February 9, 2015 - Twin Cities Health Professionals Education
TCHP Education Consortium You must print out your own course materials! None will be available at the class. Click on the link below to access: www.tchpeducation.com/coursebooks/coursebooks_main.htm If the link does not work, copy and paste the link (web page address) into your internet browser. Available 1 week prior to class. Cardiovascular Critical Care February 9th, 2015 7:30 a.m. to 4:00 p.m. Minneapolis VA Simulation Center (Building in the parking lot North of the hospital) Please read driving and parking directions carefully Description/Purpose Statement Cardiac and vascular diseases are becoming more and more common in American society. Critical care nurses routinely see patients with a wide variety of cardiovascular problems. The purpose of this class is to learn how to assess and care for the patient experiencing problems such as angina, myocardial infarction, peripheral vascular disease, hypertension, congestive heart failure, cardiomyopathy, and cardiogenic shock. Simulation will be provided to reinforce course content. Target Audience/Prerequisite This class was designed for the novice critical care or telemetry nurse; however, other health care professionals are welcome to attend. Before You Come to Class You must complete the Cardiovascular Critical Care Primer and the Shock and Infection in Critical Care Primer. Please bring your primer post-tests to class with you for processing. Schedule 7:30 - 7:45 a.m. 7:45 - 9:15 a.m. 9:15- 9:30 a.m 9:30 – 10:00 a.m. 10:00 a.m. -12:00 p.m. 12:00 - 12:45 p.m. 12:45 - 1:45 p.m. 1:45 - 2:00 p.m. 2:00 – 4:00 p.m. Registration Hypertensive Urgencies and Emergencies; Vascular Disease Break Congestive Heart Failure and Cardiomyopathies Acute Coronary Syndrome (ACS) Lunch Cardiogenic Shock and SVO2 Break Cardiac Simulations and Debriefing Cleo Bonham Cleo Bonham Robin Rabey Robin Rabey Robin Rabey /Cleo Bonham Continuing Education Credit For attending this class, you are eligible to receive: 8.4* or 7.00** contact hours (see below). If you complete the primer for this class, you are eligible to receive an additional: 2.0* or 1.66** contact hours per primer (see below). Criteria for successful completion: All participants must attend the program and complete verification and evaluation forms to receive contact hours. If you are an ANCC certified nurse, you must attend the ENTIRE activity to receive contact hours and complete the application process with TCHP. The Twin Cities Health Professionals Education Consortium is an approved provider of continuing nursing education by the Wisconsin Nurses Association, an accredited approver by the American Nurses Credentialing Center's Commission on Accreditation. Criteria for successful completion for all: You must read the primer, complete the post-test and evaluation, and submit it to TCHP for processing. If you are an ANCC certified nurse, you must complete the application process with TCHP. *Denotes contact hours used for renewing licensure with the MN Board of Nursing or other Board that uses a 50 min/contact hour formula. These contact hours will be issued unless you request contact hours that comply with the ANCC formula. **Denotes contact hours used for renewing Nursing Certification with ANCC or other organization that uses the formula of 60 min/contact hour. You must request these contact hours if you need them. Please Read! • • • • • • • Check the attached map for directions to the class and assistance with parking. Certificates of attendance will be distributed at the end of the day. You should dress in layers to accommodate fluctuations in room temperature. Food, beverages, and parking costs are your responsibility. If you are unable to attend after registering, please notify the Education Department at your hospital or TCHP at 612-873-2225. In the case of bad weather, call the TCHP office at 612-873-2225 and check the answering message to see if a class has been cancelled. If a class has been cancelled, the message will be posted by 5:30 a.m. on the day of the program. More complete class information is available on the TCHP website at www.tchpeducation.com. Directions to the Minneapolis VA Simulation Center, Building 68, Entry Door 68-2, Room 227, One Veterans Drive, Minneapolis, MN 55417 The VA Simulation Center is located on the second floor of Building 68 in Room 227 Please allow at least TEN minutes to get to the classroom from either the hospital or parking lots. Driving Directions th Take Hwy. 55 to 54 Street and go west. Go past the stop sign on Minnehaha and turn left at the second entrance into the VA parking lot. Visitors should park in Lot 11 (overflow lot) or in Lots 9 or 10. Parking Directions Head towards the building which is northwest of the hospital. Enter using the southeast entrance that faces parking Lot 7. The door is to the right of the smoking shelter (“68-2” sign located above the door). The northwest entrance is for the daycare—do not go in this door. Entry to the second floor is only available through the stairwell or elevator. Walk through the door directly across from the elevator to the end of the hall to room 227. There is a light rail station in front of the Minneapolis VA Health Care System. Check http://www.metrotransit.org/light-rail for information on taking the light rail. NOTE: There is not a cafeteria in this building. Please bring refreshments (snacks and drinks) for break time and consider packing a lunch so that you don’t need to walk to and from the hospital. There is not a refrigerator available. Dress in layers to accommodate fluctuations in temperature. Doors to the Simulation Center Room will not be open until approximately 7:30 a.m. Doors to the building should be open by 7:00 a.m. Map of surrounding roads to the Minneapolis VA Health Care System: Sim. Center More detailed driving directions: th From the East (St. Paul): Take 35E south to West 7 /Highway 5 exit. Turn right at the top of the exit ramp. Continue on 5 to the Fort Snelling exit and stay to the right as you follow the exit around. You will “Y” into traffic coming from the Mendota Bridge. Move to the right and exit on 55 west. As you exit on 55 west, it will “Y” almost immediately. Stay th to the right and go to the next stoplight (54 ) and turn left.* From the Southeast: Take 35E to 110 west. Take the 55 west/Fort Snelling exit. Go to the far righthand lane as soon as you exit to continue on 55 west. Go over the Mendota Bridge, move to the right lane and exit to follow 55 th west. As you exit on 55 west, it will “Y” almost immediately. Stay to the right and go to the next stoplight (54 ) and turn left.* From the North: Take 35W south to 62 east. Get into the right lane on 62 and exit on 55 west. At the top of the exit nd th ramp, turn left to continue on 55 west. Go to the 2 stoplight (54 ) and turn left.* From the South: Take 35W north to 62 east. Get into the right lane on 62 and exit on 55 west. At the top of the exit nd th ramp, turn left to continue on 55 west. Go to the 2 stoplight (54 ) and turn left.* From the West: Take 494 east to 35W north. Take 62 east. Get into the right lane on 62 and exit on 55 west. At the nd th top of the exit ramp, turn left to continue on 55 west. Go to the 2 stoplight (54 ) and turn left.* *Go past the stop sign on Minnehaha and turn left at the second entrance into the VA parking lot. Visitors should park in Lot 11 (overflow lot) or in Lots 9 or 10. TCHP Education Consortium This home study is pre-reading for a class. Please complete this activity and bring your post-test and evaluation to class with you. Cardiovascular Critical Care Primer © 2000 TCHP Education Consortium. Revised 2007, 2010, 2014 This educational activity expires March 27, 2015 All rights reserved. Copying, electronic transmission and sharing without permission is forbidden. Introduction/Purpose Statement Cardiac and vascular diseases are becoming more and more common in American society. Critical care nurses routinely see patients with a wide variety of cardiovascular problems. The purpose of this home study is to increase your understanding of the anatomy, physiology, and pathophysiology of problems such as angina, myocardial infarction, peripheral vascular disease, congestive heart failure, and cardiomyopathy. Target Audience This home study was designed for the novice critical care or telemetry nurse. However, other health care professionals are invited to complete this packet. participating in the planning, writing, reviewing, or editing of this program are expected to disclose to TCHP any real or apparent relationships of a personal, professional, or financial nature. There are no conflicts of interest that have been disclosed to the TCHP Education Consortium. Expiration Date for this Activity: As required by ANCC, this continuing education activity must carry an expiration date. The last day that post tests will be accepted for this edition is March 27, 2015—your envelope must be postmarked on or before that day. Planning Committee/Editors* *Linda Checky, BSN, RN, MBA, Program Manager for TCHP Education Consortium. Content Objectives 1. 2. 3. 4. 5. 6. 7. *Lynn Duane, MSN, RN, Assistant Program Manager for TCHP Education Consortium. Identify the normal anatomy and physiology of the cardiovascular system. Describe the pathophysiology of an acute myocardial infarction. Describe the symptoms of heart failure. Describe the pathophysiology of tamponade. Identify the factors that favor the development of a venous thrombosis. Differentiate between dilated, hypertrophic, and restrictive cardiomyopathy. Differentiate between Buerger’s Disease and Raynaud’s Syndrome. Authors Marie Langer, RN, MA, CCRN, Staff Nurse in the CICU at Regions Hospital. Karen Poor, MN, RN, Former Program Manager for the TCHP Education Consortium. Content Experts/Reviewers Disclosures In accordance with ANCC requirements governing approved providers of education, the following disclosures are being made to you prior to the beginning of this educational activity: Requirements for successful completion of this educational activity: In order to successfully complete this activity you must read the home study, complete the post-test and evaluation, and submit them for processing. Conflicts of Interest It is the policy of the Twin Cities Professionals Education Consortium to balance, independence, and objectivity educational activities sponsored by TCHP. Robin Rabey, MSN, RN, Critical Care Educator at the Minneapolis VA Health Care System. Cleo Bonham, MSN, RN, Critical Care Educator at the Minneapolis VA Health Care System. Colleen Johannsen, RN, Staff Nurse in the Heart and Vascular Care Unit at Regions Hospital. Marie Langer, RN, MA, CCRN, Staff Nurse in the CICU at Regions Hospital. *Robin Rabey, MSN, RN, Critical Care Educator at the Minneapolis VA Health Care System. Sharon Stanke, MSN, RN, Critical Care Educator at the Minneapolis VA Health Care System. *Denotes reviewer of current edition Health provide in all Anyone Cardiovascular Critical Care Primer © 2000 TCHP Education Consortium; 2014 edition Page 1 Contact Hour Information For completing this Home Study and evaluation, you are