Hypertensive Emergency
A. General characteristics
- Hypertensive emergency: Systolic BP
220 and/or diastolic BP
120 in addition to
end-organ damage—immediate treatment is indicated (see Clinical Pearl 1-13).
- Elevated BP levels alone without end-organ damage—referred to as hypertensive
urgency. Hypertensive urgencies rarely require emergency therapy and can be man
aged with attempts to lower BP over a period of 24 hours.
- Whenever a patient presents with markedly elevated BP, it is critical to assess the
following systems for end-organ damage.
a. Eyes: Papilledema
b. CNS
• Altered mental status or intracranial hemorrhag- • Hypertensive encephalopathy may develop (suspect when BP is markedly elevated: 240/140 or higher, along with neurologic findings such as confusion)
- c. Kidneys: Renal failure or hematuria
- d. Heart: USA, MI, CHF with pulmonary edema, aortic dissection
- e. Lungs: Pulmonary edema
- Hypertensive emergency may lead to posterior reversible encephalopathy syndrome (PRES)—a radiographic condition which is postulated to be caused by
autoregulatory failure of cerebral vessels as well as endothelial dysfunction.
a. Despite the name, the syndrome may not always be reversible and can affect
regions other than the posterior region of the brain.
b. Symptoms include insidious onset of headache, altered level of consciousness,
visual changes, and seizures. The classic radiographic finding is posterior cerebral white matter edema.
c. Most patients are hypertensive, but may be normotensive. Elevated blood pressures overwhelm the autoregulatory mechanisms of the cerebral vessels, leading
to arteriolar dilation and extravasation of fluid into the brain.
d. Diagnose with clinical findings and brain MRI. First treatment step is to lower
BP, usually with IV medications. Other treatment steps include correcting electrolyte abnormalities and stopping seizures if they occur.
B. Causes- Noncompliance with antihypertensive therapy
- Cushing syndrome
- Drugs such as cocaine, LSD, methamphetamines
- Hyperaldosteronism
- Eclampsia
- Vasculitis
- Alcohol withdrawal
- Pheochromocytoma
- Noncompliance with dialysis
- Renal artery stenosis (atherosclerosis or fibromuscular dysplasia)
- Polycystic kidney disease
C. Clinical features- Severe headache
- Visual disturbances
- Altered mentation
D. Treatment- Hypertensive emergencies
a. Reduce mean arterial pressure by 25% in 1 to 2 hours. The goal is not to immediately achieve normal BP, but to get the patient out of danger, then reduce BP
gradually.
b. If severe (diastolic pressure >130) or if hypertensive encephalopathy is present,
IV agents such as hydralazine, esmolol, nitroprusside, labetalol, or nitroglycerin are appropriate.
c. In patients who are in less immediate danger, oral agents are appropriate.
Options include captopril, clonidine, labetalol, nifedipine, and diazoxide.- Hypertensive urgencies: BP should be lowered within 24 hours using oral agents
Aortic Dissection
A. General characteristics
- Predisposing factors
a. Long-standing systemic HTN (present in 70% of patients)
b. Cocaine use (may be remote)
c. Trauma
d. Connective tissue diseases, such as Marfan and Ehlers–Danlos syndrome
e. Bicuspid aortic valve
f. Coarctation of the aorta
g. Third trimester of pregnancy- Daily (Stanford) classification (Figure 1-17)
a. Type A (proximal) involves the ascending aorta (includes retrograde extension
from descending aorta).
b. Type B (distal) is limited to the descending aorta (distal to the take-off of the
subclavian artery).
B. Clinical features- Severe, tearing/ripping/stabbing pain, typically abrupt in onset, either in the
anterior or back of the chest (often the interscapular region)
a. Anterior chest pain is more common with proximal dissection (type A).
b. Interscapular back pain is more common with distal dissection (type B).- Diaphoresis
- Most are hypertensive, but some may be hypotensive
- Pulse or BP asymmetry between limbs
- Aortic regurgitation (especially proximal dissections)
- Neurologic manifestations (hemiplegia, hemianesthesia) due to obstruction of
carotid artery
C. Diagnosis- CXR shows widened mediastinum (>8 mm on AP view).
- TEE has a very high sensitivity and specificity; it is noninvasive and can be
performed at the bedside.
