Week 31: Hypertension, Aneurysms, and Dissections

Hypertensive emergency is defined as a markedly elevated blood pressure with evidence of acute cardiovascular, renal or neurologic end-organ damage. Rapid reduction of blood pressure is achieved with reduction of the mean arterial pressure (MAP) by 25-30%. Excessive reduction of blood pressure should be avoided as it may cause cerebral ischemia. The first-line agents for blood pressure reduction to consider are nitroprusside, nicardipine, or labetolol. Nicardipine affects both coronary and cerebral circulations and is a pure arterial vasodilator that prevents tachycardia, bradycardia and decreased preload. It reliably reduces blood pressure and is easy to titrate.

The main indication for nitroglycerin is a patient with acute pulmonary edema who needs direct vasodilation. Nitroglycerin will also lower blood pressure, although not as quickly as nitroprusside. The other medications listed are not first-line agents as they will not quickly improve pulmonary edema. Nitroprusside is a potent arterial vasodilator that reduces afterload (instead of preload), is difficult to titrate, and may cause wide fluctuations in blood pressure. Labetolol is difficult to titrate, can cause wide fluctuations in blood pressure and is contraindicated in patients with congestive heart failure. Nicardipine is a pure arterial vasodilator.

The American Heart Association/American College of Cardiology (AHA/ACC) guidelines provide recommendations on the use of antihypertensive medications in unstable angina/non-ST-segment elevation MI. Nitroglycerin can be used to control both symptoms and BP; however, it should not be used to the exclusion of other therapies that are more likely to have a beneficial effect on outcomes. Patients should be asked if they have recently used sildenafil or one of its analogues, as the combination with nitrates can cause severe hypotension. The use of oral beta-blockers in the ED is optional. The current AHA/ACC guidelines suggest that oral beta-blockers can be given any time within the first 24 hours of presentation. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers may be used for patients with hypertension and left ventricular dysfunction or pulmonary congestion. Recommendations allow ACE inhibitors to be given within 24 hours of presentation.

Aortic dissection is caused by a tear in the inner layer of the aorta, which allows blood to enter the wall and travel in a “false lumen”. Chest x-ray findings consistent with aortic dissection include a widened mediastinum, obscuration of aortic knob, presence of apical cap, lateral displacement of the trachea and depression of the left mainstem bronchus. ECG findings are variable and may depict an ST-Elevation myocardial infarction (MI) if a proximal dissection dissects into the coronary arteries. This is a rare entity that usually involves the right coronary artery, causing an inferior or posterior MI. This particular case is concerning for an ascending thoracic aortic dissection, whose treatment is surgical. However, while waiting for cardiothoracic surgical consult and radiographic imaging studies, acute control of the heart rate and blood pressure is imperative to minimize aortic wall stress and shearing. Initial acute treatment consists of an intravenous beta blocker to reduce the heart rate below 60 beats/min – while propranolol, labetalol, and esmolol can be used, esmolol has the advantage of a short half-life and use in patients with relative contraindications to beta-blockers (asthma, CHF). If systolic blood pressure remains >100mmHg despite beta-blockade, nitroprusside is classically recommended, although several other anti-hypertensive intravenous medications may be used.

This patient is presenting with symptoms concerning for acute aortic dissection.  Patients with aortic dissection (specifically type A) can show ST elevations most commonly in the inferior leads due to involvement of the right coronary artery. In addition to cardiothoracic surgery consult, treatment of aortic dissection usually involves esmolol and nitroprusside; however, labetolol can be used in isolation. The most important treatment principle is to reduce the heart rate and then lower the blood pressure. Rate reduction is important in order to reduce shear stress on the aortic wall. As a beta blocker esmolol is effective in reducing the heart rate as it is easily titratable secondary to a short half-life. Nitroprusside is preferred to nitroglycerin as it is a more potent reducer of blood pressure, and it decreases afterload. Nitroprusside should not be used in isolation as it may increase the rate of rise of aortic wall pressure by increasing shearing forces. Reflex tachycardia may also result secondary to peripheral vasodilation increasing cardiac output.