eligible to receive: 2.0* or 1.66** contact hours (see below) Criteria for successful completion: You must read the home study packet, complete the post-test and, evaluation, and submit them to TCHP for processing. The Twin Cities Health Professionals Education Consortium is an approved provider of continuing nursing education by the Wisconsin Nurses Association, an accredited approver by the American Nurses Credentialing Center’s Commission on Accreditation. *Denotes contact hours used for renewing licensure with the MN Board of Nursing or other Board that uses a 50 min/contact hour formula. These contact hours will be issued unless you request contact hours that comply with the ANCC formula. **Denotes contact hours used for renewing Nursing Certification with ANCC or other organization that uses the formula of 60 min/contact hour. You must request these contact hours on the evaluation form if you need them. Please see the last page of the packet before the post-test for information on submitting your post-test and evaluation for contact hours. Cardiovascular Critical Care Primer © 2000 TCHP Education Consortium; 2014 edition Page 2 Peripheral Vascular Disease As opposed to cardiac or cerebrovascular disease, peripheral vascular disease refers to problems within the blood vessels in the extremities, thorax, and abdomen. The majority of peripheral vascular disease problems are caused by atherosclerosis, just like cardiac and cerebral vascular disease. Arterial Vascular Disease There are three major problems that can arise in the arterial vasculature: atherosclerotic occlusion, aneurysm, and embolization. femoral) are related to the lack of arterial flow. The distal extremity becomes cool, pale or cyanotic, with poor or absent pulses. Pain often accompanies arterial insufficiency because the distal tissues are starved for oxygen. The symptoms of carotid arterial insufficiency result from brain anoxia – ranging from transient ischemic attacks to completed stroke. Bruits are common in both ileofemoral and carotid artery insufficiency. A bruit is the sound that is heard when the pressure in the vessel prior to the lumen narrowing is high, and the pressure after the narrowed area is low. The resulting turbulent blood flow causes a low-pitched “whooshing” sound. Aneurysm Atherosclerosis Atherosclerosis – or arteriosclerosis in the artery – is the primary cause of all vascular problems in the United States. In this process, there is a gradual build up of plaque on the intimal wall of the artery caused by repeated injury, clotting, and scarring. Problems in the arterial system arise when the amount of plaque build up has grown to such as an extent that blood is no longer able to pass easily through the narrowed arterial diameter. This is called arterial insufficiency. When blood cannot pass through at all, it is called arterial occlusion. Normal cross-section of an artery Beginning of atheroma Partial occlusion with clot formation An aneurysm is a weak area in an arterial wall. This weakening can be caused by hypertension, atherosclerosis, smoking, or may be congenital. There are three layers of the artery: the intima, the media, and the adventitia. Intima Adventitia Media While there is initially just a weakening in the media of the arterial wall, eventually pressure will build up and cause the weakened area of the artery to begin to balloon. There are two main types of aneurysms: Saccular and fusiform. Fusiform aneurysms appear as a nearly symmetrical bulge around the circumference of the weakened area of the affected vessel. Saccular aneurysms appear as a blister on one side of the vessel. They may be caused by trauma, such as a motor vehicle crash. Occluded vessel Fusiform aneurysm Although the most common sites of arterial insufficiency and occlusion are the carotid, renal, popliteal, aortoiliac and femoral arteries, any junction or branching area can develop problems. The symptoms of arterial insufficiency or occlusion in the arteries that supply the legs (popliteal, aortoiliac, and (side view of an artery) There is a large dilation of the artery closest to the heart with a gradual narrowing. Cardiovascular Critical Care Primer © 2000 TCHP Education Consortium; 2014 edition Page 3 Saccular aneurysm reaches a branch through which it cannot travel.. At that point, the embolus will block blood flow distal to the occlusion. (side view of an artery) There is an outpouching on one side of the artery Venous Vascular Disease The most common form of vascular disease related to the venous system is the development of deep vein thrombosis. Typically found in the lower extremities (particularly the calves), a thrombus occludes venous return to the heart. Pressure backs up from below the thrombus, causing edema to form distal to the occlusion. Many aneurysms lie dormant without symptoms for years. Other aneurysms can continue to grow in size until their mass causes symptoms or they rupture. Although any artery can develop an aneurysm, the most dangerous ones are in the aorta. The aorta is the major artery in the body. It branches from the left ventricle and traverses down through the thorax (thoracic aorta) and the abdomen (abdominal aorta), giving off branches to supply all of the body organs with blood. Symptoms from an aortic aneurysm may include dyspnea, stridor, hoarseness, hemoptysis, cough, or chest pain. All of these symptoms are related to the mass of the aneurysm impinging on other organs. Pain is the main symptom of descending thoracic aortic aneurysm: pain in the shoulder, lower back, abdomen, shoulders, arms, or neck. Finally, abdominal aneurysms usually have no symptoms until they leak or rupture. Leaking or rupture of an aortic aneurysm is usually a lifethreatening emergency. If the wall is weakened enough, the aneurysm will rupture, resulting in aortic blood being pumped into either the chest or abdominal cavity. The patient may bleed to death (exsanguinate) in a very short time. More commonly, patients who complain of severe, unrelenting pain, shortness of breath, faintness, etc., may be experiencing the leaking of blood from the aneurysm. Similar to aneurysms, an aortic dissection is more common than an aortic aneurysm rupture. A dissection is said to occur when there is a longitudinal split between the intima and the media of the thoracic aorta. A dissection may occur after trauma, or due to Marfan’s syndrome, increasing age, hypertension, or atherosclerosis. Embolization The third cause of peripheral vascular insufficiency is embolism. An embolus can begin as either a clot formed in the heart or as a piece of dislodged plaque. An embolus will travel through the arterial system until it Cardiovascular Critical Care Primer © 2000 TCHP Education Consortium; 2014 edition Page 4 The first stage of deep vein thrombosis (DVT) formation is injury. The second stage is intravascular clot formation. If that clot (thrombus) does not become detached and form an embolus, it will adhere to the vein wall within 24-48 hours and eventually be lysed. The three components needed to cause a DVT are defined in Virchow’s triad: 1. Hypercoagulability of the blood: blood dyscrasias, trauma, cancer, estrogen therapy, systemic infection, smoking 2. Venous stasis: heart disease (CHF), dehydration, immobility, incompetent leg vein valves 3. Intimal damage: trauma, infection, venipuncture, IV infusion of irritant solutions. Buerger’s Disease and Raynaud’s Syndrome Buerger’s Disease, or Thromboangiitis Obliterans, (TOA) is a rare condition that presents as an inflammation and eventual blockage of the small vessels of the extremities. In rare cases, internal organs are affected. Unlike other vascular diseases, it is neither an embolic nor an atherosclerotic disease. The classic patient is a 20-40 year old smoker, usually male. Non-smoking tobacco users are at risk as well. There is likely a genetic component to it, as it is far more prevalent in certain ethnic groups. TOA is characterized by reduced blood flow to the extremities, with collateral circulation developing in an ineffective corkscrew pattern (visible on angiogram). Symptoms are related to lack of blood flow: coldness of the extremity, intermittent claudication (pain or cramping that occurs in the legs when walking), and numbness, tingling, and burning sensations. Symptoms start at the tips of the fingers and toes and progress upward. As the disease progresses, there is ulceration of the tips of the digits, and eventually gangrene. Amputation of the digits can only be avoided by abstaining from all forms of tobacco. Exposure to cold worsens the symptoms. The extremity is sensitive to loss of blood flow caused by elevation above the level of the heart. Care to avoid cold and constricting medications is important. Treatments such as sympathectomies, (a surgical procedure that destroys nerves in the sympathetic nervous system provide only temporary relief, as do vasodilating drugs). The cause is unknown, but tobacco is thought to be a trigger for an autoimmune or inflammatory process. TOA is often accompanied by Raynaud’s Syndrome. Treatment is generally aimed at control of symptoms. This involves avoiding offending drugs, including caffeine and tobacco. Protection of the extremities by keeping warm in cold weather and when handling cold and frozen objects can prevent attacks. Patients also need to be aware that significant cooling after exercise can trigger an attack, making it important to cool down slowly. Some drugs, such as topical nitroglycerin, Viagra, ace inhibitors, and calcium channel blockers may relieve symptoms. Open wounds, blackening of the skin, breaks in the skin, and joint soreness surrounding the affected areas need to be evaluated and treated. Figure 2 Raynaud's Syndrome (eMedicine.com) Figure 1: Buerger’s Disease with thrombophlebitis of the great toe. (emedicine.medscape.com) In Raynaud’s Syndrome, the arterioles of the extremities constrict in response to exposure to cold or stress. There is a cyclical response, with the fingers, toes, and the tips of the nose and ears turning pale due to lack of blood flow. As oxygen is consumed, the color turns to bluish. Then, as the arterioles relax and blood refills, the extremity becomes flushed, and then returns to normal color. Attacks may last minutes or hours. Primary Raynaud’s occurs with no associated cause, and is generally a milder form, with little pain. Secondary Raynaud’s may be associated with vasoconstricting drugs, frostbite, repetitive motion or vibration injury, smoking, or thoracic outlet syndrome. Secondary Raynaud’s is more painful and may also be associated with Buerger’s disease. Hypertension & Hypertensive Crisis Mr. Jerome Atwater enters the Emergency Department with complaints of headache, dizziness, and chest pain. He has a 30 year history of hypertension. His initial vital signs are: HR of 145, sinus tachycardia; BP of 210/138 mm Hg; RR of 24/minute. The initial diagnosis is hypertensive crisis. What is blood pressure? The arterial blood pressure is the pressure within the arteries that drives blood into the circulation. The blood pressure is determined by the cardiac output multiplied by the systemic resistance. There are