospasm, such
as bronchitis, COPD, emphysema, cystic
fibrosis or croup. |
Hyper-sensitivity to albuterol or any of its
components. Use caution in pregnancy or history of cardiovascular disease. |
Paradoxical
broncho-spasm, palpitations, tachycardia and increase in BP, tremors or
nervousness (CNS stimulation). |
Be familiar with the following SOPs:
|
STROKE |
|
BLS/ALS 1.
Initial Medical Care. ·
Limit
scene time ·
C-spine
control for unconscious patients with suspected trauma 2.
Protect
airway, suction as necessary 3.
Maintain
head and neck in neutral alignment. DO
NOT flex neck. If SBP > 90 mmHg,
elevate head of bed 15-30° 4.
Monitor
and record neurological status using GCS, and note any changes 5.
Assess
patient using the Cincinnati Stroke Scale: ·
Facial
Droop (have patient show teeth or smile) ·
Arm
Drift (patient closes eyes and hold both arms out) ·
Speech
(have patient say “You can't teach an old dog new tricks") ALS 6.
INTUBATE if GCS ≤ 8 7. |