Herzing UniversityNF 216WEEK 2./ complete solution

WEEK 2 CABG • Description o The occluded coronary arteries are bypassed with the client’s own venous or arterial blood vessels o The saphenous vein, internal mammary artery or other arteries may be used to bypass l ...

WEEK 2 CABG • Description o The occluded coronary arteries are bypassed with the client’s own venous or arterial blood vessels o The saphenous vein, internal mammary artery or other arteries may be used to bypass lesion in the coronary artery o Coronary artery bypass grafting is performed when the client does not respond to medical management of coronary artery disease or when vessels are severely occluded o A minimally invasive direct coronary artery bypass may be an option for clients who have a lesion in the LAD artery; a sternal incision is not required, usually a 2 inch left thoracotomy incision is done and cardiopulmonary bypass is not required in this procedure • Preoperative interventions o Familiarize the client and the family with the cardiac surgical critical care unit o Inform the client to expect a sternal incision, possible arm or leg incision, 1 or 2 chest tubes, a foley catheter and several IV catheters o Inform the client that the ET will be in place for a short period of time and that they will be unable to speak o Will be on a mechanical ventilator to breath and not to fight it o Post op pain is expected, and that pain medication will be available o How to splint the chest incision, cough and deep breathe, use the incentive spirometer and perform arm and leg exercises o Discuss anxieties and fear related to surgery o Some medication like diuretics 2 to 3 days before surgery, digoxin 12 hours before surgery and aspirin and anticoagulants 1 week before surgery. o Administer medications as prescribed which may include potassium chloride, antihypertensives, antidysrhythmic and antibiotics • Cardiac surgical unit postoperative interventions o Mechanical ventilation is maintained for 6 to 24 hours as prescribed o The heart rate and rhythm, pulmonary artery and arterial pressures, urinary output and neurological status are monitored closely o Mediastinal and pleural chest tubes to the water seal drainage system with prescribed suction are present, drainage exceeding 100 to 150 mL/hr. is reported to the PCP o Epicardial pacing wires are covered with sterile caps or connected to a temporary pacemaker generator. All equipment in use must be properly grounded to prevent micro shock o Fluid and electrolyte balance are monitored closely. Fluids are usually restricted to 1500 to 2000 ml because the client has edema o The blood pressure is monitored closely because hypotension can cause collapse of a vein graft. Hypertension can cause increased pressure, promoting leakage from the suture line, causing bleeding o Temperature is monitored and rewarming procedures are initiated using warm or thermal blankets if the temp drops below 96.8. rewarm the client no faster than 1.87 degrees/hr to prevent shivering and discontinue rewarming procedures when the temp approaches 98.6. o Potassium is administered intravenously as prescribed to maintain the potassium level between 4 and 5 to prevent dysrhythmias o The client is monitored for signs of cardiac tamponade, which will include sudden cessation of previously heavy mediastinal drainage, jugular vein distention with clear lung sounds, equalization of right atrial pressure and pulmonary artery wedge pressure and pulsus paradoxus o Pain is monitored, differentiating sternotomy pain from anginal pain, which would indicate graft failure • Transfer of the client from the cardiac surgical unit o Monitor vital signs, level of consciousness and peripheral perfusion o Monitor for dysthymias o Auscultate lung and assess respiratory status o Encourage the client to splint the incision, cough deep breath and use the incentive spirometer to raise secretions and prevent atelectasis o Monitor temperature and white blood cell count which if elevated after 3 to 4 days indicate infection o Provide adequate fluids and hydration as prescribed to liquefy secretions o Assess suture line and chest tube insertion sites for redness, purulent discharge and signs of infection o Assess sternal suture line for instability, which may indicate infections o Guide the client to gradually resume activity o Assess the client for tachycardia, postural orthostatic hypertension and fatigue before, during and after activity o Discontinue activities if the BP drops more than 10 to 20 or if the pulse increases more than 10 beats per minute o Monitor signs of pain • Home care o Progressive return to activities at the home o Limiting of pushing or pulling activities for 6 weeks following discharge o Maintenance of incisional care and recording signs of redness, swelling or drainage o Sternotomy incision heals in about 6 to 8 weeks o Avoidance of crossing leg, wearing elastic hose and elevating the surgical limb if used to obtain the graft when sitting in a chair o Use of prescribed medications o Dietary measures, including the avoidance of saturated fats and cholesterol and the use of salt o Resumption of sexual intercourse if they can climb 2 flights of stairs without symptoms • Indications o To increase blood flow to heart muscle in clients with sever angina o Saphenous vein or internal mammary artery used for graft as many as five arteries may be bypassed. • Preoperative o Education and psychological preparation o Medications discontinued ▪ Digitalis 12-hour preop ▪ Diuretics 2-3 days preop ▪ Aspirin and anticoagulants 1-week preop o Medications administered ▪ Potassium chloride to maintain normal potassium levels ▪ Beta blockers ▪ Calcium channel blockers ▪ Antiarrhythmics ▪ Antihypertensives ▪ Prophylactic antibiotics 20-30 mins prior to surgery • Post op o Received mechanical vent for 6-24 hours o Connect chest tubes to water seal drainage system o Ground epicardial pacer wire and tape to client o Assess pulmonary artery and arterial pressures and heart rate and rhythm o Pain relief o Monitor for complications ▪ Fluid and electrolyte imbalance ▪ Hypotension ▪ Hypertension ▪ Hypothermia ▪ Bleeding ▪ Cardiac tamponade ▪ Altered cerebral perfusion o Be alert to psychological state, disorientation or depression o Provide activity as tolerated with progress as ordered from feet dangling over the side of the bed, to sitting in a chair to waling in a room by the third day o Provide guidance concerning long term care and follow up. • CABG • What is it? • Taking a vessel from your body and bypassing it. Harvest an artery rather than a vein. Artery is not subject to changes in arteriosclerosis. The internal mammary artery • Who is at the highest risk for getting a CABG? • Patients with coronary artery disease • 500,000 surgeries are done • Several stints • 65 and older are the most clients • Most common cardiac surgery • What is the nurses responsibility? • Fever • Redness • Tachycardia • Drainage • Infection • Bleeding • Splinting because incision is so big • Educate the UAP about sternal precautions • Put up a sign above the bed about sternal precautions • The coronary arteries supply the heart muscle with oxygenated blood, adjusting the flow according to metabolic needs. B. Coronary artery bypass grafts. One or more procedures may