three main elements to blood pressure: Cardiovascular Critical Care Primer © 2000 TCHP Education Consortium; 2014 edition Page 5 The systolic blood pressure (SBP) is the pressure in the arteries that occurs with ejection from the left ventricle. The diastolic blood pressure (DBP) is the pressure that has been “stored up” in the arteries during the relaxation of the heart. The sympathetic nervous system (SNS) maintains the muscle tone in the arteries. The mean arterial pressure (MAP) is the average blood pressure in the systemic circulation. vasoconstricts the blood vessels and stimulates the kidneys to reabsorb water. Hypertension is defined as... Although definitions may vary, the American Heart Association defines hypertension as a consistently elevated blood pressure of > 140 mm Hg systolic and/or > 90 mm Hg diastolic. What causes hypertension? How is blood pressure controlled? There are many mechanisms that work to control the blood pressure. Baroreceptors: receptors in the aortic arch and carotid artery bodies that are sensitive to pressure. Stimulation of these receptors occurs with either a low or high BP. Information sent to the medulla results in a change in the heart rate and vascular tone of the arteries. Chemoreceptors: situated near the baroreceptors, chemoreceptors are sensitive to changes in the pH, PaO 2, and PaCO2. The chemoreceptors are stimulated when the PaCO2 rises and when the pH and PaO2 falls with hypotension. Information is sent to the medulla. Autonomic nervous system: The parasympathetic nervous system decreases cardiac output (CO) and BP by decreasing the heart rate. The sympathetic nervous system increases the CO by increasing the heart rate and cardiac contractility, and by vasoconstricting the blood vessels, thus increasing BP. Renin-Angiotensin-Aldosterone system: Renin is released by the kidneys in response to a decrease in blood pressure. Renin combines with angiotensinogen to form angiotensin I, which is then converted to angiotensin II. Angiotensin II causes massive vasoconstriction and stimulates aldosterone. Aldosterone causes the kidney tubules to reabsorb water and sodium. Renal prostaglandins: These hormones weaken the action of the renin-angiotensin-aldosterone system. Vasopressin: Also known as antidiuretic hormone (ADH), vasopressin is released with a decrease in blood volume or an increase in serum osmolality. It Cardiovascular Critical Care Primer © 2000 TCHP Education Consortium; 2014 edition Page 6 Ninety to ninety-five percent of hypertension is called “primary” or “essential” hypertension. There is no known cause for primary hypertension. Risk factors that are suspected in the development of primary hypertension are: Family history Advancing age Race High sodium intake Obesity Excess alcohol consumption Low intake of potassium, calcium, magnesium Stress Use of oral contraceptive drugs The remaining cases of hypertension are lumped into the category of “secondary hypertension.” Causes for this type of hypertension include renal disease, arteriosclerosis, coarctation of the aorta, pheochromocytoma, elevated levels of adrenocortical hormones, and brain lesions. Why is hypertension harmful? The main problem with hypertension is that it places a larger burden on the heart and blood vessels than they are built for. The workload of the heart increases because it has to pump harder against resistance to push blood out. This leads to ventricular muscle hypertrophy, which increases myocardial oxygen demand. Eventually the oxygen demand outstrips the supply, leading to angina, myocardial infarction, and congestive heart failure. The arteries throughout the body are also affected by hypertension. Hypertension appears to speed the development of atherosclerosis, affecting the coronary arteries and renal vasculature. An elevated blood pressure can also cause an outpouching in a weak part of an arterial wall. This outpouching is called an aneurysm. Aneurysms can occur in any blood vessel in the body; especially the aorta, the retina, and the brain. What is occurring with Mr. Atwater? Mr. Atwater is experiencing a hypertensive crisis. Hypertension is a “crisis” when the diastolic BP increases above 120 mmHg, and when there is organ damage. It is generally accompanied by renal disorders, vascular changes and retinopathy. The extremely high pressure causes an intense reflex vasoconstriction in the brain, in the brain’s attempt to preserve itself. This measure is often not successful, and cerebral edema develops, causing papilledema (swelling of the optic nerve at the point of its entrance into the eye), headache, restlessness, confusion, stupor, motor and sensory deficits, and visual disturbances. The continued high BP injures the walls of the arterioles, especially in the kidney and retina. Retinal hemorrhage and kidney failure occur as a result. Cardiomyopathy What is cardiomyopathy? Cardiomyopathy is a term that is used to describe a problem with the functioning of the heart muscle. There are three forms: 1. Dilated (congestive) 2. Hypertrophic 3. Restrictive to dilated cardiomyopathy, sometimes called alcoholic cardiomyopathy. Other potential causes: pregnancy, viral infections, certain chemotherapy drugs, and a hereditary disposition. What causes the signs and symptoms of dilated cardiomyopathy? Some people with dilated cardiomyopathy can live for a long time without symptoms. When symptoms do begin, however, they resemble those of congestive heart failure. As the left heart fails, the left ventricle is not able to pump out the blood that is filling it. The pressure in the left ventricle rises, eventually causing fluid to back up into the pulmonary system. As the pressure in the pulmonary system rises, fluid is forced out of the capillary bed into the alveoli. Pulmonary edema ensues, with shortness of breath, cough with frothy or blood tinged sputum, and crackles bilaterally. As the right heart fails, the right ventricle cannot pump out its share of blood, leading to increased pressure in the venous system. Fluid is forced out of the venous system into the peripheral circulation, causing edema of the extremities. People with dilated cardiomyopathy can also develop cardiac dysrhythmias, particularly atrial fibrillation and ventricular dysrhythmias. Dilated Cardiomyopathy Hypertrophic Cardiomyopathy Dilated cardiomyopathy is the most common form of cardiomyopathy. In this form, the heart muscle fibers are stretched beyond their normal size. This stretching causes the heart chambers to become dilated and the walls of the heart to become thinner. The stretched muscle fibers are not able to contract well, resulting in poor cardiac contractility and inadequate ejection of blood. This eventually leads to increased dilation, and eventually, to congestive heart failure. Hypertrophic cardiomyopathy is the second most common form of cardiomyopathy. In this type of cardiomyopathy, there is an abnormal overgrowth of muscle fibers, leading to decreased ventricular chamber size and increased ventricular wall size. As the cardiomyopathy progresses, there is little room for blood in the ventricles, and limited relaxation of the ventricles during diastole, causing a decreased amount of blood to be pumped into the circulation with each beat. See how the ventricles are enlarged and the walls surrounding them are thin? Note how the ventricle chamber size is about the same as the atrial chamber size (much too small) and the walls of the ventricle are very thick. What are the causes of dilated cardiomyopathy? The majority of cases of dilated cardiomyopathy are idiopathic – that is, no one knows why they have developed this condition. Alcohol abuse has been linked Another name for hypertrophic cardiomyopathy is hypertrophic obstructive cardiomyopathy (HOCM). Cardiovascular Critical Care Primer © 2000 TCHP Education Consortium; 2014 edition Page 7 What are the causes of hypertrophic cardiomyopathy? About 50% of all cases seem to be related to a genetic abnormality transmitted by one or both parents. The other cases do not have an identifiable cause. Hypertrophic cardiomyopathy is not caused by exercise; the conditioned heart has more muscle mass, but the ventricular chamber size remains adequate, as does the ability to contract and relax. What are the signs and symptoms caused by? The cause of the symptomology of hypertrophic cardiomyopathy is related to inadequate stroke volume (the amount of blood pumped out of the left ventricle with each contraction). The patient’s heart rate may be normal or even fast, but the patient cannot get enough blood to the vital organs. Symptoms arising from inadequate blood supply are: shortness of breath, fainting during activity, palpitations, chest pain, or fatigue. Ventricular fibrillation can be the first indicator of a problem, and may lead to sudden death. Congestive Heart Failure Mr. Wood enters the hospital after a three-day history of chest pain. The EKG indicates that Mr. Wood has had an anterior wall MI. The day after admission, Mr. Wood begins to show the signs and symptoms of heart failure. He is hypotensive and tachycardic, with a respiratory rate of 26. His respirations are labored; rales are auscultated in the middle and lower lobes of his lungs. He is anxious. What is heart failure? The term “heart failure” indicates that the heart has been damaged so that it does not pump blood adequately, causing decreased tissue perfusion and back up into the peripheral circulation. Although heart failure can be classified as left or right in etiology, the failure of one side of the heart usually leads to failure on the opposite side. The pathophysiology for both left and right heart failure is the same, as shown below: As the condition progresses to the severe stage, congestive heart failure results as the pressure in the heart rises to such an extent that blood “backs up” into the lungs and periphery. Heart pumps ineffectively Blood backs up into the venous system There is insufficient blood going to the tissues Venous pressure increases Kidneys retain sodium and water Capillary pressure Blood volume Restrictive Cardiomyopathy Restrictive cardiomyopathy is rare in the United States. In this case, there is no chamber size or ventricle wall size change; rather, the walls of the ventricle become stiff and noncompliant. Abnormal tissue, caused by amyloidosis, hemochromatosis, or sarcoidosis, invades the walls of the ventricle, causing the contractility to be compromised. The chamber and wall sizes are normal; however, the wall itself is rigid and noncompliant. Fluid leaks from the capillaries into the tissues Edema develops The signs and symptoms of restrictive cardiomyopathy are essentially the same as dilated cardiomyopathy: weakness, fatigue, shortness of breath, edema, nausea and bloating. Tissues become hypoxic What is the route of blood through the heart? The right side of the heart is a low pressure, high capacity venous system. Blood enters the right atrium from the superior and inferior vena cava. Passive filling and active contraction of the atria pushes the blood through Cardiovascular Critical Care Primer © 2000 TCHP Education Consortium; 2014 edition Page 8 the tricuspid valve