Beyond the Basics: Vascular Emergencies

CEU Review Form Vascular Emergencies (PDF)Valid until May 4, 2007

Vascular diseases, specifically of the arteries, have been and continue to be one of the major contributors to death in the United States. After peaking in the late 1960s, their incidence started to drop, largely due to changes in lifestyle. It has been leveling off as Americans realize the importance of risk factors such as a high-fat diet, lack of exercise and high-risk behaviors like smoking; however, vascular disease remains the pathologic origin for nearly half of all deaths in the U.S.

Basic Anatomy
     There are three types of vascular structures in the body: arteries, veins and lymphatics. Oxygenated blood is ejected from the left ventricle into the aorta, where it travels through an extensive network of arteries that decrease in lumen size and eventually branch into arterioles. The arterioles provide oxygenated blood to the capillary bed that perfuses tissue and organs like the brain, kidneys and liver. Following gas exchange in the capillary bed, the deoxygenated blood enters a venule, which then transports the blood to a vein. The blood travels through increasingly larger veins until it eventually enters the right atrium. The lymphatic system collects fluid from the body's tissues and provides filtration to it via the lymph nodes. This fluid is eventually returned to the venous system, where it mixes with the blood and returns to the heart.

     The walls of the arterial system, as well as of the venous system, are comprised of three layers. The innermost layer, the tunica intima (Latin for covering or coat), is a smooth interior surface of the blood vessel that minimizes unnecessary resistance to blood as it travels through the vessel. The middle layer, the tunica media, is also the thickest layer of the artery. The tunica media is comprised of elastic connective tissue and smooth muscle, which are circularly positioned around the artery and regulate the diameter of the vessel's lumen by contracting and relaxing. Interestingly, in the body's larger arteries, the tunica media is dominated by elastic tissue, whereas the smaller arteries and arterioles' tunica media are dominated by smooth muscle. The outermost layer of the blood vessel is called the tunica adventitia (adventitia in Latin means from afar). This outer layer is composed mainly of collagen and loosely organized connective tissue. Not only does this layer give the blood vessel its strength, the collagen also serves to anchor the blood vessel to nearby structures for added stability.

     While the intima and media are provided with oxygenated blood by a process of diffusion from the vessels' internal lumen, the adventitia and outer portion of the media are perfused by a network of small vessels that penetrate into these layers. The vasa vasorum are known as the "vessel of vessels."

Pathogenesis
     Essentially, the same vascular pathology underlies many of the cardiovascular, neurological and pulmonary emergencies seen in the prehospital setting. One may rationalize that a patient with diminished tactile sensation does not share anything in common with the patient who just suffered a debilitating stroke. In fact, the pathology of the two problems may well be one and the same. In order to understand this concept, an overview of specific arterial disease progression is necessary.

Arteriosclerosis
     Most disease processes that damage the arterial wall result in a reduction in the elasticity and flexibility of the vessel, which is known as sclerosis. The medical term applied to this condition as it relates to the arterial network of the body is arteriosclerosis, known to the layperson as "hardening of the arteries." In recent years, this term has fallen into disfavor, as it does not distinguish between the different types of arterial diseases. If left unqualified, the term usually means atherosclerosis, which is actually a form of arteriosclerosis.

     Arteriosclerosis is described as a disease process that results in intimal thickening and hardening. The process involves a migration of collagen fibers and smooth muscle cells into the intimal layer of the blood vessel, which results in thickening of the wall and decrease in lumen size. Unlike the typical description, these changes do not cause the arteries to harden so much as they prohibit them from expanding normally, which contributes to an increase of the resistance to blood flow. The heart must overcome the increased vessel resistance during ejection of the blood, resulting in a greater myocardial workload. These changes may be expected as a normal part of aging; however, it can worsen almost every chronic disease process that may concurrently develop.

     The various types of arteriosclerosis can be distinguished more specifically by the type of artery and the layer of the artery involved, and the etiology that produced the sclerosis. Three sclerotic conditions include a very rare type known as Monckeberg's medial calcific sclerosis, a more common type known as arteriolosclerosis, and atherosclerosis, the most widely known of the conditions.

     Monckeberg's sclerosis is a rare condition that affects the medium-sized arteries found in the muscles of limbs, and, when present, usually is diagnosed in patients in their 50s or older. In this condition, an abnormal deposition of calcium in the media layer of the artery gives the superficial blood vessel a palpable rigidity. This type of sclerosis does not decrease the lumen size of the artery; thus, there is no obstruction in blood flow or deprivation of oxygen to distal tissue. However, some patients may concurrently have another form of sclerosis present in the same vessel (e.g., atherosclerosis), which may then give rise to further clinical consequences.