be performed using various veins and arteries. A. Left internal mammary artery, used frequently because of its functional longevity. B. Saphenous vein, also used as bypass graft. • Heart is not beating they are hooked up to a bypass machine • The blood is hepranised and oxygenated and then is returned to the body cooled so it reduces myocardial oxygen demand • Postoperative care of the cardiac surgical patient requires the nurse to be proficient in interpreting hemodynamics, correlating physical assessments with laboratory results, sequencing interventions, and evaluating progress toward desired outcomes. • In the preop check skin, pulses, clotting time, RBC, WBC, H and H. Educate the family that he will be on a tube during and after surgery. Assess for any reactions for anesthesia. Any immediate family had an issue with anesthesia we need to know because they are at risk. • Educate patient to report pain • Cough and deep breathing • Early ambulation • Assess for anesthesia reactions • Discuss tubes and lines that will be in postop • Postop • Assess fluid and electrolyte balance-irregular heart rhythms • Invasive lines • Assess for hypothermia-common after surgery-below 96 degrees Fahrenheit rewarm them but not to fast because it increases myocardial demand. • Monitor for hypotension-graph may have collapsed or is compromised. May be bleeding • Hypertension-nitroprusside. Strain on the heart and the new graft that was just put in. • Bleeding • Neurovascular status-temp, color, cap refill less than 3 seconds. CABG-Nursing Process Assessment: all systems because the HEART is important. Pain from surgery. Diagnosis: decreased cardiac output, ineffective perfusion, risk for infection, fluid volume and electrolyte imbalance, impaired gas exchange Planning: infection, community resources, rehab for cardiac status, 1. Activity tolerance adequate to meet self-care needs. 2. Pain alleviated or managed. 3. Complications prevented or minimized. 4. Incisions healing. 5. Post-discharge medications, exercise, diet, and therapy understood. 6. Plan in place to meet needs after discharge. Talk about sternotomy and positioning. Implementation: Monitor hemodynamic parameters to assess cardiac output, volume status, and vascular tone. Observe for persistent bleeding: excessive chest tube drainage of blood; hypotension; low CVP; tachycardia. Prepare to administer blood products, IV fluids. Maintain mechanical ventilation until the patient is able to breathe independently. ABG’s. Monitor fluid and electrolyte balance. Manage pain. Evaluation: recheck all those interventions. CARDIOMYOPATHY • Cardiomyopathy • What is it? • Means heart muscle disease. One thing common is decreased cardiac output. Fatigue, difficulty breathing. Holding on to salt and water and putting increased work load on the heart which will lead to heart failure. • dilated cardiomyopathy (DCM)-most common. Dilation of ventricles without hypertrophy • hypertrophic cardiomyopathy (HCM)-rare genetic disposition. Heart muscle has delayed relaxation time. Needs to fill up with blood, can not do it. • restrictive or constrictive cardiomyopathy (RCM)-impaired diastolic filling. • 2nd most common cause of death • Who is at risk? • What is the nurses responsibility? • Maintaining adequate perfusion • Rest periods • • Dilated Cardiomyopathy o Enlargement of all four chambers o Decreased contractility o Dilated chamber and decreased cardiac output o May be asymptomatic so they have a poor prognosis o Probably need a o Dilation without hypertrophy is the most sign o Cardiomyopathy is the second most common direct cause of sudden death; CAD is first. o Because dilated cardiomyopathy usually isn’t diagnosed until its advanced stages, the prognosis is generally poor. • Hypertrophic Cardiomyopathy o Heart muscle asymmetrically increases in size o Ventricles- more difficult to fill with blood o Decreased effectiveness of contractions o Increased risk for dysrhythmias o The hypertrophied ventricle becomes stiff, noncompliant, and unable to relax during ventricular filling. Consequently, ventricular filling is reduced and left ventricular filling pressure rises, causing increases in left atrial and pulmonary venous pressures and leading to venous congestion and dyspnea. o Ventricle is still and it can not relax o Can not fill with blood, decreased filling time RESTRICTIVE CARDIOMYOPAHTY o Rigid ventricular walls o Right HF o Decreased cardiac output o Decreased cardiac output o Increases atrial and pulmonic pressures o May order beta blocker to reduce the workload on the heart o May have a pacemaker if beta blocker is not working o May be asymptomatic for years o Fatigue o Dyspnea on exertion o Paroxysmal nocturnal dyspnea o Fluid retention o Nausea- r/t poor perfusion of GI tract. The mortality rate is highest for African Americans and older adults • Clinical Manifestations o May be asymptomatic for years o Fatigue o DOE o PND o Fluid retention o Nausea- r/t poor perfusion of GI tract. The mortality rate is highest for African Americans and older adults • Medical management o Low-sodium diet o Anticoagulation o Fluid restriction 2L/day o Alcohol Septal Ablation-happens over several weeks before they become normal. Alcohol is put in through the artery which kills the muscle of the sternum taking the pressure off the heart and reversing heart failure. For hypertrophic cardiomyopathy. o Heart transplant (nothing else works) o Cyclosporine o Tacrolimus o Amiodarone ▪ Treatment of V-tach and Atrial dysrhythmias in HF ▪ Potassium channel blocker ▪ Hypokalemia needs to be corrected first ▪ Pulmonary toxicity can be fatal ▪ Has a long half life ▪ May cause blurry vision ▪ May hurt the liver ▪ Can be necrotic to the veins so use special tubing for this drug • Cardiomyopathy- Nursing Process o Assessment: History (predisposing factors, family history), Chest pain, Review of diet (Na reduction, vitamin supplements), Psychosocial history: impact on family, stressors, depression, Physical assessment: VS pulse pressure; pulsus paradoxus; weight gain or loss; PMI; murmurs; S3 or S4; pulmonary auscultation for crackles, JVD, and edema. o Diagnosis: Decreased cardiac output, Risk for ineffective cardiac, cerebral, peripheral, and renal tissue perfusion, Impaired gas exchange, Activity intolerance, Anxiety, Powerlessness, Noncompliance with medication and diet therapies. o Planning: Goals: Improvement or maintenance of cardiac output, Increased activity tolerance, Reduction of anxiety, Adherence to the self-care program, Increased sense of power with decision making, Absence of complications. o Implementation: Improve cardiac output and peripheral blood flow, Increase activity tolerance and improving gas exchange, Reduce anxiety, Decrease the sense of powerlessness, promote home- and community-based care. o Evaluation: Maintain or improve cardiac function, Maintain or increase activity tolerance, Reduce anxiety, Decrease sense of powerlessness, Adhere to self-care program • What is the main electrolyte involved in cardiomyopathy o Calcium o Phosphorus o Potassium o Sodium********************** • The nurse is caring for a client with cardiomyopathy. Which of the following classes of drugs would the nurse expect to administer in the treatment of cardiomyopathy? o Antihypertensive o Beta-adrenergic blockers************** o Calcium channel blockers o Nitrates • The nurse is caring for a client with cardiomyopathy. The nurse understands which of the following recurring conditions is a complication? o Heart failure******************** o Diabetes mellitus o Myocardial infarction o Pericardial effusion • A nurse is reviewing the lab results for a client with a mechanical heart valve. The client is prescribed warfarin (Coumadin) since discharge from the hospital. The nurse expects the INR level to be? o 2.0 o 2.3 o 3.0 o 5.0************* • The nurse is developing a care plan for a client with a nursing diagnosis to decrease cardiac output. Which of the following statements by the client demonstrates understanding? o “I will eat enough daily fiber to prevent straining from stool.”