into the right ventricle. As the right ventricle fills, it actively expels the blood through the pulmonic valve into the pulmonary artery and into the lungs for re-oxygenation. The renin-angiotensin-aldosterone system is also stimulated, causing further vasoconstriction and the retention of water and sodium. Rales and Respiratory Rate The left side of the heart is a high pressure arterial system whose size is regulated by different muscle walls. Arteries have the ability to dilate and constrict as stimulated by the sympathetic nervous system in a response to baroreceptor reflexes, oxygenation status, presence of hypercarbia, and CNS stimulation. When the blood exits the pulmonary circulation through the pulmonary vein, it enters the left atrium. From the left atrium, the blood is expelled through the mitral valve into the left ventricle, and is then ejected through the aortic valve. The aorta is the gateway into the systemic circulation from the aorta’s origin on the left ventricle. Aorta Superior vena cava Pulmonary artery Left atrium Right atrium Left ventricle Inferior vena cava Right ventricle What are the pathophysiologic mechanisms for Mr. Wood’s symptoms? Hypotension and Tachycardia As Mr. Wood’s heart fails to pump adequately, the baroreceptors located in the aortic arch and carotid bodies sense a decreased blood pressure. This will stimulate the Sympathetic Nervous System (SNS) to release the catecholamines (epinephrine and norepinephrine), which increases the heart rate and the pumping action (contractility) of the heart, and constricts the peripheral blood vessels to attempt to get more blood into the central system. The inadequate pumping of Mr. Woods’ heart causes a backup into the lungs from the left side of the heart. The pressure inside the pulmonary blood vessels increases to such a point that fluid (plasma) escapes into an area of less pressure - the alveoli and smaller airways. This is known as cardiogenic pulmonary edema. Fluid in the airways will “bubble” with respiration, causing the crackling sound of rales. This fluid also impairs gas exchange, which triggers the medulla to increase respiratory rate and effort. Anxiety The decrease in oxygenation from pulmonary edema and the actions of the catecholamines combine to cause anxiety in the heart failure patient. In severe cases, these physiologic mechanisms can cause a feeling of “impending doom.” What signs and symptoms indicate left sided heart failure? All patients with heart failure will exhibit fatigue and weakness, and an S3 and S4 may be auscultated. The patient with left-sided heart failure will exhibit signs that relate to the arterial flow of blood. Symptoms of Left-Sided Heart Failure Anxiety Orthopnea, dyspnea, tachypnea Cough with frothy sputum Diaphoresis Basilar rales, rhonchi Cyanosis, hypoxia, respiratory acidosis Elevated Pulmonary Artery Diastolic Pressure (PA diastolic), Pulmonary Capillary Wedge Pressure (PCWP) Nocturia Mental confusion Pulsus alternans (arterial pulse waveform that has alternating strong and weak beats, and almost always indicates left ventricular systolic impairment) Cardiovascular Critical Care Primer © 2000 TCHP Education Consortium; 2014 edition Page 9 What signs and symptoms indicate right sided heart failure? Right-sided heart failure manifests in the venous side of blood flow. Symptoms of Right-Sided Heart Failure Hepatomegaly / splenomegaly Dependent pitting edema Venous distention, hepatojugular reflux (an alternative method to measure venous pressure through distension of the internal jugular vein) Bounding pulses Oliguria Dysrhythmias Elevated Central Venous Pressure (CVP), Right Atrial (RA), and Right Ventricle (RV) pressures Kussmaul’s sign (A rise in jugular venous pressure on inspiration) Abdominal pain, anorexia, weight gain From the Core Curriculum for Critical Care Nurses, J. Alspach (ed.). Angina and Myocardial Infarction Mr. Caleb Ash presents to his family physician with the complaint of chest pain that “comes and goes.” His physician suspects that Mr. Ash may have angina. He orders a stress test and echocardiogram. What is angina? Angina is a "warning sign" of myocardial damage. Because the heart has no direct pain receptors or messengers, the pain of myocardial ischemia is through nerves sent back to the spinal cord. The spinal cord sends out the urgent pain messages through other spinal nerves, which may manifest as chest pressure; tightness; arm, back or jaw pain; or GI distress may be the patients' symptoms. Whatever manifestation the warning takes, the symptoms are known as "angina." 1. 2. 3. 4. 5. Age: Males > 45 years; Females > 55 years or premature menopause without estrogen therapy History of premature coronary artery disease (CAD) in a first degree relative (parent, sibling) Current cigarette smoking Hypertension > 140/90 or on medication High density lipid (HDL) count < 35 The factor that is “negative” or is likely to subtract another risk factor is: 1. High density lipid (HDL) count > 60 How is angina diagnosed? Mr. Ash’s physician has ordered two of the most common tests for diagnosis of angina. The stress electrocardiogram is a test which combines electrical rhythm monitoring with exertion. The patient is placed on a treadmill or other exercise machine and exercises until either angina is experienced or there are EKG - ST depression/ T wave inversion changes. An echocardiogram is a noninvasive diagnostic test that bounces sound waves from the probe off of the structures below it, i.e., the heart. A visual picture forms on the echocardiogram screen. Cardiac wall movement abnormalities, chamber size, valve function, and blood flow can be assessed using this test. Although the resting echocardiogram was normal, Mr. Ash’s stress test was abnormal. His physician ordered a coronary angiogram for the next week. The most common angiographic procedure done is the coronary angiogram. The term "coronary angiogram" is commonly used to describe a number of diagnostic tests that can be performed in the cardiac catheterization lab. Included in these diagnostic tests are: What causes angina? Left main c. a. Circumflex c.a. Angina is caused by myocardial ischemia. Causes of myocardial ischemia include atherosclerosis, hypertension, anemia, dysrhythmias, shock, congestive heart failure, and coronary artery spasm. Atherosclerosis is the most common cause of myocardial ischemia. Right c.a. Left anterior descending c.a. What are the risk factors for Atherosclerosis? The risk factors that are “positive” or are likely to cause atherosclerosis include: Cardiovascular Critical Care Primer © 2000 TCHP Education Consortium; 2014 edition Page 10 Coronary arteriogram: viewing the coronary arteries through the use of dye Right heart cath: obtaining volumes and pressures in the right heart Left heart cath: obtaining volumes and pressures in the left heart Aortogram: obtaining information about the size, function, and pressure of the aorta Ventriculogram: through the use of dye, obtaining the ejection capability of the heart During the weekend, Mr. Ash had several episodes of angina. On Sunday evening, the angina was not relieved with three nitroglycerin tablets. As instructed by his physician, his wife called 911. Mr. Ash was brought into the Emergency Room, where he was evaluated for an acute myocardial infarction (AMI). What is a myocardial infarction? A myocardial infarction, or MI, is the end result of tissue ischemia. An MI indicates that cells in the myocardium have been anoxic and have died. There are three phases in the evolution of an MI: ischemia, injury, and infarction. In ischemia, the myocardium is deprived of oxygen and/or blood. At this point, if the blood supply or oxygen is returned, the myocardium will return to normal. Injury is the next phase of an MI, where the cells have become damaged from the lack of oxygen. If interventions are started in time, the myocardium will return to normal. Infarction occurs when the cells are deprived of oxygen long enough to die. Infarction is irreparable. Immediately to 7 days after an MI, the infarcted area is "mushy" and friable. The cells are dead, and no longer contract or move. After about seven days, collagen scar tissue forms over the area, making the infarcted region more stable. Stretching of the dead tissue before seven days can lead to either a ventricular aneurysm and rupture or to remodeling (thickening of the muscle) of the expanded area, which will lead to congestive heart failure. What arteries supply the heart? The heart needs oxygenated blood like any other tissue in the body. All of the coronary arterial blood supply arises from two "holes" in the root of the aorta, called coronary ostia. During contraction of the ventricles, the coronary ostia are compressed. Coronary arteries are supplied with blood only during diastole. The right coronary artery arises from the right ostia and is located between the right atrium and right ventricle. The right coronary artery is also known as the RCA. The RCA artery supplies: the sinoatrial node (SA) node in 55% of hearts the atrioventricular node (AV) node in 90% of hearts the RA and RV heart muscle the inferior-posterior wall of the LV For most people, the RCA divides into two branches: the posterior descending artery, which supplies the RV and inferior wall of the LV; and the marginal acute branch, which supplies the inferior surface of the RV. The left coronary artery comes off of the left coronary ostia as the left main coronary artery (LMCA). It quickly branches into the left anterior descending artery (LAD) and the circumflex artery. The LAD supplies the: anterior part of the interventricular septum the anterior wall of the LV the right bundle branch of the conduction system part of the left bundle branch. The circumflex artery, and its major branch, the obtuse marginal, supplies: the AV node in 10% of all hearts the SA node in 45% of all hearts the lateral posterior surface of the left ventricle. The coronary arteries supply all of the layers of the heart, which means that they do not lay just on the outside surface of the heart. The large part of the artery lies on the surface of the heart, with smaller branches entering into the myocardial and subendocardial tissue layers to supply all parts of the heart. Mr. Ash complains of severe painful pressure in the center of his chest and radiating down his left arm and up his jaw. He is diaphoretic and pale. He complains of some nausea. He is given morphine and started on a nitroglycerin drip, but does not have significant pain relief. Cardiovascular Critical Care Primer © 2000 TCHP Education Consortium; 2014 edition Page 11 What is causing Mr. Ash’s symptoms? Chest Pressure and Radiation Because the heart has no direct pain receptors or messengers, the pain of myocardial ischemia is shunted through the spinal nerves of its dermatome. The warning sent by the heart may manifest in many different ways, according to which spinal nerves were stimulated. Chest pressure, tightness; arm, back, or jaw pain; or GI distress may result. Diaphoresis and Pallor As the injury has occurred to his heart, Mr. Ash’s sympathetic nervous system has kicked into high gear. The catecholamines (epinephrine and norepinephrine) that were released in response to SNS stimulation cause peripheral vasoconstriction and sweating, resulting in cool, clammy, and pale skin. divided into the fibrous and serous pericardium. The epicardium is a component of the serous pericardium and covers the heart and great vessels. The myocardium is the muscular portion of the heart which contains conduction fibers, atrial muscle fibers, and ventricular muscle fibers. The endocardium is the innermost surface of the heart that covers the chambers of the heart. What are the possible mechanisms of tamponade in Ms. Comparo’s case? Pericarditis is an inflammation of the pericardial sac, usually as a result of a more generalized disease process, such as an MI or leukemia. Pericarditis will not cause the heart to pump less effectively; however, the complications of pericarditis will cause pericardial effusions and fibrin deposits. In a pericardial effusion, fluid leaks from the blood vessels supplying the pericardial sac into the space between the fibrous and serous layers. As the effusion grows, the sac becomes "full". When there is no further room for expansion to the outside of the heart, the effusion will either stop, or will continue to grow, causing a decreased pulse pressure and tamponade. Fibrin deposition on the serous pericardium from pericarditis causes constrictive pericarditis. The constriction does not allow expansion or effective contraction of the heart, rendering it unable to adjust to minute to minute changes in volume and pressure. Nausea Gastrointestinal distress and heartburn are two of the many symptoms of an MI. Nausea and vomiting, however, are commonly seen with an RCA occlusion. The RCA supplies the AV node, which is also stimulated by the vagus nerve. Irritation of the vagus nerve occurs when the AV node is deprived of oxygen, resulting in nausea. An inferior MI can be the direct result of an RCA occlusion and will often coincide with symptoms of GI upset. Mr. Ash is transferred to the CCU after a bolus of a thrombolytic agent is given. Pericarditis/Pericardial Tamponade Ms. Louise Comparo is a 36 year old woman who has been undergoing radiation therapy for breast cancer. She enters the ER at approximately 2:30 a.m. complaining of chest pressure, dizziness, and shortness of breath. The assessment shows: distended neck veins, normal breath sounds, distant heart sounds, BP 86/62 mm Hg, HR 156, RR 32. The preliminary diagnosis is cardiac tamponade. What structures are involved with pericarditis and cardiac tamponade? There are four layers of the heart: the pericardium, epicardium, myocardium, and endocardium. The pericardium is the outermost layer of the heart and makes up a sac that surrounds the heart. This sac is Cardiovascular Critical Care Primer © 2000 TCHP Education Consortium; 2014 edition Page 12 Pericardial tamponade is the end result of either pericardial effusion, constrictive pericarditis or pericardial hemorrhage. Cardiac tamponade occurs when the heart is unable to fill or pump adequately, leading to: Decreased filling and contractility of the heart Decreased cardiac output and BP Compensatory mechanisms for low BP results in: Vasoconstriction & Tachycardia Increased workload for the heart Decreased perfusion of the tissues as blood is shunted away from the periphery and towards central organs Tissues lack oxygen to produce ATP, forcing a change from aerobic to anaerobic cellular metabolism in an attempt to produce energy and preserve life Lactic acidosis develops from anaerobic metabolism Cardiac failure and shock results if the oxygen deprivation is not fixed What caused Ms. Comparo’s symptoms? Because the heart was being compressed by the fluid in the pericardium, it was not able to pump effectively, causing less and less blood to enter into the system. The net result: hypotension. The response of the SNS causes tachypnea, and tachycardia. Fluid in the pericardium will uniformly compress the heart, not just one side. This causes an equalization in pressures between the right side and the left side of the heart. This equalization translates into a narrow pulse pressure, or a diastolic pressure that is very close to the systolic pressure. was given to form a foundation of knowledge to apply to clinical practice. Recommended Reading and References 1. Brozenee S, Russell SS. (2004). Core Curriculum for Medical-Surgical Nursing, 3rd ed. Academy of Medical-Surgical Nurses, Janetti, NJ. 2. Phipps WJ, Sands JK, Marek JF, eds. (1999). Medical-Surgical Nursing: Concepts & Clinical Practice, 6th ed. St. Louis: Mosby, Inc. 3. Seidel HM, Ball JW, Dains JE et al, eds. (2011). Mosby's Guide to Physical Examination, 5th ed. St. Louis: Mosby, Inc. 4. Stillwell, S. (2006). Mosby’s Critical Care Nursing Reference. 3rd ed. St. Louis, Mo: Mosby/Elsevier. 5. Smeltzer SC, Bare BG, eds. (2012). Brunner & Suddarth's Textbook of Medical-Surgical Nursing, 10th ed. Philadelphia: Lippincott William and Wilkins. 6. Wiegand, D.J.L. (ed). (2011). AACN Procedure Manual for Critical Care. 7. Functional peripheral arterial disease: Raynaud’s Syndrome. (2008). Retrieved March 13, 2010, from http://www.merck.com/mmhe/sec03/ch034/ch034c.ht ml#sec03-ch034-ch034c-1045 8. Hanly, E. J. (2009, May 1). Buerger Disease (Thromboangiitis Obliterans) Retrieved March 13, 2010, from, http://emedicine.medscape.com/article/460027overview 9. Occlusive peripheral arterial disease: Thromboangiitis Obliterans. (2008). Retrieved March 13, 2010 from, http://www.merck.com/mmhe/sec03/ch034/ch034b.ht ml#sec03-ch034-ch034b-1029 10. American Association of Critical Care Nurses (2005). The Cardiovascular System. J. Alspach. Core curriculum for critical care nursing (6th edition). Philadelphia: Saunders. Summary This program presented information regarding the normal anatomy and physiology of the heart and blood vessels and compared the normal state of affairs to pathological states. Information on angina, myocardial infarction, congestive heart failure, pericarditis, and cardiomyopathy Cardiovascular Critical Care Primer © 2000 TCHP Education Consortium; 2014 edition Page 13 Directions for Submitting Your Post Test for Contact Hours You have received this packet as pre-reading to prepare you for attending a TCHP class. If you have paid to attend the class, the cost of this home study is covered by your course tuition. Please fill out the attached post-test and evaluation and bring them with you to class. The program coordinator will process your post-test for contact hours and return it to you with a certificate of completion. HCMC employees only: it is preferred that you complete this home study on the HCMC intranet if it is available. TCHP home studies can be accessed under My Learning Center. If you are unable to complete the post-test and evaluation prior to class, you can mail it in later to TCHP: HCMC – TCHP Office 701 Park Avenue – Mail Code SL Minneapolis, MN 55415* Please make a copy of your post-test prior to mailing as it will not be returned to you. Paid participants may request contact hours for this home study without a processing charge up to 3 months after you have taken the class. *Please check the TCHP website for updates to our address: www.tchpeducation.com Cardiovascular Critical Care Primer © 2000 TCHP Education Consortium; 2014 edition Page 14 Cardiovascular Critical Care Primer Post-Test Please print all information clearly and sign the verification statement. If you wish to submit your post-test electronically (preferred method), please access it from www.tchpeducation.com under home studies. 1. Name 8. Baroreceptor stimulation from decreased BP will cause: a) increased heart rate b) activation of the parasympathetic nervous system c) decreased blood pressure d) stimulation of the vagus nerve 9. A symptom of left sided heart failure is: a) pitting edema b) dysrhythmias c) basilar rales d) elevated CVP (please print legal name above) 2. Birth date (required) Format: 01/03/1999 M M D D Y Y Y Y 3. Email: (Required to return your certificate of completion to you—TCHP Hospitals must use work email) 4. Where do you work? (example: HCMC, MVAHCS, etc.). Enter N/A if you are not employed Hospital Unit 5. Personal verification of successful completion of this educational activity (required): I verify that I have read this home study and have completed the post-test and evaluation. Signature 6. 7. Which of the following can be a symptom of angina? a) chest pressure b) jaw pain c) GI distress d) all of the above The right coronary artery supplies: a) the SA node, the LA and LV b) the AV node, the LA and LV c) the AV node, the RA, and RV d) the bundle branches, the LA and RV 10. Arterial insufficiency refers to: a) total occlusion of the artery b) blood supply inadequate for tissue need c) clot formation in the artery d) arterial wall spasm 11. A bruit is caused by: a) turbulent blood flow b) arterial occlusion c) carotid artery dysfunction d) myocardial infarction 12. Which of the following is NOT a component of Virchow’s triad? a) hypercoagulability b) intimal damage c) arterial insufficiency d) venous stasis 13. Symptoms of dilated cardiomyopathy are the same as the symptoms of: a) myocardial infarction b) subaortic stenosis c) congestive heart failure d) hypertension 14. Which of the following disease may result in gangrene and possible amputation of a digit? a) Buerger’s Disease b) Raynaud’s Syndrome c) both of the above d) none of the above Expiration date: The last day that post tests will be accepted for this edition is March 27, 2015— your envelope must be postmarked on or before that day. Cardiovascular Critical Care Primer © 2000 TCHP Education Consortium; 2014 edition Page 15 Evaluation: Cardiovascular Critical Care Primer Please complete the evaluation form below by placing an “X” in the box that best fits your evaluation of this educational activity. Completion of this form is required to successfully complete the activity and be awarded contact hours. At the end of this home study program, I am able to: 1. Identify the normal anatomy and physiology of the cardiovascular system. 2. Describe the pathophysiology of an acute myocardial infarction. 3. Describe the symptoms of heart failure. 4. Describe the pathophysiology of tamponade. 5. Identify the factors that favor the development of a venous thrombosis. 6. Differentiate between dilated, hypertrophic, and restrictive cardiomyopathy. 7. Differentiate between Buerger’s Disease and Raynaud’s Syndrome. Strongly Agree Agree Neutral Disagree Strongly Disagree 8. The teaching / learning resources were effective. If not, please comment: The following were disclosed in writing prior to, or at the start of, this educational activity (please refer to the first 2 pages of the booklet). Yes 9. No Notice of requirements for successful completion, including purpose and objectives 10. Conflicts of interest, if present 11. Expiration Date for Awarding Contact Hours 12. Did you, as a participant, notice any bias in this educational activity that was not previously disclosed? If yes, please describe the nature of the bias: 13. How long did it take you to read this home study and complete the post test and evaluation: ______hours and ______minutes. 