     In arteriolosclerosis, there is a thickening of the intima and media layers of the artery that occurs from accumulation of plasma proteins and the proliferation of cells that thicken the arteriole walls. This results in a decrease in the lumen size of the arteriole and an increase in vascular resistance to blood flow. This condition often produces hypertension, resulting in a condition known as hypertensive vascular disease. It is commonly found in renal vasculature.

     The third and most prevalent form of the chronic arteriosclerotic conditions is atherosclerosis&-a systemic arterial disease that is derived from the Greek word athere, meaning gruel or porridge, and scleros, which means hard. It is the underlying pathogenic process in the majority of patients who have coronary artery disease and those who have experienced a myocardial infarction, as well as patients who have suffered a stroke. Atherosclerosis alone is the No. 1 killer worldwide in economically developed countries.

     Arteriolosclerosis is a disease process that primarily affects arterioles, whereas atherosclerosis affects the large and medium-sized arteries. The most common arterial vessels affected, in descending order of frequency, are the:

• Abdominal aorta
• Iliac arteries
• Coronary arteries
• Femoral and popliteal arteries
• Internal carotid arteries
• Major blood vessels in the base of the brain.

     Atherosclerosis is an inflammatory disease that starts with the intimal lining of the blood vessels where endothelial cells become damaged. Common risk factors that are thought to cause this endothelial injury include smoking, diabetes, hypertension, high levels of low-density lipoproteins (LDL), and low levels of high-density lipoproteins (HDL). Once injury occurs, dysfunction and inflammation of the intima occur as a result of the following basic pathophysiologic events. Intima damage allows the migration of blood platelets and serum lipoproteins into the vascular wall. As a result of the irritation and inflammation, macrophages migrate to the location, as do smooth muscle cells of the tunica media layer. Both macrophages and smooth muscle cells proliferate. As the disease progresses, longitudinal fatty streaks develop in the lumen of the blood vessels. The blood vessel weakens as the intima and media are deprived of nutrients from the expanding plaque. In an attempt to "close off" the fatty streaks, smooth muscle cells produce collagen and migrate over the fatty streak to form a fibrous cap. Fibrous caps are not stable and may rupture, which causes the body's clotting mechanism to activate with development of a thrombus that may occlude the blood vessel. It is this vascular pathoplogic progression that ties together the etiology of many of the cardiac, pulmonary and neurological conditions seen in the prehospital environment. Although this disease process can affect all arteries in the body, it is not until there is a specific organ dysfunction that the damaging effects become obvious.

There are four major locations where atherosclerosis has clinical relevance for prehospital providers.

• When an atherosclerotic disease process damages peripheral blood vessels, it is known as peripheral arterial disease, also known as peripheral vascular insufficiency.
• When an atherosclerotic disease process damages arteries within the brain, it is known as cerebrovascular disease.
• When an atherosclerotic disease process damages coronary blood vessels, it is known as coronary heart disease.
• When an atherosclerotic disease process damages the aorta, the result is emergencies such as aortic aneurysm, aortic dissection or aortic calcification.

     The damage does not affect only these four locations. As any artery becomes occluded from atherosclerotic changes, it will result in a decrease or cessation of blood flow to distal vessels. This may result in emergencies such as a renal (kidney) infarct, intestinal infarct, a loss of tactile sensation from damaged peripheral sensory nerves from a lack of perfusion, or even peripheral vascular occlusion in an extremity.

Risk Factors
     As to be expected, the risk factors for the three types of arteriosclerosis discussed thus far are the same ones that adults and children alike have been warned about for literally decades. Although the exact role of each risk factor may not be totally understood, the common theme is damage to the intimal lining of the artery with progressive changes that can eventually result in full occlusion of the artery.

Non-modifiable risk factors:

• Age&-Arteriosclerosis is typically a disease of older people.
• Gender&-Males are afflicted more often than females, although rates become closer to equal after menopause.
• Heredity&-Arteriosclerosis afflicts some families and spares others.

Modifiable risk factors:

• Lipid metabolism&-Influenced by obesity, diet, diabetes and high cholesterol levels.
• Hypertension&-Left undiagnosed or untreated, it can speed the progression of the disease.
• Cigarette use&-Known to promote vasoconstriction and speed damage to intimal lining.
• Behavior&-Although loosely related, a healthy lifestyle may reduce the risk of developing the disease.

     Attention to risk factors is extremely important for children and adolescents, as well as adults. It has been found that fatty streaks can develop in children of young ages. This is alarming, as the fatty streaks are typically subclinical, and, as such, do not create a large degree of concern for the parents, but the benign fatty streaks in childhood today will become the ruptured plaque and artery occlusion of tomorrow's adults.

     By the time many adults enter the healthcare system, there may already be a significant amount of atherosclerotic changes; however, the process of atherosclerosis may be reversible. There is an abundant amount of data from animal research and, to a lesser extent, human research that shows atherosclerotic lesions can and do regress with modifications in lifestyle and medication use.

