Week 8: Cardiology Part 4/5: Hypertension & Vascular

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.

The patient in the question stem has exertional syncope related to his severe aortic stenosis, characterized by his narrow pulse pressure, harsh systolic murmur, and findings of left bundle branch block on EKG. Syncope is a poor prognostic indicator for patients with aortic stenosis, and they require urgent surgical management. Patients with severe aortic stenosis causing syncope have a mortality rate approached 50% within 3 years if left untreated; therefore surgical consultation is neccessary prior to discharge. Although the patient is presenting with new left bundle branch block potentially representing acute coronary syndrome, he has absence of chest pain and thus would not be the best answer choice.

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.

Nicardipine and nitroprusside are effective parenteral drugs for acutely lowering blood pressure. They both reliably and quickly decrease blood pressure. The main disadvantage for nitroprusside is the cyanide byproduct, while for nicardipine is its longer half-life (more difficult to rapidly titrate).

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.

The most common forms of end-organ damage in hypertensive emergencies, in order of decreasing frequency, are (1) cerebral infarction or hemorrhage; (2) acute pulmonary edema; (3) hypertensive encephalopathy; (3) acute CHF; and (4) aortic dissection. Preeclampsia is another hypertensive state associated with very high BP, but unique goals and treatment options are associated with this condition.

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.