*********************************** o “I will drink 2-3 glasses of wine each night to dilate my vessels.” o “I will drink 3000-5000 mL of fluid daily to promote kidney function.” o “I will exercise vigorously to strengthen my heart muscles.” • The nurse notates a pulsating abdominal mass on their client. The nurse understands this usually indicates which of the following conditions? o Gastritis o Enlarged spleen o Gastric distention o Abdominal aneurysm******************** • The nurse is caring for a client who had a resection of an abdominal aortic aneurysm yesterday. The client has an intravenous infusion at a rate of 150 mL/hour, unchanged for the last 10 hours. The client’s urine output for the last 3 hours has been 90, 50, and 28 mL. The client’s blood urea nitrogen level is 35 mg/dL and the serum creatinine level is 1.8 mg/dL, measured this morning. Which nursing action is the priority? o Check the urine specific gravity. o Call the health care provider (HCP).********************* o Check to see if the client had a sample for a serum albumin level drawn. o Put the intravenous (IV) line on a pump so that the infusion rate is sure to stay stable. AORTIC ANEURYSMS o Description o An aortic aneurysm is an abnormal dilation of the arterial wall caused by localized weakness and stretching in the medial layer or wall of the aorta o The aneurysm can be located anywhere along the abdominal aorta o The goal of treatment is to limit the progression of the disease by modifying risk factors, controlling the BP to prevent strain on the aneurysm, recognizing symptoms early and preventing rupture. o Types of aortic aneurysm o Fusiform ▪ Diffuse dilation that involves the entire circumference of the arterial segment o Saccular ▪ Distinct localized outpouching of the artery wall o Dissecting ▪ Created when blood separates the layers of the artery wall, forming a cavity between them o False (pseudoaneurysm) ▪ Occurs when the clot and connective tissue are outside the arterial wall as a result of vessel injury or trauma to all 3 layers of the arterial wall o Assessment o Thoracic aneurysm ▪ Pain extending to neck, shoulders, lower back or abdomen ▪ Syncope ▪ Dyspnea ▪ Increased pulse ▪ Cyanosis ▪ Hoarseness, difficulty swallowing because of pressure from the aneurysm o Abdominal aneurysm ▪ Prominent, pulsating mass in abdomen at or above the umbilicus ▪ Systolic bruit over aorta ▪ Tenderness on deep palpation ▪ Abdominal or lower back pain o Rupturing aneurysm ▪ Sever abdominal or back pain ▪ Lumbar pain radiating to the flank and groin ▪ Hypotension ▪ Increased pulse rate ▪ Signs of shock ▪ Hematoma at flank area o Diagnostic tests o Diagnostic tests are done to confirm the presence, size, and location of the aneurysm o Test include abdominal ultrasound, computed tomography scan and arteriography o Interventions o Monitor vital signs o Obtain information regarding back or abdominal pain o Question the client regarding the sensation of pulsation in the abd o Check peripheral circulation including pulses, temp and color o Observe for signs of rupture o Note any tenderness over the abd o Monitor for abdominal distention o Nonsurgical interventions o Modify risk factors o Instruct the client regarding the procedure for monitoring BP o Instruct the client on the importance of regular PHCP visits to follow the size of the aneurysm o Instruct the client that if severe back or abdominal pain or fullness, soreness over the umbilicus, sudden development of discoloration in extremities or a persistent elevation of BP occurs, to notify the PHCP o Instruct the client with an aortic aneurysm to report immediately the occurrence of chest or back pain, shortness of breath, difficulty swallowing or hoarseness o Pharmacological interventions o Administer antihypertensives to maintain the BP within normal limits and to prevent strain on the aneurysm o Instruct the client about the purpose of the medications o Instruct the client about the side effect and schedule of the medication o Abdominal aortic aneurysm resection o Description ▪ Surgical resection or excision of the aneurysm the excised section is replaced with a graft that is sewn end to end o Preoperative interventions ▪ Assess all peripheral pulses as a baseline for postoperative comparison ▪ Instruct the client in coughing and deep breathing exercises o Postoperative interventions ▪ Monitor vital signs ▪ Monitor peripheral pulses distal to the graft ▪ Monitor for signs of graft occlusion • Changes in pulses • Cool to cold extremities below the graft • White or blue extremities or flanks • Severe pain • Abdominal distension ▪ Limit elevation of the head of the bed to 45 degrees to prevent flexion of the graft ▪ Monitor for hypovolemia and kidney failure resulting from significant blood loss during surgery ▪ Monitor serum creatinine and blood urea nitrogen levels daily ▪ Monitor respiratory status and auscultate breath sounds to identify respiratory complications ▪ Monitor urine output hourly and notify the PHCP if it is lower than 30 to 50 ml/hr ▪ Encourage turning, coughing and deep breathing and splinting the incision ▪ Ambulate as prescribed ▪ Prepare the client for discharge by providing instruction regarding pain management, wound care and activity restrictions ▪ Instruct the client not to lift objects heavier than 15 to 20 lb for 6 to 12 weeks ▪ Advise the client to avoid activities requiring pushing, pulling or straining ▪ Instruct the client not to drive a vehicle until approved by PCP ▪ Endovascular aneurysm grafting involves insertion of a graft using a vascular catheter, it does not require an abdominal incision. The preoperative and postoperative care is similar to that of a surgical abdominal aneurysm repair o Thoracic aneurysm repair o Description ▪ A thoracotomy or median sternotomy approach is used to enter the thoracic cavity ▪ The aneurysm is exposed and excised and a graft or prosthesis is sewn onto the aorta ▪ Total cardiopulmonary bypass is necessary for excision of aneurysms in the ascending aorta ▪ Partial cardiopulmonary bypass is used for client with an aneurysm in descending aorta o Postoperative interventions ▪ Monitor vital signs and neurological and renal status ▪ Monitor for signs of hemorrhage • Drop in BP • Increased pulse rate and respirations ▪ Monitor chest tubes for an increase in chest drainage, which may indicate bleeding or separation at the graft site ▪ Assess sensation and motion of all extremities and notify the PCP if deficits are notes which can occur