14. Did you feel that the number of contact hours offered for this educational activity was appropriate for the amount of time you spent on it? ____Yes ____No, more contact hours should have been offered ____No, fewer contact hours should have been offered 15. Describe how you plan to incorporate the knowledge gained in this home study into your practice (indicate all that apply): ___This information has made me more knowledgeable about my practice. ___I feel that I will be more skilled at assessing and managing elderly patients. ___I have a better understanding of the normal aging process. ___I will use this information to educate my patients. ___I will use this information to educate my colleagues. Cardiovascular Critical Care Primer © 2000 TCHP Education Consortium; 2014 edition Page 16 ___I do not plan to integrate any of this information into my practice (please explain) Other/answer explanation:______________________________________________ 16. What best describes your reason for completing this home study? (select all that apply): ___I wanted to learn more about caring for elderly patients. ___I needed contact hours. Other: ________________________________________________________________ 17. Do you think there is a continued need to have this home study available? ___Yes, this information will continue to be relevant. ___No, this information is no longer relevant. ___Don’t know. ___It depends. (please specify):_____________________________________________ If you are an ANCC-certified nurse* or need contact hours based on a 60 min/contact hour formula, fill out the information below. Please note that you will receive a follow up survey via email to track how you are using the information presented in this packet in your professional practice 3-6 months from now. Name: Email: *Certified nurses renew their certification (CCRN, PCCN, etc.) with the organization that manages their certification. Most nurses are not certified and renew licensure with their state Board of Nursing. Expiration date: March 27, 2015 Cardiovascular Critical Care Primer © 2000 TCHP Education Consortium; 2014 edition Page 17 TCHP Education Consortium This home study is pre-reading for this TCHP class: • Shock and Infection in Critical Care Please complete this activity and bring your post-test and evaluation to class with you. Shock and Infection in Critical Care Primer © 2000, 2007 TCHP Education Consortium. This educational activity expires March 27, 2015. All rights reserved. Copying without permission is forbidden. Introduction Introduction/Purpose Statement Failure of the normal regulatory mechanisms in the body can lead to rapid and profound shock. The purpose of this home study is to review the pathophysiology of cardiogenic, hypovolemic, anaphylactic, and neurogenic shock. A brief review of sepsis and septic shock is also covered. Target Audience This home study was designed for the novice critical care or telemetry nurse; however, other health care professionals are invited to complete this packet. Content Objectives 1. List the classifications of shock. 2. List the functions of the cell and the microcirculation. 3. Describe the stages of shock. 4. Describe three major mechanisms put into action to compensate for shock. 5. Define terms related to shock. Disclosures In accordance with ANCC requirements governing approved providers of education, the following disclosures are being made to you prior to the beginning of this educational activity: Requirements for successful completion of this educational activity: In order to successfully complete this activity you must read the home study, complete the post-test and evaluation, and submit them for processing. Conflicts of Interest It is the policy of the Twin Cities Health Professionals Education Consortium to provide balance, independence, and objectivity in all educational activities sponsored by TCHP. Anyone participating in the planning, writing, reviewing, or editing of this program are expected to disclose to TCHP any real or apparent relationships of a personal, professional, or financial nature. There are no conflicts of interest that have been disclosed to the TCHP Education Consortium. Relevant Financial Relationships Resolution of Conflicts of Interest: and If a conflict of interest or relevant financial relationship is found to exist, the following steps are taken to resolve the conflict: 1. Writers, content reviewers, editors and/or program planners will be instructed to carefully review the materials to eliminate any potential bias. 2. TCHP will review written materials to audit for potential bias. 3. Evaluations will be monitored for evidence of bias and steps 1 and 2 above will be taken if there is a perceived bias by the participants. No relevant financial relationships have been disclosed to the TCHP Education Consortium. Sponsorship or Commercial Support: Learners will be informed of: • Any commercial support or sponsorship received in support of the educational activity, • Any relationships with commercial interests noted by members of the planning committee, writers, reviewers or editors will be disclosed prior to, or at the start of, the program materials. This activity has received no commercial support outside of the TCHP consortium of hospitals other than tuition for the home study program by non-TCHP hospital participants. If participants have specific questions regarding relationships with commercial interests reported by planners, writers, reviewers or editors, please contact the TCHP office. Non-Endorsement of Products: Any products that are pictured in enduring written materials are for educational purposes only. Endorsement by WNA-CEAP, ANCC, or TCHP of these products should not be implied or inferred. Off-Label Use: It is expected that writers and/or reviewers will disclose to TCHP when “off-label” uses of commercial products are discussed in enduring written materials. Off-label use of products is not covered in this program. Shock and Infection in Critical Care Primer © 2007 TCHP Education Consortium Page 1 Contact Hour Information Expiration Date for this Activity: As required by ANCC, this continuing education activity must carry an expiration date. The last day that post tests will be accepted for this edition is March 27, 2015—your envelope must be postmarked on or before that day. Planning Committee/Editors Linda Checky, BSN, RN, MBA, Assistant Program Manager for TCHP Education Consortium. Lynn Duane, MSN, RN, Program Manager for TCHP Education Consortium. Author Karen Poor, MN, RN, Former Program Manager, TCHP Education Consortium Content Expert Lynelle Scullard, BSN, RN, CCRN, Clinical Care Supervisor, SICU, Hennepin County Medical Center. For completing this Home Study and evaluation, you are eligible to receive: 2.0 MN Board of Nursing contact hours / 1.66 ANCC contact hours Criteria for successful completion: You must read the home study packet, complete the post-test and evaluation and submit them to TCHP for processing. The Twin Cities Health Professionals Education Consortium is an approved provider of continuing nursing education by the Wisconsin Nurses Association, an accredited approver by the American Nurses Credentialing Center’s Commission on Accreditation. Please see the last page of the packet before the posttest for information on submitting your post-test and evaluation for contact hours. Shock and Infection in Critical Care Primer © 2007 TCHP Education Consortium Page 2 An Overview of Shock Definition Shock is a state of inadequate perfusion relative to tissue demands. Life at the Cellular Level The cell is the unit, or building block, of all living things. The cell has several structures that are vital for functioning: 1. Cell membrane: a barrier with selective permeability between plasma and interstitial fluid that allows interchanges to occur between the cell and its environment. When damaged, it becomes permeable to almost anything. 2. Nucleus: controls the biochemical reactions; site of cellular reproduction. 3. Cytoplasm: the protoplasm within the cell but outside of the nucleus; site of most cellular activity. 4. Organelles: specialized metabolic machinery of the cell that produce and store protein, detoxify contents, aid in phagocytosis, and provide cellular energy. Classification The integrity of the circulatory system is dependent on: (a) efficient cardiac pump, (b) an adequate blood volume, and (c) a healthy vascular bed. The loss of any one of these three essential components leads to one of the three major classes of shock: • Cardiogenic: loss of an efficient cardiac pump • Hypovolemic: inadequate blood volume • Distributive (neurogenic, anaphylactic, and septic): an unhealthy vascular bed The cascading events of shock begin with inadequate oxygen transport and cellular dysfunction, which proceed to tissue and vascular disturbances, and end with organ dysfunction or failure. Oxygen Transport Oxygen transport has two components: oxygen delivery (DO2) and oxygen utilization /consumption (VO2). Oxygen delivery (DO2) is the product of cardiac output and arterial oxygen content. Calculation of the arterial oxygen content depends on (1) the hemoglobin content of blood, (2) the oxygen saturation of hemoglobin, and (3) the amount of oxygen bound to hemoglobin. Changes in any of these three factors and/or changes in cardiac output alters oxygen delivery to tissues. Normally, systemic oxygen delivery is five times greater than oxygen consumption. In other words, 20 percent of DO2 is absorbed (VO2), while 80 percent of DO2 remains in returning venous blood. The body adjusts to maintain this ratio; usually by increasing or decreasing cardiac output. Tissue oxygen utilization cannot be directly measured; however, the calculation of VO2 infers utilization and serves as a guide to the adequacy of tissue perfusion and cellular metabolism. Factors that determine VO2 are: (1) DO2, (2) state of microcirculation, and (3) cellular milieu. Cellular metabolism refers to all chemical and energy transformations that occur in the body, including anabolic and catabolic reactions. Carbohydrates, proteins, and fats are oxidized, producing CO2, H2O, heat, and chemical energy. This oxidation (catabolism) is a complex, slow process which liberates energy (ATP) in small, usable amounts. The Microcirculation The term microcirculation is used to describe a group of blood vessels within the tissues that acts as an independent organ unit in regulating blood supply to the tissues. The functions of the microcirculation are to: • Deliver nutrients to, and remove wastes from, cells • Adjust blood flow in response to tissue metabolic needs • Maintain intravascular/interstitial osmotic equilibrium The portion of the vascular bed lying between the arterioles and the venules is considered the microcirculation. There are no distinct boundaries between the divisions, and the arrangement and distribution differ from tissue to tissue depending on architecture and function. The artery has a strong, smooth muscle wall, and directs blood to capillary beds and controls pressure Shock and Infection in Critical Care Primer © 2007 TCHP Education Consortium Page 