     With lifestyle and behavior changes, there is a decrease of fatty streaks and plaque in the intracellular lipids. Additionally, as cells of the plaque diminish in size and shape, and the extracellular lipids and necrotic debris are cleared, the fibrous cap remodels itself and flattens out. Eventually, the endothelial damage associated with the overlying fibrous cap heals and the lumen of the vessel returns to a more traditional size and shape. While this is not a "cure" per se, nor is it a very effective means of management in patients with extremely severe atherosclerosis, it is an endpoint worth striving for in the millions of people afflicted with the disease. Patients' arteries may not be returned to those of their adolescent years, but any improvement in distal blood flow, especially with coronary and cerebral atherosclerosis, can have a significant impact on the patient's quality of life and life expectancy.

Clinical Application
     The patient with any form of arteriosclerosis is one who is at risk for perfusion emergencies distal to the afflicted arterial site. With the changes that occur to the lumen of the blood vessel, the prehospital care provider can start to anticipate what type of emergencies may arise. Since these disease processes, especially atherosclerosis, are so widespread, understanding the type of conditions that could arise from this vascular pathology may allow the clinician to better recognize signs and symptoms and provide effective and accurate emergency care.

Arterial Stenosis
     If the lumen of a blood vessel is becoming narrowed from the disease, then blood flow distal to the site of arterial stenosis will be negatively affected. While this is not a significant problem in the aorta, due to its larger size, it can become problematic in smaller arteries. More common is stenosis of the iliac and femoral arteries. The decrease in perfusion to the legs may result in delayed wound healing, skin ulcerations and increased risk of infection. As an example, the chronic diabetes patient may suffer ulcerated lower extremities, have toes surgically removed due to gangrene, and lose sensation as nerve fibers fail from a lack in perfusion.

     Tissue that is extremely sensitive to low perfusion states will be the first to malfunction. In the brain, stenosis of vessels can precipitate a progressive deterioration in mental capability (memory loss, confusion, impaired cognition). In the kidneys, renal artery stenosis can cause renal ischemia, which triggers a cascade of events that result in fluid retention and increases in blood pressure. Over time, there is development of renal-induced hypertension, termed renovascular hypertension, that further hastens the atherosclerotic process and wears away other organs of the body. Even the heart is subject to this stenotic process. With coronary artery stenosis, the heart will not receive enough oxygenated blood to meet the myocardial demand, typically resulting in chest pain. Stable angina is due to coronary artery stenosis.

Weakening Arteries
     Emergencies can also arise from a weakened blood vessel. The enlarging atherosclerotic plaque can result in diminished blood flow to the intima and media layers of the blood vessels. The drop in perfusion over time can weaken the blood vessel to the point that the layers may start to separate, the arterial walls may weaken, or, worst of all, arterial vessels may rupture.

     An abdominal aneurysm is one such emergency caused by a weakening aorta. With detrimental changes in the aortic wall integrity from atherosclerosis, the vessel may balloon out as the systolic pressure continues to make the aneurysm larger, with only the adventitia layer of the blood vessel keeping the artery intact. The vessel may rupture, oftentimes with fatal hemorrhage into the abdominal cavity.

     An aneurysm can also occur in the brain, commonly called a berry aneurysm, when the wall of the cerebral blood vessel weakens and pouches out. If the aneurysm ruptures, the patient is said to have had a hemorrhagic stroke. The problem is not the hemorrhage resulting in hypovolemia; rather, it is rapid hemorrhage into the surrounding delicate tissue confined within a rigid skull that does not allow for any significant space-occupying lesion to expand. Compression of brain tissue and an increase in intracranial pressure may result in a decrease in brain tissue perfusion, herniation and neurologic dysfunction.

Thrombosis and Embolism
     An additional complication that can arise from the atherosclerotic disease process is the formation of a thrombus or embolism. The advance of plaques further into the lumen of the blood vessel causes turbulent blood flow and favors attachment of platelets in and around the plaque. Development of a thrombus may result in total occlusion of an already stenotic artery. Fatal myocardial infarction is commonly due to the rapid development of a thrombus at the site of a ruptured plaque in a coronary artery. Use of fibrinolytics to deconstruct the newly formed thrombus is one of the most important therapies in reducing MI mortality rates. This is why it is so important to gather a good SAMPLE history, complete a fibrinolytic checklist and transport the patient to the hospital expeditiously. The same progression of a thrombus in the coronary artery resulting in a myocardial infarction can also occur in cerebral blood vessels. Development of a thrombus in a cerebral vessel will result in a thrombotic stroke, which is a subcategory of ischemic strokes. In ischemic stroke, there is permanent damage to distal brain tissue.