because of a lack of blood supply to the spinal cord during surgery ▪ Monitor respiratory status and auscultate breath sounds to identify respiratory complications ▪ Encourage turning, coughing and deep breathing while splinting the incision ▪ Prepare the client for discharge by providing instructions regarding pain management, wound care and activity restrictions ▪ Instruct the client not to lift object heavier than 15 to 20 lb for 6 to 12 weeks ▪ Advise the client to avoid activities, pushing, pulling or straining o Aneurysm ▪ Instruct the client not to drive a vehicle until approved by the PCP o Localized sac or dilation at weak point in wall of artery o Classified by shape o Saccular o Fusiform o Abdominal aortic aneurysm (AAA)- most common o Saccular- one side of the vessel o Fusiform- Entire artery segment becomes dilated o AAA- attributed by atherosclerotic changes in the aorta o Saccular Aneurysm-one sided o Fusiform Aneurysm-two sided o Rupture is the most common and is life threatening o Check blood pressure o Establish a large bore IV o Thoracic Aneurysm o Commonly caused by atherosclerosis o Frequently in men ages 50-70 o Affects 10 out of every 100,000 older adults o High morbidity & mortality rates o Endovascular repair o This is frequently diagnosed because of size on the imaging that is not visible o Clients may have renal failure so watch it. Watch I and O and creatinine and BUN o Symptoms o Constant & boring pain o Dyspnea o Cough o Stridor o Aphonia o Boring- deep o Pain occurs when client is supine o SOB- pressure of aneurysm sac against the trachea, main bronchus or lung o Aphonia- loss of voice; hoarse voice pressure against laryngeal nerve o o Assessment and Diagnostics o CXR-chest x-ray o CTA-Computed tomography angiography (also called CT angiography or CTA) is a computed tomography technique used to visualize arterial and venous vessels throughout the body o MRA-magnetic resonance angiogram o TEE-Transesophageal echocardiography. A diagnostic test which employs ultrasound waves to make images of the heart chambers, valves and surrounding structures and which is done through the esophagus o Management-control the blood pressure because the vessel can rupture o Beta blockers o Angiotensin receptor blockers o Preoperatively o SBP maintained 90 to 120 mmHg o Beta blocker o Hydralazine-can rapidly reduce BP. May be a PRN medicine. Given IV push o Sodium nitroprusside o BB; ARBS- control BP; retard dilation o Preop- Maintain a MAP of 65 to 75 o Sodium nitroprusside- continuous IV drip to emergently lower BP. Rapid onset & short action. o Abdominal Aortic Aneurysm o Atherosclerosis o Untreated, rupture & death o Damaged layer of vessel o Tends to enlarge o Risk factors o Genetic o Tobacco use o Hypertension o Manifestations o Feel heart beating in abdomen while lying down” o Impending rupture o Severe lower back or abdominal pain o Rupture o Constant, intense back pain o Drop in b/p o Decreasing hematocrit o Rupture is rapidly fatal o Systolic Bruit o Only 40% of pts. Have symptoms o Abd pain- localized in middle or lower abdomen to left of midline o Back pain- present pressure of lumbar nerves o Rupture may result in: o Hematomas in scrotum, perineum, flank, or penis o Loud bruit suggests rupture into vena cava-do not press on it you may cause it to rupture o Mass in the upper abdomen that pulsates o Assessment and Diagnostic Findings o Pulsatile mass in middle & upper abdomen o Palpable o Bruit o Ultrasonography o CTA o U/S- 6 month intervals until reaches a size so sx to prevent rupture is more of a benefit than possible complications o Medical Management o Beta blockers o ACE inhibitors o ARBs o Calcium channel blockers o If aneurysm is stable, b/p closely monitored. Association between increased b/p & aneurysm rupture o Nursing Interventions o Inserting IV access is priority o Postoperatively o check pulses o Pt must lie supine x 6 hrs o HOB may be elevated up to 45 degrees after 2 hrs o V/S & Doppler assessment q15 mins. o Assess access site (femoral) o Temperature q4hrs o Post implantation syndrome (Acetaminophen, ibuprofen)- can have for up to 24 hours, inflammatory process due to foreign body so they may have a slight fever but it is benign. Monitor for renal failure. o Notify MD- persistent cough, sneezing, vomiting or SBP > 180mmHg o Assess- bleeding, pulsation, swelling, pain, & hematoma o Skin changes- lumbar area or buttocks may be extremely tender, irregularly shaped, cyanotic areas o Post implantation syndrome- within 24 hrs. of stent placement. Fever, leukocytosis. Immunologic o Increased risk of hemorrhage DISSEMINATED INTRAVASCULAR COAGULATION (DIC) o DIC o Not an actual disease caused by another disease like septic or septic shock, venomous snake bite, drug reactions, burns, trauma. Inflammatory response is setting off this syndrome. Worry about ischemia because of all the clots but your supply of clotting factors is also low because its being used. o “Death Is Coming” or “Disruption In Clotting” o Triggers may include sepsis, trauma, shock, cancer, abruptio placentae, toxins, and allergic reactions o Altered hemostasis mechanism causes massive clotting in microcirculation. o As clotting factors are consumed, bleeding occurs. Symptoms are related to tissue ischemia and bleeding o Massive amount of tiny clots o Platelets & clotting factors are busy forming clots, coagulation fails o Manifestations o Bleeding from mucous membranes o Venipuncture sites o GI & urinary tracts o Decline in organ function (clot= ischemia) o Thrombocytopenia o Low fibrinogen o Prolonged PT, PTT, thrombin time-reflect low circulating coagulation factors o Elevated D-dimer o 80% mortality in clients with severe DIC o Early recognition is essential o Decreased platelets and fibrinogen o Assessment & diagnostic findings o Scoring System ▪ Platelet count ▪ Fibrin degradation products ▪ PT & fibrinogen level ▪ Thromboelastography o Thromboelastography o Bedside test for coagulation studies. Done in surgery mostly, few centers have this. o Medical Management o Aggressively treat underlying cause o Improve oxygenation o Replacing fluids o Correcting electrolyte imbalances o Vasopressors o Cryoprecipitate o Fresh frozen plasma o Platelets o Heparin o Enoxaparin o Nursing Management o Monitor the patient’s cardiac, respiratory, and neurologic status closely, at least every 30 minutes initially. Assess breath sounds and monitor vital signs and cardiac rhythm. o Assess the patient for signs of hemorrhage and hypovolemic shock. Observe the patient’s skin color and check peripheral circulation and capillary refill. Inspect skin and mucous membranes for signs of bleeding. o Check all I.V. and venipuncture sites often. Apply pressure to injection sites for at least 15 minutes. o Monitor the patient’s diagnostic laboratory values and administer blood, fresh frozen plasma, or platelets as ordered. o Monitor the patient’s intake and output hourly, especially when administering blood products. Watch for transfusion reactions and signs of fluid overload. o Thrombi may cause ischemia & organ dysfunction CARDIAC RHYTHMS • Normal sinus rhythm o Atrial and ventricular rhythms are regular o Atrial and ventricular rates are 60 to 100 beats per minute o PR intervals and QRS width are within normal limits • Sinus