3 of the blood delivered to those beds. Arterioles are referred to as “resistance vessels.” Adjustments to the blood flow, and therefore, tissue perfusion pressure, is made by the sympathetic innervation and vasomotor influences. The arteries branch into the metarterioles, and from there into the pre-capillary sphincters. The capillaries at the end of the arterial system form a junction with the venous system. It is in the capillary system that nutrients, oxygen and waste products are exchanged from the arterial side to the venous side. Once that process is complete, the blood exists into the venules and finally the veins. The microcirculation is controlled by the metabolites from surrounding tissues. These metabolites have an intrinsic capacity to regulate blood flow to compensate for changes in the perfusion pressure and metabolic needs. There is a delicate balance between blood flow and tissue demand that is maintained by the (1) autonomic nervous system (modulates vascular tone), (2) humoral, (3) chemical, and (4) metabolic influences. Moment to moment redistribution of blood flow through the microcirculation is known as autoregulation. Actively metabolizing cells release local mediators such as K+, H+ ion, CO2, and lactic acid, causing local vasodilatation in order to deliver greater blood flow to vascular beds with higher metabolic activity. Pathophysiology of Shock: Initial Stage This is the stage in which there are (theoretically) cellular changes in response to shock. There are also no clinical signs or symptoms except elevated lactate levels. In the initial stage of shock, the cell switches from aerobic metabolism to anaerobic metabolism, which causes decreased energy production and increased lactic acid levels. Diminished blood flow to the microcirculation reduces oxygen delivery and sequesters metabolic by-products, thereby reducing oxygen delivery and utilization. The cell metabolism suffers, and the cell begins to deteriorate. Compensatory Stage of Shock The homeostatic compensatory mechanisms of the body are activated by decreased cardiac output. Compensation is mediated through neural, hormonal, and chemical changes. Neural Compensation Baroceptors located in the aorta and carotid bodies sense a decrease in the blood pressure. Messages are sent to the medullary vasomotor center that stimulates the sympathetic nervous system. The SNS uses the endogenous catecholamines (epinephrine and norepinephrine), which are released from the adrenal medulla, to: 1. 2. 3. 4. 5. 6. Constrict the blood vessels in the skin, GI tract and kidneys Dilate the blood vessels in the skeletal muscles and coronary arteries Sweat Increase the heart rate and contractility Increase the rate and depth of breathing Dilate the pupils Hormonal Compensation Mediated through the sympathetic nervous system, humoral compensation begins. The anterior pituitary releases ACTH, which causes a release of mineralocortocoids and glucocorticoids. The mineralocorticoids balance the sodium and water levels. The glucocorticoids regulate the metabolic function of the body through the stress response. Cortisol sensitizes the muscle of the arteriole to the effects of catecholamines. The posterior pituitary releases ADH, causing vasoconstriction and renal retention of water. The kidneys, which are flow dependent, also sense the decreased blood pressure. The kidneys release renin in response, which then stimulates the angiotensin and aldosterone systems. These hormones cause: • Retention of sodium and water • Increased blood volume in the major blood vessels because of water retention and vasoconstriction of the smaller blood vessels Shock and Infection in Critical Care Primer © 2007 TCHP Education Consortium Page 4 • • Decreased urine volume and sodium excretion Increased potassium excretion and increased urine osmolarity Chemical Compensation Hypoxemia and cellular hypoxia cause an increase in respiratory depth and rate. The acid-base balance is disturbed with the “blowing off” of CO2, which leads to respiratory alkalosis. The combination of hypoxemia and alkalosis adversely affects the level of consciousness. Progressive Stage of Shock In this stage of shock, previously helpful compensatory responses are no longer effective. Severe hypoperfusion to all organ systems causes multi-organ dysfunction syndrome (multi-system organ failure). The microcirculation loses the ability to autoregulate blood flow, leading to decreased blood volume returning to the central blood vessels. This causes further organ hypoperfusion. Refractory Stage of Shock This final and irreversible stage reflects the very last part of a patient’s life. The cellular and organ destruction has been so severe that death is inevitable. Essential versus Non-essential Organs The body long ago developed a priority list for scant amounts of blood. On the top of the list: Brain Heart Lungs Organ-Specific Effects of Shock Brain - Essential Organ Beta adrenergic stimulation dilates cerebral vessels to attempt to maintain enough flow for a MAP of 50. Late in shock, the vasomotor center fails to recognize and respond to sympathetic stimulation. Early symptoms of hypoperfusion are irritability and agitation, replaced by unresponsiveness in late stages. Heart - Essential Organ In all forms of shock except cardiogenic shock, the myocardium experiences a protective flow. Autoregulation maintains coronary flow as long as arterial pressure does not fall below 70 mm/Hg. The deterioration of heart function makes shock irreversible. All other organs are considered biologically expendable. Skeletal Muscle, Fat, Skin Vasoconstriction from alpha receptor stimulation results in muscle weakness, cramping, and fatigue. The skin becomes cool; its color ashen to cyanotic. The potential for skin breakdown is enormous. Kidneys The low blood pressure is seen as a decreased glomerular filtration rate (GFR) by the kidney. In order to increase flow, the kidneys activate the reninangiotensin-aldosterone compensatory mechanism. Metabolic acidosis created by cellular increases of lactic acid is perpetuated by the kidneys’ inability to break down and excrete lactic acid. Lungs These organs will receive the most blood possible during shock through stimulation of the beta receptors, which causes vasodilation. The other organs of the body, such as the skin and gut, have primarily alpha-receptors, which when stimulated cause vasoconstriction. They are considered to be “non-essential organs.” Hyperpnea occurs as a compensatory response to sympathetic stimulation, hypoxia, and metabolic acidosis. The increased respiratory rate increases pulmonary muscle oxygen consumption. Coupled with primary damage from centrally mediated chemicals to pulmonary capillary endothelial cells, increased capillary permeability results in interstitial and intra-alveolar edema and decreased pulmonary compliance. Resultant decreased ventilation and impeded gas exchange further decrease oxygen delivery to cells. Shock and Infection in Critical Care Primer © 2007 TCHP Education Consortium Page 5 Mesentery In early stages of shock, there is a marked decrease in blood flow to the gut manifested by nausea, vomiting, and hypoactive bowel sounds. Later, intestinal damage and necrosis by digestive enzymes cause damage to the protective mucosal barrier. Bacteria and toxins are released into the bloodstream. Hypoperfusion to the intestines also enhances the formation and absorption of endotoxins released from native gram negative bacteria. When released, these endotoxins cause extensive vascular dilatation, greatly increasing cellular metabolism despite inadequate oxygen and nutrients to cells. Impaired pumping ability of the left ventricle Decreased S.V . Inadequate systolic emptying Decreased C.O Elevated left ventricular filling pressure Decreased BP IncreasedLAP Decreased tissue perfusion Increased pulmonary venous pressure Liver The liver filters and detoxifies drugs, metabolites, and coagulation products. The liver also stores glucose as glycogen. The metabolic rate of the liver is very high with consumption of large quantities of oxygen and nutrients. In shock, the catecholamines stimulate liver activity. Glucose is made available to the cells, which are unable to use it, resulting in hyperglycemia. Hepatic ischemia results in a decrease in its metabolic and detoxification functions. Loss of clotting factors induce coagulopathies such as DIC. Pancreas Shock induces the release of amylase and lipase into the circulation. A chemical called myocardial depressant factor (MDF), released from the pancreas, decreases myocardial contractility. Cardiogenic Shock Cardiogenic shock is caused by inadequate myocardial contractility from acute myocardial infarction, coronary artery disease, or mechanical factors (valvular regurgitation, low output syndrome, arrhythmias). Pathophysiology of Cardiogenic Shock In cardiogenic shock, the left ventricle has been injured in some way, leading to impaired pumping. Increased pulmonary capillary pressure Pulmonary interstitial edema Intra-alveolar edema Because the pumping is ineffective, less blood is pushed out with each heartbeat, leading to a decreased stroke volume*. The heart rate increases to compensate for a low cardiac output and blood pressure, but will eventually be insufficient to compensate for the decreased stroke volume. The tissues begin to be inadequately perfused. The impaired pumping also leads to less blood being pushed from the ventricle during systole. The left ventricle gradually fills with more and more blood, causing an elevated pressure within the LV and left atrium. This pressure “backs up” into the pulmonary vasculature, causing an increased pulmonary capillary pressure. * Stroke volume = the amount of blood pumped out of the left ventricle with each contraction. Hypovolemic Shock In hypovolemic shock, there is a critical depletion of intravascular volume from hemorrhage (most common), plasma loss due to burns, dehydration, traumatic shock due to blood loss and major tissue damage. Shock and Infection in Critical Care Primer © 2007 TCHP Education Consortium Page 6 Pathophysiology of Hypovolemic Shock The pathophysiologic process of hypovolemic shock is straight-forward. Blood and/or fluids have left the body, causing a decreased amount of volume in the blood vessels. Pathophysiology of Neurogenic Shock Loss of sympathetic tone Massive vasodilation Decreased intravascular volume Venous dilation Arteriolar dilation Venous return Peripheral vascular resistance Decreased venous return Decreased ventricular filling Stroke volume Decreased stroke volume Cardiac output Decreased cardiac output Tissue perfusion Inadequate tissue perfusion Venous return is decreased because of the lack of fluid in the vascular space, causing decreased ventricular filling. The ventricles do not have as much blood as normal to pump out, so the stroke volume is decreased. The heart rate will increase to compensate for the diminished stroke volume and resulting poor cardiac output and blood pressure. Eventually, if the fluid or blood loss continues, the heart rate will not be able to compensate for the decreased stroke volume. The end result of hypovolemic