- CT scan and MRI are both highly accurate (MRI more so); MRI takes longer to
perform, making it less ideal in the acute setting.- Aortic angiography is invasive, but it is the best test for determining the extent of
the dissection for surgery.
D. Treatment- Initiate medical therapy immediately
a. IV β-blockers to lower heart rate and diminish the force of left ventricular
ejection
b. IV sodium nitroprusside to lower systolic BP below 120 mm Hg- For type A dissections—surgical management
a. Most cases of type A dissections should be treated as surgical emergencies to
prevent complications such as MI, aortic regurgitation, or cardiac tamponade
b. Open surgery is still the standard of care- For type B dissections—medical management
a. Lower blood pressure as quickly as possible. First-line drugs include IV
β-blockers such as labetalol, esmolol, or propranolol
b. Pain control with morphine or dilaudid
c. Unrelenting symptoms may require surgical treatment—both open and endovascular surgical options exist
Abdominal Aortic Aneurysm
A. General characteristics- Abdominal aortic aneurysm (AAA) is an abnormal localized dilation of the aorta.
Most AAAs occur between the renal arteries and iliac bifurcation.- The incidence increases with age. AAAs are rare before the age of 50. The average
age at time of diagnosis is 65 to 70 years.- AAAs are much more common in men, though more likely to rupture in women
at a given size.
B. Causes- Multifactorial—in most cases, there is atherosclerotic weakening of the aortic wall.
- Other predisposing factors include trauma, HTN, vasculitis, smoking, and positive
family history.- Syphilis and connective tissue abnormalities (e.g., Marfan disease) are associated
with thoracic aneurysms, but they may involve the lower aorta as well.
C. Clinical features- Usually asymptomatic and discovered on either abdominal examination or a radiologic study done for another reason
- Sense of “fullness”
- Pain may or may not be present—if present, located in the hypogastrium and
lower back and usually throbbing in character.- Pulsatile mass on abdominal examination
- Symptoms suggesting expansion and impending rupture include the following:
a. Sudden onset of severe pain in the back or lower abdomen, radiating to the
groin, buttocks, or legs
b. Grey Turner sign (ecchymoses on back and flanks) and Cullen sign (ecchymoses
around umbilicus)- Rupture of an AAA
a. The triad of abdominal pain, hypotension, and a palpable pulsatile abdominal mass indicates a ruptured AAA and emergent laparotomy is indicated. No
further diagnostic testing is needed with this constellation of symptoms; however, patients may present with only one or two components of this triad
b. Cardiovascular collapse
c. Syncope or near-syncope, secondary to sudden hemorrhage
d. Nausea and vomiting. Diagnosis
- Ultrasound
a. Test of choice to evaluate both the location and size of the aneurysm
b. 100% sensitive in detecting AAAs- CT scan
a. 100% sensitive in detecting AAAs
b. Takes longer to perform than plain radiographs or ultrasound; should only be
used in hemodynamically stable patients
c. CT is the scan of choice for preoperative planning
E. Treatment- Unruptured aneurysms.
a. Management largely depends on size of aneurysm.
• Data from the ADAM and UK-SAT trails have shown that if the aneurysm
is >5 cm in diameter or symptomatic, surgical resection with synthetic
graft placement is recommended. (The infrarenal aorta is replaced with a
fabric tube.) This can often be done endovascularly by accessing the femoral artery. The diameter of the normal adult infrarenal aorta is about 2 cm.