bradycardia o Atrial and ventricular rhythms are regular o Atrial and ventricular rates are less than 60 o PR intervals and QRS width are within normal limits o Treatment may be necessary if the client is symptomatic (decreased cardiac output) o A low heart rate may be normal for some individuals such as athletes • Interventions o To determine the cause of sinus bradycardia, withhold medication suspected of causing the bradycardia and notify the PCP o Administer oxygen as prescribed for symptomatic client o Administer atropine sulfate as prescribed to increase the heart rate to 60 beats per minute o Be prepared to apply a noninvasive transcutaneous pacemaker initially if the atropine sulfate does not increase the heart rate sufficiently o Avoid additional doses of atropine sulfate because this will induce tachycardia o Monitor for hypotension and administer fluids intravenously as prescribed o Depending on the cause of the bradycardia, the client may need a permanent pacemaker • Sinus tachycardia o Atrial and ventricular rates are 100 to 180 beats per minute o Atrial and ventricular rhythms are regular o PR interval and QRS width are within normal limits • Interventions o Identify the cause of the tachycardia o Decrease the heart rate to normal by treating the underlying cause • Atrial fibrillation o Multiple rapid impulses from many foci depolarize the atria in a totally disorganized manner at the rate of 350 to 600 times per minute o The atria quiver which can lead to the formation of thrombi o Usually no definitive P wave can be observed only fibrillatory waves before each QRS • Interventions o Administer oxygen o Administer anticoagulants as prescribed because of the risk of emboli o Administer cardiac medications as prescribed to control the ventricular rhythm and assist the maintenance of cardiac output o Prepare the client for cardioversion as prescribed o Instruct the client in the use of medications as prescribed to control the dysrhythmia • PVC o Early ventricular contractions result from increased irritability of the ventricles o PVCs frequently occur in repetitive patterns such as bigeminy, trigeminy and quadrigeminy o The QRS complexes may be unifocal or bifocal • Interventions o Identify the cause and treat on the basis of the cause o Evaluate oxygen saturation to assess for hypoxemia, which can cause PVCs o Evaluate the electrolytes, particularly the potassium level, because hypokalemia can cause PVCs o Oxygen and mediation may be prescribed in the case of acute myocardial ischemia or MI o For the client experiencing PVCs, notify the PCP or cardiologist if the client complains of chest pain or if the PVCs increase in frequency are multifocal occur on the T wave or occur in runs of ventricular tachycardia • Types o Bigeminy ▪ Every other beat PVC o Trigeminy ▪ Every third beat PVC o Quadrigeminy ▪ PVC every fourth o Couplet or pair ▪ Two sequential PVCs o Unifocal ▪ Uniform upward or downward deflection arising from the same ectopic focus o Multifocal ▪ Different shapes with the impulse generating from different sites o R on T phenomenon ▪ PVC falls on the T wave of the preceding beat, may precipitate ventricular fibrillation • Ventricular tachycardia o VT occurs because of a repetitive firing of an irritable ventricular ectopic focus at a rate of 140 to 250 beats per minute or more o May be present as a paroxysm of 3 self-limiting beats or more or may be a sustained rhythm o Can lead to cardiac arrest o Stable client with sustained VT, with pulse and no signs of symptoms of decreased cardiac output ▪ Administer oxygen as prescribed ▪ Administer antidysrhythmic as prescribed o Unstable client with VT, with pulse and sings and symptoms of decreased cardiac output ▪ Administer oxygen and antidysrhythmic therapy as prescribed ▪ Prepare for synchronized cardioversion if the client is unstable ▪ The PCP may attempt cough cardiopulmonary resuscitation by asking the client to cough hard every 1 to 3 seconds o Pulseless client with VT ▪ Defib and CPR • Ventricular fibrillation o Impulses from many irritable foci in the ventricles fire in a totally disorganized manner o VT is a chaotic rapid rhythm in which the ventricles quiver and there is no cardiac output o Fatal if not successfully resolved within 3 to 5 minutes o Client is unconscious with no pulse, BP, respirations or heart sounds • Interventions o Initiate COR until a defib is available o The client is defibrillated immediately with 120 to 200 biphasic defibrillator or 360 joules monophasic. Check the entire length of the client 3 times to make sure no one is touching the client or the bed. When clear, defib o CPR is continued for 2 minutes and the cardiac rhythm is reassessed to determine the need for further countershock o Administer oxygen as prescribed o Administer antidysrhythmic therapy as prescribed RHYTHM DISTURBANCES • Assessment o Dizziness, syncope o Chest pain, palpitations, abnormal heart sounds o Dyspnea o Abnormal pulse rate-increased, decreased or irregular • Diagnose o Caused by interruption in normal conduction process o Can occur at any point in the normal conduction pathway o Types of dysrhythmias ▪ Sinus dysrhythmias-originate in the sinoatrial node and are conducted along the normal conductive pathways • Tachycardia-sympathetic nervous system increases the automaticity of the SA node o Heart rate is increased above 100 o Causes-pain, exercise, hypoxia, pulmonary embolism, hemorrhage, hyperthyroidism or fever o Symptoms-dizziness, dyspnea, hypotension, palpitations o Treatment-treat underlying problem, beta blockers, calcium channel blockers or cardioversion • Bradycardia-parasympathetic nervous system (vagal stimulation) causes automaticity of the SA node to be depressed o Heart rate decreased to below 60 o Causes-MI, the Valsalva maneuver or vomiting, arteriosclerosis in the carotid sinus area, ischemia of the SA node, hypothermia, hyperkalemia or drugs such as digitalis and propranolol o Symptoms-pale, cool, hypotension, syncope, dyspnea, weakness o Treatment-atropine or possible pacemaker ▪ Atrial dysrhythmias-abnormal electrical activity that results in stimulation outside the SA node but within the atria • Premature atrial contractions o Ectopic focus within one of the atria fires prematurely o Causes-normal phenomenon in some individuals but may be caused by emotion disturbances, fatigue, tobacco or caffeine o Symptoms-senses of skipped beat o Treatment-treat the underlying cause ▪ Atrial flutter • Arises form an ectopic focus in the atrial wall causing the atrium to contract 250-400 times per minute, AV node blocks most of the impulses, thereby protecting the ventricles from receiving every impulse • Causes-stress, hypoxia, dugs, or disorders such as chronic disease, hypertension • Symptoms-chest discomfort, dyspnea hypotension • Treatment-vagal maneuvers, adenosine, cardioversion or ablation ▪ Atrial fibrillation • Uncoordinated atrial electrical activation that causes a rapid, disorganized uncoordinated twitching of the atrial muscle. Most common atrial dysrhythmia presents with grossly irregular pulse rate • Causes-chronic lung disease, heart failure, and rheumatic heart disease, chronic hypertension • Symptoms-stroke symptoms, hypotension, syncope, dyspnea • Treatment-address underlying cause, calcium channel