Aortic dissection is commonly seen in patients with long-term hypertension and connective tissue disorders, but can also be seen in pregnancy, coarctation of the aorta and a bicuspid aortic valve. Ascending aortic dissection is most common in the 50- to 60-year age range, whereas descending dissections occur more commonly in older individuals. Anatomic classification of aortic dissection is important for diagnosis and treatment. The Stanford classification system divides dissections into two types: A and B. Type A dissections involve the ascending aorta and Type B dissections involve the descending aorta. Type A dissections are more lethal, more common and require prompt surgical intervention. Commonly, Type A dissections often present with normotensive or hypotensive vitals, while Type B are hypertensive. The hypotension in Type A is usually due to cardiac tamponade, aortic rupture, or heart failure associated with severe aortic regurgitation. Pulse deficits are present only in 19% of Type A dissection and 9% of Type B dissection. Aortic regurgitation murmurs are present in 44% of Type A dissections and 12% of Type B dissections, according to the IRAAD registry (International Registry of Acute Aortic Dissection). While Type B dissections are typically treated medically, acute Type A ascending aortic dissections should be treated as a surgical emergency, given that these patients are at high risk for a life-threatening complications (e.g. aortic regurgitation, tamponade, and myocardial infarction) and high mortality rates for delayed repairs.

All of the answer choices are sites that aortic aneurysms may rupture into, but aortic aneurysms most commonly rupture into the retroperitoneum. The most rapidly fatal location is the intraperitoneum. Less common sites of rupture include the gastrointestinal tract and the inferior vena cava.

The most common factor predicting the risk of rupture is the size of the aneurysm. Aneurysms occur when a segment of the aorta is weakened, and the larger the aneurysm, the greater tension exerted on the wall. Most ruptured aneurysms are greater than 5cm. There is a high incidence of aneurysms in patients with atherosclerotic disease and men older than 65 years of age. Other risk factors include history of smoking, hypertension, and family history of abdominal aortic aneurysm.

This patient presents with asymptomatic hypertension in the setting of medical non-compliance and should berestarted on his medications and scheduled for follow up with a primary care physician. Accelerated hypertension is defined as markedly elevated blood pressure in the absence of symptoms. This is in contrast with hypertensive emergency where the patient has symptoms or evidence of end organ system dysfunction or both as a result of elevated blood pressure. Accelerated hypertension has a poor long-term prognosis if not controlled but does not pose an immediate threat. As such, it should not be aggressively treated with parenteral medications. Rapid lowering of blood pressure in patients with chronic elevated blood pressure can cause organ hypoperfusion, particularly brain hypoperfusion, and lead to serious sequelae. These patients should be restarted on their medications (if appropriate) and sent for follow up with a primary care physician to monitor and treat the elevated blood pressure.

Hypertensive encephalopathy describes reversible cerebral disorders associated with high BP in the absence of cerebral thrombosis or hemorrhage. The theoretical mechanism of hypertensive encephalopathy is a rapid rise in BP that overwhelms the autoregulatory mechanisms of the brain and leads to blood-brain barrier permeability and brain edema. The symptoms of hypertensive encephalopathy can include headache, seizures, visual disturbances, nausea, and vomiting. The diagnosis must be made only after other potential hypertensive emergencies are excluded. A PubMed search for clinical trials, meta-analyses, and randomized controlled trials of hypertensive encephalopathy yielded 22 articles. None of the trials dealt directly with treatment or prognosis, and no studies suggested which agent is best for short-term reduction of BP in hypertensive encephalopathy. However, nitroprusside should be avoided in patients with this disorder, as the drug has been shown to decrease systemic pressure while preserving intracranial perfusion pressures. In the absence of data, the consensus goal of treatment is often stated as a 20% to 25% reduction in mean arterial pressure or a DBP of 100 to 110 mg Hg.