The same plaque that is implicated in thrombus formation is also a factor in embolic development. The plaque, as it extends into the lumen of the blood vessel, is commonly irregularly shaped. As it distorts the blood flow, the turbulence may cause a piece of the plaque to detach or may release necrotic debris into the blood. In either case, the material can travel downstream and result in occlusion of a smaller distal artery or capillary bed. Even though the distal artery may not have any atherosclerotic changes itself, it may become occluded due to the proximal plaque debris that has broken off and formed an embolism.

     The embolism can result in organ dysfunction and tissue death. Common emergencies known to prehospital providers from this pathology include pulmonary embolism (where a pulmonary vein becomes occluded from an embolism) or embolic stroke. In both conditions, distal perfusion deficits may result in cellular dysfunction and possible tissue death. A dislodged embolism could also occlude a distal coronary artery, causing a myocardial infarction.

Management Considerations
     With vascular diseases, it is important to remember that the pathogenesis causing the emergency is not what your management is aimed at correcting. The arteriosclerotic damage cannot be treated in the prehospital environment with a specific drug or intervention; rather, it is the end organ dysfunction that determines prehospital emergency care. Following are some common emergencies that occur as a result of vascular disease.

     Myocardial infarction is one of the more common emergencies seen in the prehospital environment. EMS providers should be aware of the typical and atypical presentation of symptoms and remember that management is geared toward improving myocardial oxygenation and coronary blood flow. This is achieved by early administration of high-flow oxygen, nitroglycerin and aspirin. Establish intravenous access prior to medication administration. A 12-lead ECG should be acquired to identify ischemic areas of the heart. Administration of nitroglycerin or morphine in a patient with a right-sided myocardial infarction may result in significant hypotension. Additional management may include completing a fibrinolytic checklist.

     Stroke is another complication of arteriosclerosis. This patient may present with a sudden or gradual onset of cognitive, motor or sensory deficits. Prehospital management includes diligent airway control, administration of oxygen, ventilatory support if breathing is inadequate and intravenous access. Hypertension management is typically not a prehospital consideration, since the true pathophysiology of the stroke is not able to be identified. Lowering systolic blood pressure may result in a decrease in cerebral perfusion pressure in the ischemic stroke. EMS providers should perform a stroke fibrinolytic checklist and protect any weak or paralyzed limbs.

     An aortic aneurysm is a life-threatening emergency, especially if the weakened aortic wall has burst. The aorta is the largest artery in the body, and the blood is under tremendous pressure; thus, significant blood loss can occur quickly with resultant hypoperfusion and severe hemorrhagic shock. The patient may be alert or unresponsive, depending on the amount of blood loss and cerebral perfusion status. If an aortic aneurysm is suspected, and especially if the patient exhibits signs and symptoms of hypovolemic shock, transport quickly to a hospital with immediate surgical capabilities. The patient should be well oxygenated and receive assisted ventilation if respirations are inadequate. The volume depletion can be initially managed with crystalloid intravenous fluids; however, be cautious not to overhydrate the patient or dramatically increase the systolic blood pressure. The goal should be to maintain perfusion of the heart, brain, lungs and kidneys, but not cause any newly formed clot to rupture. Generally, maintain a systolic blood pressure at 70-90 mmHg.

     Aortic dissection is a less common, but equally lethal, vascular emergency. The patient with a dissection may present with sharp tearing pain in the substernal or precordial regions, or between the shoulder blades; however, this symptom is not experienced by all patients. The patient may also have a difference in the amplitude in pulses in upper extremities, complain of blindness, exhibit neurological signs or symptoms, and present with significant pulmonary edema. The goal of prehospital management is to provide a high concentration of oxygen, ventilatory support if needed and intravenous access. If the patient is hypertensive with a normal or tachycardic heart rate, beta blocking agents may be used to reduce cardiac output and blood pressure to potentially reduce progression of the dissection. If the patient has an elevated blood pressure and is bradycardic, beta blockers are contraindicated. A rapid-acting vasodilator, such as sodium nitroprusside, may be used.

CEU Review Form Vascular Emergencies (PDF)Valid until May 4, 2007

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Randall W. Benner, Med, MICP, NREMT-P, is an instructor in the Department of Health Professions at Youngstown (OH) State University. He currently serves as the director of the Emergency Medical Technology Program at Youngstown.

Joseph J. Mistovich, Med, NREMT-P, is a professor and chair of the Department of Health Professions at Youngstown (OH) State University.

Daniel D. Limmer, AS, EMT-P, is a paramedic with Kennebunk Fire-Rescue in Kennebunk, ME, and EMS Program Coordinator at York County Community College in Wells, ME.

William S. Krost, BSAS, NREMT-P, is an operations manager and flight paramedic with the St. Vincent/Medical University of Ohio/St. Rita's Critical Care Transport Network (Life Flight) in Toledo, OH.