blockers, beta blockers, digoxin, cardioversion, warfarin o Ventricular dysrhythmias-occur when one or more ectopic foci arise within the ventricles ▪ PVCs • One or more ectopic foci stimulate a premature ventricular response • Causes-ischemia due to a myocardial infarction, infection, mechanical damage due to pump failure, deviations in concentrations of electrolytes (potassium, calcium) nicotine, coffee, tea, alcohol, drugs such as digitalis and reserpine, psychogenic factors such as stress anxiety, fatigue and acute or chronic lung disease. • Symptoms-angina, shortness of breath, heart flip feeling • Treatment-amiodarone, beta blocker, procainamide ▪ Ventricular tachycardia • Three or more PVCs occurring in a row at a rate exceeding 100 bpm, severer myocardial irritability • Causes-large MI, low ejection fraction, same as PVCs • Symptoms-hypotension, pulmonary edema, confusion, cardiac arrest • Treatment-determine if monomorphic (procainamide, sotalol, amiodarone) or polymorphic (magnesium, isoproterenol) pulseless (CPR, defib, epinephrine, amiodarone) ▪ Ventricular fibrillation • Several ectopic foci within the ventricles are discharged at a very rapid rate. Most serious of all dysrhythmias because of the potential cardiac standstill • Causes-acute myocardial infarction, hypertension, rheumatic or arteriosclerotic heart disturbances or hypoxia. • Symptoms-unresponsive, pulseless, apneic • Treatment-CPR unless blood flow is restored and the dysrhythmia is interrupted by defib, death will result within 90 seconds to 5 mins o Heart blocks-delay in the conduction if impulses withing the atrioventricular system ▪ First degree • AV junction conducts all impulses but at a slower than normal rate • Causes-digitalis, calcium channel blockers, beta blockers, MI, and or increased vagal tone • Symptoms-asymptotic • Treatment-address the underlying cause ▪ Second degree block-type 1 and 2 • AV junction conducts only some impulses arising in the atria • Causes-infection, digitalis toxicity, coronary artery disease • Symptoms-may not hypotension, dyspnea, syncope • Treatment-atropine, pacemaker ▪ Third degree heart block • AV junction blocks all impulses to the ventricles causing the atria and ventricles to dissociate and beat independently, each with its own pacemaker establishing a rate, ventricular rate is low 20 to 40 beats per minute • Causes-congenital defects, vascular insufficiency, fibrosis of the myocardial tissue, or myocardial infarction • Symptoms-shock symptoms, syncope • Treatment-pacemaker, atropine dopamine, epinephrine. If not treat immediately may lead to death o Determine rate ▪ Each small box-0.04 seconds ▪ 1500 small boxes – 1 minute ▪ Each large box – 0.2 seconds (5 small boxes) ▪ 15 large boxes – 3 seconds ▪ EKG paper is marked at 3 seconds intervals at the top by a vertical line ▪ If regular count the number of 0.04 second intervals between two R waves divide by 1500 ▪ If irregular count the number of R-R intervals in 6 second, multiply by 10 o Determine the rhythm ▪ Presence or absence of P wave-SA node originated impulse ▪ Measure P-R interval-normal 0.12 – 0.20 seconds ▪ Measure QRS duration-normal is less than 0.12 ▪ Check P wave, QRS complex, ST segment and T wave o Medications ▪ Antiarrhythmics • Lidocaine, quinidine, procainamide ▪ Antilipid medications • Lovastatin • Cholestyramine o Cardioversion ▪ Completely depolarizes all myocardial cells so SA node can re-establish as pacemaker ▪ Diazepam ▪ Synchronizer turned on check at the R wave ▪ Oxygen discontinued ▪ Voltage 25-360 joules ▪ Paddles place over the right sternal border and over the apex of the heart ▪ After procedure asses vital every 15 mins for 1 hours every 30 mins for 2 hours and then every 4 hours SHOCK • Shock o Hypovolemic shock ▪ The most common type defined as a shock state caused by internal or external blood or fluid loss o Cardiogenic shock ▪ Caused by heart (pump) failure resulting in diminished cardiac output o Vasogenic shock ▪ With this type the vasculature is dilated, making it difficult for the heart to move blood and fluid to the rest of the body; types include septic shock, anaphylactic shock and neurogenic shock o Obstructive shock ▪ Caused by a physical obstruction or outflow of blood from the heart that results in a reduced cardiac output. Conditions that can contribute to this type of shock include cardiac tamponade, tension pneumothorax, superior vena cava syndrome, abdominal compartment syndrome and pulmonary embolism • Vasodilation o Septic shock ▪ Massive infection leads to sepsis as a result of the release of endotoxins from bacteria. This causes vasodilation and pooling of blood. o Anaphylactic shock ▪ An allergic reaction to substances like drugs, food, and insect bites that leads to anaphylactic shock, which results in an acute and life-threatening hypersensitivity reaction. This immediate reaction causes massive vasodilation, release of vasoactive mediators and an increase in capillary permeability. o Neurogenic shock ▪ A phenomenon that results in massive vasodilation without compensation as a consequence of the loss of spinal nervous system vasoconstrictor tone, this leads to a pooling of blood in the blood vessels. • Hemodynamic monitoring o Cardiac output ▪ Reflects blood flow reaching the tissue. Normal cardiac output is 4 to 6 liters per minute o Mean arterial pressure ▪ Amount of pressure the blood is placing on the walls of the vessels as the blood leaves the heart. Normal mean arterial pressure is between 70 and 105. This measure is an important indicator of adequacy of cardiac output. Mean arterial pressure greater than 60 is needed to maintain perfusion to vital organs o Central venous pressure ▪ A measure of pressure in terms of right ventricular preload. Measure the pressure of the blood returning from the body to the heart. The normal central venous pressure is 3 to 8. An elevated central venous pressure indicates right ventricular failure and volume overload. A low central venous pressure indicates hypovolemia o Cerebral perfusion pressure ▪ A measure of perfusion to the brain, calculated by subtracting the ICP from the mean arterial pressure. The normal cerebral perfusion pressure is 70 to 100. A central perfusion pressure less than 50 is associated with ischemia and tissue death. A central perfusion pressure less than 30 is incompatible with life. • Stages of shock- it is a priority to intervene in the early stages of shock to prevent progression to the later stages o Stage 1 ▪ Restlessness, increased heart rate, cool and pale skin, agitation o Stage 2 ▪ Compensatory: cardiac output is less than 4 to 6 liters per minute, systolic blood pressure is less than 100 there is decreased urinary output, confusion and the cerebral perfusion pressure is less than 70 o Stage 3 ▪ Progressive: edema, excessively low blood pressure, dysrhythmias, weak and thread pulse o Stage 4 ▪ This stage is unresponsive to vasopressor, there is profound hypotension the heart rate slows, and multiple organ failure ensues. Most often the client will not survive • Treatments o Treatment depends on the cause of the shock and the type of shock o For clients in shock, central venous and pulmonary artery catheters are inserted to monitor hemodynamic status o Assessment of the central venous pressure, urine