• The management of asymptomatic aneurysms <5 cm is controversial. Periodic
imaging is recommended to follow up growth. No “safe” size exists, however,
and small AAAs can rupture.
b. Other factors to consider are the patient’s life expectancy (patient may be more
likely to die of other medical illnesses), and the risk of surgery.- Ruptured AAAs: Emergency surgical repair is indicated. All of these patients are
unstable.
a. While open repair remains the gold standard, some ruptured AAAs may be
repaired endovascularly as well.
Peripheral Vascular Disease (Chronic Arterial Insufficiency)
A. General characteristics- Peripheral vascular disease (PVD) is an occlusive atherosclerotic disease of the
lower extremities (see also Clinical Pearl 1-14)- Patients with PVD usually have coexisting CAD (with CHF, history of MI, and so
on) and other chronic medical problems (e.g., diabetes, lung disease)- Sites of occlusion/stenosis
a. Superficial femoral artery (in Hunter canal) is the most common site
b. Popliteal artery
c. Aortoiliac occlusive disease- Risk factors
a. Smoking is by far the most important risk factor
b. CAD, hyperlipidemia, HTN
c. Diabetes—prevalence is markedly increased in these patients- Prognosis
a. If the patient has intermittent claudication, the prognosis is generally good
b. Patients with rest pain or ischemic ulcers have the worst prognosis (especially
in diabetics or smokers)B. Clinical features
- Symptoms (see also Clinical Pearl 1-14)
a. Intermittent claudication
• Cramping leg pain that is reliably reproduced by same walking distance (distance is very constant and reproducible)
• Pain is completely relieved by rest
b. Rest pain (continuous)
• Usually felt over the distal metatarsals, where the arteries are the smallest
• Often prominent at night—awakens patient from sleep
• Hanging the foot over side of bed or standing relieves pain—extra perfusion
to ischemic areas due to gravity
• Rest pain is always worrisome—suggests severe ischemia such that frank gangrene of involved limb may occur in the absence of intervention- Signs
a. Diminished or absent pulses, muscular atrophy, decreased hair growth, thick
toenails, and decreased skin temperature
b. Ischemic ulceration (usually on the toes)
• Localized skin necrosis
• Secondary to local trauma that does not heal (due to ischemic limb)
• Tissue infarction/gangrene in end-stage disease
c. Pallor of elevation and rubor of dependency (in advanced disease)
C. Diagnosis- Ankle-to-brachial index (ABI): Ratio of the systolic BP at the ankle to the systolic
BP at the arm
a. Normal ABI is between 0.9 and 1.3
b. ABI >1.3 is due to noncompressible vessels and indicates severe disease
c. Claudication ABI <0.7
d. Rest pain ABI <0.4- Pulse volume recordings
a. Excellent assessment of segmental limb perfusion
b. Pulse wave forms represent the volume of blood per heart beat at sequential
sites down the leg
c. A large wave form indicates good collateral blood flow
d. Noninvasive using pressure cuffs- Arteriography (contrast in vessels and radiographs)
a. Gold standard for diagnosing and locating PVD
D. Treatment- Conservative management for intermittent claudication.
a. Stop smoking (the importance of this cannot be overemphasized). Smoking
is linked to progression of atherosclerosis and causes vasoconstriction (further
decreasing blood flow).
b. Graduated exercise program: Walk to point of claudication, rest, and then continue walking for another cycle.
c. Foot care (especially important in diabetic patients).
d. Atherosclerotic risk factor reduction (control of hyperlipidemia, HTN, weight,
diabetes, and so on).
e. Avoid extremes of temperature (especially extreme cold).
f. Aspirin along with ticlopidine/clopidogrel have shown slight improvements
in symptom relief. They are often used in these patients for stroke/MI prevention.
g. Cilostazol is a PDE inhibitor which acts both by suppressing platelet aggregation and by directly dilating arterioles.- Surgical treatment
a. Indications: Rest pain, ischemic ulcerations (tissue necrosis), severe symptoms
refractory to conservative treatment that affects quality of life or work.