shock is inadequate tissue perfusion. Neurogenic Shock Neurogenic shock is caused by the loss of sympathetic control (tone) of resistance vessels, resulting in the massive dilatation of arterioles and venules. Neurogenic shock can be caused by general or spinal anesthesia, spinal cord injury, pain, and anxiety. In neurogenic shock, there has been an insult to the nervous system so that impulses from the sympathetic nervous system (the fight or flight response) cannot maintain normal vascular tone or stimulate vasoconstriction. The lack of SNS stimulation causes a massive venous and arterial vasodilation. On the venous side, blood pools in the distensible veins and does not return to the larger veins. Because of this pooling, there is a diminished amount of blood that returns to the heart. Stroke volume, cardiac output, and blood pressure all fall. On the arterial side, there is decreased peripheral vascular resistance, which actually helps the heart to pump with less energy. The drawback is that with decreased peripheral pressure, there is not the driving force to get blood, oxygen, and nutrients to the cells. This also causes a small degree of arterial blood pooling, which decreases the amount of blood returning to the heart. Shock and Infection in Critical Care Primer © 2007 TCHP Education Consortium Page 7 Anaphylactic Shock Septic Shock Shock due to the severe allergic antigen-antibody reaction to substances such as drugs, contrast media, blood products, or insect or animal venom is called anaphylactic shock. Food products such as seafood, nuts, peanuts, peanut butter, and MSG can also cause anaphylactic shock. Sepsis is a condition that occurs in many critically ill patients. Sepsis is the systemic response to infection. Many types of organisms can cause sepsis, including gram-negative bacteria, gram-positive bacteria, and fungi. The infections can occur anywhere in the body; urinary tract infections are probably the most common cause of sepsis. Septic shock is said to occur when the sepsis has progressed to the point where it is affecting many organ systems. Pathophysiology of Anaphylactic Shock Exposure to antigen Activation of sensitized antibodies Antigen-antibody reaction Release of vasoactive mediators Massive vasodilation Capillary permeability Venous & arterial dilation Interstitial edema Relative hypovolemia The immune system goes “haywire” in anaphylactic shock in an extreme allergic reaction. At some point, the individual is exposed to the substance and develops antibodies against it. On subsequent exposure to the substance (the antigen), these antibodies will aggressively bind to the antigen, forming an antigen-antibody complex. This complex causes the release of chemicals that cause vasodilation (in particular, histamine). Both veins and arteries vasodilate, leading to decreased blood returning to the heart. The capillaries become permeable to nearly everything, allowing fluids, proteins, and sometimes blood to pass through into the interstitial space. This causes massive interstitial edema. The vasodilation and fluid sequestration in the interstitium causes a relative hypovolemia. Pathophysiology of Septic Shock The immune and inflammatory response begins to try to combat the organism that is causing an infection. The body releases multiple chemicals into the blood stream, including cytokines, vasodilators, complement factors, and free radicals. In septic shock, this response is not adequate to eliminate the infection and actually causes increased damage. The organism itself also releases substances called endotoxins or exotoxins, which further harm the organs and tissues. The combination of these chemicals and toxins cause: (1) peripheral vasodilation – interstitial edema and decreased blood return to the heart, and (2) decreased ability of the cells and tissues to take up oxygen and nutrients. The heart tries harder and harder to get oxygen and nutrients to the cells by increasing the heart rate and contractility initially, sometimes driving the cardiac output twice to three times its normal amount. Eventually, however, the immune response and compensatory mechanisms may not enough to combat the infection and resulting cellular destruction. The patient may develop multi-organ dysfunction syndrome (MODS); AKA multi-system organ failure (MSOF). Conclusion Patients with a wide variety of problems can develop shock. Knowing the underlying pathophysiology may help guide you in assessing and managing the care of the patient with cardiogenic, hypovolemia, and distributive types of shock. Shock and Infection in Critical Care Primer © 2007 TCHP Education Consortium Page 8 Resources 1. 2. 3. 4. 5. Barone, J., and Snyder, A. (1991). Treatment strategies in shock: Use of oxygen transport measurements. Heart and Lung, 20(1), 81-86. Rice, V. (1992). Shock, a clinical syndrome: An update. Part 1: An overview of shock. Critical Care Nurse, 11(4), 20-27. Rice, V. (1992). Shock, a clinical syndrome: An update. Part 2: The stages of shock. Critical Care Nurse, 11(5), 74-82. Rice, V. (1992). Shock, a clinical syndrome: An update. Part 3: Therapeutic Management. Critical Care Nurse, 11(6), 34-39. Rice, V. (1992). Shock, a clinical syndrome: An update. Part 4: Nursing care of the shock patient. Critical Care Nurse, 11(7), 28-38. Recommended Reading 1. 2. 3. 4. 5. 6. Brozenee S, Russell SS. (1999). Core Curriculum for Medical-Surgical Nursing, 2nd ed. Academy of Medical-Surgical Nurses, Janetti NJ. Phipps WJ, Sands JK, Marek JF, eds. (1999)..Medical-Surgical Nursing: Concepts & Clinical Practice, 6th ed. St. Louis: Mosby, Inc. Seidel HM, Ball JW, Dains JE et al, eds.(2002) Mosby's Guide to Physical Examination, 5th ed. St. Louis: Mosby, Inc. Stillwell, S. (2002). Mosby’s Critical Care Nursing Reference. 3rd ed. St. Louis, Mo: Mosby/Elsevier. Smeltzer SC, Bare BG, eds. (2002) Brunner & Suddarth's Textbook of Medical-Surgical Nursing, 10th ed. Philadelphia: Lippincott William and Wilkins. Wiegand, D.J.L. & Carlson, K.K. (eds.) (2005). AACN Procedure Manual fro Critical Care. 5th ed. Philadelphia: Elsevier. Directions for Submitting Your Post Test for Contact Hours You have received this packet as pre-reading to prepare you for attending a TCHP class. If you have paid to attend the class, the cost of this home study is covered by your course tuition. Please fill out the attached post-test and evaluation and bring them with you to class. The program coordinator will process your post-test for contact hours and return it to you with a certificate of completion. HCMC employees only: it is preferred that you complete this home study on the HCMC intranet if it is available. TCHP home studies can be accessed under My Learning Center. If you are unable to complete the post-test and evaluation prior to class, you can mail it in later to TCHP: HCMC – TCHP Office 701 Park Avenue – Mail Code SL Minneapolis, MN 55415* Please make a copy of your post-test prior to mailing as it will not be returned to you. Paid participants may request contact hours for this home study without a processing charge up to 3 months after you have taken the class. *Please check the TCHP website for updates to our address: www.tchpeducation.com Shock and Infection in Critical Care Primer © 2007 TCHP Education Consortium Page 9 Shock & Infection Critical Care Primer Post-Test in Please print all information clearly and sign the verification statement: Name (please print legal name above) Birth date (required) Format: 01/03/1999 M M D D Y Y Y Y Email: _______________________________________________ For TCHP Consortium Hospital employees only: Hospital Unit Personal verification of successful completion of this educational activity (required): I verify that I have read this home study and have completed the post-test and evaluation. Signature 1) The sympathetic nervous system will do all of the following actions in response to a low cardiac output except: a) increase cardiac rate and contractility b) constrict the pupils c) dilate blood vessels in the skeletal muscles and coronary arteries d) sweat 2) Which organ is considered essential in relation to blood supply in the shock states? a) gastrointestinal tract b) kidneys c) heart d) lungs 3) The two pathophysiologic processes that occur in cardiogenic shock are: a) anoxia and decreased tissue perfusion b) decreased stroke volume and inadequate systolic emptying c) low cardiac output and high urine output d) pulmonary edema and decreased stroke volume 4) What is the most common cause of hypovolemic shock? a) dehydration b) burns c) hemorrhage d) vomiting 5) The massive vasodilation neurogenic shock results in: a) venous dilation b) arteriolar dilation c) decreased cardiac output d) all of the above that occurs in 6) What of the following will NOT cause anaphylactic shock? a) a first bee sting b) blood products c) peanut butter d) contrast media 7) The most common cause agent of septic shock is: a) upper respiratory infection b) urinary tract infection c) central line infection d) none of the above Expiration date: The last day that post tests will be accepted for this edition is March 27, 2015— your envelope must be postmarked on or before that day. Primer completed with Class Shock and Infection in Critical Care Primer © 2007 TCHP Education Consortium Page 10 Evaluation: Shock and Infection Critical Care Primer Please complete the evaluation form below by placing an “X” in the box that best fits your evaluation of this educational activity. Completion of this form is required to successfully complete the activity and be awarded contact hours. At the end of this home study program, I am able to: 1. List the classifications of shock. 2. List the functions of the cell and the microcirculation. 3. Describe the stages of shock. 4. Describe three major mechanisms put into action to compensate for shock. Define terms related to shock. 5. Strongly Agree Agree Neutral Disagree Strongly Disagree 6. The teaching / learning resources were effective. If not, please comment: The following were disclosed in writing prior to, or at the start of, this educational activity (please refer to the first 2 pages of the booklet). Yes 7. Notice of requirements for successful completion, including purpose and objectives 8. Conflict of interest No 9. Disclosure of relevant financial relationships and mechanism to identify and resolve conflicts of interest 10. Sponsorship or commercial support 11. Non-endorsement of products 12. Off-label use 13. Expiration Date for Awarding Contact Hours 14. Did you, as a participant, notice any bias in this educational activity that was not previously disclosed? If yes, please describe the nature of the bias: 15. How long did it take you to read this home study and complete the post test and evaluation: ______hours and ______minutes. 16. Did you feel that the number of contact hours offered for this educational activity was appropriate for the amount of time you spent on it? ____Yes ____No, more contact hours should have been offered ____No, fewer contact hours should have been offered. Expiration date: March 27, 2015 Shock and Infection in Critical Care Primer © 2007 TCHP Education Consortium Page 11
© Copyright 2024