output, heart rate and clinical and mental status is done every 5 to 15 minutes o Oxygen is administered to assist in tissue perfusion o Isotonic and electrolyte intravenous solutions such as lactated ringers’ solution and normal saline are frequently used o Rapid infusion of volume expanding fluids including whole blood, plasma, and plasma substitutes such as colloid fluids o Whole blood is effective but is not used often as a treatment measure because of the risk of transfusion reactions o Administration of medications is withheld until circulating volume has been restored. o The primary goal for medication therapy with shock is to improve tissue perfusion o Medications used to improve perfusion in shock are administered intravenously via an infusion pump and often via a central line. o It is important to note that if the shock state is cardiogenic in nature the infusion of volume expanding fluids may result in pulmonary edema, therefore restoration of cardiac function is the priority for this type of shock. Cardiotonic medications such as digoxin, dopamine or norepinephrine may be administered to increase cardiac contractility and induce vasoconstriction o Once improvement of perfusion is achieved intervention are then directed toward the underlying cause of the condition. • Assessment o Cool, clammy skin, cyanosis, decreased capillary refill o Restlessness, decreased alertness, anxiety o Weakness o Tachycardia, weak or absent pulse, decreased blood pressure o Metabolic acidosis o Oliguria, increased urine specific gravity o Respirations shallow, rapid o Increased muscle weakness • Diagnose o Sudden reduction of oxygen and nutrients, decreased blood volume causes a reduction in venous return, decreased cardiac output and a decrease in arterial pressure • Types of shock o Hypovolemic shock-loss of fluid from circulation ▪ Hemorrhagic shock external or internal ▪ Cutaneous shock from burns resulting in external fluid loss ▪ Diabetic ketoacidosis ▪ Gastrointestinal obstruction like vomiting and diarrhea ▪ Diabetes insipidus ▪ Excessive use of diuretics ▪ Internal sequestration like fractures hemothorax and ascites o Cardiogenic shock-decreased cardiac output ▪ Myocardial infarction ▪ Dysrhythmias ▪ Pump failure o Distributive shock-inadequate vascular tone ▪ Neural-induced loss of vascular tone • Anesthesia • Pain • Insulin shock • Spinal cord injury ▪ Chemical-induced loss of vascular tone • Toxic shock • Anaphylaxis • Capillary leak-burns, decreased serum protein levels • Plan/ implementation o Maintain adequate oxygenation o Increase tissue perfusion o Maintain systolic BP greater than 90 o Treat acidosis o Maintain patent airway ▪ If necessary, ensure ventilation by ambu bag or ventilator assistance ▪ Provide supplemental oxygen to maintain adequate blood pO2 o Indwelling catheter, hourly outputs o Assess CVP o Assess ABG o Treat acidosis o Keep warm o Intravenous admin of blood or other appropriate fluids o Large amount of fluid may be pushed until systemic blood pressure, urine output and lactate levels return to a relatively normal level or CBP or pulmonary artery pressure or both become elevated ▪ Crystalloid-normal saline, ringers ▪ Colloid-blood, packed red cells, plasma, expanders like hetastarch o Medications ▪ Antibiotics ▪ Medications to vasoconstrict and improve myocardial contractility ▪ Medications to maintain adequate urine output like mannitol and furosemide ▪ Medications to restore blood pressure like adrenergic/sympathomimetics- dobutamine hydrochloride ▪ Low dose corticosteroids for septic shock ▪ Infuse and assess large volumes of fluid • Shock o Inadequate tissue perfusion that makes the patient at risk for death o Any infection can lead to shock o Early recognition is key o Decreased perfusion-organ damage o Risk-hemorrhage, burns, massive infection, dehydration o Cells without oxygenation switch to anaerobic metabolism-without oxygen o Lactic acid is byproduct to lactic acidosis is a hallmark sign. Level is greater than 4 if they are in shock, the higher the number the poorer the prognosis o Initially-short of breath, not feeling well. Low blood pressure o Compensatory- sympathetic nervous system takes over. Renin system holds onto the fluid and sodium. Angiotensin 2 is a vasoconstrictor. Skin and kidney perfusion is low so decreased urinary perfusion. Skin is cool and clammy o Progressive-starting to falter is the compensatory. MAP, lowest it can be is 60-65. it starts to fall, and organ begins to drop there is an issue cellularly and tissues. o Hypovolemia give fluids first before vasopressors o In cardiogenic shock give fluids but check regularly for fluid overload in increments and inotropic drugs o If it doesn’t work give IABP, balloon pushes oxygenated blood to the coronary arteries. o Septic shock inflammatory response that causes vasodilation. Blood pressure drops. Increased capillary valves, seeping out of the vascular space o Restore intravascular volume o Correct underlying cause o 2 large gauge IV lines o Intraosseous if unable to obtain IV o Crystalloid o Blood transfusion o Oxygen o Cellular metabolism is impaired, and a self-perpetuating negative situation (aka, a positive feedback loop) is initiated. o I attached a Hyperlink of a video I want you to watch.The first link is the video that you may copy and paste to view in youtube. o If there is pump failure (heart) pt not responsive to IV fluids, vasopressors etc., this will be next modality. o Explain to the patient that the doctor is going to place a catheter in the aorta to help his heart pump more easily. Tell him that, while the catheter is in place, he can’t sit up, bend his knee, or flex his hip more than 45 degrees. Attach the patient to a continuous ECG monitor and make sure he has an arterial line, a PA catheter, and a peripheral I.V. line in place. o An IABP consists of a polyurethane balloon attached to an external pump console by means of a large-lumen catheter. It’s inserted percutaneously through the femoral artery and positioned in the descending aorta just distal to the left subclavian artery and above the renal arteries. This external pump works in precise counterpoint to the left ventricle, inflating the balloon with helium early in diastole and deflating it just before systole. As the balloon inflates, it forces blood toward the aortic valve, thereby raising pressure in the aortic root and augmenting diastolic pressure to improve coronary perfusion. It also improves peripheral circulation by forcing blood through the brachiocephalic, common carotid, and subclavian arteries arising from the aortic trunk. o IABP ▪ If there is pump failure (heart) pt not responsive to IV fluids, vasopressors etc., this will be next modality. ▪ Explain to the patient that the doctor is going to place a catheter in the aorta to help his heart pump more easily. Tell him that, while the catheter is in place, he can’t sit up, bend his knee, or flex his hip more than 45 degrees. Attach the patient to a continuous ECG monitor and make sure he has an arterial line, a PA catheter, and a peripheral I.V. line in place. ▪ An IABP consists of a polyurethane balloon attached to an external pump console by means of a large-lumen catheter. It’s inserted percutaneously through the femoral artery and positioned in the descending aorta just distal to the left subclavian artery and above the renal arteries. This external pump works in precise counterpoint to the left ventricle, inflating the balloon with helium early in diastole and deflating it just before systole. As the balloon inflates, it forces blood toward the aortic valve, thereby raising pressure in the aortic root and augmenting diastolic pressure to improve coronary perfusion. It also improves peripheral circulation by forcing blood through the brachiocephalic, common carotid, and subclavian arteries arising from the aortic trunk. VASOPRESSORS • IV therapy o Hypovolemic shock o Colloids- Albumin o Crystalloids- 0.9% NS, LR • Vasopressors o Will need an A-line o Require close monitoring o Drug dose in calculating in weight o Drug is titrated down to reach a therapeutic goal will never be stopped abruptly o Sometimes they steal blood from the limbs so check pulses and skin • Norepinephrine o Sympathomimetic o Use: shock & cardiac arrest o Preferred drug for septic shock o Duration of 1-2 mins after stopped o If extravasation occurs, give phentolamine at site if the drug seeps into the tissue it can cause necrosis o Contraindicated if blood pressure is really high or if there is bleeding and we didn’t fix it yet • Dopamine o Low doses- increased blood flow to kidneys o Higher doses- vasoconstriction & increases blood pressure o Monitor for dysrhythmias & hypertension o Vesicant o Interactions- Phenytoin (Hypotension)-decreased the ethicacy of the drug • Dobutamine o Positive inotropic drug o Beneficial when cause of shock is heart failure o Only given as an IV infusion o May cause ARDS MULTIPLE ORGAN DYSFUNCTION SYNDROME Multiple organ dysfunction syndrome (MODS) is altered organ function in acutely ill patients that requires medical intervention to support continued organ function. It is another phase in the progression of shock states. The actual incidence of MODS is difficult to determine, because it develops with acute illnesses that compromise tissue perfusion. Dysfunction of one organ system is associated with 20% mortality, and if more than four organs fail, the mortality is at least 60%. Pathophysiology MODS may be a complication of any form of shock, but it is most commonly seen in patients with sepsis and is a result of inadequate tissue perfusion. The precise mechanism by which MODS occurs remains unknown. However, MODS frequently occurs toward the end of the continuum of septic shock when tissue perfusion cannot be effectively restored. It is not possible to predict which patients who experience shock will develop MODS, partly because much of the organ damage occurs at the cellular level and, therefore, cannot be directly observed or measured. The clinical presentation of MODS is insidious; tissues become hypoperfused at both a microcellular and macrocellular level, eventually causing organ dysfunction that requires mechanical and pharmacologic intervention to support organ function. Organ failure usually begins in the lungs, and cardiovascular instability, as well as failure of the hepatic, GI, renal, immunologic, and central nervous systems, follows. Clinical Manifestations While it is not possible to predict MODS, clinical severity assessment tools may be used to anticipate patient risk of organ dysfunction and mortality. These clinical assessment tools include APACHE (Acute Physiology and Chronic Health Evaluation); SAPS (Simplified Acute Physiology Score); PIRO (Predisposing factors, the Infection, the host Response, and Organ dysfunction); and SOFA score. In MODS, the sequence of organ dysfunction varies depending on the patient’s primary illness and comorbidities before experiencing shock. Advanced age, malnutrition, and coexisting disease appear to increase the risk of MODS in acutely ill patients. For simplicity of presentation, the classic pattern is described. Typically, the lungs are the first organs to show signs of dysfunction. The patient experiences progressive dyspnea and respiratory failure that are manifested as ALI or ARDS, requiring intubation and mechanical ventilation. The patient usually remains hemodynamically stable but may require increasing amounts of IV fluids and vasoactive agents to support BP and cardiac output. Signs of a hypermetabolic state, characterized by hyperglycemia (elevated blood glucose level), hyperlactic acidemia (excess lactic acid in the blood), and increased BUN, are present. The metabolic rate may be 1.5 to 2 times the basal metabolic rate. At this time, there is a severe loss of skeletal muscle mass (autocatabolism) to meet the high energy demands of the body. After approximately 7 to 10 days, signs of hepatic dysfunction (e.g., elevated bilirubin and liver function tests) and renal dysfunction (e.g., elevated creatinine and anuria) are evident. As the lack of tissue perfusion continues, the hematologic system becomes dysfunctional, with worsening immunocompromise, increasing the risk of bleeding. The cardiovascular system becomes unstable and unresponsive to vasoactive agents, and the patient’s neurologic response progresses to a state of unresponsiveness or coma. The goal of all shock states is to reverse the tissue hypoperfusion and hypoxia. If effective tissue perfusion is restored before organs become dysfunctional, the patient’s condition stabilizes. Along the septic shock continuum, the onset of organ dysfunction is an ominous prognostic sign; the more organs that fail, the worse the outcome. Medical Management Prevention remains the top priority in managing MODS. Older adult patients are at increased risk for MODS because of the lack of physiologic reserve and the natural degenerative process, especially immune compromise (Guirgis et al., 2014). Early detection and documentation of initial signs of infection are essential in managing MODS in older adult patients. Subtle changes in mentation and a gradual rise in temperature are early warning signs. Other patients at greater risk for MODS are those with chronic illness, malnutrition, immunosuppression, or surgical or traumatic wounds. If preventive measures fail, treatment measures to reverse MODS are aimed at (1) controlling the initiating event, (2) promoting adequate organ perfusion, (3) providing nutritional support, and (4) maximizing patient comfort. Nursing Management The general plan of nursing care for patients with MODS is the same as that for patients with shock. Primary nursing interventions are aimed at supporting the patient and monitoring organ perfusion until primary organ insults are halted. Providing information and support to family members is a critical role of the nurse. The health care team must address end-of-life decisions to ensure that supportive therapies are congruent with the patient’s wishes . Promoting Communication Nurses should encourage frequent and open communication about treatment modalities and options to ensure that the patient’s wishes regarding medical management are met. Patients who survive MODS must be informed about the goals of rehabilitation and expectations for progress toward these goals, because massive loss of skeletal muscle mass makes rehabilitation a long, slow process. A strong nurse–patient relationship built on effective communication provides needed encouragement during this phase of recovery